[Considerations for the development of adult vaccination in China].

Adult vaccination is an important component of the life-course immunization for all. Strengthening adult vaccination in China contributes to shrinking immunization gaps between regions and groups, enhancing the overall immunity of our population, and promoting health equity and social prosperity. Chinese adults bear the heavy burden of vaccine preventable diseases such as influenza, pneumococcal diseases and shingles, and have low coverage of vaccines against those diseases, so it is necessary to make efforts to improve adult vaccination development. This article focuses on elaborating the values of adult vaccination, introducing the current status of adult vaccination abroad, and analyzing the challenges and existing foundations for China to provide adult vaccination, and makes suggestions for the building and development of adult vaccination.

[Current status of vaccination services for adults in urban and rural areas of nine provinces in China from 2019 to 2021].

Objective: To understand the current situation of vaccination services for adults in China, explore how to establish a stable and efficient vaccination service system for adults, and provide reference for formulating corresponding policies. Methods: The vaccination information systems of nine provinces in China were used to obtain information on urban and rural vaccination of influenza vaccine, 23-valent pneumococcal polysaccharide vaccine (PPV23), and human papillomavirus vaccine (HPV) from 2019 to 2021. The indicator, vaccination rate/full vaccination rate, was used for statistical description. Results: The vaccination rate/full vaccination rate of the three vaccines in eastern China was generally higher than that in central and western China. The vaccination rate/full vaccination rate in urban areas was generally higher than that in rural areas. From 2019 to 2021, the vaccination rates of influenza vaccine among people aged 60 years and above in urban and rural areas were 2.96%, 6.29%, 6.14% and 1.29%, 2.58%, 2.94%, respectively. The vaccination rates of the PPV23 among people aged 60 years and above in urban and rural areas increased year by year, with rates of 0.38%, 1.05%, 1.15% and 0.14%, 0.49%, 0.59%, respectively. From 2019 to 2021, the HPV coverage of female adults aged 27-45 years in urban and rural areas increased year by year, with rates of 0.46%, 0.93%, 1.88% and 0.17%, 0.40%, 1.08%, respectively. Conclusion: The vaccination rates of influenza vaccine,PPV23 vaccine and HPV vaccine for adults in China are relatively low, with higher rates in the eastern region than in the central and western regions, and higher rates in urban areas than in rural areas. It is recommended to formulate corresponding health and economic policies and explore a suitable vaccination service system for adults in China to improve vaccination rates.

[Thoughts and suggestions on co-administration of seasonal influenza vaccine and COVID-19 vaccine].

In the context of the global pandemic of COVID-19, the epidemic intensity, epidemic characteristics and infection risk of influenza have presented new features. COVID-19 and influenza have simultaneously emerged in many regions of the world. COVID-19 and influenza are similar in terms of transmission mode, clinical symptoms and other aspects. There are also similarities in the mechanism of influenza virus and novel coronavirus on cells. At the same time, it is feasible and significant to do a good job in the prevention and control of COVID-19 and influenza. This paper discusses the relevant strategies and measures for the joint prevention and control of influenza and novel coronavirus from the aspects of influenza vaccination to prevent co-infection, simultaneous vaccination of influenza vaccine and novel coronavirus vaccine, etc., and puts forward corresponding thoughts and suggestions, in order to provide scientific support for the formulation of strategies on seasonal influenza vaccine and novel coronavirus vaccination.

[Application of neuroendoscopy combined with fluorescence angiography in anterior circulation aneurysm clipping].

