Abstract: Objective　To analyze the epidemiological characteristics of late diagnosed HIV/AIDS cases (LD) in Sanya from 2010 to 2021, and to provide evidence for reducing the LD rate. Methods　The database was downloaded from the AIDS Prevention and Control Information System of China's Disease Prevention and Control Information System and newly reported HIV/AIDS cases between 2010 and 2021 in Sanya were included, identified LD according to the LD criteria proposed by Chinese Center for Disease Control and Prevention in 2014 and analyzed the relevant factors of LD. Results　From 2010 to 2021, a total of 710 research objects were included in this study. The proportion of LD was 33.4% (237/710), and decreased from 95.5% to 22.4% between 2010 and 2021 (χ2trend=34.777, P<0.001). Ethnic groups, educational level, sample sources and confirmed date were the relevant factors of LD of HIV/AIDS in Sanya City. The proportion of LD was 56.8% in Li ethnic group, which was higher than that in Han ethnic (OR=2.253, 95%CI=1.361-3.670). The proportion of LD of patients who were middle school and less was 55.5%, which were more likely to be LD than high school or above (OR=1.722, 95%CI=1.072-2.765). The proportion of LD was 56.8% in patients whose samples were from medical institutions or testing consultation were more likely to be LD than MSM (OR=5.564, 95%CI=3.278-9.444; OR=2.204, 95%CI=1.239-3.923). Compared with patients who were confirmed between 2018-2021, the patients derived from 2010 to 2013 had higher LD (OR=2.246, 95%CI=1.311-4.488). Conclusion　The LD of HIV/AIDS in Sanya cannot be ignored, especially the HIV/AIDS from counseling and testing and medical institutions. We should strengthen HIV testing, strengthen health education.

Site-saturation mutagenesis is a newly-developed technology in protein engineering.By manipulating the encoding genes,it can rapidly obtain the mutants of desired proteins whose target residues are substituted by 19 other common amino acids.Site-saturation mutagenesis could serve not only as a powerful tool in protein engineering,but also as an important method in exploring the structure-function relationship of proteins.Several techniques were summarized to achieve site-saturation mutagenesis and introduce their application status in the protein engineering.The problem and promising future of its application were also discussed.

Objective:To observe the change of periphery and centra lymphocyte subsets at the crest-time of MOG_(35-55) induced EAE disease in mice,and to explore the alteration of cellular immunity and humoral immunity in the invasion process in EAE.Methods:MOG_(35-55) was used to establish EAE model in femina C57BL/6 mice.The behavioral changes and the histological scores were recorded after the mice were immuned .The changes of CD3~+CD4~+,CD3~+CD8~+,CD4~+CD25~+ and B220~+ on periphery and centra lymphocytes in spleen,brain and spinal cord were analyzed by flow cytometry.Results:The CD3~+CD4~+,CD3~+CD8~+,CD4~+CD25~+ and B220~+ lymphocytes were detected in the brain and spinal cord of EAE group mice,but they were not detected in CFA control group.The CD3~+CD4~+ and CD3+CD8+lymphocytes in the spleen of EAE crest-time group were lower than those in CFA control group(P＜0.05).The B220~+ lymphocytes were obviously higher than in the CFA control group (P＜0.01).And CD4~+CD25~+ lymphocytes were slight higher than the CFA control group.Conclusion:At the crest-time during EAE,the CD3~+CD4~+,CD3~+CD8~+lymphocytes of spleen reduced obviously,B220~+ lymphocytes increased markedly,and the CD4~+CD25~+ lymphocytes just have the increasing trend.It indicates that cellular immunity and humoral immunity coregulated the patho-process at the crest-time of EAE,T lymphocytes and B lymphocytes all played important roles in the pathogenesy of EAE.

OBJECTIVETo observe analgesic effect of electroacupuncture ( EA) on rats with chronic inflammatory pain and its regulatory mechanism on ispilateral dorsal root ganglion (DRG) and spinal dorsal horn (SDH) Mas-related G protein-coupled C receptor (MrgprC).

METHODSTotally 40 healthy male SD rats were divided into 4 groups according to random number table, i.e., the normal (N) group, the model (M) group, the acupuncture (Acu) group, the EA group, 10 rats in each group. The model of chronic inflammatory pain was established by subcutaneous injecting 0. 1 mL complete Freund's adjuvant (CFA) into right hind paw. Paw withdrawal thresholds (PWTs) were measured before modeling, at day 1, 3, 5, 7, and after CFA injection, respectively. Expression levels of MrgprC in ispilateral DRG and SDH were detected by Western blot. The content of bovine adrenal medulla 22 (BAM22) in SDH was detected by immunohistochemical assay.

