HIV-1 Vpu induces neurotoxicity by promoting Caspase 3-dependent cleavage of TDP-43.

Despite the efficacy of highly active antiretroviral therapy in controlling the incidence and mortality of AIDS, effective interventions for HIV-1-induced neurological damage and cognitive impairment remain elusive. In this study, we found that HIV-1 infection can induce proteolytic cleavage and aberrant aggregation of TAR DNA-binding protein 43 (TDP-43), a pathological protein associated with various severe neurological disorders. The HIV-1 accessory protein Vpu was found to be responsible for the cleavage of TDP-43, as ectopic expression of Vpu alone was sufficient to induce TDP-43 cleavage, whereas HIV-1 lacking Vpu failed to cleave TDP-43. Mechanistically, the cleavage of TDP-43 at Asp89 by HIV-1 relies on Vpu-mediated activation of Caspase 3, and pharmacological inhibition of Caspase 3 activity effectively suppressed the HIV-1-induced aggregation and neurotoxicity of TDP-43. Overall, these results suggest that TDP-43 is a conserved host target of HIV-1 Vpu and provide evidence for the involvement of TDP-43 dysregulation in the neural pathogenesis of HIV-1.

Density-dependent species interactions modulate alpine treeline shifts.

Species interactions such as facilitation and competition play a crucial role in driving species range shifts. However, density dependence as a key feature of these processes has received little attention in both empirical and modelling studies. Herein, we used a novel, individual-based treeline model informed by rich in situ observations to quantify the contribution of density-dependent species interactions to alpine treeline dynamics, an iconic biome boundary recognized as an indicator of global warming. We found that competition and facilitation dominate in dense versus sparse vegetation scenarios respectively. The optimal balance between these two effects was identified at an intermediate vegetation thickness where the treeline elevation was the highest. Furthermore, treeline shift rates decreased sharply with vegetation thickness and the associated transition from positive to negative species interactions. We thus postulate that vegetation density must be considered when modelling species range dynamics to avoid inadequate predictions of its responses to climate warming.

Effects of excess sodium consumption on arterial function in C57BL/6 mice.

Excess sodium consumption contributes to arterial dysfunction in humans. The C57BL/6 strain of mice has been used to identify mechanisms by which arterial dysfunction occurs after excess sodium consumption. However, there are concerns that C57BL/6 mice have strain-specific resistance to high-sodium (HS) diet-induced hypertension. To address this concern, we performed a meta-analysis to determine if excess sodium consumption in C57BL/6 mice induces arterial dysfunction. Databases were searched for HS versus standard diet studies that measured arterial function [i.e., systolic blood pressure (BP), endothelium-dependent dilation (EDD), and central arterial stiffness] in C57BL/6 mice. A total of 39 studies were included, demonstrating that the HS condition resulted in higher systolic BP than control mice with a mean difference of 9.8 mmHg (95% confidence interval [CI] = [5.6, 14], P < 0.001). Subgroup analysis indicated that the systolic BP was higher in HS compared with the control condition when measured during night compared with daytime with telemetry (P < 0.001). We also identified that the difference in systolic BP between HS and control was ∼2.5-fold higher when administered through drinking water than through food (P < 0.001). A total of 12 studies were included, demonstrating that the HS condition resulted in lower EDD than control with a weighted mean difference of -12.0% (95% CI = [-20.0, -4.1], P = 0.003). It should be noted that there was considerable variability across studies with more than half of the studies showing no effect of the HS condition on systolic BP or EDD. In summary, excess sodium consumption elevates systolic BP and impairs EDD in C57BL/6 mice.NEW & NOTEWORTHY C57BL/6 mice are perceived as resistant to high-sodium diet-induced arterial dysfunction. This meta-analysis demonstrates that excess sodium consumption elevates blood pressure and impairs endothelium-dependent dilation in C57BL/6 mice. Nighttime measurements show more pronounced blood pressure elevation. In addition, sodium administration via drinking water, compared with food, induces a greater blood pressure elevation. These findings may be influenced by outlier studies, as the majority of studies showed no adverse effect of excess sodium consumption on arterial function.

