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SOmega-3 polyunsaturated fatty acids (PUFAs) possess anti-inflammatory properties. There is a lack of consensus regarding the effects of omega-3 PUFAs on C-reactive protein (CRP), a marker of systemic inflammation, in cancer patients. Herein, a meta-analysis of randomized controlled trials was conducted to evaluate the effects of omega-3 PUFAs on CRP levels in patients with cancer. PubMed and EMBASE were searched until May 2020 to identify randomized controlled trials that examined the effects of omega-3 PUFA administration on CRP levels in cancer patients. Standardized mean differences (SMDs) with their 95% confidence intervals (CIs) were calculated to determine the differences in omega-3 PUFA administration and control conditions. Seventeen eligible studies involving 916 cancer patients were included in this meta-analysis. Significant heterogeneity was present among individual studies (Pheterogeneity = 0.000; I2 = 74.5%). The overall SMDs of CRP levels between omega-3 PUFA administration and control conditions were 0.628 (95% CI: 0.342-0.914) and 0.456 (95% CI: 0.322-0.590) by the random-effect and fixed-effect models, respectively. Sources of heterogeneity were not found through subgroup and meta-regression analyses. Existing publication bias contributed slightly to the effect size. Omega-3 PUFAs can reduce systemic inflammation, as indicated by CRP levels in cancer patients. The use of omega-3 PUFAs is recommended for cancer patients due to their anti-inflammatory properties.

Purpose The recommendation strength of the guidelines for mechanical thrombectomy among patients with large pre-treatment core infarct is weak. We evaluated the safety and outcome of endovascular treatment for acute ischemic stroke with diffusion-weighted imaging-Alberta Stroke Program Early Computed Tomography Score (DWI-ASPECTS) ≤ 5. Methods Data on acute ischemic stroke patients with DWI-ASPECTS ≤ 5 who underwent endovascular treatment within 6 h, or presented an arterial spin labeling-DWI (ASL-DWI) mismatch within 12 h, at our center were retrospectively collected. We report the clinical characteristics and outcome of every patient, and review the relevant literature. Results Among the 19 patients who were enrolled, all experienced successful reperfusion, and 10 achieved a favorable outcome (modified Rankin scale (mRS) ≤ 2). Two patients presented with symptomatic intracranial hemorrhage (sICH); both of them had a poor outcome (mRS > 2). Conclusion Acute ischemic stroke patients with large DWI lesions caused by large vessel occlusion can achieve a favorable clinical outcome with endovascular treatment if recanalization is performed within 6 h, or after 6 h in case of an ASL-DWI mismatch. Electronic supplementary material The online version of this article (10.1007/s00234-019-02177-1) contains supplementary material, which is available to authorized users.

Background and Purpose: Acute ischemic stroke (AIS) with large artery occlusion (LAO) may lead to severe disability or death if not promptly treated. To determine the source of cerebral artery occlusion thrombosis, we studied the pathological components of cerebral artery thrombosis with different etiological classifications to guide clinical formulation of preventive treatment. Materials and Methods: Eighty-eight thrombi from AIS patients with LAO, 12 atrial thrombi from patients with valvular heart disease (VHD), and 11 plaques obtained by carotid endarterectomy (CEA) from patients with carotid artery stenosis were included in this retrospective study. The hematoxylin and eosin–stained specimens were quantitatively analyzed for erythrocytes, white blood cells (WBCs) and fibrin; platelets were shown by immunohistochemistry for CD31. Results: The thrombi of VHD showed the highest percentage of fibrin, followed by those of cardioembolism (CE) and stroke of undetermined etiology (SUE), and these values were higher than those of the other groups. Plaques obtained by CEA showed the highest erythrocyte number, followed by the large artery atherosclerosis (LAA) thrombi, and showed significantly noticeable differences between other stroke subtypes. The proportions of fibrin and erythrocytes in the thrombi of CE and SUE were most similar to those in the thrombi of VHD, and the LAA thrombi were the closest to those obtained by CEA. CE thrombi and CEA plaques had a higher percentage of WBCs than thrombi of other stroke thrombus subtypes and VHD. Conclusions: CE and most cryptogenic thrombi may originate from the heart, and the formation of carotid atherosclerotic plaques may be related to atherosclerotic cerebral embolism. Inflammation may be involved in their formation.

