Emodin activates BK channel in vascular smooth muscle cells and relaxes the interlobar renal artery of rat.

AIM: The purpose of this study was to investigate the mechanical and electrophysiological effects of emodin on BK channels in the IRASMCs, of the rat. METHODS: Isolated interlobar renal artery was used for vascular reactivity measurements using a pressure myograph system. Electrophysiological measurements of single vascular smooth muscle cells were conducted using whole-cell and cell-attached patch-clamp recording. Laser scanning confocal microscope technology was used to measure cytosolic calcium ion signals. KEY RESULTS: Emodin relaxed the interlobar renal artery and enhanced the outward currents amplitude of IRASMCs in a concentration-dependent manner, and IbTX inhibited these emodin-induced outward currents. Incubation of IRASMCs in a calcium ion free medium for 30 min decreased the observed effects of emodin on IRASMCs membrane currents. Furthermore, the application of nimodipine, an L-Type calcium ion channel blocker, ryanodine, a ryanodine receptor modifier, and heparin, an IP3 receptor blocker, decreased the emodin-induced BK channel currents, respectively. BAPTA-AM, a selective calcium ion chelator, abolished the emodin-induced BK channel currents. Emodin repolarized cytomembrane and enhanced BK channel open probabilities and elevated cytosolic calcium ion concentration. CONCLUSION: The vasorelaxant effect of emodin on vessels is mediated through the activation of BK channels.

Contrasting responses in growth, photosynthesis and hydraulics of two subtropical tree species to cadmium contamination as affected by elevated CO2 and nitrogen addition.

Plant growth, photosynthesis, and hydraulics are affected by heavy metals but also by elevated atmospheric CO2 concentration (e[CO2]) and nitrogen (N) deposition. However, few studies have investigated the response of woody species to the combined effects of these three factors. We conducted an open-top chamber experiment with two common subtropical trees (Acacia auriculiformis and Syzygium hainanense) to explore the effects of cadmium (Cd)-contamination, e[CO2], and N addition on plant eco-physiological traits. We found that the growth of A. auriculiformis was insensitive to the treatments, indicating that it is a Cd-tolerant and useful afforestation species. For S. hainanense, in contrast, e[CO2] and/or N addition offset the detrimental effects of Cd addition by greatly increasing plant biomass and reducing the leaf Cd concentration. We then found that e[CO2] and/or N addition offset the detrimental Cd effects on S. hainanense biomass by increasing its photosynthetic rate, its N concentration, and the efficiency of its stem water transport network. These offsetting effects of e[CO2] and/or N addition, however, came at the expense of reduced xylem hydraulic safety resulting from wider vessels, thinner vessel walls, and therefore weaker vessel reinforcement. Our study suggests that, given future increases in global CO2 concentration and N deposition, the growth of Cd-tolerant tree species (like A. auriculiformis) will be probably stable while the growth of Cd-sensitive tree species (like S. hainanense) might be enhanced despite reduced hydraulic safety. This also suggests that both species will be useful for afforestation of Cd-contaminated soils given future global change scenarios.

Remediation of petroleum hydrocarbons-contaminated soil: Analysis based on Chinese patents.

Increasing soil petroleum hydrocarbons (PHs) pollution have caused world-wide concerns. The removal of PHs from soils mainly involves physical, chemical, biological processes and their combinations. To date, most reviews in this field based on research articles, but limited papers focused on the integration of remediation technologies from the perspective of patents. In this study, 20-years Chinese patents related to the remediation of soil PHs were comprehensively analyzed. It showed an increasing number of patent applications and the patents' quantity were positively correlated with Chinese GDP over the years, suggesting the more the economy developed the more environmental problems and corresponding solutions emerged. In addition, chemical technologies were mostly used in a combination to achieve faster and better effects, while the physical technologies were often used alone due to high costs. In all PHs remediation techniques, bacteria-based bioremediation was the most used from 2000 to 2019. Bacillus spp. and Pseudomonas spp. were the most used bacteria for PHs treatment because these taxa were widely harboring functions such as biosurfactant production and hydrocarbon degradation. The future research on joint technologies combining microbial and physicochemical ones for better remediation effect and application are highly encouraged.

The relationship between serum levels of S-100ß and anxiety symptoms in patients with acute stroke.

