Breast Neoplasms ; genetics ; Disease Susceptibility ; Female ; Genes, BRCA1 ; Genes, BRCA2 ; Humans ; Mutation ; Ovarian Neoplasms ; genetics

Objective To compare the accuracy of spectrophotometer under different color measurement conditions, so as to provide evidence for clinical color measurement. Methods Spectrophotometer was used to obtain the chromatic value L*, a* and b*(L*:Lightness; a*:Saturation on the red and green axile; b*:Saturation on the yellow and blue axile) of all color pieces in the medium 1/3 of vita classical shade guide under the natural light, incandescent lamp and dark room; the values of chromatism were calculated under different color measurement conditions, and the results were fed to statistical software for analysis. Results The L*, a* and b* values were not significantly different under natural light, incandescent lamp and dark room. The composition ratios of ΔE <1.5 NBS for the natural light and incandescent light, natural light and dark room, incandescent lamp and dark room were 87.50%, 100%, and 93.75%, respectively. Conclusion The measurement accuracy of CM-700d spectrophotometer is high and the environment light has slight effe0ct on the accuracy. The chromatism values of shade guide measured in the dark room is the most true ones, so dark room is recommended for CM-700d spectrophotomete.

OBJECTIVETo explore the molecular mechanism of exocrine immune inflammatory injury of Sjögren's Syndrome and the intervention of Banxia Qinlian Decoction (BQD).

METHODSTotally 18 female NOD mice were randomly divided into the model group, the positive drug group, and the BQD group, 6 in each group. Six female BALB/c mice were recruited as a blank control group. Mice in the blank control group and the model group were gavaged with deionized water at the daily dose of 0.1 mL/10 g body weight. Tripterygium Tablet was administered by gastrogavage to mice in the positive group at the daily dose of 10 mg/kg. BQD was administered by gastrogavage to mice in the BQD group at the daily dose of 60 g crude drugs/kg. After 12 weeks of medication, mice were sacrificed. Their eyeballs were excised and blood collected. Tissues of bilateral parotids and submandibular glands were kept. mRNA transcriptional levels of IL-17, IL-6, type 3 muscarinic acetylcholine receptors (M3R), aquaporin protein-5 (AQP5) were detected by RT-PCR. Expression levels of M3R and AQP5 protein were detected by Western blot. Protein expression levels of IL-17 and IL-6 were detected by ELISA.

RESULTSCompared with the normal group, mRNA transcriptional levels and protein expression levels of IL-17, IL-6, M3R, and AQP5 were significantly up-regulated in the model group (P < 0.01). Compared with the model group, mRNA transcriptional levels and protein expression levels of IL-17, IL-6, M3R, and AQP5 were significantly down-regulated in the positive drug group and the BQD group with statistical difference (P < 0.01, P < 0.05). Compared with the BQD group, mRNA-transcriptional levels of IL-17, IL-6, and M3R, as well as M3R and AQP5 protein expression levels were significantly down-regulated in the positive drug group (all P < 0.01).

CONCLUSIONThe molecular mechanism of BQD in inhibiting SS exocrine neurotoxic injury might be possibly related to regulating Th17/IL-17 immune inflammatory way.

Animals ; Aquaporin 5 ; metabolism ; Disease Models, Animal ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Female ; Interleukin-17 ; metabolism ; Interleukin-6 ; metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred NOD ; Sjogren's Syndrome ; drug therapy ; immunology ; Submandibular Gland ; Th17 Cells ; Up-Regulation

Objective To investigate the clinical significance of intraportal vein anticoagulation for the prevention of portal vein thrombosis after portaazygous devascularization and splenorenal shunt. Methods In this study 67 patients of portal hypertension undergoing surgery were randomly divided into two groups,receiving respectively intraportal vein heparin injection by 100 U?kg~(-1)?d~(-1)?7 d in group A (32 patients)and placebo in group B(35 patients).Portal vein thrombosis,the recurrent bleeding after operation and portal hypertensive gastropathy were compared between the two groups.Results The occurrence of portal vein thrombosis after operation in group A(0)was significantly lower than that in group B(20%,X~2=5.169,P

