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Human Behavior

Views Active-choice: An enrollment alternative worth considering – Employee Benefit Adviser (registration)

Advisers to retirement plans are familiar with the biggest challenge facing their retirement plan sponsor clients: How to motivate employees to participate?

Various enrollment methods have been developed to encourage participation and consider basic human behavior, but each carries tradeoffs. Standard enrollment and auto-enrollment have been widely adopted, but active-choice enrollment has been an area somewhat unexplored.

A traditional enrollment process allows participants to choose to participate in, or opt-in to, a retirement plan.

This method requires employee initiation. Unfortunately, when this decision is left entirely up to employees, some basic behaviors take over. These include loss aversion, present bias and procrastination.

Loss aversion happens when employees weigh out the costs and benefits of setting aside part of their paycheck every month to save for retirement. The perceived losses receive undue importance when compared with the expected benefits. In simpler terms, giving up income today is a bigger deal than receiving income in the future.

Present bias is this same idea of unequal importance of costs and benefits, but compounded by time. The costs are borne immediately and the benefits are not realized until much further in to the future. The delay in benefit when it comes to retirement savings is decades long. Employees may not be able to extrapolate their decisions this far into the future.

Procrastination will also come into play, causing decisions about saving for retirement to be put off until employees feel they make enough money to save, know enough about how much to save, or have enough time to make these crucial savings decisions.

These psychological forces are hard for all humans to overcome and the default of not enrolling in the retirement savings plan is, to many potential participants, the path of least resistance.

One solution to the motivation conundrum is the auto-enrollment process. This process allows a plan sponsor to automatically enroll eligible employees into the plan unless an employee affirmatively elects otherwise.

When employees do not have to act to be enrolled, participation can increase by up to 50% as compared to traditional enrollment, while giving employees the flexibility to not participate if they decide the retirement plan or automatic savings rate is not right for them.

However, many default savings rates prove to be sticky; participants consider them an implicit recommendation and are reluctant to stray from it. Default savings rates are most commonly set at 2-4%, which is not the optimal long-term savings rate for most participants. Loss aversion and present bias appear when participants weigh the costs and benefits of increasing savings above the default rate. Conversely, these same default savings rates may not be affordable for certain participants.

In addition to the psychological struggles that auto-enrollment presents, certain plan sponsors feel that auto-enrolling participants is too paternalistic. The politics of a plan sponsor taking the choice out of participation can be tricky or impossible to navigate.

A different pathActive-choice enrollment requires employees to actively make the decision to participate, or not, in their retirement plan.

This differs from the other enrollment processes, which allow participants to default into a state of participation. By mandating employees to decide, plan sponsors may better serve employees who might struggle with procrastination, and can offer more tailored engagement than an auto-enroll process may provide.

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The retirement, technology, voluntary, wellness and overall winners are taking charge of the future of benefits.

Usually, the active choice is presented to employees along with other new-hire materials that must be completed or returned within a specified period. Employees decide between two options: Enroll or Waive; Yes, I want to participate or No, I do not want to participate, etc. If participants choose to participate, they are prompted to make contribution rate decisions immediately or in the near future.

By making the decision time-bound, employees are more likely to make an instant decision regarding their savings. This can result in a positive or negative effect. On the one hand, it starts employee saving as early as possible, maximizing compounding. Additionally, employees enrolled through active choice have been found to immediately choose a savings rate that took traditional enrolled participants more than two years to reach through contribution increases.

But the immediate decision can place unprepared employees in a situation where they are not informed enough to make the proper savings rate decision for their specific circumstance. Financially illiterate employees may be better served through a carefully chosen default savings rate and auto-enrollment.

Enhanced active voiceActive choice can be elaborated upon to include language that invokes an emotional response from potential participants. Known as enhanced active choice, this process adds descriptive language to the decision. Instead of choice between Enroll, or Waive, the participant must choose between such statements as Yes, I want to plan for a successful retirement by saving and investing money today. and No, I do not want to save today and understand that this choice may negatively affect my retirement.

This style of active choice taps into human instinct, highlighting the possible positive and negative effects of this choice in a visceral way. Plan sponsors who adopt enhanced active choice should be sure to not use language that implies any guarantee of success or failure.

The principles behind active-choice enrollment relieve many pain points that exist in other enrollment methods. Active-choice enrollment increases plan participation. By allowing employees to choose, plans will have more engaged, empowered participants. By requiring employees to choose for themselves, and making it easy to enroll, plans can help participants sidestep behavioral roadblocks and end up on track for a more successful retirement.

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Views Active-choice: An enrollment alternative worth considering - Employee Benefit Adviser (registration)

Anatomy

Anatomy and physiology of ageing 8: the reproductive system – Nursing Times

Abstract

In men and in women, middle age brings about changes to the reproductive system that eventually lead to infertility although men stay fertile for longer. These changes are partly due to dramatic fluctuations in the production of sex hormones such as oestrogen, progesterone and testosterone. In the perimenopause and menopause, most women experience physical and psychological symptoms that can be extremely disruptive. Although less dramatic, the changes prompted in men by the andropause can lead to erectile dysfunction and a loss of libido. Article 8 in our series on the effects of ageing explores the changes occurring in the female and male reproductive systems, and the role of hormone replacement therapy.

Citation: Knight J, Nigam Y (2017) Anatomy and physiology of ageing 8: the reproductive system. Nursing Times [online]; 113: 9, 44-47.

Authors:John Knight is senior lecturer in biomedical science; Yamni Nigam is associate professor in biomedical science; both at the College of Human Health and Science, Swansea University.

Throughout the fertile years, the male and female reproductive organs (testes and ovaries) produce gametes (sperm and ova) which, through sexual intercourse, may fuse to form an embryo. The production of gametes is orchestrated by a cascade of hormones and growth factors, many of which have complex effects on the body. In middle and old age, the reproductive systems undergo significant changes: a gradual decline in fertility and fluctuations in the production of sex hormones, the latter triggering anatomical and physiological changes in distant organs and tissues. This article examines these changes and explores some of the treatments available to alleviate their consequences.

As women age, there is a progressive decline in the number of ovarian follicles, which gains speed in the fourth decade of life; the number and quality of ova diminish and oestrogen production declines, which in most women triggers the menopause around the age of 51. The speed of ovarian ageing is determined primarily by genetics, although oxidative stress, apoptosis and environmental factors also play a role. Premature ovarian failure (POF) can be triggered by surgery, radio- or chemotherapy, autoimmune reactions, and infections caused, for example, by the mumps virus and cytomegalovirus (Amanvermez and Tosun, 2016; Broekmans et al, 2009).

In women, the first episode of menstrual bleeding (menarche) marks the onset of puberty. The prime child-bearing years correspond to the period between menarche and perimenopause (Dutton and Rymer, 2015). Before the menopause, when menstruation ceases and women become infertile, the hormones that drive the menstrual cycle start to fluctuate. This perimenopausal phase, which can last 2-10 years, is often accompanied by increasing irregularity of the menstrual cycle. Although perimenopausal women are still fertile, pregnancy becomes more difficult.

