When someone has a heart attack…

If immediate first-aid is not given to a heart attack patient, there may be permanent damage or a cardiac arrest.

Heart attack is one of the leading causes of death the world over. Most of these deaths take place, because proper first-aid or medical attention is not given between the time the person has the attack and the time the person reaches a hospital. That is why it is important for everyone to know how and what to do, as soon as a person is suspected to have had a heart attack.

Remember the following:
Every moment is precious in case of heart attack, so act fast. Do not leave the person alone and don’t try to manage at home. Do not give anything orally. Even if he feels little better, lift him to reach the nearest hospital as early as possible.There is no household remedy for heart attack. Keep him in lying down posture, loosen his clothing and rush him to the nearest hospital. Make him chew one full tablet of apirin and swallow.

Give him one Sorbitrate tablet under the tongue. If there is profuse sweating, ie, drop in blood pressure, then don’t give it.
You can give glucose powder in spoonful dosages on or under the tongue frequently. Don’t give sweet drinks.

If short of breath, then recline the patient partially and make him cough intermittently.

If the person is unconscious and unresponsive, CPR (cardio pulmonary resuscitation) should be performed. Give chest thrust and mouth-to-mouth respiration.

Do not depend on the first-aid to benefit. Reach the nearest facility, which has ICU or advanced treatment facilities for heart

High white blood cell ratio linked to recurrence risk in early stage breast cancer

A high ratio of two types of immune system cell is linked to an increased risk of disease recurrence after a diagnosis of early stage breast cancer, finds the first study of its kind, published on the eve of international Women’s Day (March 8) in the online journal ESMO Open.

The finding might guide future treatment and monitoring strategies, if prospective studies confirm the link, say the researchers.

A mounting body of evidence indicates that inflammation has a role in the development and progression of several types of cancer, with studies suggesting that the ratio of neutrophils to lymphocytes, or NLR for short, may be important.

Neutrophils and lymphocytes are white blood cells that are despatched as part of the body’s immune system response to harmful invaders, including cancer cells.

Several studies have reported that a high NLR is associated with a poor outcome in several different types of cancer. But the few studies carried out in women with breast cancer have been inconclusive–possibly because they have included mostly women of Asian ethnicity whose survival is generally longer than that of women from other ethnic backgrounds, say the researchers.

To find out if NLR was associated with disease free survival, the research team tracked the health of 300 white women, all but nine of whom were older than 35, for up to 15 years (1999-2015) following their diagnosis.

All the women had early stage breast cancer, defined as stages I or II, with no spread to other parts of the body.

On the basis of their blood counts taken after diagnosis, but before treatment, 134 of the women had a low NLR (1.97 or lower) and 166 had a high NLR (above 1.97).

After 15 years, cancer had returned in another part of the body in 37 (12%) of the women.

Women with a low NLR fared better at each of the subsequent check-ups at 1, 3, 6, 9, 12, and 15 years, with, respectively, 100%, 98.9%, 91.7%, 82.7%, 82.7%, and 82.7% of them free of recurrence.

This compares with comparable figures of 99.4%, 94.3%, 84.5%, 69.2%, 66%, and 51.4% at the same time points in those with a high NLR.

The researchers undertook further analysis to take account of other potentially influential factors. They found that not having yet gone through menopause, nodes with cancerous cells in the armpit (N1), and a high NLR were independently associated with the risk of recurrence.

To corroborate the findings further, the researchers carried out a propensity score matched analysis–a statistical matching technique that attempts to estimate the effect of an intervention by accounting for the factors that predict receiving it.

This technique was applied to 226 patients (half with a high NLR and half with a low NLR).The results confirmed that not having gone through the menopause, having armpit lymph nodes with cancerous cells, and a high NLR were each independently associated with a worse prognosis.

This is an observational study so no firm conclusions can be drawn about cause and effect, and it was retrospective. But the statistical matching strengthens the associations found, which have also been found in other cancers, say the researchers.

“Despite looking apparently simple, the relationship between NLR and outcome in patients with cancer is probably a complex and multifactorial process [that is] still poorly understood,” write the researchers.

“In simple terms, a high NLR may reflect the key role of systemic inflammation in enhancing angiogenesis [formation of new blood vessels], tumour growth, and development of metastasis [spread],” they say.

