First Week Pregnancy Symptoms

Human Fetal Development Timeline

Printables, coloring pages, recipes, crafts, and more from your child's favorite Nickelodeon and Nick Jr. shows..TODAY Parents is the premiere destination for parenting news, advice community. Find the latest parenting trends and tips for your kids and family on TODAY.com..Find information from BabyCenter on pregnancy, children's health, parenting more, including expert advice weekly newsletters that detail your child's development..Pill nowadays is the most popular pregnancy termination option. Medical Pill - is a method of in early pregnancy 6-7 weeks .Information on Zika virus. Provided by the U.S. Centers for Disease Control and Prevention..

Human Fetal Development Timeline

Lesbian Couples Side By Side Pregnancy Photos Go Viral Inspire

Pill nowadays is the most popular pregnancy termination option. Medical Pill - is a method of in early pregnancy 6-7 weeks .TODAY Parents is the premiere destination for parenting news, advice community. Find the latest parenting trends and tips for your kids and family on TODAY.com..Printables, coloring pages, recipes, crafts, and more from your child's favorite Nickelodeon and Nick Jr. shows..Information on Zika virus. Provided by the U.S. Centers for Disease Control and Prevention..Find information from BabyCenter on pregnancy, children's health, parenting more, including expert advice weekly newsletters that detail your child's development..

Feet first

An interesting and logical (to the non-medical reader) theory from sciencedaily.com  as to why neuropathy attacks the feet first. If acted upon, it may lead to  treatments being more specifically directed towards the mitochondria (the parts of the cells that generate energy) thus being more effective and likely to succeed. In short, since nerve cells are about a metre long, by the time mitochondria drift to the feet they are about three years old and have accumulated mutations. This could explain why neuropathies start with the feet.

Feet First? Old Mitochondria Might Be Responsible for Neuropathy in the Extremities

ScienceDaily (Mar. 4, 2011) —

The burning, tingling pain of neuropathy may affect feet and hands before other body parts because the powerhouses of nerve cells that supply the extremities age and become dysfunctional as they complete the long journey to these areas, Johns Hopkins scientists suggest in a new study. The finding may eventually lead to new ways to fight neuropathy, a condition that often accompanies other diseases including HIV/AIDS, diabetes and circulatory disorders.

Neuropathies tend to hit the feet first, then travel up the legs. As they reach the knees, they often start affecting the hands. This painful condition tends to affect people who are older or taller more often than younger, shorter people. Though these patterns are typical of almost all cases of neuropathy, scientists have been stumped to explain why, says study leader Ahmet Hoke, M.D., Ph.D., a professor of neurology and neuroscience at the Johns Hopkins University School of Medicine.

He and his colleagues suspected that the reason might lie within mitochondria, the parts of cells that generate energy. While mitochondria for most cells in the body have a relatively quick turnover -- replacing themselves every month or so -- those in nerve cells often live much longer to accommodate the sometimes long journey from where a cell starts growing to where it ends. The nerve cells that supply the feet are about 3 to 4 feet long in a person of average height, Hoke explains. Consequently, the mitochondria in these nerve cells take about two to three years to travel from where the nerve originates near the spine to where it ends in the foot.

To investigate whether the aging process during this travel might affect mitochondria and lead to neuropathy, Hoke and his colleagues examined nerve samples taken during autopsies from 11 people who had HIV-associated neuropathy, 13 who had HIV but no neuropathy, and 11 HIV-negative people who had no signs of neuropathy at their deaths. The researchers took two matched samples from each person -- one from where the nerves originated near the spine and one from where the nerves ended near the foot.

They then examined the DNA from mitochondria in each nerve sample. Mitochondria have their own DNA that's separate from the DNA in a cell's nucleus.

The researchers report in the January Annals of Neurology that in patients with neuropathy, DNA from mitochondria in the nerve endings at the ankle had about a 30-fold increase in a type of mutation that deleted a piece of this DNA compared to mitochondrial DNA from near the spine. The difference in the same deletion mutation between the matched samples in people without neuropathy was about threefold.

Since mitochondria quit working upon a person's death, the scientists looked to a monkey model of HIV neuropathy to see whether these deficits affected mitochondrial function. Tests showed that the mitochondria from the ankles of these animals didn't function as well as those from near their spines, generating less energy and producing faulty proteins and damaging free radicals.