The symptoms of the perimenopause are similar to those of the menopause. Some women experience few symptoms, but for others the perimenopause can be extremely challenging, since fluctuating hormone levels can cause physical and psychological symptoms such as hot flushes, night sweats, mood swings and feelings of sadness (Wagner, 2016).

The irregular menstrual cycles characteristic of the perimenopause eventually cease completely. Strictly speaking, the menopause is the cessation of periods for 12 months (Goodman et al, 2011). In most of the world it occurs in the early 50s, with some variation. Around 95% of women go through the menopause between 44 and 56 years, the average age being 50.7 (Freeman, 2015). Many factors that precipitate POF can also trigger early menopause (Dutton and Rymer, 2015). Since no more ova are being released, it is impossible for postmenopausal women to become pregnant without fertility treatment.

Follicle-stimulating hormone (FSH), secreted by the pituitary gland, drives the menstrual cycle. It stimulates the development of ovarian follicles, and as these enlarge they secrete the female sex hormone oestrogen. In perimenopausal and menopausal women, FSH levels remain high or are higher than in premenopausal women but FSH is unable to stimulate follicular development. Eventually, follicular activity ceases altogether, leading to a rapid decline in oestrogen secretion.

Similarly, luteinising hormone, which triggers ovulation, is secreted at normal or higher than normal levels (Burger et al, 2007), but without mature follicles, no ova can be released so menopausal women become infertile.

As during puberty and pregnancy, the transition to and through menopause is associated with dramatic fluctuations in the sex hormones oestrogen and progesterone. Symptoms are diverse and sometimes unique to the individual, but there are four that most women experience to varying degrees: hot flushes, vaginal dryness, mood changes and sleep disturbances (Santoro et al, 2015).

Hot flushesAround three in four women experience hot flushes in the perimenopause and menopause. They are described as a rapid heat increase, particularly in the face, neck and chest, often with sweating and palpitations. The length of time women experience them varies between 4 and 10 years; most experience them every day and a third have more than 10 a day (Committee on Practice Bulletins Gynecology, 2014).

Hot flushes appear to be related to increased levels of FSH and decreased levels of oestrogen. Decreased oestrogen seems to affect serotonin levels in the hypothalamus, causing fluctuations in the set point of the thermoregulatory centre; this leads to vasodilation and increased blood flow in the skin (Santoro et al, 2015).

Vaginal atrophy and drynessThe menopause is associated with a loss of elasticity and shrinkage in the length of the vagina. The epithelial lining becomes thinner and infiltrated by neutrophils, while the production of natural lubricating secretions slows down, increasing the risk of tears, bleeding and infection. In this changing environment, faecally derived species of bacteria may become dominant over the lactobacilli populations typically seen in premenopausal women. Lactobacilli produce lactic acid, so their depletion reduces the acidity of the vagina, resulting in a neutral or alkali pH that can encourage the growth of Candida albicans and other micro-organisms (Milsom, 2006). These vaginal changes can make sexual intercourse uncomfortable or painful (dyspareunia), and can reduce libido; 27-60% of menopausal women are affected by vaginal dryness and dyspareunia.

Menopausal woman are also at risk of urinary incontinence: the bladder and urethra are sensitive to oestrogen (both have oestrogen receptors), so it seems likely that decreased oestrogen levels contribute to urethral shrinkage and urinary incontinence (Santoro et al, 2015). Breast tissue is also oestrogen sensitive and women often notice a loss of supporting connective tissue in the breasts (Chahal and Drake, 2007); age-related skin thinning and loss of skin elasticity can exacerbate this.

Mood changes and depressionFluctuating concentrations of FSH, oestrogen and progesterone are often associated with mood changes. Despite inconsistencies in the literature, it is generally accepted that normal fluctuations in hormone levels whether in the premenstrual stage of the menstrual cycle, during pregnancy or in the perimenopausal years can be associated with negative psychological symptoms. The perimenopause is also associated with poor memory and concentration, problems with other people and low self-esteem. Other psychological symptoms are anxiety, irritability and rapid mood swings, but not necessarily low mood (Freeman, 2015; Cohen et al, 2005).

A previous history of depression or premenstrual syndrome is associated with an increased risk of clinical depression in the perimenopause and menopause. Women may also have pre-existing pathologies such as metabolic syndrome, osteoporosis or cardiovascular disease that are associated with depression and depressive symptoms. It is unclear if there is an increased risk of clinical depression in the perimenopause (Freeman, 2015), so clinical depression should not be regarded as a normal feature of either perimenopause or menopause.

Sleep disturbancesSleep problems become more common with age. In women, the risk of insomnia is 41% greater than in men. Around 25% of women aged 50-64 report sleep problems rising to 50% in postmenopausal women (Santoro et al, 2015; Ameratunga et al, 2012). Many reasons for sleep disturbances during the menopause have been suggested: hot flushes and night sweats, anxiety, depressive symptoms and sexual dysfunction (Jehan et al, 2015). Not all studies agree that the menopause is directly linked to sleep problems. A recent study showed no statistically significant differences in sleep quality between premenopausal and menopausal women (Tao et al, 2016).

Decreased bone healthReduced oestrogen levels can lead to a decrease in bone density and increased risk of fractures. Menopausal women lose up to 15% of their bone mass (Riggs and Melton, 1986). Significant losses in the spongy bone of the vertebrae contribute to the curvature of the spine often seen in postmenopausal women with osteoporosis.

Shrinkage in the length of the Fallopian tubes, loss of ciliated epithelia and loss of mucosa have been reported (Hwang and Song, 2004). Since the Fallopian tubes are the site of fertilisation and are responsible for transporting the fertilised ovum to the uterus, these changes contribute to the age-related reduction in fertility, and may explain why older women are at increased risk of ectopic pregnancy (Bouyer et al, 2003).

The endometrium is the inner mucosal layer of the uterus that is shed during menstruation and then rebuilt under the influence of oestrogens. When oestrogen production decreases, this rebuilding is gradually compromised, until it becomes impossible and menstruation ceases.

The myometrium, the middle layer of the uterus, is composed almost entirely of smooth muscle fibres. In childbirth its contractions push the baby through the birth canal. In the menopause, it begins to shrink. Oestrogen helps to maintain the myometrium, so its reduction is thought to contribute to the loss of smooth muscle fibres although the mechanisms of myometrial atrophy remain unclear (Mwampagatwa et al, 2013).

The perimetrium the thin outer serous layer of the uterus appears to change little with age.

The cervix (neck of the womb) consists of a smooth muscle layer overlaid by a mucus-producing cervical epithelium. Cervical mucus is essential to female fertility, aiding sperm to pass through the cervical aperture and enhancing sperm motility and maturation. The menopause is associated with a reduction in cervical secretions which contributes to reducing fertility (Gorodeski, 2000).

