Objective: Several COVID-19 patients have overlapping comorbidities. The independent role of each component contributing to the risk of COVID-19 is unknown, and how some non-cardiometabolic comorbidities affect the risk of COVID-19 remains unclear. Methods: A retrospective follow-up design was adopted. A total of 1,160 laboratory-confirmed patients were enrolled from nine provinces in China. Data on comorbidities were obtained from the patients' medical records. Multivariable logistic regression models were used to estimate the odds ratio ( Results: Overall, 158 (13.6%) patients were diagnosed with severe illness and 32 (2.7%) had unfavorable outcomes. Hypertension (2.87, 1.30-6.32), type 2 diabetes (T2DM) (3.57, 2.32-5.49), cardiovascular disease (CVD) (3.78, 1.81-7.89), fatty liver disease (7.53, 1.96-28.96), hyperlipidemia (2.15, 1.26-3.67), other lung diseases (6.00, 3.01-11.96), and electrolyte imbalance (10.40, 3.00-26.10) were independently linked to increased odds of being severely ill. T2DM (6.07, 2.89-12.75), CVD (8.47, 6.03-11.89), and electrolyte imbalance (19.44, 11.47-32.96) were also strong predictors of unfavorable outcomes. Women with comorbidities were more likely to have severe disease on admission (5.46, 3.25-9.19), while men with comorbidities were more likely to have unfavorable treatment outcomes (6.58, 1.46-29.64) within two weeks. Conclusion Besides hypertension, diabetes, and CVD, fatty liver disease, hyperlipidemia, other lung diseases, and electrolyte imbalance were independent risk factors for COVID-19 severity and poor treatment outcome. Women with comorbidities were more likely to have severe disease, while men with comorbidities were more likely to have unfavorable treatment outcomes.
Adult ; Aged ; COVID-19/virology* ; China/epidemiology* ; Comorbidity ; Female ; Humans ; Male ; Middle Aged ; Retrospective Studies ; Severity of Illness Index ; Treatment Outcome

OBJECTIVETo compare the behavioral and pathological features of SORL1 gene knockout mice with those of normal mice and APP/PSE1 mice to verify the feasibility of using SORL1 knockout mice as a model of sporadic Alzheimer disease.

METHODSSORL1 gene of fertilized mouse eggs were edited using Crispr/Case9 technique. SORL1 mice were screened and identified by detecting the DNA sequence, and Western blotting was used to detect the expression of SORL1. SORL1 mice, control mice and APP/PSE1 mice all underwent Morris water maze test to assess their learning and memory abilities with positioning navigation and space exploration experiments. The expression of APP and Aβ in the brain of the mice was detected using immunohistochemistry and Western blotting, respectively.

RESULTSDNA sequencing showed CAAT deletion in SORL1 gene in two chromosomes of SORL1 mice, and the control mice had intact SORL1 gene without the deletion; Western blotting did not detect the expression of the SORL1 in the brain of SORL1 mice. Morris water maze test showed that in positioning navigation experiment, the average avoidance latency was similar between SORL1 mice and APP/PSE1 mice (P>0.05) but increased significantly in both mice as compared with the control group (P<0.05); similar results were obtained in the space exploration experiment. Immunohistochemistry and Western blotting revealed significantly increased APP and Aβ expression in the brain tissue of both SORL1 mice and APP/PSE1 mice compared with the control mice without significant differences between the two transgenic mice.

CONCLUSIONSORL1 mice exhibit similar behavioral and pathological changes with APP/PSE1 mice and can be used as a model of sporadic Alzheimer's disease.

OBJECTIVETo study the protective effect of butylphthalide in a cell model of Alzheimer's disease(AD) induced by Aβ25-35 in Neuro 2a (N2a) cells.