Objective: Chronic cerebral hypoperfusion (CCH) is a common consequence of various cerebral vascular disorders, hemodynamics and blood composition changes, which can lead to neurodegenerative injury and cognitive dysfunction. Therefore, it is important to take measures to prevent or reverse its development. Methods: Eighty Sprague-Dawley rats were randomly divided into five groups: Sham group, Vehicle groups (2-week group and 4-week group), Rosuvastatin-treated groups (2-week group and 4-week group). Both vehicle and treated group rats were treated with bilateral common carotid artery occlusion (BCCAO). Then rats in the treated group were intravenously injection with rosuvastatin (0.2 mg/kg/day) daily for 14 days beginning 24 hours after BCCAO. The vehicle groups were given the same amount of saline. The MRI ASL technique was used to scan cerebral blood flow (CBF) at pre-occlusion, BCCAO, 1, 2, 3, and 4 weeks after operation. Morris water maze test detected spatial memory abilities of the treated and vehicle rats after BCCAO. Immunofluorescence staining was used to detect the expression of CD34, GFAP, NeuN and Caspase-3 positive cells in hippocampus. Results: CBF decreased significantly after BCCAO in both rosuvastatin-treated and vehicle groups and then increased gradually. The CBF of the treated group was basically recovered to baseline levels at 1 or 2 weeks after BCCAO. But it took the vehicle group 4 weeks to restore to baseline. The vertebral artery (VA) diameter of the treated group was greater than that of the vehicle group (p+ and NeuN + cells in the hippocampus of the treated group was more than that in the vehicle group (p+ and Caspase-3 + cells was less than in the vehicle group (p Conclusion: Rosuvastatin can accelerate the recovery of cerebral blood flow in CCH rats, which may be related to the dilation of VAs and angiogenesis; and its effects on reducing astrocyte activation and neuroprotection may help to ameliorate cognitive dysfunction in CCH rats.

// Wenxian Li 1, * , Xiaomei Xie 1, * , Di Wei 5, * , Shijun Zhang 2 , Yuanling Wu 1 , Xuejun Fu 3 , Zhen Jing 1 , Weibiao Lu 1 , Xinqiang Lai 4, # and Li’an Huang 1, # 1 Department of Neurology, The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, 510632, P.R. China 2 Department of Neurology, People’s Hospital of Zengcheng District, Guangzhou, Guangdong, 510180, P.R. China 3 Department of Neurology, People’s Hospital, Second Clinical College, Jinan University, Shenzhen, 518020, P.R. China 4 Analysis and Testing Center, Jinan University, Guangzhou, Guangdong, 510632, P.R. China 5 Department of Urology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shanxi, 710032, P.R. China * These authors contributed equally to this work and share first authorship # These authors contributed equally to this study and share corresponding authorship Correspondence to: Li’an Huang, email: huanglian1306@126.com Xinqiang Lai, email: xinqianglai@126.com Keywords: mean platelet volume, platelet count, clopidogrel resistance, non-cardioembolic ischemic stroke, platelet response Received: June 11, 2017 Accepted: September 21, 2017 Published: October 07, 2017 ABSTRACT Purpose: The present study investigated whether routine baseline platelet parameters(BPPs) detected before clopidogrel therapy in acute non-cardioembolic ischemic stroke(NCIS) could predict early platelet response and future clinical outcomes. Results: The CYP2C19 polymorphisms constituted independent risk factors for LCR. The number of female patients, the incidence of diabetes mellitus (DM), the level of low-density lipoprotein(LDL) cholesterol, and the neutrophil-to-lymphocyte ratio(NLR) were significantly high in the clinical clopidogrel resistance (CCR) group. However, none of the BPPs had a significant association with laboratory clopidogrel resistance (LCR) or discriminated with the cut-off values regarding LCR or CCR. The patients were divided into two groups according to the average mean platelet volume(MPV) or platelet count(PC). We found that the HbA1c level, the number of female patients, and the CCR were higher in the groups with elevated MPV (≥ 10.6fL) and PC (≥ 235 × 10 9 /L); the LCR, the NIHSS score at discharge, and elevated MPV and PC were risk predictors for CCR. Materials and Methods: This study included 196 patients with acute NCIS who underwent routine blood tests upon admission, were treated with clopidogrel, and were followed up for 6 months. Early platelet response was assessed and the CYP2C19 genetic variants were screened for. All participants were categorized into either laboratory clopidogrel resistance(LCR) or clinical clopidogrel resistance (CCR) groups. Conclusions: Elevated baseline MPV and PC before clopidogrel therapy, as well as CYP2C19 gene variants, should be included in a risk algorithm for NCIS. Furthermore, other nongenetic clinical risk factors should be assessed for optimal prediction of the risk for thrombotic events because of individual variability in platelet response to clopidogrel.

