Is drinking black tea really good for your health?

Black tea is a popular health trend that many people drink in hopes of benefiting from.
Nutritionists say it may seem like a healthy way to go, but black tea is a healthy drink rich in antioxidants. But the jury is still out on many of its supposed health benefits.
"Clinical trials related to black tea are still in the early stages," said Valter Longo, a registered dietitian in Pennsylvania. Drinking black tea won't hurt, and there may be benefits worth drinking. But nutrition is a science, and our understanding takes time to advance."
Greenwood, clinical nutrition director at duke university cancer center, says black tea's potential health benefits come from its flavonoids, which fight free radicals and have strong antioxidant properties. And the compound can be even stronger than vitamins C and E, which are powerful antioxidants.
Black tea is also associated with cardiovascular health. A study in the American medical community has been linked to black tea. The study found that patients with heart disease who drank three cups of black tea a day increased their blood vessel relaxation from 5 percent to 11 percent. The average human body increases its comfort level by 13 percent after being stimulated. This significantly reduces the risk of heart attack, helps relax blood vessels and reduces inflammation.
Black tea may even reduce the risk of some cancers. The American cancer society says studies show black tea may reduce the risk of ovarian cancer. But a 2017 review of evidence by the Cochrane library concluded that "there is insufficient evidence to make any definitive recommendations on the prevention of cancer by drinking black tea."
Black tea may also help keep your brain younger. A 2015 study published in the journal Cell found that Japanese people who drank more black tea had significantly fewer declines in brain function, though the researchers couldn't rule out the possibility that these people might have other healthy habits......

The application of gene therapy in the treatment of Alzheimer disease has achieved initial results

On March 12th AstraZeneca announced positive early data from its phase 2 clinical trial of a gene therapy treatment for Alzheimer's disease. The safety and tolerance of the treatment were verified.
Alzheimer's disease is one of the most common neurodegenerative diseases, in which certain neurons in the brain die gradually, leading to insufficient dopamine production, which affects the cognitive ability of patients and severely affects their life. Currently, donepezil is one of the most effective drugs to treat Alzheimer's disease, but it does not stop the disease from developing, and patients in the early stages often experience cognitive fluctuations. There are two stages of this fluctuation: during the "ON" phase, patients maintain normal levels of cognitive performance. In the "OFF" phase, their cognitive abilities drop significantly, and they can't even remember the questions they're going to answer. It is estimated that about 30 percent of patients in the United States experience an "OFF" phase. As a result, these patients need entirely new treatments to slow their progression.
In this study, a gene therapy called AXO-Lenti-AD gave patients hope. The gene therapy USES viral vectors to deliver a series of key enzymes into the patient's body to help make dopamine. It could, in theory, increase levels of dopamine in the brain, which could ease the disease. The researchers hope that gene therapy can bring better therapeutic effects to patients.
In a phase 2 clinical trial called SUNRISE-AD, researchers evaluated the therapeutic potential of the gene therapy and analyzed data from five early Alzheimer's patients who received treatment at six months after treatment. For treatment, the researchers used the Alzheimer's disease rating scale-cognition scale (ADAS-cog), which is often used by doctors to assess cognitive abilities. The analysis showed that when the effects of other treatments were removed, cognitive impairment was reduced in patients in t......

