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How not to get pregnant under Trump presidency

Many women in  Facebook are talking about IUD (intra-uterine device, to prevent pregnancy) that is still covered by health insurance and might not be covered under Trump presidency. Be sure to have your doctor give you regular check up (yearly) with regards to your IUD. I will not suggest IUD to my daughter.  Some prefer IUD because they experience more side effects with birth control pills. Examine all options and research well any contraceptives in the market. My mom’s IUD caused her to have ectopic pregnancy which is life threatening.

How not to get pregnant

During the first day of your menstruation, count this day as day 1. Between day 8 to day 14, check the mucus that comes out of your OS (vagina). If it stretches by 2 cm and egg white in consistency, that day is your fertile day (day 12 -14). If that day is day 13, having sex on day 12-13 will give you a boy and a girl during days 9-11. So use condom or abstain from days 9 to 14 if you do not want to get pregnant.  Taking 6000 mg per day (500 mg every 3hrs) of Vit C during that week makes the uterus inhospitable for conception.

Adverse Effecgts of IUD from Wiki

Regardless of containing progestogen or copper, potential side effects of intrauterine devices include expulsion, uterus perforation, pelvic inflammatory disease (especially in the first 21 days after insertion), as well as irregular menstrual pattern. A small probability of pregnancy remains after IUD insertion, and when it occurs there is a greater risk of ectopic pregnancy.

Substantial pain that needs active management occurs in approximately 17% of nulliparous women and approximately 11% of parous women.[39] In such cases, NSAID are evidenced to be effective.[39] However, no prophylactic analgesic drug have been found to be effective for routine use for women undergoing IUD insertion.[39]

Also, IUDs with progestogen confer an increased risk of ovarian cysts,[40] and IUDs with copper confer an increased risk of heavier periods.

Menstrual Cup companies recommend that women with IUDs who are considering using menstrual cups should consult with their gynecologists before use. There have been rare cases in which women using IUDs dislodged them when removing their menstrual cups, however, this can also happen with tampon use.

Breast cancer types

Why does our skin causing us to age?

epi-mechskin-epi

Epigenetics studies genetic effects notencoded in the DNA sequence of an organism, hence the prefix epi- (Greek: επί– over, outside of, around).[1][2] Such effects on cellular and physiological phenotypic traits may result from external or environmental factors that switch genes on and off and affect how cells express genes.[3][4] These alterations may or may not be heritable, although the use of the term epigenetic to describe processes that are heritable is controversial.[5]

The term also refers to the changes themselves: functionally relevant changes to the genome that do not involve a change in the nucleotide sequence. Examples of mechanisms that produce such changes are DNA methylationand histone modification, each of which alters how genes are expressed without altering the underlying DNA sequence. Gene expression can be controlled through the action of repressor proteins that attach to silencer regions of the DNA. These epigenetic changes may last through cell divisions for the duration of the cell’s life, and may also last for multiple generations even though they do not involve changes in the underlying DNA sequence of the organism;[6] instead, non-genetic factors cause the organism’s genes to behave (or “express themselves”) differently.[7]

 


Connie’s skin tips: Sleep, hydrate, moisturize, use Vit C serum (DIY), wash with lemon and left over tea bags and apply sunscreen (from whole foods store).

Stop aging of your face with DIY Vitamin C serum by wellnessmama

Molecular cancer screen at a distance

cancer screen.JPG

Molecular biomarkers are independent of the presence of a detectable tumor mass or even the detection of intact transformed cells. Instead, they represent detection at a distance, using molecular signals in blood or excretia to indicate the presence of a cancer or pre-invasive lesion. These molecular biomarkers fall into four groups (Table 1).

Some are products of the neoplastic process that are shed by the tumors, such as mutated or hypermethylated DNA (‘carcinogenesis markers’). Others are molecular species generated by the host response to the cancer (‘response biomarkers’). Examples include antibodies, protein degradation products,12 and acute phase reactants.13

A third group of biomarkers, like blood in stool or PSA in serum, are released in abnormal amounts as a result of the anatomical or metabolic disruption associated with a tumor (‘released biomarkers’).

