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Retinitis Pigmentosa – The Foundation Fighting Blindness

Stell Cell Research | Posted by admin
Feb 06 2019


Retinitis pigmentosa (RP) describes a group of genetic disorders that damage light-sensitive cells in the retina, leading to gradual vision loss over time as the cells die off. While the condition is classified as a rare disease, it is one of the most common inherited diseases of the retina, affecting between 1 in 3500 to 1 in 4000 Canadians.[1]RP is often referred to as an inherited retinal disease, meaning that it is passed along genetic lines and inherited from ones parents. Though it is usually diagnosed during childhood or adolescence, a minority of patients report symptoms later in life.

Specialized cells called photoreceptors are responsible for absorbing light and translating it into signals that are interpreted by the brainit is these essential cells that gradually die off as a result of RP. The cells come in two varieties: rod cells and cone cells. Rod photoreceptors are responsible for peripheral and night vision, while cone photoreceptors are responsible for central, high-acuity vision as well as detail and colour. Since it is the rod cells that are first damaged by RP, peripheral and night vision are affected during the early stages of the disease, followed by a narrowing of the visual field, often referred to as a progressive form of tunnel vision. The death of rod cells eventually affects the cone cells as well, leading to the loss of central vision and often resulting, during the later stages of the disease, in near or total blindness. The length of this process varies from individual to individual.

RP was originally considered a single disease, but after decades of researchincluding research funded by the FFBwe now know that there are several forms of RP, and that these forms involve mutations in any one of more than 64 different genes. The gene or genes affected determine the disease type and symptoms.

There are several different ways that RP can be inherited, which is usually described as the inheritance pattern. The different RP inheritance patterns include: autosomal dominant, autosomal recessive, and x-linked recessive. A genetic counsellor can talk with you about your family history and determine which of these patterns is associated with your vision loss. With this information, the genetic counsellor may be able to tell you more about how your condition will progress, and give you and your family information about the risks of vision loss for other family members. To learn more about genetic testing for RP, please consult the FFB resource Everything You Need to Know about Genetic Testing.

Typically, each person with RP only has damage in one pair of genes. Scientists have now identified more than 64 genes that can have mutations that cause RP. It is likely that mutations in more than 100 different genes will eventually be identified. Because so many RP-causing gene mutations are still unknown, there is about a 50:50 chance that genetic testing will provide a definitive result. Given your family history and the inheritance pattern of your RP, your genetic counsellor will be able to advise you about the likelihood that a genetic test will provide a definitive result.

Different genetic mutations can damage the retina or impair its function in different ways; for example, some mutations affect how the retina processes nutrients, while others damage the photoreceptors. Its important to identify the specific gene and mutation, because many treatments being developed for RP will be for particular genetic types.

Content on this page was written by Dr. Chad Andrews and Dr. Mary Sunderland, and was most recently updated on August 23, 2018. An earlier version of the content was approved by Dr. Jane Green and Dr. Bill Stell.

The most common early symptom of RP is difficultly seeing at night and in low-light conditionsthis is called nyctalopia or night blindness. The loss of peripheral vision is also a common first symptom, and is often experienced alongside nyctalopia. As RP progresses, peripheral vision slowly diminishes, resulting in a narrow field of view or tunnel vision. By age 40, many people with RP are legally blind, with a severely constricted field of vision, although many may retain the ability to read and recognize faces. Uncomfortable sensitivity to light and glare is common, as is photopsia (seeing flashes of light or shimmering). RP can also cause a loss of visual acuity (the ability to see clearly), but the onset is more variable. Some patients retain normal visual acuity, even when their vision is reduced to a small central island; others lose acuity much earlier in the course of disease. Eventually, however, most people with RP will begin to lose central vision and some will lose all light perception.

An ophthalmologist may suspect RP on the basis of a persons symptoms and the findings of a simple eye examination. Two tests are used to clarify the diagnosis:

Currently, there is only a single approved treatment for a very rare form of RP on the market in the United States: a gene therapy called Luxturna, which can halt vision loss and even restore some sight in individuals with a biallelic mutation of their RPE65 gene (manifesting as either RP or Leber congenital amaurosis). Though the number of patients with this mutation is small, the medical effectiveness of Luxturna and its materialization as a pharmaceutical product demonstrate that there is significant potential for gene therapy to treat other forms of RP in the future.

Read Our Story About The Approval of Luxturna

Clinical trials are essential to the scientific process of developing new treatments: they test the viability and safety of experimental drugs and techniques, called interventions, on human beings. While there is no guarantee that enrolling in a clinical trial will provide any medical benefit, some patients do experience positive results after receiving an experimental therapy.

Read Our Clinical Trials Guide

The website is a centralized database of clinical trials that are offered globally. But as the disclaimer on the sites home page states, there is no guarantee that a listed trial has been evaluated or approvedthe National Institutes of Health runs the site but does not vet its content. This means that there could be bogus or dangerous trials listed that are preying on patients. It is essential that you discuss a clinical trial with your ophthalmologist before enrolling, and that you pay close attention to enrollment criteria.

If you are interested in exploring what is available on the site you can click on the button below, which will take you to and initiate a search for trials relevant for patients living with RP.

CLINICAL TRIALS FOR Retinitis Pigmentosa

For individuals living with an inherited retinal disease (a disease caused by a genetic mutation), participation in a clinical trial could be a logical next-step (for a description of clinical trials, see above). But in Canada there is no centralized, guided mechanism for enrolling in a trial; with this in mind, the Foundation Fighting Blindness has developed a secure medical database of Canadian patients living with inherited retinal diseases: we call it the Patient Registry.

By enrolling in the Patient Registry, your information will become a part of this essential Canadian database that can be used to help connect you to a relevant clinical trial. The availability of relevant trials depends on a number of factors, so this tool provides no guarantees, but signing onto it will put you in a position to be connected to something appropriate. It is also a way of standing up and being counted: the more individuals enrolled in the Patient Registry, the better our chances of showing policymakers that there is a significant need for new treatments for inherited retinal diseases. The Patient Registry also helps to drive more sight-saving research!

You can begin the process of enrolling in the Patient Registry by clicking the button below.

Patient Registry Enrollment

The Foundation Fighting Blindness is committed to advancing the most promising sight-saving research, and has invested over $33 million into cutting-edge science since the organization was founded. Recognizing that science is tied to policy frameworks, the Foundation is also actively involved in health policy activities across Canada.

Many research groups are working to develop treatments and cures for RP. Experimental treatments can be divided into three broad categories:

Protective therapies aim to stop (or at least slow) the damage caused by genetic mutations. Often protective therapies are not specific to one mutation, but may benefit people with many types of RP. These include treatments to stop the process of photoreceptor death (apoptosis), as well as cell-derived therapies that aim to help photoreceptors survive.

Some protective therapies aim specifically to prevent the death of cone cells in RP and thus, the loss of central vision in later stages of the disease.

Corrective therapies aim to reverse the underlying genetic defect that causes vision loss. If these therapies are successful they might prevent a person who is treated when first diagnosed, from ever developing vision loss. Corrective therapies might also help slow the disease in people whose vision has already been affected, especially in the earlier stages. The corrective therapies being developed now are specific to certain forms of recessively inherited RP. Gene therapies, which replace a non-functioning gene, are one type of corrective therapy. Clinical trials of gene therapies for several types of RP are underway, and the results so far are encouraging.

Sight-restoring therapies are also a growing area of research success. These therapies are intended for people who have already lost all, or much, of their vision. Stem cell therapies aim to replace the retinas lost photoreceptors. There are promising early results with stem cell trials involving other retinal degenerative diseases; trials with RP are on the horizon. Retinal prosthetics, such as the Arugus II or Bionic Eye, use computer technology to generate vision. The Foundation Fighting Blindness helped to support the first Canadian trial of the Argus II and continues to work closely with health policy experts across Canada to ensure that patients who could benefit from the Argus II device have access to this innovative treatment. Drug and gene therapies are also being developed that may give non-photoreceptor nerve cells in the retina the capacity to sense light.

Thanks to our generous donors, we are funding ground-breaking research in these areas. Click on the button below to review the full list of FFB-funded projects:


On the right side of this webpage, you will find an updating list of stories that detail new research and health policy developments relevant for individuals affected by RP.

The page you are now on provides information on RP, but the Foundation Fighting Blindness has developed additional resources that can be helpful in plotting an optimal path through vision care. Below is a list of such resources, including information on genetic testing, clinical trials, Vision Quest (the FFBs in-person educational events), and more. The list will update as new resources are added.

Must-Read Resources Vision Quest Educational Series

We know that helpful resources related to your eye disease can be difficult to find. Vision care in Canada entails a complex web of services, programs, and instructions, and little of it is centralized. The information on this site represents our attempt at providing a comprehensive, centralized resource that offers guidance and information specific to your eye disease. Our goal is to help you find your optimal path through vision care in Canada, which is why we call this initiative Vision Care Pathways.

