Genetic engeneering2 essays

Genetic engeneering2 essays Genetic engineering has some history of good and bad. In 1989as a result of the food supplement Typtophan, 37 people died, 1500 were permanently disabled, and 5000 were very ill as result of high toxin levels in the food. No one knows the future side effects. Such as in August 19994, corn crops grew three inches tall and then suddenly fell over dead, because past crops drained the soil of most nutrients. Genetics have some new applications. They have newer and better-enhanced cells to be bigger and to produce more. For example soybean companies, they try to get a cell of all or mostly protein. It didnt work to well many people had an allergic reactions. Now scientists are looking and trying to make bigger and better plants. Scientists are also looking for a way to make plants grow twice or three times as big and produce more. That will let them get more crops out of one area of land. Scientists are out to educate people about engineering in plants. To let them know what they are eating. So they dont eat something that a major problem, and most of the public agree to be produced. Since scientists dont know about the long-term effects, because no long-term tests have been able to conducted. There are some negatives that come with everything but genetic engineering on plants has some pretty good ones. People have unknown reactions to some foods that have been altered. Our public health agencies are powerless to trace problems of any kind, back to the source, because there are no labels. There are unexpected and unknown side effects yet to be discovered. Genetic engineering also has its good side. We can produce three times as many crops in one field at one time. That will make our plants three times the size. It will also make the food we produce three times as much. This will help people buy making food in good supply year round, and making it c ...

A case study diffuse non-scarring alopecia in an adult female patient and an approach to diagonossis and management female-pattern hair loss in primary care setting The WritePass Journal

