Background The accurate calculation of intraocular lens (IOL) power is essential for attaining the desired refractive outcome after cataract surgery,especially for patients with high myopia and posterior scleral staphyloma.Objective This study was to evaluate the clinical feasibility of IOL Master compared with contact A-scan in cataract patients with high myopia and posterior scleral staphyloma,then compare the accuracy of different IOL power calculation formulas.Methods This was a prospective case control clinical research.Fourty-one eyes with age-related cataract of 28 patients underwent phacoemulsification with monofocal foldable IOL implantation in Tianjin Medical University Eye Hospital were involved,who were all high myopia with posterior scleral staphyloma.Preoperative measurement was measured with IOL Master as well as with contact A-scan and manual keratometry.IOL power was calculated according to the SRK-Ⅱ,SRK-T,Haigis,Hoffer Q,Holladay 1 formulas.The refractive outcome was followed-up 3 months after operation.Results The difference was significant between the 2 methods in axial length (AL) and anterior chamber depth (ACD) measurement (P =0.005,0.000) ; In corneal curvature measurement,there was no significant difference between them (P =0.398).When mean absolute refractive error (MAE) was divided by ±1.00 D,The SRK/T and Haigis formula performed better than other formulas measured by IOL Master;The Holladay 1,Hoffer Q and Haigis formula performed better than other formulas measured by contact A-scan combined with manual keratometry,respectively.Conclusions For cataract patients with high myopia and posterior scleral staphyloma,SRK/T and Haigis formula were recommended when employing IOL Master; whereas when using contact A-scan combined with manual keratometry,we prefer Holladay 1,Hoffer Q or Haigis formula.

Objective To investigate the dynamics of the level of S100 in cerebrum, brainstem, and serum following the diffuse brain injury in rats and provide the experimental evidences for estimating injury time. Methods ELISA was used to determine whether S100 protein is changed after diffuse brain injury in rats. Forty rats were sacrificed at 0.5 hour, 2 hours, 4 hours, 12 hours, 24 hours, 3 d and 7 d after diffuse brain injury and normal rats as control. Results The level of S100 in cerebrum, brainstem, and serum increased, followed by a decrease, and then further increased. The level of S100 could be detected to increase at 30 minutes and reached the peak at 4 hours after DBI. The level decreased gradually to the normal at 1d and till 3 d formed the second peak. The level returned to the normal at 7d following injury again. In the postmortem injury groups, there were no significant changes compared to the control group. Conclusion The present study showed that the time-dependent expression of S100 is obvious following diffuse brain injury in rats and suggested that S100 will be a suitable marker for diffuse brain injury age determination.

Objective:To study the possible immune escape mechanisms of HCoV-OC43 from human dendritic cells(DC).Methods:HCoV-OC43 was isolated from clinical specimen using BSC-1 cells and identified by Real-time PCR,and the cytopathic effect was observed by phase contrast microscope.DCs were induced in vivo using hu-GM-CSF and IL-4 cytokines,and after 7 days of differentiation,DCs were infected by HCoV-OC43.The morphology of HCoV-OC43 infected DC was observed by transmission electron microscope,and the cytokines related to DC functions were detected by Real-time PCR after infection.DC proportion and function related co-stimulatory molecules were analyzed by flow cytometry.Results:In vitro HCoV-OC43 infected human DC model was successfully built.HCoV-OC43 can infect DC and generate immune response of DC in vitro,but no virus nucleonic acid could be detected in culture supernatant.The DC expression of IFN-α,IFN-β,CCL3 and CCL5 were significant decreased when infected with HCoV-OC43,but the expression of costimulatory molecules including HLA-DR,CD1c and CD86 were not affected by HCoV-OC43 infection.Conclusion:Human DC could be infected by HCoV-OC43 and generate immune response,but could not produce progeny virus.HCoV-OC43 may escape from immune response by suppressing the expression of IFN-α and other inflammatory cytokines and chemokines in DC.

