Co-Contraction of Lower Limb Muscles Contributes to Knee Stability During Stance Phase in Hemiplegic Stroke Patients.

BACKGROUND Knee stability has an important role in the gait of hemiplegic stroke patients. However, factors affecting knee stability have not been assessed concerning gait. The purpose of this study was to explore whether co-contraction of the lower limb muscles contributes to the knee stability during the stance phase of the gait cycle in hemiplegic stroke patients. MATERIAL AND METHODS A total of 30 hemiplegic stroke patients, ages 36-79 years, were instructed to walk at their natural speed. The root mean square of surface electromyography was used to measure activities of the biceps femoris and rectus femoris muscles, while the co-contraction ratio was computed based on the root mean squares. The peak angle of knee extension was acquired in the stance phase by 3D kinematic analyses. Lower limb function was evaluated using the Fugl-Meyer scale for lower limb motor assessment. RESULTS A statistically significant increase of the muscle co-contraction ratio of the involved extremity was observed compared with that of the uninvolved extremity (t=-4.066, P<0.05). The muscle co-contraction ratio was significantly correlated with the peak angle of knee extension (r=0.387, P=0.035), Fugl-Meyer scale (r=-0.522, P=0.003), and Modified Ashworth Scale (r=0.404, P=0.027) during the stance phase of the gait cycle. CONCLUSIONS Our results showed that co-contraction of the rectus femoris muscle contributes to the stability of the knee and lower limb function in hemiplegic stroke patients, and suggests that co-contraction should be considered in the rehabilitation of knee stability during gait in hemiplegic stroke patients. Appropriate rehabilitation assessment planning with hemiplegic stroke patients, such as muscle co-contraction or knee stability of, might be created based on our results.

Association of microtubule-associated protein tau gene polymorphisms with the risk of sporadic Alzheimer's disease: a meta-analysis.

BACKGROUND: Numerous epidemiological studies were published to investigate the role of microtubule-associated protein tau (MAPT) gene variations (rs7521G/A, rs242557G/A, rs1467967A/G, rs2471738C/T and rs3785883G/A) in SAD, and these genetic polymorphisms may be a risk factor for sporadic Alzheimer's disease (SAD). However, controversial results were revealed. METHODS: The MEDLINE, Embase and HuGEnet databases were searched to identify eligible studies. The odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to evaluate the genetic association of MAPT with the risk of SAD. RESULTS: A total of 30 studies were included in this meta-analysis to assess the association between five single-nucleotide polymorphisms and susceptibility to SAD. The pooled results exhibited no significant association between rs1467967A/G, rs3785883G/A, rs2471738C/T and rs7521G/A polymorphisms and the risk of SAD. However, a lower risk of SAD was observed in the GG versus (GA + AA) model of rs242557G/A polymorphism (OR = 0.86, 95% CI = 0.751-0.983, P = 0.027). CONCLUSION: The present meta-analysis showed that rs1467967A/G, rs3785883G/A, rs2471738C/T and rs7521G/A polymorphisms were not associated with the risk of SAD. However, rs242557G/A genetic polymorphism was associated with susceptibility to SAD, and individuals with a GG genotype of rs242557G/A might be at a lower risk of SAD. Further studies with a larger sample size are required to validate these conclusions.

Angiotensin converting enzyme (I/D) gene polymorphism contributes to ischemic stroke risk in Caucasian individuals: a meta-analysis based on 22 case-control studies.