A case study diffuse non-scarring alopecia in an adult female patient and an approach to diagonossis and management female-pattern hair loss in primary care setting Introduction A case study diffuse non-scarring alopecia in an adult female patient and an approach to diagonossis and management female-pattern hair loss in primary care setting IntroductionCASE STUDYDISCUSSIONHair AnatomyLifecycle of the hair Factors influencing hair growthGrowth FactorsHormonesMineralsOther factorsTypes Of Non-Scarring AlopeciaDiffuse hair lossFemale Pattern Hair LossAcute telogen EffluviumChronic telogen EffluviumTreatment of FPHLMinoxidilThe Hair ConsultationHistoryExaminationScalpHairPull testNon-scalp hair and skinLab testsCASE DISCUSSION AND CONCLUSIONREFERENCESRelated Introduction CASE STUDY Mrs   KJ, a 29 year old manager at a busy law firm, presented to her GP complaining of recent sudden onset of hair loss over a period of a few weeks. What prompted her visit to the GP, was noticing large amounts of hair on the bathroom floor whilst on honeymoon, and subsequently that her scalp hair was suddenly thinner than usual, especially around the temporal areas. She had wondered whether she should be changed back to Cilest (from the Dianette she was currently taking), her original contraception, the cessation of which had appeared to trigger the same symptoms two years before. On that occasion, after stopping Cilest, she had experienced amenorrhoea with facial hirsutism and similar hair loss, leading to investigations and a diagnosis of polycystic ovarian syndrome (PCOS). She then used Dianette oral contraception and for a short time, oral cyproterone acetate, which improved the hair loss. Mrs KJ, who was also a vegetarian, denied use of hair dye or chemicals on her hair, and on the day of her consultation her hair was not styled in a manner promoting traction. Questions regarding family history revealed that her father had died of a heart attack in his fifties. The GP agreed with Mrs KJ that the hair around the temporal and crown areas appeared less than elsewhere on her scalp. The scalp was found to be otherwise normal, with no evidence of scarring alopecia or alopecia areata. The pull test was negative (however, her hair had been washed that morning), blood results (biochemistry and haematology) were deemed normal by the GP and because of the hair shedding, a diagnosis of telogen effluvium (secondary to stress – work and wedding planning) was made. She was advised to stay on Dianette. Because of the previous history and treatment she was referred to a dermatologist with an interest in alopecia, who described a mixed picture of telogen effluvium secondary to low ferritin, and mild androgenetic alopecia. He also asked for the bloods to be repeated, and these showed a decreased ferritin level, high SHBG, and all the rest normal, including zinc, antibody screen, and thyroid tests. He too advised that Mrs KJ remain on the Dianette, and that she start taking an iron supplement. Of interest is that the initial ferritin level done by the GP was 37ng/l, and this fell to 28ng/l over a period of about a month. Haemoglobin was normal. Both these figures were within the normal range provided by the lab (normal range 13-150ug/l, with optimum ferritin for females advised at 27ug/l)1. A few weeks after starting the iron supplements, Mrs KJ came back to see her GP to discuss work related stress which had spiked. In particular she was concerned that she would not be able to manage a very important presentation to the senior partners at the firm. She was so distressed that she found the only thing that calmed her was drinking alcohol, which she was understandably not keen on using regularly! So after some discussion about stress, the GP suggested that she try low dose propranolol for performance anxiety, for only the few days leading up to the presentation, including the actual day of, then to discontinue. Hair loss was not discussed at this consultation. A month later she was back to see the GP, complaining that there had been an even bigger spike in hair loss, and on contacting the dermatologist she had been advised to continue the iron supplementation. She requested a second dermatology opinion, and was then diagnosed with androgenetic alopecia secondary to PCOS, unmasked by telogen effluvium secondary to low ferritin, and a degree of scalp seborrhoea. She was advised to continue taking Dianette, iron supplementation, Ketoconazole shampoo a few times a week, topical minoxidil and topical cyproterone. She was also put on Metformin by her gynaecologist as part of the treatment for PCOS. A number of months later there was a marked improvement in hair growth. As she was keen on starting a family, she was advised to stop oral contraception and to continue the topical treatments, but to stop both minoxidil and cyproterone once she conceived. DISCUSSION In order to understand abnormalities associated with hair loss, it is important to understand the normal hair physiology and anatomy. Having personally spoken with a group of 12 GP’s, about how they would approach a patient complaining of hair loss, all admitted that they felt underprepared to do so. They also admitted to a poor understanding of hair anatomy and physiology. Hair Anatomy Figure 1.   Structure of a hair follicle2 Types of hair There are three types of hair – terminal hairs are thick hairs found on the scalp, axilla and pubic areas; vellus hairs are finer, shorter hairs on the rest of the body; and lanugo hairs develop in utero and are shed in the first few months of life. Anatomy The hair starts to develop within the hair follicle, which is a stocking-like structure made up of an inner and an outer layer.   The hair is divided into the part that protrudes above the skin, called the shaft, and the root, which is within the follicle. The dermal papilla is a finger-like projection into the base of the follicle. It contains capillaries to allow for a rich blood supply to the hair bulb, forming the base of the hair root, the only living part of the hair, and therefore requires nutrients. The hair bulb is the enlarged lower end of the hair into which the dermal papilla projects. It is made up of living cells with a high potential for division and differentiation which divide every 23-72 hours, the fastest rate of any cells in the body3. These cells are called the hair matrix. They divide and move up the follicle to become either hair cells or cells of the inner sheath of the follicle. Among the matrix cells are melanocytes which produce dark (melanin) or red/blonde (phaeomelanin) hair pigment. Pigment is taken up by the differentiating cells of the matrix by phagocytosis. The matrix gives rise to the layers which form the hair shaft – the medulla is the inner layer(not always present in non-terminal hair), the cortex makes up the main bulk of the hair shaft and contains dead keratinocytes, and the cuticle is the layer of tightly packed overlapping cells surrounding and sealing the shaft. The matrix is fed by the dermal papilla, which plays a significant role in hair growth. The dermal papilla produces a number of substances which have an effect on matrix cell growth and differentiation. The dermal papilla is itself under the influence of hormones and regulating substances, which include growth factors. These can increase proliferation of dermal papilla cells, which release cytokines which can act as inhibitors or stimulators of matrix cell growth. The hair follicle is a component of the pilosebaceous unit – one of the other components being the sebaceous gland (as well as apocrine glands in specific areas such as the groin and axilla). The inner layer of the follicle extends up the shaft and ends below the opening of the gland into the follicle, while the outer sheath extends to the gland itself. The outer sheath has a fibrous membrane to which is attached the erector pili muscle, contraction of which causes the hair to stand upright (giving the effect of ‘goosebumps’ when someone is nervous or cold). The sebaceous gland secretes sebum, an oily substance that helps to moisturise the skin and hair, while the apocrine gland is a sweat and scent gland, and mostly becomes activated at puberty under the influence of hormones. Lifecycle of the hair There are three phases of hair growth. Anagen – is the active phase when the cells of the hair bulb are constantly dividing and causing the hair shaft to elongate. This growth phase can last between 3-4 years. Catagen – is the transitional or involutional phase which follows anagen. The hair stops growing, the follicle shrinks slightly and the root is diminished and breaks away from the dermal papilla. This phase lasts 2-3 weeks. Telogen – is the resting phase when the hair is no longer growing and the dermal papilla is not attached to the follicle. This phase lasts 6-12 weeks. When anagen phase restarts and the follicle and dermal papilla reconnect, a new hair forms and starts growing, and can push the old hair out. About 10-15% of scalp hairs are thought to be in telogen phase at any given time.3,4 There is no synchronicity in the hair cycle and so small amounts, about 100 hairs per day, are lost every day, unnoticeably for the most part.   Very occasionally, cycles can be synchronised, for example toward the latter part of pregnancy, thought to be under the influence of hormones, so that larger amounts at a time are shed a few months postpartum; this hair loss is by and large seen as physiological and not pathological, and normal hair growth pattern is usually soon re-established.5 Factors influencing hair growth Progress has been made toward understanding the processes which influence hair growth, but there is still much work to be done in this regard.3,6 Growth Factors Insulin-like growth factor (IGF) accelerates hair growth depending on its concentration at the dermal papilla. This is regulated by IGF binding protein (IGFBP) which reduces the amount of free IGF available for action, and therefore has an inhibitory effect on hair growth. There are also a number of other growth factors which play in a role in hair growth regulation.3,6,8 Hormones Androgens were proven to play a role in androgenic alopecia by Hamilton who noticed that men who were castrated before puberty never grew beards or developed baldness, unless they were treated with testosterone, and that balding men who were castrated showed no progression of balding.6 Androgens stimulate hair growth in some areas such as the beard and groin. In genetically predisposed individuals the presence of circulating androgens can also cause hair loss in areas such as the temporal and vertex areas of the scalp; the occipital area is usually spared. The reason for this is not well understood, and is thought to be related to specific receptors.6,8 The main androgens are testosterone and its metabolite dihydrotestosterone (DHT), the conversion occurring under the action of the enzyme 5 a-reductase at the site of the end organ, in the case of hair, the skin. DHT is more potent than testosterone in this area as it has a higher affinity for the receptors. Sex hormone binding globul in (SHBG) binds to free testosterone, preventing its breakdown to its more active metabolite DHT. Therefore, SHBG has an inhibitory effect on testosterone function. SHBG is in turn inhibited by IGF and insulin – these therefore help to increase the level of active testosterone and DHT.3 Testosterone reduces the anagen phase of the terminal hair, with the result that the hair is shorter and has a smaller diameter, called miniaturisation of the hair, and conversion of the terminal pigmented hair into a vellus (often) non-pigmented hair.3,6,8 The result is that with time, the areas where this occurs appears to have thinner hair growth or appear balding. In females, androgens are manufactured in the ovaries and the adrenal glands. The ovaries produce both male and female hormones, and under the influence of insulin there is increased conversion to testosterone. 3,9 In women with higher levels of circulating insulin, such as those with polycystic ovarian syndrome (PCOS), metabolic syndrome (MS) and insulin resistance, there can be higher levels of androgens due to increased conversion, and the suppressant effect on SHBG. 9 The net result would be a hyperandrogenic state, which could result in AGA, hirsutism, acne, voice changes, among other signs of virilisation. 7 The role of oestrogens appears to be more complicated. 15 The enzyme aromatase is found in oestrogen producing cells in the adrenals, ovaries, testes, fat cells, as well as a few other organs. Aromatase helps to convert testosterone into oestradiol, thereby decreasing the amount of free testosterone. Women who took aromatase inhibitors as part of treatment for other conditions, were found to develop androgenetic male pattern hair loss, indicating that aromatase has a role to play in the pathogenesis of alopecia. The exact nature of this role is unclear. 10 According to Yip et al. oestrogens are at least of equal importance to androgens in scalp hair growth.15 Minerals While iron deficiency anaemia has been widely accepted to be a cause of hair loss17, it is less clear to what extent ferritin levels without the presence of anaemia, has on hair loss. When comparing women of child-bearing age with diffuse telogen hair loss, to those without, in the presence of no nutritional supplementation or underlying medical conditions, women with the hair loss were found to have a mean ferritin level that was significantly lower than those without hair loss. The odds that someone would have ratio   TE was higher when the ferritin level was at 30ng/ml or lower. The authors concluded that serum levels at 30ng/ml or lower therefore increased the chances of TE. 14 However Olsen et al. compared   iron deficiency in women with female pattern hair loss (FPHL or AGA – difference discussed later), CTE and a control group with no hair loss, and found that while iron deficiency was common in all the women, there was no significant difference in levels between the three groups. This study cited as a limiting factor that the outcome of treating the women, who had been discovered to have iron deficiency, was unknown. 12 Theoretically then, those who had hair loss and iron defiency, could have experienced a degree of hair regrowth after the iron deficiency had been treated. While a number of studies have supported the theory that ferritin levels affect hair loss, such as the study by Kantor et al 11 a number have also. Disputed. 12 Although the effects of ferritin on hair loss is still being studied and debated, Rushton suggests it would be advisable to treat even a low normal ferritin, if it was under the level of about 30-70 ng/ml; Trost et al . also advocate that ferritin above 70ng/ml should be aimed at to optimise treatment for AGA, and that the reason for the presence of anaemia or low iron stores should be sought if appropriate, while iron overload should be avoided. 13,16 Zinc deficiency is known to play a role in alopecia, but the mechanism is unclear. 