Essential oils, which are “essences” derived from plants, are part of beauty rituals since ages and it is widely known for its wonders in skincare, body care and hair care.
Rahul Agarwal, CEO of organic personal care brand Organic Harvest, shares tips on using them in the winter season.
Oils from Essences are not only rich in nutrients but have unique healing and aromatic properties which helps to facilitate recovery from seasonal illnesses. Many essential oils are proven to be used as an effective healer, nourisher and cleanser.
Eucalyptus essential oil is one of the best for the cold weather which help fight sore throats, cough, seasonal allergies and headaches. The oil has antibacterial properties to improve immunity and blood circulation. It proves to be one of the best home remedies to reduce cough, allergies or to purify your home.
Winters can be particularly harsh on your scalp, causing dandruff and exacerbating dry skin issues. Other popular oils from essences like tea tree and rosemary work wonderfully for itchy and flaky skin. They are the best companion in winters to cure dandruff and reduce skin itching. Bonus, they also work wonderfully as a natural deodorant and fights body odour.
Other useful essential oils for cold weather includes the floral and citrus oils, such as lemon, lavender, grapefruit, jasmine and ylang ylang – which have enriching and calming scents that are said to have mood-boosting and uplifting effect on the mind. (IANS)
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.
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.
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.
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)