BACKGROUND: Stroke is a multifactorial disease in which genetic factors play an important role. Previous studies associated angiotensin converting enzyme (ACE) (insertion/deletion, I/D) gene polymorphism with ischemic stroke risk in Caucasian individuals reported conflicting results. The purpose of this study was to evaluate the association between ACE (I/D) gene polymorphism and ischemic stroke risk by a meta-analysis. METHODS: The related studies were searched in MEDLINE, EMBASE and HuGEnet databases. The odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for ischemic stroke risk associated with this polymorphism were estimated using fixed-effect or random-effects model. Twenty-two studies (5528/5081 cases/controls) were eligible in our meta-analysis. RESULTS: Overall, statistical associations of the ACE (I/D) polymorphism with ischemic stroke risk were found in dominant model (DD + ID versus II) : OR = 1.21, 95% CI = (1.06,1.38), P = 0.006, recessive model (DD versus ID + II): OR = 1.28, 95% CI = (1.05,1.55), P = 0.01, and homozygote comparison (DD versus II): OR = 1.37, 95% CI = (1.14,1.65), P = 0.001 for Caucasians. When stratifying according to stroke subtypes, there were similarly significant differences for small vessel disease in dominant model (DD + ID versus II) : OR = 1.44, 95% CI = (1.01,2.05), P = 0.04, recessive model (DD versus ID + II): OR = 1.30,95% CI = (1.09,1.55), P = 0.004, and homozygote comparison (DD versus II): OR = 1.44, 95% CI = (1.15,1.80), P = 0.001. CONCLUSION: This analysis suggests that the ACE (I/D) polymorphism may be a risk factor for ischemic stroke, genotype DD of ACE could increase the risk of ischemic stroke in Caucasians. Subgroup analyses indicate that stroke subtypes may be a genetic risk factor of ischemic stroke, and there might be a greater genetic liability with small vessel disease.

Evaluation of histopathological changes, viral load and immune function of domestic geese infected with Newcastle disease virus.

Outbreaks of Newcastle disease in flocks of geese with high morbidity and mortality in southern and eastern China have been reported frequently since the late 1990s, which broke the traditional view that geese are considered to be the natural reservoir of Newcastle disease virus (NDV) but show few or no clinical signs after infection. In this present study, geese were infected intranasally with a local strain of NDV. Clinical disease and gross pathology were observed. Serum and immune organs were collected from geese sequentially euthanized or after disease-associated death. We studied the histopathology of immune organs by haematoxylin and eosin staining and NDV fusion protein was detected in tissues by immunohistochemistry. At the same time, the SYBR Green I real-time polymerase chain reaction assay was used to detect the viral load from the collected samples. Serum samples were tested for NDV-specific antibodies and avian influenza virus (AIV)-specific antibodies by haemagglutination inhibition (HI) test. The results showed that severe lesions and numerous positive reactions of NDV antigen were detected in the immune organs. High viral loads developed in immune organs of infected geese, correlating with the severity of clinical signs and lesions in the tissues. Furthermore, the infected geese developed low HI antibody titres to both AIV and NDV. The present study showed that the replication and dissemination of the NDV isolate was widespread in immune organs of geese. The study revealed that waterfowl may not only be a natural reservoir of NDV but also become susceptible to disease and may play a major role in the epidemiology of Newcastle disease.

Genetic polymorphism of interleukin 1ß -511C/T and susceptibility to sporadic Alzheimer's disease: a meta-analysis.

A large number of epidemiological studies have been performed to investigate the association between Alzheimer's disease (AD) risk and interleukin-1ß -511C/T genetic polymorphism, however, inconsistent results have been reported. The effect of the IL-1ß -511C/T polymorphism on AD susceptibility was evaluated by a meta-analysis. Series of databases were researched. 14 studies involving 2640 AD case and 3493 control subjects were identified. The pooled results showed there were no statistical associations of interleukin-1ß -511C/T genetic polymorphism with susceptibility to AD for five analysis models in all subjects. However, obvious heterogeneity among studies was detected. When stratifying for age at onset, ethnicity and geographic distribution of population to explore the original source of heterogeneity, the meta-analysis results based on geographic distribution of population showed the significant difference (CC vs CT, OR 1.26, 95 % CI: 1.03, 1.54, z = 2.25, P = 0.025; CC vs CT+TT, OR 1.24, 95 % CI: 1.03, 1.50, z = 2.24, P = 0.025) only in non-Europe. These findings indicate that the IL-1ß -511C/T polymorphism might be associated with AD risk, and individuals with IL-1ß -511C/C genotype might be at higher risk of AD in non-Europe. Further larger sample research would be warranted to confirm these conclusions.

Case report: Myocardial noncompaction causing massive cerebral infarction in 1 patient with eyelid edema as an early manifestation and literature review.

