OBJECTIVE: To investigate the status of anxiety and depression in patients requiring emergency treatment during the epidemic of COVID-19 to identify the patients with acute psychological stress disorder. METHODS: During the COVID-19 epidemic, the medical staff divided the patients visiting the emergency department into suspected group, fever group and control group through interview of the patients at triage. Self-rating anxiety scale (SAS) and self-rating depression scale (SDS) were distributed to each patient, and a trained medical staff was responsible for assisting the patient to complete the scales. RESULTS: A total of 557 sets of scales were distributed, including 211 in suspected COVID-19 case group, 167 in fever group and 179 in the control group. A total of 516 scales were retrieved, including 197 in suspected case group, 151 in fever group and 168 in control group. In the 3 groups, the incidence rates of anxiety and depression were 57.87% and 58.88%, 48.34% and 43.71%, and 18.31% and 18.99%, respectively, and the rates were significantly higher in suspected group and fever group than in the control group ( < 0.01), and significantly higher in suspected group than in fever group ( < 0.05). The standardized anxiety and depression scale scores in suspected case group, fever group and control group were 57.38±16.25 and 42.58±14.27, 51.23±15.29 and 38.32±15.39, and 32.58±17.8 and 12.25±12.94, respectively. Compared with the control group, both suspected case group and fever group had significantly higher standard scores for anxiety and depression ( < 0.01), and suspected case group had significantly higher standardized scores than fever group ( < 0.01). CONCLUSIONS Among the patients visiting the emergency treatment, the patients with suspected COVID-19 and common fever are more likely to develop anxiety and depressive symptoms.
Anxiety ; epidemiology ; Betacoronavirus ; Coronavirus Infections ; epidemiology ; psychology ; Depression ; epidemiology ; Emergency Service, Hospital ; Humans ; Pandemics ; Pneumonia, Viral ; epidemiology ; psychology

Chimeric antigen receptor T (CAR-T) cell therapy is an emerging immunotherapy that has allowed for major breakthroughs in the treatment of hematological neoplasms. However, little progress has been made in the treatment of solid tumors, primarily due to the difficulty in homing to tumor tissues by CAR-T cells during treatment. The complex tumor microenvironment and the barrier function of tumor tissues prevent CAR-T cells from contacting tumor cells, thereby preventing them from exerting their antitumor ac-tivity. This review article summarizes not only the progress made in the study of homing disorders of CAR-T cells in the treatment of solid tumors but also the current methods to overcome these disorders.

Objective To establish a cell model mimicking Alzheimer's disease (AD) by knocking down SORL1 gene and compare the viability, apoptosis, and expressions of tumor necrosis factor-α( TNF-α) and interleukin-1β(IL-1β) in this model with a traditional Alzheimer's disease cell model. Methods A traditional cell model of AD was established by inducing N2a cells with Aβ25-35, and the optimal Aβ25-35 concentration was determined by assessing the cell viability changes. Another cell model of AD was established by transfecting N2a cells with SORL1-shRNA lentiviral vector, and SORL1 expression in the transfected cells were detected using Western blotting and qRT-PCR. With wild-type N2a cells without any treatment and cells transfected with a scramble shRNA as the control groups, the two cell models were examined for cell viability with MTT assay, cell apoptosis with flow cytometry, and TNF-αand IL-1βlevels in the culture supernatant with ELISA. Results The two cell models of AD showed obviously decreased viability and increased cell apoptosis compared with the untreated control cells or cells transfected with a scramble shRNA (P<0.05); no significant difference was found in the cell viability and apoptosis rate between the two AD cell models or between the two control groups (P>0.05). Significantly increased expressions of TNF-αand IL-1βwere observed in both of the two cell models compared with their respective control groups (P<0.05) without significant differences between the two cell models or between the two control groups (P>0.05). Conclusion A new AD cell model similar to Aβ25-35-induced AD model can be established by SORL1 knockdown in N2a cells.

Objective To establish a cell model mimicking Alzheimer's disease (AD) by knocking down SORL1 gene and compare the viability, apoptosis, and expressions of tumor necrosis factor-α( TNF-α) and interleukin-1β(IL-1β) in this model with a traditional Alzheimer's disease cell model. Methods A traditional cell model of AD was established by inducing N2a cells with Aβ25-35, and the optimal Aβ25-35 concentration was determined by assessing the cell viability changes. Another cell model of AD was established by transfecting N2a cells with SORL1-shRNA lentiviral vector, and SORL1 expression in the transfected cells were detected using Western blotting and qRT-PCR. With wild-type N2a cells without any treatment and cells transfected with a scramble shRNA as the control groups, the two cell models were examined for cell viability with MTT assay, cell apoptosis with flow cytometry, and TNF-αand IL-1βlevels in the culture supernatant with ELISA. Results The two cell models of AD showed obviously decreased viability and increased cell apoptosis compared with the untreated control cells or cells transfected with a scramble shRNA (P<0.05); no significant difference was found in the cell viability and apoptosis rate between the two AD cell models or between the two control groups (P>0.05). Significantly increased expressions of TNF-αand IL-1βwere observed in both of the two cell models compared with their respective control groups (P<0.05) without significant differences between the two cell models or between the two control groups (P>0.05). Conclusion A new AD cell model similar to Aβ25-35-induced AD model can be established by SORL1 knockdown in N2a cells.