Hoke explains that as mitochondria make the trek from near the spine to the feet, their DNA accumulates mutations with age. These older mitochondria might be more vulnerable to the assaults that come with disease than younger mitochondria near the spine, leading older mitochondria to become dysfunctional first. The finding also explains why people who are older or taller are more susceptible to neuropathies, Hoke says.

"Our mitochondria age as we age, and they have even longer to travel in tall people," he says. "In people who are older or taller, these mitochondria in the longest nerves are in even worse shape by the time they reach the feet."

Hoke notes that if this discovery is confirmed for other types of neuropathy, it could lead to mitochondria-specific ways to treat this condition. For example, he says, doctors may eventually be able to give patients drugs that improve the function of older mitochondria, in turn improving the function of nerve cells and relieving pain.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Johns Hopkins Medical Institutions, via EurekAlert!, a service of AAAS.


Journal Reference:
1.Helmar C. Lehmann, Weiran Chen, Jasenka Borzan, Joseph L. Mankowski, Ahmet Höke. Mitochondrial dysfunction in distal axons contributes to human immunodeficiency virus sensory neuropathy. Annals of Neurology, 2011; 69 (1): 100 DOI: 10.1002/ana.22150

SCIENTISTS GENERATE FIRST HUMAN TISSUE IN L AB WITH STEM CELLS

Scientists used pluripotent stem cells to generate functional, three-dimensional human stomach tissue in a laboratory -- creating an unprecedented tool for researching the development and diseases of an organ central to several public health crises, ranging from cancer to diabetes.

Scientists at Cincinnati Children's Hospital Medical Center report Oct. 29 in Nature they used human pluripotent stem cells -- which can become any cell type in the body -- to grow a miniature version of the stomach. In collaboration with researchers at the University of Cincinnati College of Medicine, they used laboratory generated mini-stomachs (called gastric organoids) to study infection by H. pylori bacteria, a major cause of peptic ulcer disease and stomach cancer.

This first-time molecular generation of 3D human gastric organoids (hGOs) presents new opportunities for drug discovery, modeling early stages of stomach cancer and studying some of the underpinnings of obesity related diabetes, according to Jim Wells, PhD, principal investigator and a scientist in the divisions of Developmental Biology and Endocrinology at Cincinnati Children's.

It also is the first time researchers have produced 3D human embryonic foregut -- a promising starting point for generating other foregut organ tissues like the lungs and pancreas, he said.

"Until this study, no one had generated gastric cells from human pluripotent stem cells (hPSCs)," Wells said. "In addition, we discovered how to promote formation of three-dimensional gastric tissue with complex architecture and cellular composition."

This is important because differences between species in the embryonic development and architecture of the adult stomach make mouse models less than optimal for studying human stomach development and disease, Wells added.

Researchers can use human gastric organoids as a new discovery tool to help unlock other secrets of the stomach, such as identifying biochemical processes in the gut that allow gastric-bypass patients to become diabetes-free soon after surgery before losing significant weight. Obesity fueled diabetes and metabolic syndrome are an exploding public health epidemic. Until now, a major challenge to addressing these and other medical conditions involving the stomach has been a relative lack of reliable laboratory modeling systems to accurately simulate human biology, Wells explained.

The key to growing human gastric organoids was to identify the steps involved in normal stomach formation during embryonic development. By manipulating these normal processes in a petri dish, the scientists were able to coax pluripotent stem cells toward becoming stomach. Over the course of a month, these steps resulted in the formation of 3D human gastric organoids that were about 3mm (1/10th of an inch) in diameter. Wells and his colleagues also used this approach to identify what drives normal stomach formation in humans with the goal of understanding what goes wrong when the stomach does not form correctly.

Along with study first author Kyle McCracken, an MD/PhD graduate student working in Wells' laboratory, and Yana Zavros, PhD, a researcher at UC's Department of Molecular and Cellular Physiology, the authors report they were impressed by how rapidly H. pylori bacteria infected stomach epithelial tissues.

