The significance of beta-2 microglobulin monitoring in early renal impairment in hypertensive patients

Essential hypertension is one of the most common chronic diseases in the world. With the improvement of living standards, life pressure, changes in nutritional structure and other factors, the prevalence rate increases year by year. Kidney is one of the target organs of essential hypertension, which can lead to renal failure and affect renal function.
Generally, obvious clinical symptoms have been developed to the end of renal damage, the treatment effect is very poor.
It is of great significance to discover the symptoms of kidney damage through medical means. Traditional renal function examination is generally to reflect the damage to the kidney parenchyma for the purpose, not a sensitive indicator. Therefore, the medical community continues to explore how to make effective and rapid diagnosis of early hypertensive nephropathy.
The discovery and clinical application of beta -2 microglobulin make the diagnosis of early renal damage easy.Beta-2 microglobulin is widely found in plasma, urine, saliva and colostrum. It is a small globulin produced by lymphocytes, platelets and polymorphonuclear white blood cells, and its molecular weight is 11.8kD. It is part of the beta (light) chain of human histocompatibility antigens (HLA) on the cell surface. The molecule contains a pair of disulfide bonds that contain no sugar and are similar in structure to the immunoglobulin stabilizer region.95% of beta 2-mg in the normal human body is filtered by glomeruli and 99.9% is reabsorbed in the proximal convoluted tubules and decomposed into amino acids, so the content of beta 2-mg in the blood and urine of normal people is extremely low. Beta 2-MG is relatively stable and can be used as an indicator of glomerular and tubular functional status.

E0260h is a ready-to-use microwell, strip plate ELI......

New cancer immunotherapy is expected to be used in clinical practice

In 2018, the Nobel Prize in physiology or medicine was awarded to two scientists for their pioneering work in the field of cancer immunotherapy for their contributions to the development of this revolutionary cancer treatment.
The mechanism of cancer immunotherapy is well understood. In the body's immune system, t-lymphocytes can attack cancer cells. But T cells have inhibitory receptors that inhibit T cell activity. Cancer cells are acutely aware of this, secreting substances that bind to these receptors and bind T cells. Immunotherapy, on the other hand, unlocks these bonds, allowing T cells to resume their ability to attack cancer cells.
As a revolutionary anti-cancer treatment, immunotherapy has two properties: on the one hand, the immune system has a "memory" for cancer. Once it works, it works for the long term. Some patients who received treatment did not relapse for nearly a decade, which is clinically equivalent to "cure". On the other hand, immunotherapy is not a panacea. According to statistics, only about 10% of patients can get long-term benefits from immunotherapy. So scientists and drug developers are developing new immunotherapies to benefit patients. Unfortunately, new drugs are not easy to develop. Several promising new drugs have failed in clinical trials. But that has not stopped innovation. A new combination of immunotherapies has emerged. The key behind this treatment is a receptor molecule called NKG2A, which is expressed in large amounts on the surface of T cells and NK cells, and the binding of NKG2A to ligands inhibits the function of T cells and NK cells. This is similar to the immune cell "brake" we mentioned above. Similarly, if NKG2A binding to ligand can be inhibited, it is expected to release the activity of immune cells. The researchers did an in vitro experiment first. They found that both NKG2A antibody and pd-l1 antibody alone increased the activity of immune cells. And both use together, can have apparent more outsta......

