Cardioprotective effects of sinomenine in myocardial ischemia/reperfusion injury in a rat model

BackgroundIschemia reperfusion (I/R) play an imperative role in the expansion of cardiovascular disease. Sinomenine (SM) has been exhibited to possess antioxidant, anticancer, anti-inflammatory, antiviral and anticarcinogenic properties. The aim of the study was scrutinized the cardioprotective effect of SM against I/R injury in rat.MethodsRat were randomly divided into normal control (NC), I/R control and I/R + SM (5, 10 and 20 mg/kg), respectively. Ventricular arrhythmias, body weight and heart weight were estimated. Antioxidant, inflammatory cytokines, inflammatory mediators and plasmin system indicator were accessed.ResultsPre-treated SM group rats exhibited the reduction in the duration and incidence of ventricular fibrillation, ventricular ectopic beat (VEB) and ventricular tachycardia along with suppression of arrhythmia score during the ischemia (30 and 120 min). SM treated rats significantly (P < 0.001) altered the level of antioxidant parameters. SM treatment significantly (P < 0.001) repressed the level of creatine kinase MB (CK-MB), creatine kinase (CK) and troponin I (Tnl). SM treated rats significantly (P < 0.001) repressed the tissue factor (TF), thromboxane B2 (TXB2), plasminogen activator inhibitor 1 (PAI-1) and plasma fibrinogen (Fbg) and inflammatory cytokines and inflammatory mediators.ConclusionOur result clearly indicated that SM plays anti-arrhythmia effect in I/R injury in the rats via alteration of oxidative stress and inflammatory reaction.     

Protective effect of creatine on amikacin-induced ototoxicity

IntroductionAminoglycosides are widely known for their ototoxic side effects. Nevertheless, they are potent antibiotics used in the treatment of life-threatening conditions because of the current concern for antibiotic resistance. We hypothesized that creatine supplements which are believed to improve mitochondrial antioxidant defense system and maintain optimal energy homeostasis may improve the ototoxic side effects.ObjectiveThis study aimed to investigate the protective effects of creatine monohydrate against ototoxicity induced by amikacin in rats in an experimental animal model, using distortion product otoacoustic emissions and auditory brainstem response.MethodsTwenty healthy rats were assigned to four groups (5 rats in each): the control group, the creatine monohydrate group, the amikacin group and the amikacin + creatine monohydrate group. The creatine monohydrate group received creatine at a dose of 2 g/kg once daily via gastric gavage for 21 days. The amikacin group received amikacin at a dose of 600 mg/kg by intramuscular injections once daily for 21 days. The amikacin + creatine monohydrate group received intramuscular injections of amikacin (600 mg/kg) once daily for 21 days and creatine monohydrate (2 g/kg) once daily via gastric gavage for 21 days. The control group received nothing. The distortion product otoacoustic emissions and auditory brainstem response measurements were performed on all rats on days 0, 7, 21.ResultsRegarding auditory brainstem response values, a significant increase in the auditory threshold was observed in the amikacin group on day 21 (p <  0.001). The amikacin+creatine monohydrate group showed significantly lower levels of auditory brainstem response auditory thresholds on day 21 in comparison to the amikacin group (p <  0.001). Additionally, the control group and the amikacin+creatine monohydrate group did not differ significantly with respect to auditory brainstem response thresholds on treatment day 21 (p >  0.05). When we compare distortion product otoacoustic emissions values, there was no significant difference between the amikacin and amikacin+creatine monohydrate groups on day 7 (p >  0.05), However significantly greater distortion product otoacoustic emissions values were observed in the amikacin+creatine monohydrate group on day 21 compared to the amikacin group (p <  0.001).ConclusionOur findings demonstrate that creatine treatment protects against amikacin ototoxicity when given at a sufficient dose and for an adequate time period.     

