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The cerebral ischemic stroke is a major type of stroke characterized by brain injury, neurological deficits, and cognitive impairments, which accounts for increased disability and mortality worldwide. The present study focusses to investigate the therapeutic efficacy of ononin against the ischemic stroke induced by ischemia–reperfusion (I/R) injury via suppression of I/R injury stimulated neuroinflammation in rat model. Animals were separated into four groups as Sham, I/R induced, I/R + ononin pretreated (10 mg/kg body weight), and I/R + ononin pretreated (20 mg/kg body weight). The ischemic stroke was stimulated in animals by middle artery occlusion method as described previously. The infarct volume, brain edema, and neurological deficits were studied by standard methods. The oxidative stress markers like SOD, CAT, GSH, GSH-Px, Cu/Zn-SOD, Mn-SOD, MDA, and acetylcholinesterase were assessed by previously described methods. The contents of TNF-α, IL-1β, and IL-6 were assessed using assay kits. The in vitro studies were performed using SH-SY5Y neuroblastoma cells. The level of Ononin given at 10 and 20 mg/kg body weight resulted in increase in water content, reduced volume of infarct, improved neurological deficit score, and exerted its antioxidant, anti-inflammatory and neuroprotective efficacy against cerebral I/R injury-induced rats. Increase in proinflammatory cytokine expression was observed in cerebral I/R injury-stimulated rats. Oxygen glucose deprivation/ reoxygenation (OGD/R) injury showed reduction in cell viability of SH-SY5Y cells which was attenuated following treatment with ononin at varying concentrations. Ononin has reduced proinflammatory cytokine expression in vitro. Thus, ononin has successfully attenuated I/R injury-induced neuroinflammation in rats and thus minimized neuronal injury. Therefore, all the findings of the study depicts that ononin can thus be used as a beneficiary move toward treatment of cerebral I/R injury.

Background: Titanium dioxide (TiO2), consisting of nanoparticles and sub-microparticles, were widely used as food additive and consumed by people every day, which has aroused a public safety concern. Some studies showed TiO2 can be absorbed by intestine and then distributed to different tissues after oral intake, which is supposed to affect the content of various elements in the body whereas led to tissue damage. However, knowledge gaps still exist in the impact of TiO2 on the disorder of elemental homeostasis. Thus, this study aimed to explore the oral toxicity of TiO2 by assessing its influence on elemental homeostasis and tissues injury. Method: ICR mice were fed with normal feed, TiO2 nanoparticles (NPs)-mixed feed or TiO2 submicron particles (MPs)-mixed feed (1% mass fraction TiO2 NPs or MPs were mixed in commercial pellet diet) for 1, 3, and 6 months. Particles used in this study were characterized. The distribution of Ti and other 23 elements, the correlation among elements, and pathological change in the liver, kidney, spleen and blood cells of the mice was determined. Result: Ti accumulation only appeared in blood cells of mice treated with TiO2 MPs-mixed feed for 6 months, but TiO2 cause 12 kinds of elements (boron, vanadium, iron, cobalt, copper, zinc, selenium, sodium, calcium, magnesium, silicon, phosphorus) content changed in organ tissue. The changed kinds of elements in blood cells (6 elements), liver (7 elements) or kidney (6 elements) were more than in the spleen (1 element). The TiO2 NPs induced more elements changed in blood cells and liver, and the TiO2 MPs induced more elements changed in kidney. Significantly positive correlation between Ti and other elements was found in different organs except the liver. Organ injuries caused by TiO2 NPs were severer than TiO2 MPs. Liver exhibited obvious pathological damage which became more serious with the increase of exposure time, while kidney and spleen had slight damages. Conclusion: These results indicated long-time dietary intake of TiO2 particles could induce element imbalance and organ injury. The liver displayed more serious change than other organs, especially under the treatment with TiO2 NPs. Further research on the oral toxicity of TiO2 NPs should pay more attention to the health effects of element imbalances using realistic exposure methods.