December 12th, 2018 by FFB Canada

Right now, over 1 million Canadians are living with blinding eye diseases and as vision fades, so too can hope. To date, donors of the Foundation Fighting Blindness (FFB) have contributed more than $32 million for vision research. And now, until the end of 2018, a generous supporter will match your gift up to a

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November 13th, 2018 by FFB Canada

On Saturday, October 20, 2018, family and friends of the Celebres came together in support of one very special little boy. Nicholas Celebre was born with Usher syndrome,a condition that causes deaf-blindness and often balance issues. Born profoundly deaf, he was fortunate enough to get cochlear implants when he was 12 months old. He also

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November 13th, 2018 by FFB Canada

Guest-written by Deborah Scott. Our daughter, Olivia was 5 years old when she was diagnosed with a blinding eye disease called retinitis pigmentosa (RP). It was difficult for us to comprehend what that diagnosis really meant. As a parent, you never get over the impact of learning that there is so much more to vision

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Retinitis Pigmentosa - The Foundation Fighting Blindness

Everything You Need To Know About The Bionic Eye – The …

Stell Cell Research | Posted by admin
Feb 06 2019

May 18th, 2016 by FFB Canada

Click here to download a printable version this article/fact sheet: PDF/Word.

What is a retinal prosthesis? A retinal prosthesis is a non-living, electronic substitute for the retina. Popular and brand names for retinal prostheses are the Bionic Eye and the Argus II. The aim is to restore vision to someone blinded by retinal eye disease. A retinal prosthesis is different from an implanted lens or a low-vision device, which works to maximize a persons existing vision.

What does it do? In people with advanced retinal disease, the light-capturing cells of the retina, called photoreceptors, have been lost, but the network of nerves that sends visual information to the brain often is intact. A retinal prosthesis bypasses the photoreceptors and sends visual signals to the brain.

Will it restore my vision? The prostheses that have been tested so far do not provide natural sight. For example, people who are using them are able to recognize a doorway or the shape of a person, or in some cases can make finer distinctions, such as the difference between a fork and a spoon. These retinal prostheses provide a simulation of sight which means that the users have to re-learn how to see. Their brains need to learn how to interpret this new kind of information.

Who could use it? Retinal prostheses are intended for people who are blind or have only minimal light perception, but who once had sight. With prostheses, the brain must interpret the devices signals. Someone blind from birth never developed this capacity, and therefore it might not benefit them.

Are any approved in Canada? Yes. The Argus II Retinal Prosthesis is approved by Health Canada. It is also approved in Europe and the USA. The Foundation Fighting Blindness played a key role in bringing the Argus II (sometimes called the Bionic Eye) to Canada by helping to fund an observational clinical trial of the device at the Toronto Western Hospital led by Dr. Robert Devenyi.

What will it cost? The Argus II Retinal Prosthesis is now being marketed in Europe for about $100,000 USD, plus the cost of the surgery to implant it. Second Sight (the manufacturer) is actively seeking coverage of the device through public insurance or government subsidies. The costs of other retinal prostheses are not yet known.

How does it work? Just as there are multiple kinds of smart phones, there are different approaches to this technology.

Camera + Epi-Retinal Chip The Argus II by Second Sight is the leader in this category. It captures images with a mini-camera embedded in glasses that also carry a batterypack. A 2D array of many tiny electrodes is implanted surgically on the front surface of the retina (epi-retinal). Images from the camera are converted into electrical pulses sent wirelessly to the implant. The pulses stimulate the retinas remaining cells to send patterns of nerve impulses, representing the images, along the optic nerve to the brain. Patients can learn to interpret the patterns and regain some functional vision. Most of the people who have received an Argus II implant have had some visual perception restored, allowing them to better orient themselves in a room or negotiate daily tasks. There appear to be significant variations in results between users.

The Intelligent Retinal Implant System is another camera/chip combo, similar to the Argus II. It is in clinical trials in Germany and the UK. Bionic Vision Australia is also working on a similar product.

Sub-Retinal Chip Retinal Implant AG has created a sub-retinal implant, which sits behind the retina instead of in front of it. This electronic chip contains tiny photocells to capture light, amplifiers to boost their signal, and electrodes to stimulate retinal nerve cells. Since photocells are part of the chip, the device does not need an external camera, and the sub-retinal placement should be more secure and stable than the epi-retinal option; but morecomplicated surgery is required to implant it. Clinical trials of this device are ongoing in Germany, Italy and the UK, and in the USA.

Other groups developing chips include Artificial Silicon Retina Microchip, the Boston Retinal Implant Project, and Nano Vision although the later two are not yet at the human trial stage.

Sub-retinal chips may allow somewhat higher resolution images than epi-retinal chips. However, since even the tiniest electrodes in these prostheses are bound to stimulate more than one retinal cell, so the wearers visual acuity may never approach normal sight. This limitation has led to hybrid strategies, in which remaining retinal nerve cells are made light-sensitive andthen stimulated by patterns of light instead of electricity.

Encoding Neural Signals Dr. Sheila Nirenberg of Cornell University is one of several researchers, who are developing this new hybrid approach to prosthetics. In Dr. Nirenbergs studies, a camera sends images to a computer, which measures local differences in intensity across the image and encodes this information in pulses of light that mimic the natural language of the central nervous system. The size of these pulses of light can be smaller than the smallest retinal nerve cells; they can be projected through the pupil onto individual retinal cells. Using a new approach called optogenetics, a form of gene therapy endows these nerve cells with the ability to respond directly to light, so that the computer-generated light pulses stimulate them to send high-resolution, realistic image representations to the brain. This approach is being tested in animals. If it proves to be effective, it should provide much higher-quality images and a more natural visual experience. Dr. Gautam Awatramani at the University of Victoria is one scientist funded by the Foundation Fighting Blindness donors to study similar therapies.

Direct to Brain Prothesis Scientists at the Monash Vision Group in Australia have developed a different type of vision prosthesis. It avoids the retina altogether. This device uses a video camera to capture images and send its electronic signals directly to the visual cortex of the brain.

While brain surgery sounds like a more difficult, and risky option, the surgery required is relatively straightforward. More importantly, if it is successful, the device could have some important advantages. For example, it could help people with retinal degenerative disease, but it might also help people whose optic nerve has been damaged due to glaucoma or injury

As well, this prosthesis would not be implanted into the retina and thus would not block or damage retinal tissue. So the prosthetic could be used to augment vision for people with some remaining sight, and would not impair their remaining vision. The Monash Vision Group and its partners have committed to having their direct to brain bionic eye ready for first patient tests very soon.

Updated May 18, 2016: Dr. Mary Sunderland, Director of Research & Education, Foundation Fighting Blindness. Initially reviewed by Dr. Bill Stell, Professor of Cell Biology and Anatomy, at the University of Calgary and Dr. Gautam Awatramani, University of Victoria.

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Everything You Need To Know About The Bionic Eye - The ...

Menstrual cycle – Wikipedia

Stell Cell Research | Posted by admin
Feb 02 2019

The menstrual cycle is the regular natural change that occurs in the female reproductive system (specifically the uterus and ovaries) that makes pregnancy possible.[1][2] The cycle is required for the production of oocytes, and for the preparation of the uterus for pregnancy.[1] Up to 80% of women report having some symptoms during the one to two weeks prior to menstruation.[3] Common symptoms include acne, tender breasts, bloating, feeling tired, irritability and mood changes.[4] These symptoms interfere with normal life and therefore qualify as premenstrual syndrome in 20 to 30% of women. In 3 to 8%, they are severe.[3]

The first period usually begins between twelve and fifteen years of age, a point in time known as menarche.[5] They may occasionally start as early as eight, and this onset may still be normal.[6] The average age of the first period is generally later in the developing world and earlier in developed world. The typical length of time between the first day of one period and the first day of the next is 21 to 45 days in young women and 21 to 35 days in adults (an average of 28 days[6][7][8]). Menstruation stops occurring after menopause which usually occurs between 45 and 55 years of age.[9] Bleeding usually lasts around 2 to 7 days.[6]

The menstrual cycle is governed by hormonal changes.[6] These changes can be altered by using hormonal birth control to prevent pregnancy.[10] Each cycle can be divided into three phases based on events in the ovary (ovarian cycle) or in the uterus (uterine cycle).[1] The ovarian cycle consists of the follicular phase, ovulation, and luteal phase whereas the uterine cycle is divided into menstruation, proliferative phase, and secretory phase.

