Humans ; Lung ; pathology ; Physical Examination ; Pneumoconiosis ; diagnosis ; Thoracotomy

The clinical values of acetoacetate ( AcAA ) and β hydroxybutyrate ( βHBA ) determination in classification of type 1 and2 diabetes were explored. 102 normal control subjects,33 cases of type 1 diabetes, and 104cases of type 2 diabetes were enrolled. Serum AcAA, βHBA, fasting plasma glucose ( FPG), C-peptide, and insulin levels were measured. The results showed that serum AcAA, βHBA, total ketone tody (TKB) levels in the diabetic groups were significantly higher than those of the normal group( P＜0. 01 ). AcAA, βHBA, TKB levels in type 1diabetes were higher as compared with those of type 2 diabetes( P＜0.01 ). The AcAA, βHBA, and TKB levels were negatively related with C-peptide and insulin in diabetic patients( P＜0. 01 ). All the type 1 diabetic patient were found to have TKB and lower C-peptide levels. TKB positive and lower C-peptide in type 2 diabetes were found in 47% and 26% respectively. Receiver operating characteristic (ROC) curve suggested that the area under the ROC curve of type 1 and type 2 diabetes was 0.926. The optimal operating point of the total ketone body was 0. 532 mmol/L with higher sensitivity and specificity. Enzymatic determination of acetoacetate and β hydroxybutyrate seems to have important clinical values for classification of type 1 and 2 diabetes.

Background:The diagnostic accuracy of APRI and FIB-4 for liver fibrosis in patients with chronic hepatitis B is nothigh,especially for significant liver fibrosis (F≥2). Noninvasive diagnosis for liver fibrosis has become a research hotspot;and the diagnostic value of APRI combined with FIB-4 is not clear. Aims:To investigate the diagnostic value ofAPRI combined with FIB-4 for significant liver fibrosis in patients with chronic hepatitis B. Methods:A total of 171patients with chronic hepatitis B from January 2011 to October 2016 at General Hospital of Xinjiang Military Region wereenrolled. Liver biochemical indices,routine blood test and liver biopsy pathology were performed. APRI and FIB-4 werecalculated,ROC curve was drawn,and cutoff value of APRI and FIB-4 for diagnosing significant liver fibrosis wasdetermined,and mode of APRI combined with FIB-4 for diagnosing significant liver fibrosis was established. Results:Withthe increase in degree of liver fibrosis,APRI and FIB-4 were gradually increased (P < 0. 05). Area under ROC curve(AUC)for APRI and FIB-4 were 0. 812 and 0. 770,respectively. The sensitivity of FIB-4 for diagnosing significant liverfibrosis was higher than that of APRI. Sensitivity,specificity,negative predictive value,positive predictive value,andaccuracy of APRI combined with FIB-4 for diagnosing significant liver fibrosis were superior to APRI or FIB-4 used alone;and the specificity,accuracy of mode 2 were superior to mode 1. Conclusions:APRI combined with FIB-4 can increasethe accuracy for diagnosing significant liver fibrosis.

OBJECTIVETo investigate the role of Xuebijing injection(XBJI, traditional Chinese medicine), in inhibiting TLR4--NF-kappaB--IL-1beta pathway of myocardial hypoxia/reoxygenation in rats.

METHODSThirty six male SD rats (280 +/- 30) g were randomly divided into six groups (n = 6): normal group (N group), balanced perfusion group (BP group), model group (M group), low dose XBJI group (XBJI(L) group), middle dose XBJI group (XBJI(M) group), high dose XBJI group (XBJI(H) group). By Langendorff isolated heart perfusion device to establish the model of myocardial hypoxia/reoxygenation in rats. ELISA was used to detect the concentration of interleukin-1beta (IL-1beta); Western blot was used to detect the expression of nuclear factor kappa B p65 (NF-kappaB p65) protein and toll like receptor 4 (TLR4) protein; and RT-PCR to determine the expression of NF-kappaB p65 mRNA and TLR4 mRNA;To observe microstructure changes of hypoxia/reoxygenation myocardial by light microscopy.

