Saturday, May 5, 2018

Diet linked to menopause timing

(Reuters Health) - A UK study suggests that diets rich in certain foods may be a factor in the timing of menopause.
Researchers who studied more than 14,000 women found that those whose diets included lots of fish and legumes entered menopause years later, on average, than women who didn’t eat much of these foods.
Conversely, eating more refined carbohydrates, including pasta and rice, was tied to earlier menopause, the research team reports in Journal of Epidemiology and Community Health.

Understanding perimenopause

Perimenopause is considered a precursor to menopause. This phase can last years before your period ceases for good. Although the length of time women spend in this transitional phase varies, the natural body processes at play are largely the same.
During perimenopause, a woman’s estrogen and progesterone start to fluctuate. Overall, these hormones levels are decreasing. Estrogen levels may go up and down a bit more before leveling out as your body settles into menopause. These natural hormone fluctuations of perimenopause can often cause different symptoms for different women.
Some common symptoms of perimenopause include:
  • irregular periods, which includes changes in flow or frequency
  • vaginal dryness
  • mood changes, including irritability or depression
  • hot flashes
  • night sweats, which may inhibit sleep


PASTA AND OILY FISH


Hot flashes, fatigue and, of course, changes to your period. The menopause can be a trying time for many women—but for some it can have serious health implications. These are the women, researchers think, that might benefit from a study investigating diet and the timing of menopause.
Researchers have linked certain foods to a delay in the start of menopause in a study including data from more than 14,150 women in the U.K. But, outside experts caution that women should not change their diets just yet. The results were revealed Monday in a study published in the Journal of Epidemiology and Community Health


Include foods that are good for the bones

After going through the menopause, your bones will begin to lose density. This can make them weaker over time, so it is important to make sure you're getting enough calcium and vitamin D, which are vital for bone health.

Can legumes and fish help you delay menopause?


When will I start menopause? It’s a question a lot of women worry about, especially if you’re over 40. While a lot of factors -- age, mother’s history, BMI -- determine when the process of menopause will eventually start for you, diet also plays an important role.
According to a recent study by researchers at the University of Leeds, links have been found between diet and the onset of menopause in British women. The study showed that high intake of healthy foods, such as oily fish and fresh legumes, such as peas and green beans were associated with a later onset of the menopause, while a high consumption of refined white pasta and rice was associated with an earlier start.
Analysis of their diet showed that high intakes of oily fish were associated with a delayed start to menopause by nearly three years. A diet with lots of refined pasta and rice showed that menopause was more likely to occur one and a half years earlier than average. Study co-author, Janet Cade, said: “The age at which menopause begins can have serious health implications for some women.” 

A diet rich in legumes—beans, peas, and lentils—and fish may put off the natural onset of menopause, a new study suggests, while foods rich in carbohydrates may accelerate it.
A woman in menopause loses ability to become pregnant, but getting menopause premature (before age 40) or early (age 40 to 45) has several complications.
A loss of bone density, a higher risk of heart disease, and a loss of sexual desire are only some of the consequences of premature or early menopause.
Pushing back your menopause to a later age, on the contrary, might have some health benefits. One recent study suggests a late-onset menopause might keep cognitive decline at bay in senior women.

Eating Fish And Legumes 'Could Delay Menopause By 3 Years'



A diet rich in fish and legumes may help to delay the menopause, while eating lots of refined carbs, such as pasta and rice, may hasten it, researchers have found.
The study of women from England, Scotland, and Wales, which is the first of its kind in the UK, found the average age of menopause to be 51 and certain foods seemed to be associated with its timing. 
The researchers found having a high intake of oily fish and fresh legumes - such as peas and beans - was associated with a menopause delay of more than three years. Higher intakes of vitamin B6 and zinc were also associated with later menopause.

Researchers from the University of Leeds looked at the effect of diet on the onset of the menopause.
Their study involved more than 35,000 women aged between 35 and 69, who provided information on their weight history, physical activity levels, reproductive history, and use of hormone replacement therapy (HRT).
They also estimated the quantities of 217 food items they ate every day by completing a food frequency questionnaire.

After analysing these women over a four year period, 914 of whom experienced a natural menopause during this time, they found that eating certain foods may influence the age at which they start experiencing symptoms.

For example, those who ate a diet heavy in foods such as beans, salmon and peas were more likely to experience delayed menopause, whereas regular consumption of foods such as pasta and rice was linked to an earlier onset of menopause by 18 months.