The association between serum S100ß levels and prognosis in acute stroke patients after intravenous thrombolysis: a multicenter prospective cohort study.

BACKGROUND: S100ß is a biomarker of astroglial damage, the level of which is significantly increased following brain injury. However, the characteristics of S100ß and its association with prognosis in patients with acute ischemic stroke following intravenous thrombolysis (IVT) remain unclear. METHODS: Patients in this multicenter prospective cohort study were prospectively and consecutively recruited from 16 centers. Serum S100ß levels were measured 24 h after IVT. National Institutes of Health Stroke Scale (NIHSS) and hemorrhagic transformation (HT) were measured simultaneously. NIHSS at 7 days after stroke, final infarct volume, and modified Rankin Scale (mRS) scores at 90 days were also collected. An mRS score ≥ 2 at 90 days was defined as an unfavorable outcome. RESULTS: A total of 1072 patients were included in the analysis. The highest S100ß levels (> 0.20 ng/mL) correlated independently with HT and higher NIHSS at 24 h, higher NIHSS at 7 days, larger final infarct volume, and unfavorable outcome at 3 months. The patients were divided into two groups based on dominant and non-dominant stroke hemispheres. The highest S100ß level was similarly associated with the infarct volume in patients with stroke in either hemisphere (dominant: ß 36.853, 95% confidence interval (CI) 22.659-51.048, P < 0.001; non-dominant: ß 23.645, 95% CI 10.774-36.516, P = 0.007). However, serum S100ß levels at 24 h were more strongly associated with NIHSS scores at 24 h and 3-month unfavorable outcome in patients with dominant hemisphere stroke (NIHSS: ß 3.470, 95% CI 2.392-4.548, P < 0.001; 3-month outcome: odds ratio (OR) 5.436, 95% CI 2.936-10.064, P < 0.001) than in those with non-dominant hemisphere stroke (NIHSS: ß 0.326, 95% CI  - 0.735-1.387, P = 0.547; 3-month outcome: OR 0.882, 95% CI 0.538-1.445, P = 0.619). The association of S100ß levels and HT was not significant in either stroke lateralization group. CONCLUSIONS: Serum S100ß levels 24 h after IVT were independently associated with HT, infarct volume, and prognosis in patients with IVT, which suggests the application value of serum S100ß in judging the degree of disease and predicting prognosis.

Complying with ISO 26262 and ISO/SAE 21434: A Safety and Security Co-Analysis Method for Intelligent Connected Vehicle.

A cyber-physical system (CPS) integrates communication and automation technologies into the operational processes of physical systems. Nowadays, as a complex CPS, an intelligent connected vehicle (ICV) may be exposed to accidental functional failures and malicious attacks. Therefore, ensuring the ICV's safety and security is crucial. Traditional safety/security analysis methods, such as failure mode and effect analysis and attack tree analysis, cannot provide a comprehensive analysis for the interactions between the system components of the ICV. In this work, we merge system-theoretic process analysis (STPA) with the concept phase of ISO 26262 and ISO/SAE 21434. We focus on the interactions between components while analyzing the safety and security of ICVs to reduce redundant efforts and inconsistencies in determining safety and security requirements. To conquer STPA's abstraction in describing causal scenarios, we improved the physical component diagram of STPA-SafeSec by adding interface elements. In addition, we proposed the loss scenario tree to describe specific scenarios that lead to unsafe/unsecure control actions. After hazard/threat analysis, a unified risk assessment process is proposed to ensure consistency in assessment criteria and to streamline the process. A case study is implemented on the autonomous emergency braking system to demonstrate the validation of the proposed method.

High-salt diet augments systolic blood pressure and induces arterial dysfunction in outbred, genetically diverse mice.

