Laparoscopic Medial-to-lateral Colon Dissection: How and Why

Laparoscopic colectomy is a difficult procedure with a long learning curve. We describe in this study our technique for right- and left-sided laparoscopic medial-to-lateral colectomy. The medial approach involves division of the vascular pedicle first, followed by mobilization of the mesentery toward the abdominal wall, and finally freeing of the colon along the white line of Toldt. This approach allows immediate identification of the plane between the mesocolon and the retroperitoneum and renders the dissection fast and safe. Our series of 50 consecutive laparoscopic colectomies supports this concept. We believe that surgeons familiar with this technique will have an important tool in their armamentarium to circumvent some of the challenges of laparoscopic colectomy.     

Soul City: a sustainable edutainment vehicle facilitating social change

This paper outlines the programming model employed by the Soul City Institute for Health and Development Communication, a South African NGO, in using ‘edutainment’ to facilitate social change. The paper refers to the intersection of this model and current thought on health promotion and various social change theories. It also discusses key challenges and factors contributing to sustainability over 12 years.     

Role of metabolism and oxidation-reduction cycling in the cytotoxicity of antitumor quinoneimines and quinonediimines

Quinone(di)imines are nitrogen analogues of quinones in which one or both quinone oxygens are replaced by an imino group. A series of quinone(di)imines with antitumor activity has been studied for its in vitro chemical reactivity, metabolism, acute toxicity to primary cultured rat hepatocytes, and growth-inhibitory activity with Chinese hamster ovary (CHO) cells. The quinone(di)imines exhibited a wide range of activity as substrates for metabolism by hepatic microsomal flavoenzymes. The maximum rate of quinone(di)imine metabolism was more than 7.5-fold greater than reported for metabolism of quinones. Some quinone(di)imines formed free radicals that could be detected by electron spin resonance spectroscopy. 2-Amino-1,4-naphthoquinoneimine gave a short-lived electron spin resonance signal that could be detected only under aerobic conditions. 2,3',6-Trichloroindophenol gave an electron spin resonance signal in air that was stable for 24 h. Most quinone(di)imines underwent oxidation-reduction cycling to form the superoxide anion radical, but some quinone(di)imines, although rapidly metabolized, formed little or no superoxide anion radical. Quinone(di)imines were relatively toxic to hepatocytes and CHO cells, and some quinone(di)imines were more toxic to one cell type than the other. The log 1-octanol/water partition coefficient showed an optimal value of 2.61 for toxicity against both cell types. In hepatocytes the more toxic quinone(di)imines were the most rapidly metabolized. For a subgroup of quinone(di)imines toxicity to hepatocytes and CHO cells appeared to be related to the ability to form a semiquinone(di)imine free radical. Toxicity of quinone(di)imines to hepatocytes and CHO cells was not related to superoxide anion radical formation, and toxicity to CHO cells was not affected by exclusion of oxygen during exposure of the cells to the compounds. The rate of chemical addition of quinone(di)imines to reduced glutathione did not correlate with toxicity. An understanding of the mechanisms of acute toxicity and growth-inhibitory activity of quinone(di)imines could lead to the design of more selective quinonoid antitumor agents.     

Comparative studies of the in vitro metabolism and covalent binding of 14C-benzene by liver slices and microsomal fraction of mouse, rat, and human

Metabolism of benzene by the liver has been suggested to play an important role in the hepatotoxicity of benzene. The role of the different benzene metabolites and the causes of species differences in benzene hepatotoxicity are, however, not known. The metabolism and covalent binding of 14C-benzene by liver microsomal fractions and liver slices from rat, mouse, and human subjects have been studied. Rat microsomal fraction formed phenol at a rate of 0.32 nmol/min/mg of protein; mouse microsomal fraction formed phenol at 0.64 nmol/min/mg and hydroquinone at 0.03 nmol/min/mg; and human microsomal fraction formed phenol at 0.46 nmol/min/mg and hydroquinone at 0.07 nmol/min/mg. Covalent binding of 14C-benzene metabolites to rat, mouse, and human liver microsomal protein was 29, 113, and 169 pmol/min/mg of protein, respectively. The rates of metabolite formation from benzene by liver slices in nmol/min/g of tissue were: rat, phenol 0.15, hydroquinone 0.26, and phenylsulfate 1.22; mouse: phenol 0.13, hydroquinone 0.29, phenylsulfate 1.37, and phenylglucuronide 1.34; and human: phenol 0.16, hydroquinone 0.27, phenylsulfate 0.83, and phenylglucuronide 0.52. trans,trans-Muconic acid formation was not detected with liver slices of any species. Covalent binding of 14C-benzene metabolites to rat, mouse, and human liver slices was 8.2, 79.7, and 27.3 pmol/min/g liver, respectively. There was no correlation between ascorbic acid levels in the human liver slices and covalent binding of 14C-benzene metabolites. The results show that phenol and hydroquinone found in extrahepatic tissues, including bone marrow, of animals exposed to benzene could originate from the liver. There was no evidence for the release of highly reactive benzene metabolites such as trans,trans-muconaldehyde or p-benzoquinone from liver cells.(ABSTRACT TRUNCATED AT 250 WORDS)