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@#Depression is one of the most common psychiatric disorders. Depression increases the risk of stroke,cardiovascular disease,and dementia. Certain types of depression may be a harbinger of cognitive impairment. Chronic stress and inflammation jointly compromise vascular and brain functions. The resulting microglial activation and increases in proinflammatory cytokines lead to depression and cognitive impairment,which may progress to dementia. Anti-inflammatory treatments can improve depressive symptoms,and anti-inflammatory and antidepressant treatments may prevent cognitive impairment in patients with inflammatory depression. This paper reviews the relationship between inflammation, depression,and cognition,aiming to provide a reference for the clinical research of inflammatory depression and dementia.
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With rapid global growth of the older population, it has been increasingly important for screening, early diagnosis, treatment and daily monitoring of cognitive function in the elderly population. Given the limited effects of pharmacological treatments, cognitive rehabilitation has the potential to improve meaningful outcomes for older people and thus comes into sight. Traditional cognitive assessment and rehabilitation require face-to-face interview, while patients with cognitive impairment are mostly elderly with difficulties in access to medical care, usually needed to be accompanied by caregivers and having other co-morbidities with limited mobility. This contradiction is especially prominent in the context of COVID-19 pandemic, which may even exacerbate cognitive decline of patients. Therefore, remote cognitive assessment and rehabilitation based on information and communication technologies have become new options. This paper introduces the widely used and validated means of remote assessment and its guiding use in cognitive rehabilitation, which can be implemented through the Internet, applications, video and telephone. The advantages of being fast, convenient and geographically agnostic lead to a wider use in large community and safeguard the health of patients with cognitive impairment.
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Cognitive impairment is one of the important clinical manifestations in depression. The particularly vulnerable cognition domains included executive function, attention, memory, and processing speed. Depression with cognitive impairment is not only a predictor of poor efficacy, but also closely related to dementia. Previous studies have suggested that multiple physiological mechanisms may be altered between depression and cognitive impairment. With the rapid development of neuroimaging technology, resting state functional magnetic resonance imaging has been widely used to explore the neurobiological mechanisms of depression and cognitive impairment. After reviewing the resting-state functional MRI manifestations of the comorbidity, it was found that the default mode network, cognitive control network, and salience network were activated or weakened in the brain. In addition, the inter-network functional connectivity was altered with the co-existence of impairment and compensation. The aforementioned changes of brain function are expected to be the therapeutic targets for depression with cognitive dysfunction.
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Objective:To investigate the factors associated with delay in anticoagulant therapy in patients with cerebral venous sinus thrombosis (CVST) and its effect on outcome.Methods:Patients with CVST admitted to Changhai Hospital, Naval Medical University from January 2010 to August 2021 were retrospectively enrolled. Patients were divided into early anticoagulation group and late anticoagulation group by the median time interval from first symptom to initiation of anticoagulation. The modified Rankin Scale was used for outcome assessment at 90 d after onset. 0-2 scores were defined as good outcome and 3-6 were defined as poor outcome. Demographic and clinical data were compared for the early versus late anticoagulation group and for the good versus poor outcome groups. Multivariable logistic regression was used to identify independent influencing factors of delay in anticoagulation and the correlation of delay in anticoagulation with poor outcome. Results:A total of 131 patients were included, their age was 40.07±15.11 years old, and 68 (51.91%) were male. Of these, 65 patients (49.62%) were in the early anticoagulation group and 14 (10.69%) were in the poor outcome group. Compared with the late anticoagulation group, the early anticoagulation group had a significantly higher proportion of patients with seizures and brain parenchymal damage as well as higher D-dimer levels on admission, while the proportion of patients with visual impairment/papilloedema was significantly lower (all P<0.05). Compared with the good outcome group, the poor outcome group had significantly higher proportions of patients with seizures, dyskinesia, impaired consciousness, low Glasgow Coma Scale score, and brain parenchymal damage as well as higher D-dimer, total cholesterol and low density lipoprotein cholesterol levels, sites of thrombus involvement were more common in the superior sagittal and straight sinuses, and significantly lower proportions of patients with headache and lower albumin levels on admission (all P<0.05). Multivariate logistic regression analysis showed that visual impairment/papilloedema (odds ratio [ OR] 0.119, 95% confidence interval [ CI] 0.030-0.473; P=0.002) and brain parenchymal damage ( OR 1.341, 95% CI 1.042-1.727; P=0.023) were independently associated with a delay in anticoagulation treatment, and a delay in anticoagulation treatment ( OR 6.102, 95% CI 1.185-30.504; P=0.030) and D-dimer level on admission ( OR 1.299, 95% CI 1.141-1.480; P<0.001) were the independent predictors of poor outcome in patients with CVST. Conclusions:Visual impairment/papilloedema and absence of brain parenchymal damage on cranial imaging are the independent risk factors for delay in anticoagulation in patients with CVST. The delay in anticoagulation is strongly associated with the poor outcome in patients with CVST.