Stimulated by gradually increasing amounts of estrogen in the follicular phase, discharges of blood (menses) flow stop, and the lining of the uterus thickens. Follicles in the ovary begin developing under the influence of a complex interplay of hormones, and after several days one or occasionally two become dominant (non-dominant follicles shrink and die). Approximately mid-cycle, 2436 hours after the luteinizing hormone (LH) surges, the dominant follicle releases an ovocyte, in an event called ovulation. After ovulation, the ovocyte only lives for 24 hours or less without fertilization while the remains of the dominant follicle in the ovary become a corpus luteum; this body has a primary function of producing large amounts of progesterone. Under the influence of progesterone, the uterine lining changes to prepare for potential implantation of an embryo to establish a pregnancy. If implantation does not occur within approximately two weeks, the corpus luteum will involute, causing a sharp drop in levels of both progesterone and estrogen. The hormone drop causes the uterus to shed its lining in a process termed menstruation. Menstruation also occurs in closely related primates (apes and monkeys).[11]

The average age of menarche is 1215.[5][12] They may occasionally start as early as eight, and this onset may still be normal.[6] This first period often occurs later in the developing world than the developed world.[8]

The average age of menarche is approximately 12.5 years in the United States,[13] 12.7 in Canada,[14] 12.9 in the UK[15] and 13.1 years in Iceland.[16] Factors such as genetics, diet and overall health can affect timing.[17]

The cessation of menstrual cycles at the end of a woman's reproductive period is termed menopause. The average age of menopause in women is 52 years, with anywhere between 45 and 55 being common. Menopause before age 45 is considered premature in industrialised countries.[18] Like the age of menarche, the age of menopause is largely a result of cultural and biological factors;[19] however, illnesses, certain surgeries, or medical treatments may cause menopause to occur earlier than it might have otherwise.[20]

The length of a woman's menstrual cycle typically varies somewhat, with some shorter cycles and some longer cycles. A woman who experiences variations of less than eight days between her longest cycles and shortest cycles is considered to have regular menstrual cycles. It is unusual for a woman to experience cycle length variations of more than four days. Length variation between eight and 20 days is considered as moderately irregular cycles. Variation of 21 days or more between a woman's shortest and longest cycle lengths is considered very irregular. [21]

The average menstrual cycle lasts 28 days. The variability of menstrual cycle lengths is highest for women under 25 years of age and is lowest, that is, most regular, for ages 25 to 39.[7] Subsequently, the variability increases slightly for women aged 40 to 44.[7]

The luteal phase of the menstrual cycle is about the same length in most individuals (mean 14.13 days, standard deviation 1.41 days)[22] whereas the follicular phase tends to show much more variability (log-normally distributed with 95% of individuals having follicular phases between 10.3 and 16.3 days).[23] The follicular phase also seems to get significantly shorter with age (geometric mean 14.2 days in women aged 1824 vs. 10.4 days in women aged 4044).[23]

Some women with neurological conditions experience increased activity of their conditions at about the same time during each menstrual cycle. For example, drops in estrogen levels have been known to trigger migraines,[24] especially when the woman who suffers migraines is also taking the birth control pill. Many women with epilepsy have more seizures in a pattern linked to the menstrual cycle; this is called "catamenial epilepsy".[25] Different patterns seem to exist (such as seizures coinciding with the time of menstruation, or coinciding with the time of ovulation), and the frequency with which they occur has not been firmly established. Using one particular definition, one group of scientists found that around one-third of women with intractable partial epilepsy has catamenial epilepsy.[25][26][27] An effect of hormones has been proposed, in which progesterone declines and estrogen increases would trigger seizures.[28] Recently, studies have shown that high doses of estrogen can cause or worsen seizures, whereas high doses of progesterone can act like an antiepileptic drug.[29] Studies by medical journals have found that women experiencing menses are 1.68 times more likely to attempt suicide.[30]

Mice have been used as an experimental system to investigate possible mechanisms by which levels of sex steroid hormones might regulate nervous system function. During the part of the mouse estrous cycle when progesterone is highest, the level of nerve-cell GABA receptor subtype delta was high. Since these GABA receptors are inhibitory, nerve cells with more delta receptors are less likely to fire than cells with lower numbers of delta receptors. During the part of the mouse estrous cycle when estrogen levels are higher than progesterone levels, the number of delta receptors decrease, increasing nerve cell activity, in turn increasing anxiety and seizure susceptibility.[31]

Estrogen levels may affect thyroid behavior.[32] For example, during the luteal phase (when estrogen levels are lower), the velocity of blood flow in the thyroid is lower than during the follicular phase (when estrogen levels are higher).[33]

Among women living closely together, it was once thought that the onsets of menstruation tend to synchronize. This effect was first described in 1971, and possibly explained by the action of pheromones in 1998.[34] Subsequent research has called this hypothesis into question.[35]

Research indicates that women have a significantly higher likelihood of anterior cruciate ligament injuries in the pre-ovulatory stage, than post-ovulatory stage.[36]

The most fertile period (the time with the highest likelihood of pregnancy resulting from sexual intercourse) covers the time from some 5 days before until 1 to 2 days after ovulation.[38] In a 28day cycle with a 14day luteal phase, this corresponds to the second and the beginning of the third week. A variety of methods have been developed to help individual women estimate the relatively fertile and the relatively infertile days in the cycle; these systems are called fertility awareness.

There are many fertility testing methods, including urine test kits that detect the LH surge that occurs 24 to 36 hours before ovulation; these are known as ovulation predictor kits (OPKs).[39] Computerized devices that interpret basal body temperatures, urinary test results, or changes in saliva are called fertility monitors. Fertility awareness methods that rely on cycle length records alone are called calendar-based methods.[40] Methods that require observation of one or more of the three primary fertility signs (basal body temperature, cervical mucus, and cervical position)[41] are known as symptoms-based methods.[40]

A woman's fertility is also affected by her age.[42] As a woman's total egg supply is formed in fetal life,[43] to be ovulated decades later, it has been suggested that this long lifetime may make the chromatin of eggs more vulnerable to division problems, breakage, and mutation than the chromatin of sperm, which are produced continuously during a man's reproductive life. However, despite this hypothesis, a similar paternal age effect has also been observed.

As measured on women undergoing in vitro fertilization, a longer menstrual cycle length is associated with higher pregnancy and delivery rates, even after age adjustment.[44]Delivery rates after IVF have been estimated to be almost doubled for women with a menstrual cycle length of more than 34 days compared with women with a menstrual cycle length shorter than 26 days.[44] A longer menstrual cycle length is also significantly associated with better ovarian response to gonadotropin stimulation and embryo quality.[44]

The different phases of the menstrual cycle correlate with women's moods. In some cases, hormones released during the menstrual cycle can cause behavioral changes in females; mild to severe mood changes can occur.[45] The menstrual cycle phase and ovarian hormones may contribute to increased empathy in women. The natural shift of hormone levels during the different phases of the menstrual cycle has been studied in conjunction with test scores. When completing empathy exercises, women in the follicular stage of their menstrual cycle performed better than women in their midluteal phase. A significant correlation between progesterone levels and the ability to accurately recognize emotion was found. Performances on emotion recognition tasks were better when women had lower progesterone levels. Women in the follicular stage showed higher emotion recognition accuracy than their midluteal phase counterparts. Women were found to react more to negative stimuli when in midluteal stage over the women in the follicular stage, perhaps indicating more reactivity to social stress during that menstrual cycle phase.[46] Overall, it has been found that women in the follicular phase demonstrated better performance in tasks that contain empathetic traits.

Fear response in women during two different points in the menstrual cycle has been examined. When estrogen is highest in the preovulatory stage, women are significantly better at identifying expressions of fear than women who were menstruating, which is when estrogen levels are lowest. The women were equally able to identify happy faces, demonstrating that the fear response was a more powerful response. To summarize, menstrual cycle phase and the estrogen levels correlates with womens fear processing.[47]

However, the examination of daily moods in women with measuring ovarian hormones may indicate a less powerful connection. In comparison to levels of stress or physical health, the ovarian hormones had less of an impact on overall mood.[48] This indicates that while changes of ovarian hormones may influence mood, on a day-to-day level it does not influence mood more than other stressors do.

