Smoking and coffee intake following alcohol withdrawal in alcoholic inpatients

The aim of this study was to assess alcoholic inpatients' smoking and coffee intake variation following withdrawal. Only moderate smokers (less than 30 cigarettes/day) showed a significant increase of cigarette consumption after alcohol withdrawal. However, their urinary cotinine level did not vary, suggesting a behavioral, and not biological, compensation through smoking following alcohol withdrawal. Heavy smokers (30 cigarettes/day or more) showed no significant clinical or biological variation of smoking behavior. Coffee consumption increased after alcohol withdrawal in all patients, irrespective of smoking habits.     

Innovative Laboratory Techniques to Facilitate Processing of Large Mohs Cases

Background Processing multiple tissue sections in large Mohs cases is time consuming and labor intensive.
Objective To present innovative laboratory techniques to facilitate processing of large Mohs cases.
Methods A method for processing a large dermatofibrosarcoma protuberans Mohs case is outlined.
Results Modifications in tissue processing and equipment employed in a large Mohs case are presented.
Conclusion Innovative modifications to the standard Mohs laboratory technique can facilitate processing of large Mohs cases, resulting in high-quality, rapid frozen sections while optimizing efficiency.     

Lipoprotein(a) concentrations in Mexican Americans and non-Hispanic whites: the San Antonio Heart Study.

There is considerable evidence that lipoprotein(a) (Lp(a)) is a strong independent risk factor for coronary heart disease. Based on their risk factor profile, Mexican Americans have an increased risk of coronary heart disease, yet Mexican Americans have coronary heart disease mortality similar to or lower than that of non-Hispanic whites. The authors therefore attempted to determine whether Mexican Americans had decreased Lp(a) concentrations relative to non-Hispanic whites in the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. Lp(a) concentrations (mg/dl) were significantly lower in Mexican Americans (n = 316) than in non-Hispanic whites (n = 242) (men: 10.4 vs. 16.3; women: 11.5 vs. 16.4). In addition, the proportion of persons with Lp(a) concentrations of > or = 30 mg/dl (the threshold at which increased risk of coronary heart disease is believed to occur) was significantly higher in non-Hispanic whites than in Mexican Americans (18.6% vs. 7.6%; Mantel-Haenszel odds ratio (adjusted for sex) = 2.79). Age, obesity, body fat distribution, cigarette smoking, alcohol consumption, and glucose and insulin concentrations were not significantly related to Lp(a) levels. Decreased Lp(a) concentrations may account in part for Mexican Americans' relative protection from coronary heart disease mortality.     

Regional Variation in Wound Contraction of Mohs Surgery Defects Allowed to Heal by Second Intention

BACKGROUND: The phenomenon of wound contraction results in a decrease in wound size and a healed scar significantly smaller than the original defect. OBJECTIVE: This study was undertaken (1) to determine the amount of wound contraction in Mohs surgery defects allowed to heal by second intention, (2) to evaluate for regional differences in wound contraction based on the facial anatomic zones for second intention healing described by Zitelli, and (3) to determine whether regional differences in wound contraction account for observed differences in cosmetic outcome. METHODS: One hundred sixty secondarily healed Mohs surgery defects limited to the head and neck having a wound age of greater than 12 weeks in 102 consecutively examined patients were carefully measured with a tissue caliper. The percent wound contraction was calculated and compared for each Zitelli anatomic subunit. The final shape of the wound (quantitatively described) and the cosmetic acceptability (subjectively rated by the patient and examiner) were also compared with the percent wound contraction for each anatomic area. RESULTS: Both NEET (concave surface of the nose, eye, ear, and temple) and FAIR (forehead, antihelix, eyelids, and the remainder of the nose, lips, and cheeks) areas were identical in terms of mean wound contraction (74%), cosmetic acceptability (97%), and conversion to a wound shape with a ratio of maximal length to width of greater than 3.0 (fusiform and linear shapes) (52%). NOCH areas (convex surface of the nose, oral lips, cheeks and chin, and the helix of the ear) demonstrated less wound contraction (66%), cosmetic acceptability (78%), and fusiform-linear conversion (29%). Subset differences and variables that appear to influence wound contraction are discussed. Secondarily healed wounds in areas with one or more positive contraction variables contract 75%, whereas defects in areas with negative contraction variables contract 55%. CONCLUSIONS: Regional differences in wound contraction of secondarily healed head and neck wounds exist and account for some differences in cosmetic acceptability. Scar location, regardless of the degree of wound contraction, is the most important factor for the final cosmetic outcome.     