Most men show an age-related reduction in testicular mass (Chahal and Drake, 2007) with an associated reduction in testosterone and sperm production. Since spermatozoa are produced in huge numbers, most men remain fertile until their 80s and 90s, although erectile dysfunction (ED) may be a problem. The sperm ducts, which carry sperm from the testes during ejaculation, gradually become less elastic because of an accumulation of collagen (sclerosis).

The secretions from the seminal vesicles and prostate gland, which form the semen in which sperm swim, decrease with age, so the volume of ejaculate is reduced. Due to the parallel decrease in sperm numbers, sperm concentration remains fairly constant, which helps maintain male fertility. Secretions from the prostate contain antibacterial factors, so their decrease may increase the risk of urinary tract infection.

A common age-related problem is benign prostatic hypertrophy (BPH), a gradual, non-malignant increase in the size of the prostate contributing to age-related micturition difficulties. BPH may cause symptoms that are similar to those of prostate cancer, so investigations may be needed to rule out malignancy.

Although most men do not experience the profound physiological and psychological changes that many women go through, they do undergo hormonal changes indicative of the so-called andropause often inaccurately referred to as the male menopause (Chahal and Drake, 2007). In their 30s, men start to experience a decline in serum testosterone levels of around 1-1.4% per year. This is thought to be due to a reduction in the number of interstitial cells that synthesise testosterone and a reduced availability of free testosterone in the blood (Matsumoto, 2002).

Compared with the literature on the perimenopause and menopause, there is little research on the andropause. Reduced testosterone levels are associated with various physiological and psychological changes:

Reduced testosterone levels can cause the penis to shrink, both in its flaccid and erect states. However, in most men, the earliest symptom of the andropause is a loss of libido, often accompanied with problems achieving an erection and maintaining it to the point of orgasm. The number of erections decreases and weaker erections become more common. Men who smoke or have pre-existing pathologies such as diabetes, blood pressure problems or atherosclerotic occlusion are at higher risk of ED. Today, ED can be treated by techniques such as counselling and medications such as sildenafil (Viagra) (Bansal, 2013).

Some effects of the perimenopause and menopause can be alleviated by hormone replacement therapy (HRT) usually either oestrogen alone or oestrogen and progesterone given orally or transdermally. HRT has been reported to be effective in:

Treating osteoporosis and reducing the risk of bone fractures;

HRT carries certain risks and there is growing evidence that HRT (particularly oestrogen plus progesterone) increases the risk of breast cancer (Sood et al, 2014). Evidence of other risks of HRT is conflicting.

There has been much research into the benefits and risks of HRT in women, but HRT in men going through the andropause has received less attention. Recent research has shown that testosterone replacement therapy (TRT) can have positive effects (Sofiajidpour et al, 2015).

However, increasing the level of circulating testosterone is associated with a variety of side-effects and risks including oily skin, acne, increased haematocrit count, gynaecomastia (breast tissue development) and increased risk of prostate cancer. The effect of TRT on cardiovascular health remains unclear (Nandy et al, 2008).

The ageing of the reproductive tracts, and the changes and symptoms brought about by the menopause and andropause, are inevitable. However, certain lifestyle changes may delay, or reduce the effects of the menopause or andropause although some of the evidence is contradictory.

Smoking is the main modifiable risk factor. The inhalation of cigarette smoke increases the risk of infertility and early menopause in women, and the same risks exist for women exposed to second-hand smoking (Hyland et al, 2016). In men, smoking increases the risk of ED and lowers sperm count and quality (Sengupta and Nwagha, 2014).

A low body mass index (BMI) and being undernourished are both associated with an earlier menopausal onset. The effect of an increased BMI is less clear: some studies show that it is linked with a later menopausal onset (Akahoshi et al, 2002), others suggest no influence (Hardy et al 2008). A high BMI and obesity seem to be associated with more severe hot flushes and other perimenopausal symptoms (Saccomani et al, 2017). In men, a high BMI is associated with lower circulating testosterone levels, which can exacerbate the effects of the andropause (Bansal, 2013).

Akahoshi M et al (2002) The effects of body mass index on age at menopause. International Journal of Obesity and Related Metabolic Disorders; 26: 7, 961-968.

Amanvermez R, Tosun M (2016) An update on ovarian aging and ovarian reserve tests. International Journal of Fertility and Sterility; 9: 4, 411-415.

Ameratunga D et al (2012) Sleep disturbance in menopause. Internal Medicine Journal; 42: 7, 742-747.

Bansal VP (2013) Andropause, a clinical entity. Journal of Universal College of Medical Sciences; 1: 2, 54-68.

Bouyer J et al (2003) Risk factors for ectopic pregnancy: a comprehensive analysis based on a large case-control, population-based study in France. American Journal of Epidemiology; 157: 3, 185-194.

Broekmans FJ et al (2009) Ovarian aging: mechanisms and clinical consequences. Endocrine Reviews; 30: 5, 465-493.

Burger HG et al (2007) A review of hormonal changes during the menopausal transition: focus on findings from the Melbourne Womens Midlife Health Project. Human Reproduction Update; 13: 6, 559-565.

Chahal HS, Drake WM (2007) The endocrine system and ageing. Journal of Pathology; 211: 2, 173-180.

Cohen LS et al (2005) Diagnosis and management of mood disorders during the menopausal transition. American Journal of Medicine. 118(Suppl 12B), 93-97.

Committee on Practice Bulletins Gynecology (2014) Management of menopausal symptoms. Obstetrics and Gynecology; 123: 1, 202-216.

Dutton PJ, Rymer JM (2015) Physiology of the menstrual cycle and changes in the perimenopause. In: Panay N et al (eds) Managing the Menopause: 21st Century Solutions. Cambridge: Cambridge University Press.

Freeman EW (2015) Depression in the menopause transition: risks in the changing hormone milieu as observed in the general population. Womens Midlife Health; 1: 2, 1-11.

Goodman NF et al (2011) American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for the diagnosis and treatment of menopause. Endocrine Practice; 17(Suppl6): 1-25.

Gorodeski GI (2000) Effects of menopause and estrogen on cervical epithelial permeability. Journal of Clinical Endocrinology and Metabolism; 85: 7, 2584-2595.

Hardy R et al (2008) Body mass index trajectories and age at menopause in a British birth cohort. Maturitas; 59: 4, 304-314.

Hwang TS, Song J (2004) Morphometrical changes of the human uterine tubes according to aging and menstrual cycle. Annals of Anatomy; 186: 3, 263-269.

Hyland A et al (2016) Associations between lifetime tobacco exposure with infertility and age at natural menopause: the Womens Health Initiative Observational Study. Tobacco Control; 25: 6, 706-714.

Jakiel G et al (2015) Andropause state of the art 2015 and review of selected aspects. Menopause Review; 14: 1, 1-6.

Jehan S et al (2015) Sleep disorders in postmenopausal women. Journal of Sleep Disorders and Therapy; 4: 5, 1000212.