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Vascular cognitive impairment (VCI) is a progressive cognitive impairment caused by cerebrovascular disease or vascular risk factors. It is the second common type of cognitive impairment after Alzheimer's disease. VCI can be caused by a variety of signal and metabolic pathways. Its core mechanism is that cerebrovascular disease destroys the neurovascular unit composed of neurons, glial cells, and cerebrovascular endothelial cells. This article summarizes and discusses the known mechanisms of VCI, in order to deepen the understanding of the molecular pathological process of VCI and provide ideas for its prevention and treatment.
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Objective:To study the relationship between somatization symptoms and body mass index (BMI), sleep and cognitive function in patients with depression.Methods:A total of 119 patients with depression were selected from January to December in 2019.According to the score of patient health questionnaire-15(PHQ15), they were divided into mild somatization group ( n=75) and moderate severe somatization group ( n=44). Hamilton depression scale-24(HAMD-24), patient health questionnaire-15, Pittsburgh sleep quality index(PSQI) and Montreal cognitive assessment(MoCA) were used to evaluate all subjects.SPSS 23.0 software was used for data analysis.Independent sample t-test was used to compare BMI, sleep and cognitive function scores between the two groups.Pearson correlation analysis was used to study the correlation between somatization symptoms and sleep quality and cognitive function. Results:There were significant differences in BMI((21.70±3.09)kg/m 2, (23.31±3.51)kg/m 2), PSQI((12.56±4.37), (14.37±3.72)), sleep quality(1.87±0.86), (2.21±0.80)), sleep disorder ((1.24±0.59), (1.65±0.53))and daytime dysfunction((2.45±0.81), (2.77±0.48)) between the two groups ( t=-3.783--2.133, all P<0.05), but no difference was found in cognition ( P>0.05). Correlation analysis showed that after controlling HAMD, PHQ-15 was positively correlated with PSQI, sleep quality, sleep disorder, daytime dysfunction and language score in MoCA ( r=0.205-0.298, all P<0.05). Conclusion:The severity of somatization in patients with depression is related to BMI, sleep quality, sleep disorder, daytime dysfunction and language function, suggesting that they may play an important role in the pathogenesis of depression with somatization.
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Cognitive impairment includes several clinical processes from mild cognitive impairment to dementia, and now it has been a serious public health problem, as there is no effective treatment, it has caused a heavy economic and psychological burden on the family and society, therefore, it seems important to find effective intervention means.Vitamin D is an essential nutrient element for the human body, more and more evidences show that it also participates in many extraskeletal biological reactions, such as nervous system regulatory processes, in addition to calcium and phosphorus metabolism.Several researches have revealed that Vitamin D deficiency is associated with impaired cognition, the mechanisms mediating this link are poorly understood, what's more, for further clinical application, we need to solve the problems like choosing the suitable populations and drug dosage, therefore, this article summarizes and analyzes the effects of serum Vitamin D levels on the cognitive function of different populations, the research progress of Vitamin D intervention research and its possible mechanism of action, hoping to provide references for the clinical application of Vitamin D in the treatment of cognitive impairment.The results show that Vitamin D deficiency is related to the decline of cognitive function in different populations, and Vitamin D can improve cognitive function through reducing Aβ toxicity, anti-inflammatory and anti-oxidative stress and other mechanisms, its supplementation is expected to be an important measure of treating cognitive impairment, in the future, large-scale longitudinal cohort studies are needed to determine the optimal dosage and duration of treatment.
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Chronic pain is a public health concern of desiderate to be solved, and analgesics is not always successful and may be difficult to tolerate in clinic.Studies have suggested that the development of chronic pain involves alterations in multiple brain regions.Central modulation mechanisms, especially those soliciting the prefrontal cortex and its related brain regions, may play an important role.Non-pharmacological therapies such as transcranial direct current stimulation, transcranial repetitive magnetic stimulation and cognitive behavior therapy have emerged to be effective interventions of great potential for chronic pain in recent years.Hereby the research progress was reviewed on the neural modulation effect of prefrontal cortex in non-pharmacological treatment of chronic pain, focusing on the related changes in brain structure and function, to further explore the underlying mechanism of pain modulation, and provide theoretical basis to optimize non-pharmacological treatment of chronic pain.
