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Colorectal cancer （CRC） is a malignant tumor of the intestinal tract with changes in bowel habits， blood in the stool， and pain as the main clinical manifestations. With the change in lifestyle and diet structure in recent years， the incidence of CRC has been increasing year by year. The pathogenesis of CRC is closely related to abnormal immune response and chronic inflammation， intestinal microbial dysbiosis， and the production of oncogenic metabolites. There is a two-way communication between the intestinal microbiota and the body's immunity， which not only plays a key role in maintaining the body's health but also has a close relationship with the development of diseases. An increasing number of studies have shown that abnormal immune responses accelerate the disease process by producing inflammatory factors， causing chronic inflammation in the body， disrupting the intestinal mucosal barrier， and increasing mucosal permeability， thus resulting in dysbiosis of the intestinal microbial ecology and a large number of pathogenic microorganisms and their metabolites. In addition， dysbiosis of intestinal microbes， by suppressing the normal immune response， leads to the disruption of multiple metabolic pathways in the body， affecting the internal and external stress response of the intestine， inducing inflammation， and thus producing disease. Therefore， the complex crosstalk mechanism between the immune response and intestinal microbial axis is closely related to the development of CRC. Based on traditional Chinese medicine theory and clinical research， it was found that dietary factors are an important causative factor in the development of CRC. The deficiency of positive energy is the root cause of the disease， and damp-heat accumulation is the key pathogenesis. Through modern medical and biological research， it is believed that abnormal immune response is the microscopic manifestation of damp-heat entrapment， while intestinal microbial dysbiosis is the biological basis of toxic injection into the large intestine， and in the pathogenesis of CRC， the imbalance of immune response-intestinal microbial axis is compatible with damp-heat accumulation in traditional Chinese medicine. This study aims to explore the biological connotation of CRC due to damp-heat accumulation from the immune response-intestinal microbial axis， so as to interpret the pathogenesis of CRC due to damp-heat accumulation with objective data and provide new ideas and theoretical basis for the pathogenesis and treatment strategies of CRC due to damp-heat accumulation.
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Objective:To clarify the distribution and composition of drug-resistant genes of carbapenem-resistant Klebsiella pneumoniae (CRKP) in Qingdao City and to provide rationale for clinical application of antibacterial treatment by screening for carbapenemase phenotype and detecting resistance genes of CRKP. Methods:Fifty-four clinically isolated non-repeating CRKP from five Third Grade & Class A Hospitals in Qingdao City from October 2016 to September 2019 were collected. Kirby-Bauer method was used for drug sensitivity tests of commonly used antibacterial drugs; modified Hodge test was used for carbapenemase phenotypic screening; and polymerase chain reaction (PCR) was used to amplify blaKPC-2, blaNDM-1, blaOXA-48, blaIMP, blaVIM target genes. The amplified products were subjected to agarose gel electrophoresis. Results:Drug susceptibility tests showed that CRKP had the lowest resistance rate to amikacin (35.2%), followed by compound sinomine (53.7%), gentamicin (55.6%), levofloxacin (75.9%), and imipenem-cilastatin (88.9%); piperacillin-tazobactam, meropenem, cefotaxime, and cefoperazone-sulbactam were all higher than 90%. There were 43 positive strains in the modified Hodge test (the positive rate was 79.63%) and 11 negative strains. A total of 40 strains with carbapenemase resistance were detected by PCR resistance gene detection. The detection rate of target drug-resistant genes was 74.07%. Among them, 35 strains carry the KPC-2 gene, 7 strains carry the OXA-48 gene, 4 strains carry the NDM-1 gene, and 1 strain carries the IMP gene. All strains carrying the OXA-48 gene also carried the KPC-2 gene, which was not detected. Strains carrying the VIM gene were identified, and the remaining 14 strains did not detect the target carbapenem gene.Conclusion:The carbapenem-producing genes carried by CRKP in five hospitals in Qingdao City are mainly KPC-2, followed by OXA-48 and NDM-1.
