Mitochondria replacement from transplanted amniotic fluid stem cells:a promising therapy for non-neuronal defects in spinal muscular atrophy

Spinal muscular atrophy(SMA)is a genetic disorder that primarily affects infants and leads to muscle weakness,atrophy,and paralysis.The main cause is the homozygous mutation or deletion of the SMN1 gene,resulting in inadequate levels of the survival motor neuron(SMN)protein.Approved treatments focus on restoring SMN levels through various approaches,but there is a need for“SMN-independent”therapies that target other pathological processes.Skeletal muscle is closely involved in SMA pathology,with impaired muscle function observed before motor neuron degeneration.Studies have revealed that SMN loss leads to skeletal muscle mitochondrial structural abnormalities,impaired respiration,and accumulation of reactive oxygen species.

Strain-dependent alpha-synuclein spreading in Parkinson's disease and multiple system atrophy

Parkinson's disease(PD) and atypical Parkinsonian syndromes,such as multiple system atrophy(MSA) and Dementia with Lewy bodies,are neurodegenerative movement disorders characterized by the accumulation of alphasynuclein(a-syn) aggregates.These a-syn aggregates propagate throughout the brain in a prion-like manner,where pathological a-syn recruits endogenous a-syn to form insoluble aggregates.Oligomeric forms representing intermediates on the way to insoluble aggregates result in the most pronounced neurotoxic effects.

Infantile Spinal Muscular Atrophy at the Albert Royer National Children’s Hospital Center in Dakar

Introduction: Infantile spinal muscular atrophy (ISA) is an autosomal recessive disease caused by primary degeneration of cells in the anterior horn of the spinal cord, leading to muscle weakness and hypotonia. Its incidence is estimated at 1 in 6000 births worldwide. In Africa, particularly in Senegal, there are few studies interested on this pathology. We therefore deemed this study necessary, which set itself the objective of describing the diagnostic, therapeutic and progressive aspects of infantile spinal muscular atrophy at the Albert Royer National Children’s Hospital Center in Dakar (CHNEAR). Methodology: We conducted a retrospective descriptive study over a period of two (2) years from December 2020 to December 2022. Included were all hospitalized patients in whom the diagnosis of spinal muscular atrophy was made with or without genetic confirmation. The data were collected on a pre-established form then entered and analyzed with the following software: Excel 2013 and R version 4.1.3. Results: During our study period, 2100 children were hospitalized, the annual incidence was 0.76%. The average age of our patients was 9 ± 9 months with a range of 3 months to 32 months and the median was 6.5 months. The sex ratio was 7. The notion of family consanguinity was found in 62.5% of cases and the notion of ISA in the family in 25% of cases. Hypotonia and respiratory distress were found at the forefront in equal proportions (50% of cases). Electromyogram (EMG) was performed in 3 patients (37.5%). Symptomatic medical treatment was administered in 100% of patients, 04 patients had benefited from respiratory physiotherapy, i.e. 50% of cases, and genetic counseling was carried out in one patient (12.5%). The evolution was immediately favorable in 2 patients or 25% of cases, unfavorable in 75% of cases with a death rate of 50% and the average age of death was 5.5 months ± 1 with extremes ranging from 3 to 7 months. Conclusion: The number of Infantile spinal muscular atrophy cases remains low in hospitals in Dakar. Diagnostic means are still difficult to access. The course is difficult to predict and is often marked in the long term by respiratory difficulties which can be fatal.

Anesthetic Management of a Patient with Spinal Muscular Atrophy Type III Undergoing Emergent Caesarean Section: A Case Report

In this case report, we describe the anesthetic management for a 36-year-old G2P0010 at 36 weeks gestation with Spinal Muscular Atrophy Type III who underwent an emergent caesarean section due to fetal footling breech position. The patient is a wheelchair-bound quadriplegic with kyphoscoliosis and a lack of cough reflex who required nasal continuous noninvasive ventilatory support (CNVS) for chronic hypercapnic respiratory failure. Surgery was done under general anesthesia due to its emergent nature, and the patient was successfully extubated and transitioned to nasal CNVS in the operating room at the end of the case. Postoperative care was provided in the medical intensive care unit for three days without complication and the patient was discharged home uneventfully.