Objective: To explore the value of neuroendoscopy combined with fluorescence angiography in anterior circulation aneurysm clipping. Methods: A total of 15 patients with anterior circulation aneurysm from Department of Neurosurgery, Zhongnan Hospital of Wuhan University between October 2018 and January 2019 were enrolled. Neuroendoscopy combined with indocyanine green fluorescence angiography (ICGA) was used to determine the shape of the aneurysm, the specific location of the aneurysm neck and its relationship with the aneurysm-bearing artery during anterior circulation aneurysm clipping. Meanwhile, Neuroendoscopy combined with ICGA can be employed to observe whether there was stenosis and incomplete clamping of the aneurysm-bearing artery after clipping the aneurysm, and whether there was misclamping of the perforating branches hidden under the posterior wall of the aneurysm. Results: The success rate of aneurysm clipping in 15 cases was 15/15. After aneurysm clipping, ICGA and neuroendoscopy were performed. The residual aneurysm neck was detected in 3 cases, and the position of aneurysm clip was adjusted or aneurysm clips were added. In one case, the anterior choroidal aneurysm was found to be mistakenly clipped. After adjusting the aneurysm clip, ICGA and neuroendoscopy showed that the anterior choroidal artery was normal. In another case, the A1 segment aneurysm was clipped. ICGA and neuroendoscopy found that the perforating branch blood vessels were mistakenly clipped. After the adjustment of the aneurysm clip, the blood vessels recovered their patency. There were no surgical-related deaths, disability and coma cases in the study. Conclusions: During aneurysm clipping, neuroendoscopy combined with ICGA can reduce cerebral vasospasm, decrease the misclipping rate of perforation of blood vessels, and avoid residual neck of aneurysm, stenosis or occlusion of aneurysm-bearing artery by using neuroendoscopy to observe whether misclipping of the perforating branch vessels exist and whether the aneurysm is clipped. Therefore, it can reduce postoperative complications.

[Analysis on genetic characteristics of H9N2 avian influenza virus isolated from human infection and external environment in Gansu province].

Objective: To analyze the genomic characteristics of human infection with H9N2 avian influenza virus in Gansu province. Methods: The etiological analysis was conducted for human infection with H9N2 avian influenza virus detected in influenza like illness cases in northwestern China in 2016. Molecular bioinformatics Mega 7.0 software was used to analyze the full genomic sequences of the viral isolate. Results: The gene fragments of HA, NA, MP, NP, NS, PA, PB1 and PB2 of the isolate were highly similar (>90%) to those of H9N2 avian influenza virus strain isolated in external environment in Gansu from 2014 to 2019. The HA gene belonged to BJ/94-like branch, PB2 and MP belonged to G1/97-like branch, and the PB1, PA, NS, and NP genes belonged to F/98-like branch. MP and PB2 were closely related to H7N9, H10N8 and H5N6 viruses. Amino acid sequence alignment showed that the HA cleavage site was arranged in PSRSSR ↓ GLF, H183N and Q226L mutated which included 7 HA glycosylated sites; 62-64 sites of NA absented 3 amino acids (ITE); and M2-31N, NS1-42S, PA-356R, and PA-409N mutated. Conclusions: Apparently, this case of human infection with human infection with H9N2 avian influenza virus was an incidental. However, the isolates of H9N2 influenza virus in external environment of Gansu had a series of mammalian adaptive molecular markers, suggesting that the risk of human infection is higher. It is necessary to strengthen the surveillance by multi departments to deal with influenza pandemic.

[Interaction between PSF and cytokeratin 18 mediates PSF relocation to cell membrane and maintains chemosensitivity of myeloid leukemia].