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Migraine is the most common type of primary headache with disabling brain dysfunction. The prevalence of the migraine in Chinese population is 9.3%, and the ratio of female to male is 3∶1, which seriously affect people′s quality of life. Depression is one of the most common psychiatric disorders in migraine comorbidity. Compared with non-migraine patients, the risk of depression comorbidity in migraine patients is more than 2.5 times higher. The frequency and severity of migraine are closely related to depressive symptoms. Depressive symptoms have different effects on headache-related pain signal transduction, which is susceptible to neuroendocrine network disorders in the process of transmission from thalamus to cortex. Neuroendocrine network plays an important role in the depression of migraine comorbidity. Therefore, exploring the pathogenesis of neuroendocrine network in comorbidity provides a theoretical basis for screening more suitable depressive drugs for migraine comorbidity.
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Depression is a common complication after stroke.It is often associated with disability,cognitive impairment,and increased mortality.This article reviews the epidemiology,risk factors,predictive factors,and pathophysiology mechanisms of post-stroke depression.
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Flavonoids are widely used today in the treatment of ischemic stroke. The therapeutic effects and functions of flavonoids are, therefore, generating more and more interest.
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Objective To analyse the spectral patterns of complementarity determining region 3 (CDR3) length distribution of T lymphocyte receptor beta chain variable (TRBV) gene families in infiltrating T cells of the liver tissues and the peripheral blood samples of patients with chronic hepatitis B (CHB) in order to evaluate the characteristics of T cell clonal expansion. Methods The spectral patterns drift of TRBV gene families (the monoclonal/oligoclonal TCR β T cells) in the peripheral blood and hepatic tissues from 11 cases of CHB patients were analyzed by the real-time fluorescence quantitative reverse transcription polymerase chain reaction (FQ-PCR) with DNA melting curve analysis, and abnormal rates of TRBV gene families were compared between CHB patients and healthy control. The comparison of rates was done by chi square test. Results The gene melting spectral pattern of 26 TRBV families of the 11 CHB patients, no matter in the peripheral blood or hepatic tissue, showed either a single peak or prominent melting peaks, even disappeared for certain TRBV families. The abnormal rate of TRBV gene families in the hepatic tissues was significantly higher than that in the peripheral blood samples (x2 = 23. 246, P<0. 01). What is more interesting was that some parts of TRBV families were identical in both the peripheral blood and the hepatic tissue in certain patients. TCR BV13.1, TCR BV17 and TCR BV22 fragments were found to be restricted used in both the peripheral blood and hepatic tissue by some CHB patients. Conclusions T cells in the peripheral blood and the hepatic tissues of CHB patients can develop clonal expansion to some extent.Parts of TRBV families are restricted used in the peripheral blood and hepatic tissue in some CHB patients, which offers a foundation for further studying the common specific spectral drift patterns of TRBV CDR3 gene in CHB patients.
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Objective To study the effects of methylmercury chloride(MMC) on protein kinase C(PKC) activities in rat developing cerebellum.Methods The animals in experimental groups were fed standard rat chow with(0.75 mg) MMC(ExpⅠ),1.5 mg MMC(ExpⅡ) and 3.0 mg MMC(ExpⅢ)respectively for 90 d before gestation to(30 d) post parturition.Cerebella of pups from each group on postnatal days(PND) 3,7,17,21 and 30 were dissected. All the samples were separated into cytosol and membrane subcellular fractions and assayed for PKC activity by the improved method from Takai′s.Results Membrane and cytosolic PKC activities of pups′ cerebella from certain experimental groups were significantly higher than those of corresponding control group,PKC activities of rats from ExpⅡ,ExpⅢ and PND 3,7,14 in ExpⅠwere significantly higher than those in control group((P
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Objective To study the inhibitory effect of methylmercury chloride(MMC) on rat C6 glioma cells in vitro.Methods The rat C6 glioma cells were cultivated in vitro and divided into control group and MMC-treated group(0.08-10.00 ?mol?L-1 MMC were divided into 8 groups with concentration gradient).MTT assay was performed to evaluate the proliferation inhibitory effect and cytotoxicity effect of MMC with different concentrations on cultured rat C6 glioma cells,and flow cytometry was used to assess the effects of MMC treatment on cell apoptosis and cell cycle in rat C6 glioma cells.Results 1.25,2.50,5.00 and 10.00 ?mol?L-1 MMC could inhibit the proliferation of cultured rat C6 glioma cells in vitro,the viabilities of MMC treated C6 glioma cells were significantly lower than those in control group(P