Excess salt consumption contributes to hypertension and arterial dysfunction in humans living in industrialized societies. However, this arterial phenotype is not typically observed in inbred, genetically identical mouse strains that consume a high-salt (HS) diet. Therefore, we sought to determine the effects of HS diet consumption on systolic blood pressure (BP) and arterial function in UM-HET3 mice, an outbred, genetically diverse strain of mice. Male and female UM-HET3 mice underwent a low-salt [LS (1% NaCl)] or HS (4% NaCl) diet for 12 wk. Systolic BP and aortic stiffness, determined by pulse wave velocity (PWV), were increased in HS after 2 and 4 wk, respectively, compared with baseline and continued to increase through week 12 (P < 0.05). Systolic BP was higher from weeks 2-12 and PWV was higher from weeks 4-12 in HS compared with LS mice (P < 0.05). Aortic collagen content was ∼81% higher in HS compared with LS (P < 0.05), whereas aortic elastin content was similar between groups (P > 0.05). Carotid artery endothelium-dependent dilation (EDD) was ∼10% lower in HS compared with LS (P < 0.05), endothelium-independent dilation was similar between groups (P > 0.05). Finally, there was a strong relationship between systolic BP and PWV (r2 = 0.40, P < 0.05), as well as inverse relationship between EDD and systolic BP (r2 = 0.21, P < 0.05) or PWV (r2 = 0.20, P < 0.05). In summary, HS diet consumption in UM-HET3 mice increases systolic BP, which is accompanied by aortic stiffening and impaired EDD. These data suggest that outbred, genetically diverse mice may provide unique translational insight into arterial adaptations of humans that consume an HS diet.NEW & NOTEWORTHY Excess salt consumption is a contributor to hypertension and arterial dysfunction in humans living in industrialized societies, but this phenotype is not observed in inbred, genetically identical mice that consume a high-salt (HS) diet. This study reveals that a HS diet in outbred, genetically diverse mice progressively increases systolic blood pressure and induce arterial dysfunction. These data suggest that genetically diverse mice may provide translational insight into arterial adaptations in humans that consume an HS diet.

Therapeutic strategies targeting the endothelial glycocalyx.

PURPOSE OF REVIEW: This review will highlight recent studies that have examined the endothelial glycocalyx in a variety of health conditions, as well as potential glycocalyx-targeted therapies. RECENT FINDINGS: A degraded glycocalyx is present in individuals that consume high sodium diet or have kidney disease, diabetes, preeclampsia, coronavirus disease 2019 (COVID-19), or sepsis. Specifically, these conditions are accompanied by elevated glycocalyx components in the blood, such as syndecan-1, syndecans-4, heparin sulfate, and enhanced heparinase activity. Impaired glycocalyx barrier function is accompanied by decreased nitric oxide bioavailability, increased leukocyte adhesion to endothelial cells, and vascular permeability. Glycocalyx degradation appears to play a key role in the progression of cardiovascular complications. However, studies that have used glycocalyx-targeted therapies to treat these conditions are scarce. Various therapeutics can restore the glycocalyx in kidney disease, diabetes, COVID-19, and sepsis. Exposing endothelial cells to glycocalyx components, such as heparin sulfate and hyaluronan protects the glycocalyx. SUMMARY: We conclude that the glycocalyx is degraded in a variety of health conditions, although it remains to be determined whether glycocalyx degradation plays a causal role in disease progression and severity, and whether glycocalyx-targeted therapies improve patient health outcomes. Future studies are warranted to investigate therapeutic strategies that target the endothelial glycocalyx.

Primary intracranial lymphomas-incidence and survival: a population-based study.

