OBJECTIVE: To observe the correlation between traditional Chinese medicine (TCM) syndromes ("deficiency of qi and yin" and "deficiency of liver yin and kidney yin") and A267G in 5'-untranslated region within exonal of megsin gene, and to search the substantial genetic basis for micro-differentiation of TCM syndromes in primary immunoglobulin A nephropathy (IgAN). METHODS: A total of 120 IgAN cases meeting the diagnostic criteria were enrolled. The sequence of single nucleotide polymorphism (SNP) of A267G in 5'-untranslated region within exonal of megsin gene was tested. The correlation between SNP and TCM syndromes was observed. RESULTS: There were 83 cases carrying GG genotype, 34 cases carrying GA genotype and 3 cases carrying AA genotype in 120 cases of primary IgAN. There was a high proportion of "deficiency of liver yin and kidney yin" in IgAN cases with AA and GA genotypes, and a high proportion of "deficiency of qi and yin" in IgAN cases with GG genotype (P<0.01). Odds ratio in TCM syndrome distribution between GG genotype and GA plus AA genotype was 9.800, and 95% confidence interval was 3.969-24.199. The discrepancy also resided in IgAN patients with different genders and ages. CONCLUSION: A267G in 5'-untranslated region within exonal of the megsin gene may be one of the substantial genetic basis for differentiating "deficiency of liver yin and kidney yin" syndrome and "deficiency of qi and yin" syndrome in primary IgAN.

Adolescent ; Adult ; China ; epidemiology ; Female ; Humans ; Male ; Middle Aged ; Occupational Diseases ; epidemiology ; Poisoning ; epidemiology ; Young Adult

Aim To determine whether AngⅡin para-ventricular nucleus (PVN)was involved in the chronic intermittent hypoxia (CIH ) induced-hypertension in rats.Methods Male Sprague-Dawley rats were ran-domly divided into Sham and CIH groups,the Sham rats were exposed to continuous normoxia,while the CIH rats were submitted to CIH (8 h per day for 15 days).The conscious noninvasive method with tail cuff was performed in rats to record the systolic blood pres-sure during establishing the model of CIH induced hy-pertension.Mean arterial pressure (MAP)and heart rate (HR)were recorded in vivo on a PowerLab data acquisition system after CIH.Rats were fixed on the stereotaxic instrument to conduct microinjection in the PVN.We used Western blot to measure Ang Ⅱ level and AngⅡtype 1 receptor (AT1 R)protein expression in PVN.Results The level of PVN Ang Ⅱin CIH rats was significantly higher than that in Sham rats,a-long with increased AT1 R protein expression.Microin-jection of Ang Ⅱ(0.03,0.3,3 nmol)in bilateral PVN dose-dependently increased MAP in both CIH and Sham rats,and this response was significantly augmen-ted in CIH rats.Losartan (50 nmol),AT1 R antago-nist,had no effect on MAP in Sham rats,but caused significant MAP decreases in CIH rats,and prevented Ang Ⅱ-induced increases in MAP in both CIH and Sham rats.Conclusion The results suggest that the increased AngⅡrelease and enhanced AT1 R activation in the PVN contribute to CIH induced-hypertension in rats.

Objective To establish multi-PCR-single strand conformational polymorphism analysis (mPCR-SSCP) for rapid detection of isoniazid (INH) and rifampin (RIF) resistance associated katG,inhA and rpoB genes of Mycobacterium tuberculosis isolates.Methods The INH-and RFP-resistance of 134 isolates was determined by using drug susceptibility test.The primers were designed for detecting INH and RFP resistance-associated katG,inhA and rpoB gene in the isolates by mPCR-SSCP.PCR-DS technique was applied to detect the mutations in katG,inhA and rpoB genes.All the results from different assays were subsequently analyzed as well as compared.Results All of the 134 tested isolates had katG,inhA and rpoB genes.Of the 134 isolates,42 (31.3％) and 45 (33.6％) strains were INH-and RFP-resistant,respectively.The results of mPCR-SSCP and PCR-DS showed that all the 92 INH-susceptible isolates had no mutation in katG and inhA genes with 100％ specificity.In the 89 RFP-susceptible isolates,2 and 1 had mutation in rpoB genes confirmed by mPCR-SSCP and PCR-DS with 97.8％ or 98.9％ specificity,respectively.Among the 42 INH-resistance isolates,33 and 36 strains had the mutations in katG and/or inhA genes due to the results of mPCR-SSCP and PCR-DS with 78.6％ or 85.7％ sensitivity,respectively.The results of mPCR-SSCP and PCR-DS also demonstrated that in the 45 RFP-resistance isolates,41 and 43 strains had the mutations in rpoB gene with 91.1％ or 95.6％ sensitivity,respectively.Conclusion The mPCR-SSCP established in this study can be used to rapidly detect INH and RFP-resistance associated mutations in katG,inhA and rpoB genes of M.tuberculosis with convenience,specificity and sensitivity,which shows a good prospect for application in clinic.

