ABSTRACT
Perfluoroalkyl and polyfluoroalkyl substances (PFASs), as a group of persistent organic pollutants among environmental endocrine disruptors, are widely used in industrial production and daily life. PFASs are widely and persistently present in the environment and organisms due to their bioaccumulation, long half-life, and low degradability properties. Published studies have proved that PFASs have immunotoxicity, endocrine toxicity, neurotoxicity, reproductive toxicity, and hepatotoxicity. At present, several epidemiological studies have been conducted on the effects of PFASs on allergic diseases, the research endpoints include asthma, allergic rhinitis, atopic dermatitis, and the expression of allergic biomarkers such as serum immunoglobulin E (IgE), but no consistent results have been observed yet. PFASs have the potential to activate several signaling pathways, including the peroxisome proliferator-activated receptor (PPAR), nuclear factor-κB (NF-κB), and JAK/STAT pathways. These mechanisms, along with increasing mast cell calcium influx and sex hormone synergistic effects, may contribute to immunomodulation in allergic diseases. At present, the exact human effect of PFASs exposure on allergic diseases and the related mechanisms are still uncertain. This review focused on the impacts of PFASs on asthma, allergic rhinitis, and atopic dermatitis and their possible mechanisms, so as to provide research ideas for the prevention, diagnosis, and treatment of allergic diseases.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of 17-AAG combined with paclitaxel (PTX) on the proliferation and apoptosis of esophageal squamous cell carcinoma cell line Eca-109 in vitro.</p><p><b>METHODS</b>Eca-109 cells were treated with 17-AAG and PTX either alone or in combination. The proliferation of Eca-109 cells was detected by MTT assay, and the cell cycle changes and cell apoptosis were determined by flow cytometry.</p><p><b>RESULTS</b>Compared with the control group, both 17-AAG and PTX significantly inhibited the proliferation of Eca-109 cells. A combined treatment of the cells with 0.5 µmol/L PTX and 0.625 µmol/L 17-AAG produced an obviously stronger inhibitory effect on the cell proliferation than either of the agents used alone (P<0.01). Flow cytometry showed that, 17-AAG and PTX used alone caused Eca-109 cell cycle arrest in G2/M phase and S phase, respectively, and their combined use caused cell cycle arrest in both G2/M and S phases. The cell apoptosis rates of Eca-109 cells treated with 17-AAG, PTX and their combination were 4.52%, 10.91%, and 29.88%, respectively, all significantly higher than that in the control group (1.32%); the combined treatment resulted in a distinct apoptotic peak that was significantly higher than that caused by either of the agents alone.</p><p><b>CONCLUSION</b>17-AAG and PTX can inhibit cell proliferation and promote apoptosis of Eca-109 cells, and their combination produces stronger effects in inhibiting cell proliferation and increasing cell apoptosis.</p>
Subject(s)
Humans , Apoptosis , Benzoquinones , Pharmacology , Carcinoma, Squamous Cell , Pathology , Cell Cycle Checkpoints , Cell Line, Tumor , Cell Proliferation , Esophageal Neoplasms , Pathology , Lactams, Macrocyclic , Pharmacology , Paclitaxel , PharmacologyABSTRACT
Objective To explore the shielding effect that Tween has made on the erythrocyte’ s surface antigen( ABO and D antigen mainly) and the stability of the RBC. Methods Various types red blood cells’ surface antigens were incubated with different concentrations of Tween,then the titers of RBC’ s surface antigen before and after incubation were compared. The erythrocyte’ s function alterations and sta-bility through the morphological obersavation,the osmotic fragility,RBC’ s own hemolysis rate,oxygen saturation( SO2 ) ,routine test of blood as well as the supernatant of free hemoglobin determination were confirmed. Results The masking effect of the Tween-20 on D antigen with the weaken titer keeping above“ +” was better and more stable than that on A,B antigen. The impact on B antigen was a little worse,and A was the worst. The advantaged concentration is about 0. 004%. Besides,the influence of Tween-80’s on B and D antigen was not apparent e-nough. Among all of the concentration,0. 74% and 0. 80% did a relatively better job,which also could keep the weaken titer above “ +”. Conclulsion The shielding effect that Tween has made on the erythrocyte’ s surface antigen( ABO and D antigen mainly) is stable,which keeps above “ +”. The morphology and function of the RBC does not change.