RESULTSCompared with N group at each time point, PWTs significantly decreased in M group (P <0. 01). Compared with M group, PWTs significantly increased at day 5 of EA and after EA in EA group (P < 0.05, P < 0.01). Compared with Acu group at each time point, post-EA PWTs significantly increased in the EA group (P < 0.05). Compared with N group, expression of MrgprC in ispilateral DRG and ratio of BAM22 positive cells in ispilateral SDH increased in M group (P < 0.01). Compared with M group, expression of MrgprC in ispilateral DRG and ratio of BAM22 positive cells in ispilateral SDH increased in the EA group (P < 0.05).

CONCLUSIONEA had favorable analgesic effect on chronic inflammatory pain induced by CFA, and its mechanism might be possibly associated with up-regulating MrgprC expression in ispilateral DRG and BAM22 content in ispilateral SDH.

Analgesia ; Animals ; Electroacupuncture ; Enkephalins ; metabolism ; Freund's Adjuvant ; Ganglia, Spinal ; drug effects ; Inflammation ; chemically induced ; drug therapy ; Male ; Pain Management ; methods ; Peptide Fragments ; metabolism ; Posterior Horn Cells ; drug effects ; Random Allocation ; Rats ; Rats, Sprague-Dawley

Adult ; China ; epidemiology ; GB virus C ; classification ; Hepatitis, Viral, Human ; epidemiology ; virology ; Homosexuality, Male ; Humans ; Male

Abstract: Objective　To investigate the drug demand and related influencing factors of AIDS non-occupational post-exposure prophylaxis (nPEP) among men who have sex with men (MSM) in Wuhan, and to provide a scientific basis for the development of subsequent intervention policies for MSM. Methods　With the assistance of social organizations in Wuhan, MSM was recruited by the snowball method to carry out an online questionnaire survey to collect information on demographics, AIDS-related knowledge, high-risk behaviors, and the need for nPEP medication. The χ2 test and unconditional Logistic regression were used to analyze the related factors of the demand for nPEP medication. Results　A total of 308 valid subjects were included in this study, with predominantly 18-29 years old (78.57%, 242/308). The self-reported sexual orientation was mainly homosexuality (82.47%, 254/308), and the awareness rate of AIDS knowledge was high (89.29%, 275/308). Among the survey respondents, 35.06% (108/308) did not know the situation of HIV infection among MSM population in Wuhan; 55.19% (170/308) had two or more same-sex sexual partners in the last six months; 90.91% (280/308) had heard of nPEP before participating in this survey. After passing nPEP and informing the protective effect of nPEP, 59.42% (183/308) of them needed nPEP. After HIV exposure, 73.38% (226/308) were willing to spend money to buy nPEP drugs, and 88.64% (273/308) were willing to take nPEP drugs because of the known side effects. Logistic regression analysis showed that in the last six months, the needs for taking nPEP medication in those who had 2 or more same-sex sexual partners (OR=2.121, 95%CI: 1.329-3.386) and who had received peer education (OR=1.740, 95%CI: 1.088-2.781) were higher than those of those who had a same-sex sexual partner in the last six months and who had not received peer education. Conclusions　The MSM population in Wuhan has a great demand for nPEP drugs, and peer education is an important way to carry out nPEP publicity and promotion. At the same time, we should continue to strengthen warning publicity and education and behavioral intervention to reduce MSM risky sexual behaviors and reduce new HIV infections.

This study was aimed to investigate the effect of arsenic trioxide (As2O3) on expression of vascular endothelial growth factor-C (VEGF-C) and its receptor VEGFR-3 in gastric cancer in order to clarify the role of As2O3 in lymphangiogenesis and metastasis of tumor. The gastric cancer model was established in nude mice by using gastric cancer cell line SGC-7901. As2O3 was injected to the two treatment groups (2.5 mg/kg and 5 mg/kg) and the same volume of saline solution was injected to the control group. Expression of VEGF-C and VEGFR-3 were detected by immunohistochemistry and were analyzed with QWin550cW image Acquiring & Analysis System. The results showed that the expression of VEGF-C and VEGFR-3 in cancer cells significantly reduced in the arsenic -treated groups. The expression of VEGF-C and VEGFR-3 in 5 mg/kg group was significantly less than that in 2.5 mg/kg group. The gray ratio analysis confirmed that there were significant difference between control group and two treated group, as well as between 2.5 mg/kg-treated group and 5 mg/kg-treated group. It is concluded that As2O3 can inhibit expression of VEGF-C and VEGFR-3 of human gastric cancer xenografts in nude mice, which suggests that As2O3 may inhibit the lymphangiogenesis by suppressing the expression of VEGF-C and VEGFR-3.
Animals ; Arsenicals ; pharmacology ; Cell Line, Tumor ; Humans ; Male ; Mice ; Mice, Nude ; Oxides ; pharmacology ; Stomach Neoplasms ; metabolism ; Vascular Endothelial Growth Factor C ; metabolism ; Vascular Endothelial Growth Factor Receptor-3 ; metabolism ; Xenograft Model Antitumor Assays

