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.     

Constant light rearing disrupts compensation to imposed- but not induced-hyperopia and facilitates compensation to imposed myopia in chicks

PURPOSE: While rearing chicks in constant light (CL) inhibits anterior segment growth, these conditions also induce excessive enlargement of the vitreous chamber. The mechanisms underlying these effects are poorly understood although it has been speculated that the enlarged vitreous chambers are a product of emmetropization, a compensatory response to the altered anterior segments. We examined the ability of eyes to compensate to defocusing lenses in CL as a direct test of their ability to emmetropize. We also studied recovery responses, i.e. from lens-induced changes in CL as well as CL-induced changes alone or combined with lens-induced changes in eyes returned to normal diurnal lighting (NL). METHODS: Hatchling White-Leghorn chicks were reared in either CL or NL (control) lighting conditions (n=36) for 2 weeks, with lenses of either +10 or -10D power fitted to one eye of all chicks at the beginning of the second week. The lenses were removed at the end of the same week, at which time some CL chicks (n=14) were shifted to NL, the rest of the chicks remaining in their respective original lighting conditions. Retinoscopy, IR photo-keratometry and high-frequency A-scan ultrasonography were used to track refractions, corneal radii of curvature and ocular axial dimensions, respectively; data were collected on experimental days 0, 7, 9, 14 and 21. RESULTS: Under CL, eyes showed near normal, albeit slightly exaggerated responses to +10D lenses while the response to -10D lenses was disrupted. With +10D lenses, lens-wearing eyes became more hyperopic (RE), and had shorter vitreous chambers (VC) and optical axial lengths (OL) relative to their fellows by the end of the lens period [RE: +10.5+/-1.5D, CL, +8.25+/-2.5D, NL; VC: -0.363+/-0.129mm, CL; -0.306+/-0.110mm, NL; OL: -0.493+/-0.115mm, CL, -0.379+/-0.106mm, NL (mean interocular difference+/-SD)]. With -10D lenses, the NL group showed a myopic shift in RE and increased elongation of both VC depth and OL (RE: -10.75+/-2.0D; VC depth: 0.554+/-0.097mm; OL: 0.746+/-0.166mm), while the CL group showed a small hyperopic shift in RE (+4.0+/-6.0D). Nonetheless, CL eyes were able to recover from lens-induced hyperopia, whether they were left in CL or returned to NL. One week of exposure to NL was sufficient to reverse the effects of 2 weeks of CL on anterior and vitreous chamber dimensions. CONCLUSION: CL impairs emmetropization. Specifically, it disrupts compensation to lens-imposed hyperopia but not imposed myopia. However, CL eyes are able to recover from lens-induced hyperopia, suggesting that the mechanisms underlying the compensatory responses to defocusing lenses are different from those involved in recovery responses. The ocular growth effects of CL on young eyes are reversible under NL.