Aims. The prognostic value of plasma D-dimer in patients with coronary artery disease (CAD) remains controversial. The study is aimed at investigating the relationship between plasma D-dimer levels and in-hospital heart failure (HF) in ST-segment elevation myocardial infarction (STEMI) patients who underwent primary percutaneous coronary intervention (pPCI). Methods. STEMI patients who underwent pPCI were enrolled in this study. Venous blood samples were collected from patients on admission before pPCI procedure. The study endpoint was the occurrence of in-hospital HF. The participants were divided into two groups according to plasma D-dimer levels and further compared baseline D-dimer levels between male and female. Logistic regression and receiver operating characteristic (ROC) curves were performed to evaluate the relationship of D-dimer and in-hospital HF. Results. A total of 778 patients were recruited in the study, of which 539 (69.3%) patients had normal D-dimer levels (≤0.5 mg/L) while 239 (30.7%) had increased D-dimer levels (>0.5 mg/L). The female patients have higher D-dimer levels and higher incident rate of in-hospital HF than that in male patients ( p < 0.001 ). The multivariate logistic regression model revealed that D-dimer was an independent predictor for in-hospital HF in overall population (adjusted odds ratio [OR]: 1.197, 95% CI: 1.003-1.429, and p = 0.046 ) and female patients (adjusted OR: 1.429, 95% CI: 1.083-1.885, and p = 0.012 ). Conclusion. Increased plasma D-dimer levels were an independent risk factor for incidence of in-hospital HF in STEMI patients who underwent pPCI, especially in female patients, which provides guidance for clinicians in identifying patients at high risk of developing HF and lowering their risk.

Purpose: To study the anti-inflammatory influence of dexmedetomidine (DEX) in mice with acute pancreatitis (AP), and to determine the underlying mechanism.Methods: A total of 75 healthy ICR male mice were randomly divided into control, mild acute pancreatitis (MAP), MAP+DEX, severe acute pancreatitis (SAP), and SAP+DEX groups, with 15 mice/group. Blood levels of inflammatory factors (TNF-α and IL-1β) and norepinephrine were assayed ineach group. Western blotting was used to assay the protein expressions of NLRP3 and norepinephrine transporter (NET) in the pancreatic tissue of each group.Results: The levels of inflammatory factors in the MAP+DEX group were markedly lower than those in the MAP group after 10 h of MAP induction (p < 0.01). Mice in MAP+DEX group had significantly lower expression of NLRP3 in pancreatic tissue, and significantly higher NET protein level, relative to the MAP mice. Following 10 h of SAP, concentrations of the inflammatory factors and the pancreatic expression of NLRP3 were lower in SAP+DEX-treated mice than in SAP mice, while NET protein was significantly higher in SAP mice (p < 0.01).Conclusion: DEX reduces the expressions of inflammation-related factors TNF-α and IL-1β, and inhibits inflammatory response in mice with AP via downregulation of NET protein expression via inhibition of NLRP3 and early sympathetic events. Keywords: Dexmedetomidine, NLRP3 inflammasome, Sympathetic nerve, Acute pancreatitis, Inflammatory response

Background In the present study, we aimed to examine the correlation of serum levels of MMP-9, ADMA, and sCD40L with the occurrence and severity of acute ischemic stroke. Methods All routines analyses were performed using a Cobas platform. MMP-9, ADMA, and sCD40L were measured using ELISA kit. Results Compared with the controls, the stroke group showed higher MMP-9,higher sCD40L and higher ADMA. There were significant positive correlations between the NIHSS scores and MMP-9, sCD40L and ADMA. Conclusions Our study indicated that serum levels of MMP-9, sCD40L, and ADMA are associated with ischemic stroke and are correlated with the NIHSS scores at admission.

Background and Purpose: This study aimed to analyze the association between hyperattenuated lesions (HALs) and postoperative intracranial hemorrhage (IH) and predict perioperative IH through quantitative analysis of HALs in acute ischemic stroke (AIS) with anterior large vessel occlusion (LVO) after endovascular therapy (ET).Materials and Methods: This retrospective, propensity-matched study enrolled AIS who received ET from a single-center registry study between August 2017 and May 2020. The enrolled patients were divided into two groups: IH and non-IH, by follow-up postoperative CT. The occurrences of HALs on immediate CT after ET were also recorded. The association between IH and HALs after propensity score matching (PSM) was determined by binary logistic regression models. The receiver operating characteristic (ROC) curve was used to determine the predictive value of the highest CT Hounsfield units (HU) value on immediate CT.Results: Initially, 1,418 patients who underwent digital subtraction angiography were reviewed and 114 AIS patients with immediate postoperative CT and follow-up CT after ET were enrolled. Forty-nine out of the 114 patients developed IH after therapy. After PSM analysis, patients with IH were more likely to have HALs on immediate CT (Odds Ratio, OR 11.9, P = 0.002, and 95% CI: 2.485–57.284). For 80 patients with HALs, ROC analysis of the highest CT value in the HALs territory showed that the cut-off value was 97 HU, the sensitivity was 70.21%, and the specificity was 81.82%.Conclusions: Patients with HALs after ET are more likely to have perioperative IH. The highest CT value in the HALs area might be used to predict IH.

