Cigarette smoking and glaucoma in the United States population.

PurposeTo evaluate the association between cigarette smoking and glaucoma in the United States population.Patients and methodsUS civilian, non-institutionalized population from 2005 to 2008 administrations of the National Health and Nutrition Examination Survey that were ≥40 years of age with visual fields and optic disc photographs were included. Diagnosis of glaucoma was based on the Rotterdam criteria. Logistic regression modeling was performed to assess the association between glaucoma and smoking history, while controlling for age, gender, ethnicity, household income, alcohol consumption, diabetes, and hypertension.ResultsIn 3864 participants, 212 (5.5%) had glaucoma (corresponds to a population weighted glaucoma prevalence of 3.7% in a total of 83 570 127 subjects). Population weighted proportion of current smokers was 20.6% and ex-smokers was 28.3%. Participants with glaucoma were older (63.0±11.6 vs 56.1±11.2, P=0.002), likely to be male (57.1% vs 49.2%, P=0.03), to be Black (36.3% vs 20.7%, P<0.001), and to have diabetes (18.9% vs 12.4%, P=0.006) and hypertension (50.5% vs 39.7%, P=0.003). Current smokers had a lower odds of glaucoma compared to non-smokers (OR=0.61, 95% CI=0.41-0.88, P=0.009), and ex-smokers (OR=0.46, 95% CI=0.28-0.76, P=0.002). The effect estimates were similar in adjusted models, but not statistically significant. Among smokers, greater pack/day of smoking history was associated with statistically significantly higher odds of glaucoma (OR=1.70, 95% CI=1.08-2.67, P=0.02).ConclusionsAmong cigarette smokers, heavy smoking defined by greater number of pack of cigarettes smoked per day is associated with higher odds of glaucoma. Health care providers should include this association when counseling patients on their smoking habit.

An Effective Cell Coculture Platform Based on the Electrospun Microtube Array Membrane for Nerve Regeneration.

Recently, a novel substrate known as an electrospun polylactic acid (PLLA) microtube array membrane (MTAM) was successfully developed as a cell coculture platform. Structurally, this substrate is made up of one-to-one connected, ultrathin, submicron scale fibers that are arranged in an arrayed formation. Its unique structure confers several key advantages which are beneficial in a cell coculture system. In this study, the interaction between rat fetal neural stem cells (NSC) and astrocytes was examined by comparing the outcome of a typical Transwell-based coculture system and that of an electrospun PLLA MTAM-based coculture system. Compared to tissue culture polystyrene (TCP) and Transwell coculture inserts, a superior cell viability of NSC was observed when cultured in lumens of electrospun PLLA MTAM (with supportive immunostaining images). Reverse transcription polymerase chain reaction revealed a strong interaction between astrocytes and NSC through a higher expression of doublecortin and a lower expression of nestin. These data demonstrate that MTAM is clearly a better coculture platform than the traditional Transwell system.

Malignant pleural effusion cells show aberrant glucose metabolism gene expression.

Malignant pleural effusion (MPE) accompanying lung adenocarcinoma indicates poor prognosis and early metastasis. This study aimed to identify genes related to MPE formation. Three tissue sample cohorts, seven from healthy lungs, 18 from stage I-III lung adenocarcinoma with adjacent healthy lung tissue and 13 from lung adenocarcinomas with MPE, were analysed by oligonucleotide microarray. The identified genes were verified by quantitative real-time PCR (qRT-PCR), immunohistochemical staining, and immunofluorescence confocal microscopy. 20 up- or down-regulated genes with a two-fold change in MPE cancer cells compared to healthy tissues were differentially expressed from early- to late-stage lung cancer. Of 13 genes related to cellular metabolism, aldolase A (ALDOA), sorbitol dehydrogenase (SORD), transketolase (TKT), and tuberous sclerosis 1 (TSC1) were related to glucose metabolism. qRT-PCR validated their mRNA expressions in pleural metastatic samples. Immunohistochemical staining confirmed aberrant TKT, ALDOA, and TSC1 expressions in tumour cells. Immunofluorescence confirmed TKT co-localisation and co-distribution of ALDOA with thyroid transcription factor 1-positive cancer cells. TKT regulated the proliferation, vascular endothelial growth factor secretion in vitro and in vivo vascular permeability of cancer cell. Glucose metabolic reprogramming by ALDOA, SORD, TKT and TSC1 is important in MPE pathogenesis.

Multifocal axonal polyneuropathy in celiac disease.

The authors report six patients with multifocal axonal polyneuropathy and the subsequent diagnosis of celiac disease (CD). Five patients did not improve or had only modest improvement following dietary intervention or immune therapies; one patient with marked weakness and mild electrodiagnostic findings had complete resolution of the neuropathy following immunomodulatory therapy. CD may be a cause of multifocal axonal polyneuropathy.

Endogenous IGF1 enhances cell survival in the postnatal dentate gyrus.

The dentate gyrus is selectively reduced in size in the insulin-like growth factor 1 (IGF1) null mouse brain. The purpose of this study was to determine whether this defect is due to reduced granule cell numbers, and if so, to determine whether altered cell proliferation, survival, or both contribute to attenuation of dentate gyrus size. At postnatal day 10 (P10), granule cell numbers were not significantly different in IGF1 null and littermate wildtype (WT) dentate gyri. The subgranular zone cell population, however, was relatively increased, and the granule cell layer population relatively decreased in the IGF1 null dentate gyrus. By P50, total dentate cell numbers were decreased by 20% (P = 0.01) in the IGF1 null mouse, although IGF1 null subgranular zone progenitor cells remained relatively increased compared with WT (38%, P < 0.05). IGF1 null dentate cell proliferation, assessed by thymidine analogue incorporation, was actually increased at P10 (33%, P < 0.05) and P50 (167%, P = 0.001). Dentate granule cell death, assessed by the appearance of pycnotic cells and DNA fragmentation, was also significantly increased in the IGF1 null dentate (61%, P < 0.05 and 101%, P = 0.03). These data suggest that endogenous IGF1 serves an important role in dentate granule cell survival during the course of postnatal brain development. In addition, this work suggests the potential of a compensatory mechanism promoting increased dentate cell proliferation in the face of impaired cell survival during postnatal neurogenesis. J. Neurosci. Res. 64:341-347, 2001. Published 2001 Wiley-Liss, Inc.