Objective:To explore the clinical characteristics of various types of severe drug eruption and common sensitized drugs,and to provide clinical references for reducing the incidence of severe drug eruption.Methods:The clinical data regarding 126 cases of severe drug eruption were analyzed retrospectively from June 2009 to May 2017 in Xiangya Hospital,Central South University.Results:In the 126 cases of severe drug eruption,the distribution of men and women ratio was 1∶1.38.The length of stay was (12.7±9.8) d.The most common type was Steven-Johnson syndrome;the most dangerous type was drug-induced bullosa epidermolysis,The most common sensitized drug category in these patients was antibiotics;the most common single sensitizing drug was carbamazepine,following by allopurinol.Conclusion:Severe drug eruption occurs mostly in young and middle-aged people.Steven-Johnson syndrome is the most common type;drug hypersensitive syndrome has the longest length of hospital course.Mortality rate of drug-induced bullosa epidermolysis is the highest.Timely stop using of allergens,early using glucocorticoids,and timely combination of non-glucocorticoids treatment (such as intravenous immunogloblin,plasma exchange and hemodialysis),can improve the efficacy and reduce the complications and mortality.

ObjectiveTo study the impact of EZH2 silence on the sensitivity of human hepatic multidrug-resistant cancer cells Bel/Fu to 5-Fu.MethodsBel/Fu cells were cultured in vitro; EZH2 siRNA was used to interfere EZH2 expression; RT-PCR and Western blot was used to detect the efficiency of interference.MTT assay was used to detect the cellular growth inhibitory rate; Annexin V-FITC/PI double staining was used to detect the apoptosis rate of cells ; Flow cytometry was to analyze cell cycle ; Western blot analysis was used to detect the expression of multidrug resistance-associated protein MDR1 after silencing EZH2.The experiment set up four groups:control group,5-Fu treatment group,EZH2 siRNA treatment group,5-Fu combined with EZH2 siRNA treatment group. ResultsThe expression of EZH2 was greatly decreased after 24 h in the combined group,the apoptotic inhibitory rate by MTT was 43.17％ ± 3.81％,higher than other three groups; the apoptotic rate in the combined group by Flow cytometry was 30.4％ ± 1.77％,markedly higher than other three groups.The cell cycle of the combined group detected by Flow cytometry was 69.16％ ±2.31％ of cells in the combined group at G1 phase,the percentage was higher than other three group,30.76％ ± 1.29％ at S,G2 and M phases,lower than other three groups,indicating the cell cycle was blocked at G1 phase.MDR1 protein level in the combined group was lower than other groups.ConclusionsSilencing EZH2 strengths the sensitivity of Bel/Fu cells to 5-Fu,probably by a mechanism decreasing the expression of MDR1.

Objective To evaluate the effect of the pulmonary stretch reflex on the lung injury in acute respiratory distress syndrome (ARDS). Method ARDS models of rabbits were induced by intratracheal infusion hydrochloric acid and ventilated with neurally adjusted ventilatory assist (NAVA) with a tidal volume ( VT) of 6 mL/kg and the electrical activity of diaphragm ( Eadi)-determined PEEP level. The rabbits were randomly ( random number) divided into two groups: ( 1 ) sham operation (Sham) group ( n = 5 ),(2) bilateral vagotom (VAG) group( n = 5 ). Gas exchange and pulmonary mechanics were determined at baseline, after lung injury and ventilation 1, 2, 3 h respectively. Indices about pulmonary permeability,pathological changes and inflammatory response were also measured. Results Compared with Sham group,the PaO2/FiO2in VAG group decreased significantly at ventilation 2 h, 3 h (P ＜0.05). There was no significant difference on PaCO2 between Sham and VAG group (P ＞ 0.05 ), and VAG group had the higher VT,peak pressure ( Ppeak), mean pressure (Pm) compared with Sham group at the time point of ventilation 1 h, 2 h, 3 h (P＜0.05). Compared with Sham group, the dead space fraction (VD/VT) and the respiratory system elastance (Ers) in VAG group increased (P ＜ 0.05 ) and the static pulmonary compliance (Cst)decreased markedly (P ＜ 0.05 ) after 3 h ventilation. The wet/dry weight (W/D), lung injury score, tumor necrosis factor-α ( TNF-α), interleukin-8 ( IL-8 ), myeloperoxidase ( M PO ) and malondialdehyde ( M DA )in VAG group elevated significantly when compared with Sham group ( P ＜ 0.05 ). Conclusions The lung injury in ARDS was aggravated after bilateral vagotomy, which demonstrated that the pulmonary stretch reflex may have the lung protective effect.