OBJECTIVE: To identify the chaperone of polypyrimidine tractor-binding protein-associated splicing factor (PSF) in myeloid leukemia cells, and to explore the mechanism and redistributive pattern to cell surface of PSF in chemo-sensitive HL60 cells and resistant HL60/DOX cells. METHODS: The eukaryotic expression vector of PSF was transfected with liposomes transiently, then flow cytometry was used to detect the expression level of PSF on the cell surface 24 h, 48 h and 72 h after vector transfections. We constructed a chimeric expression vector, streptavidin binding peptide (SBP)-PSF, meanwhile this vector was transfected and made SBP-PSF fusion protein overexpress. In addition, we used streptavidin magnetic beads to precipitate the cellular chaperonin of PSF and then identified its chaperonin by mass spectrometry (MS). Lentiviral vectors containing cytokeratin18 (K18) interference sequences were transfected into 293T cells to prepare lentivirus. HL60 and HL60/DOX cells were infected with lentivirus to obtain stable interfering K18 cell lines. Next, flow cytometry was used to test the membrane relocation level of PSF. Together, these methods confirmed the similar or different mechanisms of the PSF redistributing to membrane synergistically mediated by K18 in HL60 and HL60/DOX cells. RESULTS: The expression of membrane relocated PSF was detected every day for three days (at the end of 24 h, 48 h and 72 h) after transient overexpression. The expressing rate of PSF on the cell surface was 22.4%±3.5%, 37.9%±6.0%, 58.3%±8.8%, respectively in sensitive HL60 cells, while that was 4.7%±0.5%, 3.9%±0.6%, 2.9%±0.6% , respectively in resistant HL60/DOX cells. The difference of expressing rate on each day was significant, P<0.01. We identified K18 detected by co-immunoprecipitation and mass spectrum assay which was the cellular chaperone of PSF. We found that K18 knockdown decreased the PSF expression level which redistributed on cell surface from 48.9%±5.4% to 6.2%±1.0% in sensitive HL60 cells, and from 9.11%±1.2% to 2.21%±0.51% in resistant HL60/DOX cells, respectively. CONCLUSION: K18 is the intracellular chaperonin of PSF. The interaction of PSF and K18 mediates its redistribution to cell membrane in sensitive cells. While in resistant cells, PSF failed to relocate at the cell surface and accumulated in cells, which mediated resistance to chemotherapeutics.

[Association study of genetic variations in SLCO1B3 gene with prognosis in breast cancer patients treated with neoadjuvant chemotherapy of TA regimen].

Objective: To assess the association of single nucleotide polymorphisms (SNPs) in SLCO1B3 gene with prognosis of breast cancer (BC) patients treated with neoadjuvant chemotherapy of TA regimen (taxane and antharcycline drugs). Methods: 439 female BC patients were recruited and treated with neoadjuvant chemotherapy of TA regimen. A blood sample (2 ml) of peripheral blood was collected from each patient before chemotherapy. Tagging SNPs (tag-SNPs) were selected. We investigated the association of tag-SNPs with prognosis, by Sequenom Mass ARRAY system platform, characterizing tag-SNPs. The hazard ratio (HR) and 95% confidence interval (CI) for progression or death were calculated by multivariable-adjusted Cox regression model. Results: Seven tag-SNPs (rs11045689, rs200104106, rs3764006, rs3834935, rs4149117, rs7305323 and rs73241801) were selected for study. Compared with individuals carrying the rs11045689 GG genotype, individuals carrying rs11045689 AA genotype performed worse PFS and OS, with the HR (95% CI) for progression being 1.39 (1.11~1.75) and the HR (95% CI) for death being 1.38 (1.04~1.83). Compared with individuals carrying the rs73241801 CC genotype, individuals carrying rs73241801 TT genotype performed better OS (P=0.041), with the HR (95% CI) for death being 0.65 (0.44~0.94). The number of risk allele was significantly associated with PFS (P=0.012) and OS (P=0.017) of BC patients by accumulation analysis. Compared with individuals carrying one or less than one risk allele, individuals carrying four risk alleles performed worse PFS and OS, with the HR (95% CI) for progression being 1.37 (1.09~1.72) and the HR (95% CI) for death being 1.36 (1.02~1.81). Conclusion: The variations of rs11045689 and rs73241801 in SLCO1B3 gene were significantly associated with prognosis of BC patients treated with neoadjuvant chemotherapy of TA regimen, which might serve as biomarkers for predicting prognosis of BC patients treated with neoadjuvant chemotherapy.

Protective effect of remifentanil on myocardial ischemia-reperfusion injury through Fas apoptosis signaling pathway.