ABSTRACT
Objective:This study aimed to compare the differences in molecular subtypes between Uygur and Han patients with breast cancer. This study was also conducted to provide clinical recommendations. Methods:The new typing standard of St. Gallen International Expert Consensus on the Primary Therapy of Early Breast Cancer 2011 was used to classify the molecular subtypes of 369 breast cancer cases from the First People's Hospital of Kashgar Prefecture, Xinjiang Uygur Autonomous Region, China. Four immunohistochemical markers (ER, PR, HER-2, and Ki-67) were used to divide the patients into four intrinsic subtypes:Luminal A;Luminal B (divided into HER-2 negative subtype and HER-2 positive subtype);HER-2 enriched;and triple negative breast cancer (TNBC) subtype. Statistical analysis was then conducted to evaluate the differences in molecular subtype characteristics of Uygur and Han patients with breast cancer. Results:The proportion of Luminal A, Luminal B with HER-2 negative subtype, Luminal B with HER-2 positive subtype, HER-2 enriched, and TNBC subtype were 12.67%(36/284), 34.51%(98/284), 20.07%(57/284), 14.79%(42/284), and 17.96%(51/284) for 284 Uygur patients with breast cancer;the corresponding proportions were 16.47%(14/85), 37.65%(32/85), 10.59%(9/85), 10.59%(9/85), and 24.71%(21/85) for 85 Han patients with breast cancer, respectively. The HER-2 positive rates of Uygur and Han patients with breast cancer were 34.86%(99/284) and 21.18%(18/85), respectively. The proportions of Luminal B with HER-2 positive subtype and HER-2 positive rate were significantly higher in Uygur patients than in Han patients (P=0.045 and P=0.030, respectively).Conclusion:A larger proportion of Luminal B with HER-2 positive subtype and a higher HER-2 positive rate were observed in Uygur patients with breast cancer than in Han patients with the same disease. HER-2-targeted therapy could be more effective for Uygur patients with breast cancer than for Han patients.
ABSTRACT
Objective:To investigate the incidence and distribution of malignant tumor in Uygur People and provide a theoretical basis for epidemiological surveys. Methods:A retrospective study was conducted from November 2007 to October 2012 on inpatients with malignant tumors at The First People′s Hospital of Kashgar Prefecture. The top 10 kinds of malignant tumor were found in Uygur People and Han People. Results:A total of 7578 patients were registered, including 6840 (about 90.26%) Uygur People, 628 (nearly 8.29%) Han People, and 110 (about 1.45%) from other minority groups. The top 10 kinds of malignant tumor for Uygur People were gastric cancer, esophageal cancer, leukemia, cervical cancer, malignant lymphoma, primary hepatic carcinoma, breast cancer, head and neck cancer, lung cancer, and colorectal cancers. Meanwhile, the order for Han People were lung cancer, colorectal cancer, breast, gastric, primary hepatic, head and neck, leukemia, cervical, esophageal cancer, and pancreatic cancer. Conclusion:A different epidemic character of malignant tumor existed between Uygur People and Han People in Kashga, Xinjiang.
ABSTRACT
This study investigated the effect of epigenetic modification of maspin on extravillous trophoblastic function. The mRNA expression of maspin in placentae from normotensive and preeclamptic pregnant women was detected by RT-PCR. TEV-1 cells, a human first-trimester extravillous trophoblast cell line, were cultured and treated with CoCl(2) (300 μmol/L) to induce chemical hypoxia and with 5-aza (500 nmol/L) to induce demethylation. The mRNA expression of maspin in TEV-1 cells subjected to different treatments was determined by RT-PCR, and the proliferative and migratory abilities of TEV-1 cells were assessed by cell counting kit-8 (CCK-8) and Transwell assays. Our results showed that the maspin mRNA expression level in placentae from preeclamptic women was much higher than that from normotensive women. CoCl(2) or 5-aza could up-regulate the mRNA expression of maspin and significantly suppress the proliferation and migration of TEV-1 cells. It was concluded that the epigenetic modification in promoter region of maspin contributes to incomplete trophoblast invasion, which offers a novel approach for predicting and treating placental dysfunction.
ABSTRACT
This study investigated the effect of epigenetic modification of maspin on extravillous trophoblastic function. The mRNA expression of maspin in placentae from normotensive and preeclamptic pregnant women was detected by RT-PCR. TEV-1 cells, a human first-trimester extravillous trophoblast cell line, were cultured and treated with CoCl(2) (300 μmol/L) to induce chemical hypoxia and with 5-aza (500 nmol/L) to induce demethylation. The mRNA expression of maspin in TEV-1 cells subjected to different treatments was determined by RT-PCR, and the proliferative and migratory abilities of TEV-1 cells were assessed by cell counting kit-8 (CCK-8) and Transwell assays. Our results showed that the maspin mRNA expression level in placentae from preeclamptic women was much higher than that from normotensive women. CoCl(2) or 5-aza could up-regulate the mRNA expression of maspin and significantly suppress the proliferation and migration of TEV-1 cells. It was concluded that the epigenetic modification in promoter region of maspin contributes to incomplete trophoblast invasion, which offers a novel approach for predicting and treating placental dysfunction.
Subject(s)
Adult , Female , Humans , Pregnancy , Chorionic Villi , Physiology , Epigenesis, Genetic , Genetics , Serpins , Genetics , Trophoblasts , PhysiologyABSTRACT
The mechanism of injury on the human glomerular endothelial cells (ciGENC) induced by preeclampsia serum was investigated. Concentration of maternal serum sFlt-1 protein was detected by ELISA. Fluorescently-labeled bovine serum albumin infiltrating through lower chamber of Transwell was measured by multifunction microplate reader. Morphologic change of ciGENC was observed under inverted phase contrast microscope. The concentration of sflt-1 in preeclampsia groups was significantly increased as compared with control group (P<0.01). Permeability in preeclampsia groups was significantly increased as compared with control group (P<0.01). By contrast with severe preeclampsia group, the permeability of ciGENC monolayer in mild preeclampsia group was decreased significantly (P<0.05). Intervention of exogenous VEGF significantly decreased permeability of ciGENC in preeclampsia groups. It was concluded that sFlt-1 increased ciGENC permeability by damaging integrity of endothelial barrier function.