关节镜下肱二头肌长头腱切断术治疗老年SLAP损伤

<正>肩关节上盂唇前后部(superior labrum from anterior to posterior,SLAP)损伤是肩胛盂上盂唇从前至后的损伤,常常累及肱二头肌长头腱(long head of the biceps tendon,LHBT)附着处,是导致老年人肩关节疼痛和功能紊乱的重要原因之一,严重影响生活质量~([1])。随着肩关节疾病诊疗水平的日益提高,肩关节镜技术微创治疗SLAP损伤不断取得良好的临     

不同水平的低密度脂蛋白胆固醇人群踝肱脉搏波传导速度的研究

目的 研究不同水平低密度脂蛋白胆固醇(LDL-C)与踝肱脉搏波传导速度(baPWV)的关系,探讨影响动脉弹性的主要因素.方法 从哈尔滨医科大学附属第二医院体检中心2010年4月-2011年10月的体检人群中随机抽取1 075例(男728例)作为研究对象.按照血清LDL-C水平分为4组:LDL-C正常组(C组,LDL-C<3.42 mmol/L);LDL-C临界升高组(H1组,LDL-C 3.42 mmol/L~4.20 mmol/L);LDL-C升高组(H2组,LDL-C:4.21 mmol/L~4.97 mmol/L);LDL-C显著升高组(H3组,LDL-C≥4.98 mmol/L).测定各组体检者的baPWV和踝肱指数(ABI),及其他临床指标,并行组间比较分析.结果 高LDL-C组baPWV值显著高于LDL-C正常组(1 391.74 cm/s±224.74 cm/s比1 310.49 cm/s±222.10 cm/s,P=0.027).C组和H1组baPWV值处于正常范围,且H1组baPWV值(1 351.77 cm/s±229.88 cm/s)明显高于C组(1 310.49 cm/s±222.02 cm/s),差异有统计学意义(P=0.012),H2组baPWV值和H3组baPWV值轻度升高,与C组、Hl组差异有统计学意义(P=0.00).各组间ABI值差异无统计学意义(P=0.221).baPWV逐步线性回归分析显示,收缩压(SBP)、年龄、LDL-C、高密度脂蛋白胆固醇(HDL-C)、尿酸(UA)均是影响baPWV的独立危险因素.且在控制SBP、年龄、HDL-C、UA影响因素后,LDL-C仍然与baPWV存在相关性(r=0.078,P=0.012).结论 随着LDL-C的升高,baPWV值增高,LDL-C升高者早期动脉血管弹性下降,baPWV检测有助于发现LDL-C升高的早期动脉粥样硬化.     

不同糖耐量状态下急性冠状动脉综合征患者血清ICAM-1和VCAM-1水平变化的研究

目的 评价急性冠状动脉综合征合并糖尿病患者中ICAM-1和VCAM-1这两个直接促使白细胞与损伤血管内皮黏附,参与动脉粥样硬化斑块内炎疽反应过程。促使内皮损伤的重要因子是否为糖尿病促发炎症反应,引起斑块病变不稳定的重要机制。方法入选急性冠状动脉综合征患者148例,根据OGTF试验结果分为3组：糖耐量正常组;糖耐量减低组;2型糖尿病组。3组均于入院时即行酶联免疫吸附测定法（ELISA）检测血清可溶性ICAM—1和VCAM—1的水平。结果急性冠状动脉综合征患者在不同糖耐量状态下,3组间血清ICAM-1和VCAM-1水平有统计学差异,其中糖耐量减低组血清ICAM-1和VCAM-1水平均高于糖耐量正常组;糖尿病组明显高于糖耐量正常组;糖尿病组高于糖耐量低减组,但无统计学差畀。结论急性冠状动脉综合征糖耐量异常患者中血清ICAM-1和VCAM-1水平明显升高,血糖可能通过激活ICAM-1和VCAM-1,参与血管炎症损伤,促进急性冠状动脉综合征动脉宽块的破裂与发展。     

Isolated tuberculous abscess in biceps brachii muscle of a young male

Tuberculosis of muscles without coexistent active skeletal or extraskeletal involvement is very rare. A case of tuberculous abscess of biceps brachii muscle in a young immunocompetent male is presented. A good response was seen with antitubercular treatment. Tuberculosis should be considered in the differential diagnosis of any unexplained soft tissue swelling in people born in tubercular endemic areas, who are immunosuppressed or had an injury to the affected area.     