Objective To study the relationship between the expression of Mycobacterium tuberculosis small heat shock protein Hsp16.3 and the apoptosis of infected mouse alveolar macrophages.Methods The laboratory mice were infected with bacterial suspension of the international standard virulent strain of Mycobacterium tuberculosis H37Rv strains (H37Rv),Hsp16.3 gene deletion mutants of the international standard virulent of Mycobacterium tuberculosis H37Rv strains(△H37Rv),or sterile saline solution (normal control)by the tail vein. After successful replication of mouse infection model in each group,we cleaved the alveolus of each group of mice and collected lavage fluid to obtain alveolar macrophages of the infected mice at days 1 ,3 ,5 ,7 ,9 ,1 1 ,1 3 and 1 5 .Then the infection status of macrophages was observed with confocal laser scanning microscopy;flow cytometry was used to detect the apoptosis rate of alveolar macrophages of the infected mice;Caspase-3 and Bcl-2 expressions were examined by Western blot.Results The apoptosis rate of Hsp16.3 gene was higher in deletion strain (△H37Rv)group and H37Rv strains (H37Rv)group than in control group.The apoptosis rate of alveolar macrophages in △ H37Rv group gradually increased,peaked at day 7 ,and then gradually decreased.It was significantly higher in H3 7 Rv group than in H3 7 Rv strain group from day 1 to 7 and from day 1 3 to 1 5 (P<0 .0 5 ).Caspase-3 and Bcl-2 protein expressions in the macrophages of△H37Rv group and H37Rv group were higher than those of control group.Caspase-3 expression in the microphages of △H3 7 Rv group and H3 7 Rv group gradually increased from day 1 to 7 and peaked at day 7;it peaked again at day 13 in H37Rv group.However,Caspase-3 expression remained significantly higher in△H37Rv group than in H3 7 Rv group (P<0 .0 5 ).Bcl-2 expression in △H3 7 Rv group did not change much at the early stage of infection (P<0 .0 5 ),but gradually increased after day 9 .Bcl-2 expression in H3 7 Rv group did did not change much from day 1 to 7 (P<0.05),but gradually increased after day 7.However,it remained lower in△H37Rv group than in H37Rv group,especially after 7 days(P<0.05).Conclusion Mycobacterium tuberculosis small heat shock protein Hsp16.3 can inhibit the apoptosis of macrophages during the early and late stages of infection,and this inhibition may be achieved by inhibiting the expression of apoptotic protease Caspase-3 and promoting the expression of Bcl-2 protein.

Acute Disease ; Adult ; Aged ; Angiography ; Female ; Humans ; Male ; Middle Aged ; Phlebography ; Thrombolytic Therapy ; Tomography, X-Ray Computed ; Venous Thrombosis ; diagnostic imaging ; drug therapy

OBJECTIVETo provide a quantitative summary in estimating the association between polymorphisms of 3 loci in NRAMP1 gene and susceptibility to tuberculosis in East-Asia population by means of meta-analysis.

METHODSWe searched databases (MEDLINE, OVID and CBM disc) from January 1995 to May 2005 using "NRAMP1" or "SLC11A1", in combination with "tuberculosis", also performed a manual search of citations from relevant original studies and literature. For each study involved, information was collected concerning the characteristics of the subjects, such as mean age of cases and the size of study. These characteristics were used to evaluate the sources of variation. Summary ORs and corresponding 95% CI were estimated by fixed effects (Mantel-Haenszel) or random effects (DerSimonian and Laird) model. To check for publication bias,a funnel plot, using Egger's linear regression method, was constructed. Cumulative meta-analysis was performed to evaluate whether the summary OR for studies with the polymorphisms of the 3 loci in the NRAMP1 gene was changing along with the accumulation of more data. Chi-square goodness of fit was used to test deviation from Hardy-Weinberg equilibrium.

RESULTSEight publications, with the number of cases and controls of 1067 and 1084 respectively, were identified and all genotype frequencies were consistent with Hardy-Weinberg equilibrium. The summary ORs for studies with polymorphisms of 3' UTR, D543N and INT4 loci of the NRAMPI gene among the East-Asia population were 1.68(95% CI: 1.31-2.16, P< 0.001), 1.78(95% CI: 1.38-2.30, P< 0.001), 1.56 (95% CI: 0.72- 3.35, P = 0.26), respectively when compared with their corresponding common homozygotes. Publication bias was not found in the studies with the three loci, except for INT4 locus, by Egger linear regression method. The cumulative summary effects ORs were 1.85 (P = 0.02) in 2000, 1.35 (P = 0.12) in 2002,1.64 (P= 0.001) in 2003, and 1.68 (P<0.001) in 2004 for 3'UTR locus, 1.88 (P = 0.001) in 2000,1.65(P = 0.001) in 2002,1.70(P<0.001) in 2003,1.76(P<0.001) in 2004, and 1.78(P<0.001) in 2005 for D543N locus, and 0.88(P = 0:70) in 2002, 2.50(P = 0.41) in 2003, 1.52(P = 0.42) in 2004 and 1.56(P = 0.26) in 2005 for INT4 loucs.