Breast cancer resistance may be related to a diet rich in leucine

About one in ten American women will develop breast cancer in her lifetime. Most breast cancers rely on estrogen for growth. Estrogen-receptor-positive breast cancer is often treated with the drug tamoxifen, which blocks the hormone's effect on the tumor. However, many tumors eventually become resistant to tamoxifen, leading to cancer recurrence or metastasis.
Now, a team of researchers at duke university’s cancer institute has found a possible link between leucine levels and tamoxifen resistance in ER+ breast cancer. At the same time, the researchers further identified a key protein that can introduce leucine into cells and modulate the sensitivity of ER+ breast cancer cells to tamoxifen, revealing a mechanism for overcoming endocrine drug resistance in ER+ breast cancer patients.
"The survival of ER+ breast cancer patients with drug-resistant and metastatic tumors is very short, usually less than three years, because their treatment options are very limited," says Helen piwnica-worms, Ph.D., director of the cell biology program at the BIDMC cancer institute." Our findings in the laboratory suggest that lowering leucine levels inhibits tumor cell proliferation, while increasing leucine levels enhances cancer cell proliferation." These findings also provide evidence for the possible benefits of a low-leucine diet.
Leucine is one of the 20 amino acids that make up all proteins in the body. It is also one of the nine essential amino acids that must be obtained through food. Beef, chicken, pork and fish are rich in leucine. Because cells by themselves don't produce leucine, Helen piwnica-worms and his colleagues were able to test how controlling leucine levels can affect the growth of human-derived ER+ breast cancer cells. Lowering leucine levels inhibited division in ER+ breast cancer cells, while increasing the number of amino acids by a factor of 10 increased the division, the researchers said.

Serotonin regulates gene expression in neurons

    Serotonin or 5-hydroxytryptamine (5-HT) is an important monoamine neurotransmitter. It is responsible for transmitting signals between brain neurons and for regulating mood.
    Recently, scientists in China and the United States discovered that serotonin also regulates gene expression in neurons.
    By Western blotting and recombinant TGM2 enzyme analysis, they confirmed that histone H3 is an endogenous substrate for serotoninization. Chemical modifications of histones can mediate diverse DNAtemplated processes, including gene transcription1–3. The study proved that serotonylation of glutamine occurred at position 5 (Q5ser) on histone H3 in organisms that produce serotonin (also known as 5-hydroxytryptamine (5-HT)).
    The researchers demonstrate that tissue transglutaminase 2 can serotonylate histone H3 tri-methylated lysine 4 (H3K4me3)-marked nucleosomes, resulting in the presence of combinatorial H3K4me3Q5ser in vivo. H3K4me3Q5ser displays a ubiquitous pattern of tissue expression in mammals, with enrichment observed in brain and gut, two organ systems responsible for the bulk of 5-HT production. Genomewide analyses of human serotonergic neurons, developing mouse brain and cultured serotonergic cells indicate that H3K4me3Q5ser nucleosomes are enriched in euchromatin, are sensitive to cellular differentiation and correlate with permissive gene expression, phenomena that are linked to the potentiation of TFIID4–6 interactions with H3K4me3. Cells that ectopically express a H3 mutant that cannot be serotonylated display significantly altered expression of H3K4me3Q5ser-target loci, which leads to deficits in differentiation.
    These results identify a direct role for 5-HT, independent from its contributions to neurotransmission and cellular signalling, in the mediation of permissive gene expression. The research helps people better understand a variet......

Human cells reprogrammed to create insulin

    When blood sugar levels rise after eating, cells in the pancreas called β-cells normally respond by releasing insulin, which in turn stimulates cells to start absorbing sugars. In people with diabetes, this system breaks down, leading to high blood sugar levels that can damage the body and causes illness.
    In type 1 diabetes, the immune system attacks and destroys β-cells; in type 2, the β-cells do not produce enough insulin, or the body becomes resistant to insulin.
    Scientists have previously shown in mouse studies that if β-cells are destroyed, another type of pancreatic cell, called α-cells become more β-like and start making insulin. These α-cells normally produce the hormone glucagon, and are found alongside β-cells in clumps of hormone-secreting cells called pancreatic islets or islets of Langerhans. Previous studies showed that two proteins that control gene expression seemed to have an important role in coaxing α-cells to produce insulin in mice: Pdx1 and MafA.
    Researchers at the University of Geneva first took islet cells from human pancreases, and separated out the individual cell types. They then introduced DNA that encoded Pdx1 and MafA proteins into the α-cells, before clumping them back together.
    After one week in culture, almost 40% of the human α-cells were producing insulin, whereas control cells that hadn’t been reprogrammed were not. The reprogrammed cells also showed an increase in the expression of other genes related to β-cells. “They have a hybrid personality” said the researcher.
    The team then implanted the mass of cells into diabetic mice, which had their β-cells destroyed, and found that blood-sugar levels went down to normal levels. When the cell grafts were removed, the mice’s blood sugar shot back up.
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