Continuing Medical Education Program in Echocardiography

Article Title: Study of Left Ventricular Rotation and Torsion in the Acute Phase of ST-Elevation Myocardial Infarction by Speckle Tracking Echocardiography (Echocardiography 2010;27:44)     

索拉非尼抑制肝癌细胞增殖中自噬的作用及其机制

目的：研究分子靶向药物索拉非尼在体外对人肝癌细胞株HepG_2增殖抑制过程中自噬的表达及作用,并探讨其可能机制。方法：以吖啶橙染色荧光显微镜对自噬进行定性观察;cell counting kit-8检测活性氧（reactiveoxygen species,ROS）抑制前后HepG_2细胞成活率的变化;RT-PCR检测自噬基因Beclin-1表达的变化。Western印迹检测自噬相关蛋白Beclin-1的变化：荧光分光光度计检测胞内二氯荧光素DCF的荧光强度。结果：索拉非尼对肝癌细胞HepG_2具有显著的抑制作用;索拉非尼可诱导肝癌细胞HepG_2产生自噬及ROS,自噬在基因及蛋白水平表达均增加;抑制ROS的产生可减少索拉非尼诱导的肝癌细胞HepG_2自噬的表达量,自噬的抑制增强了索拉非尼对肝癌细胞的抑制作用。结论：ROS参与索拉非尼诱导肝癌细胞HepG_2的自噬表达,索拉非尼在抑制肝癌细胞自噬过程中自噬可能起到保护作用,抑制自噬可能为提高进展期肝癌病人索拉非尼分子靶向治疗敏感性提供新的思路。     

Novel antitubercular diallyl/dibenzylthiosemicarbazones endowed with high activity toward multi-drug-resistant tuberculosis

Novel diallyl and dibenzylthiosemicarbazones were prepared by three-step reactions. The compounds were tested for their in vitro activity against Mycobacterium tuberculosis H37Rv (MTB) and multi-drug-resistant Mycobacterium tuberculosis (MDR-TB). Most of the compounds showed excellent activity toward MDR-TB. Among the thirty compounds (4,5a–o) tested N,N-dibenzyl-2-((5-nitrofuran-2-yl)methylene)hydrazinecarbothioamide (5g) was found to be the most potent compound MICs of 0.55 and 0.12 μM against MTB and MDR-TB.     

Myxoinflammatory Fibroblastic Sarcoma: An Uncommon Tumour at an Unusual Site

Myxoinflammatory fibroblastic sarcoma is a low grade sarcoma that is composed of a mixed inflammatory infiltrate along with spindled, epithelioid and bizarre appearing cells in a background of hyaline and myxoid zones. Seen affecting the distal extremities commonly, with an equal sex predilection, these tumors are rare and require an extensive immunohistochemical work up for proper diagnosis. They have a tendency to recur.     

The albino chick as a model for studying ocular developmental anomalies, including refractive errors, associated with albinism

Albinism is associated with a variety of ocular anomalies including refractive errors. The purpose of this study was to investigate the ocular development of an albino chick line. The ocular development of both albino and normally pigmented chicks was monitored using retinoscopy to measure refractive errors and high frequency A-scan ultrasonography to measure axial ocular dimensions. Functional tests included an optokinetic nystagmus paradigm to assess visual acuity, and flash ERGs to assess retinal function. The underlying genetic abnormality was characterized using a gene microarray, PCR and a tyrosinase assay. The ultrastructure of the retinal pigment epithelium (RPE) was examined using transmission electron microscopy. PCR confirmed that the genetic abnormality in this line is a deletion in exon 1 of the tyrosinase gene. Tyrosinase gene expression in isolated RPE cells was minimally detectable, and there was minimal enzyme activity in albino feather bulbs. The albino chicks had pink eyes and their eyes transilluminated, reflecting the lack of melanin in all ocular tissues. All three main components, anterior chamber, crystalline lens and vitreous chamber, showed axial expansion over time in both normal and albino animals, but the anterior chambers of albino chicks were consistently shallower than those of normal chicks, while in contrast, their vitreous chambers were longer. Albino chicks remained relatively myopic, with higher astigmatism than the normally pigmented chicks, even though both groups underwent developmental emmetropization. Albino chicks had reduced visual acuity yet the ERG a- and b-wave components had larger amplitudes and shorter than normal implicit times. Developmental emmetropization occurs in the albino chick but is impaired, likely because of functional abnormalities in the RPE and/or retina as well as optical factors. In very young chicks the underlying genetic mutation may also contribute to refractive error and eye shape abnormalities.     

Growth hormone deficiency in children: From suspecting to diagnosing

Isolated Growth hormone deficiency is an important and treatable cause of short stature. However, it is often difficult to diagnose the condition with certainty due to the lack of a single robust diagnostic test. Short children, other than those with the classical phenotype of immature chubby facies, truncal obesity and micropenis in boys, or those with history of cranial lesions with known association with hypopituitarism, should be evaluated for growth hormone deficiency only after excluding the other more common conditions. These children typically have height markedly below that expected for their midparental height with low height velocity and delayed bone age. Growth hormone levels should be checked by provocative testing, after ensuring that the child is euthyroid, and after priming with sex steroids if indicated. Low levels of Insulin-like growth factor 1 and Insulin-like growth factor binding protein 3 and pituitary abnormalities on neuroimaging provide important corroborative evidence to the diagnosis.