Objective To explore the effect of central venous pressure waveforms on the location of power PICC tip. Methods From January 2015 to December 2015, we placed power PICC for 47 patients in our intensive care unit. The CVP waveforms were applied to detect any displacement into small thoracic veins after a four-step localization method. The position of the catheter tip was finally confirmed by X-ray inspection. Results Among the 47 cases undergoing PICC implantation, 45(95.75%) displayed a typical CVP waveform, with the catheter tip positions were located in the superior vena cava inferior segment, 1 (2.13%) displayed a typical CVP waveform, with the catheter tip was misplaced into axillary vein and retraced and 1(2.13%) did not display typical CVP waveforms and CVP value was negative, with the catheter tip was in left internal jugular vein. To locate the catheter tip position with CVP waveform and chest X-rang were 100.00%the same. Conclusions The central venous pressure waveform can be used to determine whether the catheter tip is located in the inferior segment of the superior vena cava or not immediately after the placement of a power PICC. However, chest X-ray inspection conformation is still needed.

Objective To study the cognitive impairment in SD rats after intermittent hypoxia (IH),and explore the relation of miR-26b up-regulated expression and neuron apoptosis in the hippocampus of SD rats after IH.Methods Eight-week-old male SD rats (n=20,each weighing approximately 300±10 g) were randomly divided into normal oxygen control group,IH 1-week group,IH 2-weeks group and IH 4-weeks group (n=5).Rats in the later three groups were given IH for different times,and rats in the normal oxygen control group were given normal oxygen.The spatial learning and memory abilities were detected by Morris Water Maze (MWM) in the normal oxygen control group and IH 4-weeks group.The levels of apoptosis proteins Caspase3 and Bax and anti-apoptosis protein Bcl-2 in the hippocampus of 4 groups were detected by Western blotting.The miR-26b expression level in the 4 groups was detected by real time-PCR.Results (1) The results of MWM revealed that the mean escape latency in the IH 4-weeks group was significantly prolonged as compared with that in the normal oxygen control group (P＜0.05);the time entering into the target quadrant in the IH 4-weeks group ([22.0±6.7] s) was significantly shorter than that in the normal oxygen control group ([39.8±8.8] s,P＜0.05).(2) Western blotting indicated that up-regulated expressions of apoptosis proteins Bax and Casepase3 and down-regulated expression of anti-apoptosis protein Bcl-2 in the IH 1-week group,IH 2-weeks group and IH 4-weeks group were noted as compared with those in the control group,with significant differences (P＜0.05);significantly higher apoptosis protein Bax and Casepase3 expressions in the IH 1-week group were noted as compared with those in the IH 2-weeks group and IH 4-weeks group (P＜0.05),while significantly decreased Bcl-2 expression in the IH 1-week group was noted as compared with that in the IH 2-weeks group and IH 4-weeks group (P＜0.05).(3) The results of real time-PCR revealed that the miR-26b expression level in the hippocampus was up-regulated in the IH 1-week group,IH 2-weeks group and IH 4-weeks group as compared with that in the control group,with significant differences (P＜0.05);miR-26b expression level in the IH 1-week group was significantly higher as compared with that in the IH 2-weeks group and IH 4-weeks group (P＜0.05).Conclusion The miR-26b up-regulated expression in the hippocampus might refer to Bax /Bcl-2-related mitochondrial apoptotic signaling pathway after IH brain injury;miR-26b could be a potential mean ofgene therapy after IH brain injury.

