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The coronavirus disease 2019 (COVID-19) pneumonia is a recent outbreak in mainland China and has rapidly spread to multiplecountries worldwide. Pulmonary parenchymal opacities are often observed during chest radiography. Currently, few caseshave reported the complications of severe COVID-19 pneumonia. We report a case where serial follow-up chest computedtomography revealed progression of pulmonary lesions into confluent bilateral consolidation with lower lung predominance,thereby confirming COVID-19 pneumonia. Furthermore, complications such as mediastinal emphysema, giant bulla, andpneumothorax were also observed during the course of the disease.
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Objective To explore the pathogenesis of ovarian cancer by investigating the function of Toll-like receptor 1 (TLR1),TLR2 and TLR6 in peripheral blood mononuclear cell(PBMC) from patients with ovarian cancer.Methods PBMC,SK OV 3 co culture system and anti-TLR1,anti-TLR2,anti-TLR6 mAb blocking experiment were used to explore the relationship between TLR1,TLR2 or TLR6 signaling and inflammation in ovarian cancer.Quantitative real time PCR was used to measure interleukin(IL)-1β,IL-6,IL-8,and tumor necrosises factor(TNF)-α in the PBMC.MyD88,TRAF6,TANK,NF-κB and P-NFκB were observed by Western blotting.Results In the PBMC and SK-OV-3 coculture system,we found the activation of TLR signaling pathways,including significantly increased MyD88,TRAF6,TANK and P-NF-κB levels following cocultured with SK-OV-3 in PBMC from ovarian cancer patients.PBMC derived from ovarian cancer patients led to a increase in IL-1β,IL-6 and IL-8 mRNA levels after 24 hours of co-incubation with SK-OV-3 (Fold=1.74,Fold=1.92,Fold=1.65,P＜0.05),though there was no difference of TNF-a mRNA expression.In contrast to the ovarian cancer patients,coculture of PBMC derived from benign diseases controls and healthy normal controls decreased IL-1β at the mRNA level (Fold=0.71,P＜0.05;Fold=0.72,P＜0.05),furthermore the expression of MyD88,TRAF6,TANK,P-NF-κB,and NF-κB showed no changes.PBMC which treated with anti-TLR1,anti-TLR2 or-TLR6 mAb could inhibite inflammatory IL-1β (Fold=0.16,Fold=0.31,Fold=0.29,P＜0.05) and IL-6 (Fold=0.14,Fold=0.20,Fold=0.28,P＜0.05).Conclusion TLR1/TLR2/TLR6 in PBMC of ovarian cancer patients participate in the recognition of the factors.
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Objectives To study the effect of ubiquitin proteasome inhibitor bortezomib on apoptosis and Caspase-3 expression in human umbilical arterial vascular smooth muscle cells. Methods Human umbilical artery vascular smooth muscle cells were cultured in vitro. Different doses of bortezomib (0, 4, 10, 40nmol/L) were used to treat cell. Cell proliferation activity were detected by using CCK8 method. Western Blot assay was used to measure the expression of Pro-caspase-3 and Cleaved-PARP protein. Morphology of cells in different groups are observed by confocal microscopy and apoptosis rate were detected by flow cytometry analysis. Results Bortezomib inhibits proliferation activity of vascular smooth muscle cells. With increasing of drug concentration and treating time, cell viability are reduced (P < 0.01). Cells treated with different concentrations bortezomib for 48 h showed increased apoptosis rate (P < 0.01), decreased pro-caspase-3 protein expression and increased cleaved-PARP protein expression (P < 0.01). Laser confocal microscope found that with the increase of drug concentration, the number of apoptotic cells showed an upward trend under per high-power vision. Conclusion The ubiquitin proteasome inhibitor bortezomib may decrease the expression of pro-caspase-3 and increase Cleaved-PARP expression in human umbilical artery vascular smooth muscle cells. Additionally , it could induce apoptosis in a dose-dependent manner.
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Objective To investigate the phenotype and function of CD8+T cells cultured with SK-OV-3. Methods Transwell coculture experiments were conducted in 24-well plates with inner wells to separate CD8+ T cells and SK-OV-3. After 5 days of culture, CD8+ T cells were washed, and 1 × 106 cells were collected for Foxp3, CD25, CD28, CTLA-4 and GITR mRNA analysis and 2 × 106 cells were collected to detect expression of Foxp3, CD25, CD28, CTLA-4 and GITR in CD8+ T cells by flow cytometry. CD8+T cells that cultured alone or with SK-OV-3 were added at ratios of 1∶0 , 1∶1 , 1∶5 , 1∶10 , and 0∶1 to na?ve CD4+ T cells in 96-well plates. All wells were cultured with the presence of irradiated PBMCs and anti-CD3 antibody. After 72 h, [3H]-thymidine was added for 16 h prior to the determination of proliferation by scintillation counting. Results Compared with CD8+ T cells cultured without SK-OV-3 , the expression of Foxp3 and CTLA-4 was increased and CD28 expression was decreased in CD8+ T cells cultured with SK-OV-3 (both P < 0.001). We found that CD8+T cells cultured with SK-OV-3 significantly suppressed the na?ve CD4+ T cell proliferation induced by the anti-CD3 stimulation in a dose-dependent manner. In contrast, CD8+ T cells cultured without SK-OV-3 did not suppress na?ve CD4+ T cell proliferation. Conclusion Ovarian cancer cell can induce the suppressive CD8+Treg, which is an important link of the immunosuppressive microenvironment in ovarian cancer.
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At present,stroke has become one of the diseases seriously harming the human life and the quality of life with its high morbidity,disability,and mortality.Therefore,clinicians need to find more effective indicators to identify the clinical conditions and outcomes,and guide the treatment.Studies in recent years have suggested that the biological markers have important clinical value for guiding the treatment of stroke.
