Intensive attention has been drawn to macrophages in obesity after the discovery of macrophage infiltration in adipose tissue. This review updates of adipose tissue macrophages in the immune-pathophysiology of obesity, including new progression on the adipose tissue macrophages phenotype and the potential of beige fat induction by M2 macrophage, which inspires a novel therapy for obesity and insulin resistance.

To study the antisensitiZation of Chinese drug, Inodel gUinea pigS with hypersensitive thinilistabbed with Kebindn Sray Served as Group l, and substance P(SP) contents in lung and plasma ofGroup I were detected and compared with normal coned group (Group 11),model control groUp(Group ill) and poSitive medicine control group(GrouP ac).The resultS showed that SP content inlung and plasma of Group ill were higher than thais of GrouP 11(P 0.05).SP is an active neuropeptide and over release of SP Inay result in hperetion of the nose.It is indicated that Kebimin SPlaycan inhibit type I alleds by decreasing SP contents in lung and plasma.

AIM: To study the effects of oxidative modification lipoproteins on blood coagulation and fibrino (lysis) in vitro. METHODS: Normal human plasma VLDL, LDL and HDL, which were isolated by density gradient ultracentrifugation method, were oxidatively modified by Cu~(2+) and HOCl method. N-VLDL, Ox-VLDL, N-LDL, Ox-LDL, N-HDL, Ox-HDL were added to the reaction system which consisted of mixed fresh normal plasma respectively, prothrombin time (PT), activated partial thrombplastin time (APTT), plasminogen activator inhibitor 1 (PAI-1), tissue plasminogen activator (t-PA) and platelet aggregation were measured according to the direction of the kits. RESULTS: The relative electrophoretic mobility (REM), absorbance at 234nm and TBARS of oxidized VLDL, LDL and HDL mediated by HOCl or Cu~(2+) were significantly higher than that of the control group (P

With the widespread application of diving technology, the safety of long-term diving has become a research focus. Research on the chronic health effects of long-term diving on divers mainly focuses on the respiratory system, circulatory system, nervous system, skeletal system, urinary system, as well as psychological health and sleep. Long-term diving can lead to increased lung capacity, thickening of nasal mucosa, myocardial hypertrophy, changes in heart rhythm, and hearing loss in divers. The impact of long-term diving on health is influenced by diving exposure index such as diving mode, maximum diving depth, underwater stay time, diving frequency, and number of dives, as well as individual factors such as years of diving experience, age, and medical history of divers. However, research on the effects of diving on health are inconsistent, and the potential mechanisms of health damage are unclear. Future large-scale research should be conducted under strict experimental conditions and with standardized inclusion criteria for subjects. Establishing a scientific and systematic assessment method for decompression is crucial for studying the chronic health effects of divers and enhancing understanding of relevant mechanisms to promote the development of diving industry and sport.

Objective: To explore the genetic basis for a patient with autism. Methods: High-throughput sequencing was carried out to detect copy number variations in the patient. Results: DNA sequencing found that the patient has carried a 0.11 Mb deletion in distal 2p16.3 spanning from genomic position 50 820 001 to 50 922 000, which resulted removal of exon 6 and part of intron 7 of the NRXN1 gene. The same deletion was not found his parents and brother. Conclusion Partial deletion of the NRXN1 gene may underlie the disease in this patient.

OBJECTIVE: To explore the genetic basis for a patient with autism. METHODS: High-throughput sequencing was carried out to detect copy number variations in the patient. RESULTS: DNA sequencing found that the patient has carried a 0.11 Mb deletion in distal 2p16.3 spanning from genomic position 50 820 001 to 50 922 000, which resulted removal of exon 6 and part of intron 7 of the NRXN1 gene. The same deletion was not found his parents and brother. CONCLUSION Partial deletion of the NRXN1 gene may underlie the disease in this patient.
Autistic Disorder ; genetics ; Cell Adhesion Molecules, Neuronal ; genetics ; DNA Copy Number Variations ; Gene Deletion ; Humans ; Male ; Nerve Tissue Proteins ; genetics