阴道锥体训练联合生物反馈盆底肌治疗尿失禁老年人盆底肌康复研究现状

目的研究阴道锥体训练联合生物反馈盆底肌治疗尿失禁老年人的临床疗效及对盆底肌的影响。方法选取84例从2016年9月至2018年3月本院收治的尿失禁老年患者进行研究,以随机抽签法将其均分为联合组及对照组,每组42例。对照组予以常规盆底肌训练治疗,联合组则予以阴道锥体训练联合生物反馈盆底肌治疗。对比两组在临床疗效、治疗前后盆底肌力情况、治疗前后尿动力学参数指标水平以及生活质量变化情况等方面的差异。结果联合组与对照组在总有效率方面比较,前者高于后者(P<0.05)。治疗后联合组盆底肌力分级为Ⅳ级、Ⅴ级的人数占比相比对照组较高(P<0.05)。治疗后联合组与对照组在VLPP、PMUC水平方面比较,前者高于后者(P<0.05)。治疗后联合组与对照组I-QOL评分相比治疗前较高,且联合组相比对照组较高(P<0.05)。结论阴道锥体训练联合生物反馈盆底肌治疗老年尿失禁患者的疗效显著,有利于促进盆底肌力的恢复,且有效改善患者尿动力学参数,提高生活质量,具有较高的临床推广应用价值。     

Vibratory stimulus to the masseter muscle impairs the oral fine motor control during biting tasks

PurposeTo investigated the effect of vibratory stimulus on masseter muscles during oral fine motor biting tasks.MethodsSixteen healthy individuals (age: 24.5 ± 2.4 years) participated in experiment I during which the participants were asked to “hold and split” half a roasted peanut placed on a force transducer with their front teeth. The participant performed ten series with ten trials of the “hold and split” behavioral task while vibratory stimulus was applied on the masseter muscle every alternate series. Further, fourteen participants participated (age: 25.2 ± 4.8 years) in experiment II during which they performed a series each of the behavioral task at baseline, an adjusted baseline without and with vibration as well as with and without visual feedback. Hold and split forces along with the variability of hold force and duration and force rate during the split were measured.ResultsThe results of the study showed an increase in the magnitude of the hold force (P = 0.002), force rate during the split (P < 0.001) and a significant decrease in the duration of split (P < 0.001) due to the vibratory stimulus. However, there was no significant effect of the vibratory stimulus on the variability of hold forces (P = 0.879) or mean split force (P = 0.683) during the “hold and split” behavioral task. The results of experiment II also showed an increase in hold force due to the vibratory stimulus (P < 0.001).ConclusionsVibratory stimulus to the masseter muscles impairs the oral force control during a standardized biting task and provide further insight into the sensorimotor regulation of the masticatory system.     

INAUGURAL ARTICLE by a Recently Elected Academy Member:Functional redundancy of type I and type II receptors in the regulation of skeletal muscle growth by myostatin and activin A

Myostatin (MSTN) is a transforming growth factor-β (TGF-β) family member that normally acts to limit muscle growth. The function of MSTN is partially redundant with that of another TGF-β family member, activin A. MSTN and activin A are capable of signaling through a complex of type II and type I receptors. Here, we investigated the roles of two type II receptors (ACVR2 and ACVR2B) and two type I receptors (ALK4 and ALK5) in the regulation of muscle mass by these ligands by genetically targeting these receptors either alone or in combination specifically in myofibers in mice. We show that targeting signaling in myofibers is sufficient to cause significant increases in muscle mass, showing that myofibers are the direct target for signaling by these ligands in the regulation of muscle growth. Moreover, we show that there is functional redundancy between the two type II receptors as well as between the two type I receptors and that all four type II/type I receptor combinations are utilized in vivo. Targeting signaling specifically in myofibers also led to reductions in overall body fat content and improved glucose metabolism in mice fed either regular chow or a high-fat diet, demonstrating that these metabolic effects are the result of enhanced muscling. We observed no effect, however, on either bone density or muscle regeneration in mice in which signaling was targeted in myofibers. The latter finding implies that MSTN likely signals to other cells, such as satellite cells, in addition to myofibers to regulate muscle homeostasis.