Newborn hearing screening is not designed to detect delayed-onset prelingual hearing loss or aminoglycoside-antibiotic-induced ototoxicity. Cases with severe to profound hearing loss have been reported to have been missed by newborn hearing screens. The aim of this study was to evaluate the efficacy of concurrent hearing and genetic screening in the general population and demonstrate its benefits in practice. Enrolled newborns received concurrent hearing and genetic screens between September 1, 2015 and January 31, 2018. Of the 239,636 eligible infants (median age, 19 months), 548 (0.23%) had prelingual hearing loss. Genetic screening identified 14 hearing loss patients with positive genotypes and 27 patients with inconclusive genotypes who had passed the hearing screens. In addition, the genetic screen identified 0.23% (570/239,636) of the newborns and their family members as at-risk for ototoxicity, which is undetectable by hearing screens. In conclusion, genetic screening complements newborn hearing screening by improving the detection of infants at risk of hereditary hearing loss and ototoxicity, and by informing genotype-based clinical management for affected infants and their family members. Our findings suggest that the practice should be further validated in other populations and rigorous cost-effectiveness analyses are warranted.

A meta-analysis of prospective cohort studies was conducted to clarify the association between obstructive sleep apnoea (OSA) and future risk of all-cause mortality.Eligible studies were identified by searching the PubMed and EMBASE databases up to July 2015. Pooled hazard ratios (HRs) and their corresponding 95 % confidence intervals (CIs) were calculated to estimate the association between OSA and risk of all-cause mortality. Sources of heterogeneity were identified by subgroup and meta-regression analyses.Twelve prospective cohort studies involving 34,382 participants were included in this meta-analysis. The pooled HR of all-cause mortality was 1.262 (95 % CI 1.093-1.431) with significant heterogeneity. Subgroup analyses indicated that the pooled HRs of all-cause mortality in patients with mild, moderate and severe OSA were 0.945 (95 % CI 0.810-1.081), 1.178 (95 % CI 0.978-1.378) and 1.601 (95 % CI 1.298-1.902), respectively. OSA severity could be a possible sources of heterogeneity. Existing publication bias produced a minor contribution to effect size.Severe, but not mild to moderate, OSA is significantly associated with increased risk of all-cause mortality.

Previous findings have demonstrated, in a rat model, that chronic cerebral hypoperfusion (CCH) decreases cortical cerebral blood flow (CBF) while Dl-3-n-Butylphthalide (DNB) accelerates the timely recovery of CBF. However, potential biomarkers, therapeutic targets, and underlying mechanisms for these processes are unclear. In this study, a solid-phase antibody microarray for simultaneously detecting multiple proteins was used to search cortex biotargets in CCH compared to a sham control group, and these results were further examined by biological functional analysis. After DNB treatment, western blot and immunostaining were used to verify candidate protein expression. Importantly, we identified seven proteins that may serve as novel biotargets contributing to CCH. The levels of Tie-2, CNTFRα, IL-4, IL-10, ITGAM, MDC, and TROY were uniquely altered in the CCH. The Tie-2 level was significantly decreased and identified in CCH 2 week (W), CCH 4 W and CCH 8 W. In addition, Ang-1 level and Ang-1/Ang-2 ratio were significantly decreased in CCH 2 W and CCH 4 W while Ang-2 level was increased in the CCH, whereas DNB treatment created the inverse effect to some extent. Moreover, the expression of VEGF and CD34 in the earlier stage of CCH and the diameters of bilateral vertebral arteries (VAs), were significantly enlarged by DNB treatment. Together, we found that the Ang-1/Ang-2/Tie-2 signaling axis was altered in the CCH rat cortex, and DNB treatment could timely regulate this angiopoietin/Tie signaling axis to promote neovascularization in early stages.