BACKGROUND: Post-stroke anxiety (PSA) is a common neuropsychiatric affective disorder occurring after a stroke. Animal experiments have indicated that serum S-100ß levels are closely related to anxiety disorder. No clinical study has been done to explore the relationship between serum S-100ß levels and anxiety symptoms in patients with acute stroke. The aim of our study was to investigate the association between serum S-100ß levels and PSA. METHODS: One hundred twenty-six acute stroke patients were recruited and followed up for 1 month. Blood samples were collected within 24 h after admission. The levels of serum S-100ß were measured by enzyme-linked immunosorbent assays. Patients with significant clinical symptoms of anxiety and a Hamilton Anxiety Rating Scale score >7 at 1 month after stroke were diagnosed as PSA. RESULTS: Serum S-100ß levels in the non-PSA group were lower than the PSA group (838.97 (678.20-993.59) ng/L vs. 961.87 (796.09-1479.59) ng/L, Z = -2.661, P = 0.008). In multivariate analyses, we found that decreased risk of PSA was associated with low tertile serum S-100ß levels (≤753.8 ng/L, OR 0.062, 95% CI 0.008-0.475, P = 0.007). CONCLUSIONS: Low serum S-100ß levels at admission may be associated with the decreased risk of PSA.

Physiological and proteomic analyses reveal the effects of exogenous nitrogen in diminishing Cd detoxification in Acacia auriculiformis.

Cadmium (Cd) has toxic effects on plants. Nitrogen (N), an essential element, is critical for plant growth, development and stress response. However, their combined effects on woody plants, especially in N-fixing tree species is still poorly understood. Our previous study revealed that the fast-growing Acacia auriculiformis showed strong Cd tolerance but the underlying mechanisms was not clear, which constrained its use in mine land reclamation. Herein, we investigated the physiological and proteomic changes in A. auriculiformis leaves to reveal the mechanisms of Cd tolerance and toxicity without N fertilizer (treatment Cd) and with excess N fertilizer (treatment CdN). Results showed that Cd tolerance in A. auriculiformis was closely associated with the coordinated gas exchange and antioxidant defense reactions under Cd treatment alone. Exogenous excessive N, however, inhibited plant growth, increased Cd concentrations, and weaken photosynthetic performance, thus, aggregated the toxicity under Cd stress. Furthermore, the aggregated Cd toxicity was attributed to the depression in the abundance of proteins, as well as their corresponding genes, involved in photosynthesis, energy metabolism (oxidative phosphorylation, carbon metabolism, etc.), defense and stress response (antioxidants, flavonoids, etc.), plant hormone signal transduction (MAPK, STN, etc.), and ABC transporters. Collectively, this study unveils a previously unknown physiological and proteomic network that explains N diminishes Cd detoxification in A. auriculiformis. It may be counterproductive to apply N fertilizer to fast-growing, N-fixing trees planted for phytoremediation of Cd-contaminated soils.

Effects of elevated CO2 concentration and nitrogen addition on the chemical compositions, construction cost and payback time of subtropical trees in Cd-contaminated mesocosm soil.

Rising atmospheric CO2 concentration ([CO2]) and nitrogen (N) deposition are changing plant growth, physiological characteristics and chemical compositions; however, few studies have explored such impacts in a heavy metal-contaminated environment. In this study, we conducted an open-top chamber experiment to explore the impacts of 2 years of elevated atmospheric [CO2] and N addition on the growth, physiological characteristics and chemical compositions of five subtropical tree species in a cadmium (Cd)-contaminated environment. Results showed that N addition significantly increased concentration of leaf N and protein in five tree species and also decreased payback time (PBT) and leaf carbon:nitrogen ratios and increased tree relative height growth rate (RGR-H) and basal diameter growth rate (RGR-B) in Liquidambar formosana Hance and Syzygium hainanense Chang et Miau. Elevated [CO2] increased leaf maximum photosynthetic rate (Amax) and concentration of total non-structural carbohydrates and shortened PBT to offset the negative effect of Cd contamination on RGR-B in Acacia auriculiformis A. Cunn. ex Benth. The combined effects of elevated [CO2] and N addition did not exceed their separate effects on RGR-H and RGR-B in Castanopsis hystrix Hook. f. & Thomson ex A. DC. and Cinnamomum camphora (L.) presl. The addition of N significantly increased the concentration of leaf Cd by 162.1% and 338.0%, and plant Cd bio-concentration factor by 464% and 861% in C. hystrix and C. camphora, respectively, compared with only Cd addition. Among the five tree species, the decrease in PBT and the increase in Amax, RGR-B and concentrations of leaf protein in response to N and Cd addition under elevated [CO2] were on average 86.7% higher in A. auriculiformis than other species, suggesting that the mitigation of the negative effects of Cd pollution by elevated [CO2] and N addition among five species was species-specific. Overall, we concluded that N addition and elevated [CO2] reduced Cd toxicity and increased the growth rate in A. auriculiformis, S. hainanense and L. formosana, while it maintained the growth rate in C. hystrix and C. camphora by differently increasing photosynthetic rate, altering the leaf chemical compositions and shortening PBT.