17,18,19 Lack of essential fatty acids can help cause a diffuse alopecia with some lightening in colour of the remaining hair. Selenium deficiency can cause a hair loss similar to zince deficiency. Biotin deficiency can be genetic or acquired (medications like valproic acid, adult excessive consumption of raw eggs) and is also thought to play a part in causing hair loss, but there have been no clinical trials to support biotin supplementation to improve this. 19 Other factors Hair loss is also a well known side effect of thyroid problems, inflammatory illnesses such as lupus, malnutrition, anorexia nervosa, among other conditions, all of which can be picked up as part of the differential diagnosis when evaluating someone with hair loss. 17,20 Stress has also been known to cause hair loss, such as following major surgery or emotional trauma. 17,20 A long list of medications also affects the hair. Heparin, Warfarin, Ace inhibitors, Beta Blockers, Allopurinol, and levodopa, among many other drugs, have been found to cause hair loss 20 Age is also an important determinant, as balding increases with age 21, as is genetics – baldness appears to run in families. There is a marked difference between races in manifestation of androgenic hair loss, with Caucasians exhibiting this the most. 8,15 Types Of Non-Scarring Alopecia Hair loss can be broadly classified as scarring (or cicatricial) alopecia and non-scarring alopecia. There are some occurrences when there is some overlap between these two. Non-scarring alopecia can be further divided into a diffuse hair loss, or localised/patchy hair loss (alopecia areata, not discussed further). Diffuse hair loss This problem is not an uncommon presenting complaint to a GP. It can be noticed by the patient as either decreased hair density/thickness, or as increased hair shedding. The main causes for this would be acute telogen effluvium (ATE), chronic telogen effluvium (CTE) and female pattern hair loss (FPHL). 17 FPHL, together with male pattern hair loss (MPHL) is also known as androgenetic alopecia (AGA), but more authors are now referring to separate nomenclature for the sexes. 8,15,17,20 Although MPHL and FPHL are histologically identical the age of onset in females is later than in males. Also the patterns of hair loss between the sexes differ. The progression of the problem is not as rapid with women or as severe and there is not as good a response to anti-androgen therapy with women, as there is with men.15, 20 Many authors have therefore suggested that in women there is therefore a very complex, multifactorial aetiology. Female Pattern Hair Loss This is the most common type of hair loss affecting women, with prevalence increasing with age. It affects about 12% of women aged 20-29, to about 50% of women over 40, and over 50% by the age of 80. 20, 28 FPHL is an under-recognised entity.20 Androgenetic alopecia has been defined as progressive hair loss in genetically susceptible people in the presence of circulating androgens. Histologically, there is miniaturisation of the terminal hair follicle with progressive transformation of the terminal hair follicle (with central medulla) into a vellus hair follicle (no medulla). 15,17, 20 The role of androgens and androgen receptors is much more established in MPHL, and therefore finasteride and minoxidil are established treatments for MPHL. Androgens definitely have their role to play in FPHL, but there are other factors which influence the disorder as well, which are not clearly understood, such as oestrogens and iron. Many women with FPHL do not have demonstrable elevated androgen levels or other features of hyperandrogenism. 17 Women with hyperandrogenism respond better to anti-androgen treatment. 20 MPHL commonly follows the pattern described by Hamilton, with temporal recession initially, followed by vertex balding, with eventual fusion of the temporal and vertex balding areas and sparing of the occipital area).23 In women, only a small number present with this pattern of hair loss and the degree of balding is not usually as severe as in men. 20 The pattern in FPHL follows three main distributions: Diffuse central-frontal hair loss with sparing of the frontal hairline. In 1977 Ludwig described this in three scales – mild, moderate and severe (almost completely bald at vertex, this is very rare). 17, 20, 24 Diffuse, mainly frontal hair loss (frontal accentuation) with breach of the frontal hairline. The Olsen scale or Christmas tree pattern – this is demonstrated by parting the hair in the midline and noting the part widening, with the narrowest part at the vertex and the widest part toward the frontal hairline. 17, 20, 24 Fronto-temporal and vertex hair thinning, in other words a male pattern of hair loss or Hamilton-Norwood- type. 17, 20, 24 Hamilton-Norwood  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚     Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ludwig  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚     Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚   Olsen  Ã‚  Ã‚  Ã‚   (male pattern)  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚     Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  (diffuse central)  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚     Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚   (frontal accentuation)drawing, courtesy ref.24 More recently the Sinclair 5 point scale has been adapted and introduced, and may become more widely used as it allows more subtle description; this may become more necessary as women start to present more early with their hair loss. 20, 24 Sinclair 5-point scale for FPHL drawing courtesy ref. 24 (drawing by L. Tosti) Because it is a progressive problem, without effective treatment the condition will worsen. However the rate of the progression is variable and unpredictable. Diagnosis is usually clinical, based on history and examination. Correct diagnosis is imperative so that the correct treatment can be commenced to try to at least slow down/halt the progression of hair loss, or at best bring about some degree of hair regrowth.17, 20 Progression tends to be slow, with hair loss quite diffuse. It mainly occurs in the distributions mentioned above. Miniaturised hairs are seen in the affected areas, hair shaft diversity is noted more easily on dermoscopic examination. Very occasionally peripilar halos/atrophy is seen as well.   If shedding is present it is not as significant as in ATE or CTE, and the hair pull test is usually negative. Biopsy shows the abovementioned miniaturisation and a decreased terminal:vellus hair ratio, with a lower anagen:telogen ratio. The biopsy, which is not necessary unless doubt exists as to the diagnosis, should be taken from three sites, as a horizontal section and be about 4mm in diameter.17,20,24 By the time a biopsy is contemplated a patient would probably be seen by a dermatologist. While the diagnosis of FPHL is usually clinical, a biopsy should be performed when the diagnosis is uncertain.17,24The main differential diagnosis is CTE.17,20,23 The main difference is that CTE occurs as a rapid hair loss (FPHL is slower), lots of shedding is noted (as opposed to the presenting complaint being thinning hair). With CTE there is a positive pull test (patient should not shampoo their hair for 24 hours prior to test), when the effluvium is in an active shedding phase. Examination of the scalp in CTE does not show widening of the part, or miniaturisation, and biopsy is normal in CTE (apart from showing an increase in telogen hairs).17, 20 Acute telogen Effluvium ATE is also a diffuse type of hair loss which has an abrupt onset, usually seen 2-3 months after a trigger event, and usually does not last for longer than 6 months. About 15% of adult scalp hairs are in telogen phase – when telogen hairs are shed the bulb or club-shaped tip can usually be seen. Anagen hairs have a more tapered tip – there is no bulb because it is attached to the dermal papilla as the hair is still growing. 25 At the time of the precipitating event or trigger for the effluvium, as many as 75% of anagen hairs can be pushed into telogen. 20 A few months later the new anagen hairs starting to grow in the follicle push the old hairs out, and the hair shedding is noticed by the person as hair loss. In actual fact, this shedding is really a sign that new hair is growing. 25 Shedding reaches a peak and hair thickness gradually returns to normal over months in the majority of cases things are largely back to normal by about 1 year. 17 Sometimes the precipitati ng event causes a corresponding Beau’s line in the nail. 25 Potential causes of ATE would include: (febrile) illness, surgery, trauma/accident, childbirth, emotional trauma. Severe and sudden weight loss can also precipitate this. A number of drugs, including beta blockers, can cause an effluvium. Discontinuing the oral contraceptive can also cause hair to fall out, as can jetlag and excessive sun exposure.25 Chronic telogen Effluvium In CTE, the cause tends not be a single event that acts as a one-off trigger, but something that allows the hair loss to be perpetuated for longer than 6 months. 17 Many cases of CTE are idiopathic, but iron deficiency anaemia, hyper/hypothyroidism, zinc deficiency and malnutrition have been implicated as causative/contributory factors by a number of studies. 17,20 In CTE the hair shedding can fluctuate in severity, for example as an animal might moult. 25 Both acute and chronic telogen effluvium does not cause baldness as there is no miniaturisation or conversion of terminal hairs to vellus hairs, only decreased anagen hair growth. However, it can unmask an individual’s genetic tendency to bald. 20    Treatment of Diffuse hair loss Treatment of telogen Effluvium Treatment of acute and chronic telogen effluvium involves treating the underlying causes, if found. Removing the trigger factor for acute telogen effluvium should allow for an improvement in hair growth in most cases by about one year; most people will see an improvement after a few months already. 17,20 If no cause for CTE is found, a biopsy to rule out FPHL should be considered. 20 The course for CTE is that shedding occurs in phases, but never leads to balding. 20 It is thought to potentially take up to 3-10 years to resolve, but there are insufficient studies that have looked properly at this condition over time. 17 Empiric use of minoxidil 2% has been suggested, in the hope of decreasing telogen and increasing anagen. 20 Treatment of FPHL While a general practitioner may not be expected to able to offer all of the therapies available for the treatment of FPHL, it is very helpful to have a good understanding of the therapeutic processes so that patient questions can be dealt with a knowledgeable manner; this improves the therapeutic relationship. The primary care doctor should be able to initiate medical treatment in an uncomplicated case of FPHL. Minoxidil Minoxidil was first discovered to improve AGA while undergoing development as an oral antihypertensive drug, when it was seen to cause hypertrichosis, and hair growth in balding men. 8, 22, 26 It is now used as a topical treatment for AGA in a 2% and 5% strength. The exact mechanism of action is unclear. It is converted into its active metabolite by an enzyme present in the outer follicle of the hair sheath. In its activated form the drug opens potassium channels to bring about a vasodilatory effect, but studies looking at this effect after topical application of minoxidil, have been inconclusive. 22, 27 Other potential mechanisms of action could include induction of new blood vessel formation by increasing vascular endothelial growth factor gene expression at the site of the dermal papilla. Another theory is that it could stimulate activity of an enzyme (cytoprotective prostaglandin synthase I) which stimulates hair growth. 22, 27 It could also increase expression of the gene for he patocyte growth factor, which stimulates hair growth. Messenger and Rundegren 2004 have proposed that the mechanism of action is to cause premature end to telogen and prolong anagen.20, 27 Ongoing studies are needed into the mechanism of action of minoxidil, as this could help with development of better treatments. Although not enough is known about the mechanism of action to improve alopecia, it has been proven to be efficacious for both men and women. 17, 20, 22, 23, 26, 27 The European Dermatology Forum (EDF) performed an extensive literature review (of specific databases) with the aim of formulating evidence-based treatment guidelines for the treatment of AGA (it differentiates between male and female treatments but calls the conditions AGA). Based on the studies reviewed, it recommends topical application of minoxidil 2% or 5% applied twice daily for mild to moderate AGA, with the 5% strength favoured if greater efficacy required. A foam application (as opposed to the solution) is also available, but further studies comparing efficacy to the solution, are needed. 20 For women, the recommendation is also to use the 2% solution twice daily, but there is no evidence currently available to support the use of 5% strength in females.20, 22, 28 In a study by Lucky et al. female patients were foun d to show psychosocial improvement after using 2% and5% minoxidil respectively, compared with placebo. More pruritis, local irritation and hypertrichosis were reported by women using the 5% solution.28 Patients should always be counselled thoroughly before starting medication. This is vital for compliance, as the progression of the hair loss is only halted/reversed for the duration of compliance. Counselling should include how to apply the medication (1ml in   a dropper, applied to dry scalp morning and night and not washed for at least 4 hours – if hair/scalp get wet within an hour the medication should be reapplied), the importance of compliance for results,   when to expect an improvement, as well as potential side effects. 20 There are three main side effects. One is an apparently paradoxical shedding of hairs – if minoxidil does indeed shorten telogen and stimulate anagen then any new hairs forming would ‘push out’ the old. It is very important that the patient is informed to continue with the treatment, and they could be reassured that this is a sign of the medication working; this effect usually occurs in the first 2-8 weeks of treatment.17, 20 , 22, 23 The other main side effects are related to contact, so it is important to warn the patient to wash their hands immediately after application. Hypertrichosis can occur, mainly because of incorrect application (usually disappears about 4 months after cessation of the treatment). 17, 20, 22, 28 The patient should be advised to apply the medication 2 hours before going to bed at night so that there is less risk of transfer to the pillow, and subsequently to the face. 22Contact dermatitis, either allergic or irritant, has also been reported. 17, 20, 22, 28The main causative agent is the vehicle for the drug, called propyleneglycol, in higher concentration in the 5% solution. 20,22, 28 If contact irritant dermatitis is confirmed then the vehicle should be changed (for example to the foam application – positive results have been produced by Lucky et all with regards to equal efficacy to the solution, and better tolerability from subjects). 20 However if an allergy to minoxi dil is confirmed then the treatment needs to be abandoned/changed completely. 20, 22 The EDF has advised that efficacy should be assessed at 6 months for cessation of shedding and 12 months for regrowth.   