Biopsy is recommended for patients with primary intracranial lymphoma to confirm the diagnosis, but the effect of tumor resection is still controversial. We conducted this retrospective study to better understand the epidemiology of primary intracranial lymphoma in the USA and explore the relationship between surgical resection and prognosis. Data regarding primary intracranial lymphoma, including incidence, were extracted from the SEER database. We analyzed the difference in incidence between different groups of people. We explored the effect of surgery on the survival of patients by the Kaplan-Meier method and evaluated the possible prognostic indicators by multivariate Cox proportional hazards models. The incidence significantly increased with age. The non-Hispanic Asian or Pacific Islander population exhibited the highest incidence, and the incidence was significantly higher in males than females. A total of 6428 cases were included in the cohort study, and most of the patients were diagnosed in the sixth to seventh decade of life. Sixty percent of tumors were supratentorial tumors. Surgery, especially total resection, significantly improved overall survival and cancer-specific survival. The survival of female patients, patients diagnosed before reaching 60 years of age, patients diagnosed after 2010, and patients with supratentorial lymphomas was better than that of their counterparts. The survival of patients with diffuse large B-cell lymphoma was worse than that of their counterparts. We conducted a comprehensive retrospective analysis of patients with primary intracranial lymphoma. We analyzed the difference in incidence between different groups of people. Surgery significantly improved overall and cancer-specific survival. The results of our research can help clinicians and patients better understand the epidemiology and management of primary intracranial lymphoma.

Acute cardiovascular responses to unilateral bicep curls with blood flow restriction.

A consensus on the acute cardiovascular responses to low intensity (LI) resistance exercise (RE) combined with blood flow restriction (BFR) has not yet been reached. This study was designed to compare acute cardiovascular responses to a single bout of LIRE, high intensity (HI) RE, and LIRE with BFR in physically active young males. Participants completed 3 RE sessions in random order, where each session consists of 4 sets of unilateral dumbbell bicep curls. Cardiovascular hemodynamics were measured at baseline and right after each set of RE. Aortic augmentation index (AIx) was significantly higher after set 2,3,4 of RE in LI + BFR session compared to LI session (P < 0.05). Brachial systolic blood pressure (SBP), heart rate (HR), brachial rate pressure product (RPP), and central RPP responses did not differ between LI and LI + BFR sessions (P > 0.05). HI session had a higher central SBP, brachial RPP, central RPP, and aortic AIx compared to LI session after each set of RE (P < 0.05), but not brachial SBP (P > 0.05). Taken together, this study showed that LIRE combined with BFR acutely augmented aortic stiffness, as also observed in HI session, but myocardial oxygen consumption was only higher in HI session when compared to LI session. Thus, although BFR did not exaggerate cardiovascular responses nor cause extra myocardial oxygen consumption, it should be prescribed with caution when control of acute aortic stiffening is necessary during RE.

[Shenfu Injection alleviates sepsis-associated lung injury by regulating HIF-1α].

Shenfu Injection(SFI) is praised for the high efficacy in the treatment of septic shock. However, the precise role of SFI in the treatment of sepsis-associated lung injury is not fully understood. This study investigated the protective effect of SFI on sepsis-associated lung injury by a clinical trial and an animal experiment focusing on the hypoxia-inducing factor-1α(HIF-1α)-mediated mitochondrial autophagy. For the clinical trial, 70 patients with sepsis-associated lung injury treated in the emergency intensive care unit of the First Affiliated Hospital of Zhengzhou University were included. The levels of interleukin(IL)-6 and tumor necrosis factor(TNF)-α were measured on days 1 and 5 for every patient. Real-time quantitative polymerase chain reaction(RT-qPCR) was performed to determine the mRNA level of hypoxia inducible factor-1α(HIF-1α) in the peripheral blood mononuclear cells(PBMCs). For the animal experiment, 32 SPF-grade male C57BL/6J mice(5-6 weeks old) were randomized into 4 groups: sham group(n=6), SFI+sham group(n=10), SFI+cecal ligation and puncture(CLP) group(n=10), and CLP group(n=6). The body weight, body temperature, wet/dry weight(W/D) ratio of the lung tissue, and the pathological injury score of the lung tissue were recorded for each mouse. RT-qPCR and Western blot were conducted to determine the expression of HIF-1α, mitochondrial DNA(mt-DNA), and autophagy-related proteins in the lung tissue. The results of the clinical trial revealed that the SFI group had lowered levels of inflammatory markers in the blood and alveolar lavage fluid and elevated level of HIF-1α in the PBMCs. The mice in the SFI group showed recovered body temperature and body weight. lowered TNF-α level in the serum, and decreased W/D ratio of the lung tissue. SFI reduced the inflammatory exudation and improved the alveolar integrity in the lung tissue. Moreover, SFI down-regulated the mtDNA expression and up-regulated the protein levels of mitochondrial transcription factor A(mt-TFA), cytochrome c oxidase Ⅳ(COXⅣ), HIF-1α, and autophagy-related proteins in the lung tissue of the model mice. The findings confirmed that SFI could promote mitophagy to improve mitochondrial function by regulating the expression of HIF-1α.

