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1.
Int J Psychiatry Clin Pract ; 25(2): 109-114, 2021 Jun.
Article in English | MEDLINE | ID: mdl-32662692

ABSTRACT

OBJECTIVES: Coronavirus disease 2019 (COVID-19) first broke-out in Wuhan China in December 2019, and spread throughout the entire country within a short time. This cross-sectional study investigated the prevalence of depression and anxiety and associated risk factors were analysed in patients with COVID-19. METHODS: This single-center cross-sectional study focussed on measuring depression and anxiety using self-report scales. Linear regression was used to determine independent predictors for depression and anxiety. RESULTS: A total of 78 patients who were confirmed to have COVID-19 were enrolled in the study. Prevalence of depression and anxiety symptoms were diagnosed in 35.9% and 38.5% of the patients, respectively. Multivariate linear regression analysis found female gender was an independent predictor for higher depression severity index. Having family members who were diagnosed with COVID-19 and family members who died from COVID-19 were independently associated with higher depression severity index and anxiety score. CONCLUSIONS: Patients with COVID-19 especially those who had family members diagnosed with COVID-19 or died from COVID-19 were more susceptible to depression and anxiety than were other patients. Effective strategies should be pursued to improve the mental health of this patient population.Key pointsPatients with COVID-19 showed a significantly high prevalence of depression and anxiety.Female patients were associated with higher risk of depression.Patients with family members diagnosed as COVID-19 or died from this disease were associated with higher risk of depression and anxiety.


Subject(s)
Anxiety/etiology , COVID-19/psychology , Depression/etiology , Anxiety/epidemiology , China/epidemiology , Cross-Sectional Studies , Depression/epidemiology , Family , Female , Humans , Linear Models , Male , Middle Aged , Prevalence , Psychiatric Status Rating Scales , Risk Factors , Sex Factors
2.
Commun Biol ; 3(1): 575, 2020 10 15.
Article in English | MEDLINE | ID: mdl-33060834

ABSTRACT

Although disturbed phosphate metabolism frequently accompanies chronic kidney disease (CKD), its causal role in CKD progression remains unclear. It is also not fully understood how excess salt induces organ damage. We here show that urinary phosphate-containing nanoparticles promote kidney injury in salt-sensitive hypertension. In Dahl salt-sensitive rats, salt loading resulted in a significant increase in urinary phosphate excretion without altering serum phosphate levels. An intestinal phosphate binder sucroferric oxyhydroxide attenuated renal inflammation and proteinuria in this model, along with the suppression of phosphaturia. Using cultured proximal tubule cells, we confirmed direct pathogenic roles of phosphate-containing nanoparticles in renal tubules. Finally, transcriptome analysis revealed a potential role of complement C1q in renal inflammation associated with altered phosphate metabolism. These data demonstrate that increased phosphate excretion promotes renal inflammation in salt-sensitive hypertension and suggest a role of disturbed phosphate metabolism in the pathophysiology of hypertensive kidney disease and high salt-induced kidney injury.


Subject(s)
Hypertension, Renal/etiology , Hypertension, Renal/urine , Nanoparticles , Nephritis/etiology , Nephritis/urine , Phosphates/urine , Animals , Biomarkers , Cardiomegaly/etiology , Cardiomegaly/metabolism , Cardiomegaly/pathology , Chemokine CCL2/genetics , Chemokine CCL2/metabolism , Disease Models, Animal , Fluorescent Antibody Technique , Gene Expression Profiling , Gene Expression Regulation , Glomerulonephritis/diagnosis , Glomerulonephritis/etiology , Glomerulonephritis/urine , Hypertension, Renal/diagnosis , Hypertension, Renal/metabolism , Immunohistochemistry , Macrophages/immunology , Macrophages/metabolism , Macrophages/pathology , Models, Biological , Nanoparticles/chemistry , Nephritis/diagnosis , Nephritis/metabolism , Phosphates/blood , Phosphates/chemistry , Rats , Rats, Inbred Dahl , Transcriptome , Urinalysis
3.
J Photochem Photobiol B ; 205: 111805, 2020 Apr.
Article in English | MEDLINE | ID: mdl-32092661

