Objective To explore the effect of smoking on the triglyceride ( TG ) , cholesterol ( TC ) , high density lipoprotein-cholesterol(HDL-C) and low density lipoprotein-cholesterol(LDL-C) with the male type 2 diabetes. Methods Selected 144 male patients with type 2 diabetes, then divided them into four groups, including non-smokers, former smokers,current mild(≤20 per day) smokers and current heavy ( >20 per day) smokers. All of them were investigated about the age, diabetes pathogenesis, exercise, diet, smoking, lipid-lowering drugs used and checked with TG, TC, HDL-C, LDL-C and so on. The difference of TG, TC, HDL-C, LDL-C among these four groups was compared by the methods of covariance analysis, regression analysis and partial correlation to evalu-ate the relationships of smoking with blood lipid. Results TG of heavy smokers was higher than the non-smokers and HDL-C was lower after correcting the effects of other possibly relative factors(P<0. 05). HDL-C of the former smokers was higher than smokers and TG was lower than heavy smokers(P<0. 05). Smoking was an independent risk factor for HDL-C ( P<0. 05 ,β= -0. 213 ) , and there was a significantly negative relationship between daily cigarette consumption and HDL-C ( r= -0. 223 , P<0. 05 ) . Conclusion Smoking is an important risk factor for the diabetic male patients’ metabolism of the TG and HDL-C,independent of age, body mass index, blood pres-sure,exercise,diabetes pathogenesis, percentage of body fat and blood glucose. Smoking promotes the type 2 diabet-ics’ disorder of blood lipid and smoking cessation is of significance for the diabetics’ regulation of blood lipids.

Objective:The aim of this study was to investigate the mechanism underlying transforming growth factor-β1 ( TGF-β1 ) induced differentiation of bone marrow-derived mesenchymal stem cells (BMSCs)into myofibroblasts.Methods:Primary mouse BMSCs were isolated from bone marrow by flushing the tibias and femurs of mice , and passage 3 to passage 5 of BMSCs were used in the experiments . BMSCs differentiation into myofibroblast was induced by different doses of TGF-β1.In addition, reactive oxygen species (ROS) inhibitor (N-acetylcysteine, NAC) was added to test its effect on the action of TGF-β1.Expressions of BMSCs differentiation parameters , α-smooth muscle actin (α-SMA), collagenα1(Ⅰ) [Col α1(Ⅰ)] and collagen α1(Ⅲ) [Col α1(Ⅲ)] were measured by real-time quantitative PCR (RT-qPCR) and Western blot analysis.BMSCs were preloaded for 15 min with 2’, 7’-dichlorohydro-fluorescein diacetate ( DCFH-DA) , then stimulated with TGF-β1 for different times , and fluorescence of ROS was measured using high content analysis .Results:TGF-β1 stimulated differentiation of BMSCs into myofibroblasts and up-regulated expression of α-SMA, Col α1(Ⅰ) and Col α1(Ⅲ) in a dose-dependent manner , which blocked by ROS inhibitor NAC .In addition , TGF-β1 could induce a significant rapid and transient increase in ROS production in BMSCs , and the effect of TGF-β1 on ROS production was peaked at 30 min.Conclusion:TGF-β1 induced differentiation of BMSCs into myofibroblasts via production of ROS.