22 The treatment should be continued for as long as the therapeutic benefit is required. This is lost with cessation of treatment, with hair loss recommencing about 3 months after cessation. Pregnant and lactating women are advised not use minoxidil, even though no adverse outcomes were noted after a large study.17, 20, 22, 23 5 a-reductase inhibitors These drugs were initially aimed at treating men with prostatic hypertrophy, and both licensed 5 a-reductase inhibitors, finasteride and dutasteride, are currently used to treat this condition. Of the two, finasteride is also registered to treat AGA in men.22 The mechanism of action of finasteride is to act as on 5 a-reductase II, the receptors of which are mainly found in the scalp, skin and liver. Dutasteride acts on both types I (gut and prostate) and II 5 a-reductase. Finasteride reduces serum DHT by about 58-60% 17, 22 while dutasteride reduces serum DHT by about 90% 22 In all the clinical trials assessed by the European Dermatology Forum, 1mg of finasteride taken daily showed a significant improvement by 6 months, compared to placebo, and the same was true at 12 months, and up to a 60 months follow-up. Dutasteride was also looked at by a number of authors and showed an improvement in hair loss but at a much higher dose than that needed to treat benign prostatic hypertrophy. 22 Further studies comparing its efficacy to 1mg finasteride are needed. There are not many studies assessing the efficacy of finasteride in females – in a study of post menopausal women taking finasteride, further hair loss was noted.22, 23 Finasteride is therefore not indicated in women, although one study has shown positive results in women with FPHL and hyperandrogenism. 17, 20 There have also been sporadic reports of finasteride improving hair loss in individual female patients.20, 23More studies into finasteride for use in FPHL, are needed. If finasteride is used off licence in a female of reproductive age, adequate contraception needs to be taken to avoid feminisation of a male foetus. 17, 20, 22, 23   For this reason it is completely contraindicated in pregnancy. Finasteride also lowers PSA levels, so a baseline PSA blood test should be done on men aged 45 years or older, who are starting finasteride.20, 22, 23, 26 Finasteride also has a number of side effects which have potential psychosocial impact – it can cause erectile dysfunction in men and decreased libido. As with minoxidil, counselling is therefore indicated as compliance is important for outcome. For those who do not tolerate the 1mg dosage, a 0.2mg dosage can also be effective. 22 Studies looking at combining the above therapies were done. Khandpur et al showed that 2% minoxidil applied twice daily, and 1mg of oral finasteride daily, taken together, was superior to each therapy used by itself. Taking finasteride with Ketoconazole shampoo was also reported to be superior to the abovementioned monotherapies.20, 29 Combination therapies can therefore be considered if monotherapies are insufficient. Compliance is of course important. Hormone Treatment According to the European Dermatology Forum, evidence for the efficacy of hormonal treatment is limited. Anti-androgens act by blockading androgen receptors (AR) – these are therefore contraindicated in men as they cause feminisation. There is no evidence to support the use of oestrogens in men. (ref. 22) The Forum also decided that, based on their literature review, there was insufficient evidence to support the use of oestrogens, progesterones or anti-androgens in FPHL , although there was a place for anti-androgens in the treatment of some women with hyperandrogenism.22 Use of Spironolactone to treat hirsutism and FPHL is common, especially in the US.20 Spironolactone acts by binding to AR and also acts at the site of the ovary to reduce manufacture of androgens. In a study spironolactone was shown to be as effective as cyproterone acetate in FPHL, but only a small percentage of women showed improvement; the majority of women in the study showed no response. 20 Spironolacto ne   is taken at a dosage of 100mg 200mg per day, with concurrent use of contraception. Cyproterone acetate is taken at a dosage of 25-100mg per day for 10 days of every menstrual cycle, also with concurrent use of contraception.17, 20 Cyproterone inhibits gonadotrophin-releasing hormone (GnRH) and blocks AR; it is also used for treatment of acne, prostate cancer and hirsutism. Vexiau compared minoxidil 2%   and cyproterone – the former was more effective in women who had no hyperandrogenism, and the latter was more effective for those who had, 20, 30 suggesting some role for anti-androgens. Flutamide is another anti-androgen; it compared favourably against finasteride and cyproterone for treatment of FPHL, and also compared favourably against Spironolactone for treatment of acne, seborrhoea, FPHL and hirsutism. 20 However, this drug has a significant side effect profile in that it can potentially cause hepatotoxicity – ongoing monitoring is therefore required and the medication should be stopped or not commenced in the face of significant abnormality.20 Anti-androgen therapy can cause disturbances of the menstrual cycle, breast tenderness, and are contraindicated in pregnancy due to feminisation of male foetus. Spironolactone increases potassium levels, so monitoring of electrolytes is required, as well as hypotension. Adequate counselling prior to commencement of treatment is paramount.20 Surgery There are two types of surgical procedures used to treat alopecia – these are hair transplantation and scalp reduction surgery; they can also be used in conjunction with each other. Because AGA is pattern hair loss, as mentioned earlier, there will be certain areas on the scalp that have a greater tendency to balding than others, for example the occipital area does not have a tendency to bald in pattern hair loss. It makes sense therefore, that for hair transplantation to be effective, the donor site needs to be from an area that is less androgen sensitive or prone to shedding, such as the occipital scalp. The process involves microsurgical techniques of implanting harvested terminal hair follicles under local anaesthetic, into areas of scalp needing more hair. Donor sites must be carefully chosen, the grafts harvested, prepared and implanted without any damage, in order to obtain optimal results. Certain techniques show superiority of efficacy 22.   One study showed a combi nation of hair transplantation surgery with 1mg of oral finasteride had superior results at one year compared with surgery alone. 22 In women the ideal candidate has thick occipital hair and decreased hair density over the frontal scalp. 20 Between one and three sessions are usually required 6 months apart to allow adequate assessment of each surgery. 20 Occasionally there is an effluvium a few weeks after the procedure, but this can often be avoided with concurrent use of 2% minoxidil 20. The best results are achieved in controlled/stabilized AGA and when there is optimal, sufficient donor site. Women with concurrent diffuse effluvium are not good candidates as there is not an optimal donor site. In a good candidate, surgery can result in as good a result as in men. 20 Scalp reduction surgery is not as widely practiced as hair transplant surgery. In scalp reduction surgery the area of scalp with alopecia is surgically removed and two areas of scalp with hair growth are surgically approximated. Scarring and the need for revision surgery, are disadvantages. 20,22 Supplementation A number of trials looking at amino acid supplementation, trace element supplementation (zinc, copper, iron), vitamins like biotin and niacin, antioxidants and millet seed, were assessed by the EDF who found the most of the studies flawed in some way and therefore inconclusive. 22 An improvement in hair growth with use of a herbal treatment containing hibiscus, polygonum, fennel chamomile, thiya and menthe was reported by one author 22Another study also showed some improvement in hair growth after application of a Chinese herbal treatment for six months. 22Retinoids were not proven to show a significant improvement. 22 Saw Palmetto was also looked at by some studies and showed improvements that were significant when compared with placebo.22 Cosmetic Aids While treatments for FPHL are ongoing, or if the patient may for some reason choose not to pursue treatment, or if these were perhaps contraindicated in someone, discussing ways of coping cosmetically may be useful. One study 22 noted that both males and females suffer psychologically when afflicted with hair loss, but for men it was more socially acceptable to be balding than for women, and so the psychological impact can be higher for women who face more pressure to have a ‘normal’ physical appearance. Another study looked at the difference between a woman’s perception of the severity of her hair loss, compared with the clinician’s assessment of this 31.   It found that women consistently rated the severity of their hair loss as higher than the clinician. The study also found that the decrease in quality of life was disproportionate to the degree of hair loss. 31 It is therefore important to consider the patient’s psychological and mental health as well when approaching the issue of hair loss. For this reason it is important to address cosmetic aids and discuss practical issues which may help camouflage the problem in a way that makes the patient feel less conspicuous. Sinclair makes the point that a good hairstylist can be invaluable 20; styling hair in a way to create volume and hide the problem, and learning washing, drying and styling techniques that discourage damage to remaining hair is important. Camouflaging products to create the illusion of thickness include hair building fibres, spray hair thickeners, masking lotion, and topical shading. Fibres can be shaken onto the affected scalp and works in about 30 seconds to create the illusion of thickness. Spray thickeners also create the illusion of increased thickness but can be messy to apply. Tinted lotion and topical shading are less messy and help to create thicker looking hair. Another option, especially if the hair loss is very   advanced or if the application of products is unacceptable for whatever reason, is to use hair extensions, hair weaves/integration pieces or wigs. These depend on choice, and on the quality and amount of remaining hair 20. Hair accessories such as hats, scarves and other fashion accessories can also be useful. The Hair Consultation History After noting gender and age, it is important to determine the nature of the complaint. Has the hair been falling out, breaking off, appearing thinner without noticeable hair loss, or does the quality of the hair appear different.   23 Conditions like monilethrix can result in short fragile hair that breaks easily; in some protein energy malnutritional states such as kwashiorkor hair also breaks easily; with thyroid disorders hair can appear dry and course. Has the problem occurred in the past, or is this the first episode? Has it appeared to improve before? In other words, what is the course of the problem? In CTE, the problem can occur for short periods of time, intermittently for a number of years.   Spontaneous regrowth occurs in TE postpartum. Is there a seasonal variation? Also determine the age at which the problem was first noted. 23,24 Have there been associated symptoms related to the hair problem, such as dandruff, itching of the scalp, burning or painful sensation of the scalp, any rashes occurring simultaneously on the body, any systemic features such as tiredness (anaemia, thyroid problems). Initial signs of AGA can be itching or trichodynia. 24 Any inflammatory condition of the scalp can cause hair loss which can be precluded by itching, scaling or flaking of the scalp. An oily skin can indicate increased activity of the seborrhoeic glands which could indicate increased androgen sensitivity/levels. 24 What is the patient’s past medical history (including any change in health in the year before noticing the hair loss)– severe infections, chronic disease which can cause anaemia of chronic disorder, thyroid problems, medications taken, eczema, any autoimmune disorders, and any chemotherapy or radiation therapy in the past. 23,24 Treatment for breast cancer involving anti-oestrogen therapy can be associated with male pattern hair loss. 10 Gynaecological history for women is also important – menorrhagia, PCOS, amenorrhoea, hormonal contraception, whether post-menopausal and if so has/is hormone replacement therapy used. Discuss past pregnancies – was there difficulty in conceiving, miscarriages, was delivery particularly stressful/complicated. Discuss future family planning. Is there a tendency toward acne, hirsutism, and scalp/skin seborrhoea/oiliness?   23,24 Mental health – issues such as trichillomania, anorexia, and taking antipsycholtic or antidepressant medication. Medications can affect hair growth – beta blockers, anti-epileptics, chemotherapy, thyroid medication, oral contraceptions.   20, 23, 24 Social history is also important – some studies have pointed at smoking exacerbating hair loss. 24 Diet can affect nutritional status, which can affect hair. Sudden weight loss can trigger hair loss. 24Being overweight has been connected with hyperinsulinaemia and metabolic syndrome. The use of anabolic steroids can be significant. 24Enquire about hair products and styling methods – traction can cause problems. Family medical history can indicate an autoimmune problem, family history of male or female pattern balding, skin disorders such as atopy or psoriasis, PCOS, hirsutism. 23,24 It is also important to note from the history how the condition has affected the patient. In the study by Reid et al. mentioned earlier, 31 the clinician’s assessment of severity of hair loss did not predict the patient’s perception of severity of the problem, or their quality of life. While mental health may not always be present as a causative factor, hair loss can cause psychosocial problems such as depression, loss of self esteem and social isolation. 26 It is also important to find out what the patient’s expectations, and hopes, for treatment are. 23 Examination The clinician’s initial impressions are important – is the patient wearing a hairstyle with lots of traction on the scalp, is the person over/underweight, is there obvious hirsutism or acne, is the face looking a bit shiny? Does the person appear emotionally distressed/shy and recalcitrant? It is important to clinically evaluate the whole scalp, including skin and actual hair, facial skin and hair growth (are eyelashes present, is there hirsutism, is there appropriate beard growth), body skin and hair growth, and nails (in alopecia areata the nails can appear pitted). 23,24 Scalp With non-scarring alopecia the scalp should appear normal. Sometimes increased seborrhoea can aggravate AGA. (ref. 26) Scaling, erythema and crusting can indicate inflammation.   With scarring alopecia there is loss of the follicular os. 24 Sun damage in longstanding baldness can be significant. 24 Yellow dots are seen in alopecia areata on dermoscopy, which is thought to represent follicular openings plugged with a keratinous and sebum debris mixture. This can help to distinguish FPHL and TE, from alopecia areata incognita. 32 Hair Note the hairstyle, and whether the hair shafts appear damaged/ dry/ brittle/ broken. 23,24 Part the hair and compare width of the parting at the vertex, frontal, temporal and occipital areas – this is important when describing pattern of hair loss. Use a sheet of white paper for dark hair, and black paper for light/grey hair, over a parting in the hair, to look for miniaturised hair, broken hairs or variations among the hairs. 