Sexual feelings and behaviors change during the menstrual cycle. Before and during ovulation, high levels of estrogen and androgens result in women having an increased interest in sexual activity.[49] Unlike other animal species, women show interest in sex across all days of the menstrual cycle, regardless of fertility.[50]

Behavior towards potential mating partners changes during different phases of the menstrual cycle.[51][52][53] Near ovulation, women may have increased physical attraction and interest in attending social gatherings with men.[54] During the fertile phase of the cycle, women appear to prefer males who are more masculine.[55] The intensity of mate guarding differs across the phases of the cycle, with increased mate guarding occurring when women are fertile.[53][56][57]

During the fertile phase, many women experience more attraction, fantasies and sexual interest for extra pair men but not for the primary partner.[54][53][58] They also engage in extra-pair flirtations and demonstrate a preference for extra pair copulation.[54][58]

Preferences for voice pitch change across the cycle.[58] When seeking a short term mating partner, women may prefer a male with a low voice pitch, particularly during the fertile phase.[58] During the late follicular phase, it is common for women demonstrate a preference for mates with a masculine, deep voice.[59] Research has also been conducted on the attractiveness of the female voice throughout the cycle.[60] During their most fertile phase of the menstrual cycle, there is some evidence that female voices are rated as significantly more attractive.[60] This effect is not found with women on the birth control pill.[60]

Women's preference for male's body odor can change across the menstrual cycle.[61] Males who score highly on dominance have been rated as sexier by females during the fertile phase of the menstrual cycle. Additionally, during their most fertile phase of the menstrual cycle, women may show preference for the odor of symmetrical men.[53] This effect is not found for women on the birth control pill.[62] Also, during the late follicular and ovulatory phases, women prefer the scent of masculine men.[58] The scent of androsterone (responsible for testosterone levels) is highly preferred by women during the peak of their fertility in the menstrual cycle.[58] Moreover, women may demonstrate preference for men with a scent that indicates developmental stability.[58]

With regard to women's smell across the cycle, some evidence indicates that men use olfactory cues in order to know if a woman is ovulating.[61] Using a rating of women's odors, women who are ovulating have been rated as more attractive by men.[61] Men demonstrate preferences for the scent of fertile women.[61]

Preferences for facial features in mates can also change across the cycle.[58] There has been no difference found in preference for long-term mating partners during the menstrual cycle; however, those seeking a short-term relationship were more likely to choose a partner with more masculine features than usual.[54][59] This was found to be the case especially during the woman's high conception risk stage and when salivary testosterone was high.[63] However, when women are in the luteal (non-fertile) phase, they tend to prefer men (and females) with more feminine faces.[59] A preference is also shown for self-resembling faces and apparent health in faces during the luteal phase of the cycle.[64] Apparent health preferences were found to be strongest when progesterone levels were high.[64] Additionally, during the fertile phase, many women show a preference for men with darker skin pigmentation.[58] Research on facial symmetry is mixed.[65]

Preferences for body features can change during the fertile phase of the cycle. Women seeking a short-term partner demonstrate a preference for taller and muscular males.[58] Women also show preferences of males with masculine bodies at peak fertility.[58][63] Mixed research has been found regarding body symmetry preferences throughout different phases of the cycle.[58]

In short term mates, during the fertile phase, women may show more attraction to dominant men who display social presence.[58] For long-term mates, shifts in desired trait preferences do not occur throughout the cycle.[58]

Females have been found to experience different eating habits at different stages of their menstrual cycle, with food intake being higher during the luteal phase than the follicular phase.[66][67] Food intake increases by approximately 10% during the luteal phase compared to the follicular phase.[67]

Various studies have shown that during the luteal phase woman consume more carbohydrates, proteins and fats and that 24-hour energy expenditure shows increases between 2.5-11.5%.[68] The increasing intake during the luteal phase may be related to higher preferences for sweet and fatty foods, which occurs naturally and is enhanced during the luteal phases of the menstrual cycle.[68] This is due to the higher metabolic demand during this phase.[69] In particular, women tend to show a cravings for chocolate, with higher cravings during the luteal phase.[68]

Females with premenstrual syndrome (PMS) report changes in appetite across the menstrual cycle more than non-sufferers of PMS, possibly due to their oversensitivity to changes in hormone levels.[67] In women with PMS, food intake is higher in the luteal phase than follicular.[70] The remaining symptoms of PMS, including mood changes and physical symptoms, also occur during the luteal phase. No difference for preference of food types has been found between PMS sufferers and non-sufferers.[66]

The different levels of ovarian hormones at different stages of the cycle have been used to explain eating behaviour changes. Progesterone has been shown to promote fat storage, causing a higher intake of fatty foods during the luteal phase when progesterone levels are higher.[67] Additionally, with a high estrogen level dopamine is ineffective in converting to noradrenaline, a hormone which promotes eating, therefore decreasing appetite.[67] In humans, the level of these ovarian hormones during the menstrual cycle have been found to influence binge eating.[71]

It is theorized that the use of birth control pills should affect eating behaviour as they minimise or remove the fluctuations in hormone levels.[66] The neurotransmitter serotonin is also thought to play a role in food intake. Serotonin is responsible for inhibiting eating and controlling meal size,[72] among other things, and is modulated in part by ovarian hormones.[73]

A number of factors affect whether dieting will affect these menstrual processes: age, weight loss and the diet itself. First, younger women are likely to experience menstrual irregularities due to their diet. Second, menstrual abnormalities are more likely with more weight loss. For example, anovulatory cycles can occur as a result of adopting a restricted diet, as well as engaging in a high amount of exercise.[67] Finally, the cycle is affected more by a vegetarian diet compared to a non-vegetarian diet.[74]

Studies investigating effects of the menstrual cycle on alcohol consumption have found mixed evidence.[75] However, some evidence suggests that individuals consume more alcohol during the luteal stage, especially if these individuals are heavy drinkers or have a family history of alcohol abuse.[69]

The level of substance abuse increases with PMS, mostly with addictive substances such as nicotine, tobacco and cocaine.[69] One theory behind this suggests this higher level of substance abuse is due to decreased self-control as a result of the higher metabolic demands during the luteal phase.[69]

Infrequent or irregular ovulation is called oligoovulation.[76] The absence of ovulation is called anovulation. Normal menstrual flow can occur without ovulation preceding it: an anovulatory cycle. In some cycles, follicular development may start but not be completed; nevertheless, estrogens will be formed and stimulate the uterine lining. Anovulatory flow resulting from a very thick endometrium caused by prolonged, continued high estrogen levels is called estrogen breakthrough bleeding. Anovulatory bleeding triggered by a sudden drop in estrogen levels is called withdrawal bleeding.[77] Anovulatory cycles commonly occur before menopause (perimenopause) and in women with polycystic ovary syndrome.[78]

Very little flow (less than 10 ml) is called hypomenorrhea. Regular cycles with intervals of 21 days or fewer are polymenorrhea; frequent but irregular menstruation is known as metrorrhagia. Sudden heavy flows or amounts greater than 80 ml are termed menorrhagia.[79] Heavy menstruation that occurs frequently and irregularly is menometrorrhagia. The term for cycles with intervals exceeding 35 days is oligomenorrhea.[80]Amenorrhea refers to more than three[79] to six[80] months without menses (while not being pregnant) during a woman's reproductive years. The term for painful periods is Dysmenorrhea.

The menstrual cycle can be described by the ovarian or uterine cycle. The ovarian cycle describes changes that occur in the follicles of the ovary whereas the uterine cycle describes changes in the endometrial lining of the uterus. Both cycles can be divided into three phases. The ovarian cycle consists of the follicular phase, ovulation, and the luteal phase, whereas the uterine cycle consists of menstruation, proliferative phase, and secretory phase.[1]

The follicular phase is the first part of the ovarian cycle. During this phase, the ovarian follicles mature and get ready to release an egg.[1] The latter part of this phase overlaps with the proliferative phase of the uterine cycle.

Through the influence of a rise in follicle stimulating hormone (FSH) during the first days of the cycle, a few ovarian follicles are stimulated.[81] These follicles, which were present at birth[81] and have been developing for the better part of a year in a process known as folliculogenesis, compete with each other for dominance. Under the influence of several hormones, all but one of these follicles will stop growing, while one dominant follicle in the ovary will continue to maturity. The follicle that reaches maturity is called a tertiary or Graafian follicle, and it contains the ovum.[81]

Ovulation is the second phase of the ovarian cycle in which a mature egg is released from the ovarian follicles into the oviduct.[82] During the follicular phase, estradiol suppresses release of luteinizing hormone (LH) from the anterior pituitary gland. When the egg has nearly matured, levels of estradiol reach a threshold above which this effect is reversed and estrogen stimulates the production of a large amount of LH. This process, known as the LH surge, starts around day12 of the average cycle and may last 48 hours.[83]

The exact mechanism of these opposite responses of LH levels to estradiol is not well understood.[84] In animals, a gonadotropin-releasing hormone (GnRH) surge has been shown to precede the LH surge, suggesting that estrogen's main effect is on the hypothalamus, which controls GnRH secretion.[84] This may be enabled by the presence of two different estrogen receptors in the hypothalamus: estrogen receptor alpha, which is responsible for the negative feedback estradiol-LH loop, and estrogen receptor beta, which is responsible for the positive estradiol-LH relationship.[85] However, in humans it has been shown that high levels of estradiol can provoke 32 increases in LH, even when GnRH levels and pulse frequencies are held constant,[84] suggesting that estrogen acts directly on the pituitary to provoke the LH surge.

The release of LH matures the egg and weakens the wall of the follicle in the ovary, causing the fully developed follicle to release its secondary oocyte.[81] If it is fertilized by a sperm, the secondary oocyte promptly matures into an ootid and then becomes a mature ovum. If it is not fertilized by a sperm, the secondary oocyte will degenerate. The mature ovum has a diameter of about 0.2mm.[86]

Which of the two ovariesleft or rightovulates appears essentially random; no known left and right co-ordination exists.[87] Occasionally, both ovaries will release an egg;[87] if both eggs are fertilized, the result is fraternal twins.[88]

After being released from the ovary, the egg is swept into the fallopian tube by the fimbria, which is a fringe of tissue at the end of each fallopian tube. After about a day, an unfertilized egg will disintegrate or dissolve in the fallopian tube.[81]

Fertilization by a spermatozoon, when it occurs, usually takes place in the ampulla, the widest section of the fallopian tubes. A fertilized egg immediately begins the process of embryogenesis, or development. The developing embryo takes about three days to reach the uterus and another three days to implant into the endometrium.[81] It has usually reached the blastocyst stage at the time of implantation.