RESULTSCompared with M group, the IL-1beta concentration, NF-kappaB p65 and TLR4 protein,NF-kappaB p65 and TLR4 mRNA of XBJIL group, XBJI(M) group, XBJI(H) group expression decreased in varying degrees,and decreased most obviously all in XBJI(M) group (P < 0.05, P < 0.01); Myocardical structural damage was serious in M group, and improved after treatment XBJI, the most obvious was the XBJI(M).

CONCLUSIONDifferent dose of XBJI can inhibit TLR4--NF-kappaB--IL-1beta signal transduction pathway and reduce several inflammatory reaction after myocardial hypoxia/reoxygenation injury, the 4 ml/100 ml of XBJI is the best.

Animals ; Drugs, Chinese Herbal ; pharmacology ; Heart ; drug effects ; Inflammation ; Interleukin-1beta ; metabolism ; Male ; Myocardium ; pathology ; RNA, Messenger ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; drug therapy ; Signal Transduction ; Toll-Like Receptor 4 ; metabolism ; Transcription Factor RelA ; metabolism

OBJECTIVETo study the inhibition of maxizyme (Mz) directed against the mutant-type p53 gene (mtp53) at codon 249 in exon 7 (AGG --> AGT) both in cell-free system and in MHCC97 cell lines.

METHODSMaxizyme and control mutant maxizyme (G5 --> A5) were designed by computer and cloned into the eukaryotic expression vector pBSKneoU6 (pU6Mz, pU6asMz). Mz was driven by T7 RNA polymerase promoter in vitro. In the cell lines, U6 promoter was driven by RNA PolIII. The mutant type p53 gene fragment was cloned into the pGEM-T vector under the T7 promoter control. The 32P-labeled mtp53 transcript was the target RNA. Cold maxizyme transcripts were incubated with 32P-labeled target RNA in vitro. pU6Mz was introduced into MHCC97 cells by Lipofectamine2000 and mtp53 expression was analyzed by RT-PCR and Western blot.

RESULTSIn vitro cleavage showed that pU6Mz was very active with cleavage efficiency of 42% while pU6asMz was not. The wild type p53 was not cleaved. Partial down-regulation of mtp53 mRNA and mtp53 protein were observed in MHCC97 cells transfected with pU6Mz but not those with pU6asMz. The proliferation of MHCC cells was inhibited by MTT analysis.

CONCLUSIONOur findings suggest that the chimeric U6 maxizyme against the mtp53 is a new promising gene therapeutic agent in treating hepatocellular carcinoma.

Carcinoma, Hepatocellular ; genetics ; Cell Line, Tumor ; Genetic Therapy ; methods ; Genetic Vectors ; Humans ; Liver Neoplasms ; genetics ; Nucleic Acid Conformation ; Point Mutation ; Protein Conformation ; RNA, Catalytic ; RNA, Messenger ; chemical synthesis ; metabolism ; Recombinant Fusion Proteins ; Ribonuclease T1 ; pharmacology ; Tumor Suppressor Protein p53 ; genetics