33 Exclamation hairs (tapering broken hairs) indicate alopecia areata. 32 Miniaturisation indicates AGA. 32 Note the pattern of hair loss – in MPHL, there is thinning and recession bitemporally initially, then in the vertex. In FPHL the pattern can demonstrate the Ludwig, Olsen (Christmas tree pattern) or the Sinclair description, or the Hamilton distribution. 20, 23, 24 Diffuse thinning of the hair can also be caused by diffuse alopecia areata or diffuse telogen effluvium. 20, 26, 24, 32 Pull test This is an important test to help differentiate at the initial consultation between the types of non-scarring alopecia, when not clinically obvious. It is important to determine when hair was washed, as a head washed more recently would be more likely to have lost telogen hairs and have fewer to yield. 17, 20 About 50-60 hairs are pulled between the thumb, forefinger and middle finger. A positive test occurs when more than 10% of the hairs can be pulled out.17, 20, 23, 24 Performing the test on different areas of the scalp is useful in excluding diffuse telogen effluvium; often this can co-exist with a pattern hair loss. 17 The test is usually negative for pattern hair loss, except when performed during a telogen phase in the affected area, when there would be more hairs than usual in the telogen phase. If the pull test is positive, a diagnosis other than pattern hair loss should at least be considered. 24 Non-scalp hair and skin Abnormal distribution of body hair is important to note as can indicate a hormonal problem which may need further investigations. An increased amount of body hair can be hormonal or genetic or related to medication. 24 Absent sexual hair can indicate a hormonal problem, and absent or scanty eyebrows or eyelashes can be associated with alopecia areata or frontal fibrosing alopecia. 24 Acne and seborrhoea can be hormonal. 26 Nails are affected by a number of dermatoses, but of the non-scarring alopecias, only alopecia areata has been known to cause nail changes. 24 Mentioned above is that the trigger causing ATE can sometimes cause Beau’s lines in the nails. 25 Lab tests The history and clinical examination should allow a diagnosis of non-scarring alopecia to be made, and for the problem to be classified as either pattern hair loss, telogen effluvium, or alopecia areata (or a combination). Because confounding factors may also be present which can exacerbate hair loss or prevent treatment, it is reasonable to do some laboratory tests, if suggested by the findings of the history and examination.17, 20, 23, 24 Serum ferritin and thyroid hormone levels should be done. 17, 20, 23, 24 In men it has been advised that after the age of 45, a PSA level should performed prior to treatment with finasteride, as this drug can lower PSA. The patient should be made aware of this side effect.23, 26 If on history and examination there is a suspicion of a virilising tumour, PCOS, or hyperandrogenism in women, then additional tests such as a free androgen index (FAI) (total testosterone x 100 / SHBG) test, and prolactin level as screening tests for hyperandrogenaemia – for example levels of FAI of 5 and above indicate that someone may have PCOS (reference). Depending on findings, FSH, or cortisol levels may also be needed, and the patient referred to either a gynaecologist or endocrinologist (or both if needed). 17, 20, 23, 24 Hormone levels are affected by ingestion of exogenous hormones so should be tested if no hormones taken for 2 months at least, and the time of the menstrual cycle noted for adequate interpretation of hormone results. 23 Oestrogens can increase the level of SHBG, and therefore improve FAI. 23 Other investigative tools available to dermatologists are  ·Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚   dermoscopy    in FPHL it shows increased hair diameter diversity and an increased number of vellus hairs. 32 Global photography – helps to evaluate the course of hair changes in clinical studies in an objective fashion – set regions of the scalp are photographed using standardised procedure and equipment 23,24 Trichoscan – for diagnostic and follow-up purposes, it measures hair density and anagen/telogen ratios. For reproducibility tattoos of the sample areas in frontal and occipital regions are needed. 23,24 Trichogram – to be used by a dermatologist experienced in its use. 24 Biopsy – not usually required for diagnosis of non-scarring alopecia, but may be helpful if there is doubt about the diagnosis. Much more relevant for cases of scarring alopecia. 17, 20, 23, 24 CASE DISCUSSION AND CONCLUSION The case of Mrs KJ is interesting because of the complexities involved. Her initial hair loss had occurred on cessation of Cilest. She therefore believed that stopping this had caused the problem, and helped maintain hair thickness, hence her request to be put back on Cilest when she saw her GP. As mentioned above, cessation of the combined oral contraceptive has been noted to cause transitory hair loss. However, at the time of the initial presentation she was put on Dianette and cyproterone as she was found to have PCOS. This is one of the potential causes of hyperandrogenism. Although her blood results did not show any hormonal imbalances, she mentioned that she had had facial hirsutism at the time, so was clinically hyperandrogenous without being biochemically hyperandrogenous. It may be that in the presence of normal hormone levels, she was more responsive to existing hormones, possibly with increased receptor sensitivity. The blood results could also not accurately be relied on as she was not taken off the oral contraception. The fact that there was hair growth with cyproterone suggests that androgens had their role to play in her case. When she presented to the GP for the second time, there were a number of issues to note. She had a very stressful and demanding job. It must be noted that Mrs KJ’s personality was that of a perfectionist, and it could be argued that people like this, who are driven to succeed might be more susceptible to stress. She had also planned her wedding and honey moon in the months leading up to the dramatic hair shedding which occurred whilst on honey moon. Added to this was her vegetarian diet, and although she was not anaemic, her ferritin level was below ‘the optimum’ levels discussed above, even though normal according to the lab reference range. The plot thickens. Based on the above the GP had correctly made the diagnosis of a telogen effluvium. However Mrs KJ had the compounding problem of PCOS. The underlying problem for Mrs KJ was the PCOS, a syndrome affecting about 5-10% of women. 34 PCOS symptoms are related to abnormal levels of sex hormones – high/high-normal Luteinising Hormone (LH) and androgens (including testosterone), and low Follicle Stimulating Hormone (FSH) and progesterone. The cause for PCOS is not known but there is an association with insulin resistance. 35 Insulin resistance causes the body to increase the amount of insulin produced. Higher insulin levels increase ovarian production of androgens, which inhibit ovarian follicular maturation, hence the menstrual abnormalities. 35 Higher androgen production also has an effect on hair growth, specifically, thinning of scalp hair in a pattern of hair loss. Although there was no history of baldness in the family, male or female, she presented with a typical male pattern of baldness with bilateral thinning of the temporal areas (Hamilton I). The second dermatologist noted increased seborrhoea, which can indicate clinical hyperandrogenism, and treated with Ketoconazole. This bitemporal thinning could have been occurring unnoticed as FPHL tends to be slowly progressive. Her hair loss shot to her attention with the abrupt onset of the telogen effluvium. One more interesting point to note is that when she saw her GP to discuss stress, neither considered the impact of the propranolol on her hair loss. She did present a few weeks after the short period of having used the propranolol, with a sudden increase in her hair loss, which may well have contributed to by the beta blocker. Whether a few days at a low dose would have made such an impact, is uncertain. The interesting case of Mrs KJ serves as a perfect example of why primary care physicians need to have a good approach to dealing with the rather complex problem of diffuse hair loss. Once each of the (potential) contributory factors had been treated, Mrs KJ started to grow a thicker, more dense, head of hair. Lastly, there is a small subset of patients in whom non-scarring hair loss serves to uncover more serious medical problems such as thyroid disease, hyperinsulinaemia, PCOS, Metabolic Syndrome and potential for heart disease.   This link has been the subject of numerous studies. Matilainen et al. investigated whether early AGA could serve as a marker for insulin resistance, and concluded that further research was needed, but suggested that people with early AGA could benefit from cardiovascular screening.   36 This was supported by Arias-Santiago et al. who investigated lipid levels in women with AGA, and found that women with AGA were shown to have significantly higher levels than women with no AGA. 37   Abdel Fattah and Darwish found that people with metabolic syndrome, regardless of the presence of AGA, were more likely to be have insulin resistance, compared with people with AGA and normal controls. 38 This serves to highlight the point that while much work is still needed t o clarify the above, the vigilant GP, presented with the problem of FPHL, should also be on the lookout for comorbid disease or potential for these.   Mrs KJ’s father had died of a heart attack in his early fifties, but she maintained a healthy lifestyle, normal lipid and glucose profile, and low-normal blood pressure and so had a low risk for cardiovascular disease. There is much on hair loss that was not discussed in this paper, such as cicatricial or scarring alopecia, localised hair loss (alopecia areata) and hair loss in children and adolescents. If the latter occurs, and appears to be non-scarring, it is best discussed with a paediatric endocrinologist and dermatologist. Dr Yumnah Ras MBChB, June 2011 REFERENCES 1. The Doctors Laboratory reference range for normal ferritin levels,2010. tdlpathology.com 2. Gray, Henry. Anatomy of the Human Body. Philadelphia: Lea Febiger, 1918; Bartleby.com, 2000   www.bartleby.com/107/.June 2011 3. Slobodan M.Jankovic and Snezana V.Jankovic. The control of hair growth. Dermatology Online Journal 4(1):2 http://dermatology.cdlib.org/DOJvol4num1/original/jankovi.html 4. http://emedicine.medscape.com/article/835470 Author Samer Alaiti 5. http://emedicine.medscape.com/article/259724 Author Suzanne R Trupin, 6. Messenger, A. The control of Hair Growth: An overview.Journal of Investigative Dermatology Vol.101 No.1supplement,July 1993 7. http://emedicine.medscape.com/article/273153   Author Mohamed Yahya Abdel-Rahman, 8. Trueb, R. Molecular mechanisms of androgenic Alopecia. Experimental Gerontology 37 (2002) 981-990 9. Apridonidze et al.Prevalence and Characteristics of the Metabolic Syndrome in Women with Polycystic Ovary Syndrome. The Journal of Clinical   Endocrinology Metabolism April 1, 2005 vol. 90 no. 4 1929-1935 10. Carlini, et al. Alopecia in a premenopausal breast cancer woman treated with letrozole and triptorelin. Ann Oncol (2003) 14 (11): 1689-1690. doi: 10.1093/annonc/mdg444 11. Kantor et al. Decreased Serum Ferritin is Associated with Alopecia in Women. Journal of Investigative Dermatology (2003) 121, 985–988; oi:10.1046/j.1523-1747.2003.12540.x 12. Olsen et al. Iron deficiency in female pattern hair loss, chronic telogen effluvium, and control groups. Journal Am. Acad. Derm 2010 Dec 63 (6):991-9 Epub 2010 Oct 13. Rushton, D. Decreased Serum ferritin and Alopecia in Women. Journal of Investigative Dermatology (2003) 121, xvii–xviii; doi:10.1046/j.1523-1747.2003.12581.x 14. Moeinvaziri et al.   Iron status in diffuse telogen hair loss among women. Acta Dermatovenerol Croat. 2009;17 (4):279-84. 15. Yip et al. Role of genetics and sex steroid hormones in male androgenetic alopecia and female pattern hair loss: An update of what we now know. Australian Journ derm (2011) 52, 81-88 16. Trost et al. The diagnosis and treatment of iron deficiency and its potential relationship to hair loss. Journ. Am. Acad. Dermatol. Vol (54) No.5 824-844 17. Shrivastava et al. Diffuse Hair loss in an adult Female: Approach to diagnosis and management. 18. Prasad, A. Clinical, endocrinological and biochemical effects of zinc deficiency. Clinics in Endocrinology and Metabolism Volume 14, Issue 3, August 1985, Pages 567-589 19. Goldberg et al. Nutrition and Hair. Clinics in Dermatology, Volume 28, Issue 4, July-August 2010, Pages 412-419 20. Dinh, Q and Sinclair, R. Female pattern hair loss: current treatment concepts. Clin Interv Aging. 2007 June; 2(2): 189-199. Published online 2007 June. 21. Gan, D and Sinclair, R. Prevalence of male and female pattern hair loss in Maryborough. J Investig Dermatol Symp Proc. 2005 Dec;10(3):184-9. 22.European Dermatology Forum, S3-Guideline on Androgenetic Alopecia. euroderm.org/edf/images/stories/guidelines/S3_guideline_androgenetic_alopecia.pdf 23. Blume-Peytavi, U and Vogt, A. Current Standards in the diagnostics and therapy of hair diseases. JDDG; 2011 9:394-412 24. Blume-Peytavi et al. S1 guideline for diagnosic evaluation in androgeentic alopecia in men, women and adolescents. Br J Dermatol. 2011 Jan;164(1):5-15. doi: 10.1111/j.1365-2133.2010.10011.x. Epub 2010 Dec 8. 25. http://dermnetnz.org/hair-nails-sweat/telogen-effluvium.html June 2011 26. Hordinsky, M. Medical Treatment of Noncicatricial Alopecia. Seminars in Cutaneous Medicine and Surgery Volume 25, Issue 1, March 2006, Pages 51-55 27. Messenger, A and Rundegren, J. Minoxidil: Mechanisms of Action on Hair Growth. British Journal of Dermatology Vol 150 (2):186–194, Feb 2004 28. Lucky et al. A randomized, placebo-controlled trial of 5% and 2% topical minoxidil solutions in the treatment of female pattern hair loss. J Am Acad Dermatol Vol 50 (4) p 541-553 29. Khandpur et al. Comparative efficacy of various treatment regimens for androgenetic alopecia in men.J Dermatol. 2002 Aug;29(8):489-98. 30. Vixiau et al. Effects of minoxidil 2% vs. cyproterone acetate treatment on female androgenetic alopecia: a controlled, 12-month randomized trial. British Journal of Dermatology Volume 146, Issue 6, pages 992–999, June 2002 31. Reid et al. Clinical Severity does not reliably predict quality of life in women with alopecia areatam telogen effluvium, or androgenenic alopecia. Journal of the American Academy of Dermatology, In Press, Corrected Proof, Available online 24 May 2011. 32. Tosti, A and Duque-Estrada, B. Dermoscopy in Hair Disorders. J Egypt Women Dermatol Soc. Vol. 7, No. 1, 2010 33. Course Notes on Hair, QMUL post.grad. Dip.Derm 2010/2011. 34. verity-pcos.org.uk/guidetopcos/whatispcos 35. Kovacs,P. Metabolic Syndrome amd PCOS. Medscape Ob/Gyn 2003; 8(2) medscape.com/viewarticle/456221 36. Matileinen et al. Early Androgenetic Alopecia as a marker of Insulin Resistance. The Lancet Vol(356) p1165-1166 Sept 30, 2000. 37. Arias-Santiago et al. Lipid levels in women with angrogenetic alopecia. International Journal of Dermatology 2010, 49, 1340-1342 38. Abdel Fattah, N and Darwish Y. Androgenetic alopecia and insulin reistance: are they truly associated? International Journal of Dermatology 2011, 50, 417-421