In some women, ovulation features a characteristic pain called mittelschmerz (German term meaning middle pain).[89] The sudden change in hormones at the time of ovulation sometimes also causes light mid-cycle blood flow.[90]

The luteal phase is the final phase of the ovarian cycle and it corresponds to the secretory phase of the uterine cycle. During the luteal phase, the pituitary hormones FSH and LH cause the remaining parts of the dominant follicle to transform into the corpus luteum, which produces progesterone. The increased progesterone in the adrenals starts to induce the production of estrogen. The hormones produced by the corpus luteum also suppress production of the FSH and LH that the corpus luteum needs to maintain itself. Consequently, the level of FSH and LH fall quickly over time, and the corpus luteum subsequently atrophies.[81] Falling levels of progesterone trigger menstruation and the beginning of the next cycle. From the time of ovulation until progesterone withdrawal has caused menstruation to begin, the process typically takes about two weeks, with 14 days considered normal. For an individual woman, the follicular phase often varies in length from cycle to cycle; by contrast, the length of her luteal phase will be fairly consistent from cycle to cycle.[91]

The loss of the corpus luteum is prevented by fertilization of the egg. The syncytiotrophoblast, which is the outer layer of the resulting embryo-containing structure (the blastocyst) and later also becomes the outer layer of the placenta, produces human chorionic gonadotropin (hCG), which is very similar to LH and which preserves the corpus luteum. The corpus luteum can then continue to secrete progesterone to maintain the new pregnancy. Most pregnancy tests look for the presence of hCG.[81]

The uterine cycle has three phases: menses, proliferative, secretory.[92]

Menstruation (also called menstrual bleeding, menses, catamenia or a period) is the first phase of the uterine cycle. The flow of menses normally serves as a sign that a woman has not become pregnant. (However, this cannot be taken as certainty, as a number of factors can cause bleeding during pregnancy; some factors are specific to early pregnancy, and some can cause heavy flow.)[93][94][95]

Eumenorrhea denotes normal, regular menstruation that lasts for a few days (usually 3 to 5 days, but anywhere from 2 to 7 days is considered normal).[89][96] The average blood loss during menstruation is 35 milliliters with 1080 ml considered normal.[97] Women who experience Menorrhagia are more susceptible to iron deficiency than the average person.[98] An enzyme called plasmin inhibits clotting in the menstrual fluid.[99]

Painful cramping in the abdomen, back, or upper thighs is common during the first few days of menstruation. Severe uterine pain during menstruation is known as dysmenorrhea, and it is most common among adolescents and younger women (affecting about 67.2% of adolescent females).[100] When menstruation begins, symptoms of premenstrual syndrome (PMS) such as breast tenderness and irritability generally decrease.[89] Many sanitary products are marketed to women for use during their menstruation.

The proliferative phase is the second phase of the uterine cycle when estrogen causes the lining of the uterus to grow, or proliferate, during this time.[81] As they mature, the ovarian follicles secrete increasing amounts of estradiol, and estrogen. The estrogens initiate the formation of a new layer of endometrium in the uterus, histologically identified as the proliferative endometrium. The estrogen also stimulates crypts in the cervix to produce fertile cervical mucus, which may be noticed by women practicing fertility awareness.[101]

The secretory phase is the final phase of the uterine cycle and it corresponds to the luteal phase of the ovarian cycle. During the secretory phase, the corpus luteum produces progesterone, which plays a vital role in making the endometrium receptive to implantation of the blastocyst and supportive of the early pregnancy, by increasing blood flow and uterine secretions and reducing the contractility of the smooth muscle in the uterus;[102] it also has the side effect of raising the woman's basal body temperature.[103]

While some forms of birth control do not affect the menstrual cycle, hormonal contraceptives work by disrupting it. Progestogen negative feedback decreases the pulse frequency of gonadotropin-releasing hormone (GnRH) release by the hypothalamus, which decreases the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) by the anterior pituitary. Decreased levels of FSH inhibit follicular development, preventing an increase in estradiol levels. Progestogen negative feedback and the lack of estrogen positive feedback on LH release prevent a mid-cycle LH surge. Inhibition of follicular development and the absence of a LH surge prevent ovulation.[104][105][106]

The degree of ovulation suppression in progestogen-only contraceptives depends on the progestogen activity and dose. Low dose progestogen-only contraceptivestraditional progestogen only pills, subdermal implants Norplant and Jadelle, and intrauterine system Mirenainhibit ovulation in about 50% of cycles and rely mainly on other effects, such as thickening of cervical mucus, for their contraceptive effectiveness.[107] Intermediate dose progestogen-only contraceptivesthe progestogen-only pill Cerazette and the subdermal implant Nexplanonallow some follicular development but more consistently inhibit ovulation in 9799% of cycles. The same cervical mucus changes occur as with very low-dose progestogens. High-dose, progestogen-only contraceptivesthe injectables Depo-Provera and Noristeratcompletely inhibit follicular development and ovulation.[107]

Combined hormonal contraceptives include both an estrogen and a progestogen. Estrogen negative feedback on the anterior pituitary greatly decreases the release of FSH, which makes combined hormonal contraceptives more effective at inhibiting follicular development and preventing ovulation. Estrogen also reduces the incidence of irregular breakthrough bleeding.[104][105][106] Several combined hormonal contraceptivesthe pill, NuvaRing, and the contraceptive patchare usually used in a way that causes regular withdrawal bleeding. In a normal cycle, menstruation occurs when estrogen and progesterone levels drop rapidly.[103] Temporarily discontinuing use of combined hormonal contraceptives (a placebo week, not using patch or ring for a week) has a similar effect of causing the uterine lining to shed. If withdrawal bleeding is not desired, combined hormonal contraceptives may be taken continuously, although this increases the risk of breakthrough bleeding.

Breastfeeding causes negative feedback to occur on pulse secretion of gonadotropin-releasing hormone (GnRH) and luteinizing hormone (LH). Depending on the strength of the negative feedback, breastfeeding women may experience complete suppression of follicular development, but no ovulation, or normal menstrual cycle may resume.[108] Suppression of ovulation is more likely when suckling occurs more frequently.[109] The production of prolactin in response to suckling is important to maintaining lactational amenorrhea.[110] On average, women who are fully breastfeeding whose infants suckle frequently experience a return of menstruation at fourteen and a half months postpartum. There is a wide range of response among individual breastfeeding women, however, with some experiencing return of menstruation at two months and others remaining amenorrheic for up to 42 months postpartum.[111]

The word "menstruation" is etymologically related to "moon". The terms "menstruation" and "menses" are derived from the Latin mensis (month), which in turn relates to the Greek mene (moon) and to the roots of the English words month and moon.[112]

Even though the average length of the human menstrual cycle is similar to that of the lunar cycle, in modern humans there is no relation between the two.[113] The relationship is believed to be a coincidence.[114][115] Light exposure does not appear to affect the menstrual cycle in humans.[11] A meta-analysis of studies from 1996 showed no correlation between the human menstrual cycle and the lunar cycle[116], nor did data analysed by period-tracking app Clue, submitted by 1.5m women, of 7.5m menstrual cycles[117].

Dogon villagers did not have electric lighting and spent most nights outdoors, talking and sleeping, so they were apparently an ideal population for detecting a lunar influence; none was found.[118]

In a number of countries, mainly in Asia, legislation or corporate practice has introduced formal menstrual leave to provide women with either paid or unpaid leave of absence from their employment while they are menstruating.[119] Countries with policies include Japan, Taiwan, Indonesia, and South Korea.[119] The practice is controversial due to concerns that it bolsters the perception of women as weak, inefficient workers,[119] as well as concerns that it is unfair to men.[120][121]

Media related to Menstrual cycle at Wikimedia Commons

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Cigarette lighter using rechargeable AA batteries …

Stell Cell Research | Posted by admin
Jan 28 2019

NiCads have a lower internal resistance than NiMH. SLA even lower.

Having said that, I'd approach this as an academic exercise rather than as a practical project opportunity

This page (and I think they mean milliohms rather than milliwatts in the table) gives you some indication of internal resistances for cell types. (remember to divide these figures by the number of cells to get the per-cell internal resistance)

I think you'd have a better chance with D cells (certainly SLA cells are available in that size)

A major issue would be the connection to the cells. You would have to use cells that are terminated with solder tags rather than bare cells -- the connection resistance would be far too high.

You would need to look at the datasheets on individual cells to determine if the discharge rates are possible for the cell.