Objective:To investigate the correlation of cognitive dysfunction with intracranial lesions and symptoms of depression and anxiety in patients with neuromyelitis optica spectrum disorders (NMOSD).Methods:Thirty-one NMOSD patients (7/24 males/females) were enrolled in the Department of Neurology of the Sixth Medical Center of the PLA General Hospital from August 2019 to August 2022. The average age was 42±13 years, and the average education level was 12 (9, 12) years. There were 30 healthy controls, 11/19 males/females, with an average age of 47±9 years and an average education of 12 (9, 15) years. The general clinical data and imaging data were collected, and the subjects were assessed on their cognition, anxiety and depression using the assessment scale approved at home and abroad. A cross-sectional study was conducted on them. The t-test or Wilcoxon test was used for inter-group comparison, and Pearson test or Spearman test was used to explore the correlation between the cognition of NMOSD patients and their intracranial lesions, depression and anxiety. Results:Compared with the healthy control group, NMOSD patients had significantly lower scores on MoCA ( Z=-3.10, P=0.002), CRAVLT-N7 ( Z=-5.12, P<0.001), CRAVLT-N8 ( t=-4.40, P<0.001), ROCF-R ( t=-3.10, P<0.01), ROCF-C ( Z=-2.72, P<0.01), PASAT-3 ( Z=-2.71, P<0.01), PASAT-2 ( Z=-3.14, P<0.01), and CWT-A ( Z=-3.10, P<0.01)scales. Frontal lobe lesions were negatively correlated with PASAT-2 ( r=-0.448, P=0.012) scores, temporal lobe lesions were negatively correlated with CRAVLT-N9 ( r=-0.564, P=0.001), and parietal lobe lesions were negatively correlated with MoCA ( r=-0.374, P=0.038), PASAT-3 ( r=-0.426, P=0.017), and PASAT-2 ( r=-0.459, P=0.009) scores; The scores of MoCA ( r=-0.392, P=0.029), CRAVLT-N6 ( r=-0.396, P=0.028), CRAVLT-N7 ( r=-0.415, P=0.020), CRAVLT-N8 ( r=-0.406, P=0.023), PASAT-3 ( r=-0.537, P=0.002) and PASAT-2 ( r=-0.495, P=0.005) scales were negatively correlated with the scores of HAMD assessment, and the scores of PASAT-3 ( r=-0.499, P=0.004) and PASAT-2 ( r=-0.452, P=0.011) were negatively correlated with the scores of HAMA. Conclusions:The cognitive function of patients with NMOSD is significantly reduced, involving multiple cognitive domains. The cognitive function is affected by the distribution of intracranial lesions and the degree of depression and anxiety.

BACKGROUND: Carbapenem-resistant Klebsiella pneumoniae (CRKP) is considered a serious global threat. However, little is known regarding the multidrug resistance (MDR) mechanisms of CRKP. This study investigated the phenotypes and MDR mechanisms of CRKP and identified their clonal characteristics. METHODS: PCR and sequencing were utilized to identify antibiotic resistance determinants. Integron gene cassette arrays were determined by restriction fragment length polymorphism (RFLP) analysis. Multi-locus sequence typing (MLST) and pulsed-field gel electrophoresis (PFGE) were used for epidemiological analysis. Plasmids were typed by using a PCR-based replicon typing and analyzed by conjugation and transformation assays. RESULTS: Seventy-eight strains were identified as resistant to at least one carbapenem; these CRKP strains had a high prevalence rate (38.5%, 30/78) of carbapenemase producers. Additionally, most isolates harbored MDR genes, including Extended spectrum β-lactamases (ESBLs), AmpC, and quinolone and aminoglycoside resistance genes. Loss of porin genes was observed, and Class 1 integron was detected in 66.7% of the investigated isolates. PFGE and MLST results excluded the occurrence of clonal dissemination among these isolates. CONCLUSIONS: A high prevalence of NDM-1 genes encoding carbapenem resistance determinants was demonstrated among the K. pneumoniae isolates. Importantly, this is the first report of bla(NDM-1) carriage in a K. pneumoniae ST1383 clone in China and of a MDR CRKP isolate co-harboring bla(NDM-1), bla(KPC-2), bla(CTX-M), bla(SHV), acc(6′)-Ib, rmtB, qnrB, and acc(6′)-Ib-cr.
China* ; Clone Cells ; Drug Resistance, Bacterial ; Drug Resistance, Microbial ; Drug Resistance, Multiple* ; Electrophoresis, Gel, Pulsed-Field ; Genes, MDR ; Integrons ; Klebsiella pneumoniae* ; Klebsiella* ; Molecular Epidemiology ; Phenotype ; Plasmids ; Pneumonia ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Prevalence ; Replicon