Objective To study the inhibitory effects of δ-opioid receptor activation in serumdeprivation induced apoptosis of human liver cells and the proposed protein kinase C(PKC)pathway mechanism.Methods MTT assay was used to detect the survival rate of human liver cells in vitro and Annexin V-FITC/PI double staining was used to detect the cell apoptosis rate.Flow cytometry was used to analyze cell cycle,RT PCR used to analyze the PKC mRNA and Western Blot analysis was used for detecting the protein expression of PKC and Caspase-3.Results After serum-deprivation for 48h of cultured human liver cells in vitro,significant liver cell apoptosis occurred.The apoptosis was suppressed by δ-opioid receptor activation,which manifested as a slower rate of apoptosis,decreased expression of Caspase-3and increased expression of PKC.After GF109203X was added,the inhibitory effects of DADLE decreased markedly.Conclusion Activation of δ-opioid receptor on the membrane of human liver cells has inhibitory effects on serum-deprivation induced apoptosis of liver cells.The underlying mechanism may be associated with PKC pathway activation.

Human tissue kallikrein-binding protein (Kallistatin, KAL), a secretory protein that participates in the regulation of multiple signaling pathways by binding to the extracellular receptor, however, at present has not been reported about the intracellular activity, and whether it has the similar biological activity with extracellular activity. Here we constructed no signal peptide KAL (NSK) into the adeno-associated virus vector to explore the intracellular activity of KAL. Both the endothelial cell and lung cancer cells could express KAL, but not secreted after rAAV2-NSK transfection. The proliferation and migration of human umbilical vein endothelial cells (HUVECs) were inhibited, but the apoptosis rate was not affected. The proliferation rates, mobility and tubule formation of all the three tested lung cancer cells, such as NCI-H446, NCI-H460 and A549, were inhibited to different extents. This cellular study not only confirmed the intracellular activity, but also suggested it may serve as a kind of "balance factor" in multi-targeted controlling, which may provide a new train of thoughts to explain the regulatory contradiction in PI3K-Akt signaling pathways by KAL.
Apoptosis ; Cell Proliferation ; Dependovirus ; Genetic Vectors ; Human Umbilical Vein Endothelial Cells ; metabolism ; Humans ; Lung Neoplasms ; metabolism ; Serpins ; metabolism ; Signal Transduction ; Transfection

Abstract: Schistosomiasis, an important zoonotic parasitic disease, is one of the six major tropical diseases identified by WHO, and also one of the most important parasitic diseases for prevention and control in China. After more than 70 years of efforts, the prevention and control of schistosomiasis in China has made great achievements, and the current epidemic of schistosomiasis in China has entered an extremely low epidemic state, but the distribution base of the only intermediate host of schistosomiasis, Oncomelania hupensis, is still large. For now, the techniques used to monitor schistosomiasis have shortcomings such as time-consuming, laborious and low sensitivity, which cannot meet the current needs of China. Environmental DNA (eDNA) refers to DNA that can be extracted from environmental samples (such as soil, water or air) without isolating any target organisms, which is a complex mixture of genomic DNA and its degradation products from different organisms in the same environment. eDNA technology can reflect the community or species composition information in the ecosystem through DNA extraction and detection of environmental samples. Compared with traditional biological monitoring methods, eDNA technology has the advantages of high efficiency, high sensitivity and environmental friendliness. eDNA has been successfully used for the specific detection of Schistosoma mansoni, Schistosoma haematobium and Schistosoma japonicum. This paper reviews the current detection methods of eDNA, the application and technical limitations of eDNA technology in schistosomiasis monitoring, aiming to provide scientific reference for research in the field of schistosomiasis surveillance.

Antioxidants ; pharmacology ; Ascorbic Acid ; pharmacology ; Carbon Disulfide ; adverse effects ; antagonists & inhibitors ; Cells, Cultured ; Endothelium, Vascular ; drug effects ; Humans ; Umbilical Veins ; cytology ; drug effects ; metabolism