Another issue would be that you would almost certainly need to generate another higher voltage source to power your regulator. It is difficult to imagine any of the more efficient designs starting up on their own from 1.5V. You might need a more specialised "joule thief" type of inverter to generate an initial 12V rail to power the main inverter before using the generated 12V rail for continuous operation (or not -- you could use 2 regulators, it's not like a bit of inefficiency here would be a real issue).

More practically, you may be better off creating your own specialised "cigarette lighter" from a coil of nichrome wire of sufficient length to glow red hot from just a 1.2V supply. Since this device would be small enough to turn on when brought to the cigarette, it need not require the relatively large thermal mass of a conventional car cigarette lighter.

I would estimate that you could probably create a device that used perhaps only 10W (i.e. 8A) and would only need to be operated for a couple of seconds. The major issue here would be the contact resistance and the switch. It may be sensible to use a small inverter to provide gate voltage for a high current mosfet that has a very low RDSon.

At a minimum, I think you'd still be looking at a sub-C sized cell.

OK, here's the specs I found on a sub-C cell. It is rated for up to 30A discharge. Note the voltage at 30A, also note that the effective capacity is much lower, still it looks like you'd get 6 minutes use at 30A which is pretty good.

This page has more battery types listed:

From a quick look, it appears that the AA sized cells top out at a recommended max of 6.6A. (D cells go to 50A)

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Cigarette lighter using rechargeable AA batteries ...

Stell Cell Research | Posted by admin
Jan 28 2019

Doris White, 1923 2019

Doris May Chinery White, 95, died January 5, 2019, in Rocky Face, Georgia. Doris was the youngest of two daughters born to Daniel Henry and Dora May Decker Chinery on June 3, 1923, on Staten Island, one of the five boroughs of New York City. Around the age of three years, Doris lost her mother to influenza. Raised by their father, with the help of nearby maternal aunts, Doris and her sister, Constance Henrietta (Connie), enjoyed a happy, comfortable childhood in their home on Rainbow Avenue.

In 1942 Doris graduated from Port Richmond High School, just months after her beloved father died of a stroke. She and her sister were required by circumstances to support themselves, though Doris still managed to take some courses at Seton Hall College. During World War II, Doris worked in the Empire State Building for the Electric Boat Company, which produced PT boats for the Navy. After a time, Doris older sister Connie pursued a career overseas, working for an electric company, Marconi's Wireless Telegraph Company. Connie never married and died in 1973 in New York City.

Following WW II, Doris was introduced to William C. White by her friend and his younger sister, Catherine (Kitty). A graduate of the College of the Holy Cross in Worcester, Massachusetts, and a returning Army officer who had served in England for five years, Bill White was the son of a New York City physician who practiced medicine from an office in his brownstone home in the Irish neighborhood of Hells Kitchen near Times Square. Bill and his sister Kitty were among the youngest of ten siblings; their oldest sister, Bessie, was a nun in the order of the Cenacle Sisters.

On June 14, 1947, Doris and Bill were married in Manhattan, New York City, and they enjoyed over 50 years of marriage, until Bill died on August 28, 1997, in Thomaston, Georgia. In their early married life, they lived in Manhattan and also in Danbury, Connecticut, and in Freeport, New York, on Long Island, as Bill pursued a business career. In 1955, they moved briefly to Jacksonville, Florida, and then on to Atlanta, Georgia, where they lived in the Chamblee and Dunwoody areas.

In 1964, Doris and Bill moved their family to Yatesville, Georgia, seventy miles south of Atlanta, in Upson County (west of Macon). There, Bill began an almost 20-year career with the Federal Paper Board Company in the county seat of Thomaston; he also served a term on the Yatesville City Council. As her children grew older, Doris worked in a clerical capacity at the Marist School in Atlanta, Upson Regional Hospital in Thomaston, and Shallowford Hospital in Atlanta.

Doris was the mother of 7 children: Frances Mary (deceased as a newly born infant), Daniel C. (Sarah Wynn), Mary A., William C. Jr. (Penny), Paul J. (Sue), Theodore M., and John F. (Carolyn). Also known as Gram (while her husband was known as Pop), Doris delighted in her role as grandmother to eleven grandchildren: Leslie Carter, Chas White, Katie White, Kelie White, Kimberly Mann, Kristin White, Erin White, Garrett Mann, Gina White, Jeff Mann, and Henry White. Doris is also survived by nine great-grandchildren.

A memorial service will be held at a later date. In lieu of flowers, memorial contributions may be made to the Bill and Doris White Scholarship at Gordon State College ( and As the parents of six children who were educated in the Upson County, Georgia, Public School System, Bill and Doris White developed a deep respect for the rural teachers and administrators who made the education of their children such a rich and rewarding experience. Realizing the importance for all students to continue onto higher education and realizing that many rural students are economically challenged and that not all students reach their full academic potential in high school, it is the intention of the Bill and Doris White Scholarship to provide financial assistance and recognition to students who might not otherwise receive it.

Donations may be made on-line or mailed to Gordon State College Foundation at: GSC Foundation, 419 College Drive, Barnesville, GA 30204. Donation checks may be made out to the Gordon State College Foundation. In memory of Doris White may be written on the FOR line of the check or a note may be enclosed with the donation indicating the intended scholarship.


YNS Cosmeceutical Skincare – Top Skin Care Products

Stell Cell Research | Posted by admin
Jan 28 2019

Hi, I would like to express my extreme pleasure in Anne's product's. I have very sensitive skin and Anne's products are the only products that I have been able to use that do not cause irritation and/ or further damage. I could be wrong by a year but I do believe I have been a client for at least ten years. I would highly recommend her services and products to everyone.. I promise you will not be disappointed. I use radiance, infusion, cell tight and the cleansing gel. All 4 of these products either singularly or 2 or 3 or all 4 in the same day at the right time have an amazing ability to be effective for all the necessary needs my skin requires. In addition, I have tried many other products spending thousands of dollars, prior to meeting Anne. I am perfectly happy and have not tried another product since. In addition, after so many years of raw skin, blotchy, uneven, and ruddy red skin, I am pain free with beautiful healthy skin. Finally, I am stopped on a regular basis with compliments about my skin and what do I do. I say YNS that the answer and I share Anne's number. Natasha and Anne thank you so much. God Bless you and your company. Beat Regards, Tammyread more

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YNS Cosmeceutical Skincare - Top Skin Care Products

Best Bourbon. Rankings of Best Bourbon – Bourbon Reviews

Stell Cell Research | Posted by admin
Jan 28 2019

Evan Williams 23 year Old

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Basil Haydens 8 year old Kentucky Straight Bourbon

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Parkers Heritage Collection "Golden Anniversary" Bourbon

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1792 Ridgemount Reserve

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Pappy Van Winkles Family Reserve 23yr

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Baker's Kentucky Straight Bourbon Whiskey

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Jim Beam Original

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Glen Garioch 46 years old 1958

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Booker's True Barrel Bourbon

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Angel's Envy

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Best Bourbon. Rankings of Best Bourbon - Bourbon Reviews

Practical Statistics for Medical Research (Chapman & Hall …

Stell Cell Research | Posted by admin
Dec 21 2018

PQk0|Pn2(](A/AB,#I[I%v|; y' -x^OJ0*qr mNC.S.B_[hh3h|jh]wDV`&b%hU8Yd"| ts4KWSJ6[2z NVW?o]=|t52sEZ?C'[X7! p^+fe0'JHTt%j,xHEgocz&^il# YP&+=d6^AYbON(kH`9o7HzR-4)uf{`Ys6E$!jr8nqvgC /|I~e;Z!?G I]Ity-2j3pLofl^X">*)4UllM(ehOV>;+e07&O?|DRhF$TlHdN#wYicEvN.NO`-Z#c 78:xa*.3|LFjT 6zXk7bIn@GdL# x>`!EU} ?,^3|guW$q0~ hT3~EFNrm~):'-A^ZBz0BRE.9#| Pc0|DM*?>C&A:kdH~%Vr68:zl#m9-LJ$c7bS;31}T`:5_^Ji%S+Rl:# `m-/N D4cf&BelhS#E fT1msa_UETfr44ga3T^Gb% FX':ui8n}m, :9m#4` BJ5U3dH4MK;2m!T}oSge;)O m -0(u)+i!o=k1>Xa~F_J%IhQ4Od,#@vs3a gp@Y57fNIAOa"-VkZ&IZn0Hz)Lp+GHgH.~"2PP88ugE!KhF{wL?MnAAwjSP,*XXodjd|LZ7&[[W@r6_[,t,#8GIyNZv5l +O

A Rare Side Effects of Stem Cell Therapy: A Case Study

Stell Cell Research | Posted by admin
Oct 11 2018

By: Ian Murnaghan BSc (hons), MSc - Updated: 28 Sep 2018 | *Discuss

There is no doubt that stem cell therapy holds enormous potential. Unfortunately, this potential also brings with it side-effects, some particularly severe. Such was the case during a therapy that used human foetal stem cells.