Context: Cervical spinal cord infarction is a rare and severe complication of vertebral artery dissection (VAD). We report a case of VAD in an acute stage followed by cervical spinal cord infarction that was treated using direct endovascular tirofiban infusion via digital subtraction angiography (DSA) monitoring. Findings: A 48-year-old man presented with vertigo, neck pain, numbness and weakness in four limbs with subsequent cardiac and respiratory arrest. Neurological examination revealed hypoesthesia below the neck with grade one myodynamia on the right side of the limbs and zero on the left side. The diagnosis of VAD-related cervical spinal infarction was confirmed using DSA imaging and cervical vertebra magnetic resonance imaging (MRI). The patient received timely treatment with endovascular tirofiban infusion and achieved good outcome without any sequelae. Conclusion: Endovascular treatment with tirofiban may be a selective choice for cervical spinal cord infarction due to VAD in acute stage and warrants further study.

The role of leptin in the development of obstructive sleep apnoea (OSA) has been identified. However, the effects of OSA treatment using continuous positive airway pressure (CPAP) on serum leptin levels remain controversial. To address this issue, a meta-analysis was conducted to evaluate the effects of CPAP therapy on serum leptin levels in OSA.A comprehensive literature search was performed to identify studies that focused on the effects of CPAP therapy (treatment duration, ≥4 weeks) on the serum leptin levels of OSA patients. Standardised mean difference (SMD) was used to analyse the summary estimates for CPAP therapy.Fifteen studies involving 427 patients were included in the meta-analysis. Results indicate that the overall SMD of the leptin levels before and after CPAP therapy was 0.137 (95% confidence interval (CI) 0.002 to 0.272); test for overall effect z=1.99 (P=0.046). Sources of heterogeneity were not found by subgroup and meta-regression analyses. Subgroup analyses showed that differences in OSA severity, baseline body mass index, compliance, CPAP duration and leptin assay did not affect the effectiveness of CPAP therapy.The evidence for the use of CPAP therapy on decrease of leptin levels in OSA patients is low, and stronger evidence is needed.

Background: Inflammation plays a critical role in the progression of atherosclerosis, and hyperglycemia is a common feature in patients with ACS. We investigated the relationship between fasting plasma glucose (FPG) levels and the levels of the inflammatory factor, myeloperoxidase (MPO), in patients with acute coronary syndrome (ACS). Method: A total of 85 patients with no prior history of diabetes mellitus were recruited. The patients were divided into three groups based on their FPG levels as follows: group A, FPG < 5.6 mmol/l; group B, 5.6 mmol/l ≤ FPG < 6.1 mmol/l; and group C, FPG ≥6.1 mmol/l. The FPG concentrations and plasma MPO levels were determined, coronary angioplasty was performed, and the Gensini scores were used to evaluate the severity of the coronary lesion. The MPO expression in peripheral blood mononuclear cells (PBMCs) in patients with ACS was determined using western blot analysis. Result: The results demonstrated that the levels of FPG were significantly and positively correlated with plasma MPO levels, Gensini scores, high sensitive C reaction protein(hs-CRP)levels, leukocyte and neutrophils count. In multivariate regression analyses the FPG levels were positively correlated with plasma MPO levels, Gensini score and hs-CRP. The plasma MPO levels in the group C [68.68(52.62–91.88) U/L] were significantly higher than in the group A [63.04(26.18–97.75) U/L] and group B [58.22(23.95–89.54) U/L]. The plasma hs-CRP concentrations are also higher in group C [42.28 (0.31–169.40) mg/L] than in the group A [12.51(0.28–176.25) mg/L] and group B [14.7 (0.14–89.68) mg/L]. Conclusion: This study demonstrates that FPG values are positively correlated with plasma MPO levels, suggesting MPO may play a role in the proatherogenesis of high FPG.

We report here a case of nasal natural killer/T-cell lymphoma with metastasization into the pancreas. A 43-year-old Chinese female patient presented with right nasal obstruction and purulent rhinorrhea that lasted for the past half year and worsened gradually despite antibiotic medical treatment. Physical examination revealed a mass in the right nasal cavity and an enlarged lymph node in the right submandibular region. A PET/CT scan and immunostaining of the resectate led to a diagnosis of nasal natural killer/T-cell lymphoma, clinical stage IIE, and the International Prognostic Index score of 1. The patient received radiotherapy followed by four cycles of the CHOP chemotherapy. A complete remission was achieved, and the patient was disease-free for 9 months. On a subsequent follow-up, abdominal ultrasound scan, enhanced abdominal CT scan, and ultrasound-guided fine-needle aspiration biopsy revealed pancreatic metastasis secondary to nasal lymphoma. Radiotherapy (40 Gy) to the whole pancreas was done, followed by two courses of the SMILE regime chemotherapy, leading to a complete remission. At the moment, the patient is undergoing subsequent chemotherapy.