Cinema in Egypt Term Paper Example | Topics and Well Written Essays - 750 words

Cinema in Egypt - Term Paper Example First, it is important to consider major milestones in the development of the Egyptian cinematography. It is noteworthy that the first â€Å"purpose-built cinema house† was built in Egypt in 1907 (Gamal 2). It suggests that Egyptians were interested in the new form of art and the industry could easily pave its way. Initially, foreign films were shown. The first national film was produced in 1917 (Danielson 87). However, those were first attempts, though they were quite successful. The industry started developing rapidly in 1925 when Tal’at Harb, a successful banker, started his own film company. Importantly, the banker employed only nationals and he even sent the most promising ones to Europe for the necessary training (Danielson 87). Unshudat al-Fu’ad / Song from the Heart (1932) was one of the first Egyptian sound films (Shafik 45). This musical film was very successful and it inspired many Egyptian filmmakers. Another musical, al-Warda al-Badha / The White Rose produced in 1933, was also the first Egyptian movie â€Å"to be successfully exported to other Arab countries† (Shafik 45). Muhammad Karim, Ahmad Badrakhan, Fatima Rushdi were among those directors who shaped the Egyptian cinematography and created or rather identified its most significant conventions. The middle of the 20th century is regarded as the golden age of the Egyptian cinematography. Numerous brilliant films were created at that period. It is necessary to note that major themes and genres remained the same. Those were often musical films and comedies that promulgated universal values. They will be considered in detail below. However, during the 1970-1980s, the industry was declining and the number of films produced decreased significantly (Russell 344). Their quality was often very low. At present, the Egyptian industry is on its rise and numerous talented filmmakers manage to produce highly successful national films. As has been mentioned above,

The role of innocence in the exoneration process Essay

The role of innocence in the exoneration process - Essay Example However, this is not always to be, and there is always the likelihood that an innocent person is convicted2. This paper attempts to explain ways that people wrongly convicted get proof of their innocence. The causes of wrong convictions are wide ranging and comprise all features of the pre-trial and trial stages of the criminal justice process ranging from false allegations, incompetent police investigation, police misconduct, erroneous forensic science and evidence, and poor representation from criminal defense lawyers. Once an alleged victim of an unjust conviction has lost their appeal, there is a slight opportunity that the courts will be in a position to stop the conviction3. In these cases, victims of wrongful convictions are likely to have exhausted the legal aid unit and it will be up to them, their friends, supporters, families, pro-bono lawyers and voluntary groups to uncover the evidence of innocence and present it to the relevant authorities such as the Criminal Cases Review Commission (CCRC). 2Investigating a suspected wrongful conviction is a long and challenging process. Cases of high profile injustices like the Cardiff Newsagent Three and Sean Hodgson show that it can take several years of investigation before the evidence that leads to the quashing of the conviction is found4. Many projects that attempt to exonerate innocent people out of prison have come up. One such project is the Innocence Network project founded in 1992 whose principle objective is to get as many innocent people out of prison as possible and turn the experience of these people into a learning experience that could help repair the systematic failings in the criminal justic e system5. The project exonerates people by use of post-conviction DNA where the DNA from the crime scene is tested against the DNA of the accused. Often, people wrongly convicted of serious crimes like homicide or abuse has

Oral Presentation on Australian Aboriginal Families Essay Example for Free

Oral Presentation on Australian Aboriginal Families Essay We are doing the Traditional Australian Aboriginal families. The traditional Aboriginals were located in Australia and Tasmania. It is believed that Australian Aboriginals travelled from Africa to Asia around 60 000 years ago and arrived in Australia 50 000 years ago. Today, about 1% of Australian people are Aboriginal. Religion was a very large part of the Aboriginal culture. They do not have a formal religion but they were very spiritual. They believed in The Dreaming, which was when the Ancestral Beings moved across the land and created life and features in the land. Dreamtime stories are told by songs, dance, stories or paintings and pasted through the generations. Aboriginals had a complex family system; it varies from tribe to tribe. But a typical Aboriginal family consisted of grandparents, men and their wives and children. The women played the main role in educating the children but the men and women both shared the roles of healers, law makers, performers and painters. CHANGE PP. The main role of the women was to gather food. They would collect seeds, vegetables, fruits, insects and larvae. It was then their job to cook and prepare the meal. Women took care of the children until they reached the age of six. CHANGE PP. Until around age 6, children would get looked after by their mother. After this age, boys would learn hunting with their fathers and girls would learn food gathering with their mothers. Children would help and care for elders when they needed help physically. The elders of a group were the roles models. Elders would educate and teach the children and children helped them physically. Everyone had a lot of respect for the elders as they had a lot of knowledge and experience. They would decide if the group was to move camp. A typical Aboriginal family used to hunt, craft and tell stories each day. Each day the aboriginal men would go hunting for food using tools they had made themselves. The women and children would spend the day gathering foods. As they did this the women would educate the children on religion and tell them dream stories. At the end of the day the women would cook the meal for the large family around a camp fire. Aboriginal children and families played a lot of games and music together. They would play traditional music that was handed down through generations. Didgeridoos, rattles, clapping sticks and boomerangs were all used as instruments. Ceremonies were a huge part of Aboriginal life. The main ceremonies they conduct are for health of crops and land, initiation of children to adulthood and funerals. These ceremonies can go for days and even months and almost the entire community are involved. They sing songs, decorate themselves and tell stories during ceremonies. The head of a typical clan is usually one of the eldest and talented men and is followed by younger men. The leader position was passed down from father to son. In conclusion, traditional Aboriginal families were very respectful of each other. They each have a specific role in society and each contribute to the life of the community. Thank you for listening. We hope you learnt lots about the traditional Aboriginal families.

Essay --

Montanna Williams Mrs. Songer World Literature 12 October 2013 Death In the writings The Snows of Kilimanjaro and The Death of Ivan Ilyich both Ernest Hemmingway and Leo Tolstoy have a prominent theme of death. These two works do not only show strong images of death, but also a sense of death’s presence. Throughout the two writings it is presented that chasing money, how both Ivan and Harry treat the people around them, and their egotistical life style can lead to an unpleasant death. In The Snows of Kilimanjaro Harry’s fondness for money causes him to lose sight of what is critical in life. He gave up writing which is something he appreciated and was good at, for a wealthy woman that he truly did not love. Harry was more concerned with how he should act in his society instead of what he enjoys doing. He has a bad habit of falling in love with woman who were wealthy instead of looking for essential things like a woman’s beliefs and her values. â€Å"It was strange too wasn’t it? That when he fell in love with another woman, that woman should always have more money than the last one?† Harry knows what he missed out on and in the end he regrets that he stopped doing what he loved. On the other hand in The Death of Ivan Ilyich Tolstoy portrays almost every character in the book to be concerned with social class. Once Ivan’s colleges found out he died, after asking simple details, they immediately asked about if Ivan was wealthy or n ot. â€Å"Had he any property?† I think his wife had a little – but something quite trifling.† (1.12-13). Ivan and his family were not in the upper class of society, they were in the middle, and because they owned property it made them higher up in their social classe because that was very rare in Russia at that ... ... a person should look at their life and how they should face their death. In The Snows of Kilimanjaro Harry was not content with the life he had lived. He made sacrifices and in result he was just not happy, and because of his sacrifices he had many regrets as he was dying. On the other hand Ivan Ilyich was too engaged in his work life and ignored his family matters. He didn’t step up to the plate; instead he ran away from the issues and hid behind his work, therefore resulting in a very non-loving family life. Luckily Ivan found peace in himself as he was about to die, even becoming joyful. Both of these writings teach that going after materialistic things, the way a person treats the people around them, and being self-absorbed can cause a distasteful death. Living life to the fullest and making the most of it can enrich your life and cause a more pleasant passing.

