Francis por siempre!!!.


“No vencimos, pero tampoco pudieron vencernos”. F.A.C.

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Todos vamos a morir.


A propósito de la nueva ley en la organización del tránsito: las indicaciones de trafico jamás deben servir de base para publicidad.
“Todos vamos a morir, pero nadie merece morir en un accidente de tráfico”.

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Combinación de dos vacunas para prevenir la pneumonia


This infectious disease can pose a serious health risk for those age 65 and older, but two vaccines can offer sound protection.

pneumonia vaccine for adult

By Matthew Solan
Executive Editor, Harvard Men’s Health Watch

One of the leading health dangers for older adults is pneumonia. It is the most common cause of hospital admissions after childbirth. In fact, adults age 65 and older have a higher risk of death from pneumonia hospitalization than any other reason.

Pneumonia is an infection of the lungs by bacteria, viruses, or other microbes. Most cases are caused by the bacteria Streptococcus pneumoniae, Mycoplasma pneumonia, Chlamydia pneumoniae, Chlamydia psittaci, and Legionella pneumophila. A similar inflammation of the lung, called pneumonitis, can be caused by an inhaled chemical and is more common in people who have had strokes and have difficulty swallowing. A physical exam, chest x-ray, and blood test can confirm a diagnosis.


Pneumonia symptoms are similar to the flu: fever, muscle aches, headache, fatigue, and cough. However, with pneumonia, the cough often produces yellow, green, or even bloody mucus. You also may have trouble breathing after activities like climbing a few stair steps, and experience pain when taking a deep breath.

Risk factors

Besides bacterial infections and viruses, these factors also can further increase your risk for pneumonia, according to the Harvard Medical School Special Health Report A Guide to Men’s Health: Fifty and Forward:

Age. Although pneumonia can infect anyone, especially infants and young children, people age 65 and older are at higher risk for complications.
Smoking. Smokers are more likely to get pneumonia than nonsmokers, probably because smoking damages the lungs and leaves them more vulnerable.
Medical conditions. Immunodeficiencies like leukemia, chemotherapy, radiation, diabetes, and malnutrition can suppress the immune system and increase your risk of developing pneumonia. Others conditions that make you more vulnerable include Parkinson’s disease; stroke, which affects swallowing; asthma; chronic obstructive pulmonary diseases (COPD); and heart disease.

The main treatment for pneumonia is antibiotics. Pneumonia can last from a few days to a week or longer depending on when you begin drug therapy and if you have other medical issues. In addition to antibiotics, other treatments include rest, adequate fluids, and supplemental oxygen to raise the level of oxygen in the blood.

Most people can be treated safely with antibiotics at home. Yet those who are at higher risk of complications, such as those 65 and older or who have other high-risk factors, may need to be hospitalized for two days to a week.

Two pneumonia vaccines

The CDC recommends two preventive pneumonia vaccines for adults: Pneumovax (PPSV23) and Prevnar (PCV13). The combination stimulates the immune system more effectively than either alone.

The two vaccines build immunity against different types of the bacteria that causes pneumonia. Pneumovax protects against 23 common types and Prevnar protects against 13 types.

Adults 65 and older should receive Prevnar first, followed by Pneumovax six months to one year later. If you have already had Pneumovax, you can still get Prevnar and it will still be effective. Medicare Part B covers pneumonia vaccines for adults.

Beside getting vaccinated, you can reduce your risk of pneumonia by washing your hands frequently through the day, and seeing your doctor if you do get the flu so you can receive prompt treatment and avoid having it turn into pneumonia.

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Antibióticos en las enfermedades virales.

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Avanzar en la educación para el progreso es imperativo.


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Como es afectado el metabolismo hepatico por una comida de alto contenido graso.


Individuals who consume higher levels of saturated fats are more likely to feel the effects of a range of health conditions, including non-alcoholic fatty liver disease. Although this link is well-known, exactly how and why it develops is not yet clear.
[Realistic liver illustration]
The recent research investigates the effects of a single high-fat meal on the liver.
Non-alcoholic fatty liver disease (NAFLD), as the name suggests, is a condition in which excess fat is stored in the liver of an individual who drinks little or no alcohol.

Marked by liver inflammation, NAFLD most commonly affects people in their 40s and 50s, and especially those who are obese. It can cause scarring of the liver and permanent damage. At its worst, it can lead to liver failure.

NAFLD is primarily characterized by an increased buildup of fat in the liver, and this buildup is often accompanied by insulin resistance, thereby increasing the risk of type 2 diabetes and cardiovascular disease.

Although a diet high in saturated fats is linked to NAFLD, it is not clear how fatty foods initiate these changes in the liver.

Because of the unerring rise in obesity, NAFLD is predicted to become the number one reason for liver transplantation in the near future. It is already the most common chronic liver disease; NAFLD affects an estimated 20-30 percent of the Western population and 90 percent of individuals who are morbidly obese.

Currently, the reasons why high-fat diets cause NAFLD and metabolic disorders are not known. Similarly, it is not understood why certain people who eat a high-fat diet do not develop these conditions, and why some people who eat a healthful diet, do. Since the burden of metabolic disorders in Western countries is rising sharply, researchers are working to understand the exact processes behind these metabolic changes in the liver.

The effect of one high-fat meal on the liver
A recent study, published in The Journal of Clinical Investigation, set out to investigate this interaction at a molecular level.