Objectives Our meta-analysis was performed to estimate the effect of continuous positive airway pressure (CPAP) therapy on systemic inflammation in patients with obstructive sleep apnea (OSA). Methods A comprehensive literature search of PubMed and EMBASE was performed for literature published up to January 2013. Standardized mean difference (SMD) was calculated to estimate the treatment effects of pre- and post-CPAP therapy. Results A total of 35 studies involving 1985 OSA patients were included in the meta-analysis. Each study investigated one or more inflammatory markers: 24 studies on C-reactive protein (CRP), 16 studies on IL-6, 3 studies on IL-8, and 12 studies on tumor necrosis factor α (TNF-α). The results showed that the SMD (95% confidence interval [CI]) for CRP, IL-6, IL-8, and TNF-α were 0.452 (95% CI, 0.252–0.651), 0.299 (95% CI, 0.001–0.596), 0.645 (95% CI, 0.362–0.929), and 0.478 (95% CI, 0.219–0.736) in pre- and post-CPAP therapy, respectively. The subgroup analyses seemed to support better benefits with therapy duration of ⩾3months and more adequate compliance (⩾4h/night). Conclusions CPAP therapy could partially suppress systemic inflammation in OSA patients, and substantial differences were present among the various inflammatory markers.

C-reactive protein (CRP) is associated with the development of obstructive sleep apnea (OSA) and cardiovascular diseases. Continuous positive airway pressure (CPAP) is an effective treatment for OSA, but the impact of CPAP therapy on CRP levels in patients with OSA remains unclear. To obtain this information, we performed a meta-analysis to determine whether effective CPAP therapy could reduce serum CRP levels.A comprehensive literature search was performed to identify studies that examined the impact of CPAP on serum CRP levels in OSA patients who were treated with CPAP for at least 4 weeks. Standardized mean difference (SMD) was used to analyze the summary estimates for CPAP therapy.Fourteen self-control design studies involving 1199 patients with OSA met the inclusion criteria. Meta-analysis indicated that the overall SMD for the CRP levels was 0.64 units (95 % confidence interval (CI) 0.40 to 0.88) before and after CPAP therapy; test for overall effect z = 5.27 (P = 0.000). Subgroup analysis showed that evolution of CRP decreased non-significantly in less than 3 months (SMD, 0.26, 95 % CI -0.08 to 0.60, P = 0.138), significantly decreased after 3 months (SMD, 0.68, 95 % CI 0.34 to 1.02, P = 0.000), and further declined after 6 months (SMD, 0.74, 95 % CI 0.43 to 1.05, P = 0.000).The systemic inflammation, as measured by CRP, was present and significantly reduced by effective CPAP therapy in patients with OSA. The use of CRP levels may be clinically recognized as a valuable predictor for OSA treatment monitoring.

BACKGROUND: Anabolic steroids are known to improve body composition and muscle strength in healthy people. However, whether anabolic steroids improve the physical condition and function in patients with chronic obstructive pulmonary disease (COPD) remains undetermined. A meta-analysis was conducted to review the current evidence regarding the effects of anabolic steroids on COPD patients. METHODS: A comprehensive literature search of PubMed and EMBASE was performed to identify randomised controlled trials that examine the effects of anabolic steroids on COPD patients. Weighted mean differences (WMDs) with 95% confidence intervals were calculated to determine differences between anabolic steroid administration and control conditions. RESULTS: Eight eligible studies involving 273 COPD patients were identified in this meta-analysis. Significant improvements were found in body weight (0.956 kg), fat-free mass (1.606 kg), St. George's Respiratory Questionnaire total score (-6.336) and symptom score (-12.148). The apparent improvements in maximal inspiratory pressure (2.740 cmH2O) and maximal expiratory pressure (12.679 cmH2O) were not significant. The effects on handgrip strength, forced expiratory volume in one second (FEV1), predicted FEV1 percent, PaO2, PaCO2 and six-min walk distance were negative, with WMDs of -0.245 kg, -0.096 L/sec, -1.996% of predicted, -1.648 cmHg, -0.039 cmHg and -16.102 meters, respectively. CONCLUSIONS: Limited evidence available from the published literature suggests that the benefit of anabolic steroids on COPD patients cannot be denied. However, further studies are needed to identify the specific benefits and adverse effects of anabolic steroids on COPD patients and to determine the optimal populations and regimes of anabolic steroids in COPD patients.