Friday, April 20, 2018

HIV

HIV Classification

Comparison of HIV species
SpeciesVirulenceInfectivityPrevalenceInferred origin
HIV-1HighHighGlobalCommon chimpanzee
HIV-2LowerLowWest AfricaSooty mangabey
HIV is a member of the genus Lentivirus,[12] part of the family Retroviridae.[13]Lentiviruses have many morphologies and biological properties in common. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period.[14] Lentiviruses are transmitted as single-stranded, positive-senseenveloped RNA viruses. Upon entry into the target cell, the viral RNA genome is converted (reverse transcribed) into double-stranded DNA by a virally encoded enzyme, reverse transcriptase, that is transported along with the viral genome in the virus particle. The resulting viral DNA is then imported into the cell nucleus and integrated into the cellular DNA by a virally encoded enzyme, integrase, and host co-factors.[15] Once integrated, the virus may become latent, allowing the virus and its host cell to avoid detection by the immune system, for an indiscriminate amount of time.[16] The HIV virus can remain dormant in the human body for up to ten years after primary infection; during this period the virus does not cause symptoms. Alternatively, the integrated viral DNA may be transcribed, producing new RNA genomes and viral proteins, using host cell resources, that are packaged and released from the cell as new virus particles that will begin the replication cycle anew.
Two types of HIV have been characterized: HIV-1 and HIV-2. HIV-1 is the virus that was initially discovered and termed both LAV (Lymphadenopathy Associated Virus) and HTLV-III (Human T cell Lymphotropic Virus III). HIV-1 is more virulent and more infective than HIV-2,[17]and is the cause of the majority of HIV infections globally. The lower infectivity of HIV-2 compared to HIV-1 implies that fewer of those exposed to HIV-2 will be infected per exposure. Due to its relatively poor capacity for transmission, HIV-2 is largely confined to West Africa.[18]

Structure and genome


Diagram of the HIV virion
HIV is different in structure from other retroviruses. It is roughly spherical[19] with a diameter of about 120 nm, around 60 times smaller than a red blood cell.[20] It is composed of two copies of positive-sense single-stranded RNA that codes for the virus's nine genes enclosed by a conical capsid composed of 2,000 copies of the viral protein p24.[21] The single-stranded RNA is tightly bound to nucleocapsid proteins, p7, and enzymes needed for the development of the virion such as reverse transcriptaseproteasesribonuclease and integrase. A matrix composed of the viral protein p17 surrounds the capsid ensuring the integrity of the virion particle.[21]
This is, in turn, surrounded by the viral envelope, that is composed of the lipid bilayer taken from the membrane of a human host cell when the newly formed virus particle buds from the cell. The viral envelope contains proteins from the host cell and relatively few copies of the HIV Envelope protein,[21] which consists of a cap made of three molecules known as glycoprotein (gp) 120, and a stem consisting of three gp41 molecules that anchor the structure into the viral envelope.[22][23] The Envelope protein, encoded by the HIV env gene, allows the virus to attach to target cells and fuse the viral envelope with the target cell's membrane releasing the viral contents into the cell and initiating the infectious cycle.[22]
As the sole viral protein on the surface of the virus, the Envelope protein is a major target for HIV vaccine efforts.[24] Over half of the mass of the trimeric envelope spike is N-linked glycans. The density is high as the glycans shield the underlying viral protein from neutralisation by antibodies. This is one of the most densely glycosylated molecules known and the density is sufficiently high to prevent the normal maturation process of glycans during biogenesis in the endoplasmic and Golgi apparatus.[25][26] The majority of the glycans are therefore stalled as immature 'high-mannose' glycans not normally present on human glycoproteins that are secreted or present on a cell surface.[27] The unusual processing and high density means that almost all broadly neutralising antibodies that have so far been identified (from a subset of patients that have been infected for many months to years) bind to or, are adapted to cope with, these envelope glycans.[28]
The molecular structure of the viral spike has now been determined by X-ray crystallography[29] and cryo-electron microscopy.[30] These advances in structural biology were made possible due to the development of stable recombinant forms of the viral spike by the introduction of an intersubunit disulphide bond and an isoleucine to proline mutation in gp41.[31] The so-called SOSIP trimers not only reproduce the antigenic properties of the native viral spike but also display the same degree of immature glycans as presented on the native virus.[32] Recombinant trimeric viral spikes are promising vaccine candidates as they display less non-neutralising epitopes than recombinant monomeric gp120, which act to suppress the immune response to target epitopes.[33]
Structure of the RNA genome of HIV-1
The RNA genome consists of at least seven structural landmarks (LTRTARRRE, PE, SLIP, CRS, and INS), and nine genes (gagpol, and envtatrevnefvifvprvpu, and sometimes a tenth tev, which is a fusion of tatenv and rev), encoding 19 proteins. Three of these genes, gagpol, and env, contain information needed to make the structural proteins for new virus particles.[21] For example, envcodes for a protein called gp160 that is cut in two by a cellular protease to form gp120 and gp41. The six remaining genes, tatrevnefvifvpr, and vpu (or vpx in the case of HIV-2), are regulatory genes for proteins that control the ability of HIV to infect cells, produce new copies of virus (replicate), or cause disease.[21]
The two Tat proteins (p16 and p14) are transcriptional transactivators for the LTR promoter acting by binding the TAR RNA element. The TAR may also be processed into microRNAs that regulate the apoptosis genes ERCC1 and IER3.[34][35] The Rev protein (p19) is involved in shuttling RNAs from the nucleus and the cytoplasm by binding to the RRE RNA element. The Vif protein (p23) prevents the action of APOBEC3G (a cellular protein that deaminates Cytidine to Uridine in the single stranded viral DNA and/or interferes with reverse transcription[36]). The Vpr protein (p14) arrests cell division at G2/M. The Nef protein (p27) down-regulates CD4 (the major viral receptor), as well as the MHC class I and class IImolecules.[37][38][39]
Nef also interacts with SH3 domains. The Vpu protein (p16) influences the release of new virus particles from infected cells.[21] The ends of each strand of HIV RNA contain an RNA sequence called the long terminal repeat (LTR). Regions in the LTR act as switches to control production of new viruses and can be triggered by proteins from either HIV or the host cell. The Psi element is involved in viral genome packaging and recognized by Gag and Rev proteins. The SLIP element (TTTTTT) is involved in the frameshift in the Gag-Pol reading frame required to make functional Pol.[21]