Researchers from Michael Roden’s laboratory at the German Diabetes Center in Germany, led by Elisa Álvarez Hernández, examined how a single episode of high saturated fat intake would affect insulin sensitivity and other markers of metabolism in humans and mice.

In total, 14 lean and healthy participants were involved in the study. The researchers provided a quantity of fat (palm oil) equivalent to a single rich meal. Following the meal, they analyzed each individual’s hepatic metabolism. They carried out a similar, parallel experiment on mice.

An immediate increase in fat accumulation and changes in liver metabolism were observed. This single meal also led to elevated triglycerides, insulin resistance, and increased glucagon (a hormone that increases glucose levels) in the bloodstream.

The high-fat palm oil meal was found to decrease insulin sensitivity across the board. Findings show that:

Whole body insulin sensitivity decreased 25 percent
Hepatic insulin sensitivity decreased 15 percent
Adipose (fat) tissue insulin sensitivity decreased 34 percent.
Hepatic triglycerides – the main constituent of body fat in humans and a marker for metabolic and cardiovascular disease – also rose by 35 percent.

The study shows that consuming saturated fat lays the foundation for metabolic disease by influencing liver metabolism and the storage of fat. As the authors conclude:

“Saturated fat ingestion rapidly increases hepatic lipid storage, energy metabolism, and insulin resistance. This is accompanied by regulation of hepatic gene expression and signaling that may contribute to development of NAFLD.”

Because the current study only utilized male mice and human participants, the team hope to extend their findings in females. It is possible that the uptake of fatty acids by the liver is greater in men. In future investigations, the team also plan to make changes to their choice of control; in the current study, they compared saturated fat intake to water, but their next project will compare saturated fat with unsaturated fat and protein.

By understanding the metabolic machinery behind NAFLD, medical science may uncover novel ways to treat this prevalent and destructive condition.

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Protein may help prevent fatty liver.


Researchers in Spain have discovered that a protein called CPEB4 may help to prevent fatty liver, a condition in which fat builds up in the liver. They showed that mice with low levels of CPEB4 developed fatty liver as they aged, and they also found that the protein plays an important role in how liver cells respond to stress.
mouse liver section hires
Researchers found a protein that plays a key role in the development of fatty liver. This image shows a section of a mouse’s liver affected by the disease, with accumulated fat or lipid droplets (in red) inside cells. The blue dots are cell nuclei.
Image credit: C. Maíllo, IRB Barcelona
The team – led by researchers from the Institute for Research in Biomedicine (IRB Barcelona) and the IDIBAPS Biomedical Research Institute, which is part of the Hospital Clínic de Barcelona – reports the findings in the journal Nature Cell Biology.

The researchers hope that the discovery will lead to treatments that fight and even prevent fatty liver – also known as a nonalcoholic fatty liver disease – which is the most common chronic liver disease in developed countries.

Dr. Mercedes Fernández, one of the study co-leaders and head of the IDIBAPS group, says that while their study “does not have a direct and immediate clinical application,” it does, however, lay down “the foundation for the applied science that follows.”

Nonalcoholic fatty liver disease (NAFLD) is a condition in which too much fat builds up in hepatocytes, the most common cell in the liver. It is similar to an alcoholic liver disease, except that it is also found in people who drink little or no alcohol.

NAFLD can progress to nonalcoholic steatohepatitis (NASH) where, in addition to fat deposits, the liver also shows signs of inflammation and cell damage. NASH can also lead to fibrosis, cirrhosis, and eventually liver cancer.

CPEB4 depletion led to fatty liver in mice
Nobody knows exactly what causes fatty liver, although we do know that it tends to develop in people who are obese or overweight or those who have diabetes, high cholesterol, or high triglycerides. It can also result from rapid weight loss and poor eating habits.

However, some people without these risk factors also develop NAFLD. Estimates suggest that up to 25 percent of people in the United States have NAFLD.

Dr. Fernández and colleagues note that some large genomics studies have linked variants of the gene that codes for the CPEB4 protein with disruption of fat metabolism.

For their investigation, they studied mice with low expression of CPEB4 gene in their livers.

They found that the mice developed fatty liver as they aged. They also found that feeding young CPEB4-depleted mice a high-fat diet led them to develop a more pronounced form of a fatty liver disease.

Further investigation into how CPEB4 behaves at the molecular level suggests that the protein plays a key role in the liver’s stress response.

Putting liver cells under stress – as a result of a high-fat diet, for example – upsets the equilibrium in a cell component called the endoplasmic reticulum (ER).

Without CPEB4, the ER responds ineffectively to stress
The ER carries out many tasks, including making proteins and lipids, as well as clearing away accumulated excess.

The researchers found that the ER adapts to stress by releasing CPEB4 to restore equilibrium – for instance, by boosting the clean-up of accumulated excess.

They also found that circadian rhythm influences the release of CPEB4; it is more active during the day (when the liver has the most work to do) and least active at night.

The team suggests that without CPEB4, the ER cannot properly restore equilibrium in response to stress, which results in the buildup of lipids and leads to fatty liver.

In a final set of experiments, the researchers showed that a drug called Tudca, currently used to treat other liver complaints, reversed fatty liver in the mice. The drug appears to trigger the same cleanup function as the proteins (called chaperones) that are activated by CPEB4.

The researchers suggest that their findings could lead to studies that show people with certain variants of CPEB4 are more susceptible to fatty liver. These people can then be advised to improve their diets or change their eating times.

The discovery could also lead to new treatments that target CPEB4 to boost the cleanup process in the ER.

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