OBJECTIVE: The aim of this study was to investigate the protective effect of remifentanil (RFT) on myocardial ischemia-reperfusion (IR) injury through Fas apoptosis signaling pathway. MATERIALS AND METHODS: A total of 36 Sprague-Dawley (SD) rats were randomly divided into 3 groups, including the sham operation (Sham) group, IR model (IR) group and RFT pretreatment (RFT) group, with 12 rats in each group. Myocardial tissues of rats in each group were collected. Hematoxylin and eosin (H&E) staining was used to examine the pathological differences of the myocardium in the three groups. The levels of lactate dehydrogenase (LDH), creatine kinase (CK), superoxide dismutase (SOD) and malondialdehyde (MDA) in the serum of rats in each group were detected by enzyme-linked immunosorbent assay (ELISA). Meanwhile, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was adopted to detect the apoptosis level of myocardial cells in each group. Furthermore, Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western blotting were applied to measure the mRNA and protein expression levels of Fas and its pathway indexes, respectively. RESULTS: Compared with the Sham group, LDH and CK activities and MDA level in the IR group were significantly increased, whereas the level of SOD was remarkably decreased (p<0.05). Compared with the IR group, RFT pretreatment could significantly reduce the release of LDH and CK-muscle/brain (CK-MB), increase SOD level and decrease MDA level (p<0.05). TUNEL results manifested that the apoptosis rate of myocardial cells in the IR group was markedly increased than that of the Sham group (p<0.05). Meanwhile, the apoptosis rate of myocardial cells in the RFT group was notably decreased when compared with that of the IR group (p<0.05). ELISA results demonstrated that the levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) proteins in the RTF group were significantly lower than those of the IR group (p<0.05). RT-PCR and Western blotting results indicated that the expressions of Fas, Fas ligand (FasL), and Fas-associated protein with death domain (FADD) in IR and RFT groups were significantly higher than those of the Sham group (p<0.05). However, RTF pretreatment could markedly reduce the levels of Fas, FasL, and FADD (p<0.05). CONCLUSIONS: RFT can reduce the apoptosis of myocardial cells as well as IR-induced oxidative stress and inflammation by inhibiting the Fas/FasL signal transduction pathway.

LncRNA-UCA1 promotes PD development by upregulating SNCA.

OBJECTIVE: The study aims to investigate whether Long non-coding RNA (LncRNA)-UCA1 can regulate the progression of Parkinson's disease (PD) by mediating a-synuclein (SNCA) expression. MATERIALS AND METHODS: PD mouse model was first constructed by intraperitoneal injection of MPTP. SH-SY5Y cells were treated with MPP+ for inducing in vitro PD model. Expression levels of lncRNA-UCA1 and SNCA in brain tissues extracted from PD mice and MPP+-induced SH-SY5Y cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Protein expression of SNCA was accessed by Western blot. After transfection of pcDNA-NC+DMSO, pcDNA-UCA1+DMSO, pcDNA-NC+α-amantin or pcDNA-UCA1+α-amanitin in SH-SY5Y cells, SNCA expression was detected. Cell viability and SNCA expression were determined after UCA1 overexpression or knockdown in SH-SY5Y cells. Neuronal apoptosis in MPP+-induced SH-SY5Y cells was detected by flow cytometry after the UCA1 knockdown. RESULTS: UCA1 and SNCA were highly expressed in brain tissues extracted from PD mice and MPP+-induced SH-SY5Y cells. UCA1 overexpression remarkably upregulated mRNA and protein expressions of SNCA in SH-SY5Y cells. Higher viability was seen after the UCA1 knockdown in MPP+-induced SH-SY5Y cells. UCA1 knockdown remarkably inhibited caspase-3 activity and decreased MPP+-induced neuronal apoptosis in SH-SY5Y cells. CONCLUSIONS: LncRNA-UCA1 promotes the occurrence and progression of PD by upregulating SNCA expression.

Telmisartan inhibits Ang II-induced MMP-9 expression in macrophages in stabilizing atheromatous plaque.

