National Health and Family Planning Commission

About: National Health and Family Planning Commission is a government organization based out in Beijing, China. It is known for research contribution in the topics: Population & Kashin–Beck disease. The organization has 2379 authors who have published 1440 publications receiving 20078 citations. The organization is also known as: Ministry of Health of the People's Republic of China.

Deregulated MicroRNA-21 Expression in Monocytes from HIV-Infected Patients Contributes to Elevated IP-10 Secretion in HIV Infection

Abstract: Persistent activation and inflammation impair immune response and trigger disease progression in HIV infection. Emerging evidence supports the supposition that excessive production of interferon-inducible protein 10 (IP-10), a critical inflammatory cytokine, leads to immune dysfunction and disease progression in HIV infection. In this study, we sought to elucidate the cause of the upregulated production of IP-10 in HIV infection and explore the underlying mechanisms. Bolstering miR-21 levels using mimics resulted in the obvious suppression of lipopolysaccharide (LPS)-induced IP-10 in monocyte leukemia cells THP-1 and vice versa. The analysis of the primary monocytes of HIV patients revealed significantly less miR-21 than in healthy controls; this was opposite to the tendency of IP-10 levels in plasma. The secretion of IP-10 due to LPS stimulation was not affected by miR-21 modulation in the differentiated THP 1 macrophages (THP-1-MA). We found a novel switch, IFN stimulated gene 15 (ISG15), which triggers the expression of IP-10 and is significantly upregulated during the differentiation of THP-1 into THP-1-MA. The inhibition of ISG15 can restore the regulation of IP-10 by miR-21. In summary, IP-10 expression in monocytes is regulated by miR-21, whereas in macrophages, this fine-tuning is attenuated by the enhanced expression of ISG15. This study paves the way to a comprehensive understanding of the molecular regulatory mechanism of IP-10, a key point in immune intervention strategy.

Effects of metformin on metabolism of white and brown adipose tissue in obese C57BL/6J mice.

Abstract: To investigate effects of metformin on the regulation of proteins of white adipose tissue (WAT) and brown adipose tissue (BAT) in obesity and explore the underlying mechanisms on energy metabolism. C57BL/6J mice were fed with normal diet (ND, n = 6) or high-fat diet (HFD, n = 12) for 22 weeks. HFD-induced obese mice were treated with metformin (MET, n = 6). After treatment for 8 weeks, oral glucose tolerance test (OGTT) and hyperinsulinemic–euglycemic clamp were performed to evaluate the improvement of glucose tolerance and insulin sensitivity. Protein expressions of WAT and BAT in mice among ND, HFD, and MET group were identified and quantified with isobaric tag for relative and absolute quantification (iTRAQ) coupled with 2D LC–MS/MS. The results were analyzed by MASCOT, Scaffold and IPA. The glucose infusion rate in MET group was increased significantly compared with HFD group. We identified 4388 and 3486 proteins in WAT and BAT, respectively. As compared MET to HFD, differential expressed proteins in WAT and BAT were mainly assigned to the pathways of EIF2 signaling and mitochondrial dysfunction, respectively. In the pathways, CPT1a in WAT, CPT1b and CPT2 in BAT were down-regulated by metformin significantly. Metformin improved the body weight and insulin sensitivity of obese mice. Meanwhile, metformin might ameliorate endoplasmic reticulum stress in WAT, and affect fatty acid metabolism in WAT and BAT. CPT1 might be a potential target of metformin in WAT and BAT.

Histidine Alleviates Impairments Induced by Chronic Cerebral Hypoperfusion in Mice.

Abstract: Chronic cerebral hypoperfusion is one of the fundamental pathological causes of brain disease such as vascular dementia. Exploration of effective treatments for this is of great interest. Histidine has been reported to be effective in anti-apoptosis, antioxidant, and against excitotoxicity. In the present study, we aim to investigate whether histidine could have a therapeutic effect on the impairments induced by chronic cerebral hypoperfusion. Cerebral hypoperfusion model was established through bilateral common carotid arteries stenosis (BCAS) operation in Tie2-GFP mice. Radial arm maze and Morris water maze revealed that histidine showed potential improvement of the tendency of cognitive impairments induced by hypoperfusion. The possible mechanisms were further investigated. After administration of histidine in hypoperfusion mice, immunofluorescent BrdU staining revealed more new-born nerve cells. In vivo observation through a cranial window under two-photon laser-scanning microscopy demonstrated that the blood flow velocity in capillary was improved, the distance between the astrocytes and the penetrating artery was shortened. Histidine administration also significantly increased the protein expression level of zonula occludens protein 1, an indicator of the integrity of blood-brain barrier (BBB). These results suggest that histidine could alleviate the impairments induced by chronic cerebral hypoperfusion in mice, and this effect may be related to the neurogenesis, astrocytes, and the integrity of the BBB.