Matsumoto AM (2002) Andropause: clinical implications of the decline in serum testosterone levels with aging in men. Journals of Gerontology. Series A, Biological Sciences and Medical Sciences; 57: 2, M76-99.

Milsom I (2006) Menopause-related symptoms and their treatment. In: Erkkola R (ed) European Practice in Gynaecology and Obstetrics. No 9. The Menopause. Edinburgh: Elsevier.

Mwampagatwa IH et al (2013) Morpho-physiological features associated with menopause: recent knowledge and areas for future work. Tanzania Journal of Health Research; 15: 2, 93-101.

Nandy PR (2008) Male andropause: a myth or reality. Medical Journal Armed Forces India; 64: 3, 244-249.

National Institute for Health and Care Excellence (2017) Benefits and risks of hormone replacement therapy.

Riggs BL, Melton LJ (1986) Involutional osteoporosis. New England Journal of Medicine; 314: 26, 1676-1686.

Saccomani S et al (2017) Does obesity increase the risk of hot flashes among midlife women? A population-based study. Menopause [Epub].

Santoro et al (2015) Menopausal symptoms and their management. Endocrinology and Metabolisn Clinics of North America; 44: 3, 497-515.

Sengupta P, Nwagha U (2014) The aging sperm: is the male reproductive capacity ticking to biological extinction? Journal of Basic and Clinical Reproductive Sciences; 3: 1, 1-7.

Sofimajidpour H et al (2015) The effect of testosterone on men with andropause. Iranian Red Crescent Medical Journal; 17: 12, e19406.

Sood R et al (2014) Prescribing menopausal hormone therapy: an evidence-based approach. International Journal of Womens Health; 6: 47-57.

Tao MF et al (2016) Poor sleep in middle-aged women is not associated with menopause per se. Brazilian Journal of Medical and Biological Research; 49: 1, e4718.

Wagner D (2016) Perimenopause: The untold story. Obstetrics and Gynecology International Journal; 5: 1, 00139.

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Anatomy and physiology of ageing 8: the reproductive system - Nursing Times

Embryology

What is Embryology? – news-medical.net

Embryology is the study of development of an embryo from the stage of ovum fertilization through to the fetal stage.

The ball of dividing cells that results after fertilization is termed an embryo for eight weeks and from nine weeks after fertilization, the term used is fetus.

Once an egg is released from the ovary during ovulation, it meets with a sperm cell that was carried to it via the semen. These two gametes combine to form a zygote and this process is called fertilization. The zygote then begins to divide and becomes a blastula.

The blastula develops in one of two ways, which actually divides the whole animal kingdom in half. The blastula develops a pore at one end, called a blastopore. If that blastopore becomes the mouth of the animal, the animal is a protostome, and if it forms an anus, the animal is a deuterostome.

Protosomes are invertebrate animals such as worms, insects and molluscs while deuterostomes are vertebrates such as birds, reptiles, and humans.

The blastula continues to develop, eventually forming a structure called the gastrula. The gastrula then forms three germ cell layers, from which all of the bodys organs and tissues are eventually derived. From the innermost layer or endoderm, the digestive organs, lungs and bladder develop; the skeleton, blood vessels and muscles are derived from the middle layer or mesoderm and the outer layer or ectoderm gives rise to the nervous system, skin and hair.

Reviewed by Sally Robertson, BSc

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What is Embryology? - news-medical.net

Embryology

Dr Brian Iddon details his life as a Bolton MP in second volume of … – The Bolton News

FROM being put into stocks in Bolton to campaigning to ensure people with Downs Syndrome are not discriminated against, Dr Brian Iddon has given a detailed insight into his life as a Bolton MP in the second volume of Science & Politics: An Unlikely Mixture.

Volume One of Dr Iddons autobiography was published in 2015 in which he told of his remarkable career as a scientist and, in his recently released second part, he explains how he found himself representing Bolton South East at Westminster for three years.

Volume Two is billed as the most detailed account of a Parliamentary career written in modern times by a back-bench MP and, says Dr Iddon, has been written to help dispel the myth that MPs have an easy life.

He said: A lot of people do not know what MPs do. That is why I have produced this - we have family lives as well.

Some MPs are lazy but I did not want to be like that I wanted to go to Parliament and do something.

It was killing me, the pace I was going, I could not keep it up. It was my fault I got involved in far too many things and I went to too many meetings. I was just weighed down in the end.

I was almost 70 when I retired. I promised myself that I would go at 70. I wanted a life beyond Parliament, but my constituency members wanted me to do at least one more term, which was nice.

He added: Volume One of the autobiography is all about my chemistry career, my education and early life in the village of Tarleton. Volume Two is all about my political career and the rest of my family life.

Its is a heftier tome than first one was but there is a lot of humour in the book.

The opening chapter of the book is about Dr Iddons move to Bolton in 1972 in the Firwood Fold area, from Boothstown.

I came to Bolton because I loved the people, and the service in the shops was exceptional. People talked to you in the shops, he said.

Thats what brought me to Bolton, the friendliness of the people.

Dr Iddon writes about how he became involved in community politics after he disagreed with changes in his neighbourhood and started Tonge Moor Residents Association.

He said: I was a member of the Labour Party when I came here and joined Tonge Ward Labour Club.

My family has always been Labour and my family has always been immersed in the community.

He soon became vice-chairman and chairman of the local constituency party and found himself standing in local elections after the candidate who had been selected forgot to sign important paperwork and had gone on a pilgrimage to Lourdes.

But it was not until 1977 that he was elected councillor for Church, East and North Ward, which until then had been strongly Conservative.

I won accidentally, third time lucky, he said.

During his council years he started Bolton Bond Board, which celebrates its 25th anniversary next year, and Careline, which is now run by Bolton at Home. The first public sector neighbourhood dispute service, which he proposed be set up in Bolton, has been extended.

Dr Iddon and his colleagues would help out in other ways.

He said: I dressed up as Biggles and we did all kinds of things to raise money for charity, usually Mencap.

There would be a flan a councillor day. We built some stocks or borrowed some and put them in the precinct and gave people custard pies.

They had to pay a fortune for shoving one in our face but some people were nasty and banged them in our faces. We produced ducking stools for a duck a councillor day we did all this stuff in the 70s.

Dr Iddon said: I built my entire political career on what I did in Bolton but I was never seeking a Parliamentary seat.

Councillors, party members and members of the public kept asking me to stand for Parliament. I had been asked why I wouldnt stand 1,000 times. In the end I thought where am I going at Salford University?

It was a big decision but I took it. I wouldnt have done it in a marginal seat, because I was loving what I was doing at the time and it was a big change in direction.

He was elected to the safe Labour seat with a 21,311 majority in 1997 after the previous sitting Labour MP, David Young was deselected by the constituency.

As MP, Dr Iddon enlisted the help of John Prescott to allow Fred Dibnah to operate his house as a museum - producing smoke legally.

He also enhanced protection for tenants, who would find themselves homeless because the landlord had defaulted on mortgage payments.