Purpose: Radiation pneumonitis (RP) frequently occurs during a treatment course of chest radiotherapy, which significantly reduces the clinical outcome and efficacy of radiotherapy. The ability to easily predict RP before radiotherapy would allow this disease to be avoided.Methods and Materials: This study recruited 48 lung cancer patients requiring chest radiotherapy. For each participant, RNA sequencing (RNA-Seq) was performed on a peripheral blood sample before radiotherapy. The RNA-Seq data was then integrated into a genome-scale flux analysis to develop an RP scoring system for predicting the probability of occurrence of RP. Meanwhile, the clinical information and radiation dosimetric parameters of this cohort were collected for analysis of any statistical associations between these parameters and RP. A non-parametric rank sum test showed no significant difference between the predicted results from the RP score system and the clinically observed occurrence of RP in this cohort.Results: The results of the univariant analysis suggested that the tumor stage, exposure dose, and bilateral lung dose of V5 and V20 were significantly associated with the occurrence of RP. The results of the multivariant analysis suggested that the exposure doses of V5 and V20 were independent risk factors associated with RP and a level of RP ≥ 2, respectively. Thus, our results indicate that our RP scoring system could be applied to accurately predict the risk of RP before radiotherapy because the scores were highly consistent with the clinically observed occurrence of RP.Conclusion: Compared with the standard statistical methods, this genome-scale flux-based scoring system is more accurate, straightforward, and economical, and could therefore be of great significance when making clinical decisions for chest radiotherapy.

Background Previous work indicated that benzo[a]pyrene (B(a)P) exposure in utero might adversely affect neurodevelopment and cause Parkinson's Disease (PD)-like symptoms. However, the effect of utero exposure to B(a)P on PD-like α-synucleinopathy and the mechanism under are unclear. Objective The A53T human alpha-synuclein (α-syn) transgenic mice (M83+/−) were used in this study to gain insights into the role of B(a)P exposure in utero in the onset of α-syn pathology and neuronal damage. Method Timed-pregnant M83+/− dams were exposed to 1) corn oil (vehicle) or 2) 5 mg/kg bw/d B(a)P or 3) 20 mg/kg bw/d B(a)P at gestational day 10–17 by oral gavage and then the SNCA transcription, α-syn accumulation and aggregation, neuroinflammation and nigral dopaminergic neurodegeneration of 60-day-old pups were evaluated. Result SNCA mRNA and α-syn protein expression in the midbrain of 60 days adult mice were found to be remarkably elevated after B(a)P exposure in utero, the protein degradation capacity was injured (in 20 mg/kg dose group) and α-syn aggregation could be observed in the substantia nigra (SN); Enhanced Iba1 expression in the midbrain and microglial activation (in 20 mg/kg dose group) in the SN were also figured out; Besides, dopaminergic neurons in the SN of 60 days adult mice were significantly decreased. Conclusions Our findings demonstrated that B(a)P exposure in utero could exacerbate α-syn pathology and induce activation of microglia which might further lead to dopaminergic neuronal loss in the SN.

BACKGROUND Our previous study found that lower lymphocyte-to-monocyte ratio (LMR) is an independent risk factor of clinical outcome of acute ischemic stroke (AIS). However, whether lower LMR is independently associated with adverse prognosis of AIS treated with thrombolysis has not been determined. In this study, we explored the relationship between LMR and prognosis of AIS treated with thrombolysis. MATERIAL AND METHODS We retrospectively enrolled 108 patients treated with thrombolysis. LMR was calculated according to lymphocyte count and monocyte count on admission. Patients were classified into 3 groups according to LMR values on admission (group 1 LMR >4.34, group 2 LMR 2.79 to 4.34, group 3 LMR