The final group of molecular markers comprises factors associated with or supporting the underlying carcinogenesis (‘risk biomarkers’). Examples are high estradiol levels in relation to breast cancer or markers of human papilloma virus in relation to cervical cancer.

These classes of biomarkers will probably behave differently in early detection. Carcinogenesis markers are likely to be relatively specific for invasive or pre-invasive neoplasia, as they are essentially found only in on-going carcinogenesis.

Testing for PSA or blood in stool has already shown that released biomarkers can be non-specific: pathology other than cancer often leads to their release into blood and stool respectively.

Risk biomarkers are often abnormal in individuals without cancer; these are really risk factors, markers of cancer risk rather than markers of cancer itself.

Typically only a minority of individuals with the risk factors actually develop the associated disease.

Thus, just as benign masses can mimic tumors or obscure cancers in anatomical screening, pathological and metabolic processes will affect the specificity of molecular screening, especially if it is not based on carcinogenesis markers. PSA provides many examples: hemodilution of PSA levels in obese men,14, 15distortion of levels by medication,14 and increases in levels from prostatitis.16 Inflammation – a risk factor for cancer in many organs — may be a particular problem as it shares molecular mediators with carcinogenesis.

One is that the tests are convenient and safe – typically requiring only the donation of blood, urine or stool. Measuring these molecular biomarkers does not involve tests that deliver radiation, a visit to the clinic, or unpleasant procedures as is needed for colonoscopy. Thus, the use of molecular biomarkers is likely to improve the uptake of screening by the general population and make repeated testing practical and affordable. This would increase the sensitivity of the screening process, and correspondingly increase the chances of detecting early cancers. However, it would also increase the potential for false positives, with the adverse downstream consequence of unnecessary diagnostic follow-ups.

Another advantage of molecular biomarkers is that they can easily be combined into panels using mathematical techniques such as logistic models or recursive partitioning to enhance sensitivity and specificity. Such combinations might be less susceptible to measurement artifacts than the individual markers. Also, the quantitative nature of many molecular markers means that they can potentially be personalized, using age, sex and race-specific norms, for example.

Pre-malignant lesions

Since the molecular defects of early cancer are often similar to those of intraepithelial neoplasia,40molecular screening for cancers will likely identify substantial numbers of pre-invasive lesions. In organs such as the colorectum and cervix, these can be removed relatively easily to reduce risk of future cancer. Excision of pre-invasive lesions identified in less accessible tissues, such as the pancreas, entails considerable morbidity. It may not be clear what should be done to address the increased risk of invasive cancer, particularly as the natural history of these screen-detected lesions may not be well characterized.

Some risk biomarkers and some reaction biomarkers (such as antibodies) might remain in the abnormal range even after the responsible lesions are completely removed. For example, long-term hormonal patterns that promoted carcinogenesis presumably would continue, and some antibodies generated by a tumor may persist. Markers that do revert to normal after successful treatment could be used to follow disease recurrence and progression, as PSA (for prostate cancer) CEA (for colorectal cancer) and CA-125 (for ovarian cancer) are used now. Here again, advanced anatomical detection may aid the molecular screen to locate recurrent neoplasia that is not otherwise evident. Ideally, the validation of molecular screening markers would include study of their behavior as markers of disease progression after excision of the tumors that are detected.

In some organs, it may even be a challenge to find the cancers indicated by molecular biomarkers.

Some of the cancers detected may not need to be treated.


Do you want to know more about a molecular cancer screen many years before an actual cancer can be detected? Email motherhealth@gmail.com as need at least 25,000 people who wanted to be cancer screen early 20yrs before a real threat appears and another tests to determine the molecular age of your cells.

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‘Brain wi-fi’ reverses leg paralysis in primate first

monk

By James Gallagher

An implant that beams instructions out of the brain has been used to restore movement in paralysed primates for the first time, say scientists.