Dr Iddon said: In Westminster I got three Acts of Parliament through.

I am proud of my case work what we did for people like putting the Womens Land Army on the map, getting Fred Dibnah his licence, even if he was a Tory all his life

The most important piece of work I was involved with was The Human Fertilisation and Embryology Act.

We realised that the technology was way ahead of the legislation.

Practitioners were doing things that hadnt been legalised. They were not illegal, but some people considered they were immoral. It was ethics versus science and we had to put this right. It was one of the most controversial bills ever considered during my 13 years in Parliament.

Dr Iddon also helped put an end to people with Downs Syndrome being denied medical treatment and the European Parliament from getting rid of MRI scanners the only European regulation or directive that I have known to be stopped and it was rejigged because of us, said Dr Iddon.

He said: The best part of the job was being able to open doors for people.

I miss the excitement. Parliament is an exciting place there were no dull days.

I miss being able to help people. Thats the reason I went down in the first place and boy did we help people thousands of them.

I could write another book about that but I cant, I am sworn to secrecy.

I feel immensely privileged to have served in Parliament.

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Dr Brian Iddon details his life as a Bolton MP in second volume of ... - The Bolton News

Genetics

Hospital to boost genetic testing for newborn babies – Belfast Telegraph

Hospital to boost genetic testing for newborn babies

BelfastTelegraph.co.uk

One of the UK's largest women's hospitals is to increase its ability to genetically test newborn babies 12-fold.

http://www.belfasttelegraph.co.uk/news/northern-ireland/hospital-to-boost-genetic-testing-for-newborn-babies-36079324.html

http://www.belfasttelegraph.co.uk/news/northern-ireland/article36079323.ece/c3338/AUTOCROP/h342/PANews%20BT_P-013b5e7c-4e66-4b0a-b8d6-04b3c11abd37_I1.jpg

One of the UK's largest women's hospitals is to increase its ability to genetically test newborn babies 12-fold.

Liverpool Women's NHS Foundation Trust will be able to screen all infants for inherited conditions or illnesses and plan for early treatment as part of a major new IT project.

It will also contribute to a major population health programme in Liverpool analysing genetic information by location, identifying and enabling work to prevent localised health issues.

IT firm Novosco will introduce the computing system.

Novosco managing director Patrick McAliskey said: "We are delighted to secure this contract which will enable the trust to take genetic testing to the next level and play an important role in the identification and prevention of conditions and illnesses in new-born babies and the wider population."

This role of genetics in healthcare is one of the most rapidly expanding areas of development for Liverpool Women's.

It provides a regional clinical genetics service based at Alder Hey Hospital, covering a population of around 2.8 million people from across Merseyside, Cheshire and the Isle of Man, chief executive Kathryn Thomson posted on the trust's website.

She added: "To discover that you or any child you have or plan to have may be at risk of a genetic disorder which could cause disability or a rare condition is traumatic.

"People are sometimes shocked and anxious and wonder what the future might hold.

"They need as much information and support as possible to help them cope.

"That is why the often unsung work of our clinical genetics team is so important, providing diagnosis and supporting families when they need it most."

Liverpool Women's NHS Foundation Trust specialises in the health of women and their babies - both within the hospital and in the community. It is one of only two such specialist trusts in the UK - and the largest women's hospital of its kind.

Novosco is an IT infrastructure and managed cloud computing company and employs over 150 people. It has its headquarters in Belfast, with offices in Manchester, Dublin, and Cork.

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Hospital to boost genetic testing for newborn babies - Belfast Telegraph

Genetics

Genetics put some older women at higher risk than men for Alzheimer’s – USC News

White women whose genetic makeup puts them at higher risk for Alzheimers disease are more likely than white men to develop the disease during a critical 10-year span in their lives, according to a study headed by Keck School of Medicine of USC researchers.

The findings from one of the worlds largest big-data studies on Alzheimers counter long-held beliefs about who is at greatest risk for the disease and when, suggesting new avenues for clinical trials.

Study results show genetically vulnerable 55- to 85-year-old white men and women have the same odds of developing the memory-erasing disease. One exception: From their mid-60s to mid-70s, these women still face significantly higher risk. That may provide clues to disease causes and potential interventions among these women.

Our discovery is important because it highlights how clinical trials could be weighted toward women a susceptible part of the population to help scientists more rapidly identify effective drug interventions to slow or cure Alzheimers, said Arthur Toga, director of the USC Stevens Neuroimaging and Informatics Institute at the Keck School of Medicine among the nations leaders in innovative scientific discovery.

The study was published Aug. 28 in the Journal of the American Medical Association Neurology. It included data from 57,979 North Americans and Europeans in the Global Alzheimers Association Interactive Network (GAAIN). This big-data project provides scientists around the world with shared data and sophisticated analysis tools to address a disease that makes up about 65 percent of the 47 million cases of dementia worldwide.

The results contradict a seminal 20-year-old study that found women with one copy of ApoE4, a gene variant linked to Alzheimers, were diagnosed with the disease 50 percent more often than men with the same genetic profile.

The findings presented in the USC-led study expand the number of participant data by ninefold and indicate the critical decade falls between 65 and 75, more than 10 years after the start of menopause. Previous studies in animals and humans have reported a relationship between ApoE4, menopause and cognitive decline.

So much work has been dependent on one 1997 finding, but with tools like GAAIN, we now have the ability to reinvestigate with increased statistical power, Toga said.

The new findings are significant because almost two-thirds of the more than 5 million Americans now with Alzheimers disease today are women.

The new findings are significant because almost two-thirds of the more than 5 million Americans now living with Alzheimers disease are women, according to the Alzheimers Association.

Many attribute the imbalance in disease risk to the fact that women, on average, live longer than men. However, a growing body of evidence suggests other reasons also contribute to the difference. For instance, men have higher rates of heart disease and stroke. So, men who live longer may be healthier than women of the same age and may face less risk of developing Alzheimers, according to the USC-led study.

In the future, doctors who want to prevent Alzheimers may intervene at different ages for men and women, said Judy Pa, co-author of the study and an assistant professor of neurology at the USC Stevens Neuroimaging and Informatics Institute.

Menopause and plummeting estrogen levels, which on average begins at 51, may account for the difference, Pa said. However, scientists still dont know what is responsible. Researchers need to study women 10, 15 or even 20 years before their most vulnerable period to see if there are any detectable signals to suggest increased risk for Alzheimers in 15 years.

Only some women are at increased risk of developing Alzheimers in their mid-60s to mid-70s compared to men. To find out, women could have their DNA analyzed. However, Pa cautions that genetic testing for the ApoE4 variant is no crystal ball.

There is controversy in terms of whether people should know their ApoE status because it is just a risk factor, Pa said. It doesnt mean youre going to get Alzheimers disease. Even if you carry two copies of ApoE4, your chances are greatly increased, but you could still live a long life and never have symptoms.

Even if some women discover they are at heightened risk, they can improve their odds by making life changes.

Get more exercise. Work out your mind, especially in old age.