Objective To determine the long term outcomes of laryngomalacia infants with anomalies and to determine the clinical practice guideline for these infants.Methods The charts of infants with moderate to severe laryngomalacia,who were admitted to our hospital between January 2013 and December 2015,were retrospectively reviewed.These infants were divided into two groups,anomaly(A) group(n=37) and non-anomaly (NA) group(n=19).Results Fifty-six cases were enrolled.Infants in A group were older at symptom relief than those in NA group[(10.00±3.56) months vs.(7.89±3.03) months,P＜0.05],and the weight percentiles of infants in A group were lower at 3,6 and 12 months than those in NA group(P＜0.05).There was no statistically significant difference between the two groups on the weights percentiles in infants at 24 months after diagnosis.Five of 37 cases in A group and 3 of 19 cases in NA group had supraglottoplasty.One infant in A group had tracheotomy.Conclusion Both breathing difficulty and development retardations of infants with moderate or severe laryngomalacia could gradually improved with age.There is not enough evidence to support the aggressive supraglottoplasty for infants with anomalies and laryngomalacia.

Objective:To explore the protective effect of puerarin on hypoxia/reoxygenation (H/R)-induced acute kidney injury(AKI)in vitro.Methods:HK-2 cells were treated with H/R for simulating ischemia reperfusion injury(IRI)in vivo. The experimental groups included control group, H/R treatment group(0/6/12/24 h), H/R 24 h + puerarin treatment group(puerarin, Pue), H/R 24 h + Pue+ 3-methyladenine(3-MA)treatment group and H/R 24 h+ 3-MA treatment group. Immunoblotting was employed for detecting the expression changes of autophagy-related proteins, CCK-8 for examining cell proliferation, electron microscopy for observing autophagosome formation and TUNEL for detecting apoptosis.Results:As compared with control group, the expression of LC3-II rose in H/R 24 h group, the expression of autophagy marker P62 declined, count of autophagosome increased, cell viability decreased and cellular inflammation occurred. Puerarin had similar effects to 3-MA. As compared with H/R 24 h group, puerarin could reverse the changes in the expression levels of LC3 and P62 induced by H/R( P<0.05). There were greater cell viability, reduced autophagosome count and lessened cell apoptosis( P<0.05). At the same time, protein expression levels of HMGB1, TLR4 and NF-κB dropped( P<0.05). Conclusions:Puerarin suppresses autophagy through HMGB1/TLR4/NF-κB axis for lessening ischemia-reperfusion injury an in vitro model.

Objective:To evaluate the role of P2X 7 receptor in microglia in the medial prefrontal cortex (mPFC) in neuropathic pain (NP) and the relationship with autophagy in rats. Methods:Sixty-four healthy SPF male Sprague-Dawley rats, aged 6-8 weeks, weighing 200-250 g, were divided into 4 groups ( n=16 each) using a random number table method: sham operation group (S group), NP group, sham operation+ P2X 7 receptor blocking group (SP group), and NP+ P2X 7 receptor blocking group (NP+ P group). The NP model was established by ligation of the sciatic nerve.Fourteen days later a cannula was placed in the mPFC with a brain stereotactic instrument, P2X 7 receptor blocker A-740003 0.5 μg/0.5 μl was injected into bilateral mPFC for 3 consecutive days starting from the 14th day in SP and NP+ P groups, and DMSO 0.5 μl was injected instead of A-740003 in S and NP groups.The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured at 3, 7 and 10 days after establishing the model and 14, 15 and 16 days after administration.Then the rats were sacrificed, and the mPFC was removed for determination of the expression of P2X 7 receptor and mRNA and autophagy-related proteins Beclin1 and LC3Ⅱ/Ⅰ (by quantitative real-time polymerase chain reaction or by Western blot) and co-expression of P2X 7R and microglia (by immunofluorescence) and the number of autophagosomes in mPFC (with a transmission electron microscope). Results:Compared with group S, MWT was significantly decreased, and TWL was shortened at 3, 7 and 10 days after establishing the model, the expression of P2X 7 receptor and mRNA, Beclin1 and LC3Ⅱ/Ⅰ was up-regulated at 30 min after administration on 16 days after establishing the model, and the number of cells co-expressing P2X 7 receptor and IBA-1 and the number of autophagosomes were increased in NP and NP+ P groups ( P<0.05), and no significant change was found in the indexes mentioned above in group SP ( P>0.05). Compared with group NP, MWT was significantly increased, and TWL was prolonged at 30 min after administration on 14, 15 and 16 days after establishing the model, the expression of P2X 7 receptor and mRNA, Beclin1 and LC3Ⅱ/Ⅰ was down-regulated, and the number of cells co-expressing P2X 7 receptor and Iba-1 and the number of autophagosome were decreased in group NP+ P ( P<0.05). Conclusion:Up-regulation of P2X 7 receptor expression in microglia in mPFC is involved in the process of NP in rats, which is associated with the promotion of autophagy.