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OBJECTIVE To explore the sterilizing effect of low-temperature vacuum formaldehyde.METHODS The test group used the own-produced 140 L low-temperature vacuum formaldehyde sterilizer for sterilization;and the control group used "Xinhua" hydrogen peroxide plasma sterilizer.Sterilization effect of the two groups was monitored by biological indicator.RESULTS After 50 sterilization procedures run in test group,the biological indicators the bacterial were all killed,the qualification rate of sterilization was 100%.But after 30 sterilization procedures run in control group,only 8 procedures were qualified,the qualification rate of sterilization was 26%.The sterilizing effect of the two groups was significantly different(P
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BACKGROUND: Endothelin(ET) -1 is a peptide with potent actions on blood vessels and nerve system. Its expression increases in the central nervous system(CNS) in a variety of pathological conditions, inducing harmful effects on the nervous tissue. However it is not clearly elucidated whether the over-expressed ET-1 can directly induce neuronal apoptosis.OBJECTIVE: To investigate whether ET-1 can directly induce apoptosis in primarily cultured brain neurons of rat, and which ET receptor subtype(s) is involved in this action.DESIGN: Completely randomized and controlled experimental study based on cells.SETTING: Neurological department in a university hospital, pathological department of a university and laboratory center of tissue transplantation and immunology, life science and technology college.MATERIALS: This study was completed in the Pathology Department, the Institute of Tissue Transplantation and Immunology, the Life Science and Technology College of Jinan University. The subjects were primarily-cultured neurons obtained from cerebral cortex of newborn rats that were provided by the Experimental Animal Center of the Medical College, Sun Yat-sen University.INTERVENTIONS: After culturing for five days, the neurons were treated with ET-1 (0. 2 nmol/L and 20 nmol/L) for 24 hours. Apoptotic neurons were semi-quantitatively measured with Annexin V and Hoechst 33258 staining respectively. ET-1(20 nmol/L), with BQ123(a selective antagonist for ET receptor A, 1 mmol/L) or with BQ788(a selective antagonist for ET receptor B, 1 mmol/L), was added respectively into the cultures simultaneously. And the apoptotic neurons were quantitatively measured with flow cytometry 24 hours later. Equal amount of PBS, instead of ET-1, waw added into the control subjects.MAIN OUTCOME MEASURES: The effect of ET-1 on apoptosis rate of cultured rat cortical neurons, and the ET receptor subtypes involved in this action.RESULTS: Twenty-four hours after treated with 0.2 nmol/L ET-1, the Annexin-V, and Hoechest 33258 positive stained cell rates[ (23.00 ± 9.96)%,(9.82 ±0.95)% ] were of no difference as compared with those of the controls[ (13.50 ± 3.35)%, (8.21 ± 2. 17)% ]. By contrast, after incubation with the higher dose of ET-1 (20 nmol/L), significant higher rate of apoptosis was measured in Annexin V staining[(50.50 ± 10.78)%, P=0.01, n=4] and Hoechest 33258 staining[(13.78±1.52)%, P= 0. 000, n = 8] . Analyzed with flow cytometry, the apoptosis rate was (0.20±0. 15)% in the control group, (26. 11 ±3.28)% in 20 nmol/LET-1 group, and(13.58 ±4. 92)% in BQ123 +ET-1 and(9.99 ±3.30)% in BQ788 +ET-1 respectively, indicating that BQ123 and BQ788 partially-blocked the apoptosis effect of ET-1 on. cultured neurons(BQ123 + ET-1 vs ET-1, P = 0. 005; BQ788 + ET-1 vs ET-1, P = 0. 001, n = 4, respectively).CONCLUSION: The higher dose of ET-1 (20 nmol/L) can directly induce apoptosis of primarily-cultured cerebral neurons of rats. The effect of ET-1 inducing neuronal apoptosis may be mediated via both ET receptors A and B.