This study was aimed to investigate on effect of As(2)O(3) on expressions of COX-2, MMP-2 and MMP-9 in SGC7901 and K562 cells. SGC7901 and K562 cells were cultured in RPMI 1640 medium and were inoculated in culture medium with different concentrations of As(2)O(3) and at different times. Expressions of COX-2, MMP-2 and MMP-9 in SGC7901 and K562 cells were measured by using Western blot, while the levels of COX-2 mRNA and MMP-2 mRNA were measured with fluorescence quantitative RT-PCR. The results showed that the expression of COX-2, MMP-2 and MMP-9 decreased in dose- and time-dependent manners after treating with As(2)O(3). The levels of COX-2 mRNA and MMP-2 mRNA reduced in groups treated with As(2)O(3). In conclusion, As(2)O(3) inhibits expressions of COX-2, MMP-2 and MMP-9 in K562 and SGC7901 cells, suggesting that As(2)O(3) inhibits tumor development through its effect on angiogenesis involved in solid and hematologic malignancies.
Arsenicals ; pharmacology ; Cyclooxygenase 2 ; metabolism ; Gene Expression Regulation, Leukemic ; Humans ; K562 Cells ; Matrix Metalloproteinase 2 ; metabolism ; Matrix Metalloproteinase 9 ; metabolism ; Oxides ; pharmacology

Arthritis ; surgery ; Arthroplasty ; methods ; Arthroplasty, Replacement, Hip ; Female ; Humans ; Middle Aged

OBJECTIVETo determine the mechanism underlying the therapeutic activities of glycogen synthase kinase 3b (GSK3b) against hepatic ischemia-reperfusion (H-IR) injury by investigating the inhibitive effects of GSK3b on inflammation mediated by Toll-like receptor 4 (TLR4).

METHODSC57BL/6 male mice were subjected to 90 min of warm liver cephalad lobe ischemia, followed by reperfusion for various lengths of time. The mice were divided into three groups: the H-IR untreated model (control group), and the H-IR inflammation-induced models that received an intraperitoneal injection of purified lipopolysaccharide (LPS) endotoxin alone (inflammation group) or with pretreatment of the SB216763 GSK3b-specific inhibitor (intervention group). To create a parallel isolated cell system for detailed investigations of macrophages, marrow-derived stem cells were isolated from femurs of the H-IR control group of mice and used to derive primary macrophages. The cells were then divided into the same three groups as the whole mouse system: control, LPS-induced inflammation model, and inflammation model with SB216763 intervention. Differential expressions of inflammation-related proteins and genes were detected by Western blotting and real-time quantitative PCR, respectively.

RESULTSThe phosphorylation levels of ERK, JNK and p38 MAPK were induced in liver at 1 h after reperfusion, but then steadily decreased and returned to baseline levels by 4 h after reperfusion. In addition, the phosphorylation levels of ERK and JNK were induced in macrophages at 15 min after LPS stimulation, while the phosphorylation level of p38 MAPK was induced at 1 h; SB216763 pretreatment suppressed the LPS-stimulated ERK, JNK and p38 phosphorylation in macrophages. In the mouse model, GSK3b activity was found to promote the gene expression of anti-inflammatory cytokine IL-10 (control: 0.21 ± 0.08, inflammation: 0.83 ± 0.21, intervention: 1.76 ± 0.67; F = 3.16, P = 0.027) but to significantly inhibit the gene expression of pro-inflammatory cytokines IL-12 (control: 0.11 ± 0.05, inflammation: 0.85 ± 0.11, intervention: 0.43 ± 0.10; F = 2.67, P = 0.038), TNF-a, (control: 0.052 ± 0.012, inflammation: 8.11 ± 0.98, intervention: 3.9 ± 0.82; F = 4.13, P = 0.016), IL-6 (control: 0.22 ± 0.08, inflammation: 6.37 ± 0.81, intervention: 2.11 ± 0.63; F = 3.21, P = 0.024), and IL-1b (control: 0.12 ± 0.07, inflammation: 2.51 ± 0.62, and intervention: 1.28 ± 0.33; F = 2.22, P = 0.030).

CONCLUSIONInhibition of GSK3b selectively regulates the expression of anti-inflammatory and pro-inflammatory cytokines in liver Kupffer cells (liver macrophages). This process may be one of the mechanisms underlying the ability of GSK3b to ameliorate hepatic ischemia-reperfusion injury, possibly because inhibition of pro-inflammatory cytokines may indirectly mediate liver cell apoptosis.

Animals ; Cells, Cultured ; Cytokines ; metabolism ; Glycogen Synthase Kinase 3 ; metabolism ; Glycogen Synthase Kinase 3 beta ; Inflammation ; metabolism ; pathology ; Lipopolysaccharides ; adverse effects ; Liver ; pathology ; Macrophages ; metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Reperfusion Injury ; Toll-Like Receptor 4 ; metabolism