Microcirculatory and glycocalyx properties are lowered by high-salt diet but augmented by Western diet in genetically heterogeneous mice.

Many individuals in industrialized societies consume a high-salt, Western diet(WD); however, the effects of this diet on microcirculatory properties and glycocalyx barrier function are unknown. Young genetically heterogeneous male and female mice underwent 12 wk of normal chow (NC) diet, NC diet with 4% salt (NC4%), Western diet (WD), or WD with 4% salt (WD4%). Microcirculatory properties and glycocalyx barrier function were evaluated in the mesenteric microcirculation, using an intravital microscope equipped with an automated capture and analysis system. Total microvascular density summed across 4- to 25-µm microvessel segment diameters was lower in NC4% than in NC and WD (P < 0.05). Perfused boundary region (PBR), a marker of glycocalyx barrier function, averaged across 4- to 25-µm microvessel segment diameters was similar between NC and NC4%, as well as between WD and WD4% (P > 0.05). PBR was lower in WD and WD4% than in NC and NC4% (P < 0.05), indicating augmented glycocalyx barrier function in WD and WD4%. There were strong, inverse relationships between PBR and adiposity and blood glucose (r = -0.44 to -0.61, P < 0.05). In summary, NC4% induces deleterious effects on microvascular density, whereas WD augments glycocalyx barrier function. Interestingly, the combination of high-salt, Western diet in WD4% resulted in lower total microvascular density like NC4% and augmented glycocalyx barrier function like WD. These data suggest distinct microcirculatory adaptations to high-salt and Western diets that coincide when these diets are combined in young genetically heterogeneous male and female mice.NEW & NOTEWORTHY Many individuals in industrialized societies consume a combination of high-salt and Western diet; however, the effects of this diet on microcirculatory and glycocalyx properties are unknown. This study reveals that a high-salt diet lowers microcirculatory and glycocalyx properties, whereas a Western diet augments glycocalyx barrier function and thickness. Taken together, these data indicate that there are distinct microcirculatory adaptations to high-salt and Western diets that coincide when high-salt and Western diets are combined.

Enhanced bacterial inactivation by activated carbon modified with nano-sized silver oxides: Performance and mechanism.