Inverse relationship between platelet Akt activity and hippocampal atrophy:A pilot case-control study in patients with diabetes mellitus

BACKGROUND Akt plays diverse roles in humans.It is involved in the pathogenesis of type 2 diabetes mellitus(T2DM),which is caused by insulin resistance.Akt also plays a vital role in human platelet activation.Furthermore,the hippocampus is closely associated with memory and learning,and a decrease in hippocampal volume is reportedly associated with an insulin-resistant phenotype in T2DM patients without dementia.AIM To investigate the relationship between Akt phosphorylation in unstimulated platelets and the hippocampal volume in T2DM patients.METHODS Platelet-rich plasma(PRP)was prepared from the venous blood of patients with T2DM or age-matched controls.The pellet lysate of the centrifuged PRP was subjected to western blotting to analyse the phosphorylation of Akt,p38 mitogen-activated protein(MAP)kinase and glyceraldehyde 3-phosphate dehydrogenase(GAPDH).Phosphorylation levels were quantified by densitometric analysis.Hippocampal volume was analysed using a voxel-based specific regional analysis system for Alzheimer’s disease on magnetic resonance imaging,which proposes the Z-score as a parameter that reflects hippocampal volume.RESULTS The levels of phosphorylated Akt corrected with phosphorylated p38 MAP kinase were inversely correlated with the Z-scores in the T2DM subjects,whereas the levels of phosphorylated Akt corrected with GAPDH were not.However,this relationship was not observed in the control patients.CONCLUSION These results suggest that an inverse relationship may exist between platelet Akt activation and hippocampal atrophy in T2DM patients.Our findings provide insight into the molecular mechanisms underlying T2DM hippocampal atrophy.

Mitochondrial dysfunction in type 2 diabetes:A neglected path to skeletal muscle atrophy

Over the course of several decades,robust research has firmly established the significance of mitochondrial pathology as a central contributor to the onset of skeletal muscle atrophy in individuals with diabetes.However,the specific intricacies governing this process remain elusive.Extensive evidence highlights that individuals with diabetes regularly confront the severe consequences of skeletal muscle degradation.Deciphering the sophisticated mechanisms at the core of this pathology requires a thorough and meticulous exploration into the nuanced factors intricately associated with mitochondrial dysfunction.

External anal sphincter electromyography in multiple system atrophy:implications for diagnosis,clinical correlations,and novel insights into prognosis

Multiple system atrophy is a sporadic,progressive,adult-onset,neurodegenerative disorder characte rized by autonomic dysfunction symptoms,parkinsonian features,and cerebellar signs in va rious combinations.An early diagnosis of multiple system atrophy is of utmost impo rtance for the proper prevention and management of its potentially fatal complications leading to the poor prognosis of these patients.The current diagnostic criteria incorporate several clinical red flags and magnetic resonance imaging marke rs supporting diagnosis of multiple system atrophy.Nonetheless,especially in the early disease stage,it can be challenging to differentiate multiple system atrophy from mimic disorders,in particular Parkinson’s disease.Electromyography of the external anal sphincter represents a useful neurophysiological tool for diffe rential diagnosis since it can provide indirect evidence of Onuf’s nucleus degeneration,which is a pathological hallmark of multiple system atrophy.However,the diagnostic value of external anal sphincter electromyography has been a matter of debate for three decades due to controve rsial reports in the literature.In this review,after a brief ove rview of the electrophysiological methodology,we first aimed to critically analyze the available knowledge on the diagnostic role of external anal sphincter electromyography.We discussed the conflicting evidence on the clinical correlations of neurogenic abnormalities found at external anal sphincter electro myography.Finally,we repo rted recent prognostic findings of a novel classification of electromyography patterns of the external anal sphincter that could pave the way toward the implementation of this neurophysiological technique for survival prediction in patients with multiple system atrophy.