OBJECTIVE: To investigate the effects of telmisartan on matrix metalloproteinase-9 (MMP-9) expression in macrophages induced by angiotensin II (Ang II) and its mechanism. MATERIALS AND METHODS: THP-1 cells were adopted for research, and phorbol-12-myristate-13-acetate (PMA) was utilized to induce THP-1 cells to be transformed into macrophages, with Ang II as a stimulating factor and telmisartan as a therapeutic drug. Cell counting kit-8 (CCK8) and lactate dehydrogenase (LDH) were applied to detect cell viability and toxicity. Enzyme-linked immunosorbent assay (ELISA) was performed to measure the MMP-9 release level. Polymerase Chain Reaction (PCR) and Western blotting were conducted to detect the expressions of MMP-9 messenger ribonucleic acid (mRNA) and protein, respectively. The mechanism of action was further studied, and the activity of cyclooxygenase-2 (COX2)/macrophage-expressed gene 1 (mPEG1) pathway was determined via PCR and Western blotting. RESULTS: The 1 mM Ang II could remarkably activate the synthesis and release of MMP-9 as well as the COX2/mPEG1 pathway in macrophages. However, telmisartan could effectively repress the Ang II-induced MMP-9 synthesis and release in the macrophages, and suppress the COX2/mPEG1 pathway in the macrophages activated by Ang II. CONCLUSIONS: Telmisartan can inhibit the activation of MMP-9 in the macrophages by suppressing the COX2/mPEG1 pathway.

[Role of TNF-α in vascular remodeling in rats with chronic thromboembolic pulmonary hypertension].

Objective: To analyze the relationship between TNF-α and pulmonary vascular remodeling in order to explore the pathogenesis of CTEPH. Methods: Autologous blood clots were repeatedly injected into the left jugular vein of rats to establish the CTEPH model. Then mean pulmonary artery pressure (mPAP), histopathology, the plasma level of TNF-α, and the expressions of mRNA and protein of TNF-α in pulmonary artery were measured. Results: In the experiment group, the mPAP and vessel wall area/total area (WA/TA) ratio gradually increased as emblism extended, and increased significantly compared with the sham operation group. The plasma TNF-α concentration in the experimental group increased significantly (P<0.05). The TNF-α proteins expressed in pulmonary artery in the 1-week, 2-week, and 4-week subgroups of experimental group increased significantly compared with the sham operation group (1.62±0.08 vs 0.85±0.12, P<0.05; 1.85±0.08 vs 0.89±0.13, P<0.05; 1.37±0.12 vs 0.91±0.15, P<0.05, respectively). Immunohistochemical results showed that TNF-α expression was higher in pulmonary artery endothelial cells of the experimental group compared with the sham operation group. The expression of pulmonary artery TNF-α protein was positively related with mPAP (r=0.605, P<0.01), and with WA/TA (r=0.629, P<0.01). The expression of serum TNF-α was positively related with that of pulmonary artery TNF-α protein (r=0.721, P<0.01). Conclusion: A rat model of CTEPH can be established by repeatedly introducing autologous blood clots into the pulmonary artery with injecting TXA. Thrombosis induced higher expression of TNF-α in pulmonary arterial endothelial cells, and released into the blood. TNF-α may play an important role in the development of CTEPH, especially by contributing to vascular remodeling and PH.

[Epidemiological and clinical characteristics of 109 patients with crayfish-related rhabdomyolysis].

A total of 109 in patients with crayfish-related rhabdomyolysis were enrolled in our hospital from July to August 2016,including 31.2%(34/109)males and 68.8% (75/109)females.The number of home-cooked crayfish accounted for 60.6% (66/109). Main symptom was back pain 96.3% (105/109). The misdiagnosis rate was 15.6% (17/109). On day 1, 2, 3 after admission and the day before discharge,serum creatine kinase were 1 175(446, 2 258)IU/L,3 710(2 137, 8 875)IU/L,1 899(1 063, 4 595)IU/L and 317(152, 532)IU/L,respectively(P<0.001).Serum myoglobin were (603±484)µg/L,(313±284)µg/L,(104±74)µg/L and (55±20)µg/L,respectively(F=39.1, P<0.001).Females were more susceptible to crayfish-related rhabdomyolysis. Home-cooked crayfish is prone to induce rhabdomyolysis and easily to be misdiagnosed. Creatine kinase and myoglobin showed characteristic dynamic changes.

