Post-stroke arrhythmia could be a potential predictor for post-stroke depression.

Post-stroke depression (PSD) is regarded as the consequence of multiple contributors involving the process of cognition, mood and autonomic system, with the specific mechanism unclear yet. As a common type of stroke-heart syndromes, post-stroke arrhythmia shared some common pathogenesis with PSD. We presumed that post-stroke arrhythmia might be an early distinguishable marker for the presence of PSD and aimed to verity their association in this study. Patients with first-ever ischemic stroke were enrolled. The presence of post-stroke ectopic arrhythmia and the symptoms of arrhythmia were recorded with anti-arrhythmia drugs prescribed when necessary. Patients were followed up 3 months later to identify their presence and severity of PSD using Hamilton Depression Scale (HAMD) and also presence and severity of arrhythmia. Characteristics including the prevalence of various types of arrhythmias were compared between PSD and non-PSD groups. The HAMD scores were compared between patients with and without arrhythmia in PSD group. Logistic regression was used to identify the independent predictor of PSD. Patients with PSD had higher prevalence of post-stroke arrhythmia especially newly-detected arrhythmia, symptomatic arrhythmia and poor-controlled arrhythmia. In PSD group, patients of post-stroke arrhythmia had higher scores of HAMD than those without arrhythmia. Presence of newly-detected, symptomatic and poor-controlled arrhythmias were independent predictor of PSD. post-stroke arrhythmia especially newly-detected arrhythmia and symptomatic arrhythmia could be an early predictor of PSD. Successful control of arrhythmia was associated with reduced prevalence and severity of PSD.

Ginsenoside Rg1 Improves Inflammation and Autophagy of the Pancreas and Spleen in Streptozotocin-Induced Type 1 Diabetic Mice.

Background: Ginsenoside Rg1 (Rg1) is one of the key bioactive components of the precious Traditional Chinese Medicine that has been used to treat diabetes in China. Ginsenosides have been reported to protect diabetics from tissue damage, inflammation, and insulin resistance. Type 1 diabetes (T1D) is an organ-specific autoimmune disease that occurred frequently among adolescents over the world, its development was related to inflammation and ß-cells immunodeficiency. The aim of this study is to explore the biological mechanism of Rg1 on inflammation and autophagy of ß-cells in T1D and its therapeutic potential. Methods: The model of T1D mice was established by injecting Streptozotocin (STZ) (55 mg/kg) or citric acids once a day for 5 days and from the fourth day of injection, mice were administered with Rg1 (20 mg/kg) or saline by gavage once a day for 12 days. Hematoxylin-eosin staining, immunofluorescence, ELISA, quantitative real-time PCR, and Western blot were used to observe the histopathological changes, inflammatory factor levels, and autophagy markers after administration of ginsenoside Rg1. Results: Compared to the T1D mice, Rg1 improved the weight (p < 0.05) and blood glucose (p < 0.01) of mice, advanced the injury and apoptosis of ß-cells in islets (p < 0.01), and markedly inhibited the protein expression degrees of CD45, CXCL16, ox-LDL, and TF in the pancreas and spleens (p < 0.01), also activated the degrees of insulin in serum (p < 0.01). Besides, in T1D mice' pancreas and spleen, Rg1 markedly repressed the IL-1ß, TNF-α, and NOS2 mRNA levels (p < 0.05 or p < 0.01), inhibited the CXCL16, NF-κB, and TF proteins (p < 0.05 or p < 0.01), while elevating the ratio of LC3 II/I (p < 0.01) and P62 (p < 0.05) protein level. Conclusions: This study proved that Rg1 protected mice against T1D possibly by improving islet injury and tissue inflammation, raising serum insulin, and tissue autophagy marker.

Ginsenoside Rg1 Ameliorates Pancreatic Injuries via the AMPK/mTOR Pathway in vivo and in vitro.