Kallikrein-kinin system of the kidneys in hypertension under different conditions of examination

Changes are observed in the renal kallikrein-kinin system in hypertensive disease, which are displayed by compensatory increase in its activity in patients with labile hypertension and decrease in the activity of this system in patients with a stable stage of the disease. An inadequate reaction to a load experienced from walking or from a reduced volume of extracellular fluid and sodium balance in the body was noted in all stages. The absence of a reaction or the inhibition of the activity of the renal kallikrein-kinin system in response to the intake of furosemid may be a manifestation of its altered sensitivity to the electrolyte shifts in the organism and the decrease in the volume of extracellular fluid. The kallikrein-kinin system is concerned with the noted shifts in renal function linked with the transport of sodium and water in patients with the labile stage of the disease, to which the correlative connection between kallikrein excretion and natriuresis and urine excretion attests. It is suggested that the renal kallikrein-kinin system in patients with the initial stage of hypertensive disease contributes to the adaptation of renal function to the altered conditions of hemodynamics and the increased activity of the renin-angiotensin-aldosterone system.     

Quantification of the contractile response to injury: assessment of the work-length relationship in the intact heart

We used a sonomicrometric determination of ventricular dimension to examine the effect of ischemia and reperfusion on the work-length relationship in the intact heart to develop a useful and precise variable of ventricular contractile response to injury. Twenty anesthetized dogs were instrumented with epicardial ultrasonic dimension transducers to record right ventricular free wall chord length and left ventricular minor-axis length, micromanometers to record ventricular pressures, and an electromagnetic probe to record pulmonary arterial (n = 8) or aortic (n = 7) flow. Dogs were subjected to either 20 min (n = 7) or 30 min (n = 13) of global cardiac ischemia supported by cardiopulmonary bypass. Data were acquired over a range of end-diastolic volumes produced by transient (5 to 10 sec) vena caval occlusion before and after ischemia. In both ventricles, systolic epicardial dimensional shortening correlated with flow probe-measured stroke volume (mean r = .969) and regional stroke work calculated as the integral of instantaneous ventricular pressure and epicardial dimension correlated with measured global stroke work (mean r = .960), confirming the validity of dimensional measurements. Regression analysis demonstrated a highly linear relationship between calculated regional stroke work and end-diastolic length in the right ventricle (mean r = .973) and left ventricle (mean r = .967), quantifiable by a slope (Mw) and x intercept (Lw). Change in afterload produced by pulmonary arterial or aortic constriction resulted in no significant changes in Mw or Lw in either ventricle. Ischemia and reperfusion decreased Mw and shifted Lw to the right in both ventricles. The decrease in Mw with 30 min ischemia exceeded the decrease with 20 min ischemia by 29% in the right ventricle and by 32% in the left (p less than .04) with up to 1 hr of reperfusion. Changes in Lw were not related to severity of injury. After ischemia, infusion of calcium increased Mw by 177% in the right ventricle and by 67% in the left (p less than .03) without significant changes in Lw. Independent of load conditions, the slope Mw, of the linear stroke work vs end-diastolic length relationship is a valid and precise index of right and left ventricular contractile response to global ischemia in the intact circulation. This variable may be useful in evaluating therapies designed to limit myocardial injury and enhance ventricular functional performance.     