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Objective To study the anti-neuroglioma effect of methyl-mercuric chloride(MMC) by observing the morphological changes of apoptotic neuroglioma cells induced with MMC in rats with brain neuroglioma.Methods The rat models of neuroglioma were established,and divided into two groups.The rats in experimental group were lavaged with MMC 1 week after injected with C6 glioma cells,10 mg?kg-1every day,the rats in control group were treated with sodium chloride at the same dose.24 d after inoculation all rats were sacrificed except natural death,the brain tissues were obtained,and the pathohistological changes were observed under light microscope and transmission electron microscope.Results The macropathological result showed that the tumor volume in experimental group was smaller than that in control group.Under light microscope,in experimental group the growth density of C6 ghioma cells was lower than that in control group,and the apoptotic cells with smaller volume and karyopyknosis were found.The result of transmission electron microscope showed that in experimental group,the glioma cells had some changes such as karyopyknosis,chromoplasm margination,nuclear fragmentation and vacuolar degeneration and so on.Conclusion MMC has inhibitory effect on the proliferation of C6 glioma in rats in vivo,its mechanism may be related to inducing the apoptosis of neuroglioma cells.
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Objective To study the inhibitory effect of triethyltin chloride(TETC) on proliferation of rat C6 glioma cells in vitro and its mechanism and provide basis for research on TETC in treatment for glioma.Methods MTT assay was performed to determine the inhibitory rate of 0.5,1.0 and 2.0 ?mol?L-1 TETC on rat C6 glioma cells for 24 and 48 h.The changes of nucleus of C6 glioam cells treated with 0.5,1.0 and 2.0 ?mol?L-1 TETC for 48 h were observed by fluorescent microscope.Flow cytometry was used to assess the effects of 0.5,1.0 and 2.0 ?mol?L-1 TETC on cell cycle and apoptosis in rat C6 glioma cells for 48 h.Results 0.5,1.0 and 2.0 ?mol?L-1 TETC inhibited the proliferation of C6 glioma cells in vitro,and the inhibitory rates were 7.92%,9.51%,19.03% and 15.62%,36.16%,41.92% in 24 h TETC treated group and 48 h TETC treated group,respectively.The inhibitory rate of TETC on C6 glioma cells determined by MTT assay increased in a dose-dependent and time-dependent manner,and there were significant differences of the inhibitory rates at 48 h between control and various doses groups as well as between various doses groups(P
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Objective To study the inhibitory effects of triethyltin chloride(TETC) on proliferation and the morphological changes of rat C6 glioma cells in vivo.Methods C6 glioma cells were autotransplanted into 16 Wistar rats,and the rats were divided into experiment group and control group.TETC was injected into each rat through intraperitoneal route at the dose of 1 mg?kg-1?d-1 and the injection lasted 4 d in experiment group,and the physiological saline was injected into each rat in the same way as experiment group in control group.The weights of C6 glioma were measured and the proliferation rate of the tumor was calculated after 14 d.The morphological changes of C6 glioma cells were observed by HE staining and electron microscope.Results The weight of C6 glioma in TETC group was lighter than that in control group(P
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<p><b>OBJECTIVE</b>To observe trinucleotide repeat number, (CTG)n in the 3'-untranslated region of the myotonic protein kinase (MTPK) gene in a clinically suspected woman with myotonic dystrophy (DM) family history and her abortus, in order to confirm the necessity of exerting antenatal examination in patients or suspected individuals with DM family history.</p><p><b>METHODS</b>Long Expand Template polymerase chain reaction (PCR) system was used to analyze CTG trinucleotide repeat numbers located in the 3' untranslated region of MTPK on chromosome 19q13.2-3 in both peripheral white cells and muscles of the suspected mother and the other two DM patients in the family. The tissues of her abortus and blood of a health woman were detected, too.</p><p><b>RESULTS</b>CTG repeats in both peripheral white cells and muscles of the suspected mother and the tissue of abortus were higher than normal range of CTG repeat number. There is no significant difference between blood and muscle samples. High CTG repeats were detected in blood and muscles of the typical DM members in the family, but in the blood sample of control, CTG repeats is normal.</p><p><b>CONCLUSION</b>CTG trinucleotide analyses and antenatal examination should be done in pregnant with a DM family history, in order to reduce the birth rate of DM offspring.</p>