ESMO Open Editor in Chief, Professor Christoph Zielinski, comments: “It is inspirational to see the results of this study showing that there may be a potential new way to support women with early breast cancer. We hope that it will encourage more researchers active in this area to establish collaborations around the world with a view to confirming these findings.”


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The above post is reprinted from materials provided by BMJ.Note: Materials may be edited for content and length.

Unconventional treatment strategy controls — rather than eradicates — cancer

Can we learn to live with–rather than kill–cancer? A new study suggests that frequent, low-dose chemotherapy that keeps tumor growth under control may be more effective than standard high-dose chemotherapy that seeks to eradicate cancer cells completely. The treatment strategy, which was tested in mice, flies in the face of conventional cancer therapy, which generally hits patients with the maximum drug dose possible to kill off the largest number of tumor cells.

Despite aggressive treatment, complete cancer eradication is rare and toxic side effects all too common. Recently, researchers have questioned the benefits of standard chemotherapy because while it destroys drug-sensitive tumor cells, it leaves behind drug-resistant cells. By eliminating the former population of tumor cells, the drug allows resistant cells to take over and drive tumor growth uncontrolled.

Taking into account the evolutionary forces that drive cancer resistance, Pedro Enriquez-Navas and colleagues designed an evolution-based treatment strategy that adjusts the drug dose based on how the tumor responds. Rather than trying to shrink the tumor completely, the so-called adaptive therapy seeks to stabilize the tumor by maintaining a small population of drug-sensitive tumor cells to suppress the growth of resistant cells.

The researchers tested the approach with the chemotherapy drug paclitaxel in mice with two different types of breast cancer. Standard chemotherapy shrunk the mouse breast tumors, but only to have them grow back as soon as treatment stopped. Another treatment regimen that skips doses whenever the tumor shrunk also inevitably resulted in tumor progression.

In contrast, adaptive therapy consisting of high initial drug doses followed by progressively lower doses as the tumor responded was more effective in controlling tumor growth than either standard therapy or dose skipping.

In fact, the treatment allowed between 60 and 80% of the mice to be weaned off the drug completely without relapsing for an extended period of time. A related Focus by Giannoula Klement discusses how the study’s eco-evolutionary model of cancer may prompt researchers and clinicians to rethink current therapeutic strategies for cancer.


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The above post is reprinted from materials provided byAmerican Association for the Advancement of Science.Note: Materials may be edited for content and length.

New discoveries on the connection between nicotine and type 2 diabetes

Researchers at Lund University in Sweden have made two new discoveries with regard to the beta cells’ ability to release insulin. The findings can also provide a possible explanation as to why smokers have an increased risk of type 2 diabetes.

The study was conducted on mice and donated beta cells from humans, and is now published in the scientific journal Cell Reports.

The researchers have discovered that so-called nicotinic acetylcholine (nicotine-sensitive) receptors influence the normal release of insulin. They also show that a specific genetic alteration renders dysfunctional nicotine-receptors affecting the number of functional nicotine-sensitive receptors found in beta cells. A reduced number of functional receptors leads to a decrease in insulin secretion, thereby increasing the risk of developing type 2 diabetes.

“The receptors in the beta cells that stimulate the release of insulin are normally activated by the signal substance acetylcholine, but they can also be activated by nicotine. Never before has the importance of nicotine-sensitive receptors been shown in terms of the function of beta cells. Our research indicates that people who lack these receptors are at higher risk of developing type 2 diabetes,” says Isabella Artner, researcher at Lund University responsible for the study.

Isabella Artner and her colleagues have also discovered that the gene MafA (muscoloaponeurotic fibrosacoma oncogene family A) found in insulin-producing beta cells control the number of nicotine-sensitive receptors and thereby their ability to receive signals from the central nervous system.

“The effect that this single gene, MafA, alone has on insulin secretion was previously unknown, and nicotine receptors have never before been connected to type 2 diabetes,” says Isabella Artner, and continues:

“We know that smokers have an increased risk of developing type 2 diabetes, but the reason why has not been firmly established. Perhaps it has to do with the nicotine-sensitive receptors we describe. Our findings increase knowledge about the connection between smoking and type 2 diabetes.


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The above post is reprinted from materials provided by Lund University. Note: Materials may be edited for content and length.