Judy Pa

Get more exercise. Work out your mind, especially in old age, Pa said. Pick up hobbies that are cognitively or physically challenging. Reduce processed sugar intake because its linked to obesity, which is associated with many chronic diseases.

Alzheimers disease is the fifth-leading cause of death for Americans 65 and older, but it may one day outpace the nations top two killers heart disease and cancer. Alzheimers-related deaths increased by nearly 39 percent between 2000 and 2010 while heart disease-related deaths declined 31 percent and cancer deaths fell 32 percent, according to the Centers for Disease Control and Prevention.

Because Alzheimers disease has a huge impact on lifelong health, USC has more than 70 researchers dedicated to the prevention, treatment and potential cure of the memory-erasing disease. Big data projects like this require experts across disciplines computer science, biology, pathophysiology, imaging and genetics to coordinate.

For this study, the researchers examined data from 27 different studies that assessed participants ApoE gene variation, as well as characteristics such as sex, race, ethnicity, diagnosis (normal, mild cognitive impairment or Alzheimers disease) and age at diagnosis.

The records of nearly 58,000 people were scrutinized. Meta-analyses were performed on 31,340 whites who received clinical diagnoses sometime between ages 55 and 85.

The proportion of minorities was so small that analysts could not draw statistically significant conclusions about their disease risk. Because of this, the study focused on whites only.

Most of the archives around the world have insufficient numbers of underrepresented groups, Toga said. One of the take-home messages from our study is people of all races and ethnicities need to be involved in Alzheimers clinical trials because this disease is a problem that affects all of us.

The current findings need to be confirmed in more diverse study populations.

USC is working to build more diverse population studies related to Alzheimers. Established in 1984, the Alzheimer Disease Research Center at the Keck School of Medicine reaches out to communities in the greater Los Angeles area to educate the citys diverse population about Alzheimers and the clinical trials they might be interested in joining. Previous studies, for example, have focused on Latinos.

Historically, women have not been adequately represented in clinical trials, especially in studies on heart disease. Women need to be represented equally to men or even overrepresented, Pa said.

The bottom line is women are not little men, Pa said. A lot more research needs to target women because gender-specific variations can be so subtle that scientists often miss them when they control for gender or use models to rule out gender differences. Most research today is ignoring a big part of the equation.

The study was made possible because of lead author Scott Neu, a leader in the development of a federated approach to analyzing metadata and assistant professor of research at the Laboratory of Neuro Imaging at the Keck School of Medicine.

GAAIN the free resource we created in conjunction with the Alzheimers Association allows anyone to explore data sets around the world and conduct preliminary analyses to test scientific hypotheses, Neu said. Our goal is to connect scientists with those who have collected data to create new collaborations to further research and understanding of Alzheimers disease.

Analysts excluded people with a history of stroke, cerebrovascular disease, abnormal proteins that contribute to Parkinsons disease and dementia, gene mutations leading to higher levels of toxic amyloid brain plaques and any known neurological diseases.

Scientists did not adjust for known Alzheimers risk factors such as education, family history of Alzheimers or dementia because that information was not provided in all data sets. They also were unable to adjust for sex-dependent differences such as cigarette smoking, hormonal changes with age and alcohol usage.

The study was supported by the Alzheimers Association through the Global Alzheimers Association Interactive Network initiative (GAAIN-14-244631) via a $5 million grant and a portion of two National Institutes of Health grants: $12 million from Big Data to Knowledge (U54-EB020406) and $5 million from neuroimaging and genetics (P41-EB015922).

More stories about: Alzheimer's Disease, Research

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Genetics put some older women at higher risk than men for Alzheimer's - USC News

Genetics

New Genetics: The Gold Seal of Approval – Cannabis Now

Nightmare Cookies | Photos Ron Goldman via Stock Pot Images

While youve probably never encountered strains like Gorilla Grip or Nightmare Cookies, Goldman and a select group of other growers have been diligently laboring over trial gardens scanning them for anomalies and difficulties or possibly the next cannabis superstar like Northern Lights or Jack Herer.

I really like pushing the boundaries to get plants to reach their full genetic potential, he says.

Strain: Frozen Tangerines

A cannabis cultivator with overfour decades of experience, Goldmans initial farming experience began as a grower of greenhouse produce in the 1980s. More recently,his talents have been sought after by a number of marijuana seed breeders looking totest out new creations.

The same way that most manufacturers put their products through rigorous testing, says Goldman, cannabis seeds need to be tested toobefore theyre released to the world.

Because breeders are basically putting their reputations on the line every time they release a newly developed strain, testers like Goldman are absolutely essential to the process. The seed sellers that he consults for want to hear all the pros and cons of their new strains how they handle heat, synthetic versus organic fertilizers or small versus large habitats. They want a full picture of the plants inherent strengths, weaknesses and peculiarities to know whether its back to the drawing board or ready for consumer release.

Strain: Purple Frog

With every trial run, Goldman creates a detailed grow log from the time seeds germinate all the way through harvest. Being an avid photographer and a teacher of photography besides all of his very detailed scientific methodology is accompanied by close photo documentation week after week as the plants mature.

Ill document the structure of the plant and flowers. Looking at things like flower density and calyx to leaf ratio as well as yield and cannabinoid levels.

Some of Goldmans most recent work has been with Sin City Seeds, testing potential new releases such as Nightmare Cookies, a cross of White Nightmare and Platinum Girl Scout Cookies. He says its not only a beautiful plant with rich colors but at 26 percent THC, it packs a potent punch.

Strain: West Seattle

With Washington state now allowing medical and recreational cultivation, says Goldman, I can legally put together my passion for photography with my passion for growing.

The following photos were all taken from Goldmans medical cannabis test gardens and are strains we hope the public will soon have a chance to sample.

Originally published in Issue 18 of Cannabis Now. LEARN MORE

TELL US,does cannabis breeding interest you?

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New Genetics: The Gold Seal of Approval - Cannabis Now

Biochemistry

UAH welcomes Dr. Sharifa Love-Rutledge to the College of Science – UAH News (press release)

Dr. Sharifa Love-Rutledge is a new faculty member in the UAH College of Science.

Michael Mercier | UAH

Sharifa Love-Rutledge developed a keen interest in science when she and her younger brother shared a lab kit for Christmas one year. "We made borax (super bouncy) balls first, and went on to complete all the experiments in the kit, and I wanted to do more," said Love-Rutledge, an incoming faculty member at The University of Alabama in Huntsville (UAH) College of Science. She is also the first African-American woman to earn a PhD from The University of Alabama Department of Chemistry.

When Love-Rutledge entered college, she started out as a biology major, but after completing general chemistry and organic chemistry courses, she made the "switch" to chemistry.

"I was drawn to chemistry because of my love for creative problem-solving. Biochemistry was the subject that allowed me to utilize my analytical thought processes to pursue biological questions. It didn't dawn on me that chemistry was a male dominated field until graduate school. By then, it was too late because I was already hooked."