Three siblings with gyrate atrophy of the choroid and retina:a case report

Dear Editor,We report the cases of three siblings with gyrate atrophy(GA)of the choroid and retina with foveoschisis,anterior subcapsular cataracts,and capsular bag contraction.GA is a rare autosomal recessive degenerative disorder of the choroid and retina.About one-third of all reported cases are from Finland where the incidence is estimated to be around 1:50000 whereas the theoretical global incidence is only 1:1500000[1].

Pharmacological effects of denervated muscle atrophy due to metabolic imbalance in different periods

Denervation-induced skeletal muscle atrophy can potentially cause the decline in the quality of life of patients and an increased risk of mortality.Complex pathophysiological mechanisms with dynamic alterations have been documented in skeletal muscle atrophy resulting from innervation loss.Hence,an in-depth comprehension of the key mechanisms and molecules governing skeletal muscle atrophy at varying stages,along with targeted treatment and protection,becomes essential for effective atrophy management.Our preliminary research categorizes the skeletal muscle atrophy process into four stages using microarray analysis.This review extensively discusses the pathways and molecules potentially implicated in regulating the four stages of denervation and muscle atrophy.Notably,drugs targeting the reactivare oxygen species stage and the inflammation stage assume critical roles.Timely intervention during the initial atrophy stages can expedite protection against skeletal muscle atrophy.Additionally,pharmaceutical intervention in the ubiquitin-proteasome pathway associated with atrophy and autophagy lysosomes can effectively slow down skeletal muscle atrophy.Key molecules within this stage encompass MuRF1,MAFbx,LC3II,p62/SQSTM1,etc.This review also compiles a profile of drugs with protective effects against skeletal muscle atrophy at distinct postdenervation stages,thereby augmenting the evidence base for denervation-induced skeletal muscle atrophy treatment.

Functional recovery and muscle atrophy in pre-clinical models of peripheral nerve transection and gap-grafting in mice:effects of 4-aminopyridine

We recently demonstrated a repurposing beneficial effect of 4-aminopyridine(4-AP),a potassium channel blocker,on functional recove ry and muscle atrophy after sciatic nerve crush injury in rodents.However,this effect of 4-AP is unknown in nerve transection,gap,and grafting models.To evaluate and compare the functional recovery,nerve morphology,and muscle atrophy,we used a novel stepwise nerve transection with gluing(STG),as well as 7-mm irreparable nerve gap(G-7/0)and 7-mm isografting in 5-mm gap(G-5/7)models in the absence and presence of 4-AP treatment.Following surgery,sciatic functional index was determined wee kly to evaluate the direct in vivo global motor functional recovery.After 12 weeks,nerves were processed for whole-mount immunofluorescence imaging,and tibialis anterior muscles were harvested for wet weight and quantitative histomorphological analyses for muscle fiber crosssectional area and minimal Feret's diameter.Average post-injury sciatic functional index values in STG and G-5/7 models were significantly greater than those in the G-7/0 model.4-AP did not affect the sciatic functional index recovery in any model.Compared to STG,nerve imaging revealed more misdirected axons and distorted nerve architecture with isografting.While muscle weight,cross-sectional area,and minimal Feret's diameter were significantly smaller in G-7/0 model compared with STG and G-5/7,4-AP treatment significantly increased right TA muscle mass,cross-sectional area,and minimal Feret's diameter in G-7/0 model.These findings demonstrate that functional recovery and muscle atrophy after peripheral nerve injury are directly related to the intervening nerve gap,and 4-AP exerts diffe rential effects on functional recove ry and muscle atrophy.