Rhesus monkeys were paralysed in one leg due to a damaged spinal cord.

The team at the Swiss Federal Institute of Technology bypassed the injury by sending the instructions straight from the brain to the nerves controlling leg movement.

Experts said the technology could be ready for human trials within a decade.

Dr Andrew Jackson talks about the primate brain chip

Spinal-cord injuries block the flow of electrical signals from the brain to the rest of the body resulting in paralysis.

It is a wound that rarely heals, but one potential solution is to use technology to bypass the injury.

In the study, a chip was implanted into the part of the monkeys’ brain that controls movement.

Its job was to read the spikes of electrical activity that are the instructions for moving the legs and send them to a nearby computer.

It deciphered the messages and sent instructions to an implant in the monkey’s spine to electrically stimulate the appropriate nerves.

The process all takes place in real time.

The results, published in the journal Nature, showed the monkeys regained some control of their paralysed leg within six days and could walk in a straight line on a treadmill.

Monkey on treadmill

Dr Gregoire Courtine, one of the researchers, said: “This is the first time that a neurotechnology has restored locomotion in primates.”

He told the BBC News website: “The movement was close to normal for the basic walking pattern, but so far we have not been able to test the ability to steer.”

The technology used to stimulate the spinal cord is the same as that used in deep brain stimulation to treat Parkinson’s disease, so it would not be a technological leap to doing the same tests in patients.

“But the way we walk is different to primates, we are bipedal and this requires more sophisticated ways to stimulate the muscle,” said Dr Courtine.

Jocelyne Bloch, a neurosurgeon from the Lausanne University Hospital, said: “The link between decoding of the brain and the stimulation of the spinal cord is completely new.

“For the first time, I can image a completely paralysed patient being able to move their legs through this brain-spine interface.”

Using technology to overcome paralysis is a rapidly developing field:

Dr Mark Bacon, the director of research at the charity Spinal Research, said: “This is quite impressive work.

“Paralysed patients want to be able to regain real control, that is voluntary control of lost functions, like walking, and the use of implantable devices may be one way of achieving this.

“The current work is a clear demonstration that there is progress being made in the right direction.”

Dr Andrew Jackson, from the Institute of Neuroscience and Newcastle University, said: “It is not unreasonable to speculate that we could see the first clinical demonstrations of interfaces between the brain and spinal cord by the end of the decade.”

Brain chip

However, he said, rhesus monkeys used all four limbs to move and only one leg had been paralysed, so it would be a greater challenge to restore the movement of both legs in people.

“Useful locomotion also requires control of balance, steering and obstacle avoidance, which were not addressed,” he added.

The other approach to treating paralysis involves transplanting cells from the nasal cavity into the spinal cord to try to biologically repair the injury.

Following this treatment, Darek Fidyka, who was paralysed from the chest down in a knife attack in 2010, can now walk using a frame.

Neither approach is ready for routine use.

Birth Year May Affect Your Flu Risk

By Maggie Fox

A new study explains why children and young adults are more likely to be infected with H5N1, shown here, while H7N9 disproportionately affects older adults.

People’s birth years can affect their risk of catching certain strains of influenza — probably because their first case of flu somehow sets their immune system, researchers reported Thursday.

Their findings could be good news for what scientists predict about the risk of a killer flu pandemic, and they could also help researchers find better flu vaccines, the researchers said.

A new study explains why children and young adults are more likely to be infected with H5N1, shown here, while H7N9 disproportionately affects older adults. CYNTHIA GOLDSMITH / UCLA

“Our work implies that we have never seen a true ‘virgin soil’ influenza pandemic,” the team wrote in their report, published in the journal Science. “Virgin soil” means a population that has no immunity at all to a new infection.

The teams were looking at the puzzling characteristics of two strains of bird flu that keep popping up in people: the H5N1 and H7N9 avian influenza viruses.