Lymphocyte-to-monocyte ratio (LMR) is associated with diverse malignancies and cardiovascular diseases. However, it has not yet been identified whether LMR is correlated with stroke severity and prognosis. We aimed to explore the relationship between LMR and stroke severity, prognosis, and the predictive value of LMR on a 3-month functional outcome in patients with acute ischemic stroke (AIS).A total of 512 patients were enrolled in this study. Baseline demographic and clinical data of all patients were collected. Based on the LMR value on admission (4.83, 2.97-4.83,2.97), patients were divided into 3 groups. Moderate to severe stroke was defined as a National Institutes of Health Stroke Scale score of 6 or higher. Poor outcome was defined as a modified Rankin Scale score of 3 or higher. We used the Spearman rank correlation to evaluate the relationship between LMR and stroke severity. Binary logistic regression analysis was used to assess risk factors of stroke severity and prognosis. The receiver operating characteristic (ROC) curve was used to estimate the predictive value of LMR on prognosis.LMR was inversely correlated with stroke severity (r = -.014, P = .019). Moreover, LMR was an independent protective factor of stroke severity (odds ratio [OR] .891, 95% confidence interval [CI] .815-.973, P = .010) and prognosis (OR .507, 95% CI .437-.590, P .001). ROC indicated that an LMR lower than 2.99 predicted a poor outcome, with a sensitivity of 69.3% and a specificity of 86.6%.A lower LMR on admission was independently associated with severe stroke and 3-month poor outcome in patients with AIS.

OBJECTIVE The optimal time to initiate antihypertensive therapy among patients with acute ischemic stroke remains uncertain. We tested the effects of blood pressure reduction among patients with acute ischemic stroke according to time from onset to initiation of antihypertensive treatment. METHODS We randomly assigned 4071 acute ischemic stroke patients with elevated SBP to receive antihypertensive treatment or to discontinue all antihypertensive medications during hospitalization. The primary outcome was a combination of death and major disability, and secondary outcomes included the modified Rankin score, recurrent stroke, vascular disease events, and all-cause mortality. RESULTS At 24 h after randomization, the differences in SBP reductions were 8.7, 9.5, and 9.6 mmHg between the antihypertensive treatment and control groups among patients receiving treatment within less than 12, 12-23, and 24-48 h after stroke onset, respectively (P

Background: Surgical resection is the recommended procedure for colorectal cancer (CRC), but majority of the patients were diagnosed with advanced or metastatic CRC. Currently, there were inconsistent results about the diagnostic value of magnetic resonance colonography (MRC) and computed tomography colonography (CTC) in early CRC diagnosis. Our study conducted this meta-analysis to investigate the diagnostic value of MRC and CTC for CRC surveillance. Methods: A comprehensive literature search was conducted in PubMed, Embase, and the Cochrane library to select relevant studies. The summary sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic odds ratio (DOR), and the area under the receiver operating characteristic curves (AUC) were calculated to evaluate the diagnostic value of MRC and CTC, respectively. Result: Twenty-five studies including 2985 individuals were selected in the final analysis. Eight studies evaluated the diagnostic value of MRC, and 17 studies assessed CTC. The summary sensitivity, specificity, PLR, NLR, DOR, and AUC in MRC for early detection of CRC were 0.98 (95% confidence interval, CI: 0.80–1.00), 0.94 (95% CI: 0.85–0.97), 15.48 (95% CI: 6.30–38.04), 0.02 (95% CI: 0.00–0.25), 115.09 (95% CI: 15.37–862.01), and 0.98 (95% CI: 0.97–0.99), respectively. In addition, the sensitivity, specificity, PLR, NLR, DOR, and AUC of CTC for diagnosing CRC were 0.97 (95% CI: 0.88–0.99), 0.99 (95% CI: 0.99–1.00), 154.11 (95% CI: 67.81–350.22), 0.03 (95% CI: 0.01–0.13), 642.51 (95% CI: 145.05–2846.02), and 1.00 (95% CI: 0.99–1.00). No significant differences were found between MRC and CTC for DOR in all the subsets. Conclusion: The findings of meta-analysis indicated that MRC and CTC have higher diagnostic values for early CRC diagnosis. However, the DOR for diagnosing CRC between MRC and CTC showed no significance.