In this study, nano-sized silver oxides were loaded on activated carbon (nAg2O/AC) through a facile impregnation-calcination method for enhanced bacterial inactivation from drinking water, in which Escherichia coli (E. coli) was used as target bacteria. XRD and SEM characterization confirmed that nano-sized Ag2O particles (50-200 nm) were successfully prepared and uniformly distributed on the surfaces and pores of AC. Due to the structural reducing groups of AC, surface-bound Ag(I) was partially converted to Ag in the nAg2O matrix and the resulted Ag could sterilize E. coli directly. More importantly, surface-bound Ag could catalyze O2 and H2O to generate reactive oxygen species (ROS) for oxidation sterilization, thus significantly enhanced the inactivation efficiency from 0.8 log10 CFU/mL (nAg2O control) and 0.2 log10 CFU/mL (AC control) to 6.0 log10 CFU/mL in the nAg2O/AC system. The inactivation process was highly pH-dependent, and neutral pH was favorable for sterilization. A sterilization efficiency of 5.2 log10 CFU/mL could still be achieved after 5 running cycles, indicating stable sterilization performance of nAg2O/AC. In addition, the nAg2O/AC also exhibited excellent renewability since a sterilization efficiency of 5.8 log10 CFU/mL was obtained after nAg2O being stripped and reloaded on the AC. These results demonstrated that nAg2O-modified AC is an efficient material for sterilization in water treatment.

KLF15 negatively regulates cardiac fibrosis by which SDF-1ß attenuates cardiac fibrosis in type 2 diabetic mice.

Diabetic cardiomyopathy (DCM) is a serious diabetic complication that lacks effective preventive or therapeutic approaches. Wild-type and Klf15 knockout (Klf15-KO) mice were fed with either high fat diet (HFD, 60% kcal from fat) or normal diet (ND, 10% kcal from fat) for 3 months and then injected with streptozotocin or vehicle, to induce type 2 diabetes (T2D). All T2D and age-matched control mice were treated with or without SDF-1ß at 5 mg/kg body-weight twice a week and also continually received HFD or ND for 3 months. At the end of 6-month study, after cardiac functions were measured, mice were euthanized to collect heart tissue. For in vitro mechanistic study, H9c2 cells were exposed to palmitate to mimic in vivo condition of T2D. SDF-1ß prevented T2D-induced cardiac dysfunction and fibrosis and T2D-down-regulated KLF15 expression in wild-type diabetic heart tissue. However, the preventive effects of SDF-1ß on both KLF15 expression and fibrosis was abolished, with partial cardiac protection in Klf15-KO/T2D mice. These results demonstrate partial KLF15-dependence for SDF-1ß's cardiac fibrotic protection from T2D, but not on SDF-1ß's protective effects on T2D-induced cardiac dysfunction. Further study showed that SDF-1ß inhibited palmitate-induced cardiomyocyte fibrosis through its receptor CXCR7-mediated activation of p38ß MAPK signaling pathway.

Effective immobilization of hexavalent chromium from drinking water by nano-FeOOH coating activated carbon: Adsorption and reduction.

In this study, nano α-FeOOH (nFeOOH, 100-500 nm) was coated onto activated carbon (nFeOOH@AC) through a dipping means for enhanced Cr(VI) immobilization from drinking water. The nFeOOH@AC significantly improved the Cr(VI) removal from 19.9% (AC control) to 93.4%. XPS spectra and chromium speciation demonstrated that about 90% of adsorbed Cr(VI) was converted to Cr(III) by the nFeOOH@AC, accompanying with a reduction-oxidation of Fe3+/Fe2+ in the nFeOOH matrix due to electrons delivering between AC and surface-bound Cr(VI). The resultant Cr(III) subsequently reacted with Fe(III) to generate stable (CrχFe1-χ)(OH)3 precipitates, leading to a much lower Cr(III) release of 7.5% back to solution by the nFeOOH@AC as compared to the AC control of 33.8%, indicating that the nFeOOH@AC had a prospective potential for Cr(VI) immobilization and decreased Cr residue in treated drinking water. Results from column experiment also showed that the nFeOOH@AC afforded a 3.5 times higher capacity for Cr(VI) immobilization and a 3.4 times longer life-span than the pristine AC. Besides, Cr(VI) immobilization by the nFeOOH@AC was a pH-dependent process and the adsorbed Cr on the nFeOOH@AC could be readily desorbed with acetic acid. The disabled nFeOOH@AC could be refreshed by recoating nFeOOH particles with the above dipping method after stripping all the iron oxides with hydrochloric acid. This study demonstrated that nFeOOH coating is an efficient approach to enhance Cr(VI) elimination by AC during drinking water treatments.