Background: The main propanaxatriol-type saponin found in ginseng (Panax ginseng C. A. Mey), ginsenoside Rg1 (G-Rg1), has bioactivities that include anti-inflammatory, antioxidant, and anti-diabetic properties. This study aimed to investigate the effects of G-Rg1 on streptozotocin (STZ)-induced Type 1 Diabetes mellitus (T1DM) mice and the insulin-secreting cell line in RIN-m5F cells with high-glucose (HG) treatment. Methods: The STZ-induced DM mice model was treated with G-Rg1 alone or combined with 3-Methyladenine (3-MA, an autophagy inhibitor)/rapamycin (RAPA, an autophagy activator) for 8 weeks, and levels of glucose and lipid metabolism, histopathological changes, as well as autophagy and apoptosis of relevant markers were estimated. In vitro, the HG-induced RIN-m5F cells were treated with G-Rg1, 3-MA, and Compound C (CC), an AMPK inhibitor, or their combinations to estimate the influences on cell apoptosis, autophagy, and AMPK/mTOR pathway-associated target gene levels. Results: G-Rg1 treatment attenuated glucose and lipid metabolism disorder and pancreatic fibrosis in diabetic mice. In addition, subdued autophagy and p-AMPK protein expression, and enhanced p-mTOR protein expression and apoptosis levels in TIDM mice and HG-induced RIN-m5F cells were ameliorated by G-Rg1 treatment. Furthermore, these anti-apoptosis effects of G-Rg1 were partially abolished by 3-MA and CC. Conclusion: Our findings revealed that G-Rg1 exhibits strong anti-apoptosis ability in pancreatic tissues of type 1 diabetic mice and HG-induced RIN-m5F cells, and the mechanisms involved in activating AMPK and inhibiting mTOR-mediated autophagy, indicating that G-Rg1 may have the therapeutic and preventive potential for treating pancreatic injury in diabetic patients.

The etiologies of post-stroke depression: Different between lacunar stroke and non-lacunar stroke.

OBJECTIVES: Depression is common after both lacunar stroke and non-lacunar stroke and might be associated with lesion locations as proven by some studies. This study aimed to identify whether lesion location was critical for depression after both lacunar and non-lacunar strokes. METHODS: A cohort of ischemic stroke patients was assigned to either a lacunar stroke group or a non-lacunar stroke group after a brain MRI scan. Neurological deficits and treatment response was evaluated during hospitalization. The occurrence of depression was evaluated 3 months later. Logistic regressions were used to identify the independent risk factors for depression after lacunar and non-lacunar stroke respectively. RESULTS: 83 of 246 patients with lacunar stroke and 71 of 185 patients with non-lacunar stroke developed depression. Infarctions in the frontal cortex, severe neurological deficits, and a high degree of handicap were identified as the independent risk factors for depression after non-lacunar stroke, while lesion location was not associated with depression after lacunar stroke. CONCLUSION: The main determinants for depression after lacunar and non-lacunar stroke were different. Lesion location was critical only for depression after non-lacunar stroke.

The etiologies of post-stroke depression: Different between lacunar stroke and non-lacunar stroke

Abstract Objectives: Depression is common after both lacunar stroke and non-lacunar stroke and might be associated with lesion locations as proven by some studies. This study aimed to identify whether lesion location was critical for depression after both lacunar and non-lacunar strokes. Methods: A cohort of ischemic stroke patients was assigned to either a lacunar stroke group or a non-lacunar stroke group after a brain MRI scan. Neurological deficits and treatment response was evaluated during hospitalization. The occurrence of depression was evaluated 3 months later. Logistic regressions were used to identify the independent risk factors for depression after lacunar and non-lacunar stroke respectively. Results: 83 of 246 patients with lacunar stroke and 71 of 185 patients with non-lacunar stroke developed depression. Infarctions in the frontal cortex, severe neurological deficits, and a high degree of handicap were identified as the independent risk factors for depression after non-lacunar stroke, while lesion location was not associated with depression after lacunar stroke. Conclusion: The main determinants for depression after lacunar and non-lacunar stroke were different. Lesion location was critical only for depression after non-lacunar stroke.

Genome editing of CCR5 by AsCpf1 renders CD4+T cells resistance to HIV-1 infection.