Within 24 hours, the bacteria had triggered biochemical changes to the organ, according to McCracken. The human gastric organoids faithfully mimicked the early stages of gastric disease caused by the bacteria, including the activation of a cancer gene called c-Met and the rapid spread of infection in epithelial tissues.

Another significant part of the team's challenge has been the relative lack of previous research literature on how the human stomach develops, the authors said. Wells said the scientists had to use a combination of published work, as well as studies from his own lab, to answer a number of basic developmental questions about how the stomach forms. Over the course of two years, this approach of experimenting with different factors to drive the formation of the stomach eventually resulted in the formation of 3D human gastric tissues in the petri dish.

Wells emphasized importance of basic research for the eventual success of this project, adding, "This milestone would not have been possible if it hadn't been for previous studies from many other basic researchers on understanding embryonic organ development."

Oh my my first drum

For my Birthday, (July 7) my Mother and Godfather/stepfather gifted me a gift far more than an object.

My first Drum.

I am just taken. I've never had a drum of my own, nor taken classes. In fact I never felt worthy of a drum because I fear the cultural appropriation it implies and I think there is an initiation process that earns one a drum; a sort of rite of passage.... or something I can't put my finger on.

But this drum sings right to my soul ..... the resonance of it's sound vibrates quite literally, right through my skin and blood, into the very marrow of my bones.

I never in a million years expected to be gifted with my own drum. What does this mean? Am I worthy? Can I use this to it's best power? How? What is the drums name? Her medicine? Her gift?

Is it a milestone that I don't see? I'm always changing .... everything either feels like a milestone or a great painful waiting. What shall I learn? What new song will she teach me?

I'm listening, for sure.

FIRST PICTURES OF BRCA2 PROTEIN SHOW HOW IT WORKS TO REPAIR DNA

Scientists have taken pictures of the BRCA2 protein for the first time, showing how it works to repair damaged DNA

Mutations in the gene that encodes BRCA2 are well known for raising the risk of breast cancer and other cancers. Although the protein was known to be involved in DNA repair, its shape and mechanism have been unclear, making it impossible to target with therapies.

Researchers at Imperial College London and the Cancer Research UK London Research Institute purified the protein and used electron microscopy to reveal its structure and how it interacts with other proteins and DNA. The results are published today in Nature Structural and Molecular Biology.

Around one in 1000 people in the UK have a mutation in the BRCA2 gene. The lifetime risk of breast cancer for women with BRCA2 mutations is 40 to 85 per cent, depending on the mutation, compared with around 12 per cent for the general population. Many women who test positive for BRCA1 and BRCA2 mutations choose to undergo surgery to reduce their risk of breast cancer. Mutations can also raise the risk of other cancers, such as ovarian, prostate and pancreatic cancer.

The BRCA1 and BRCA2 genes encode proteins involved in DNA repair. The DNA in our cells undergoes damage thousands of times a day, caused by toxic chemicals, metabolic by-products and ultraviolet radiation. Repair mechanisms correct most of this damage, but unrepaired damage can lead to cancer.

The study was led by Professor Xiaodong Zhang from the Department of Medicine at Imperial College London and Dr Stephen West at the London Research Institute.

"This study improves our understanding of a fundamental cause of cancer," said Professor Zhang, a Wellcome Trust Senior Investigator. "It's our first view of how the protein looks and how it works, and it gives us a platform to design new experiments to probe its mechanism in greater detail.

"Once we have added more detail to the picture, we can design ways to correct defects in BRCA2 and help cells repair DNA more effectively to prevent cancer. We can also think about how to make the repair process less effective in cancer cells, so that they die."

The study found that BRCA2 proteins work in pairs -- which the researchers found surprising since BRCA2 is one of the largest proteins in the cell.

BRCA2 works in partnership with another protein called RAD51. BRCA2 helps RAD51 molecules to assemble on strands of broken DNA and form filaments. The RAD51 filaments then search for matching strands of DNA in order to repair the break.

The findings showed that each pair of BRCA2 proteins binds two sets of RAD51 that run in opposite directions. This allows it to work on strands of broken DNA that point in either direction. They also show that BRCA2's job is to help RAD51 form short filaments at multiple sites along the DNA, presumably to increase the efficiency of establishing longer filaments required to search for matching strands.