Quantification of immobilization-induced changes in human calf muscle using speed-of-sound ultrasound: An observational pilot study

Short-term immobilization leads to fatty muscular degeneration, which is associated with various negative health effects. Based on literature showing very high correlations between MRI Dixon fat fraction and Speed-of-Sound (SoS), we hypothesized that we can detect short-term-immobilization-induced differences in SoS.Both calves of 10 patients with a calf cast on one side for a mean duration of 41 ± 26 days were examined in relaxed position using a standard ultrasound machine. Calf perimeters were measured for both sides. A flat Plexiglas-reflector, placed vertically on the opposite side of the probe with the calf in-between, was used as a timing reference for SoS. SoS was both manually annotated by two readers and assessed by an automatic annotation algorithm. The thickness values of the subcutaneous fat and muscle layers were manually read from the B-mode images. Differences between the cast and non-cast calves were calculated with a paired t test. Correlation analysis of SoS and calf perimeter was performed using Pearson''s correlation coefficient.Paired t test showed significant differences between the cast and non-cast side for both SoS (P < .01) and leg perimeter (P < .001). SoS was reduced with the number of days after cast installment (r = −0.553, P = .097). No significant differences were found for muscle layer thickness, subcutaneous fat layer thickness, mean fat echo intensity, or mean muscle echo intensity.Short-term-immobilization led to a significant reduction in SoS in the cast calf compared to the healthy calf, indicating a potential role of SoS as a biomarker in detecting immobilization-induced fatty muscular degeneration not visible on B-mode ultrasound.     

Evaluation of different metrics as an index for the assessment of arterial stiffness

Elevated intravascular pressure is a contributing factor to increased arterial stiffness, and is a risk factor for cardiovascular morbidity and mortality. Assessment of arterial stiffness is of importance in evaluating cardiovascular risk. Pulse wave velocity (PWV) has been broadly used in the assessment of arterial stiffness. We compared three different metrics of arterial stiffness to PWV. Hemodynamic recordings were carried out in anesthetized hypertensive and normotensive rats (n = 25; 13–14 weeks old). Four parameters were calculated (PWV, elastic modulus (E_inc), stiffness index (β), and pressure-strain modulus (E_p)) as metrics of arterial stiffness. Hypertensive in comparison to normotensive rats had significantly higher systolic and diastolic blood pressures. Metric for arterial stiffness were significantly (p < 0.002) higher in hypertensive animals: PWV (8.46 ± 2.01 vs. 6.39 ± 1.28 m/s), E_p (0.246 ± 0.019 vs. 0.137 ± 0.010 dyn/cm² × 10^–6), E_inc (17.5 ± 1.8 vs. 10.1 ± 0.9 dyn/cm² × 10^–6), and β (2.43 ± 0.11 vs. 1.98 ± 0.08) (mean±SE). Bland-Altman analysis revealed β as the only metric aligned with PWV in hypertensive state. We find in state of reduced arterial compliance associated with high systemic pressure, β but not E_inc or E_p is an index of arterial stiffness showing agreement with PWV.     

Regulation of skeletal muscle stiffness and elasticity by titin isoforms: a test of the segmental extension model of resting tension.

To explore the role of titin filaments in muscle elasticity, we measured the resting tension-sarcomere length curves of six rabbit skeletal muscles that express three size classes of titin isoform. The stress-strain curves of the split fibers of these muscles displayed a similar multiphasic shape, with an exponential increase in tension at low sarcomere strain followed by a leveling of tension and a decrease in stiffness at and beyond an elastic limit (yield point) at higher sarcomere strain. Significantly, positive correlations exist between the size of the expressed titin isoform, the sarcomere length at the onset of exponential resting tension, and the yield point of each muscle. Immunoelectron microscopic studies of an epitope in the extensible segment of titin revealed a transition in the elastic behavior of the titin filaments near the yield point sarcomere length of these muscles, providing direct evidence of titin's involvement in the genesis of resting tension. Our data led to the formulation of a segmental extension model of resting tension that recognizes the interplay of three major factors in shaping the stress-strain curves: the net contour length of an extensible segment of titin filaments (between the Z line and the ends of the thick filaments), the intrinsic molecular elasticity of titin, and the strength of titin thick filament anchorage. Our data further suggest that skeletal muscle cells may control and modulate stiffness and elastic limit coordinately by selective expression of specific titin isoforms.