Racial discrimination in the Workplace Essay

Racial discrimination has long been a problem in social history. The discrimination of ethnic minorities has been a controversial issue, existent in society, and workplaces for many years. The implementation of ethnic monitoring and positive discrimination in employment has increased the number of ethnic employees and gone a long way to mend the bridge of inequality which has burdened society for a long time. Another method introduced to try and counter the racial inequality in employment is that of Affirmative Action. Affirmative action calls for minorities and women to be given special consideration in employment, education and contracting decisions, to increase their number in the workplace. Affirmative action is a controversial issue which has been debated by many. In this essay I am going to look at the advantages and disadvantages of affirmative action and what affect it has on society. I will also debate whether I think affirmative action is a fair method to implement in organisations, and also whether it can be considered to be fair from a philosophical perspective. Affirmative action was defined as an attempt to enlarge opportunity for everyone, it was designed to redress the imbalances caused by long-standing discrimination. Defenders of affirmative action argue that granting modest advantages to minorities and women is more than fair, given hundreds of years of discrimination that benefited whites and men. This implies that as blacks have previously suffered from detrimental racist discrimination and wrongdoings, including slavery and not having the right to vote, they now deserve extra benefits to compensate. This is known as â€Å"reverse racism†. It argues that as whites once set themselves apart from blacks and claimed privileges for themselves while denying them to others, now, on the basis of race, blacks are able to claim special status and reserving for themselves privileges they deny to others. The question then arises: Do two wrongs make a right? This is what affirmative action is condoning. It says that we are allowed to overlook  suitable white candidates if a black candidate is available. This means that even if the white candidate were a better choice and more qualified for the job, the black person would be hired because of the past injustices his race has suffered. People say affirmative action is acceptable because it cures past discrimination (Keyes 1996). However, discrimination was not acceptable when blacks were the ones discriminated against, therefore it’s not ok when whites are discriminated against (DeWit 1996). The answer is that two wrongs do not make a right – affirmative action does not make discrimination acceptable, just because it is now against whites instead of blacks. It has been said that job discrimination is grounded in prejudice and exclusion, whereas affirmative action is an effort to overcome prejudicial treatment through inclusion. The most effective way to cure society of exclusionary practices is to make special efforts at inclusion, this is what affirmative action does. We can explain the theory behind affirmative action with this example; the logic of affirmative action is no different than the logic of treating a nutritional deficiency with vitamin supplements. For a healthy person, high doses of vitamin supplements may be unnecessary or even harmful, but for a person whose system is out of balance, supplements are an efficient way to restore the body’s balance. The equal opportunities law was introduced into society due to the discrimination ethnic minorities had received in history. The policies were implemented to counter racial discrimination and bias. Thus, the equal opportunities law was not created to treat different races differently, its purpose was to treat all people as equals. Affirmative action, however, does not adhere to this principal as by dismissing perfectly capable white candidates for a role in order to employ a less qualified black person, we are not treating everyone as equals. (Hacker 1990). A major disadvantage of affirmative action in the workplace is the affect it has on the organisation and its employees. Affirmative action can be very detrimental to the organisation as hiring an under qualified worker puts  others at risk if he or she doesn’t have enough experience. It is also financially dangerous and a company should not pay inexperienced people to do work they’re not qualified for. Affirmative action will only work short term because if you hire a minority who is under qualified they will eventually lose their job. Another problem arises as organisations can only hire so many people, and this may result in too many under qualified people working for you and will eventually have to abandon affirmative action all together. Affirmative action means that employees who benefit from it bear the mark of not being the best pick, but only the best pick from a limited group (DeWit 1996) It would be better for an employees self-esteem if they knew they got a job because they were the best person for the job, not because they were black and under-represented. It is also possible that because of affirmative action, racism within an organisation will increase. If a company hires a black person who is not as good as another white candidate, employees will begin to resent him/her. If they gained their job based on their skin colour, rather than because they were the most qualified, they may become disliked and resented because of their skin colour. This could also lead to lack of respect for a black boss which would be detrimental to the organisation and the happiness of employees. One of the arguments for affirmative action is that blacks should be compensated for injustices done to their ancestors by white people. This idea contradicts the human right of individuality. It implies that if a white persons ancestor showed racist behaviour, they will be discriminated against because of this. The reality of this is completely unfair, why should one person be punished for something they had no control over, and similarly why should black people receive preferential treatment for behaviour they have not suffered from. That is to say, a black man will be treated in a better way than a white man, as his grandfather was the victim of slavery. The implementation of this is unrealistic and immoral,  especially as we should aim to promote equality among all. As discussed above this kind of preferential treatment will only cause resentment and ultimately the resentment of the black man, purely for being black. The real factor in affirmative action, is that are blacks getting their jobs because they are qualified and able, or because they are black? If the decisive factor is their skin colour and not their ability to work, then affirmative action is a flawed method. Businesses will only ever survive and be profitable if they employ the most suitable and qualified candidate for the job. For this to happen and for the organisation to ensure they have hired the best person for the job, recruitment methods must be colour-blind. This means the people in charge of recruitment should assess each application based on its merits and qualifications, not on the ethnic background of the applicant. Discrimination can only be rooted out by enforcing strictly anti-discrimination rules, without engaging in reverse discrimination which would alienate good white male candidates for employment and promotion who, after all, are not to be blamed by past injustices. From a philosophical point of view affirmative action does not comply with deontological theory, which states that it is our duty to do what is right whatever its consequences, and what is right consists in treating all human beings with respect and due consideration for their rights and liberties. This shows us that racial discrimination goes against these deontological beliefs. However, as deontology shows us that racism is wrong, as it does not treat all human beings with respect, does this mean affirmative action is the right way to go? In my opinion, affirmative action is not a solution to the deontological problem of racism. That is because affirmative action does not treat all human beings with respect and due consideration. Affirmative action disregards the consideration of the white men applying for the jobs, as its aim is to employ black people. From a utilitarian point of view, affirmative action has some key flaws. Utilitarianism says in effect that the rightness of an action (or practical  policy) consists in its tendency to produce the greatest amount of happiness for the greatest number of people than any alternative. Affirmative action would therefore only work if the people within a company were for the idea. Taking a more likely situation, based on historical facts, there are more likely to be a greater number of white males in an organisation. If this is the case and one of them is overlooked for promotion because of a less qualified black man, as the company is employing affirmative action, this goes against utilitarianism ideologies of promoting the greatest happiness for the greatest number of people. In conclusion, I do not agree with affirmative action, the unfair treatment of ethnic minorities has been a harsh reality on society for a long time and it needs to be addressed. However, the method of affirmative action, which goes out of its way to hire a black man, purely because he is black, leads us to the same racial inequality that was a problem when blacks were not hired, for being black. Although the idea of affirmative action was implemented to give black people better opportunities it is still a form of discrimination. When an employer hires someone because he or she is a minority, even if someone else if more qualified to do the job, it is discrimination. Just because it is reverse discrimination, when whites are discriminated against and minorities are being discriminated for, doesn’t make it right. â€Å"Affirmative action legalizes discrimination†. (Steele 1990) The efforts of affirmative action are no different from the policies that created the disadvantages in the first place, although the idea is trying to redress the balance of inequality, I feel it is causing more harm than good in the work place. It is undemocratic to give one class of citizen’s advantages at the expense of other citizens; the truly democratic way is to have a level playing field to which everyone has access and where everyone has a fair and equal chance to succeed purely on the basis of his or her merit. Hard work and merit, not race or religion or gender or birthright, should determine who prospers and who does not.

Analyzing the Formation of Habits Using Behavioral and Social/Cognitive Approaches

The habit to be analyzed is cigarette smoking. Around the age of 13 is when I probably had my first cigarette. The habit developed from a learned behavior from the adults around me and peer pressure. I can remember many of the adult figures around me, more so the adult males, smoked cigarettes, and cigars. At the time when I was a girl there was not an age limit on buying cigarettes. My father, who ran his body and fender shop out the garage in the back yard would send me and my siblings to the corner drugstore to buy his KOOL cigarettes. The seventh grade is when the peer pressure began.I remember sneaking the KOOL cigarettes out of my father’s pack and smoking on the way to school with friends. Smoking did not become a habit then. I had older sisters and always wanted to follow them. So once I was in high school they let me hang out with them. I smoked to pretend I was as grown as they were. It still had not become a habit. After high school about the age of 19 is when it be came a habit. I moved away from home and wanted to do the things that grown-ups do. Because smoking has formed into a habit my body craved the nicotine and this is what fed the habit and caused it to continue.The habit continued until my 29th year when I became pregnant with my daughter. The smoking probably would have continued through pregnancy, but it made me sick. The smoking resumed after birth for the next 15 years. During the period after birth I tried to stop smoking once or twice unsuccessfully, convincing myself that I enjoyed smoking and was not ready to quit. It was the nicotine addiction talking to me. Most of my friends smoke and it was something we did together When comparing this habit to the behavioral personality theory, it makes complete sense.The behavioral personality theory only deals with externally observable things. This habit came about from watching and observing others. Trying to do as others to fit in or be someone different than who I was at the time, n ot knowing how addicting this habit could be. As a person gets older the body does not allow one to continue the habits that started in their younger years without consequences. The effects of aging start taking over. Because of operant conditioning this habit had to be change. The effect of smoking in people with diabetes cause a high cardiovascular risk, Diabeticnephropathy which causes kidney disease, high blood pressure, and genetic predisposition. Every visit to the doctor reminded me of the consequences of smoking. Operant conditioning (sometimes referred to as instrumental conditioning) is a method of learning that occurs through rewards and punishments for behavior. Through these rewards and punishments, an association is made between a behavior and a consequence for that behavior (Kendra Cherry, 2013). This conditioning caused me to quit this habit. First I had to make the conscience decision that this was going to be the end of smoking.The plan was to quit smoking cold tur key; I did not want to substitute one drug to give up another. I no longer allowed myself to buy cigarettes. If I had the urge to smoke a cigarette, I would get one from someone else, preferably non-menthol or not my brand so it would not be satisfying. All money that was to be spent on cigarettes went into a savings account. After six months I had a savings of $360. 00. This is where the operant conditions plays a part, that was a great reward. This was a hard habit to change but not as hard as I thought it would be.Like any habit or addiction I believe the person has to want to make the change. People who â€Å"relapse† make the conscience decision to continue the habit. Social cognitive theory (SCT) refers to a psychological model of behavior that started primarily from the work of Albert Bandura (1977; 1986). It was first developed with an emphasis on the cognitive process or acquiring knowledge of social behaviors, social cognitive theory continues to single out that lea rning happens in a social setting and that much of what is learned is acquired through watching others (The Gale Group, 2013).Cognitive-behavioral theory (CBT) refers to the basic principle that a person’s perceptions play a substantial and important role in the development and maintenance of emotional and behav ¬ioral responses to life situations. In CBT models, cognitive processes, in the form of meanings, judgments, appraisals, and assumptions associated with specific life events, are the primary determinants of one’s feelings and actions in response to life events and thus either enable or hold back the process of adaptation (A. Antonio Gonzalez-Prendes and Stella M.  Resko, 2013)After understanding both the social and behavioral cognitive theories, I believe the cognitive-behavioral theory has the most influence in the makeup of my personality. The cognitive behavioral theory comes into play when I am trying to reach self-actualization motives as described in Maslow’s hierarchy of needs. I tend to react on feelings in most situations, which will either enable or hold back the process of adaptation. In conclusion, I am finding that studying the different theories of behavior is giving me a better understanding of the way people act and think. This hase been a very informative class.

