Is it all down to a cup of joe then?

People who drink coffee regularly, with or without sugar, both seem to benefit from the beverage as it cuts down on the risk of early death, * The Guardian* reported.

Grabbing a cup of coffee may just be something you do almost unconsciously as you sit down with your morning newspaper or before you start your workday. As the day wears on, you might be down three cups or maybe even five without giving it a second thought. However, scientists have been very conscious of the world’s coffee consumption.

Estimates suggest that over 400 million cups of coffee are consumed every day) in the U.S. That’s literally more than a cup of coffee for every inhabitant of the country. Since not everybody consumes coffee every day, the numbers suggest that an average American coffee consumer drinks three cups of coffee a day.

## How does coffee affect your health?

The critical component of coffee, caffeine is a stimulant of the central nervous system. Every time you consume caffeine or a soft drink that is also pumped with caffeine, the chemical blocks the action of adenosine on the neuronal receptors and stops you from feeling drowsy.

While this helps you feel more active and energized, caffeine is an addictive drug and researchers have warned against excessive consumption of it. Strangely though, consumption of coffee has also been linked to positive outcomes such as limiting the growth of prostate cancers or warmer brews being packed with antioxidants.

Researchers have, therefore, tapped into the UK Biobank to find out the impact of drinking coffee over a long period of time.

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A group of Chinese researchers accessed this database and selected a cohort of 171,000 participants for their study and tracked them over a period of seven years during which 3,177 people died, The Guardian reported.

Analyzing factors such as age, body mass index, amount of physical activity, and ethnicity among other various variables, the researchers found that individuals who consumed unsweetened coffee were at the lowest risk of death while those who did not consume coffee at all had higher risks. It was revealed that the individuals who consumed between 2.5 and 4.5 cups of coffee a day were at a 29% lower risk of death.

Even for individuals who consumed coffee with sugar, the risk of death was comparatively lower than for those who did not consume the beverage. The results were similar irrespective of whether the participants consumed instant, ground, or decaffeinated coffee. The data did not provide a clear correlation among people who used artificial sweeteners instead.

Remote inflammation in rheumatoid arthritis spreads by neuron crosstalk, and the molecule adenosine triphosphate (ATP) plays a key role in this.

Rheumatoid arthritis is a chronic inflammatory autoimmune disorder that mainly causes painful joints. It’s estimated to affect over 450,000 Australians.

Remote inflammation is a key feature – where inflammation spreads from one joint to another. Research has shown that factors involved include cells migrating from the joints and neural circuits, but until now the mechanism behind this spread had not been explained.

Now, a new study in mice has found that remote inflammation spreads by neuron crosstalk, and that the molecule adenosine triphosphate (ATP) plays a key role in this by acting as a neurotransmitter and inflammation enhancer.

Using a new gene therapy technique, researchers at the University of California San Diego reduced neuropathic pain resulting from spinal cord or other nerve injuries in mice — and with no detectable side effects.

The research is highly intriguing because it could lead to new treatment options for the untold numbers of patients who experience chronic pain, numbness or weak muscles as a result of spinal cord injuries.

Treating nerve damage or dysfunction, otherwise known as neuropathy, with drugs can often lead to side effects. These drugs also have to be administered continuously, and opioids — which are particularly effective painkillers — can often lead to addiction issues.

Background An attempt was made to reprogram peripheral blood cells into human induced pluripotent stem cell (hiPSCs) as a new cell source for cartilage repair. Methods We generated chondrogenic lineage from human peripheral blood via hiPSCs using an integration-free method. Peripheral blood cells were either obtained from a human blood bank or freshly collected from volunteers. After transforming peripheral blood cells into iPSCs, the newly derived iPSCs were further characterized through karyotype analysis, pluripotency gene expression and cell differentiation ability. iPSCs were differentiated through multiple steps, including embryoid body formation, hiPSC-mesenchymal stem cell (MSC)-like cell expansion, and chondrogenic induction for 21 days. Chondrocyte phenotype was then assessed by morphological, histological and biochemical analysis, as well as the chondrogenic expression.

An attempt was made to reprogram peripheral blood cells into human induced pluripotent stem cell (hiPSCs) as a new cell source for cartilage repair.

We generated chondrogenic lineage from human peripheral blood via hiPSCs using an integration-free method. Peripheral blood cells were either obtained from a human blood bank or freshly collected from volunteers. After transforming peripheral blood cells into iPSCs, the newly derived iPSCs were further characterized through karyotype analysis, pluripotency gene expression and cell differentiation ability. iPSCs were differentiated through multiple steps, including embryoid body formation, hiPSC-mesenchymal stem cell (MSC)-like cell expansion, and chondrogenic induction for 21 days. Chondrocyte phenotype was then assessed by morphological, histological and biochemical analysis, as well as the chondrogenic expression.

HiPSCs derived from peripheral blood cells were successfully generated, and were characterized by fluorescent immunostaining of pluripotent markers and teratoma formation in vivo. Flow cytometric analysis showed that MSC markers CD73 and CD105 were present in monolayer cultured hiPSC–MSC-like cells. Both alcian blue and toluidine blue staining of hiPSC–MSC-chondrogenic pellets showed as positive. Immunohistochemistry of collagen II and X staining of the pellets were also positive. The sulfated glycosaminoglycan content was significantly increased, and the expression levels of the chondrogenic markers COL2, COL10, COL9 and AGGRECAN were significantly higher in chondrogenic pellets than in undifferentiated cells. These results indicated that peripheral blood cells could be a potential source for differentiation into chondrogenic lineage in vitro via generation of mesenchymal progenitor cells.