A native of Moss Point, MS, Love-Rutledge attended Moss Point High School. An Advanced Placement student in English and Mathematics, she went on to graduate from Tougaloo College (Tougaloo, MS) with a Bachelor of Science degree in Chemistry. Love-Rutledge earned a Master's degree and PhD from The University of Alabama (UA) in Chemistry and Biochemistry, respectively.

Love-Rutledge said she "felt hopeful," when she realized she would be the first African American woman to earn a PhD in chemistry from UA. "It was bittersweet because the reality of it all is that I wasn't the first African American female capable of the accomplishment but opportunities weren't afforded in the past. It allowed me to view myself as part of the culmination of the sacrifices made by those like Vivian Malone and James Hood," she added.

The student in lockstep with Love-Rutledge in the Department of Chemistry at UA was Dr. Melody Kelley, now Assistant Professor of Chemistry at Georgia State University. Love-Rutledge said she continues to find "inspiration in seeing other African American women who are persevering and making progress toward the completion of advanced degrees."

Early mentors for Love-Rutledge were her older siblings. "They poured their knowledge into me to ensure that I made wise decisions. If it wasn't for my older brother, I don't think I would've survived some of my math courses," she said. "Once I left home, I started to rely on advice from my uncle Dr. Claude McGowan, who was Director of Toxicology at Johnson & Johnson, along with professors like Dr. Candice Love-Jackson, Acting Provost and Vice President for Academic Affairs at Kentucky State University."

Additionally, Love-Rutledge was encouraged through the graduate school application process by dedicated Ronald McNair Scholars Coordinator, Demetria Hereford. And, as a graduate student, she was able to enlist the tutelage of several professors at UA. "It was also in graduate school that I was reminded of how important my parents' guidance is. Their constant support and dedication was important in forming my personal and professional abilities."

Love-Rutledge learned about UAH from Dr. Emanuel Waddell, Associate Dean of the College of Science while attending graduate school at UA. "The deciding factors for me to further my teaching and research career at UAH included the size of the student population and access to resources that I would need to be successful. I have always wanted to work at a university where students are viewed as more than numbers."

"We are excited to have Dr. Love-Rutledge join us in the chemistry department. Her research will be attractive to students and we look forward to her establishing her research laboratory in the coming months," said Dr. Emanuel Waddell, Associate Dean of the UAH College of Science.

At UAH Love-Rutledge will teach biochemistry classes. "I have a lab and I am currently working on research projects related to identifying biomarkers for Type 1 Diabetes, and studying the changes cells producing insulin undergo before disease onset." As a teacher, Love-Rutledge said she loves students' lightbulb moments the best. At UA she served as a graduate teaching assistant for the majority of her graduate career. "I love reaffirming students' passion for their chosen field of study. There is no greater joy for me than to see my students go on to be successful in their fields of choice. I have taught students who wanted to be nurses and are nurses now, and students who wanted to be doctors who are now in residency programs. I love seeing students reach their goals."

As a Ronald E. McNair Scholar, Love-Rutledge's first bona fide research project studied the enzymes that activate colon cancer drugs. The project's Principal Investigator was Dr. Randy Wadkins, Associate Professor of Chemistry and Biochemistry at The University of Mississippi. "In my graduate research, I worked on projects that helped show Chromium, (hard, brittle metal) is not an essential element for mammalian nutrition. The research findings were published in a paper that led The European Food and Safety Authority to remove Chromium from the list of elements that 'require daily intake'."

Love-Rutledge freely offers words of wisdom for young women interested in entering academic fields of specialization. "Recently Ive been exposed to the slogan, 'You cant do UAH alone'. I think it's awesome advice for young women to adapt who are interested in chemistry 'You cant do Chemistry alone'," she said. "Even when you seem alone, you never are. Find mentors to give you advice, utilize your peers on and off campus to get through the tough times. Some of my best academic advice came from taking a risk and emailing a professor who I thought was out of reach. You will be surprised at how much help you could receive if you just ask for it."

***EDITOR'S NOTE: The McNair Scholars Program is a federal program funded at 51 institutions across the United States and Puerto Rico by the U.S. Department of Education. It is designed to prepare undergraduate students for doctoral studies through involvement in research and other scholarly activities. Dr. Ronald E. McNair was the second African American to fly in space. Two years later he was selected to serve as mission specialist aboard the ill-fated U.S. Challenger space shuttle. He was killed on Jan. 28, 1986, instantly when the Challenger exploded one minute, 13 seconds after it was launched.

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UAH welcomes Dr. Sharifa Love-Rutledge to the College of Science - UAH News (press release)

Cell Biology

Research reveals how estrogen regulates gene expression | Baylor … – Baylor College of Medicine News (press release)

Binding of steroid estrogen hormones to estrogen receptor (ER) in the cell nucleus triggers the sequential recruitment different coactivators to regulate gene transcription.

Estrogen hormones regulate gene expression. They achieve this by first binding to estrogen receptor in the cell nucleus, which triggers the recruitment of different molecules called coactivators in specific order. In a study published in Molecular Cell, a team of researchers at Baylor College of Medicine, the University of Texas MD Anderson Cancer Center and the University of Texas Health Science Center at Houston shows that the sequential recruitment of coactivators is not simply adding molecules to the complex, it results in dynamic specific structural and functional changes that are necessary for effective regulation of gene expression.

Estrogens are a group of hormones that are essential for normal female sexual development and for the healthy functioning of the reproductive system. They also are involved in certain conditions, such as breast cancer. Estrogen also plays a role in male sexual function. Estrogens carry out their functions by turning genes on and off via a multi-step process. After estrogen binds to its receptor, different coactivators bind to the complex in a sequential manner.

Experimental evidence suggests that different estrogen-receptor coactivators communicate and cooperate with each other to regulate gene expression, said corresponding author Dr. Bert OMalley, chair and professor of molecular and cellular biology and Thomas C. Thompson Chair in Cell Biology at Baylor College of Medicine. However, how this communication takes place and how it guides the sequence of events that regulate gene expression was not clear.

In this study, OMalley, Dr. Wah Chiu, Distinguished Service Professor and Alvin Romansky Professor of Biochemistry and Molecular Biology at Baylor during the development of this project, and their colleagues combined cryo-electron microscopy structure analysis and biochemical techniques and showed how the recruitment of a specific coactivator CARM1 into the complex guides the subsequent steps leading to gene activation.

For the estrogen receptor complex to be able to regulate gene expression, the coactivator CARM1 needs to be added after other coactivators have been incorporated into the complex, said first author Dr. Ping Yi, assistant professor of molecular and cellular biology at Baylor. We discovered that when CARM1 is added, it changes the complex both chemically and structurally, and these changes guide subsequent steps that lead to gene activation.

We now have a better understanding of how this molecular machine works and of what role each one of the components plays. We are better prepared to understand what might have gone wrong when the machine fails, OMalley said.