HIV


The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and over time acquired immunodeficiency syndrome (AIDS).[1][2] AIDS is a condition in humans in which progressive failure of the immune system allows life-threatening opportunistic infections and cancersto thrive. Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.[3] In most cases, HIV is a sexually transmitted infection and occurs by contact with or transfer of bloodpre-ejaculatesemen, and vaginal fluids. Non-sexual transmission can occur from an infected mother to her infant through breast milk.[4][5][6] An HIV-positive mother can transmit HIV to her baby both during pregnancy and childbirth due to exposure to her blood or vaginal fluid.[7]Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells.
HIV infects vital cells in the human immune system such as helper T cells (specifically CD4+ T cells), macrophages, and dendritic cells.[8] HIV infection leads to low levels of CD4+ T cells through a number of mechanisms, including pyroptosis of abortively infected T cells,[9] apoptosis of uninfected bystander cells,[10] direct viral killing of infected cells, and killing of infected CD4+ T cells by CD8+ cytotoxic lymphocytes that recognize infected cells.[11] When CD4+ T cell numbers decline below a critical level, cell-mediated immunity is lost, and the body becomes progressively more susceptible to opportunistic infections, leading to the development of AIDS.



Human immunodeficiency virus
HIV-budding-Color.jpg
Scanning electron micrograph of HIV-1 (in green) budding from cultured lymphocyte. Multiple round bumps on cell surface represent sites of assembly and budding of virions.
Virus classification
Group:Group VI (ssRNA-RT)
Order:Unassigned
Family:Retroviridae
Subfamily:Orthoretrovirinae
Genus:Lentivirus
Species
  • Human immunodeficiency virus 1
  • Human immunodeficiency virus 2

Monday, April 16, 2018

What causes breast cancer?