ABSTRACT

In recent days, reported researches demonstrated that encapsulation of natural hydrophobic drug molecules (Piperine) into the biodegradable polymer system with nanoformulations opens a novel prospect in bio-nanomedicine field. Generally, the nanostructured materials embedded with the drug molecules could render enhanced efficiency in therapies. Piperine is a chief alkaloid compound of natural black pepper exhibits excellent anti-convulsant efficiency in the anti-epileptic treatment. Nonetheless, the poor water solubility of the piperine molecules has some difficulties in drug delivery and clinical applications. Herein we report the synthesis of Copper oxide quantum dots coated Hyaluronic acid (HA)/ Poly(lactic-co-glycolic acid) (PLGA) with for the effective delivery of piperine in the targeted drug delivery for epilepsy treatment. The physicochemical characterization was performed using the as prepared material. The crystal structure, surface morphology and the elemental composition were investigated from XRD, SEM, TEM and EDX analyses respectively. The surface morphology clearly stated the loading of CuO QDs loaded HA/PLGA microspheres. The capping of the polymer matrix was also studied using FTIR analysis. A Photoluminescence spectrum is also recorded. This study was illustrating that Piperine loaded CuQDs@HA/PLGA nanostructures exhibit improved neuroprotection and encourage the activation of astrocytes in chemical kindling model of epilepsy. This proposed material could be a novel and effective therapeutic platform for the targeted drug delivery systems.


Subject(s)
Alkaloids/administration & dosage , Anticonvulsants/administration & dosage , Benzodioxoles/administration & dosage , Copper/administration & dosage , Drug Delivery Systems , Epilepsy/drug therapy , Piperidines/administration & dosage , Polylactic Acid-Polyglycolic Acid Copolymer/administration & dosage , Polyunsaturated Alkamides/administration & dosage , Quantum Dots/administration & dosage , Alkaloids/chemistry , Animals , Anticonvulsants/chemistry , Benzodioxoles/chemistry , Cell Line , Cell Survival/drug effects , Copper/chemistry , Drug Design , Drug Liberation , Epilepsy/chemically induced , Humans , Luminescence , Male , Pentylenetetrazole , Piperidines/chemistry , Polylactic Acid-Polyglycolic Acid Copolymer/chemistry , Polyunsaturated Alkamides/chemistry , Quantum Dots/chemistry , Rats, Wistar
4.
Perit Dial Int ; 39(5): 465-471, 2019.
Article in English | MEDLINE | ID: mdl-31501292

ABSTRACT

Background:Depression has been recognized as a risk factor for cognitive impairment (CI) from cross-sectional datasets. This multicenter prospective study investigated the association between depression and cognitive decline in peritoneal dialysis (PD) patients.Methods:This multicenter prospective cohort study included 458 PD patients who were followed up for 2 years. The Modified Mini-Mental State Examination (3MS) was used for assessment of global cognitive function, Trail-Making Tests A and B for executive function, subtests of the Battery for the Assessment of Neuropsychological Status for immediate and delayed memory, visuospatial skill, and language ability. Depression was assessed using Zung's Self-Rating Depression Scale.Results:During the 2-year follow-up, patients with moderate/severe depression at baseline showed a significant decline in global cognitive function (80.5 ± 15.2 vs 76.6 ± 15.5, p = 0.008), while patients without depression or with mild depression kept a stable global cognitive function. In the meantime, patients without depression showed significant improvements in immediate memory, visuospatial skill, and language ability. However, no significant improvement in these parameters was shown in depression groups. In multivariable linear regression analysis, depression at baseline was a significant predictor of worsening global cognitive function, whether depression was analyzed as a continuous variable (odds ratio [OR] = -0.14, 95% confidence interval [CI] -0.27, -0.01, p = 0.031) or a rank variable (OR = -1.88, 95% CI -3.30, -0.45, p = 0.010). Moreover, higher depression score or more severe depression degradation was significantly associated with decline of immediate memory, delayed memory, and language skill.Conclusion:Depression was a significant risk factor for worsening of CI in PD patients.