The boy in the case suffered from a rare genetic disease known as Ataxia Telangiectasia. This disorder affects many areas of the body and can cause significant disability. The body does not coordinate properly and those who suffer from the disease have a weak immune system as well as problems with their respiratory system.

While there have been some cases reported where experimentation on rodents resulted in the growth of tumours after stem cell injection, this hadn't been documented in humans after foetal stem cell therapy. Researchers also knew that this risk in rodents could be reduced if the stem cells were differentiated before they were injected. This means that the stem cells were coaxed into the desired body cell for the therapy prior to injection.

In a person who has a healthy immune system, the normal 'checks' on the body would be more likely to prevent a tumour from establishing itself. We have known for some time now that there is the potential for stem cells to trigger the growths of tumours but the reality has been that this is a rarity.

Rather than put a stop to stem cell research, it has been suggested that we need to spend more time looking at the Safety of Stem Cells. We should try to find out more about what can potentially go wrong and then develop safeguards to reduce any risks associated with stem cell therapies. This way, we can get the most benefits from stem cells while minimising any chances of side-effects along the way.

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Interstellar Trade – Atomic Rockets

Stell Cell Research | Posted by admin
Oct 11 2018

(ed note: This is talking about sea-going trade in the 1600s, but it can be applied to a science fictional universe. Isaac Kuo says "When the rocket equation applied to the crew")

Gemelli Careri, an Italian adventurer, circled the world in the late 17th century. No part of his journey was more dangerous than the trip from Manila to Acapulco, made in 1697 on one of the deep-drafted, many-sailed boats known as the Manila Galleons. These trading ships spent more than two centuries delivering spices and luxury goods from Asia to the New World and Europe, earning enormous profits for their financiers, mostly Spanish colonists in Manila. But here is Careris description from Giro del Mondo (1699) of what life was like for their sailors:

There is Hunger, Thirst, Sickness, Cold, continual Watching, and other Sufferings [The sailors] endure all the plagues God sent upon Pharaoh to soften his hard heart; the Ship swarms with little Vermine, the Spaniards call Gorgojos, bred in the Bisket if Moses miraculously converted his Rod into a Serpent, aboard the Galeon a piece of Flesh, without any Miracle is converted into Wood, and in the shape of a Serpent.

The journey was interminable, the sea was unruly, the food infested. Abundance of poor Sailors fell Sick, Careri writes. As a paying passenger, he would have had slightly better conditions than most of the crew. But status didnt provide much safety: by the end of his journey, two officers, one pilots mate and the Captain Commander were buried at sea, their bodies dragged down by earthen jars tied around their ankles.

The captain died of a disease known as Berben, which according to Careri swells the Body, and makes the Patient dye talking. The second disease, and the most dangerous to the galleons sailors, is called the Dutch Disease, which makes the Mouth sore, putrefies the Gums, and makes the Teeth drop out. This one is more familiar we know it as scurvy. For most of its two and a half centuries in operation, the galleons sailors died in droves of these and other heinous maladies, teeth rattling from their heads, boils blooming on their limbs like black flowers.

The Berkeley historian Jan DeVries found that some 2 million Europeans made trading voyages to Asia between 1580 and 1795. Of these, only 920,412 survived: an overall mortality rate of 54 per cent. European companies, DeVries concludes, sacrificed one human life for every 4.7 tons of Asian cargo returned to Europe. Of course, the Europeans spread their diseases when they travelled, and made liberal use of violence, so the suffering of the people they discovered was even more awful than their own. But no less than colonialism itself, the unrelenting horrors of these sailors lives helped forge the world we live in.

The first Manila Galleon made the round trip between Acapulco and Manila in 1565, and then did it nearly every year until 1815. It was the last link connecting the Earths human populations. As soon as the Spanish arrive in Manila, says Arturo Girldez, professor of Spanish literature at the University of the Pacific in California, we have a permanent connection between all the landmasses.

Though much of the history of European exploration is told through fantastic tales of overland quests for cities of gold, the galleons, their owners and their crews had no more mythical or lofty goals than Maersk or other giant merchant shipping concerns do today. It was the seaborne quest for trade that bound the far reaches of the globe together, and it is trade that has kept the world connected.

Foremost among the objects of trade were spices. After being introduced to benighted Europe from the Middle East during the Crusades, Asian spices became spectacularly prized for both their taste and their purported medical benefits. For decades, the most desired spices, including nutmeg and clove, were grown only on tiny Pacific islands called the Moluccas. They came to Europe through complex overland chains of Asian and Arab middlemen, who each took exorbitant premiums.

Europeans soon realised that they had the means to cut out those middlemen: spectacularly advanced maritime technology. Trade in the Mediterranean had relied since antiquity on slow-moving galleys, driven by oars, hard to steer, and with shallow drafts that made them unfit for the open ocean. But advances starting in the seventh century had deepened keels, multiplied sails, and made rudders sturdier. This new breed of ship, which would become the backbone of the galleon trade, was fast and manoeuvrable, able to withstand stormy seas while carrying huge amounts of cargo and large cast guns.

Leveraging this new technology, the Portuguese reached the spice islands of Southeast Asia by sailing around Africa in the 15th century. The 1494 Treaty of Tordesillas prevented the worlds other then-great power, Spain, from taking the same route so they started searching for a westward path, by way of the New World.

The first to confront the task was Ferdinand Magellan, one of the explorers least due the reverence granted by grade-school history lessons. Magellans Spanish fleet (he himself was Portuguese, real name Ferno de Magalhes) left Seville in 1519, rounding the tip of South America and crossing to Asia in 99 days. Even that brief journey was more than Magellan had prepared for: by the time the fleet reached Guam, his sailors were gnawing on the leather fittings of their sails out of hunger.

Worse, Magellan didnt know how to sail back to Mexico. Todays carbon-fuelled ships can largely ignore the forces swirling around them, and simply follow the straightest possible line to their destination. But in the age of sail, wind and currents were a ships fuel. Corralled by the great forces of lunar gravitation, climate, and the Earths rotation, the oceans travel great looping paths that remain steady for centuries. These were the highways of European exploration and trade. While Magellan had known where to find the westward current to Asia, he didnt know the way back.

On 27 April 1521, Magellan got himself killed in a local conflict in the Philippines, and his fleet fell apart. His ship, the Trinidad, attempted to sail back across the Pacific the way it had come. It spent months being pushed back to Asia the naval equivalent of trying to climb up the down escalator before the crew finally surrendered in despair to local Portuguese forces. The second ship, the Victoria, took an existing westward route home, rounding Africa and returning to Spain in September 1522, completing the first full circumnavigation of the Earth.

It was a historic milestone, but no model for a profitable trade route. For that, the Spanish needed to find the return route from Manila to Mexico, the eastward leg of the Pacific Gyre. They spent decades searching for it, before finally succeeding thanks to the sailor-monk Andrs de Urdaneta. A different breed altogether from Magellan, and far more deserving of memorialisation, Urdaneta was thoughtful and devout. He had stayed for 9 years on the Moluccas after an ill-fated 1525 Spanish expedition, so he knew the region well. He was 66 and a man of the cloth in Mexico City when, in 1564, the Spanish crown drafted him to help finish Magellans work.

Urdaneta served as pilot of a small fleet under the command of Miguel Lpez de Legazpi. The fleet, first following Magellans route westward from Mexico, captured the Philippines for Spain, and established Manila as a Spanish commercial base. In 1565, acting on local knowledge gleaned during his lengthy stranding on the Moluccas, he guided one ship, the San Pablo, north from Manila along the coast of Japan. There, he found the northward Kuroshio Current the first leg of a great watery highway that soon turned eastward, towards Mexico. This, at last, was the long-dreamed of tornaviaje, or return. Finding it was Urdanetas greatest accomplishment.

The narrow thread of force that connected Manila to Acapulco was, as it turns out, much less friendly to humans than its westward counterpart. The 11,500 miles Urdaneta crossed while returning to Mexico was then the longest sea journey ever made without landing. He took on no fresh water or food for more than four months. Much of the journey, as Careri would attest more than a century later, was both stormy and frigid. By the time they reached land again, Urdanetas crew was exhausted and malnourished. What they werent, mostly, was dead. In light of what followed, this is astounding.

One or two ships sailed Urdanetas route each year for the next two and a half centuries. The Manila Galleons were immensely profitable, with the lions share of the proceeds flowing to the Spanish colonists in Manila who financed and organised the trade. The ships arrived from Mexico laden with silver, which the Chinese badly needed for their rapidly expanding monetary system. They returned carrying not just Indonesian spice Spains original object but Chinese silk and porcelain, and Japanese jewels and preserves.

In Manila, life was leisurely, even beautiful. The work of administering the galleons took up only two or three months of a year, with the rest of the colonists time given purely to lavish parties, carriage rides, and social intrigue. The Spanish were singularly indolent occupiers, developing no aspect of the local economy except the galleon trade. They couldnt even be bothered to dig up the Philippines gold, currently calculated as the third largest reserve in the world. They were interested in profit, not in shaping the lives of the people they colonised.

