Wednesday January 22, 2020

Here’s Why E-Cigarettes May Develop The Risk Of Pulmonary Diseases

A study also found that switching from smoked tobacco to e-cigarettes lowered the risk of developing lung disease, fewer than one per cent of the smokers had completely switched to e-cigarettes

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Pulmonary
A Chemical analyses showed that e-cigarettes contain higher levels of certain toxic chemicals than conventional cigarettes. But the new study shows that these are not the only health threats posed by e-cigarettes leading to Pulmonary Diseases. Pixabay

E-cigarette use significantly increases a person’s risk of developing chronic lung diseases like asthma, bronchitis, emphysema or chronic obstructive pulmonary disease, says a new study.

The study, published in the American Journal of Preventive Medicine, also found that people who used e-cigarettes and also smoked tobacco — by far the most common pattern among adult e-cigarette users — were at an even higher risk of developing chronic lung disease than those who used either product alone.

“What we found is that for e-cigarette users, the odds of developing lung disease increased by about a third, even after controlling for their tobacco use and their clinical and demographic information,” said study senior author Stanton Glantz, PhD, Professor at the University of California in the US.

“We concluded that e-cigarettes are harmful on their own, and the effects are independent of smoking conventional tobacco,” Glantz said.

The findings are based on an analysis of publicly available data from the Population Assessment of Tobacco and Health (PATH), which tracked e-cigarette and tobacco habits as well as new lung disease diagnoses in over 32,000 American adults from 2013 to 2016.

Though several earlier population studies had found an association between e-cigarette use and lung disease at a single point in time, these cross-sectional studies provided a snapshot that made it impossible for researchers to say whether lung disease was being caused by e-cigarettes or if people with lung disease were more likely to use e-cigarettes.

By starting with people who did not have any reported lung disease, taking account of their e-cigarette use and smoking from the start, and then following them for three years, this study offers stronger evidence of a causal link between adult e-cigarette use and lung diseases than prior studies.

Though current and former e-cigarette users were 1.3 times more likely to develop chronic lung disease, tobacco smokers increased their risk by a factor of 2.6.

“Dual users — the most common use pattern among people who use e-cigarettes — get the combined risk of e-cigarettes and conventional cigarettes, so they’re actually worse off than tobacco smokers,” said Glantz.

The study also found that switching from smoked tobacco to e-cigarettes lowered the risk of developing lung disease, fewer than one per cent of the smokers had completely switched to e-cigarettes.

Importantly, the results reported in this study are unrelated to EVALI (E-cigarette or Vaping Product Use-Associated Lung Injury), the acute lung disease first reported last summer, severe cases of which sent several e-cigarette users to the hospital and others to an early grave.

Pulmonary
E-cigarette use significantly increases a person’s risk of developing chronic lung diseases like asthma, bronchitis, emphysema or chronic obstructive pulmonary disease, says a new study. Pixabay

Though scientists are still working to determine the cause of EVALI, prior physiological studies in both animals and humans found that e-cigarettes suppress the immune system and increase the levels of stress-related proteins in the lungs.

And chemical analyses showed that e-cigarettes contain higher levels of certain toxic chemicals than conventional cigarettes. But the new study shows that these are not the only health threats posed by e-cigarettes.

ALSO READ: Artificial Intelligence Can Better Help Doctors To Recognize Cancer Cells

“This study contributes to the growing case that e-cigarettes have long-term adverse effects on health and are making the tobacco epidemic worse,” Glantz added. (IANS)

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Drugs That Treat Arthritis in Dogs Can Kill Cancer Cells: Study

Drug for arthritis in dogs can fight cancer in people

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Cancer Cells
Drugs for diabetes, inflammation, alcoholism and even for treating arthritis in dogs can also kill cancer cells. Pixabay

Drugs for diabetes, inflammation, alcoholism — and even for treating arthritis in dogs — can also kill cancer cells in the lab, according to a new health news and study.

The researchers systematically analysed thousands of already developed drug compounds and found nearly 50 that have previously unrecognised anti-cancer activity.

The findings, which also revealed novel drug mechanisms and targets, suggest a possible way to accelerate the development of new cancer drugs or repurpose existing drugs to treat cancer.

“We thought we’d be lucky if we found even a single compound with anti-cancer properties, but we were surprised to find so many,” said study researcher Todd Golub from Harvard University in the US.

Cancer Cells
Most of the non-oncology drugs that killed cancer cells in the study did so by interacting with a previously unrecognized molecular target. (Representational Image). Pixabay

The study, published in the journal Nature Cancer, yet to employ the Broad’s Drug Repurposing Hub, a collection that currently comprises more than 6,000 existing drugs and compounds that are either FDA-approved or have been proven safe in clinical trials (at the time of the study, the Hub contained 4,518 drugs).

Historically, scientists have stumbled upon new uses for a few existing medicines, such as the discovery of aspirin’s cardiovascular benefits.

“We created the repurposing hub to enable researchers to make these kinds of serendipitous discoveries in a more deliberate way,” said study first author Steven Corsello, from Dana-Farber Cancer Institute and founder of the Drug Repurposing Hub.

The researchers tested all the compounds in the Drug Repurposing Hub on 578 human cancer cell lines from the Broad’s Cancer Cell Line Encyclopedia (CCLE).

Using a molecular barcoding method known as PRISM, which was developed in the Golub lab, the researchers tagged each cell line with a DNA barcode, allowing them to pool several cell lines together in each dish and more quickly conduct a larger experiment.

The team then exposed each pool of barcoded cells to a single compound from the repurposing library, and measured the survival rate of the cancer cells.

They found nearly 50 non-cancer drugs — including those initially developed to lower cholesterol or reduce inflammation — that killed some cancer cells while leaving others alone.

Some of the compounds killed cancer cells in unexpected ways.

“Most existing cancer drugs work by blocking proteins, but we’re finding that compounds can act through other mechanisms,” said Corsello.

Cancer Cells
The researchers tested all the compounds in the Drug Repurposing Hub on 578 human cancer cells lines from the Broad’s Cancer Cell Line Encyclopedia. (Representational Image). Pixabay

Some of the four-dozen drugs researchers identified appear to act not by inhibiting a protein but by activating a protein or stabilising a protein-protein interaction.

For example, the team found that nearly a dozen non-oncology drugs killed cancer cells that express a protein called PDE3A by stabilising the interaction between PDE3A and another protein called SLFN12 — a previously unknown mechanism for some of these drugs.

These unexpected drug mechanisms were easier to find using the study’s cell-based approach, which measures cell survival, than through traditional non-cell-based high-throughput screening methods, Corsello said.

Also Read- Mothers Find Gaps in Accessibility of Breastfeeding Resources at Work: Research

Most of the non-oncology drugs that killed cancer cells in the study did so by interacting with a previously unrecognized molecular target.

For example, the anti-inflammatory drug tepoxalin, originally developed for use in people but approved for treating osteoarthritis in dogs, killed cancer cells by hitting an unknown target in cells that overexpress the protein MDR1, which commonly drives resistance to chemotherapy drugs. (IANS)