METHODSN2a cells were divided into AD group, butylphthalide (NBP) group and control group. AD cell model was established by adding 20 µmol/L Aβ25-35 to cultured N2a cells. The cells in NBP group were treated with 0.1, 1, 10, or 100 µmol/L NBP 4 h prior to treatment with 20 µmol/L Aβ25-35. The cell viability were determined by MTT assay, the cell apoptotic rate were detected by AnnexinV-FITC flow cytometry, and the cell morphological changes were observed under inverted phase contrast microscope. The expression of TNF-α and IL-1β mRNA were determined by qRT-PCR.

RESULTSCompared with those in the control group, the number of adherent cells was significantly decreased, neurite structures were reduced, and the cell viability was decreased, while the apoptotic rate and expressions of TNF-α and IL-1β mRNA were increased in AD group (P<0.05). Compared with that in AD group, the number of adherent cells was increased in NBP group and the cell morphology was similar to the normal control cells. The cell viability of N2a cells was increased in NBP group with decreased apoptotic rate and expression of TNF-αand IL-1β mRNA (P<0.05).

CONCLUSIONButylphthalide can protect against AD in the cell model induced by Aβ25-35 possibly by inhibiting the expression of inflammatory cytokines.

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.
Antidepressive Agents ; pharmacology ; Depression ; drug therapy ; Humans ; Ketamine ; pharmacology ; Receptors, N-Methyl-D-Aspartate

OBJECTIVETo investigate serum adiponectin level in patients with Alzheimer's disease (AD) and its correlation with the patients' cognitive function.

METHODSThis 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.

RESULTSSerum 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).

CONCLUSIONSerum adiponectin levels are reduced in AD patients and associated with the degree of cognitive impairment.

Adiponectin ; blood ; Alzheimer Disease ; blood ; Case-Control Studies ; Cognition ; Cognitive Dysfunction ; blood ; Enzyme-Linked Immunosorbent Assay ; Humans

Drowning ; Humans ; Male ; Middle Aged ; Organothiophosphorus Compounds ; poisoning

OBJECTIVETo summarize the clinical effects of the manipulative reduction and splint fixation for the treatment of fracture-dislocation of ankle.

METHODSFrom April 1990 to June 2010, 53 patients with fracture dislocation of ankle were treated with non-operative treatment including manipulative reduction, splint fixation, oral herbal soup and early functional exercises. There were 32 males and 21 females with an average age of 42.5 years (ranged, 25 to 60). There were 30 cases in left and 23 cases in right. Ankle joint function was evaluated according to standard of Mazur.

RESULTSFollow up time was from 6 to 60 months with an average of 33 months; all the fractures healed with an average of 4 months (ranged, 3 to 5). The mean of Mazur scoring was 90.11+/- 8.40, 36 cases got excellent results, 11 good, 3 fair and 3 poor.

CONCLUSIONWith non-operative treatment such as manipulative reduction and splint external fixation for fracture-dislocation of ankle can obtain satisfactory effects, which has advantage of simple operation, less trauma.

Adult ; Ankle Injuries ; therapy ; Female ; Follow-Up Studies ; Fractures, Bone ; therapy ; Humans ; Joint Dislocations ; therapy ; Male ; Manipulation, Orthopedic ; Medicine, Chinese Traditional ; Middle Aged ; Splints

OBJECTIVETo observe the effect of willed movement therapy on the expression of neurotrophin 3 (NT-3) and growth associated protein 43 (GAP-43) in rats with cerebral ischemia-reperfusion (IR) and investigate the neuroprotective mechanism of willed movement therapy in nerve regeneration and repair.

METHODSCerebral IR model was established by middle cerebral artery occlusion (MCAO) in SD rats. The rats were randomly divided into MCAO group, environment modification group (EM group) and willed movement therapy group (WM group). The rats were evaluated for neurological deficits and decapitated on days 3, 7 and 15 after the reperfusion to examine the expressions of NT-3 and GAP-43 in the ischemic brain tissues by immunohistochemistry.