Though just as one-dimensional as the conquer-and-plunder approach taken elsewhere by the Spanish, the Philippine occupation was different in one crucial way: the resource they were exploiting was not Manilas metal, spice or opium, but its location between the spice islands, China and the New World. Europe was still in the grip of a mercantilist economic ideology that valued exports over multilateral trade. But the galleons amazing profitability showed, long before Adam Smith wrote it down, that national specialisation was the source of wealth, and those who conquered the distance between regions could reap that wealth.

The galleons ushered in global capitalism in another, bleaker way. Friedrich Engels, observing the disease, malnourishment and suffering rampant in Londons nightmarish 19th-century slums, would write that everything which here arouses horror and indignation is of recent origin, belongs to the industrial epoch. Engels was wrong. The age of sail gave us the same kind of horror, or worse.

The crossing that Urdaneta first completed in four months took longer for the less savvy sailors who followed in his wake: five months, sometimes as many as eight, with no fresh water but from rain, and no fresh food but from the sea. Never before had humans been so isolated from their natural environment, for so long, in such numbers. Centuries before the slums of industrial Europe, the trade ships of the Pacific were full of sailors rolling in their own shit, starving to death, and ravaged by disease a Breugellian vista of Hell, compacted into a boat. At times, the dangers grew too great. In 1657, the San Jose was found drifting off the coast of Acapulco, every last crewman and passenger dead.

The typical provisions of a trading ship consisted of salted, preserved meat, a variety of beans, wine, oil and vinegar and, usually in scant portions, luxuries such as honey, chocolate, rice, almonds, and raisins. But the most famous staple was hardtack, or ships biscuit. This was a sort of primitive granola bar made by baking a dense dough until it was hard as a rock. The process was supposed to preserve it, but the sea was merciless. In every Mouthful, said Careri, There went down abundance of Maggots, and Gorgojas chewd and bruisd.

Gorgojo now means weevil, but there are multiple contemporary accounts of them feeding on crewmembers, so that meaning might have shifted. Regardless, various tiny creatures constantly besieged sailors veins and food supplies. Careri also describes soups swimming with worms of several sorts, and beans infested with maggots. The sailors had little option but to dig in.

Fishing provided psychological relief from this nightmare, but didnt solve the underlying, disastrous problem: the total lack of fruit and vegetables. A certain amount was loaded on departure from Manila, but this was reserved almost exclusively for officers, and consumed within weeks. Those aboard could not have understood the chemistry or biology that made this so deadly. They saw only the consequences.

At around the third month without landfall, the sailors gums would begin to swell, while their energy flagged. As their condition progressed, the gum tissue became so swollen that sailors sometimes cut large chunks from their own mouths and felt nothing. As lethargy overwhelmed them, the rest of their flesh began to decompose before their eyes, skin taking on the soft touch of fungus, and black ulcers swelling from it. This was followed by multiple organ failure and, ultimately, death.

Many between the 16th and 19th century reckoned scurvy a consequence of the malodorous vapours of the Pacific. Careri and many others knew that the best remedy against it, is going ashore but exactly why wasnt known. A scattered few had observed that fresh fruit cured the disease, but many seamen thought burying a victim up to the neck in dirt was also a powerful cure.

Even as their crews rotted alive, the galleons often carried Chinese ginger as part of their payload of prized spices. Though ginger was generally known for its medicinal as well as culinary properties, it was not understood that it is a source for ascorbic acid, or vitamin C, which is crucial to the bodys synthesis of collagen, the basic building block of our connective tissues and skin. In its absence, humans literally fall apart.

Those not killed by scurvy were at risk from another inescapable element of life on the galleons: severe crowding. Priests, who had free passage as missionaries, were sometimes crammed into cabins so small they had to rest their heads on one anothers feet. In 1767, aboard the San Carlos, 62 Jesuits were confined to a space meant for 20. They were then joined by 25 soldiers and a small herd of pigs. And these were the privileged: most sailors were expected to simply cram themselves into any available corner.

While all sea vessels are necessarily confined, the galleons had a particular problem. Space on these ships, especially on the return trip to Acapulco, was astronomically valuable. Their crowding embodied what the historian Jack Turner calls the law of increasing exoticism: The further they travelled from their origins, the more interesting [spices and trade goods] became, the greater the passions they aroused, the higher their value. The returns on even small cargos from the East could be huge.

This led to some amazingly inhumane decisions by those in charge. Careri describes huge shipboard cisterns, designed to both store and collect water on the journey, being smashed to make room for goods belonging to an officers friends. This was practically an act of murder: sailors ration of water was already a mere two pints a day. Frequently, ships sailed without backup sails and repair supplies, and it was common practice to store the guns to save space, making them useless for repelling pirates, which often lurked in wait of the galleons precious cargo.

The most common product of severe crowding was infectious disease. Microbiotic fiends traversed the constantly moist membranes of passengers and sailors, breeding typhus (known as ship fever) and typhoid (a disease spread by fleas and ticks). These were later joined by new diseases of exploration such as yellow fever and syphilis, the latter discovered in the New World before spreading to Europe and, primarily by the galleons themselves, to Asia.

Disease was exacerbated by a primitive view of cleanliness among Europeans of the age. Though latrines that cantilevered over the ocean were available on some galleons, many sailors didnt use them, instead shitting into the ships bilge, or even in the general hold. In part, Careri tells us, that was because of the incessant, brutal cold. But this indifference was widespread. The French sailor Franois Pyrard de Laval wrote in 1610 that typical Portuguese ships around India were mighty foul and stink withal; the most men not troubling themselves to go on deck for their necessities.

The lack of basic hygiene on ships illustrates the vast gap between early modern knowledge of geography and sailing on the one hand, and of the internal frontiers of the human body on the other. It was well-known that the world was round, part of the basis for the galleons amazing navigational leap. But few educated Europeans of the 16th and 17th century had more than the vaguest concepts of nutrition, infection, germs or the role of cleanliness in health. Most ships, even as late as the 18th century, relied for rudimentary medical help on a multitasking barber whose most effective tools were his enema syringe and tooth-puller.

This had deep intellectual roots. For the 15th and most of the 16th century, medical authorities were engaged in a kind of backwards march, blindly deferential to the second-century Greek physician Galen. Galenistic medicine was based on the theory of the humours, a set of materials with various qualities that had to be balanced within the body.

Advancement past this theory was hampered by a Papal ban on human dissection for research, not lifted until 1482. But a rationalistic approach to illness was, even then, centuries away. The Manila Galleons launched more than 30 years before the birth in 1596 of Ren Descartes, whose thinking would prove foundational for the very concept of an experiment. They launched precisely a century before Robert Boyle, in 1665, became the first to make biological use of the word cell. The connection between cleanliness and contagion wasnt persuasively argued until John Pringles Observations on the Diseases of the Army (1752). The first controlled experiments showing the effectiveness of citrus fruits in preventing scurvy were performed by James Lind in 1747. In fact, they were the first properly controlled medical experiments ever conducted.

But there was more than simple ignorance behind the suffering of the galleons sailors. The ships were often suspiciously overcrewed. They could be sailed by 40 or fewer, but carried crew complements of between 75 and, as the ships grew larger, 200. In Vanguard of Empire (1993), Roger C Smith points out that this overcrewing was due to the (correct) assumption that many of the crew would die.

Providing better food was known to decrease mortality emergency rations of higher quality were packed on all ships to aid the recovery of the ill (though Careri observed that most of that quickly ended up at the captains table). But providing higher quality food would have been a major expense for financiers, without greatly increasing the likelihood that a ships cargo would arrive intact which is all that really mattered to them. In fact, since the bulk of salaries was paid only at the end of a round trip, allowing half of all crew to die would have been a double cost saving. And so the sailors wore the yoke of global commerce, were worked to death, and then forgotten.

The Manila Galleon was ultimately undone by its own success. The route was eventually worked by ships of almost every European power, albeit illegally. Merchant competition for Asian goods drove up prices, while cheaper manufactured textiles undercut demand. In 1770, the Frenchman Pierre Poivre began successfully cultivating nutmeg and clove in the Indian Ocean, ending the spice monopoly of the Moluccas. The final decades of the Manila line were marked by frequent losses (both maritime and economic) and half-filled ships. The last galleon ran in 1815.

By then, it was just one part of an expansive network of global shipping. Commercial steam power, which emerged in 1807 on the Hudson River, would eventually make that trade faster, more efficient and much less deadly. The months-long Pacific crossing that killed a million men can now be made, even by the most leisurely of diesel container ships, in two weeks.

Reliable global trade underpins the unprecedented affluence now shared by many humans. In a better world, it might have spread its benefits even more widely. But todays robust network, and the technology that underpins it, would likely never have appeared without a template to guide their growth. That template was crude, exploitative, unreliable and very often, for the men whose bodies fuelled it, gruesomely lethal.

Read more from the original source:
Interstellar Trade - Atomic Rockets