Objective: To summarize and analyze the early clinical manifestations, risk factors, treatment and prognosis of myocardial noncompaction in children, and to provide scientific basis for early and effective intervention. Methods: Combined with a case of myocardial noncompaction with massive cerebral infarction in a child, the related research reports of myocardial noncompaction in children were analyzed retrospectively. Results: Myocardial noncompaction in children is cardiomyopathy caused by abnormal myocardial compaction during embryonic development. Feeding intolerance, dyspnea, chest tightness, fatigue, eyelid edema and other non-specific manifestations may occur in the early stage. It is easy to miss the diagnosis and misdiagnosis in clinical diagnosis and treatment, leading to intractable heart failure, nausea and arrhythmia, thromboembolism and even sudden death and other serious complications. Early diagnosis, symptomatic treatment, control of complications and regular follow-up can prevent the occurrence of serious complications and reduce mortality. Conclusion: There is no specific clinical manifestation in the early stage of myocardial noncompaction in children. If it is not detected early and treated symptomatically, the prognosis is poor and the mortality is high. Therefore, clinicians should fully improve the understanding of the early clinical manifestations of this disease, give early diagnosis and early intervention to children, reduce the occurrence of serious complications and improve the survival rate.

Surgical outcomes of acute type A aortic dissection in dialysis patients: lessons learned from a single-center's experience.

There is a paucity of data describing the safety and efficacy of acute type A aortic dissection (ATAAD) repair surgeries in dialysis patients. Our study aimed to investigated the influence of dialysis on early and late outcomes in end-stage renal disease (ESRD) patients who received repair surgery for ATAAD. A total of 882 ATAAD patients who received emergency aortic dissection repair at our center from January 2015 to December 2019 were retrospectively screened in this study and divided into the dialysis group (n = 16) and the non-dialysis group (n = 866), depending on whether they required dialysis for preoperative ESRD. No significant difference of age, preoperative hemodynamics, organ ischemia conditions, operative variables as well as the 30-Day mortality and in-hospital complications was discovered between two groups. However, the survival rates and the proportion of late aortic event (sudden death and reoperation) free population at 1 and 3 years after surgery were significantly decreased in dialysis patients compared to non-dialysis patients. Our study indicated that the short-term surgical outcomes of ATAAD in dialysis patients were comparable to non-dialysis patient. However, the dialysis patients were associated with a worse long-term prognosis.

NOL6 Regulates the Proliferation and Apoptosis of Gastric Cancer Cells via Regulating TP53I3, CDK4 and MCM7 Expression.

Background: Gastric cancer (GC) is a prevalent cancer with high mortality and strong invasiveness, and the entire regulatory networks of GC is still unclear. Objective: The aim of this study was to explore the specific mechanism of the effect of nucleolar protein 6 (NOL6) on the proliferation and apoptosis of GC cells. Methods: The human gastric adenocarcinoma cell line HGC-27 and AGS were cultured. qRT-PCR was used to verify the expression level of NOL6 in GC cells; MTT and EdU were used to test cell proliferation; TUNEL staining and Flow cytometry were used to detect cell apoptosis; The downstream genes and pathways following NOL6 knockdown were explored through the microarray assay and ingenuity pathway analysis, and the downstream genes were finally verified by qRT-PCR and Western blotting. The xenograft mice were used to investigate the effect of NOL6 on GC in vivo. Results: TCGA data analysis showed that NOL6 expression level was higher in GC cells than adjacent normal cells. Over-expression of NOL6 increased proliferation and colony formation, and inhibited the apoptotic rate in AGS and HGC-27 cells, while NOL6 knockdown induced the opposite effects. Through microarray assay and IPA analysis, NOL6-related downstream genes and critical signaling pathways were found. And we verified the relationship between downstream genes and GC. Additionally, NOL6 knockdown could decrease the weight and volume of tumor in the mice. Conclusion: NOL6 knockdown could inhibit cell proliferation and induce cell apoptosis of GC, suggesting that NOL6 may serve as a potential therapeutic target for treating GC.

Risk factors for 30-day mortality in patients who received DeBakey type I aortic dissection repair surgery.