Effects of elevated CO2 concentration and nitrogen addition on foliar phosphorus fractions of Mikania micranatha and Chromolaena odorata under low phosphorus availability.

Invasive plants rapidly spread in habitats with low soil phosphorus (P) availability and have triggered a sharp decline in the diversity of native species. However, no studies have explored how widespread invasive species acclimate to low soil P availability via changing foliar P fractions, especially under elevated atmospheric CO2 concentrations ([CO2 ]) and nitrogen (N) deposition. Here, an open-top chamber experiment was conducted to explore the effect of nutrient addition and elevated [CO2 ] on leaf traits and foliar functional P fractions (i.e., Pi, metabolite P, lipid P, nucleic acid P, and residual P) of two aggressive invasive species (Mikania micranatha and Chromolaena odorata). We found that foliar N/P ratios were more than 20, and P addition significantly increased plant biomass. Both results indicated P-limited plant growth at our studied site. Elevated [CO2 ], N and N + P addition greatly increased plant biomass, photosynthetic rates, and photosynthetic P-use efficiency (PPUE) in invasive species, but PPUE decreased with increasing P addition. Nitrogen addition slightly decreased the concentration of leaf total P, decreased foliar residual P, but increased metabolite P concentrations in invasive species. Similar changes in foliar P fractions were found under N + P addition. Phosphorus addition increased foliar P concentrations, which was strongly correlated with an increase in metabolite P concentrations in invasive species. Elevated [CO2 ] alleviated these effects and increased PPUE. The present results suggest that future elevated [CO2 ] and N deposition allow the invasive species to acclimate to low soil P availability and support their successful invasion by greatly reducing P allocation to non-metabolite foliar P fractions (i.e., nucleic acid P and residual P) to meet their demand of metabolite P for photosynthesis and exhibit a high PPUE.

The Relationship of the Type of Intracerebral Hemorrhage to Early Disease Evolution and Long-Term Prognosis After r-tPA Thrombolysis.

To investigate the relationship of different subtypes of intracerebral hemorrhage (ICH) to early disease evolution and long-term prognosis in patients with acute cerebral infarction after intravenous recombinant tissue plasminogen activator(r-tPA). Seventy ischemic stroke patients treated with intravenous r-tPA who underwent computed tomography (CT) within 24 hours after thrombolysis were divided into 4 types (hemorrhagic infarction type 1 [HI-1], HI-2, parenchymal hemorrhage type 1 [PH-1], or PH-2 which according to the size of the hematoma and the presence or absence of space-occupying effect). Early evolution of the disease was observed by the change in the National Institutes of Health Stroke Scale (NIHSS) score within 24 hours after thrombolysis. The long-term prognosis was assessed by the modified Rankin Scale (mRS) score at the third month. There were 17 (24.3%) patients with ICH. Compared with patients in the non-ICH group, HI did not affect early neurological function or clinical outcome at the third month. PH-1 did not increase the risk of early neurological deterioration; however, PH-1 has a tendency to increase the risk of death at the third month (50% vs 11.3%, P = 0.090). PH-2 was significantly related to early neurological deterioration (66.7% vs 3.8%, P < 0.001) and mortality at the third month (50.0% vs 11.3%, P = 0.040). Patients with different subtypes of ICH after thrombolysis have different clinical outcomes. PH-2 is significantly associated with early neurological deterioration and increases mortality at the third month.

The therapeutic effects and safety of bright light therapy combined with escitalopram oxalate on insomnia in patients with poststroke depression.