Abstract: Objective To investigate the current status of streptomycin resistance of Yersinia pestis caused by point mutations of rpsL gene in Qinghai, so as to provide theoretical basis for precise clinical medication and prevention of drug resistance of human plague outbreak in South area of Qinghai Province in the future. Methods A total of 104 representative strains of Yersinia pestis collected from plague patients, vector insects and intermediate hosts in South area of Qinghai Province from 1957 to 2009 were screened, isolated and cultured by Hiss agar plates. The DNA of representative Yersinia pestis was extracted by sodium dodecyl sulfate lysis and phenol-chloroform method. The primers forward primer and reverse primer and TaqMan-MGB probes probe1 [FAM] and probe2 [VIC] were designed for the rpsL gene of streptomycin resistance gene in China. Real-time PCR with TaqMan-MGB fluorescent probe was used to detect the mutations of rpsL gene in streptomycin resistance locus of 104 strains of Yersinia pestis in South area of Qinghai Province. Results The FAM test results of 104 strains in South area of Qinghai Province were positive, corresponding to the detection of rpsL (128 : A ), RFU peak >1 000,negative <200. VIC test results of all tested strains were negative, corresponding to the detection of rpsL (128:G), RFU peak <200, positive >1 000. That is, no strains with rpsL gene mutation related to streptomycin resistance were found in the 104 strains of Yersinia pestis in Qingnan Province. Conclusion This study provides basic data on the distribution of streptomycin resistance of Yersinia pestis in South area of Qinghai Province, and lays a foundation for preventing the occurrence of drug resistance and clinical treatment of Yersinia pestis in South area of Qinghai Province.

To investigate the role and mechanism of ceramide (Cer) regulation in alcohol-induced neuronal proliferation and the newborn neurons formation, we used sphingomyelin synthase 2 (predominant enzyme of Cer metabolism) knockout (SMS2(-/-)) and wild type (WT) female mice to establish the model of prenatal alcohol exposure. In 24 h after being given birth (postnatal day 0, P0), the offspring of model mice received blood sphingomyelin (SM) measurement with enzymatic method. On P0, P7, P14 and P30, the proliferation of granule cells in the dentate gyrus and newborn neurons were investigated with immunofluorescent labeling. The expression of protein kinase Cα (PKCα) in the hippocampus was tested with Western blot analysis. The results showed that the SM level of blood in SMS2(-/-) pups was significantly lower than that in WT pups. No matter in SMS2(-/-) or WT mice, the prenatal alcohol exposure down-regulated the SM levels in pups with dose-dependency. In both SMS2(-/-) and WT pups, the number of proliferative neurons and newborn neurons in the dentate gyrus gradually decreased with the growing age. Compared with the WT pups, SMS2(-/-) pups showed significantly more proliferative neurons and newborn neurons in the dentate gyrus. Notably, prenatal alcohol exposure dose-dependently increased proliferative neurons and newborn neurons in the dentate gyrus in both WT and SMS2(-/-) pups. The hippocampal expression of PKCα protein in SMS2(-/-) mice was lower than that in WT mice, and prenatal alcohol exposure could up-regulate the PKCα protein expression in both WT and SMS2(-/-) mice with dose dependency. These results suggest that alcohol exposure during pregnancy can induce the compensatory neural cell proliferation and the production of newborn neurons in offspring, and the Cer-ceramide-1-phosphate (C1P) pathway is involved in alcohol-induced neural cell proliferation. The activation of PKCα may be a key step to start the Cer-C1P pathway and up-regulate the alcohol-induced neural cell proliferation and the newborn neurons formation.
Animals ; Animals, Newborn ; Cell Proliferation ; drug effects ; Cells, Cultured ; Ceramides ; metabolism ; Dentate Gyrus ; cytology ; Ethanol ; toxicity ; Female ; Mice ; Mice, Knockout ; Neurons ; cytology ; Pregnancy ; Prenatal Exposure Delayed Effects ; physiopathology ; Protein Kinase C-alpha ; metabolism ; Signal Transduction ; Transferases (Other Substituted Phosphate Groups) ; genetics