OBJECTIVE: This study aimed to identify risk factors for 30-day mortality in patients who received DeBakey type I aortic dissection (AD) repair surgery. METHODS: A total of 830 consecutive patients who received acute DeBakey type I AD surgery between 2014 and 2019 were included in the study. The associations between 30-day mortality and perioperative parameters were examined in order to identify risk factors. RESULTS: Our data suggested that the overall 30-day mortality rate of all enrolled patients was 11.7%. Unsurprisingly, non-survivors were older and more frequently accompanied with histories of cardiovascular diseases. For intraoperative parameters, the prevalence of coronary artery bypass grafting and cardiopulmonary bypass times were increased in non-survivors. In addition, acute kidney injury (AKI), dialysis, stroke, and deep sternal wound infection were more commonly seen among non-survivors. The multivariate logistic regression analysis suggested that cardiovascular disease history, preoperative D-dimer level, drainage volume 24 h after surgery, and postoperative AKI were independent risk factors for 30-day mortality after DeBakey type I aortic dissection repair surgery. CONCLUSIONS: Our study demonstrated that cardiovascular disease history, preoperative D-dimer level, drainage volume 24 h after surgery as well as postoperative AKI were risk factors for 30-day mortality after DeBakey type I aortic dissection repair surgery.

Complement receptor 1 genetic polymorphism contributes to sporadic Alzheimer's disease susceptibility in Caucasians: a meta-analysis.

Complement receptor 1 (CR1) plays an important role in the development of sporadic Alzheimer's disease (SAD) in Caucasians. However, the influence of CR1 (rs6656401A/G and rs3818361T/C) genetic polymorphisms on the risk of SAD remains controversial. A meta-analysis of 18 case-control studies was performed to derive a more precise association of CR1 (rs6656401A/G or rs3818361T/C) genetic polymorphism with the risk of SAD in Caucasians. A statistical difference was found in the dominant model (odds ratio (OR): 1.23, 95% confidence interval (CI): 1.16-1.30, P=0.00), recessive model (OR: 1.28, 95% CI: 1.05-1.56, P=0.02), homozygote comparison (OR: 1.36, 95% CI: 1.12-1.66, P=0.002) or heterozygote comparison (AG versus GG) (OR: 1.21, 95% CI: 1.15-1.29, P=0.00) of CR1 rs6656401A/G. For CR1 rs3818361T/C, a statistical difference was observed in the dominant model (OR: 1.21, 95% CI: 1.13-1.31, P=0.00), recessive model (OR: 1.28, 95% CI: 1.07-1.53, P=0.006), homozygote comparison (OR: 1.35, 95% CI: 1.13-1.62, P=0.001) or heterozygote comparison (TC versus CC) (OR: 1.20, 95% CI: 1.11-1.29, P=0.00). In summary, despite some limitations, the present meta-analysis indicated that rs6656401A/G or rs3818361T/C polymorphism was related to SAD risk. Moreover, a carrier of rs6656401A/G or T carrier of rs3818361T/C in CR1 genetic polymorphism might be an increased factor for SAD in Caucasians.

The association of three BACE1 gene polymorphisms (exon5 C/G, intron 5 T/G and 3'UTR T/A) with sporadic Alzheimer's disease susceptibility: a meta-analysis.

Despite biological support for a role of Beta-site APP-cleaving enzyme 1 (BACE1) in sporadic Alzheimer's disease (SAD), studies about the BACE1 genetic polymorphisms in SAD are inconsistent. To explore whether the BACE1 polymorphisms confers susceptibility to SAD, the current meta-analysis was conducted to evaluate the gene-disease association in relevant studies. The serious databases were researched to identify studies. The association between BACE1 (exon5 C/G, intron 5 T/G or 3'UTR T/A) polymorphism and SAD risk was evaluated by odds ratios (ORs) together with their 95% confidence intervals (CIs). The combined results showed no significant difference in all models on the basis of all studies for BACE1 (exon5 C/G, intron 5 T/G or 3'UTR T/A) polymorphisms. When subgroup analysis was performed based on ethnicity and the epsilon 4 allele of apolipoprotein E (APOEε4) carriers status, significant associations were demonstrated (CC versus CG+GG: OR=1.37, 95% CI=1.04-1.82, P=0.03<0.05 and CC versus CG: OR=1.49, 95% CI=1.11-2.01, P=0.01<0.05) for APOEε4 carriers status. The pooled results suggest the BACE1 (exon5 C/G, intron 5 T/G or 3'UTR T/A) polymorphism could be not a risk factor for SAD. However, individuals with CC genotype have higher risk of SAD with APOEε4 carrier status, and gene-gene interaction might affect on the association. Further studies with large sample size, especially in subgroup analysis, should be done to confirm these findings.