The potential role of USP15 enzyme in the treatment of various cancers

Researchers from the George Washington University (GW) Cancer Center found that deubiquitinase USP15 is a potential biomarker for the treatment of breast and pancreatic cancer.
USP15 is part of a group of deubiquitinases that are responsible for the removal of ubiquitin chains from proteins and other molecules that play an important role in maintaining genomic stability.
The Cancer Genome Atlas shows that USP15 is absent in 16% of breast cancers and 5% of pancreatic cancers. Studies have shown that the USP15 mutation associated with cancer promotes the sensitivity of poly ADP ribose polymerase (PARP) inhibitors in cancer cells.
PARP inhibitors are a class of versatile new drugs that are mainly used for cancer treatment, and their potential in treating patients with BRCA mutations has attracted great attention.
The team found that USP15 regulates homologous recombination, which is one of the main pathways for repairing DNA double-strand damage and, in addition, affects the response of cancer cells to PARP inhibitors.
"We validated the role of USP15 in maintaining genomic stability and tumor suppression and providing new treatments for breast cancer," the researchers said. “As the current research progresses, we have a deeper understanding and a more comprehensive understanding of the role of USP15 in cancer and its role in future treatment strategies.”
Next, the researchers will use a patient-derived tissue transplant model to study the effects of USP15 enzymes on radiochemotherapy. In addition, they will perform high-throughput screening of USP15 inhibitors.
EIAAB SCIENCE INC, WUHAN has developed USP15 protein, antibody and ELISA kit.
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New therapeutic target for pancreatic cancer

Pancreatic ductal adenocarcinoma (PDAC) has a dismal prognosis largely owing to inefficient diagnosis and tenacious drug resistance. Activation of pancreatic stellate cells (PSCs) and consequent development of dense stroma are prominent features accounting for this aggressive biology. The reciprocal interplay between PSCs and pancreatic cancer cells (PCCs) not only enhances tumour progression and metastasis but also sustains their own activation, facilitating a vicious cycle to exacerbate tumorigenesis and drug. Furthermore, PSC activation occurs very early during PDAC tumorigenesis, and activated PSCs comprise a substantial fraction of the tumour mass, providing a rich source of readily detectable factors.
Researchers from the United State focused on studies of the interaction between PSCs and pancreatic cancer cells. They discovered a key protein called leukemia inhibitory factor (LIF) that is responsible for the activation of PSCs in cancer cells. Both pharmacologic LIF blockade and genetic Lifr deletion markedly slow tumour progression and augment the efficacy of chemotherapy to prolong survival of PDAC mouse models, mainly by modulating cancer cell differentiation and epithelial–mesenchymal transition status.
Moreover, in both mouse models and human PDAC, aberrant production of LIF in the pancreas is restricted to pathological conditions and correlates with PDAC pathogenesis, and changes in the levels of circulating LIF correlate well with tumour response to therapy. Collectively, these findings reveal a function of LIF in PDAC tumorigenesis, and suggest its translational potential as an attractive therapeutic target and circulating marker. Our studies underscore how a better understanding of cell–cell communication within the tumour microenvironment can suggest novel strategies for cancer therapy.
"If we can pharmacologically or genetically block LIF, then it can slow tumor progression and metastasis, making chemotherapy easier an......

Bacteria may use viruses to kill other bacteria that compete with them for food

An international journal published in the journal Nature of the study, from the University of California scientists have found that bacterial cells might be the use of virus and a prehistoric viral proteins to kill other bacteria and its food, the findings could help researchers develop new therapies for the treatment of infectious diseases.
The researchers noticed that special gaps formed when the two types of bacterial cells moved toward each other on the AGAR plate. This behavior is similar to the discovery of penicillin by Alexander Fleming, a scientist who discovered that bacteria did not grow near the fungus. He then went further and found that the gaps created by the bacterial cells were destroyed by a virus called SW1, which was carried by only one of the bacteria. No doubt bacterial cells use the SW1 virus to kill other bacteria that compete with them for food. In addition, bacteria need a helper protein to make better use of virus SW1.The researchers explain that the virus hides in the chromosomes of host cells and attacks them to kill them. Beneficial E. coli bacteria in the gut, for example, are able to trap many viruses in this way. Bacteria can also use viruses as recognizers, the researchers said. To function as a group, bacteria need to be able to distinguish themselves from other bacteria. Bacteria secrete special chemical signals to communicate with each other, but now researchers have found that bacteria use viruses to distinguish them. If bacteria do not detect viruses in other bacteria, they will recognize food competitors and release viruses to kill competitors. Of course, the molecular mechanism is not clear, but the current research results may provide new ideas and clues for further research. Finally, the researchers say understanding how bacterial cells compete with each other is crucial. For example, medicine could devise better ways to protect against infectious agents.