Screening and verification of the lncRNA-miRNA-mRNA regulatory network in muscle atrophy after spinal cord injury

Objective:To find the key targets of muscle atrophy after spinal cord injury(SCI)were excavated,to construct the lncRNA-miRNA-mRNA regulatory network based on bioinformatics analysis,and to verify the expression changes of key regulatory networks in muscle atrophy after SCI by animal experiments,so as to seek new research directions for the pathogenesis and treatment of muscle atrophy after SCI.Methods:The GSE21497 data set was downloaded from the GEO database for differential expression gene screening and WGCNA treatment.Combined with the online prediction database,key mRNAs were screened out.GO and KEGG enrichment analyses of key mRNAs were performed using the DAVID database to construct the lncRNA-miRNA-mRNA regulatory network.The key regulatory genes were selected and then verified by RT-qPCR.Results:A total of 1405 differentially expressed genes were screened,and 30 key mRNAs were predicted by the WGCNA and online database.GO and KEGG enrichment analyses showed that it was mainly enriched in the functions of neuron regeneration,protection,signal transmission,the HIF signaling pathway,PD-L1 expression and the PD-1 checkpoint pathway.Four key regulatory networks were identified(LINC00410/miR-17-5p/KCNK10,LINC00410/miR-17-5p/PCDHA3,LINC00410/miR-20b-5p/KCNK10,LINC00410/miR-20b-5p/PCDHA3).The results of RT-qPCR showed that,compared with the control group,the expression of miR-17-5p and miR-20b-5p in the observation group increased,and the expression of KCNK10 and PCDHA3 decreased.Conclusions:MiR-17-5p,miR-20b-5p,KCNK10,and PCDHA3 may play an important regulatory role in the regeneration,protection,and signal transmission of neurons,which is expected to become a new target for the diagnosis and treatment of muscle atrophy after SCI.

Imaging misdiagnosis and clinical analysis of significant hepatic atrophy after bilioenteric anastomosis: A case report

BACKGROUND The occurrence of long-term bilioenteric anastomotic stenosis can readily induce liver atrophy and hyperplasia,thereby causing significant alterations in the anatomical and morphological aspects of the liver.This condition significantly hampers the accuracy of preoperative imaging diagnosis,while also exacerbating the complexity of surgical procedures and the likelihood of complications.CASE SUMMARY A 60-year-old female patient was admitted to the hospital presenting with recurring epigastric pain accompanied by a high fever.The patient had a history of cholecystectomy,although the surgical records were not accessible.Based on preoperative imaging and laboratory examination,the initial diagnosis indicated the presence of intrahepatic calculi,abnormal right liver morphology,and acute cholangitis.However,during the surgical procedure,it was observed that both the left and right liver lobes exhibited evident atrophy and thinness.Additionally,there was a noticeable increase in the volume of the hepatic caudate lobe,and the original bilioenteric anastomosis was narrowed.The anastomosis underwent enlargement subsequent to hepatectomy.As a consequence of the presence of remaining stones in the caudate lobe,the second stage was effectively executed utilizing ultrasound-guided percutaneous transhepatic catheter drainage.Following the puncture,three days elapsed before the drain tip inadvertently perforated the liver,leading to the development of biliary panperitonitis,subsequently followed by pulmonary infection.The patient and her family strongly refused operation,and she died.CONCLUSION The hepatic atrophy-hypertrophy complex induces notable alterations in the anatomical structure,thereby posing a substantial challenge in terms of imaging diagnosis and surgical procedures.Additionally,the long-term presence of hepatic fibrosis changes heightens the likelihood of complications arising from puncture procedures.

The role of 5′-adenosine monophosphate-activated protein kinase(AMPK)in skeletal muscle atrophy

As a key coordinator of metabolism,AMP-activated protein kinase(AMPK)is vitally involved in skeletal muscle maintenance.AMPK exerts its cellular effects through its function as a serine/threonine protein kinase by regulating many downstream targets and plays important roles in the development and growth of skeletal muscle.AMPK is activated by phosphorylation and exerts its function as a kinase in many processes,including synthesis and degradation of proteins,mitochondrial biogenesis,glucose uptake,and fatty acid and cholesterol metabolism.Skeletal muscle atrophy is a result of various diseases or disorders and is characterized by a decrease in muscle mass.The pathogenesis and therapeutic strategies of skeletal muscle atrophy are still under investigation.In this review,we discuss the role of AMPK in skeletal muscle metabolism and atrophy.We also discuss targeting AMPK for skeletal muscle treatment,including exercise,AMPK activators including 5-amino-4-imidazolecarboxamide ribonucleoside and metformin,and low-level lasers.These studies show the important roles of AMPK in regulating muscle metabolism and function;thus,the treatment of skeletal muscle atrophy needs to take into account the roles of AMPK.