Myostatin (MSTN) is a secreted signaling molecule that normally acts to limit skeletal muscle growth (for review, see ref. 1). Mice lacking MSTN exhibit dramatic increases in muscle mass throughout the body, with individual muscles growing to about twice the normal size (2). MSTN appears to play two distinct roles in regulating muscle size, one to regulate the number of muscle fibers that are formed during development and a second to regulate the growth of those fibers postnatally. The sequence of MSTN has been highly conserved through evolution, with the mature MSTN peptide being identical in species as divergent as humans and turkeys (3). The function of MSTN has also been conserved, and targeted or naturally occurring mutations in MSTN have been shown to cause increased muscling in numerous species, including cattle (3–5), sheep (6), dogs (7), rabbits (8), rats (9), swine (10), goats (11), and humans (12). Numerous pharmaceutical and biotechnology companies have developed biologic agents capable of blocking MSTN activity, and these have been tested in clinical trials for a wide range of indications, including Duchenne and facioscapulohumeral muscular dystrophy, inclusion body myositis, muscle atrophy following falls and hip fracture surgery, age-related sarcopenia, Charcot–Marie–Tooth disease, and cachexia due to chronic obstructive pulmonary disease, end-stage kidney disease, and cancer.The finding that certain inhibitors of MSTN signaling can increase muscle mass even in Mstn^−/− mice revealed that the function of MSTN as a negative regulator of muscle mass is partially redundant with at least one other TGF-β family member (13, 14), and subsequent studies have identified activin A as one of these cooperating ligands (15, 16). MSTN and activin A share many key regulatory and signaling components. For example, the activities of both MSTN and activin A can be modulated extracellularly by naturally occurring inhibitory binding proteins, including follistatin (17, 18) and the follistatin-related protein, FSTL-3 or FLRG (19, 20). Moreover, MSTN and activin A also appear to share receptor components. Based on in vitro studies, MSTN is capable of binding initially to the activin type II receptors, ACVR2 and ACVR2B (also called ActRIIA and ActRIIB) (18) followed by engagement of the type I receptors, ALK4 and ALK5 (21). In previous studies, we presented genetic evidence supporting a role for both ACVR2 and ACVR2B in mediating MSTN signaling and regulating muscle mass in vivo. Specifically, we showed that mice expressing a truncated, dominant-negative form of ACVR2B in skeletal muscle (18) or carrying deletion mutations in Acvr2 and/or Acvr2b (13) have significantly increased muscle mass. One limitation of the latter study, however, was that we could not examine the consequence of complete loss of both receptors using the deletion alleles, as double homozygous mutants die early during embryogenesis (22). Moreover, the roles that the two type I receptors, ALK4 and ALK5, play in regulating MSTN and activin A signaling in muscle in vivo have not yet been documented using genetic approaches. Here, we present the results of studies in which we used floxed alleles for each of the type II and type I receptor genes in order to target these receptors alone and in combination in muscle fibers. We show that these receptors are functionally redundant and that signaling through each of these receptors contributes to the overall control of muscle mass.     

Psychosocial mechanisms of a behavioral treatment for urinary incontinence of prostate cancer survivors

Abstract

Purpose: We examined underlying psychosocial processes of a behavioral treatment for urinary incontinence (UI) of prostate cancer survivors.

Design: Secondary analysis of data collected from a clinical trial.

Sample: Two hundred forty-four prostate cancer survivors who participated in a clinical trial of behavioral intervention to UI as intervention or control subjects.

Methods: The participants had a 3-month behavioral intervention or usual care and were followed up for an additional 3?months. They were assessed at baseline, 3, and 6?months. Latent growth curve models were performed to examine trajectories of each study variable and relationships among the variables.

Findings: Increasing self-efficacy and social support were significantly and independently associated with more reduction of urinary leakage frequency over time.

Implications for psychosocial oncology: Providing problem-solving skills and social support, including peer support, are essential for empowering patients to reduce UI.     

重症心源性肺水肿伴休克患者的机械通气治疗

目的研究重症心源性肺水肿伴休克患者机械通气(MV)治疗时通气压力的选择对预后的影响。方法将符合标准的22例患者分为两组对照组9例,常规给予较低通气压力和加强药物治疗;治疗组13例,适当增加通气压力。观察血压、临床症状和动脉血气的变化。结果调整MV后30分钟时,治疗组收缩压迅速由(95±12)mmHg升至(130±15)mmHg(P<0.001),呼吸频率(RR)由(38±11)次/min降至(27±6)次/min(P<0.005),心率(HR)由(126±15)次/min降至(105±12)次/min(P<0.001);对照组上述指标变化不明显。2小时后治疗组的升压药用量减少(70±15)%,对照组则增加(20±5)%;同时在吸氧浓度不变的情况下,治疗组的PaO2由(81±12)mmHg升至(140±15)mmHg(P<0.001),明显高于对照组PaO2的改善。24~48小时内治疗组11例患者(85%)停用升压药,对照组2例(22%)停用。最终治疗组100%的患者好转出院,对照组为45%(P<0.05)。结论与低压力通气相比,适当增加MV通气压力不仅可迅速改善重症心源性水肺肿伴休克患者的低氧血症,也可迅速升高血压,改善心功能,降低病死率。     