INTRODUCTION: Bright light therapy (BLT) is known to treat depression and sleep disorders in clinical practice, but its efficacy on poststroke depression (PSD) has not been studied. OBJECTIVE: To investigate the therapeutic effects and safety of BLT combined with escitalopram oxalate (ESC) on insomnia in patients with PSD. METHODS: Ischemic stroke patients with depressive symptoms and a score of ≥8 on the Hamilton Depression Scale (HAMD-17) while meeting DSM-IV criteria were diagnosed as having PSD. A total of 112 PSD patients with symptoms of insomnia were randomly assigned to polytherapy (BLT plus ESC) and monotherapy (ESC only) groups. Each regimen continued for 6 weeks. The primary outcomes were a change in scores on the Pittsburgh Sleep Quality Index (PSQI) and a remission rate (PSQI ≤7 at the endpoint). The secondary outcomes included changes in the HAMD-17 and Barthel Index (BI) scores. Adverse effects were assessed by the Adverse Events Scale. RESULTS: The endpoint assessment included 106 patients (monotherapy, 54; polytherapy, 52). The mean changes in the PSQI scores for the monotherapy and polytherapy groups were 4.85 (1.47) and 5.87 (1.72) (P = 0.001), respectively. Compared to monotherapy, polytherapy improved PSQI remission rate (71.4% vs 50.0%; χ2 = 5.390; P = 0.020), and HAMD-17 score (6.70 [2.12] vs 4.75 [1.98]; P < 0.001). Both treatments improved BI score, with no statistical difference, and were well tolerated, with few significant differences in treatment-associated adverse events. CONCLUSION: BLT combined with ESC is effective and well tolerated for the treatment of PSD-associated insomnia.

Impact of sleep quality on post-stroke anxiety in stroke patients.

OBJECTIVE: To explore whether poor sleep is associated with post-stroke anxiety (PSA) in Chinese patients with acute ischemic stroke (AIS) and to verify whether poor sleep is a predictor of PSA. METHODS: A total of 327 patients with AIS were enrolled and followed up for 1 month. Sleep quality within 1 month before stroke was evaluated using the Pittsburgh Sleep Quality Index (PSQI) at admission. The patients were divided into the poor sleep group (PSQI > 7, n = 76) and good sleep group (PSQI ≤ 7, n = 251). One month after stroke, patients with obvious anxiety symptoms and a Hamilton Anxiety Scale score >7 were diagnosed with PSA. RESULTS: Eighty-seven patients (26.6%) were diagnosed with PSA. Compared to the good sleep quality group, the incidence of PSA in patients with poor sleep quality was higher (42.1% vs. 21.9%, p = .001). Poor sleep quality is more common in patients with PSA (35.6% vs. 18.8%, p = .001). A logistic regression analysis indicated that poor sleep quality was significantly associated with PSA (OR: 2.265, 95% CI: 1.262-4.067, p = .003). After adjusting for conventional and identified risk factors, poor sleep quality was found to be independently associated with PSA (OR: 2.676, 95% CI: 1.451-4.936, p = .001). CONCLUSIONS: Poor sleep quality before stroke was associated with PSA and may be an independent risk factor of PSA 1 month after AIS onset.

2-(-2-Benzofuranyl)-2-imidazoline reciprocally regulates Th17/Treg balance induced by ischemic stroke in rats.

Our group previously showed that 2-(-2-benzofuranyl)-2-imidazoline (2-BFI) is a potent neuroprotective agent in the treatment of ischemic stroke in rats. As its mode of action was not well defined, we determined if its therapeutic effect includes altering an immune response to experimental ischemic stroke in rats. In the current study, 2-BFI significantly reduced stroke-induced brain infarct volume and it also decreased neurological deficits. Its anti-immune effects were determined based on flow cytometry measurements of both the 2-BFI-induced changes in the Th17/ Treg cell balance ratio and ELISA measurements of proinflammatory IL-17A and anti-inflammatory IL-10 cytokine expression levels in the brain and peripheral blood following ischemic strokes. 2-BFI blunted the stroke-induced increases in this ratio, which resulted from suppression of the rises in the Th17 cell number whereas the proportion of Treg cells increased. Stroke also induced increases in IL-17A expression levels whereas the IL-10 expression levels declined. 2-BFI treatment inhibited the rises in IL-17A expression levels whereas the corresponding declines in IL-10 were suppressed by this agent. Therefore, one of the neuroprotective effects of 2-BFI in the treatment of cerebral strokes stems from its suppression of rises in the Th17/Treg balance along with corresponding changes in related cytokines modulating development of this condition.

High platelet-to-lymphocyte ratio are associated with post-stroke depression.