Subject(s)
Cognitive Dysfunction/epidemiology , Cognitive Dysfunction/etiology , Depression/complications , Peritoneal Dialysis/psychology , Adult , Aged , Cohort Studies , Female , Humans , Male , Middle Aged , Prospective Studies , Risk Factors
5.
Mol Med Rep ; 19(2): 1139-1149, 2019 02.
Article in English | MEDLINE | ID: mdl-30535439

ABSTRACT

The neurological disorders and neural pathology brought about by chronic alcoholism are difficult to be reversed. Increasing evidence highlights the protective roles of erythropoietin (EPO) in neurodegenerative diseases and injuries of the central nervous system. In the present study, we investigated the therapeutic effects of EPO on the neurological function deficits and neural pathology caused by chronic alcoholism and the regulatory mechanisms. Using the canonical mouse model of chronic alcohol exposure designed to mimic the repeated cycles of heavy abuse typical of chronic alcoholism, it was found that EPO delivered via intranasal route effectively restored the alcohol­impaired motor cooperation in rotarod and beam walk tests, reversed alcoholic cognitive and emotional alterations in the novel location recognition task and open­filed test, and rescued alcohol­disrupted nervous conduction in the somatosensory­evoked potential (SSEP) test. Consistently, the intranasally administered EPO promoted the remyelination and synapse formation in chronic alcohol­affected neocortex and hippocampus as evidenced by immunofluorescence staining and transmission electron microscopy. Additionally, we discovered that the exogenous rhEPO, which entered the cerebrum through intranasal route, activated the erythropoietin receptor (EPOR) and the downstream ERKs and PI3K/AKT signaling, and suppressed autophagy­related degradation of nuclear factor, erythroid 2­like 2 (Nrf2). Furthermore, the intranasal EPO­exerted neuroprotection was almost abolished when the specific Nrf2 antagonist ATRA was administered intraperitoneally prior to intranasal EPO treatment. Collectively, our data demonstrated the repairing potential of EPO for the neurological disorders and neural pathology caused by chronic alcoholism, and identified the Nrf2 activity as the key mechanism mediating the protective effects of EPO.


Subject(s)
Alcoholism/drug therapy , Alcoholism/metabolism , Autophagy/drug effects , Erythropoietin/administration & dosage , Erythropoietin/metabolism , NF-E2-Related Factor 2/metabolism , Administration, Intranasal/methods , Animals , Disease Models, Animal , Hippocampus/drug effects , Hippocampus/metabolism , Male , Mice , Mice, Inbred C57BL , Neurodegenerative Diseases/drug therapy , Neurodegenerative Diseases/metabolism , Neuroprotective Agents/administration & dosage , Phosphatidylinositol 3-Kinases/metabolism , Receptors, Erythropoietin/metabolism , Signal Transduction/drug effects , Signal Transduction/physiology
6.
PLoS One ; 10(10): e0138973, 2015.
Article in English | MEDLINE | ID: mdl-26431046

ABSTRACT

Neural stem cells are self-renewing, multipotent and undifferentiated precursors that retain the capacity for differentiation into both glial (astrocytes and oligodendrocytes) and neuronal lineages. Neural stem cells offer cell-based therapies for neurological disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease and spinal cord injuries. However, their cellular behavior is poorly understood. MicroRNAs (miRNAs) are a class of small noncoding RNAs involved in cell development, proliferation and differentiation through regulating gene expression at post-transcriptional level. The role of miR-381 in the development of neural stem cells remains unknown. In this study, we showed that overexpression of miR-381 promoted neural stem cells proliferation. It induced the neural stem cells differentiation to neurons and inhibited their differentiation to astrocytes. Furthermore, we identified HES1 as a direct target of miR-381 in neural stem cells. Moreover, re-expression of HES1 impaired miR-381-induced promotion of neural stem cells proliferation and induce neural stem cells differentiation to neurons. In conclusion, miR-381 played important role in neural stem cells proliferation and differentiation.


Subject(s)
Basic Helix-Loop-Helix Transcription Factors/genetics , Cell Differentiation/genetics , Cell Proliferation/genetics , Gene Expression Regulation/genetics , Homeodomain Proteins/genetics , MicroRNAs/physiology , Neural Stem Cells/cytology , Animals , Astrocytes/cytology , Rats , Rats, Wistar , Transcription Factor HES-1
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