Time and Love essays

Time and Love essays Corporations or Consumers, Who is Responsible? The lives and daily routines of many Americans are affected by corporate activities. Corporations provide the basic necessities like food and water as well as luxuries and pleasures of everyday living. These corporations generate wealth for the economy and their shareholders, and provide employment for much of the population. One of these powerful corporations is Philip Morris who manufactures and distributes tobacco products such as Marlboro (Morris, 1). This tobacco manufacturer not only generates wealth but also generates health hazardous risks for the consumer. Despite increasing warnings about the health hazards of smoking and widespread bans on smoking in public places, Americans disregard these warnings and still continue to smoke (Smoking, 4). Later then finding themselves dealing with the consequences of their poorly made decisions. Therefore, a corporation should not be held responsible for providing a product. It is the users who should be held accountable for the ir choices. The American people have the right to choose whether to smoke or not to smoke. There is a lot of information of cancer risks from using tobacco available to Americans, particularly in the media. The American Cancer Society estimates that cigarettes are responsible for more than 400,000 deaths in the United States each year (Smoking, 2). American consumers have been informed that tobacco contains nicotine, an addictive drug. They also know that by smoking tobacco, it causes lung cancer, emphysema, and other respiratory diseases. It also contributes to heart disease and low birth weight of newborns. Chewing tobacco and inhaling snuff causes cancer of the mouth, nose, and throat (Tobacco, 8). Regardless of these astonishing facts, forty-seven million people still continue to use tobacco products (Smoking, 1). Therefore, corporations should not be blamed for consumers po...

Scallop Facts

Scallop Facts Found in saltwater environments like the Atlantic Ocean, scallops are bivalved mollusks that can be found around the world. Unlike their relative the oyster, scallops are free-swimming mollusks that live inside a hinged shell. What most people recognize as a scallop is actually the creatures adductor muscle, which it uses to open and close its shell in order to propel itself through the water. There are more than 400 species of scallops; all are members of the Pectinidae family. Fast Facts: Scallops Scientific Name: PectinidaeCommon Name(s): Scallop, escallop,  fan shell,  or  comb shellBasic Animal Group:  InvertebrateSize: 1–6 inch valves (width of shell)Weight: Varies depending on speciesLifespan: Up to 20 yearsDiet:  OmnivoreHabitat:  Shallow marine habitats around the worldConservation  Status:  Varies depending on species Description Scallops are in the phylum Mollusca, a group of animals that also includes snails, sea slugs, octopuses, squid, clams, mussels, and oysters. Scallops are one of a group of mollusks known as  bivalves. These animals have two hinged shells that are formed of calcium carbonate. Scallops have anywhere from 50 to 100 eyes that line their  mantle. These eyes may be a brilliant blue color, and they allow the scallop to detect light, dark, and motion. They use their retinas to focus light, a job the cornea does in human eyes. Atlantic sea scallops can have very large shells, up to 9 inches in length. Bay scallops are smaller, growing to about 4 inches. The gender of Atlantic sea scallops can be distinguished. The females reproductive organs are red while the males are white. Bobby Ware/Getty Images   Habitat and Range Scallops are found in saltwater environments worldwide, ranging from the intertidal zone to the deep sea. Most prefer beds of seagrass amid shallow sandy bottoms, although some attach themselves to rocks or other substrates. In the United States, two kinds of scallops are sold as food. Atlantic sea scallops, the larger kind, are harvested wild from the Canadian border to the mid-Atlantic and are found in shallow open waters. Smaller bay scallops are found in estuaries and bays from New Jersey to Florida. There are large scallop populations in the Sea of Japan, off the Pacific coast from Peru to Chile, and near Ireland and New Zealand. The majority of farmed scallops are from China. Diet Scallops eat by filtering small organisms such as krill, algae, and larvae from the water they inhabit. As water enters the scallop, mucus traps plankton in the water, and then cilia move the food into the scallops mouth.   DEA PICTURE LIBRARY/De Agostini Picture Library/Getty Images Behavior Unlike other bivalves such as mussels and clams, most scallops are free-swimming. They swim by clapping their shells quickly using their  highly developed adductor muscle, forcing a jet of water past the shell hinge, propelling the scallop forward. Theyre surprisingly speedy. Scallops swim by opening and closing their shells using their powerful adductor muscle. This muscle is the round, fleshy scallop that anyone who eats seafood will instantly recognize. The adductor muscle varies in color from white to beige. The Atlantic sea scallops adductor muscle may be as big as 2 inches in diameter. Reproduction Many scallops are hermaphrodites, which means that they have both male and female sex organs. Others are only male or female. Scallops reproduce by spawning, which is when organisms release eggs and sperm into the water. Once an egg is fertilized, the young scallop is planktonic before settling to the sea floor, attaching to an object with byssal threads. Most scallop species lose this byssus as they grow and become free-swimming.​ Conservation Status There are hundreds of species of scallops; in general, they are not endangered. In fact, according to NOAA: U.S. wild-caught Atlantic sea scallop is a smart seafood choice because it is sustainably managed and responsibly harvested under U.S. regulations. Bivalves such as scallops, however, are threatened by  ocean acidification, which affects the ability of these organisms to build strong shells. Species Scallops are marine  bivalve  mollusks of the family Pectinidae; the best-known are species  of the  genus  Pecten. The family Pectinidae includes about 50 genera and subgenera and more than 400 species which live around the world. Scallop species vary in their habitats; while some prefer coastal areas and intertidal zones, others live deep under the ocean. All scallops are bivalves, and in most species, the two valves of the shell are fan-shaped. The two valves may be ribbed or smooth or even knobbed. Scallop shells vary radically in color; some are white while others are purple, orange, red, or yellow. Scallops and Humans Scallop shells are easily recognized and have been a symbol since  ancient times. The fan-shaped shells have deep ridges, and two angular protrusions called auricles, one on either side of the shells hinge. Scallop shells range in color from drab and gray  to vivid and multihued. Scallop shells are an emblem of St. James, who was a  fisherman in Galilea before becoming an apostle. James is said to be buried at Santiago de Compostela in Spain, which became a shrine and pilgrimage site. Scallop shells mark the road to Santiago, and pilgrims often wear or carry scallop shells. The scallop shell is also the corporate symbol for the petrochemical giant Royal Dutch Shell. Scallops are also a major commercially harvested seafood; certain species (Placopecten magellanicus, Aequipecten irradians, and A. opercularis) are highly prized. The large adductor muscle is the part of the scallop that is typically cooked and eaten. Scallops are harvested around the world; the most productive scallop grounds are off the coast of Massachusetts and in the Bay of Fundy off the coast of Canada. Romona Robbins Photography/Getty Images   Sources Foster, Kelli. Whats the Difference Between Bay Scallops and Sea Scallops? TheKitchn.com.  13 May 2016.  Goff, Stanley. What Do Sea Scallops Eat Where Do They Live?​  Ã¢â‚¬â€¹Sciencing.com.  Ã¢â‚¬â€¹25 April 2017.Madrigal, Alexis C. Did You Know Scallops Have *Eyes*? Me Neither, but Look. TheAtlantic.com. 28 March 2013.Ramos, Juan. What Exactly Are Scallops? ScienceTrends.com. 17 Jan. 2018.

A Critical Evaluation of a Screening Event (The Kurdish Winter) Essay

A Critical Evaluation of a Screening Event (The Kurdish Winter) - Essay Example Nonetheless, this paper presents a critical evaluation of a screening event involving the documentary â€Å"The Kurdish Winter.† The documentary â€Å"The Kurdish Winter,† bears the story of the Kurdish people. These are considered to be the largest nation in the world, but without a state of their own (Gendercide n.d). Documentaries are one of the major ways of revisiting genocide and its effects, in an effort to prevent such future occurrences (Wilson & Crowder-Taraborrelli 2012). In the 1980’s, and years before, the Kurdish people suffered continuous genocides in Iraq. This therefore, had a negative impact on their life and heritage (Ibrahim & Gurbey 2000). Nonetheless, this documentary aims at collecting evidence from the Kurds that are alive today, and lived in the 1970’s. This will eventually help in shaping the truth about the Kurdish genocide, as witnesses testify in the documentary. Although the Kurdish people during that period suffered a lot of atrocities, the media publicised the events that unfolded, but the world closed its eyes and ears to the situation and cries of the Kur dish people. Being the director of the documentary, I had the responsibility of ensuring that the filming process was successful, and making sure that the content of the documentary was on point and convincing. For filming, I travelled to various parts of the world, identifying the key people that I would include in the documentary. The conditions for these people was that they had to be Kurdish, and must have been alive when the genocides occurred, as well as been affected in one way or another by the detrimental events that made up the genocide. I gained diverse insights into the situation of the Kurdish people from different parties, including political prisoners, politicians, leaders of different calibre, as well as the common Kurdish people that were victims of the genocide. As the director of the documentary, I shared the pains of these people, since I was