Objective:To evaluate the role of cold-inducible RNA-binding protein (CIRP) in acute renal injury in a mouse model of myocardial ischemia-reperfusion (I/R) and the relationship with nuclear factor kappa B (NF-κB) signaling pathway.Methods:Twenty-four SPF-grade healthy male C57BL/6 mice, aged 6-8 weeks, with body mass index of 24-28 g, were divided into 3 groups ( n=8 each) using a random number table method: sham operation group (Sham group), myocardial I/R group (I/R group) and myocardial I/R + CIRP-derived peptide C23 group (I/R+ C23 group). The model of myocardial I/R was developed by ligation of the left anterior descending coronary artery for 30 min followed by 120-min reperfusion in anesthetized animals. CIRP-derived peptide C23 8 mg/kg was intraperitoneally injected before myocardial ischemia and reperfusion in I/R+ C23 group, while Sham group was only threaded without ligation. Blood samples were collected from the right internal carotid artery at 120 min of reperfusion for determination of the serum creatine kinase isoenzymes (CK-MB), lactic dehydrogenase (LDH), creatinine (Cr) and blood urea nitrogen (BUN) concentrations. Renal tissues were obtained for examination of the pathological changes, and the tubular injury score was assessed. The expression of NF-κB, phosphorylated NF-κB (p-NF-κB), Nod-like receptor protein 3 (NLRP3), interleukin-1beta (IL-1β) and IL-18 in renal tissues was detected by Western blot. The expression of Toll-like receptor 4 (TLR4), NLRP3, IL-1β, TNF-α and IL-6 mRNA was determined by real-time polymerase chain reaction. Results:Compared with Sham group, the levels of serum CK-MB, LDH, Cr and BUN and renal tubule injury score were significantly increased, the expression of p-NF-κB, NLRP3, IL-1β and IL-18 was up-regulated, the expression of TLR4, NLRP3, IL-1β, TNF-α and IL-6 mRNA was up-regulated ( P<0.05), and the pathological injury to renal tissues was aggravated in I/R group. Compared with I/R group, the serum CK-MB, LDH, Cr, BUN and renal tubular injury score were significantly decreased, and the expression of p-NF-κB, NLRP3, IL-1β and and IL-18 was down-regulated, the expression of TLR4, NLRP3, IL-1β, TNF-α and IL-6 mRNA was down-regulated ( P<0.05), and the pathological injury to renal tissues was alleviated in I/R+ C23 group. Conclusions:CIRP is involved in the process of acute renal injury in a mouse model of myocardial I/R, which is associated with activation of NF-κB signaling pathway and promotion of inflammatory responses.

Objective To evaluate the scientific research efficiency of tertiary hospitals and analyze the influencing factors, providing reference for the decision-making of scientific research managers in China. Methods Evaluation indicators were collected from 100 tertiary hospitals in China, and their research efficiency was evaluated using Bootstrap data envelopment analysis (DEA) method. The influencing factors were analyzed using ordinary least square ( OLS) regression model. Results The averaged scientific research efficiency of these hospitals using Bootstrap DEA method was 0. 5224, lower than that using conventional DEA method (0. 0676), yet with a great variation (from 0. 1103 to 0. 8790) among them. Linear regression analysis showed that factors such as R&D input and output, and hospital types has statistical significance on the saentific research efficiency (P < 0. 05). Conclusions These hospitals are inefficient in scientific research with sizable room for improvement. Conventional DEA method should be used with caution, as deviations should be corrected with Bootstrap DEA method. The research development level and hospital types of their province can influence the research efficiency the hospitals significantly.

AIM: To study the pathological change in mouse organs immunitied by inactivated SARS-CoV vaccine. METHODS: Inactivated SARS-CoV vaccine was injected into BALB/c and C57BL/6 mice. Anti-SARS antibody was analyzed by ELISA. After 8 weeks, the immunitied mice were killed and those organs were analyzed by pathological methods. RESULTS: Anti-SARS antibody in mice was positive after 8 days. Only minimal injury was observed in a few lungs and livers, but the other organs were not. CONCLUSIONS: Inactivated SARS-CoV vaccine induced mice to create antibody, whereas they did not cause severe injury. This result will be valuable for vaccine into clinical research. [