Acute rhabdomyolysis following viral infection with coxsackie A4 in a 50-day-old infant with Fukuyama congenital muscular dystrophy

BackgroundFukuyama congenital muscular dystrophy (FCMD), which is characterized by generalized muscle weakness, hypotonia, and motor delay during early infancy, gradually progresses with advanced age. Although acute rhabdomyolysis following infection in patients with FCMD has occasionally been reported, no studies have investigated rhabdomyolysis following viral infection in FCMD patients during early infancy.Case reportWe report the case of a 50-day-old girl with no apparent symptoms of muscular dystrophy who developed severe acute rhabdomyolysis caused by viral infection, resulting in quadriplegia and respiratory failure therefore requiring mechanical ventilation. Brain magnetic resonance imaging incidentally showed the typical characteristics of FCMD, and FCMD was confirmed by genetic analysis, which revealed a 3-kb retrotransposon insertion in one allele of the fukutin gene and a deep intronic splicing variant in intron 5 in another allele. The virus etiology was confirmed to be Coxsackie A4.ConclusionWe report a severe case of acute rhabdomyolysis with the earliest onset of symptoms due to the Coxsackie A4 virus in a patient with FCMD. The present findings indicate that physicians should consider FCMD with viral infection a differential diagnosis if the patient presents with acute rhabdomyolysis following a fever.     

Changes in urinary titin N-terminal fragments as a biomarker of exercise-induced muscle damage in the repeated bout effect

ObjectivesMuscle damage symptoms induced by unaccustomed eccentric contraction exercise can be reduced by repeating the experience several times. This phenomenon is termed the repeated bout effect. Although traditional biochemical markers require invasive blood sampling, biochemical measurements have recently been developed that can be non-invasively performed using urinary titin N-terminal fragment (UTF). However, it is unclear whether UTF can reflect the repeated bout effect. Therefore, the aim of the present study was to clarify whether UTF decreased with the repeated bout effect.DesignThis study compared changes in muscle damage markers between bouts of exercise performed for the first and second time.MethodsEight young men performed 30 eccentric exercises of the elbow flexor on the first day of the first week (Bout 1). A second bout of eccentric exercises, same as the first, was performed 2 weeks later, (Bout 2). The dependent variables were muscle soreness (SOR), maximal voluntary isometric contraction (MVIC), range of motion (ROM), creatine kinase (CK), and UTF. All dependent variables were analyzed using two-way analysis of variance.ResultsNo significant difference was observed in workload or peak torque between the first and second exercise bouts. SOR as well as CK and UTF were significantly lower and ROM and MVIC were significantly higher in Bout 2 in comparison to Bout 1.ConclusionsThese results suggest that UTF sensitively reflects the repeated bout effect and exercise-induced muscle damage can be non-invasively measured.     

Abnormal liver function tests associated with severe rhabdomyolysis

Rhabdomyolysis is a syndrome of skeletal muscle injury with release of cellular constituents such as potassium,phosphate,urate and intracellular proteins such as myoglobin into the circulation,which may cause complications including acute kidney injury,electrolyte disturbance and cardiac instability.Abnormal liver function tests are frequently observed in cases of severe rhabdomyolysis.Typically,there is an increase in serum aminotransferases,namely aspartate aminotransferase and alanine aminotransferase.This raises the question of liver injury and often triggers a pathway of investigation which may lead to a liver biopsy.However,muscle can also be a source of the increased aminotransferase activity.This review discusses the dilemma of finding abnormal liver function tests in the setting of muscle injury and the potential implications of such an association.It delves into some of the clinical and experimental evidence for correlating muscle injury to raised aminotransferases,and discusses pathophysiological mechanisms such as oxidative stress which may cause actual liver injury.Serum aminotransferases lack tissue specificity to allow clinicians to distinguish primary liver injury from muscle injury.This review also explores potential approaches to improve the accuracy of our diagnostic tools,so that excessive or unnecessary liver investigations can be avoided.     