CONCLUSIONPolymorphisms at 3' UTR and D543N loci had statistically significant association between the NRAMP1 variants and susceptibility to tuberculosis in the East-Asia descendants, and variant in the INT4 locus failed to show statistically significant association in the East-Asia population.

Asian Continental Ancestry Group ; genetics ; Cation Transport Proteins ; genetics ; Far East ; Genetic Predisposition to Disease ; Humans ; Odds Ratio ; Polymorphism, Genetic ; Tuberculosis ; genetics

BACKGROUNDAccurate prediction for prognosis is important for hospitalized patients with chronic obstructive pulmonary disease (COPD) requiring invasive mechanic ventilation (IMV) and for their family members to make end-of-life decisions. The response to therapy in such a patient population has rarely been investigated. The aim of the study was to evaluate the risk factors in these patients and investigate their response to IMV and the relationship between their responses and prognosis.

METHODSA cohort of 138 patients with COPD requiring IMV >or= 12 hours for acute respiratory failure of diverse etiological factors during a 4-year period were retrospectively studied using prospectively gathered data. All variables potentially related to hospital mortality were evaluated by univariate and multiple stepwise logistic regression analysis.

RESULTSThe mean age of all patients investigated was (65.7 +/- 11.6) years and the hospital mortality was 39.9% (31.1% with COPD exacerbation). Correction of acidosis (pH >or= 7.30) was seen in 58 patients (69.9%) in survivors but only 12 patients (21.8%) in nonsurvivors (P < 0.05) after ventilation. Using multivariate logistic analysis, the variables independently associated with hospital mortality were a higher acute physiology score before intubation, lower pH value measured 24 hours after the onset of ventilation and development of multiorgan dysfunction syndrome (MODS).

CONCLUSIONSIn COPD patients requiring IMV, the postintubation pH value can not only reflect patients' response to treatment, but also serve as an independent determinant of hospital mortality apart from other risk factors such as a higher preintubation APACHE II score and development of MODS. A close correlation between the response to IMV and prognosis was proved in these patients.

Adult ; Aged ; Cohort Studies ; Female ; Forced Expiratory Volume ; Hospital Mortality ; Humans ; Hydrogen-Ion Concentration ; Logistic Models ; Male ; Middle Aged ; Pulmonary Disease, Chronic Obstructive ; mortality ; physiopathology ; therapy ; Respiration, Artificial ; Retrospective Studies ; Risk Factors

Objective: To study the prevalence of rush poppers use among men who have sex with men (MSM) in Urumqi and to analyze the mediating effect of high-risk sexual behavior between the use of rush poppers and human papillomavirus (HPV) infection. Methods: From January to June 2018, 651 MSM were recruited through network and publicity. Data was collected by using online questionnaire and anal swab were collected from them for HPV genotyping. According to Baron and Kenny's criterion, multivariate logistic regression models was used to analyze the mediation effect of high-risks sexual behaviors (multiple sexual partners, anal intercourse condom use) between rush poppers use and HPV infection. Results: A total of 651 subjects were (32.0±8.0) years old, and 174 subjects (26.7%) had ever used rush poppers in the past 6 months, while 350 subjects (46.9%) had more than 2 sexual partners and 188 subjects (28.9%) did not use anal condom. After adjusting age and marital status, rush poppers use was associated with HPV infection (OR (95%CI) was 2.34 (1.63-3.36), P<0.05), and sexual partners in the past 6 months (OR (95%CI) was 2.72 (1.89-3.93), P<0.05).After adjustment for age, marital status, sexual partners in the past 6 months, and anal condom use, rush poppers use was still associated with HPV infection (OR (95%CI) was 2.21 (1.53-3.19), P<0.05).After adjustment and adjustment of age, marital status, rush poppers use and anal sex condom use, the number of sexual partners at nearly 6 months was still associated with HPV infection (OR (95%CI) was 1.46 (1.05-2.04), P<0.05). Conclusion Sexual partners in the past 6 months have a mediation effect between rush poppers use and HPV infection in Urumqi. For the prevention of sexually transmitted diseases, we should focus on rush poppers use.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.