Effects of corona virus disease-19 control measures on air quality in North China.

Corona virus disease-19 (COVID-19) has substantially reduced human activities and the associated anthropogenic emissions. This study quantifies the effects of COVID-19 control measures on six major air pollutants over 68 cities in North China by a Difference in Relative-Difference method that allows estimation of the COVID-19 effects while taking account of the general annual air quality trends, temporal and meteorological variations, and the spring festival effects. Significant COVID-19 effects on all six major air pollutants are found, with NO2 having the largest decline (-39.6%), followed by PM2.5 (-30.9%), O3 (-16.3%), PM10 (-14.3%), CO (-13.9%), and the least in SO2 (-10.0%), which shows the achievability of air quality improvement by a large reduction in anthropogenic emissions. The heterogeneity of effects among the six pollutants and different regions can be partly explained by coal consumption and industrial output data.

Different EPHX1 methylation levels in promoter area between carbamazepine-resistant epilepsy group and carbamazepine-sensitive epilepsy group in Chinese population.

BACKGROUND: Epigenetics underlying refractory epilepsy is poorly understood. DNA methylation may affect gene expression in epilepsy patients without affecting DNA sequences. Herein, we investigated the association between Carbamazepine-resistant (CBZ-resistant) epilepsy and EPHX1 methylation in a northern Han Chinese population, and conducted an analysis of clinical risk factors for CBZ-resistant epilepsy. METHODS: Seventy-five northern Han Chinese patients participated in this research. 25 cases were CBZ-resistant epilepsy, 25 cases were CBZ-sensitive epilepsy and the remaining 25 cases were controls. Using a CpG searcher was to make a prediction of CpG islands; bisulfite sequencing PCR (BSP) was applied to test the methylation of EPHX1. We then did statistical analysis between clinical parameters and EPHX1 methylation. RESULTS: There was no difference between CBZ-resistant patients, CBZ-sensitive patients and healthy controls in matched age and gender. However, a significant difference of methylation levels located in NC_000001.11 (225,806,929.....225807108) of the EPHX1 promoter was found in CBZ-resistant patients, which was much higher than CBZ-sensitive and controls. Additionally, there was a significant positive correlation between seizure frequency, disease course and EPHX1 methylation in CBZ-resistant group. CONCLUSION: Methylation levels in EPHX1 promoter associated with CBZ-resistant epilepsy significantly. EPHX1 methylation may be the potential marker for CBZ resistance prior to the CBZ therapy and potential target for treatments.

The Detection of the Negative Effects of Interictal Epileptiform Discharges on Cognition: An Event-Related Potential Study.

Evidence from a neuropsychological test revealed that interictal epileptiform discharges (IEDs) may have significant impact on cognitive performance. Sometimes, neuropsychological tests may not be sensitive to detection of mild cognitive changes. We applied P300 and mismatch negativity (MMN) to detect mild cognitive changes caused by small amount of IEDs. Sixty-seven adult epilepsy patients and participants were divided into six groups according to different IEDs index. The patients with IED index greater than 7.5% showed longer latency and lower amplitude in the test of P300 and MMN than patients with IED index less than 7.5%, which indicated mild impaired cognitive function. The negative effect of IED index greater than 10% on cognitive has been found by neuropsychological test, whereas the mild negative effect of IED index greater than 7.5% has only been found by P300 and MMN. So, P300 and MMN may be more sensitive than neuropsychological tests to detect mild cognitive impairment caused by IEDs.

Tonic Seizure as a Different Seizure Type Presented in Autoimmune Epilepsy Caused by Systemic Lupus Erythematosus.