穴位埋线治疗进行性肌营养不良的疗效观察

目的观察穴位埋线联合糖皮质激素及神经营养药物治疗进行性肌营养不良的临床疗效。方法 50例进行性假肥大性肌营养不良患者,随机分为治疗组和对照组,每组25例。对照组采用糖皮质激素及神经营养药物治疗,治疗组在对照组基础上采用穴位埋线治疗。观察两组治疗前后10米步行时间和登梯时间及血清肌酸磷酸激酶(CPK)、乳酸脱氢酶(LDH)水平的变化,并比较两组临床疗效。结果两组治疗后及随访10米步行时间和登梯时间与同组治疗前比较,差异有统计学意义(P<0.05);两组治疗后及随访10米步行时间和登梯时间比较,差异有统计学意义(P<0.05)。两组治疗后及随访血清CPK、LDH水平较同组治疗前明显下降,差异有统计学意义(P<0.01);治疗组治疗后及随访血清CPK和LDH水平低于对照组(P<0.01)。治疗组总有效率为96.0%,对照组总有效率为72.0%,治疗组总有效率高于对照组(P<0.05)。结论穴位埋线联合糖皮质激素治疗进行性肌营养不良的临床疗效显著,可作为临床治疗进行性肌营养不良方案的优选方法。     

核磁共振结合血清甲胎蛋白、肌酸激酶水平诊断凶险型前置胎盘合并胎盘植入的价值

目的对核磁共振(MRI)结合血清甲胎蛋白(AFP)、肌酸激酶(CK)表达诊断凶险型前置胎盘合并胎盘植入的价值进行探讨。方法选取2015年1月-2016年10月收治的90例凶险型前置胎盘患者,根据手术和术后病理结果分为凶险型前置胎盘合并胎盘植入组(简称植入组,53例)和凶险型前置胎盘非胎盘植入组(简称非植入组,37例),比较两组患者静脉血中AFP、CK的水平,并将所有患者的MRI结果、血清学检查结果及两者联合检查结果与病理结果进行比较。结果植入组血清AFP和CK表达水平显著高于非植入组(P<0.05)。MRI、血清学检查及二者联用的诊断灵敏度(71.74%vs.67.92%)、漏诊率(28.3%vs.32.13%)、阴性预测值(63.34%vs.63.0%)和符合率(71.12%vs.72.25%)之间比较,差异具有统计学意义(P<0.05),联合诊断的灵敏度(90.56%)、阴性预测值(86.84%)和符合率(90.00%)均显著高于单独的MRI或血清学检查(P<0.05),漏诊率(9.43%)低于单独的MRI或血清学检查(P<0.05)。结论 MRI联合血清AFP、CK表达检测能提高诊断的灵敏度和诊断符合率,优于单项检测,具有一定的诊断价值。     

用双位点单抗免疫酶法测定CK—MB质量

应用免疫单抗ＥＬＩＳＡ法测定ＣＫ－ＭＢ的质量，与免疫抑制法及电泳法进行了比较，其准确性和精密性均符合临床要求。急性心肌梗塞（ＡＭＩ）２５份血标本测定结果与免疫抑制法相关方程为Ｙ＝１．０７７Ｘ－４．３，ｒ＝０．９９６，免疫酶法比免疫抑制法更具有特异性。     

Urine screening for patients with developmental disabilities detected a patient with creatine transporter deficiency due to a novel missense mutation in SLC6A8

Creatine transporter deficiency (CTD) is an example of X-linked intellectual disability syndromes, caused by mutations in SLC6A8 on Xq28. Although this is the second most frequent genetic cause of intellectual disabilities in Europe or America after Fragile X syndrome, information on the morbidity of this disease is limited in Japan. Using the HPLC screening method we have established recently, we examined samples of urine of 105 patients (73 males and 32 females) with developmental disabilities at our medical center. And we have found a family with three ID boys with a novel missense mutation in SLC6A8. This is the second report of a Japanese family case of CTD. A systematic diagnostic system of this syndrome should be established in Japan to enable us to estimate its frequency and treatment.