Effects of Neuromuscular Electrical Stimulation in Combination with Glutamine Administration on Skeletal Muscle Atrophy in Colon-26 Tumor-Bearing Mice

The depressed protein synthetic response,a phenomenon termed anabolic resistance,has been shown to be involved in muscle wasting induced by cancer cachexia.Moreover,a positive relationship between the protein synthetic rate and intracellular glutamine(GLN)concentration has been found in skeletal muscles.This study investigated the effects of neuromuscular electrical stimulation(ES)and GLN administration on muscle wasting and GLN metabolism in colon-26(C-26)tumor-bearing mice.CD2F1 mice were divided into 8 groups:control(CNT),CNT+ES,CNT+GLN,CNT+ES+GLN,C-26,C-26+ES,C-26+GLN,C-26+ES+GLN.Cancer cachexia was induced by subcutaneous injection of C-26 cells and developed for four weeks.ES was performed on the left plantar flexor muscles every other day,and GLN(1 g/kg)was administered daily intraperitoneally starting one day after the C-26 injection.Tumor-free body mass and fast-twitch gastrocnemius(Gas)muscle weight were lower in the C-26 group than in the CNT group(-19%and-17%,respectively).Neither ES training nor GLN administration,alone or in combination,ameliorated the loss of Gas muscle weight in the C-26 mice.However,ES training in combination with GLN administration inhibited the increased expression of GLN synthetase(GS)in the C-26 muscles.Thus,it is likely that GLN plays a critical role in muscle protein metabolism and,therefore,can be targeted as a tentative treatment of cancer cachexia.

基于“阳化气,阴成形”理论辨治痿证

津气两伤是痿证的病变基础,亦是“阳化气,阴成形”失衡的结果。阳化气不足,阴成形失衡,而致脏腑功能失调,水饮痰瘀内生,四肢九窍失养,发为痿证。本文基于“阳化气,阴成形”理论,探讨高颖教授采用助阳化气法治疗阳化气不足的重症肌无力,益肾调形法治疗阴成形失衡的多发性硬化,阴阳双补法治疗阴阳俱损的运动神经元病。治疗痿证,需审证求因,明辨阴阳,调整偏颇,在疾病早期给予中医药治疗,以延缓疾病演变进程、改善预后。

游泳运动对大鼠创伤性关节挛缩的影响及机制

背景:早期运动是预防创伤性关节挛缩的主要方式,也是近期研究热点。游泳运动借助水的特殊物理特性,可能是潜在有益的干预方式。目的:观察游泳运动对大鼠关节挛缩发展的影响,探究游泳运动预防关节挛缩的相关机制。方法:24只SD大鼠随机分为空白对照组(n=8)和关节挛缩造模组(n=16),手术制备膝关节挛缩模型后,再随机分为手术对照组(n=8)和游泳干预组(n=8)。游泳干预组在术后第2周开始游泳干预,共干预5周。在术后第6周,测试各组大鼠体质量、术侧膝关节活动度、股四头肌直径,计算直径-体质量指数;苏木精-伊红染色观察膝关节囊和股四头肌病理变化;Masson染色观察关节囊胶原纤维化改变;免疫组化检测膝关节囊中转化生长因子β1和Ⅰ型胶原蛋白表达;Western blot检测股四头肌中MuRF1蛋白的表达。结果与结论:①与空白对照组比较,手术对照组和游泳干预组大鼠膝关节活动度下降,总伸膝受限角度和关节源性伸膝受限角度均明显增加(P<0.01),股四头肌直径下降(P<0.01),关节囊出现明显纤维化表现,股四头肌萎缩,手术对照组直径-体质量指数降低(P<0.01);与手术对照组比较,游泳干预组大鼠膝关节活动度和股四头肌直径明显增加(P<0.01),关节囊纤维化病变和股四头肌萎缩明显改善;②与空白对照组比较,手术对照组和游泳干预组大鼠关节囊中胶原纤维含量、转化生长因子β1和Ⅰ型胶原蛋白表达均增加(P<0.01);与手术对照组比较,游泳干预组大鼠关节囊中胶原纤维含量、转化生长因子β1和Ⅰ型胶原蛋白表达均降低(P<0.01);③与空白对照组比较,手术对照组和游泳干预组大鼠股四头肌中MuRF1蛋白表达增加(P<0.05);与手术对照组比较,游泳干预组大鼠股四头肌中MuRF1蛋白表达降低(P<0.05)。结果表明:早期游泳干预能够降低创伤性挛缩大鼠关节囊中转化生长因子β1和Ⅰ型胶原蛋白表达,降低股四头肌中MuRF1蛋白表达,提高关节活动度和股四头肌直径,抑制关节挛缩的发展。