The diagnosis of autoimmune epilepsy is often challenging, and may be misdiagnosed as epileptic disorders or viral encephalitis. Autoimmune epilepsy has a strong association with other autoimmune diseases, especially systemic lupus erythematosus (SLE). In addition, autoimmune epilepsy was reported to present with complex partial seizure (CPS), simple partial seizure (SPS), and secondarily generalized tonic-clonic seizure (sGTCS). In our case, we present a different seizure type of tonic seizure in autoimmune epilepsy caused by SLE, which has not been reported, and it will provide with a new understanding of autoimmune epilepsy. A 17-year-old Chinese girl was diagnosed as having SLE for 1 month but with no epilepsy history. After this admission, she presented with different seizure types. Then EEG, magnetic resonance imaging, and lumbar puncture were performed. We have found generalized tonic seizure and excluded CNS infection and lupus encephalopathy. After antiepileptic therapy, no improvement has been found in seizure control. According to the previous history, clinical manifestation, and relevant examinations, we have made a clinical diagnosis of autoimmune epilepsy (tonic seizure) and SLE has been confirmed again by the immunological test. After the hormonotherapy, anti-inflammatory, and anti-tuberculosis therapy, the tonic seizure decreased significantly, and patient's consciousness improved. Autoimmune epilepsy should call the attentions of the clinicians, especially when the patient presented with SLE. Tonic seizure has not been described in autoimmune epilepsy before, which was different from other seizures reported, such as SPS, CPS, and sGTCS, and may bring a new insight into the autoimmune epilepsy.

Preparation and Characterization of Bletilla striata Polysaccharide/Polylactic Acid Composite.

Polylactic acid (PLA) is limited in its application due to its high price, high brittleness and low glass-transition temperature. Modification methods are currently used to overcome these shortcomings. In this study, Bletilla striata polysaccharide (BSP) was blended with PLA by a solvent method. DMA data showed that the BSP/PLA film had a higher glass-transition temperature, and the glass-transition temperature of the film showed an extreme value of 68 °C when the proportion of the chalk polysaccharide was 0.8%. TG data indicates that the composite film material has good thermal stability. Tensile tests show that the composite film is improved in rigidity and elasticity compared to the pure PLA film. The blending modification of PLA with white peony polysaccharide not only reduces the cost of PLA, but also improves the thermal and mechanical properties of PLA.

Preparation, In Vivo and In Vitro Release of Polyethylene Glycol Monomethyl Ether-Polymandelic Acid Microspheres Loaded Panax Notoginseng Saponins.

In order to enrich the types of Panax notoginseng saponins (PNS) sustained-release preparations and provide a new research idea for the research and development of traditional Chinese medicine sustained-release formulations, a series of Panax notoginseng saponins microspheres was prepared by a double emulsion method using a series of degradable amphiphilic macromolecule materials polyethylene glycol monomethyl ether-polymandelic acid (mPEG-PMA) as carrier. The structure and molecular weight of the series of mPEG-PMA were determined by nuclear magnetic resonance spectroscopy (1 HNMR) and gel chromatography (GPC). The results of the appearance, particle size, drug loading and encapsulation efficiency of the drug-loaded microspheres show that the mPEG10000-PMA (1:9) material is more suitable as a carrier for loading the total saponins of Panax notoginseng. The particle size was 2.51 ± 0.21 µm, the drug loading and encapsulation efficiency were 8.54 ± 0.16% and 47.25 ± 1.64%, respectively. The drug-loaded microspheres were used for in vitro release and degradation experiments to investigate the degradation and sustained release behaviour of the drug-loaded microspheres. The biocompatibility of the microspheres was studied by haemolytic, anticoagulant and cytotoxicity experiments. The pharmacological activity of the microspheres was studied by anti-inflammatory and anti-tumour experiments. The results showed that the drug-loaded microspheres could be released stably for about 12 days and degraded within 60 days. At the same time, the microspheres had good biocompatibility, anti-inflammatory and anti-tumour activities.