Background Disk herniation and disk bulge are two common disorders of lumbar intervertebral disks (IVDs) that often result in numbness, pain in the lower limbs, and lower back pain. Magnetic resonance (MR) imaging is one of the most efficient techniques for detecting lumbar diseases and is widely used for making clinical diagnoses at hospitals. However, there is a lack of efficient tools for effectively interpreting massive amounts of MR images to meet the requirements of many radiologists. Objective The aim of this study was to present an automatic system for diagnosing disk bulge and herniation that saves time and can effectively and significantly reduce the workload of radiologists. Methods The diagnosis of lumbar vertebral disorders is highly dependent on medical images. Therefore, we chose the two most common diseases—disk bulge and herniation—as research subjects. This study is mainly about identifying the position of IVDs (lumbar vertebra [L] 1 to L2, L2-L3, L3-L4, L4-L5, and L5 to sacral vertebra [S] 1) by analyzing the geometrical relationship between sagittal and axial images and classifying axial lumbar disk MR images via deep convolutional neural networks. Results This system involved 4 steps. In the first step, it automatically located vertebral bodies (including the L1, L2, L3, L4, L5, and S1) in sagittal images by using the faster region-based convolutional neural network, and our fourfold cross-validation showed 100% accuracy. In the second step, it spontaneously identified the corresponding disk in each axial lumbar disk MR image with 100% accuracy. In the third step, the accuracy for automatically locating the intervertebral disk region of interest in axial MR images was 100%. In the fourth step, the 3-class classification (normal disk, disk bulge, and disk herniation) accuracies for the L1-L2, L2-L3, L3-L4, L4-L5, and L5-S1 IVDs were 92.7%, 84.4%, 92.1%, 90.4%, and 84.2%, respectively. Conclusions The automatic diagnosis system was successfully built, and it could classify images of normal disks, disk bulge, and disk herniation. This system provided a web-based test for interpreting lumbar disk MR images that could significantly improve diagnostic efficiency and standardized diagnosis reports. This system can also be used to detect other lumbar abnormalities and cervical spondylosis.

Background Subcortical ischemic vascular dementia (SIVD) is a subtype of dementia associated with abnormalities in the subcortical white matter regions. Recent imaging techniques can be used to detect such abnormalities in vivo. Purpose To examine morphological changes of the corpus callosum in patients with SIVD by using magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI). Material and Methods MRI was performed to explore changes of cerebral white matter, especially corpus callosum. Brain matter diffusivity was examined with DTI by measuring the fractional anisotropy (FA). Results of 30 patients diagnosed with SIVD and 30 healthy subjects were analyzed and compared. Results The thicknesses of the genu, the anterior third, middle, and posterior third of the body, and the splenium of the corpus callosum were smaller in SIVD patients compared to healthy controls (0.54 ± 0.08 vs. 0.68 ± 0.09 cm, P = 0.0011; 0.27 ± 0.06 vs. 0.38 ± 0.07 cm, P = 0.002; 0.28 ± 0.05 vs. 0.38 ± 0.08 cm, P = 0.009; 0.18 ± 0.04 vs. 0.26 ± 0.06 cm, P = 0.013; 0.54 ± 0.07 vs. 0.72 ± 0.09 cm, P = 0.003, respectively). The FA values of the genu and splenium of the corpus callosum in patients with SIVD were decreased compared to healthy controls (0.664 ± 0.042 vs. 0.778 ± 0.041, P Conclusion Patients with SIVD exhibit corpus callosum atrophy and morphological changes, and these characteristics may be useful for diagnosis.

This study was aimed to explore whether the omentin-1, a novel adipokine marker, could be a biomarker for stroke, as well as its association with stroke severity.This study included 239 patients with ischemic stroke. The serum omentin-1 level was determined and the stroke was evaluated when the patients were hospitalized. The control groups consisted of 108 patients with matched age, gender and prior vascular risk factors and 120 health control with matched age and gender. The stroke severity was assessed with National Institutes of Health Stroke Scale (NIHSS) when the patients were hospitalized, and NIHSS score 6 was evaluated as moderate-to-severe stroke.Omentin-1 level in serum samples of 239 stroke patients was determined, with the median value of 109.5 ng/ml [Inter Quartile Range (IQR), 78.4-142.9 ng/ml]. There was a negative relation between omentin-1 level and the infarct volume (r = -0.289, P = 0.001). The level of omentin-1 was significantly reduced in stroke patients than that of in control group 1 [125.3 (IQR, 95.8-158.7); P = 0.002] and control group 2 [146.5 (IQR, 116.2-177.3); P 0.001]. With the analysis of multivariate model, omentin-1 as a continuous variable was related to lowered stroke risk (odds ratios [OR] 0.994, 95% confidence interval (CI): 0.990-0.998; P = 0.006). In addition, omentin-1 was an independent indicator for stroke severity (OR 0.992, 95% CI: 0.989-0.996). Levels of omentin-1 in the Q1 showed a relative risk of 2.66 (95% CI: 1.52-4.18) for moderate-to-severe stroke after adjusting for above possible confounders compared to reference category [Quartile (Q): 2-4].The data indicated a negative relation between omentin-1 level and risk of ischemic stroke. The omentin-1 could be promising indicator of stroke and its severity.