Objective:To investigate the collateral circulation compensation model in patients with favorable prognosis of basilar artery occlusion/severe stenosis treated with drugs or endovascular therapy.Methods:Clinical data of patients with basilar artery occlusion/severe stenosis and good clinical outcome were retrospectively collected in the Department of Neurology, Sixth Medical Center of PLA General Hospital from January 2019 to January 2020. They were divided into intensive drug therapy group and combined endovascular therapy group. The number and ways of collateral compensation pathway described by digital substraction angiography (DSA) were analyzed, and the characteristics of the collateral compensation model were summarized. SPSS22.0 software was used for statistical analysis, and the constituent ratio (%) was used for statistical description of the enumeration data.Results:A total of 32 eligible patients were included, including 27 males and 5 females, with an average age 45-76 (59±10) years. The compensation model included posterior communicating artery-posterior cerebral artery (13 cases, 40.6%), posterior communicating artery-posterior cerebral artery-basilar artery (10 cases, 31.2%), cerebellar artery-anastomotic branches of superior cerebellar artery (8 cases, 25.0%), anterior choroid artery-anastomotic branches of posterior choroid artery (2 cases, 6.2%), collateral circulation not established (11 cases, 34.4%).In drug treatment group, collateral compensation was found in the majority (14/15), with mainly posterior communicating artery (10/14).Most patients in combined treatment group did not develop collateral compensation (10/17), anastomotic branches of PICA-SCA were the main routes (6/7).Conclusion:In patients with basilar artery occlusion/severe stenosis, favorable clinical outcome can be achieved in both groups of patients treated with intensive drug therapy or endovascular therapy.

Potential complications arising from yttrium-90 (90Y) radioembolization are often related to inadvertent embolization of non-target vasculature during particle administration.Therefore,careful pretherapeutic planning with arterial mapping is especially important to help identify potential high-risk arteries and vascular communications.A complete pre-therapeutic evaluation of hepatic arterial vasculature includes selective arteriography,precautionary embolization of potential risk arteries and identification of occurrences of hepatopulmonary shunting secondary to tumor-related pathologic arteriovenous channels.The aim of this review is to discuss the pertinent arterial anatomy during 90Y radioembolization therapy and strategies on how to evaluate the risk and prevent the occurrence of non-target embolization through those vascular structures.

Accurate doses of yttrium-90 (90Y) microspheres are critical for the treatment of liver malignancies,because it is closely related to the clinical efficacy and adverse reactions.The dose calculationis primarily based on the type of ~Y delivery medium,whether it is glass microsphere (TheraSpheres) or resin microsphere (SIR-Spheres).The dose calculation of glass microspheres is based on the assumption that the expected radiation dose of the liver and the microspheres can be evenly distributed throughout the liver,while the dose calculation of resin microspheres is based on the assumption that the microspheres are not uniformly distributed throughout the liver,and the degree of this inhomogeneous distribution depends on the extent to which the normal liver is replaced by the tumor tissue.Many other factors may also potentially affect the therapeutic dose of 90Y microspheres.This review will introduce the calculation methods of 90Y microsphere dose,and describe the factors that need to be considered in order to achieve maximum efficacy and avoid adverse effects.

【Objective】 To study the effect of RHAG variants identified in Chinese population on mRNA splicing by minigene splicing assay(MSA) in vitro. 【Methods】 The pSplicePOLR2G minigene expression plasmids were constructed for 10 RHAG mutations with relatively high distribution frequency in Chinese population near splicing sites or synonymous mutations by analyzing the RHAG gene data in the KMxD database. Then, the wild-type and mutant plasmids were transfected into HEK 293T cells, and RNA was extracted 48 hours after transfection. After reverse transcription, specific primers were used for PCR amplification, and then agarose gel electrophoresis and capillary electrophoresis were performed to determine whether the mutations will affect the normal splicing of exons. 【Results】 MSA in vitro showed that 2 mutations (c.158-5delT, c. 807+ 3A>C) near the splicing site reduced the amount of normal transcripts slightly. The remaining 8 synonymous mutations(c.312G>A, c. 341+ 3G>A, c. 609C>T, c. 681G>A, c. 861G>A, c. 957T>A, c. 984T>C and c. 1139-7G>A) had no impact on the splicing of RHAG mRNA. 【Conclusion】 This study showed that RHAG gene was conservative in terms of splicing, and the mutations near splicing sites and synonymous mutations were less likely to cause abnormal splicing of RHAG gene.