颈椎椎旁肌退变与颈椎疾病的发生和手术预后相关性的研究进展

颈椎椎旁肌作为颈椎周围重要的附着结构,其功能状态与颈椎疾病的发生、发展及手术预后均有着密切关联。颈椎椎旁肌的退变往往会通过影响颈椎稳定性、矢状位平衡等方面进而诱发颈椎疾病,并与颈椎手术预后存在一定的相关性,颈椎疾病则通过去神经支配、炎症、失平衡等不同机制亦能加速颈椎椎旁肌的退变。本文将从多个方面对颈椎椎旁肌退变与颈椎疾病的发生和手术预后相关性进行综述,以期为剖析颈椎疾病的病因及其治疗方面提供参考。

糖尿病前期及2型糖尿病皮层萎缩与认知功能的相关性研究

目的探讨糖尿病前期(pre-diabetes mellitus,PDM)和2型糖尿病(type 2 diabetes mellitus,T2DM)大脑皮层的改变模式及其与认知功能的关系,以期探寻血糖代谢异常被试早期脑损害的影像标志物。材料与方法本研究纳入96例T2DM患者、30例PDM被试以及48名正常对照(normal control,NC),对被试进行了认知功能测试、临床生化检查及高分辨率3D-T1WI磁共振扫描。使用CAT12软件进行基于体素的形态学分析和基于表面的形态学分析得到全脑灰质体积和皮层厚度、局部回指数等皮层结构参数,并比较3组间的差异,结果均使用P<0.05的阈值和FWE校正进行多重比较校正。进一步提取组间具有差异的参数,与生化指标及认知量表得分进行相关分析。结果与NC相比,PDM被试右侧额下回眶部及左侧中央后回灰质萎缩(P<0.05,FWE校正),T2DM患者出现更多灰质萎缩,特别是右侧颞上回、右侧额下回眶部、右侧颞中回及左侧中央后回,右侧前额叶皮层厚度减小(P<0.05,FWE校正)。在血糖代谢异常被试中全脑灰质体积与胰岛素抵抗指数(r=−0.227,P=0.012,未校正)及连线测试A得分(r=−0.250,P=0.001,FDR校正)呈负相关,与数字广度-倒背得分呈正相关(r=0.267,P=0.003,FDR校正);皮层厚度与糖化血红蛋白(r=−0.181,P=0.040,未校正)及餐后2 h血糖(r=−0.272,P=0.020,未校正)呈负相关,与餐后2 h胰岛素(r=0.236,P=0.010,未校正)及胰岛β细胞功能指数(r=0.207,P=0.022,未校正)呈正相关。结论本研究发现PDM人群已存在脑区灰质萎缩,T2DM患者出现更多的灰质萎缩,且与注意和工作记忆功能相关,因此皮层萎缩有可能是糖尿病相关脑损伤早期的影像标志物。