Objective:To investigate the co-expression of leukocyte immunoglobulin-like receptor subfamily B member 2 (LILRB2) and immune surface-related molecules in different monocyte subgroups of HIV-1 patients, and analyze the correlation between LILRB2 and poor immune reconstruction in HIV-1 infection.Methods:Men who have sex with men (MSM) with chronic HIV-1 infection presenting to the Infection Center of Beijing You′an Hospital from January 2021 to September 2022 were enrolled in this study. They were categorized into four groups: healthy controls (HCs, n=22), treatment-naive patients (TNs, n=22), immune responders (IRs, n=22), and immune non-responders (INRs, n=22). Flow cytometry was used to analyze LILRB2 expression in classical (CD14 + + CD16 -), intermediate (CD14 + + CD16 + ), and non-classical (CD14 + CD16 + + ) monocyte subsets, and the co-expression of LILRB2 with CD80, CD86, CD163, human leukocyte antigen-DR (HLA-DR), and PD-L1. Kruskal-Wallis test and Dunn′s post-hoc analysis were used for statistical analysis. Results:The expression of LILRB2 in CD14 + CD16 + + monocytes increased significantly in the INRs group as compared with that in the IRs group ( P<0.05), the TNs group ( P<0.05), and the HCs group ( P<0.001). Additionally, the co-expression of LILRB2 and CD80 on CD14 + CD16 + + monocytes increased significantly in the TNs group than that in the HCs group ( P<0.001), the IRs group ( P<0.01), and the INRs group ( P<0.001); the co-expression of LILRB2 and CD86 on CD14 + CD16 + + monocyte subsets was enhanced in the INRs group than in the HCs group ( P=0.001), the TNs group ( P<0.05), and the IRs group ( P<0.05); the co-expression of LILRB2 and CD163 on CD14 + + CD16 + monocytes represented the most significant variation among the groups, with the INRs group exhibiting significantly lower level compared to both the IRs group ( P<0.01) and the HCs group ( P<0.01). In contrast, the co-expression of HLA-DR and LILRB2 on CD14 + CD16 + + monocytes was comparable between the INRs and the TNs groups, yet significantly elevated as compared with that in the HCs group ( P<0.01, P<0.05). Conclusions:LILRB2 is associated with abnormal activation of monocytes in HIV-1-infected individuals, and the changes in its expression in monocyte subsets may have a potential correlation with the occurrence of poor immune reconstruction.

Objective To investigate the changes of microglia cell phenotypes in the injured brains of rats following repetitive mild traumatic brain injury (rmTBI).Methods Sixty male SD rats were randomly divided into sham-operated group,injury of one-week group,injury of two-week group,injury of four-week group,and injury of six-week group (n=12).Rats in the injury groups were induced rmTBI models by controlled cortical impact (CCI),and rats in the sham-operated group were only performed bone window opening without hitting.Six rats from each group were sacrificed;immunofluorescent staining was used to detect the Iba-1 positive microglial cells in the injured cortex and changes ofmicroglia subsets in the injured brain after rmTBI were analyzed by flow cytometry.Results As compared with the sham-operated group,the injury of one-week group and injury of six-week group had significantly increased percentages of Iba-1 positive microglial cells in the injured cortex (19％ and 12％,P＜0.05).flow cytometry indicated that CD451ow/CD11b+ cells were the microglial cells,accountting for 90％ ofCD11b+ cells;as compared with the sham-operated group,the injury of one-week group,injury of two-week group,injury of four-week group,and injury of six-week group had significantly increased M1 type microglial cells (P＜0.06),with injury of six-week group enjoying the highest level;as compared with the sham-operated group,the injury of one-week group,injury of two-week group and injury of four-week group had significantly increased M2 type microglial cells (P＜0.06),with injury of two-week group enjoying the highest level.Conclusion Dynamic changes ofmicroglia subsets after rmTBI are noted,which reveals that different subsets of microglia phenotypes might play their unique roles in the acute or chronic phases after rmTBI.

γδ T cells are a unique type of natural immune cells that recognize antigens without the limitation of the major histocompatibility complex (MHC). They are of great significance in anti-infection immunity, serving as the important defense for maintaining immune homeostasis. Human immunodeficiency virus (HIV) infection induces the imbalance of γδ T cell subsets. A long-term antiretroviral therapy (ART) significantly damages the number and function of γδ T cells, eventually result ing in disease progression and immune reconstitution of HIV-infected patients. In the present study, we aimed to review the phenotypic function of γδ T cells, the biological role of γδ T cells in HIV infection, and γδ T cell-based immunotherapy.