冠心病合并其他器质性心脏病的外科治疗

目的分析冠心病合并其他器质性心脏病的临床特点,探讨一期外科治疗的方法和临床疗效。方法分析2004年4月至2006年4月冠心病合并其他器质性心脏病患者13例,其中风湿性心脏病联合瓣膜病1例,二尖瓣病变4例,二尖瓣退行性病变3例,主动脉瓣关闭不全3例,升主动脉瘤1例,继发孔房缺1例。因冠心病首诊入院5例,以其他器质性心脏病首诊入院8例。术前有心绞痛症状者8例,无心绞痛5例。体外循环下一期外科治疗。结果无死亡病例,13例均顺利出院。冠脉搭桥+瓣膜置换8例,冠脉搭桥+瓣膜成形3例,冠脉搭桥+Bentall+室壁瘤切除1例,冠脉搭桥+房缺修补1例。手术中搭桥1～3支,平均(1.92±0.73)支。术后1周,左心室舒张末内径(LVDD)为(51.77±2.64)mm,较术前[(58.92±3.81)mm]明显缩小(P<0.05)。随访3个月,心绞痛症状完全消失,心功能(NYHA)明显提高(P<0.05)。结论冠心病合并其他器质性心脏病临床症状无特异性,容易漏诊。虽然手术风险性和难度增加,但未得到血液重建,对患者更将是致命性的灾难,应争取一期手术。     

外科治疗56例心脏非黏液性肿瘤的临床分析

目的探讨心脏非黏液性肿瘤临床特点,总结外科治疗经验。方法对我院1996年10月至2005年3月进行外科治疗的56例心脏非黏液性肿瘤的临床资料进行回顾性分析,总结其临床表现、发生部位、肿瘤性质和外科治疗特点等。结果心脏非粘液性肿瘤占本院同期手术患者的0.14%,良性肿瘤28例,恶性肿瘤28例,其中继发性心脏肿瘤8例。良性肿瘤最常见的是生长在心室,共18例;恶性肿瘤最常见的生长部位是心房,共15例。外科治疗行急诊手术者12例。心包开窗引流术2例,探查术1例,术中肿瘤全部切除者26例,部分切除27例,术后住院期间死亡1例。结论心脏非黏液性肿瘤临床表现各异、病理类型多样、病变广泛,手术原则为尽可能切除肿瘤和保持心脏结构的完整性和功能。     

自体血预充技术对血液保护作用的研究

目的研究采用自体血预充技术对体外循环下心脏手术的血液保护作用。方法40例非急诊手术的首次接受体外循环下心脏冠脉搭桥的患者,依性别(男女比例)、年龄、体重、身高、体表面积(BSA)和射血分数(EF)进行配对后分为两组:自体血预充组(n=20)和经典预充组(n=20)。自体血预充组:用1250ml晶体液和8000IU肝素预充,体外循环开始前先采用自体血预充技术置换出大部分最初预充液,维持平均动脉压(MAP)在50mmHg以上。经典预充组:1250ml晶体液和8000IU肝素预充。心肌保护均采用Calafiore温血停跳液灌注。体外循环中保持温度35.0℃～35.5℃,流量2.5～2.8L·min-·1m-2。所有患者按标准手术步骤进行手术。手术结束前将体外循环系统中余血全部回输给患者。结果自体血预充组平均置换出(894±171)ml的最初预充液,患者体外循环中,手术结束时,术后6h、1d、2d的HCT水平均明显高于经典预充组(P<0.05)。自体血预充组围术期人均输血量明显低于经典预充组[(0.16±1.09)U/人和(0.97±2.18)U/人,P<0.05]。自体血预充组患者术后胸腔引流量较经典预充组明显减少(303±89ml和495±112ml,P<0.05)。结论自体血预充技术的应用能减少血液稀释,减少围术期输血量,保护血液。     

Impact of Transcatheter Occlusion of a Patent Ductus Arteriosus on Atrial Septal Defect Diameter in Children

Background. A persistent patent ductus arteriosus (PDA) may delay closure of a coexisting atrial septal defect (ASD) due to volume loading and enlargement of the left atrium. The purpose of this study was to investigate the natural history of ASD size in patients with a PDA following transcatheter PDA occlusion. Methods. All patients with an ASD and a PDA who underwent transcatheter PDA occlusion at Texas Children’s Hospital were identified. Patients with ASD diameter <3 mm, or additional cardiac defects were excluded. Eight patients (7 females) with small‐ to moderate‐sized ASDs and a PDA were identified. Patient demographics, echocardiographic data, and cardiac catheterization data were recorded. Data were analyzed by 1‐tailed t‐test. Results. Following PDA occlusion, ASD diameter decreased in 6 of 8 patients by a mean of 3.8 mm (±2.3 mm), including 2 that closed. The median duration of follow‐up was 689 days. One ASD remained unchanged and 1 increased in size. The mean maximum ASD diameter decreased from 6.4 mm (±2.2 mm) to 3.9 mm (±3.4 mm) (P = .03). Two patients underwent subsequent transcatheter ASD occlusion. Conclusion. Following transcatheter PDA occlusion, small‐ to moderate‐sized ASDs have significant probability to decrease in size, and possibly close. In infants and children, we recommend transcatheter PDA occlusion, and serial follow‐up of the size of the ASD. This will allow many small‐ to moderate‐sized ASDs to either close, or become smaller, obviating the need for future intervention.