Breast cancer is caused by a genetic mutation in the DNA of breast cancer cells. How or why this damage occurs isn’t entirely understood. Some mutations may develop randomly over time, while others are inherited or may be the result of environmental exposures or lifestyle factors.
Most breast cancers are diagnosed in women over age 50, but it’s not clear why some women get breast cancer (including women with no risk factors) and others do not (including those who do have risk factors).
Some breast cancer risks may be preventable. Of course, you cannot control every variable that may influence your risk. Here are the key breast cancer risk factors to know.
  • Age and gender. If you are a woman and you’re getting older, you may be at risk of developing breast cancer. The risk begins to climb after age 40 and is highest for women in their 70s.
  • Family history. Having a close blood relative with breast cancer increases your risk of developing the disease. A woman’s breast cancer risk is almost double if she has a mom, sister, or daughter with breast cancer and about triple if she has two or more first-degree relatives with breast cancer.
  • A breast cancer gene mutation. Up to 10% of all breast cancers are thought to be inherited, and many of these cases are due to defects in one or more genes, especially the BRCA1 or BRCA2 genes. (Scientists are studying several other gene mutations as well.) In the U.S., BRCA1 and BRCA2 mutations are more common in Jewish women of Eastern European descent. Having these defective genes doesn’t mean you will get breast cancer, but the risk is greater: A woman’s lifetime risk of breast cancer with a BRCA1 gene mutation, for example, may be more like 55% to 65% compared to the average 12%.
  • Breast changes and conditions. Women with dense breasts or with a personal history of breast lumps, a previous breast cancer, or certain non-cancerous breast conditions are at greater risk of developing breast cancer than women who do not have these conditions.
  • Race/ethnicity. White women are slightly more likely to develop breast cancer than Asian, Hispanic, and African American women. But African American women are more likely to develop more aggressive breast cancer at a younger age and both African American and Hispanic women are more likely to die from breast cancer than white women.
  • Hormones. Women with early menstrual periods(starting before age 12) and late menopause (after age 55) are at greater risk of getting breast cancer. Scientists think their longer exposure to the female hormone estrogen may be a factor, because estrogen stimulates growth of the cells of the breast. Likewise, use of hormone therapy after menopause appears to boost the risk of breast cancer. Oral birth control pills have been linked to a small increase in breast cancer risk compared with women who never used hormonal contraception. But that risk is temporary: More than 10 years after stopping the pill, a woman’s breast cancer risk returns to average.
  • Weight. Women who are overweight or obese after menopause are more likely to get breast cancer. The exact reason why isn’t clear, but it may be due to higher levels of estrogen produced by fat cells after menopause. Being overweight also boosts blood levels of insulin, which may affect breast cancer risk.
  • Alcohol consumption. Studies suggest women who drink two or more alcoholic beverages a day are 1 1/2 times more likely than non-drinkers to develop breast cancer. The risk rises with greater alcohol intake, and alcohol is known to increase the risk of other cancers too. For that reason, the American Cancer Society (ACS) recommends that women stick to one drink a day–or less.
  • Radiation exposure. A woman’s risk of developing breast cancer may be higher than normal if she had chest radiation for another disease as a child or young adult.
  • Pregnancy history. Having no children or having a first child after age 30 may increase your risk of breast cancer.
  • DES exposure. Women who were given the now-banned drug diethylstilbestrol to prevent miscarriage decades ago face a slightly increased risk of breast cancer, as do their daughters.


  • Symptoms Of Breast Cancer That Most Women Miss :-
     https://www.youtube.com/watch?       v=I9oo2AR59dM

What is breast cancer?

Breast cancer is the most common cancer among women, after skin cancer. One in eight women in the United States (roughly 12%) will develop breast cancer in her lifetime. It is also the second leading cause of cancer death in women after lung cancer. Encouragingly, the death rate from breast cancer has declined a bit in recent years, perhaps due to greater awareness and screening for this type of cancer, as well as better treatments.
Breast cancer is a disease that occurs when cells in breast tissue change (or mutate) and keep reproducing. These abnormal cells usually cluster together to form a tumor. A tumor is cancerous (or malignant) when these abnormal cells invade other parts of the breast or when they spread (or metastasize) to other areas of the body through the bloodstream or lymphatic system, a network of vessels and nodes in the body that plays a role in fighting infection.
Breast cancer usually starts in the milk-producing glands of the breast (called lobules) or the tube-shaped ducts that carry milk from the lobules to the nipple. Less often, cancer begins in the fatty and fibrous connective tissue of the breast.
New cases of breast cancer are about 100 times more common in women than in men, but yes, men can get breast cancer too. Male breast cancer is rare, but anyone with breast tissue can develop breast cancer.

In video see 
https://www.youtube.com/watch?v=VsviAPGfPUo

Saturday, April 14, 2018

What is the birth control implant?

The birth control implant (AKA Nexplanon) is a tiny, thin rod about the size of a matchstick. The implant releases hormones into your body that prevent you from getting pregnant. A nurse or doctor inserts the implant into your arm and that’s it — you’re protected from pregnancy for up to 4 years. It’s get-it-and-forget-it birth control.

Diet linked to menopause timing (Reuters Health) - A UK study suggests that diets rich in certain foods may be a factor in the timing o...