Sertraline, one of the oldest antidepressants, remains to be the most efficacious treatment for depression. However, major depression disorder (MDD) is characterized by altered emotion processing and deficits in cognitive control. In cognitive interference tasks, patients with MDD have shown excessive hypothalamus activity. The purpose of this study was to examine the effects of antidepressant treatment (sertraline) on hypothalamus-anchored resting brain circuitry. Functional magnetic resonance imaging was conducted on depressed patients(n=12)both before and after antidepressant treatment. After eight weeks of antidepressant treatment, patients with depression showed significantly increased connectivity between the hypothalamus and dorsolateral prefrontal cortex, orbitofrontal cortex, anterior cingulate cortex, insula, putamen, caudate, and claustrum. By contrast, decreased connectivity of the hypothalamus-related areas was primarily located in the inferior frontal gyrus, medial frontal gyrus, cingulated gyrus, precuneus, thalamus, and cerebellum. After eight weeks of antidepressant therapy, 8 out of the 12 depressed subjects achieved 70% reduction or better in depressive symptoms, as measured on the Hamilton depression rating scale. Our findings may infer that antidepressant treatment can alter the functional connectivity of the hypothalamus resting brain to achieve its therapeutic effect.

Although the benefit of reducing blood pressure for primary and secondary prevention of stroke has been established, the effect of antihypertensive treatment in patients with acute ischemic stroke is uncertain.To evaluate whether immediate blood pressure reduction in patients with acute ischemic stroke would reduce death and major disability at 14 days or hospital discharge.The China Antihypertensive Trial in Acute Ischemic Stroke, a single-blind, blinded end-points randomized clinical trial, conducted among 4071 patients with nonthrombolysed ischemic stroke within 48 hours of onset and elevated systolic blood pressure. Patients were recruited from 26 hospitals across China between August 2009 and May 2013.Patients (n = 2038) were randomly assigned to receive antihypertensive treatment (aimed at lowering systolic blood pressure by 10% to 25% within the first 24 hours after randomization, achieving blood pressure less than 140/90 mm Hg within 7 days, and maintaining this level during hospitalization) or to discontinue all antihypertensive medications (control) during hospitalization (n = 2033).Primary outcome was a combination of death and major disability (modified Rankin Scale score ≥3) at 14 days or hospital discharge.Mean systolic blood pressure was reduced from 166.7 mm Hg to 144.7 mm Hg (-12.7%) within 24 hours in the antihypertensive treatment group and from 165.6 mm Hg to 152.9 mm Hg (-7.2%) in the control group within 24 hours after randomization (difference, -5.5% [95% CI, -4.9 to -6.1%]; absolute difference, -9.1 mm Hg [95% CI, -10.2 to -8.1]; P .001). Mean systolic blood pressure was 137.3 mm Hg in the antihypertensive treatment group and 146.5 mm Hg in the control group at day 7 after randomization (difference, -9.3 mm Hg [95% CI, -10.1 to -8.4]; P .001). The primary outcome did not differ between treatment groups (683 events [antihypertensive treatment] vs 681 events [control]; odds ratio, 1.00 [95% CI, 0.88 to 1.14]; P = .98) at 14 days or hospital discharge. The secondary composite outcome of death and major disability at 3-month posttreatment follow-up did not differ between treatment groups (500 events [antihypertensive treatment] vs 502 events [control]; odds ratio, 0.99 [95% CI, 0.86 to 1.15]; P = .93).Among patients with acute ischemic stroke, blood pressure reduction with antihypertensive medications, compared with the absence of hypertensive medication, did not reduce the likelihood of death and major disability at 14 days or hospital discharge.clinicaltrials.gov Identifier: NCT01840072.