Background: The position of the eyebrows is critical when planning blepharoptosis surgery. However, insufficient scholarly attention has been paid to the details of postoperative eyebrow height changes at each anatomical landmark. This study investigated the effect of blepharoptosis surgery on brow height and evaluated the change in brow position. Methods: After a retrospective review of 247 patients, this study analyzed 53 patients (106 eyelids) who underwent levator and Müller’s complex advancement between March 2010 and January 2022. Brow heights were measured from the distance between the upper brow margin of each landmark and horizontal line of pupillary center on a digital photograph. Results: The mean change of eyebrow lowering was 1.54 mm (P<0.001) at the medial canthus, 1.29 mm (P<0.001) at the medial limbus, 1.44 mm (P<0.001) at the center of the pupil, 1.40 mm (P<0.001) at the lateral limbus, 1.15 mm (P=0.001) at the lateral canthus, and 0.75 mm (P=0.021) at the lateral eyebrow end. The brow change was most prominent at medial canthus and least prominent at the lateral brow end. The preoperative brow position was only statistically significant factor predicting brow height descent after surgery according to multiple linear regression analysis (R2=0.305, B=–0.375, P<0.001). Conclusions The eyebrows lowered in most patients after blepharoptosis surgery. The preoperative brow position is the most important factor in predicting the change in brow height after blepharoptosis surgery.

OBJECTIVETo study the variation and significance of serum and stool IL-18 and IFN-gamma levels in children with rotavirus enteritis.

METHODSSerum and stool specimens from 50 children with acute rotavirus enteritis were collected before treatment. Serum and stool levels of IL-18 and IFN-gamma were measured using ELISA. Serum and stool specimens from 21 age and gender-matched healthy children were used as the Control group.

RESULTSSerum and stool levels of IL-18 and IFN-gamma in patients with rotavirus enteritis were significantly higher than those in the Control group. There was a negative correlation between the serum IFN-gamma level and the frequency of vomiting (r=-0.368, P < 0.05). The stool IL-18 level negatively correlated to the frequency of diarrhea (r=-0.414, P < 0.05). A positive correlation was found between the serum levels of IL-18 and IFN-gamma (r=0.416, P < 0.05).

CONCLUSIONSSerum and stool levels of IL-18 and IFN-gamma were increased and associated with the severity in children with rotavirus enteritis. IL-18 and IFN-gamma might have protective effects against acute rotavirus infection at the early stage.

Child, Preschool ; Enteritis ; immunology ; Feces ; chemistry ; Female ; Humans ; Infant ; Interferon-gamma ; blood ; physiology ; Interleukin-18 ; blood ; physiology ; Male ; Rotavirus Infections ; immunology

OBJECTIVETo investigate the effect of chemically synthetic small interfering RNA (siRNA) targeting connective tissue growth factor (CTGF) on the synthesis and secretion of extracellular matrix (ECM) in hepatic stellate cells (HSC).

METHODSChemically synthetic siRNA targeting CTGF was transfected into HSC T6 (an active HSC line in rats) by oligofectamine package, and untreated HSC T6 were used as control. Total RNA and protein of the cells, after their incubation with siRNA for 24, 48 and 72 hours, were extracted, and the supernatants were collected. The expressions of CTGF and type I and III collagen genes were detected by means of reverse transcription-polymerase chain reaction (RT-PCR) and/or Western blot. Contents of hyaluronic acid and type III pro-collagen in the supernatants were determined by radioimmunoassay.

RESULTSThe expression of CTGF at mRNA and protein level and type I and III collagen at mRNA levels were markedly down-regulated in siRNA-transfected HSCs. The contents of hyaluronic acid and type III pro-collagen in the supernatants decreased by 46%+/-7%, 52%+/-7%, 53%+/-7% and 29%+/-18%, 29%+/-7%, 27%+/-5%, compared with those of the blank control at 24, 48 and 72 hours.

CONCLUSIONSChemically synthetic anti-CTGF siRNA can significantly inhibit CTGF gene expression in HSC, and markedly reduce the synthesis and secretion of ECM including type I and III collagen and hyaluronic acid. The siRNA-directed suppression of CTGF gene in HSC was maintained for 72 hours. This suggests that chemically synthetic siRNA may be a potential in preventing and treating liver fibrosis and may have a promising future for development

Cell Line ; Connective Tissue Growth Factor ; Extracellular Matrix ; metabolism ; Gene Targeting ; Humans ; Immediate-Early Proteins ; genetics ; Intercellular Signaling Peptides and Proteins ; genetics ; Liver ; cytology ; metabolism ; RNA, Small Interfering ; genetics