BACKGROUND: Post-stroke depression (PSD) is the most common psychological consequence among stroke patients, and inflammatory cytokines have cited as risk factors in PSD. We aimed to evaluate the predictive value of stratification of PLR (platelet-to-lymphocyte ratio), an inflammatory marker, in PSD patients. METHODS: A total of 363 acute ischemic stroke (AIS) patients were screened in the study and received 1-month follow-up. All of the patients were categorized into equal tertiles according to the number of patients and the distribution of PLR. PSD status was evaluated by 17-item Hamilton Depression Rating Scale at 1 month after stroke RESULTS: The optimal cut-off points of PLR were: (T1) 42.15-99.60, (T2) 99.72-127.92, (T3) 127.93-259.84. A total of 77 patients (21.2%) were diagnosed with PSD at 1-month follow-up. Significant differences were found between the PSD and non-PSD groups in PLR tertiles of patients (P < 0.001). After adjustment for conventional confounding factors, the odds ratio of PSD was 5.154 (95% CI, 1.933-13.739) for the highest tertile of PLR compared with the lowest tertile. In multiple-adjusted spline regression, continuously PLR showed linear relation with PSD risk after 95 (P < 0.001 for linearity). LIMITATIONS: We excluded patients with severe aphasia or serious conditions. In addition, the PLR was recorded only at admission, which limited us explore the correlation of the change of PLR over time with PSD CONCLUSIONS: Increased PLR at admission is a significant and independent biomarker to predict the development of PSD, and stratified PLR could strengthen the predictive power for PSD patients.

Impact of prediabetes on poststroke depression in Chinese patients with acute ischemic stroke.

OBJECTIVE: It is unknown whether prediabetes is a predictor of poststroke depression (PSD). We aimed to explore the relationship between prediabetes and PSD in Chinese patients with acute ischemic stroke. METHODS: This is a prospective cohort study, and a total of 358 patients with acute ischemic stroke were recruited and enrolled. Patients were divided into 3 groups: normal glucose group (NGT, n = 96), prediabetes group (preDM, n = 134, impaired fasting glucose (IFG), and/or impaired glucose tolerance (IGT) and/or HbA1c (A1c) 5.7%-6.4%), and the diabetes mellitus group (DM, n = 128). At 1 month after stroke, patients with a Hamilton Depression Scale score of ≥8 were diagnosed as PSD. RESULTS: In post hoc comparisons, the risk of PSD in patients with diabetes and prediabetes was higher than patients with NGT (37.5% vs 31.3% vs 14.6%, P = .001). Compared with NGT, the incidence rate of PSD in patients with prediabetes with HbA1c 5.7% to 6.4% and patients with prediabetes with IFG/IGT + HbA1c 5.7% to 6.4% was higher (35.3% vs 14.6%, 38.0% vs 14.6%; P = .006; P = .003, respectively). In logistic regression, prediabetes with HbA1c 5.7% to 6.4% and prediabetes with IFG/IGT + HbA1c 5.7% to 6.4% were a significant independent predictor of PSD after adjusting for potential confounding factors, with odd ratios of 1.731 and 1.978, respectively. CONCLUSIONS: Our study showed that prediabetes was associated with PSD and may predict its development at 1 month poststroke. In prediabetes subgroups, patients with HbA1c 5.7% to 6.4% were more likely to develop PSD compared to NGT and IFG/IGT groups.

Derivation and Validation of a Clinical Prediction Scale for Isolated Distal Deep Venous Thrombosis in Patients after Acute Ischemic Stroke.

BACKGROUND: Isolated distal deep venous thrombosis (IDDVT) is a common complication after ischemic stroke. However, there is a paucity of evidence regarding the clinical features and risk factors of IDDVT in patients with acute ischemic stroke. This study aimed to establish and validate a clinical prediction scale of IDDVT at an early stage of ischemic stroke development. METHODS: We retrospectively studied consecutive patients with stroke admitted to our neurology department between January and December 2016. Selected clinical variables were assessed by multivariable logistic regression to determine the independent risk factors for IDDVT. A prediction scale was developed and verified by the receiver operating characteristic curve. RESULTS: A total of 671 patients with ischemic stroke were included in the study, with 450 patients allocated into the derivation group and 221 patients into the validation group. A substantial proportion (22.1%) of patients developed IDDVT. A 16-point prediction scale (female gender = 2, older age [≥60 years] = 3, atrial fibrillation = 2, acute infection = 2, active cancer = 5, and higher [≥2.6 mmol/L] level of low-density lipoprotein = 2) derived from a multivariable logistic regression model was highly predictive of 10-day risk of IDDVT in both the validation group (c statistic = .70, 95% confidence interval [CI], .63-0.78, P < .0001) and the derivation group (c statistic = .68, 95% CI, .63-0.74, P < .0001). CONCLUSIONS: This prediction scale may help to identify patients with ischemic stroke who are at a higher risk of developing IDDVT.