RESULTSCompared with MCAO and EM groups, the rats in WM group showed significantly lowered grade of neurological deficits (P<0.05) at 15 days and significantly increased the expressions of NT-3 and GAP-43 (P<0.05) at 7 and 15 days after the reperfusion. No significant difference was found in the expression of NT-3 and GAP-43 between MCAO and EM groups (P>0.05). The expression of NT-3 was positively correlated to that of GAP-43 in the ischemic tissues.

CONCLUSIONSWilled movement therapy increases the expression of NT-3 and GAP-43 in the ischemic brain area in rats with cerebral ischemia-reperfusion, which is probably related to nerve regeneration and repair.

Animals ; Brain Ischemia ; metabolism ; therapy ; Exercise Therapy ; methods ; GAP-43 Protein ; metabolism ; Infarction, Middle Cerebral Artery ; metabolism ; therapy ; Male ; Movement ; physiology ; Nerve Regeneration ; Neuronal Plasticity ; physiology ; Neurotrophin 3 ; metabolism ; Physical Exertion ; physiology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; therapy

OBJECTIVETo determine the effect of willed movement on the expression of glial fibrillary acidic protein (GFAP) and synaptophysin (SYP) in adult rats with cerebral ischemia-reperfusion, and explore the mechanism of willed movement in promoting nerve repair and regeneration.

METHODSAdult rat models of cerebral ischemia-reperfusion injury were established by middle cerebral artery occlusion (MCAO) for 2 h followed by a 24-h reperfusion. The models were then divided randomly into 3 groups, namely the model group, environmental modification (EM) group, and willed movement (WM) group. In each group, neurological deficits were evaluated at 3, 7 and 15 days after reperfusion. Immunohistochemistry and immunofluorescence assay were employed to examine the expression of GFAP and SYP in the brain tissue near the ischemic foci.

RESULTSThe rats in WM group showed lessened neurological deficits at 15 days and lowered expression of GFAP and SYP at 7 and 15 days after reperfusion compared with the model and EM groups (P<0.05). No significant difference was found in the expression of GFAP or SYP between the model group and EM group at any time points.

CONCLUSIONWilled movement can promote the functional recovery of neurological deficits following cerebral ischemia-reperfusion probably in relation to enhanced GFAP and SYP expressions in the ischemic brain tissues.

Animals ; Brain Ischemia ; metabolism ; therapy ; Disease Models, Animal ; Exercise Therapy ; methods ; Glial Fibrillary Acidic Protein ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; therapy ; Synaptophysin ; metabolism

OBJECTIVETo determine the effect of butylphthalide on the expressions of protein disulfide isomerase (PDI) and P53 in the brain tissue of rats with Alzheimer's disease (AD).

METHODSSixty male adult rats were randomly divided into AD model group, butylphthalide group and control group (n = 20). AD models were established by injecting beta-amyloid protein 1-42 into the hippocampus of rats. Sixty days later, the learning and memory abilities of the rats were evaluated using Y-maze test, and the expressions of PDI and P53 in the brain tissue of the rats were measured by immunohistochemistry.

RESULTSCompared with the control group, the rats in AD model group exhibited significantly reduced learning and memory abilities, lowered expressions of PDI in the hippocampus and increased expression of P53 in the cortex (P > 0.01). In comparison with the model group, the rats in the butylphthalide group showed significantly increased PDI-positive cells in the hippocampus and decreased expression of P53 in the cortex (P < 0.01).

CONCLUSIONButylphthalide improves the learning and memory abilities of rats with experimental AD, the mechanism of which may involve inhibition of P53 expression and enhancement of PDI expression in the brain tissues.

Alzheimer Disease ; physiopathology ; Animals ; Apoptosis ; drug effects ; Benzofurans ; pharmacology ; Brain ; enzymology ; metabolism ; Disease Models, Animal ; Learning ; drug effects ; Male ; Memory ; drug effects ; Protein Disulfide-Isomerases ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Tumor Suppressor Protein p53 ; metabolism