Objective To investigate serum adiponectin level in patients with Alzheimer's disease (AD) and its correlation with the patients' cognitive function. Methods This case-control study was conducted in 90 patients with a highly probable diagnosis ofAD, who were divided into mild, moderate and severe group saccording to the MMSE score. Ninety healthy subjects matched for age and gender with the AD patients were selected as the control group. The serum levels ofadiponectin in the participants were detected using enzyme-linked immunosorbent assay. Results Serum adiponectin level was significantly lower in the AD group than in the control group (P<0.05). Of the 3 subgroups of the AD patients, the moderate and severe AD groups showed significantly lower serum adiponectin level sthan the control group (P<0.05), but the difference in adiponectin levels was not significant between the mild AD group and the control group (P>0.05);serum adiponectin levels also differed significantly among the 3 subgroups of AD patients (P<0.05). Serum adiponectin level was positively correlated with the MMSE score in the AD patients (r=0.683, P<0.001). Conclusion Serum adiponectin levels are reduced in AD patients and associated with the degree of cognitive impairment.

The pathogenesis and etiology of still remain unknown. Current evidence suggests that the occurrence of depression may be related to a reduced secretion of neurotransmitters, neuronal apoptosis, inflammation, intestinal flora and other factors. Although the commonly used antidepressants such as SSRIs, SNRIs, NaSSA, and SARIs produce some therapeutic effects, they fail to relieve the full spectrum of the symptoms of depression. In recent years, esketamine was found to produce a potent and a long-lasting antidepressant effect by acting on the NMDA receptors. Herein the authors review the progress in the study of the pathogenesis and drug therapies of depression, the efficacy of esketamine treatment and the underlying mechanism, and the prospect of esketamine treatment. Currently the mechanism of the antidepressant effect of esketamine remains indeterminate and its clinical application is limited, but its effect in rapidly alleviating the symptoms of depression suggests its bright prospect for clinical applications.

Objective To investigate serum adiponectin level in patients with Alzheimer's disease (AD) and its correlation with the patients' cognitive function. Methods This case-control study was conducted in 90 patients with a highly probable diagnosis ofAD, who were divided into mild, moderate and severe group saccording to the MMSE score. Ninety healthy subjects matched for age and gender with the AD patients were selected as the control group. The serum levels ofadiponectin in the participants were detected using enzyme-linked immunosorbent assay. Results Serum adiponectin level was significantly lower in the AD group than in the control group (P<0.05). Of the 3 subgroups of the AD patients, the moderate and severe AD groups showed significantly lower serum adiponectin level sthan the control group (P<0.05), but the difference in adiponectin levels was not significant between the mild AD group and the control group (P>0.05);serum adiponectin levels also differed significantly among the 3 subgroups of AD patients (P<0.05). Serum adiponectin level was positively correlated with the MMSE score in the AD patients (r=0.683, P<0.001). Conclusion Serum adiponectin levels are reduced in AD patients and associated with the degree of cognitive impairment.

The pathogenesis and etiology of still remain unknown. Current evidence suggests that the occurrence of depression may be related to a reduced secretion of neurotransmitters, neuronal apoptosis, inflammation, intestinal flora and other factors. Although the commonly used antidepressants such as SSRIs, SNRIs, NaSSA, and SARIs produce some therapeutic effects, they fail to relieve the full spectrum of the symptoms of depression. In recent years, esketamine was found to produce a potent and a long-lasting antidepressant effect by acting on the NMDA receptors. Herein the authors review the progress in the study of the pathogenesis and drug therapies of depression, the efficacy of esketamine treatment and the underlying mechanism, and the prospect of esketamine treatment. Currently the mechanism of the antidepressant effect of esketamine remains indeterminate and its clinical application is limited, but its effect in rapidly alleviating the symptoms of depression suggests its bright prospect for clinical applications.

Objective To study the changes of white matter fiber tracts in mild traumatic brain injury(mTBI)patients by using DTI technique on 3.0T MR system,and evaluate the clinical diagnostic value of DTI.Methods Thirty mTBI and 30 matched health-y controls underwent conventional CT,MRI and DTI examinations.FA values and ADC values in the genu of the corpus callosum, the splenium of the corpus callosum,bilateral internal capsule,the cingulum bundle,the bilateral superior longitudinal fasciculus and the inferior longitudinal fasciculus of mTBI were measured in mTBI patients and controls at acute phase,subacute phase,5 weeks and 3 months post-trauma.The temporal changes of MRI data were observed.Results The FA values in the part of the white mat-ter fiber tracts reduced in the acute and subacute phase in mTBI patients (all P <0.05)in relative to controls (all P <0.05),At 5 weeks and 3 months post-trauma,the FA values also slightly lower in patients than controls.As for the genu of the corpus callosum and the splenium of the corpus callosum,the FA values in mTBI patients increased slightly at the acute stage (all P >0.05),but de-creased at 5 weeks-3 months post-trauma phase,though there was no significantly difference(all P >0.05).ADC values significantly decreased in the acute and subacute phase in mTBI patients,while they recovered thereafter (all P >0.05).Conclusion The sensi-tivity of DTI in detecting the lesions of mild traumatic brain damage is high,and it can display the damage of white matter.DTI could play an important role in the diagnosis of mTBI.