[Efficacy and safety of ultrasound-guided or neurostimulator-guided bilateral axillary brachial plexus block].

Objective: To explore the efficacy and safety of bilateral axillary brachial plexus block under the guidance of ultrasound or neurostimulator. Methods: From February 2012 to April 2014, 120 patients undergoing bilateral hand/forearm surgery in Beijing Jishuitan Hospital were enrolled and anaesthetized with bilateral axillary brachial plexus block. All patients were divided into two groups randomly using random number table: the ultrasound-guided group (group U, n=60) and the neurostimulator-guidedgroup (group N, n=60). The block was performed with 0.5% ropivacaine. Patients' age, sex and operation duration were recorded. Moreover, success rate, performance time, onset of sensor and motor block, performance pain, patient satisfaction degree and the incidence of related complications were also documented. Venous samples were collected at selected time points and the total and the plasma concentrations of ropivacaine were analyzed with HPLC. Results: The performance time, the onset of sensor block and the onset of motor block of group U were (8.2±1.5), (14.2± 2.2)and (24.0±3.5)min respectively, which were markedly shorter than those in group N( (14.6±3.9), (19.9±3.8), (28.8±4.2)min, respectively), and the differences were statistically significant(t=11.74, 10.09, 6.73, respectively, all P<0.01). The performance pain score of group N was (25.5± 13.2), which was obviously more serious than group U (31.7± 11.2) and a significant statistical difference was detected (t=2.856, P<0.05). The patient satisfaction degree of group U was 95.0%, which was significantly higher than group N (83.3%) and a markedly statistical difference was detected (χ(2)=4.227, P<0.05). Fifty min after performance, the total plasma concentration of ropivacaine of group U was(1.76±0.48)mg/L, which was significantly lower than group N (1.88±0.53)mg/L and a significant statistical difference was detected (t=2.43, P<0.05), while no significant differences were detected at the other time points between two groups (P>0.05). No analgesic was superadded and no other anesthesia methods were applied. No complications were detected perioperatively. Conclusions: The bilateral axillary brachial plexus block under the guidance of ultrasound or neurostimulator are both effective and safe for bilateral hand/forearm surgery. However, the ultrasound-guided block may be more clinically beneficial because of its shorter performance time, rapid onset and higher patient satisfaction degree.

MicroRNA-181c functions as a protective factor in a 1-methyl-4-phenylpyridinium iodide-induced cellular Parkinson's disease model via BCL2L11.

OBJECTIVE: Parkinson is one of the most common neurodegenerative diseases. At present, many studies have pointed out that miRNAs play a very important role in Parkinson's development and process. MiR-181c has been shown to have a significant low expression in blood samples and brain tissues of Parkinson's patients. MATERIALS AND METHODS: We used 1-Methyl-4-Phenylpyridinium Iodide (MPP(+)) as a tool for constructing the Parkinson's cell model, using mir181c mimics to construct an experimental model of acquisition. The cell viability of PC12 was detected by MTT and CCK8. Reactive oxygen species (ROS) and caspase-3 activity were analyzed. The apoptosis of PC12 was detected by flow cytometry (FCM), and luciferase was used to study the binding of target genes. The protein levels of BCL2L11were measured by Western-blot. RESULTS: There was a significant low expression of mir181c in MPP(+)-morbid cells. PC12 cell viability was rescued by miR-181c overexpression. Flow cytometry showed that apoptosis in PC12 cells overexpressing miR-181c was significantly decreased. Also, ROS and caspase-3 activity were significantly decreased. Luciferase experiments showed that miR-181c may bind to the 3-'UTR side of BCL2L11 and inhibited its expression. By Western-blot, the BCL2L11 level was markedly decreased by miR-181c. CONCLUSIONS: miR-181c could promote the cell viability and inhibit the apoptosis of PC12 cells induced by MPP (+) by downregulating BCL2L11, which may play a protective role and provide a new target for PD drug resistance research.