BACKGROUND: The chemokine receptor CCR5 is one of the co-receptor of HIV-1 infection. People with homozygous CCR5Δ32 deletion resist HIV-1 infection, which makes the CCR5 an important target for HIV-1 gene therapy. Although the CRISPR/Cas9 has ever been used for HIV-1 study, the newly developed CRISPR/AsCpf1 has never been utilized in HIV-1 co-receptor disruption. The CRISPR/Cpf1 system shows many advantages over CRISPR/Cas9, such as lower off-target, small size of nuclease, easy sgRNA design for multiplex gene editing, etc. Therefore, the CRISPR/Cpf1 mediated gene editing will confer a more specific and safe strategy in HIV-1 co-receptor disruption. RESULTS: Here, we demonstrated that CRISPR/AsCpf1 could ablate the main co-receptor of HIV-1 infection-CCR5 efficiently with two screened sgRNAs via different delivery strategies (lentivirus, adenovirus). The edited cells resisted R5-tropic HIV-1 infection but not X4-tropic HIV-1 infection compared with the control group in different cell types of HIV-1 study (TZM.bl, SupT1-R5, Primary CD4+T cells). Meanwhile, the edited cells exhibited selective advantage over unedited cells while under the pressure of R5-tropic HIV-1. Furthermore, we clarified that the predicted off-target sites of selected sgRNAs were very limited, which is much less than regular using sgRNAs for CRISPR/Cas9, and no evident off-target was observed. We also showed that the disruption of CCR5 by CRISPR/AsCpf1 took no effects on cell proliferation and apoptosis. CONCLUSIONS: Our study provides a basis for a possible application of CCR5-targeting gene editing by CRISPR/AsCpf1 with high specific sgRNAs against HIV-1 infection.

Statin Pretreatment Might Be Associated with Decreased Myocardial Injury After Ischemic Stroke.

BACKGROUND: Myocardial injury is a complication of stroke associated with unfavorable outcome, with the elevation of cardiac troponin as the most sensitive marker. In this study, we aimed at investigating the association between statin pretreatment and poststroke myocardial injury. METHODS: Six hundred seventy-one patients diagnosed as acute ischemic stroke were enrolled. According to the histories of statin pretreatment before stroke, patients were categorized into nonstatin (n = 474) and statin groups (n = 197), with the latter further divided into low-dosage, standard-dosage, and high-dosage subgroups according the dosages of statins. The level of troponin-T was tested and troponin-T level ≥14 ng/l was identified to indicate the presence of myocardial injury. The level of troponin-T and the prevalence of myocardial injury was compared between groups. Logistic regression was used to identify the effect of statin pretreatment for the presence of post-stroke myocardial injury. RESULTS: Statin users had lower levels of troponin-T after stroke, with the level of troponin-T being the lowest in the high-dosage subgroup. The results of logistic regression showed that statin pretreatment and high-dosage statin were independent protective factors for the elevation of troponin-T levels. CONCLUSIONS: Statin pretreatment might be associated with the decreased myocardial injury after ischemic stroke.

[Design of Multifunctional Automated External Defibrillator Based on STM32].

This paper presents a design of multifunctional portable automated external defibrillator based on STM32F103VC SCM. The defibrillator mainly realizes the defibrillation and ECG analysis function, and according to the clinical actual need, increases information storage and transmission function, query of local records, the function of synchronous LCD display and voice prompt in the defibrillation process. The device uses the defibrillating electrodes to measure body resistance, ECG and so on. We detailedly researched and achieved the discharge module of biphasic defibrillation apparatus based on the damping of two order discharge circuit, and finished the real-time LCD display and voice prompt modules of defibrillation information based on the control of PIC24FJ256DA210 chip.

[Research and Design of a System for Detecting Automated External Defbrillator Performance Parameters].

OBJECTIVES: In order to regularly detect the performance parameters of automated external defibrillator (AED), to make sure it is safe before using the instrument, research and design of a system for detecting automated external defibrillator performance parameters. METHODS: According to the research of the characteristics of its performance parameters, combing the STM32's stability and high speed with PWM modulation control, the system produces a variety of ECG normal and abnormal signals through the digital sampling methods. RESULTS: Completed the design of the hardware and software, formed a prototype. CONCLUSIONS: This system can accurate detect automated external defibrillator discharge energy, synchronous defibrillation time, charging time and other key performance parameters.

Steady copropagation mode of laser pulse and plasma wave.

Stimulated Raman scattering is investigated using a nonperturbative method. The existence of steady copropagation modes of laser field and plasma wave is discussed. The plasma wave strength is analyzed through its relation with the total energy of the laser-plasma system. It is found that at a sufficiently high laser intensity there exist stable copropagating modes with non-zero-strength plasma waves. The strength of plasma wave in a stable steady copropagation mode is found to have an exact expression in terms of the frequency, the wave vector of the plasma wave and the laser intensity.