They’ve been spilling over into people for years and scaring scientists who see the potential for a pandemic of flu that could kill tens or even hundreds of millions of people. But this hasn’t happened yet.

And, oddly, while H5N1 has hit young people and children especially hard, H7N9 seems to attack older people.

H5N1 has infected 856 people since 2003 and killed 452 of them, WHO reports. H7N9 has infected 452 people and killed 124 of them, according to the Center for Infectious Disease Research and Policy at the University of Minnesota.

The team at the University of Arizona and the University of California Los Angeles dove into the numbers, examining the reports of each case, who was affected and how severely.

They found an almost startling link with birth year.

“It’s ridiculously predictive,” said Michael Worobey, an expert in viral genetics at the University of Arizona.

Worobey thinks he knows why. Other research suggests that early infections “imprint” the body’s immune system. It makes sense — the human immune system makes cells and antibodies that “learn” to recognize and react more quickly to microbial invaders the next time they infect someone.

Worobey has also found that influenza viruses that commonly infect people can be categorized into two groups. Group 1 consists of subtypes H1, H2, and avian H5, while group 2 includes seasonal H3 and avian H7.

Influenza A viruses all are named for two proteins found on their surfaces: hemagglutinin (the H in a flu name) and neuraminidase (the N in a flu name). Thus flu strains get names such as H5N1 or H1N1 or H3N2. So human H1N1, H2N2 and the H5N1 bird flu virus are all related in Group 1, while the H3N2 seasonal flu virus is related to the H7N9 bird flu strain.

Play

Can You Catch Bird Flu?

Every few decades, the predominant flu strain changes. So the H1N1 flu strain that killed tens of millions of people in 1918 hung around infecting people until 1957, when a pandemic of H2N2 flu swept the world and took over. Then H2N2 predominated until 1968, when the H3N2 “Hong Kong” flu took over.

Most recently, the H1N1 “swine flu” caused a minor pandemic in 2009. Now H1N1 and H3N2 both regularly circulate as seasonal flu viruses.

What Worobey and colleagues found was that people born in 1968 and later are less likely to be made severely ill by H7N9. They believe this is because the first flu strain that would have infected them would have been H3N2, which is in the same group as H7N9.

And people born before 1968 are less likely to die or be made severely ill by H5N1, because their first flu infection would have been an H1N1 or H2N2 strain.

“Roughly half of the people are quite well-protected against one of these potential pandemic viruses but not the other,” Worobey said.

“Our findings show clearly that this ‘childhood imprinting’ gives strong protection against severe infection or death from two major strains of avian influenza,” added James Lloyd-Smith, a UCLA professor of evolutionary biology who worked on the study. “These results will help us quantify the risk of particular emerging influenza viruses sparking a major outbreak.”

“It’s imprinting. Not the virus, not the behavior of people, but being exposed to different viruses at an early age,” Worobey said.

Flu strains mutate all the time, which is why people need a fresh flu shot every year. But Worobey and other researchers say there are unchanging, or “conserved” parts of the flu virus on the “stem” of the mushroom-shaped hemagglutinin structure that the human immune system can recognize.

It obviously does not provide perfect protection, but enough to protect most people with this immune imprinting from the most severe disease, he said.

“It is an extra barrier that is probably protecting us from even more frequent influenza pandemics,” he said.

More importantly, later flu infections do not seem to alter this mechanism, although this theory needs testing.

The researchers cannot say whether regular flu vaccination affects this “imprinting” effect. People are now encouraged to get annual flu vaccines starting as infants, and they get a cocktail of vaccines that protect against both the Group 1 H1N1 and Group 2 H3N2 viruses.

They also cannot say whether peoples’ susceptibility to seasonal flu is affected by imprinting. Flu is so very common that it will be hard to say which virus first infected someone and then follow them through life to see which strains make them sicker.

But it might be possible to use the findings to make better vaccines, Worobey said.

“This is really the first evidence out in the real world that this kind of cross-protection is possible,” Worobey said.