LPS resistance in monocytic cells caused by reverse signaling through transmembrane TNF (mTNF) is mediated by the MAPK/ERK pathway

The transmembrane form of tumor necrosis factor (mTNF), expressed on activated monocytes (MO) and macrophages (MPhi), is able to induce apoptosis in human endothelial cells (EC). Apoptosis is mediated by two distinct mechanisms: direct cell contact and a yet-unidentified soluble protein, death factor X. In addition, mTNF acts as a receptor that transduces a "reverse signal" into MO/MPhi when bound to the TNF receptor on EC. Reverse signaling by mTNF confers resistance to bacterial lipopolysaccharide (LPS). Stimulation of reverse signaling by mTNF blocks the ability of MO/MPhi to produce death factor X and proinflammatory cytokines. We have investigated which signaling pathways are used by mTNF acting as receptor. Reverse signaling triggers two independent pathways that can be distinguished by protein kinase C (PKC) inhibitors. The suppression of LPS-induced death factor X is dependent on PKC, whereas the suppression of LPS-mediated cytokine release is not. LPS and reverse signaling stimulate the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway. It is interesting that the activation of reverse signaling by mTNF renders MO/MPhi refractory to a subsequent activation of the MAPK/ERK pathway by LPS. Thus, reverse signaling achieves LPS resistance in monocytic cells through interference with key signal-transduction pathways.     

Ghrelin expression in hyperplastic and neoplastic proliferations of the enterochromaffin-like (ECL) cells

Ghrelin, a recently discovered peptide isolated from the gastric corpus mucosa, is believed to be important in the regulation of growth hormone secretion and has been shown to increase appetite and food intake as well. It may also have other gastrointestinal and cardiac functions. Because a cell of origin for ghrelin has not been convincingly identified in the gastric mucosa thus far, we studied the immunohistochemical expression of ghrelin in proliferative lesions of the enterochromaffin-like (ECL) cells—a cell that is not only exclusively confined to the gastric corpus mucosa but is its dominant endocrine cell type as well. Formalin-fixed, paraffin embedded tissues from three cases of gastric ECL cell hyperplasia and five ECL carcinoids (three with coexisting foci of diffuse, linear, and micronodular hyperplasia) were immunohistochemically stained for ghrelin, using a commercially available antibody. The Sevier-Munger stain for ECL cells and immunohistochemical stains for chromogranin, gastrin, serotonin, somatostatin, and vesicular monoamine transporter-2 (VMAT-2) were performed on parallel sections for correlation with the ghrelin staining results. All ECL cell carcinoids and hyperplastic lesions were positive for both the Sevier-Munger and the immunohistochemical stains for chromogranin and VMAT-2. Immunoreactivity for ghrelin was seen in 4/5 ECL carcinoids, all cases of ECL cell hyperplasia, as well as in all areas with linear and micronodular hyperplasia adjacent to the ECL cell carcinoids. In each instance, such staining was confined to the Sevier-Munger, and VMAT-2 positive cells only. Our findings indicate that the ECL cells are either the ghrelin-producing cells of the gastric mucosa or acquire the capability to synthesize ghrelin during proliferative states encompassing the entire hyperplasia to neoplasia spectrum. In view of the orexigenic and other known actions of ghrelin, the functional and/or biologic significance of ghrelin production in such ECL cell proliferations needs to be investigated further.     

Cloning and developmental expression analysis of the murine homolog of the spinocerebellar ataxia type 1 gene (Sca1)

Spinocerebellar ataxia type 1 (SCA1) is an autosomal dominant neurodegenerative disorder caused by the expansion of a CAG trinucleotide repeat which encodes glutamine in the novel protein ataxin-1. In order to characterize the developmental expression pattern of SCA1 and to identify putative functional domains in ataxin-1, the murine homolog (Sca1) was isolated. Cloning and characterization of the murine Sca1 gene revealed that the gene organization is similar to that of the human gene. The murine and human ataxin-1 are highly homologous but the CAG repeat is virtually absent in the mouse sequence suggesting that the polyglutamine stretch is not essential for the normal function of ataxin-1 in mice. Cellular and developmental expression of the murine homolog was examined using RNA in situ hybridization. During cerebellar development, there is a transient burst of Sca1 expression at postnatal day 14 when the murine cerebellar cortex becomes physiologically functional. There is also marked expression of Sca1 in mesenchymal cells of the intervertebral discs during development of the spinal column. These results suggest that the normal Sca1 gene, has a role at specific stages of both cerebellar and vertebral column development.