PURPOSE: The purpose of this study was to observe the effects of metformin on human esophageal cancer cell and to investigate its possible mechanisms. MATERIALS AND METHODS: Cell viability was detected by using a Cell Counting Kit-8, while cell cycle and apoptosis were assessed by flow cytometry and western blot was used to measure the expression of the related proteins. RNAi was used to knockout pyruvate kinase muscle isozyme 2 (PKM2). An Eca109 tumor model was established to evaluate the antitumor effect in vivo. Immunohistochemistry was determined based on the expression of PKM2 and Bim in tumor tissues. Tunnel was used to assess tumor cell apoptosis. RESULTS: Esophageal cancer cells viability was reduced after metformin treatment. The cell cycle was arrested in the G0/G1 phase, apoptosis was induced, caspase 3 was activated, caspase 9 was downregulated, and the pro-apoptotic protein Bim increased. Further study revealed that metformin could suppress the expression of insulin-like growth factor 1 receptor and its downstream proteins, phosphoinositide 3-kinase (PI3K), protein kinase B (AKT/PKB), phosphorylation of AKT (pAKT), mammalian target of rapamycin (mTOR), p70S6K, and PKM2. Insulin-like growth factor 1 partly reversed metfromin-induced apoptosis and attenuated the repression effect of metfomin to PI3K, pAKT, and PKM2. Knockout PKM2 resulted in the activation of caspase 3, down-regulation of caspase 9, and increased expression of Bim. In the Eca109 xenograft model, metformin significantly reduced tumor growth. Furthermore, we found that metformin treatment increased the rate of apoptosis, down-regulation of PKM2, and up-regulation of Bim in tumor tissues. CONCLUSION: Metformin restrained esophageal cancer cell proliferation partly by suppressing the PI3K/AKT/mTOR pathway.
Apoptosis ; Blotting, Western ; Caspase 3 ; Caspase 9 ; Cell Count ; Cell Cycle ; Cell Proliferation ; Cell Survival ; Down-Regulation ; Esophageal Neoplasms* ; Flow Cytometry ; Heterografts ; Humans ; Immunohistochemistry ; In Vitro Techniques* ; Metformin* ; Phosphorylation ; Proto-Oncogene Proteins c-akt ; Pyruvate Kinase ; Repression, Psychology ; Ribosomal Protein S6 Kinases, 70-kDa ; RNA Interference ; Sirolimus ; Up-Regulation

PURPOSE: The purpose of this study was to observe the effects of metformin on human esophageal cancer cell and to investigate its possible mechanisms. MATERIALS AND METHODS: Cell viability was detected by using a Cell Counting Kit-8, while cell cycle and apoptosis were assessed by flow cytometry and western blot was used to measure the expression of the related proteins. RNAi was used to knockout pyruvate kinase muscle isozyme 2 (PKM2). An Eca109 tumor model was established to evaluate the antitumor effect in vivo. Immunohistochemistry was determined based on the expression of PKM2 and Bim in tumor tissues. Tunnel was used to assess tumor cell apoptosis. RESULTS: Esophageal cancer cells viability was reduced after metformin treatment. The cell cycle was arrested in the G0/G1 phase, apoptosis was induced, caspase 3 was activated, caspase 9 was downregulated, and the pro-apoptotic protein Bim increased. Further study revealed that metformin could suppress the expression of insulin-like growth factor 1 receptor and its downstream proteins, phosphoinositide 3-kinase (PI3K), protein kinase B (AKT/PKB), phosphorylation of AKT (pAKT), mammalian target of rapamycin (mTOR), p70S6K, and PKM2. Insulin-like growth factor 1 partly reversed metfromin-induced apoptosis and attenuated the repression effect of metfomin to PI3K, pAKT, and PKM2. Knockout PKM2 resulted in the activation of caspase 3, down-regulation of caspase 9, and increased expression of Bim. In the Eca109 xenograft model, metformin significantly reduced tumor growth. Furthermore, we found that metformin treatment increased the rate of apoptosis, down-regulation of PKM2, and up-regulation of Bim in tumor tissues. CONCLUSION: Metformin restrained esophageal cancer cell proliferation partly by suppressing the PI3K/AKT/mTOR pathway.
Apoptosis ; Blotting, Western ; Caspase 3 ; Caspase 9 ; Cell Count ; Cell Cycle ; Cell Proliferation ; Cell Survival ; Down-Regulation ; Esophageal Neoplasms* ; Flow Cytometry ; Heterografts ; Humans ; Immunohistochemistry ; In Vitro Techniques* ; Metformin* ; Phosphorylation ; Proto-Oncogene Proteins c-akt ; Pyruvate Kinase ; Repression, Psychology ; Ribosomal Protein S6 Kinases, 70-kDa ; RNA Interference ; Sirolimus ; Up-Regulation

A new and a known anthraquinone glycosides were isolated from the ethanol extract of the roots of Rheum officinale Baill. The extract was purified by various chromatographies, such as silica gel, Sephadex LH-20, RP-C18 column chromatography and HPLC. Two compounds were identified by the spectroscopic techniques of NMR, MS, and chemical method. In addition, they were tested for their cytotoxic effects against HepG2 cell. Unfortunately, they showed no or weak activity.
Anthraquinones ; chemistry ; isolation & purification ; pharmacology ; Glycosides ; chemistry ; isolation & purification ; pharmacology ; Hep G2 Cells ; Humans ; Molecular Structure ; Plant Roots ; chemistry ; Plants, Medicinal ; chemistry ; Rheum ; chemistry