Curcumin protects against stroke and increases levels of Notch intracellular domain.

OBJECTIVES: To investigate whether curcumin regulates Notch signaling to cause neuroprotection and neurogenesis after focal ischemia reperfusion injury. METHOD: Focal ischemia reperfusion injury was modeled in rats by occluding the middle cerebral artery. These animals were given either curcumin (300 mg/kg) or corn oil (vehicle) by intraperitoneal injection starting 1 h after stroke and continuing for 7 d. In parallel, sham-operated control animals received vehicle. All animals were killed on day 12. The different treatment groups were compared in terms of neurobehavioral deficits, BrdU incorporation, and levels of doublecortin (DCX) and Notch intracellular domain (NICD) using immunohistochemistry, immunofluorescence and Western blotting. RESULTS: Animals treated with curcumin showed significantly smaller neurobehavioral deficits than vehicle-treated animals after 3, 7, and 12 d of reperfusion (all p < 0.05). Tissue sections from curcumin-treated animals contained significantly greater numbers of BrdU-positive cells (p < 0.05) and BrdU/DCX-positive cells (p < 0.01), as well as significantly higher NICD levels (p < 0.01). CONCLUSION: Curcumin may protect from focal cerebral ischemia reperfusion injury as well as stimulate neurogenesis by activating the Notch signaling pathway.

Three-year prognosis of first-ever primary pontine hemorrhage in a hospital-based registry.

Our aim was to evaluate the mortality rate of primary pontine hemorrhage (PPH) and to determine the factors related to the prognosis. Limited data exist on the long-term prognosis and determinants of death in patients with PPH in China. Our study analyzed consecutive cases of first-ever PPH from April 2007 to March 2011 in a hospital-based stroke registry. Mortality rates during 30 day and 3 year follow-ups were analyzed. We used the Kaplan-Meier method to estimate the event rates and binary logistic regression analysis, and Cox proportional hazard regression analysis to identify predictors of short-term and long-term prognosis, respectively. A total of 76 patients were identified, 44 (57.89%) were men. Both 30 day and 3 year overall mortalities in men were higher than women but this different was not statistically significant. Coma on admission, hematoma ⩾ 4 mL and a massive hemorrhage were significantly related to 30 day mortality of PPH. Multivariate Cox proportional hazard regression revealed that coma on admission (hazard ratio [HR] 2.18; 95% confidence interval [CI] 1.16-4.13; p = 0.02) and hematoma ⩾ 4 mL (HR 2.23; 95% CI 1.25-3.96; p = 0.01) were independent predictors of 3 year mortality. In conclusion, the short-term mortality rate and factors related to the prognosis of Chinese patients with PPH are similar to those reported for other populations. A low Glasgow coma scale score on admission and a large hematoma volume may be related to poor 3 year prognosis after PPH.

Noncardiogenic stroke patients with metabolic syndrome have more border-zone infarction and intracranial artery stenosis.

BACKGROUND: Little is known about the clinical character of stroke patients with metabolic syndrome (MetS) in Chinese population. In this hospital-based cross-sectional study, we elucidated the prevalence of MetS among patients with acute noncardiogenic cerebral infarction from south China, the topographic infarction patterns in magnetic resonance imaging, and vascular angiography findings of stroke patients with MetS. METHODS: The patients with acute noncardiogenic stroke were clinically evaluated including waistline circumference, blood pressure, glycemia, serum triglyceride, high-density lipoprotein cholesterol level, magnetic resonance imaging, and angiography evaluation, including magnetic resonance angiography, computed tomography angiography, or digital subtraction angiography for intracranial (IC) and extracranial arteries. According to the National Cholesterol Education Program Adult Treatment Panel III criterion, the patients were classified into the MetS and non-MetS groups. RESULTS: Among 222 patients studied, the prevalence of MetS was 54.5%, and there were more women in the MetS group than in the non-MetS group (P < .05). Frequency of all the individual factors of MetS was higher in the MetS group than in the non-MetS group (P < .05). The lesion pattern of border-zone (BZ) infarction was more prevalent in MetS patients (P < .05). The frequency of IC artery stenosis was higher in the MetS group than in the non-MetS group (odds ratio [OR], 1.8; 95% confidence interval [CI], 1.0-3.0). After adjustment for age and gender, IC stenosis was significantly associated with large waistline circumference (OR, .95; 95% CI, .91-.99). CONCLUSIONS: According to our findings, MetS was of high prevalence in noncardiogenic stroke patients in China, and female patients were more likely to have MetS. The MetS patients tended to have more BZ infarctions and more IC artery stenosis than the non-MetS stroke patients.