Objective To understand the occurrence of surgical site infection(SSI)following caesarean section,analyze risk factors,implement intervention measures,and evaluate intervention efficacy. Methods All puerperas who underwent caesarean section in the obstetric department of a hospital from January to December 2013 were mo-nitored,investigation were performed in two stages:evaluation stage(January-June,2013)and intervention stage (July-December,2013). Targeted intervention and clinical intervention were combined to intervene the risk factors. Occurrence of SSI,length of hospital stay,and hospitalization expense before and after intervention were compared. Results A total of 1 593 patients with caesarean section were monitored,31(1.95%)had SSI,incidence of SSI in evaluation stage and intervention stage were 3.40% and 0.95% respectively;incidence of SSI before and after inter-vention was significantly different(χ2= 12.02,P<0.01). Univariate analysis on evaluation stage showed that risk factors for SSI in patients with caesarean section were duration of operation≥1 hour,body mass index≥26 kg/m2,intraoperative blood loss ≥300 mL,underlying diseases,premature rupture of membranes,and without antimicro-bial prophylaxis(all P<0.05). In evaluation stage,648 patients received post-operative antimicrobial prophylaxis for>48 hours(n= 395,60.96%);in intervention stage,945 patients received post-operative antimicrobial prophy-laxis for<24 hours(n= 776,82.12%),different time distribution of post-operative antimicrobial prophylaxis in two stages after intervention was compared,difference was statistically significant(χ2= 673.26,P<0.01). The mean length of hospital stay of 31 SSI patients were(13.83±3.26)days,non-SSI patients were(7.06±1.66) days,difference was statistically significant(t= 7.86,P<0.01);the average hospitalization expenses for patients with SSI were(9 044.77±2 649.19)yuan,non-SSI patients were(6 254.73±638.52)yuan,difference was statis-tically significant(t= 4.344,P<0.01).Conclusion Intervention measures for risk factors of SSI after caesarean section can effectively reduce the incidence of SSI in caesarean section.

Humans ; Immunoglobulin D ; Multiple Myeloma ; Rupture, Spontaneous ; Spleen

OBJECTIVETo investigate the molecular mechanism of adiponectin inhibiting activation of hepatic stellate cells in non-alcoholic fatty liver fibrosis.

METHODSThe rat models of non-alcoholic fatty liver fibrosis were successfully established by fat-rich diet administration. The expression of adiponectin mRNA and protein were respectively detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. LX-2 cells were cultured in an adipogenic differentiation mixture to induce quiescent adipocytic phenotypes, and then they were treated with TGFβ1, adiponectin and TGFβ1 + adiponectin, respectively. RT-PCR and Western blot were used to determine the expressions of mRNAs and proteins of a-smooth muscle actin (a-SMA), Collagen, adenosine monophosphate-activated protein kinase (AMPK), inducible nitric oxide synthase (iNOS), and endothelial NOS (eNOS). The results were analyzed using one-way ANOVA, Student-Newman-Keuls test, and linear correlation analysis. A P value of less than 0.05 was considered as statistically significant.

RESULTSIn vivo, with the progress of non-alcoholic fatty liver fibrosis, the model rats gradually showed hepatic steatosis, inflammation, necrosis and fibrosis. Compared with the control group, the level of serum adiponectin (2.49 ± 0.86 vs 5.81 ± 0.87, P < 0.05) and hepatic expressions of adiponectin mRNA and protein (0.26 ± 0.04 vs 0.72 ± 0.08; 0.64 ± 0.07 vs 0.21 ± 0.07, all P < 0.05) were all decreased in the 24th week group, and were negatively correlated with the level of Collagen which increased gradually. In vitro, TGFβ1 could activate quiescent LX-2 cells by decreasing mRNA and protein expression of eNOS (0.30 ± 0.10 vs 0.44 ± 0.08; 0.30 ± 0.09 vs 0.46 ± 0.07, all P < 0.05) and increasing the expression of iNOS (0.53 ± 0.07 vs 0.37 ± 0.04; 0.55 ± 0.07 vs 0.39 ± 0.05, all P < 0.05). Recombinant adiponectin not only maintained the quiescent phenotype of LX-2 cells but also inhibited LX-2 cells activation due to TGFβ1 by increasing the expression of eNOS (0.43 ± 0.08 vs 0.30 ± 0.10; 0.42 ± 0.07 vs 0.30 ± 0.09, all P < 0.05) and phosphorylation of AMPK (0.43 ± 0.07 vs 0.24 ± 0.04, P < 0.05) and decreasing the expression of iNOS (0.44 ± 0.05 vs 0.53 ± 0.07; 0.46 ± 0.07 vs 0.55 ± 0.07, all P < 0.05).