人参皂苷Rg1干预小鼠巨大肩袖损伤后的肌肉退变

背景:肩袖肌退变(肌肉萎缩、纤维化和脂肪浸润)是肩袖撕裂后出现的常见问题,严重影响肩关节功能和手术预后。人参皂苷Rg1具有抗氧化、抗细胞凋亡、降血脂等生物效应,然而人参皂苷Rg1对肩袖损伤后肌肉退变的影响未见报道。目的:探讨人参皂苷Rg1对巨大肩袖损伤小鼠肌肉退变的影响。方法:将60只C57BL/6J小鼠随机分为假手术组、模型组、人参皂苷Rg1低剂量组、人参皂苷Rg1高剂量组,每组15只。假手术组小鼠切开右肩皮肤后缝合,其余3组小鼠均行右侧肩关节肩袖损伤造模,模拟巨大肩袖撕裂手术切断冈上肌肌腱和肩胛上神经压迫。术后假手术组和模型组腹腔注射生理盐水0.5 mL;人参皂苷Rg1低、高剂量组予以腹腔注射人参皂苷Rg130,60 mg/kg,1次/d,共注射6周。末次注射后次日予以步态分析评估小鼠肢体功能,安乐死后取术侧冈上肌测量肌肉萎缩率、肌肉收缩力,肌肉组织进行油红O染色、Masson染色,RT-PCR检测萎缩、纤维化、脂肪浸润相关基因的表达。结果与结论:①与模型组相比,人参皂苷Rg1低、高剂量组爪印面积、步长显著增加(P<0.05);②与模型组相比,人参皂苷Rg1低、高剂量组肌纤维横截面积、冈上肌收缩力显著增加(P<0.05),湿肌质量减少比率、脂肪浸润面积比率、胶原纤维面积比率显著下降(P<0.05);③与模型组相比,人参皂苷Rg1低、高剂量组肌肉组织中萎缩、纤维化和脂肪浸润相关基因的表达显著下降(P<0.05);④人参皂苷Rg1低、高剂量组爪印面积、冈上肌收缩力、肌纤维横截面积无统计学差异(P>0.05),人参皂苷Rg1高剂量组其他指标均优于低剂量组(P<0.05);⑤结果说明,人参皂苷Rg1能显著减轻小鼠巨大肩袖撕裂后肩袖肌萎缩、纤维化和脂肪浸润,并有利于肌肉力量及肢体功能的改善。

颞浅动脉-大脑中动脉搭桥与颞肌贴覆治疗缺血性烟雾病术后颞肌血运及并发症的比较

目的 比较颞浅动脉-大脑中动脉搭桥与颞肌贴覆术对成年缺血性烟雾病(MMD)患者神经功能和脑血流的改善作用,以及对颞肌血运、术后相关并发症的影响。方法 以2020-09—2022-12秦皇岛市第一医院收治的39例MMD患者为研究对象,其中单纯实施颞肌贴覆术20例为对照组,实施颞浅动脉-大脑中动脉搭桥术19例为研究组。采用改良Rankin量表(mRS)比较2组患者治疗前后神经功能恢复情况,采用经颅多普勒检测2组患者治疗前后脑动脉血流的平均流速(Vm)和脉动指数(PI),CT影像比较2组患者手术前后颞肌厚度,记录2组患者术后并发症发生率。结果 2组患者术后7 d、3个月m RS评分均明显低于术前1 d(P<0.05);与对照组相比,研究组3个时间点的mRS评分均明显降低(P<0.05)。2组患者术后7 d、3个月PI评分均明显低于术前1 d(P<0.05);与对照组相比,研究组3个时间点的PI评分均明显降低(P<0.05)。2组患者术后7 d、3个月Vm均明显高于术后1 d(P<0.05);与对照组相比,研究组3个时间点的Vm均显著升高(P<0.05)。对照组术后颞肌萎缩及咀嚼无力发生率明显高于研究组(30.0%比5.3%,45.0%比15.8%),颞肌厚度明显小于研究组(4.16±0.14比5.04±0.22),差异均有统计学意义(P<0.05)。结论 颞浅动脉-大脑中动脉搭桥术治疗缺血性烟雾病相比颞肌贴覆术,能够有效促进脑血流的恢复,改善缺血性烟雾病的脑血流状况,缓解缺血症状。而颞肌贴覆术,由于没有影响颞浅动脉对于颞肌的血运,因此术后出现颞肌萎缩相关并发症的概率明显减低,临床上需要重视开颅过程中对颞浅动脉的保护,必要时予以重建。