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Remote ischemic preconditioning and postconditioning are two new ways to reduce ischemia-reperfusion injury.Studies in recent years have shown that it also has significant protective effect for cerebral ischemia.At the appropriate time to give appropriate strength of remote ischemic preconditioning or postconditioning may induce brain ischemic tolerance and thus produce neuroprotection.The procedures of limb ischemic preconditioning and postconditioning are simple,and the clinical application value is higher.This article reviews the protective effect of limb ischemic preconditioning and postconditioning on cerebral ischemia.
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Objective To investigate the effects of local mild hypothermia on the expression of EMAP-Ⅱ and proEMAP-Ⅱ after cerebral ischemia and reperfusion in rats and to explore the possible neuroprotection mechanism of mild hypothermia.Methods Forty-four male Wistar rats were divided randomly into a sham-operation group (Sham),a normothermia group (NT) and a hypothermia group (HT).Middle cerebral artery occlusion was performed using Longa's method,and reperfusion was allowed after 2 hours of occlusion.Mild hypothermia (33.0 ± 0.5)℃ for 6 hours was initiated at the start of reperfusion,followed by rewarming.Brains were harvested after 6,12,24,48 and 72 hours of reperfusion and used for HE staining to evaluate cellular apzoptosis and immunohistochemical staining for detecting the expression EMAP-Ⅱ and proEMAP-Ⅱ.Results The expression of EMAP-Ⅱ and proEMAP-Ⅱ in the ischemic penumbra was significant at 6 hours in the normothermia and hypothermia groups.It peaked at 12 hours in the normothermia group and 24 hours in the hypothermia group,and then decreased gradually.At 72 hours the expression of EMAP-Ⅱ and proEMAP-Ⅱ in the ischemic penumbras was very close to that in the sham group.EMAP-Ⅱ-positive cells were significantly fewer in the hypothermia group than in the normothermia group at all time points.ProEMAP-Ⅱ-positive cells were significantly more numerous in the normothermia group than in the hypothermia group at 6,12 and 24 hours.Conclusions Mild hypothermia (33.0 ± 0.5) ℃ has a valid neuroprotective effect which involves reducing EMAP-Ⅱ and proEMAP-Ⅱ expression in the ischemic penumbra and inhibiting apoptosis and inflammatory reactions after cerebral ischemia and reperfusion,at least in rats.
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Atherosclerosis (AS) is a common underlying disease that hazard to human health.It is closely associated with stroke,hypertension,coronary artery disease,and diabetes.AS on the premise of vascular intimnal injury,excessive smooth muscle cell proliferation,inflammatory cell infiltration,oxidative stress,apoptosis and other mschanisms participate together.In eucaryotic organisms,most proteins are degraded by ubiquitin-proteasome system (UPS).An increasing number of evidence indicates that UPS is associated with the occurrenee and development of AS and complications.This article reviews the relationship between.UPS and AS,as well as the effect of ubiquitin-proteasome inhibitor on AS.
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Objective To evaluate the efficacy of deanxit in treatment of post-stroke depression (PSD).Methods60 patients with PSD were randomly divided into treatment group ( plus with deanxit) and control group (plus with estazolam necessarily). At the baseline and at 2 weeks,4 weeks, 8 weeks after the treatment, the efficacy was assessed with HAMD, SSS, and ADL rating scale respectively. Results After 2,4,8 weeks treatment, HAMD and SSS scores of the treatment group significantly decreased compared with the control group ( all P ＜ 0. 01 ), and ADL scores of the treatment group increased significantly compared with the control group ( P ＜ 0. 01 ). Conclusion Deanxit could effectively relieve depressing symptoms and neurological impairment of PSD, and clinical side effects of deanxit were less. Deanxit was suitable for acute phase and long-term maintenance therapy in PSD.
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Objective To explore the effect of fenofibrate and atorvastatin on hyperlipoidemia and hyperuricemia.Methods 55 cases were randomly divided into 2 groups. 30 cases in the treatment group were give Fenofibrate (200rmg/d) and 25 cases in control group were given atorvastatin(10mg/d). And two groups given 8 days for all patients. The therapeutic effect, blood-fat and blood uric acid levd, and complication in two groups were compared. Results There were conspicuous effect of fenofibrate and atorvastatin on hyperlipoidemia and hyperuricemia. The index of TG, TC had significant differences between the two groups. The index of acidum uricum was higher in control group.The complication had no significant differences between two groups. Conclusion Both fenofibrate and atorvastain were effective drug for hyperuricemia and hyperlipoidemia,and could reduce TC,TG, HDLC and LDLC in the short time,and could decrease the risk factor of cerebrovascular disease.
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Objective To explore the diagnostic value of quantitative test of 14-3-3 protein content in cerebrospinal fluid(CSF)in sporadic Creutzfeldt-Jakob disease(sCJD).Methods The Capture Assay was used to detect the level of CSF 14-3-3 protein in 14 cases of sCJD(sCJD group),10 cases of other dementia(OD group),12 cases of non dementia(ND group).Results The media of 14-3-3 protein content was 40.00 ng/mg in sCJD group,2.65 ng/mg in OD group,and 3.10 ng/mg in ND group,respectively.It was significantly higher in sCJD group than that in groups OD and ND(all P
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24 ng/ml,sensitivity and specificity were 90% and 92.9% respectively.Conclusions The diagnosis value of 14-3-3 protein in CSF is higher than that of NSE. The combination of CSF 14-3-3 protein and NSE can improve the sensitivity and specificity in diagnosis of CJD.