心肌

The cardiac abnormalities of echocardiography in the patients with acromegaly are the marked left ventricular hypertrophy and the increased left ventricular mass.

肢端肥大症患者超声心动图表现为明显的心肌肥厚和心肌重量的增加，伴发高血压的患者心肌肥厚有加重的趋势。

With the development of cardiac tissue engineering, it is feasible to repair the injured cardiac muscle by the cell transplantation vivo.

随着心肌组织工程学的发展，通过细胞体内移植的方法而进行的细胞心肌成形术，为病损的心肌提供了修复的可能性。

Cardiac toxicity of excessive alcohol intake has long been recognized. Alcohol can cause abnormal function of heart muscle, known as alcohol cardiomyopathy, and result in arrhythmia, cardiomegaly, congestive heart failure, which in some cases can be life-threatening.

长期过度摄取酒精会造成心脏之毒性，乃由於酒精所导致心肌功能异常与酒精所引起的心肌疾病，其包含心律不整、心肌症、充血性心脏衰竭。

The recent experimental studies have shown that bone marrow stem cells are capable of regenerating infracted myocardium and inducing myogenesis and angiogenesis, which improving myocardial perfusion and cardiac function.

目前的研究表明，移植的骨髓干细胞可以分化为心肌细胞，使心肌梗死瘢痕区血管和心肌再生，改善缺血心肌血供，改善心脏功能。

Others injected MSCs into autoallergic myocardial tissue directly, observed some caridomyocyto-like cells formation capable of cardiomyocyte specific marking of troponin T and myoglobulin heavy-chain positive staining, which proved that MSCs can be induced into myocardial cells in microenviroment in vivo.

另有学者将MSCs直接注入自体心肌组织内，发现有心肌样细胞形成，具有肌钙蛋白T和肌球蛋白重链染色阳性的心肌细胞特异性标志，表明MSCs在体内微环境条件下可以诱导分化为心肌细胞。

Results: Xuesetong protected the acute myocardial injury in rats by ligaturing the left descending coronary artery and reduced myocardial infarct range. Xuesetong decreased the CPK, LDH and the production of MDA, improved the activity of SOD in myocardium.

结果：血塞通可对抗结扎大鼠冠状动脉左前降支所致的大鼠急性心肌损伤，使心肌缺血大鼠的CPK及LDH降低，并可增加心肌组织SOD的活性，减少MDA生成且能显著缩小心肌梗死的范围。

RESULTS:(1) ET-1 could increase total protein production, surface area, ERKs activity and ［Ca2+］i in cultured cardiomyocyte in dose-dependent manner at concentrations ranging from 10-9 to 10-7 mol/L. And this effect could be abolished by BQ123, an antagonist of ETA receptor, partly inhibited by PTX, but not by BQ788, an antagonist of ETB receptor.（2）The activation of ERKs and the increase of ［Ca2+］i induced by ET-1 were obviously inhibited by PD98059, a selective ERKs kinase inhibitor, and nifedipine, a calcium channel blocker, respectively. Both antagonists partially inhibited ET-1-stimulated cardiomyocyte hypertrophic response.(3) Staurosporine, a selective PKC inhibitor, could inhibit ET-1-stimulated cardiomyocyte hypertrophic response and increase of ［Ca2+］i, but not affect the activation of ERKs.

结果： ①ET-1浓度依赖性增加新生大鼠心肌细胞蛋白质含量和心肌细胞表面积、ERKs活性及［Ca2+］i浓度，以上作用可被ETA受体拮抗剂BQ123所完全抑制，被百日咳毒素部分抑制，而ETB受体拮抗剂BQ788则无效；②ERKs激酶特异性抑制剂PD98059可完全抑制ET-1激活ERKs的作用，钙通道拮抗剂硝苯地平可明显抑制ET-1介导的［Ca2+］i浓度增加，但二者皆仅部分抑制ET-1介导的心肌细胞肥大反应；③蛋白激酶C选择性抑制剂staurosporine并不能明显抑制ET-1介导的ERKs激活，但可抑制ET-1介导的的［Ca2+］i浓度增加及心肌细胞肥大反应。

BMSCs could differentiate into CLCs in vitro induced by the supernatant liquid of the cardiomyocytes, 30% of which can make the induction effects reach the top.

心肌细胞的培养上清能够诱导BMSCs分化为心肌样细胞，且30%心肌细胞培养上清是诱导BMSCs向心肌样细胞分化的最适浓度。

Cardiac hypertrophy is a common complication of clinical cardiovascular diseases, and one of fatal factors of cardiovascular diseases' incidences and mortalities. So it is very beneficial to prevent cardiac hypertrophy for the people.

心肌肥厚是临床上心血管疾病常见的并发症，是心血管病发生率和死亡率增高的重要危险因素，因此，防止心肌肥厚的发生具有重要的意义。L-甲状腺素诱发的大鼠心肌肥厚是研究缺血性肥厚心肌的适宜模型。

Beating heart during openheart surgery is a good method to protect the myocardium being close to physiological condition, and the protective effect may be attributed to alleviation of ischemia/reperfusion injury.

浅低温体外循环心脏跳动中心内直视手术是一种较接近生理状态的心肌保护方法，能最大程度地减轻心肌缺血、缺氧损伤，避免再灌注损伤，最大程度地保持心肌细胞形态结构的完整性，从而获得较理想的心肌保护效果。

Breath, muscle contraction of the buttocks; arch body, as far as possible to hold his head, right leg straight towards the ceiling (peg-leg knee in order to avoid muscle tension).

呼气，收缩臀部肌肉；拱起身体，尽量抬起头来，右腿伸直朝向天花板（膝微屈，以避免肌肉紧张）。

The cost of moving grain food products was unchanged from May, but year over year are up 8%.

粮食产品的运输费用与5月份相比没有变化，但却比去年同期高8％。