CONCLUSIONSData suggested that adiponectin could play a protective role on the pathogenesis of non-alcoholic fatty liver fibrosis by inhibiting the activation of hepatic stellate cells via up-regulating the expression of eNOS, which might associate with increased phosphorylation of AMPK.

Adiponectin ; metabolism ; pharmacology ; Animals ; Disease Models, Animal ; Fatty Liver ; metabolism ; Hepatic Stellate Cells ; metabolism ; Liver Cirrhosis ; metabolism ; pathology ; Nitric Oxide Synthase Type III ; metabolism ; Non-alcoholic Fatty Liver Disease ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction ; Transforming Growth Factor beta1 ; metabolism ; pharmacology

This study was aimed to investigate the expression and activity of membrane surface tissue factor (TF) of monocytes and platelets in peripheral blood cells from patients with cerebral infarction and their clinical significance. The TF expressions in monocytes and platelets from 25 patients with cerebral infarction were detected by flow cytometry, the TF activity was detected by chromogenic reaction method, and compared with 24 normal people used as control. The results showed that the TF expressions of monocytes and platelets in peripheral blood cells from patients with cerebral infarction were significantly higher than that in normal controls (p<0.01), and TF activity was also higher in patients than that in controls (p<0.01). In conclusion, the expression and activity of membrane surface in patients with cerebral infarction were enhanced, the hematocyte-derived tissue factor as a trigger in coagulation pathway is involved in pathological thrombosis in patients with cerebral infarction.
Aged ; Blood Cells ; metabolism ; Case-Control Studies ; Cerebral Infarction ; blood ; metabolism ; Erythrocyte Membrane ; metabolism ; Female ; Flow Cytometry ; Humans ; Male ; Middle Aged ; Monocytes ; metabolism ; Thromboplastin ; metabolism

OBJECTIVE: To study the occurrence of serious adverse events (SAEs) related to chemotherapy with CCCG-ALL-2015 regimen in children with acute lymphoblastic leukemia (ALL) and the risk factors for death after the SAEs. METHODS: A retrospective analysis was performed on the medical data of 734 children with ALL. They were treated with CCCG-ALL-2015 regimen from January 2015 to June 2019. The occurrence of SAEs during the treatment was investigated. The children with SAEs were divided into a death group with 25 children and a survival group with 31 children. A multivariate logistic regression analysis was used to analyze the risk factors for death after the SAEs. RESULTS: Among the 734 children with ALL, 56 (7.6%) experienced SAEs (66 cases) after chemotherapy, among which 41 cases occurred in the stage of remission induction therapy. Of all 66 cases of SAEs, 46 (70%) were infection-related SAEs, including 25 cases of septic shock (38%), 20 cases of severe pneumonia (30%), and 1 case of severe chickenpox (2%), and 87% of the children with infection-related SAEs had neutrophil deficiency. The most common infection sites were blood and the lungs. The most common pathogens were Gram-negative bacteria, viruses, fungi, and Gram-positive bacteria. There were 16 cases (24%) of hemorrhage-related SAEs, with 11 cases of gastrointestinal bleeding (17%), 4 cases of pulmonary bleeding (6%), and 1 case of intracranial bleeding (2%). Of all 734 children with ALL, 66 (9.0%) died, among whom 25 died due to SAEs. The treatment-related mortality rate was 3.4%, and infection (72%) and bleeding (24%) were the main causes of death. Severe pneumonia was an independent risk factor for treatment-related death in ALL children (OR=4.087, 95%CI: 1.161-14.384, P=0.028). CONCLUSIONS SAEs often occur in the stage of remission induction therapy, and infection-related SAEs are more common in ALL children accepting chemotherapy with CCCG-ALL-2015 regimen. The development of severe pneumonia suggests an increased risk for death in these children.
Antineoplastic Agents ; adverse effects ; Child ; Gram-Negative Bacteria ; Humans ; Neutrophils ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; drug therapy ; Retrospective Studies ; Risk Factors