Objective To explore the efficacy difference of diffusion kurtosis imaging (DKI) and ultrasound elastography (UE) in the diagnosis of liver fibrosis. Methods Thirty-five patients whose serological examination showed hepatitis B or hepatitis C virus infection, disease course≥ 1 year, and finally liver biopsy confirmed pathological fibrosis grade in Tianjin Second People's Hospital from December 2015 to April 2017 were prospectively enrolled as patient group. During the same period, twenty healthy volunteers who matched the age, sex and BMI with patient group and showed normal liver function within the last month were enrolled as control group. All of the subjects underwent DKI experiment, and subjects in patient group underwent UE experiment in addition. Liver mean apparent diffusion (MD) and mean kurtosis (MK) were obtained in all subjects and liver stiffness measurement (LSM) was obtained in patient group. The patient group was staged for hepatic fibrosis based on liver biopsy results (S0 to S4). Differences in liver MD and MK values between control and patient groups were tested using independent sample t test (normal distribution) or Mann-Whitney U test (skewed distribution). Differences in liver MD, MK, and LSM between patients with different fibrosis stages were tested using One-way ANOVA (normal distribution) or Kruskal-Wallis test (skewed distribution). The correlation between liver MD, MK and LSM values with fibrosis stages were analyzed using Pearson correlation test. The diagnostic performance in staging fibrosis was analyzed using ROC analysis. Results Liver MD in patient group was lower than that in control group, and the difference was statistically significant (P<0.01). There was no significant difference in liver MK between the two groups (P>0.05). The AUC value for the diagnosis of liver fibrosis by MD was 0.950 (95％CI:0.855 to 0.990). Of the 35 patients, 15 were S1 (mild fibrosis), 13 were S2 (moderate fibrosis), 4 were S3, 3 were S4 (S3+S4 were severe fibrosis). The difference of MD and LSM between different stages of liver fibrosis was statistically significant (P<0.05), and there was no significant difference in MK (P>0.05). Liver fibrosis stages was highly correlated with MD (r=-0.757, P<0.01), and had no correlation with MK (r=-0.010, P=0.956), and moderately correlated with LSM (r=0.440, P<0.01). The AUC values of liver MD and LSM for characterization of ≥S2 stage liver fibrosis were 0.867 and 0.800, respectively, without statistically significant difference (P=0.486). The AUC values for characterization of≥S3 stage liver fibrosis were 0.918 and 0.653, respectively, with a statistically significant difference (P=0.032). Conclusion MD derived from DKI can be used for noninvasive assessment of liver fibrosis, and it is superior to LSM in distinguishing different fibrosis stages and detecting severe fibrosis.

【Objective】 To explore the characteristics of the D antigen epitope of individuals with RhD variants and the genetic molecular mechanism of gene mutations in Guangzhou. 【Methods】 A total of 59 samples of RhD variants were collected from blood donors and hospitals in Guangzhou from January to August 2019. Serological characteristics of D epitopes were further analyzed using two kinds of monoclonal anti-D reagents and D epitope detection kits, and RHCE phenotypic typing was performed. QuickGene DNA extraction kit was used to extract the genomic DNA of the samples, and PCR-RFLP method was used to analyze the RHD gene zygote type. The RHD gene sequence was detected by multiple ligation-dependent probe amplification(MLPA) genotyping, and the RHD exon(1~10) Sanger sequencing was performed on the samples still in doubt after the above detection. DNAStar/SeqMan analysis software was used for comprehensive analysis. 【Results】 In this group of individuals with RhD variants in Guangzhou, 27.12%(16/59) were detected from blood donors [accounting for 0.007%(16/232 793) of blood donors in Guangzhou during the same period], and difficult samples of patients sent by hospitals for determination accounted for 72.88%(43/59). RHD genotype detection: 40.68%(24/59) were RHD^*weak partial 15, 25.42%(15/59) were RHD^* DⅥ.3 and 33.90%(20/59) were rare RHD variants [76.92%(10/13) were RhD variants with 2 different alleles]. Serological D-screen revealed a relatively fixed pattern of RHD^*DⅥ.3 in anti-D antibody(clone: P3^*212 23B10), while the others was negative. The phenotypic distribution of RhD variant CE was Ccee 38.98%(23/59), ccEe 35.59%(21/59), CcEe 25.42%(15/59). 【Conclusion】 Weak partial D15 and DⅥ.3 were the most common RhD variants in Guangzhou Han population, and DⅥ can be preliminarily identified by serological methods such as D-Screen anti-D reagent, while the remaining RhD variants can only be identified by molecular biological methods, and >95% of the RhD variants were C+ or E+ phenotypes.