Use of khat in lactating women: a pilot study on breast-milk secretion

Nor-pseudoephedrine, one of the active ingredients of khat (Catha edulis), was found to be excreted in breast-milk in several lactating women who were chewing the leaves of the shrub according to the local customs. The compound could be traced in the urine of one breast-fed infant. It is concluded that the use of khat during lactation should be discouraged until further research has clearly elucidated the potential health hazards.     

Suramin induces and enhances apoptosis in a model of hyperoxia-induced oligodendrocyte injury

Recent evidence suggests oxygen as a powerful trigger for cell death in the immature white matter, leading to periventricular leukomalacia (PVL) as a cause of adverse neurological outcome in survivors of preterm birth. This oligodendrocyte (OL) death is associated with oxidative stress, upregulation of apoptotic signaling factors (i.e., Fas, caspase-3) and decreased amounts of neurotrophins. In search of neuroprotective strategies we investigated whether the polysulfonated urea derivative suramin, recently identified as a potent inhibitor of Fas signaling, affords neuroprotection in an in vitro model of hyperoxia-induced injury to immature oligodendrocytes. Immature OLs (OLN-93) were subjected to 80% hyperoxia (48 h) in the presence or absence of suramin (0, 30, 60, 120 microM). Cell death was assessed by flow cytometry (Annexin V, caspase-3 activity assay) and immunohistochemistry for activated caspase-3. Immunoblotting for the death receptor Fas, cleaved caspase-8 and the phosphorylated isoform of the serine-threonin kinase Akt (pAkt) was performed. Suramin lead to OL apoptosis and potentiated hyperoxia-induced injury in a dose-dependent manner. Immunoblotting revealed increased Fas and caspase-8 expression by suramin treatment. This effect was significantly enhanced when suramin was combined with hyperoxia. Furthermore, pAkt levels decreased following suramin exposure, indicating interference with neurotrophin-dependent growth factor signaling. These data indicate that suramin causes apoptotic cell death and aggravates hyperoxia-induced cell death in immature OLs. Its mechanism of action includes an increase of previously described hyperoxia-induced expression of pro-apoptotic factors and deprivation of growth factor dependent signaling components.     

Two types of mitochondrial crystals in diseased human skeletal muscle fibers

Mitochondrial crystalline inclusions, frequently found in mitochondrial myopathies, were analyzed by crystallographic techniques and computer-aided image processing. It could be shown that these structures were real crystals. There are two distinct types of crystal, which can be distinguished by shape, size, and pattern. So-called type I crystals are usually present in the intracristal space, whereas the type II crystals are preferentially located in the intermembrane space between outer and inner mitochondrial membranes. The unit cell dimensions were found to be 38 x 34 x 8 nm for the type I crystals and 20 x 17 x 8 nm for the type II crystals. These results strongly suggest that the crystals are composed of macromolecules, presumably proteins. Arguments are presented that indicate that type I crystals occur only in type 1 muscle fibers and type II crystals in type 2 muscle fibers.     

血清胸苷激酶1检测对恶性肿瘤诊断及疗效评估的意义

目的探讨血清胸苷激酶1（TK1）作为肿瘤细胞增殖标志物对恶性肿瘤诊断及疗效评估的意义。方法应用免疫印迹-增强化学发光法检测恶性肿瘤组（53例）治疗前后、体格检查组（49例）以及健康对照组（18名）的血清TK1水平。治疗前与治疗后比较用配对t检验,治疗前和后分别与健康对照组、体格检查组比较采用两独立样本均数比较t检验。结果恶性肿瘤组治疗前STK1为0．3—11．3（2．4±2．0）pmol／L;恶性肿瘤组治疗后STK1为0．3～5．0（0．9±0．8）pmol／L;体格检查组STK1为0．1～2．1（0．8±0．3）pmol／L;健康对照组STK1为0．5～1．2（0．7±0．2）pmol／L。恶性肿瘤组治疗前与治疗后之间STK1水平差异有统计学意义（t=5．257,P〈0．0001）。恶性肿瘤组治疗前与健康对照组和体格检查组STK1水平比较,差异均有统计学意义（t=3．568和5．460,P=0．001和〈0．0001）,而恶性肿瘤组治疗后与健康对照组和体格检查组STK1水平比较,差异均无统计学意义（t=1．056和0．715,P均〉0．05）。结论血清TK1检测细胞增殖有较高的特异性和灵敏度,对临床监测恶性肿瘤疗效和在体格检查中进行恶性肿瘤风险筛查具有重要意义。