Chronic subdural hematoma management: clarifying the definitions of outcome measures to better understand treatment efficacy - a systematic review and meta-analysis.

OBJECTIVE: A long history of inconsistencies in the definitions of the outcome measures for chronic subdural hematomas (CSDHs) has contributed to the controversy over the optimal surgical strategy for CSDH treatment. Clarifying these definitions, reassess the available data, and systematically review the prior literature may provide better insight into the differences in treatment efficacy for CSDH. MATERIALS AND METHODS: The clinical course of CSDH was described with a series of strictly defined outcome measures. PubMed, Cochrane Library, and ScienceDirect databases were searched for comparative studies of two main surgical techniques for CSDH, including burr hole craniotomy (BHC) and twist drill craniotomy (TDC). Data were collected with uniform criteria and analyzed using a random-effects model to estimate the mortality, recurrence, operative failure, and cure rates of each treatment. RESULTS: Twelve comparative studies that examined 2,027 CSDH patients were included. The analysis results indicated that TDC and BHC treatments were similar in the mortality rates (RR, 1.25; 95% CI, 0.83-1.87; I2 = 0%; p = 0.28) and the recurrence rates (RR, 1.29; 95% CI, 0.87-1.92; I2 = 13%; p = 0.21) for CSDH patients. However, TDC had a significantly higher operative failure rate compared with BHC (RR, 0.35; 95% CI, 0.15-0.83; I2 = 0%; p = 0.02), whereas patients treated by a TDC approach tended to achieve higher cure rates compared with BHC (RR, 0.92; 95% CI, 0.86-0.99; I2 = 55%; p = 0.02). CONCLUSIONS: The clarification of the definitions related to CSDH outcome facilitates the interpretation of differences in treatment efficacy. The TDC approach manifested a significantly higher operative failure rate compared with the BHC approach; however, TDC showed a tendency in achieving a long-term neurologic cure.

P2X7 receptor in the hippocampus is involved in gp120-induced cognitive dysfunction.

To investigate the role of the P2X7 receptor in learning and memory dysfunction induced by HIV-1 envelope glycoprotein gp120 (gp120), we established HIV-1-associated dementia (HAD) animal models by intracerebroventricular (ICV) infusion of gp120 in rats. We observed gp120-induced cognitive dysfunction in the radial arm water maze test. Results showed that rats in the gp120 groups had longer escape latencies and more errors compared to those in the control group. For example, the average trial time in the 50-ng/day-gp120 group on day eight (16.57 ± 1.71 s, N = 90) was significantly longer than that of control rats (9.93 ± 0.68 s, N = 90). The relative expression of P2X7 mRNA in the control, 50-, 70-, and 100-ng/day-gp120 groups were 0.43 ± 0.06, 0.48 ± 0.07, 0.83 ± 0.05, and 0.84 ± 0.10, respectively; relative P2X7 protein expression in those groups was 0.63 ± 0.07, 1.08 ± 0.06, 0.90 ± 0.07, and 1.03 ± 0.11, respectively. According to immunohistochemistry analysis, the staining intensity values for P2X7 protein expression in the control, 50-, 70-, and 100-ng/d-gp120 groups were 0.88 ± 0.07, 1.41 ± 0.12, 1.28 ± 0.13, and 1.31 ± 0.10, respectively. The above results showed that the expression of P2X7 increased significantly in the hippocampus of gp120 rats compared to that of the control group. These results suggest that ICV infusion of gp120 can successfully mimic HAD in rats, and P2X7 may be involved in gp120-induced cognitive dysfunction. This could provide a theoretical foundation and potential drug target for research and treatment of ADC.