Neurovascular protection conferred by 2-BFI treatment during rat cerebral ischemia.

Stroke is caused by vascular dysfunction and currently there are no effective therapeutics to stroke induced brain damage. In contrast to an intense emphasis on neuroprotection, relatively few studies have addressed means of vascular protection in cerebral ischemia. Here we discovered that the ligand to immidazolin receptor, 2-BFI, not only provided potent neuroprotection during middle cerebral artery occlusion in rat, which confirmed our previous reports, but also protected the integrity of the cerebral vasculature. Treatment with 2-BFI twice daily after the occlusion of the middle cerebral artery for 14 d significantly improved the neurological deficits, reduced brain infarction, and importantly, protected the cerebral vasculature as evidenced by the increased expression of an endothelial marker, von Willebrand factor, and better preservation of the cerebral vasculature, as viewed under a confocal microscope on rat brain perfused with FITC-labeled dextran. These results indicated that 2-BFI contributes to protection of neurovasculature. Understanding the molecular mechanisms could eventually lead to development of more effective therapies for stroke.

Attenuation of ischemia-induced rat brain injury by 2-(-2-benzofuranyl)-2-imidazoline, a high selectivity ligand for imidazoline I(2) receptors.

OBJECTIVE: The aim of this study was to determine whether 2-(2-benzofuranyl)-2-imidazoline, an imidazoline I(2) receptor ligand, could protect against cell death from brain injury and improve the functional outcome after focal cerebral ischemia in rats. METHODS: Transient focal ischemia was induced by suture occlusion of the middle cerebral artery. Rats were intraperitoneally treated with a vehicle, 2-(2-benzofuranyl)-2-imidazoline or idazoxan immediately after focal ischemia. Infarct volume was assessed by 2,3,5-triphenyltrazolium chloride staining and neurobehavioral deficits were monitored. The volume of cell death in the penumbra after ischemia was determined by immunostaining using anti-cleaved caspase-3 antibody and terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL). RESULTS: Both 2-(2-benzofuranyl)-2-imidazoline and idazoxan significantly improved the neurological score compared with the vehicle at 24 hours after focal ischemia. Treatment with 2-(2-benzofuranyl)-2-imidazoline or idazoxan also significantly reduced infarct volume and the number of both caspase-3- and TUNEL-positive cells in the penumbra compared with vehicle-treated rats (p<0.01 and p<0.05, respectively). CONCLUSION: The results suggest the neuroprotective role of 2-(2-benzofuranyl)-2-imidazoline and idazoxan in focal cerebral ischemia, and may therefore represent useful targets for developing new treatments for stroke.

Notch signaling and neurogenesis in normal and stroke brain.

Adult neuronal stem cells (NSCs) hold great promise for brain repair because of their unique location within the central nervous system, their potential to proliferate and to differentiate into all major neural lineages, and their ability to functionally incorporate into existing neuronal circuitry after stroke. Nevertheless, the ability to exploit these cells for therapeutic purposes is hampered by the lack of knowledge about the signals that control the generation of a functional neuron from adult NSCs after stroke, particularly in the aged brain. Therefore, to further define the regulatory mechanisms that underlie neurogenesis after stroke, it is critically important to develop future NSC-based repair strategies. Notch signaling defines a fundamental pathway controlling cell fate acquisition. Studies have shown that Notch signaling pathways play critical roles during the maintenance, proliferation, and differentiation of NSCs in the developing brain. Recent evidence shows that Notch1 signaling is conserved in the regulation of adult neurogenesis. Here we summarize current knowledge about the role of Notch signaling in the regulation of neurogenesis in the normal and stroke brain.