Other contributors to this work include Zhao Wang, Qin Feng, Chao-Kai Chou, Grigore D. Pintilie, Hong Shen, Charles E. Foulds, Guizhen Fan, Irina Serysheva, Steven J. Ludtke, Michael F. Schmid, Mien-Chie Hung and Wah Chiu.

Support for this study was provided by the Komen Foundation (5PG12221410), the Department of Defense (R038318-I and W81XWH-15-1-0536); National institutes of Health grants (HD8818, NIDDK59820, P41GM103832 and R01GM079429); CNIHR, R21AI122418 and R01GMGM072804; CPRIT grants (RP150648 and DP150052); and a National Cancer Institute Cancer Center Support grant (P30CA125123) to the BCM Monoclonal Antibody/recombinant Protein Expression Core Facility.

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Research reveals how estrogen regulates gene expression | Baylor ... - Baylor College of Medicine News (press release)

Anatomy

Gray’s Anatomy – 9780702052309 | US Elsevier Health Bookshop

Preface

Preface Commentary: The continuing relevance of anatomy in current surgical practice and research, R Shane Tubbs

Acknowledgements

Contributors

Historical introduction: A brief history of Gray's Anatomy, Ruth Richardson

Anatomical nomenclature

Bibliography of selected titles

Section 1 - CELLS, TISSUES AND SYSTEMS

Section Editor: Caroline B Wigley

1 Basic structure and function of cells, Abraham L Kierszenbaum

2 Integrating cells into tissues, Caroline B Wigley

3 Nervous system, Helmut Kettenmann

4 Blood, lymphoid tissues and haemopoiesis, Andrew JT George

5 Functional anatomy of the musculoskeletal system, Michael A Adams

6 Smooth muscle and the cardiovascular and lymphatic systems, Jeremy PT Ward

7 Skin and its appendages, John A McGrath, Joey E Lai-Cheong

Commentaries

1.1 Fluorescence microscopy in cell biology today, Dylan M Owen

1.2 Stem cells in regenerative medicine, Jonathan M Fishman, Paolo De Coppi, Martin A Birchall

1.3 Merkel cells, Ellen A Lumpkin

1.4 Metaplasia, Jonathan MW Slack, Leonard P Griffiths, David Tosh

1.5 Electron microscopy in the twenty-first century, Roland A Fleck

1.6 The reaction of peripheral nerves to injury, Rolfe Birch

Videos

Video 1.1 - Mitosis in a cell with fluorescently-labelled chromosomes and microtubules, Jonathon Pines, Daisuke Izawa

Video 1.5.1 - Diagnostic histopathology by electron microscopy, Roland A Fleck

Video 1.5.2 - Serial block face scanning electron microscopy(SBFSEM), Roland A Fleck

Section 2 - EMBRYOGENESIS

Section Editor: Patricia Collins

8 Preimplantation development, Alison Campbell, Patricia Collins

9 Implantation and placentation, Eric Jauniaux, Graham J Burton

10 Cell populations at gastrulation, Patricia Collins

11 Embryonic induction and cell division, Patricia Collins

12 Cell populations at the start of organogenesis, Patricia Collins

13 Early embryonic circulation, Patricia Collins

14 Pre- and postnatal development, Patricia Collins, Girish Jawaheer

15 Development of the limbs, Cheryll Tickle

Commentaries

2.1 Human anatomy informatics, Jonathan BL Bard, Paul N Schofield

2.2 An evolutionary consideration of pharyngeal development, Anthony Graham, Victoria L Shone

Videos

Video 8.1 - Human in vitro fertilization and early development, Alison Campbell

Video 9.1 - Ultrasound features of the maternal placental blood flow, Eric Jauniaux

Video 14.1 - Ultrasound features of the fetus at 26 weeks, Jonathan D Spratt, Patricia Collins

Section 3 - NEUROANATOMY

Section Editor: Alan R Crossman

16 Overview of the nervous system, Alan R Crossman, Richard Tunstall

17 Development of the nervous system, Zoltn Molnr

18 Ventricular system and subarachnoid space, Jacob Bertram Springborg, Marianne Juhler

19 Vascular supply and drainage of the brain, Paul D Griffiths

20 Spinal cord: internal organization, Monty Silverdale

21 Brainstem, Duane E Haines

22 Cerebellum, Jan Voogd

23 Diencephalon, Ido Strauss, Nir Lipsman, Andres M Lozano

24 Basal ganglia, Tipu Aziz, Erlick AC Pereira

25 Cerebral hemispheres, Guilherme C Ribas

Commentary

3.1 The resting human brain and the predictive potential of the default mode network, Stefano Sandrone

Videos

Video 18.1 - Interactive 3D rotation of the subarachnoid space, Jose C Rios

Video 18.2 - Interactive 3D rotation of the ventricles and cisterns, Jose C Rios

Video 19.1 - Rotational angiography of an intracranial aneurysm, Paul D Griffiths

Section 4 - HEAD AND NECK

Section Editor: Michael Gleeson

26 Head and neck: overview and surface anatomy, Michael Gleeson, Richard Tunstall

Head and Neck

27 External skull, Sue Black

28 Intracranial region, Juan C Fernandez-Miranda

29 Neck, John C Watkinson, Michael Gleeson

30 Face and scalp, Simon Holmes

Upper Aerodigestive Tract

31 Oral cavity, Barry KB Berkovitz

32 Infratemporal and pterygopalatine fossae and temporomandibular joint, Barrie T Evans

33 Nose, nasal cavity and paranasal sinuses, Claire Hopkins

34 Pharynx, Stephen McHanwell

35 Larynx, Stephen McHanwell

36 Development of the head and neck, Gillian M Morriss-Kay

Special Senses

37 External and middle ear, Michael Gleeson

38 Inner ear, David N Furness

39 Development of the ear, Susan Standring

40 Development of the eye, Jane C Sowden

41 Orbit and accessory visual apparatus, John G Lawrenson, Ronald H Douglas

42 Eye, Ronald H Douglas, John G Lawrenson

Commentaries

4.1 Surgery of the skull base, Juan C Fernandez-Miranda

4.2 The role of three-dimensional imaging in facial anatomical assessment, Vikram Sharma, Bruce Richard

4.3 Anatomy of facial ageing, Bryan C Mendelson, Chin-Ho Wong

Videos

Video 28.1 - 3D surface rotation of the sella turcica in the horizontal plane, Michael D Luttrell

Video 28.2 - 3D surface rotation of the sella turcica in the multiaxial plane, Michael D Luttrell

Video 28.3 - 3D surface rotation of the sella turcica in the vertical plane, Michael D Luttrell

Video 30.1 - Pan-facial fractures, Simon Holmes

Video 30.2 - Postoperative cranio-orbital imaging, Simon Holmes

Video 30.3 - A comminuted zygomatic fracture (plus Le Fort I) pattern, Simon Holmes

Video 30.4 - A comminuted zygomatic fracture pattern - post reduction, Simon Holmes

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Gray's Anatomy - 9780702052309 | US Elsevier Health Bookshop