Lung infection rates in two sympatric Tropiduridae lizard species by pentastomids and nematodes in northeastern Brazil

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Beneficial Effects of Physical Training on the Cardio-Inflammatory Disorder Induced by Lung Ischemia/Reperfusion in Rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Effects of temperature on lung and blood gases in the South American rattlesnake Crotalus durissus terrificus

The effects of temperature on lung and blood gases were measured in the South American rattlesnake (Crotalus durissus terrificus). Arterial blood and lung gas samples were obtained from chronically cannulated animals at 15, 25, and 35 degrees C. As expected for reptiles, arterial pH fell with increased temperature (0.018 U degrees C-1 between 15 and 25 degrees C and 0.011 U degrees C-1 between 25 and 35 degrees C) while lung gas PCO2 rose from 5.8 mmHg at 15 degrees C to 13.2 mmHg at 35 degrees C. Concurrently, lung gas PO2 declined from 132 mmHg at 15 degrees C to 120 mmHg at 35 degrees C, and arterial PO2 increased from 33 to 76 mmHg in that temperature range. Arterial haemoglobin O-2 saturation rose from 0.53 at 15 degrees C to 0.83 at 25 degrees C but became slightly reduced (0.77) with a further elevation of temperature to 35 degrees C. Arterial haemoglobin concentration increased from 1.96 to 2.53 mM between 15 and 35 degrees C, consistent with higher demands on oxygen delivery to tissues at elevated temperatures. Moreover, the substantial increase of haemoglobin O-2 saturation between 15 and 25 degrees C conforms to the idea that reduction of the central vascular right-to-left shunt (pulmonary bypass of systemic venous return) is associated with high metabolic demands. (C) 1998 Elsevier B.V. All rights reserved.

Effect of annexin-A1 peptide treatment during lung inflammation induced by lipopolysaccharide

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Reduced allergic lung inflammation in rats following formaldehyde exposure: Long-term effects on multiple effector systems

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Endogenous annexin A1 counter-regulates bleomycin-induced lung fibrosis

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Malignant ameloblastoma metastasis to the lung: a case report

Ameloblastoma is an odontogenic tumor, usually benign, which rarely metastasizes to distant organs. The case of a 27-year-old white woman is described, who presented a metastatic pulmonary ameloblastoma 7 years after the removal of a mandibular ameloblastoma. She presented no pulmonary symptoms, but a lung nodule was found in a chest x-ray during a routine check-up for job admission. Computed tomography (CT) revealed a 2-cm well-defined solitary round nodule without calcifications, leading to the hypothesis of a metastatic tumor. Clinical and CT investigation confirmed no ameloblastoma recurrence in the jaw and no other primary tumor. The diagnosis of metastatic ameloblastoma was confirmed by microscopic evaluation of the pulmonary nodule.

Burnt sugarcane harvesting: Particulate matter exposure and the effects on lung function, oxidative stress, and urinary 1-hydroxypyrene

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Indoor NO2 air pollution and lung function of professional cooks

Studies of cooking-generated NO2 effects are rare in occupational epidemiology. In the present study, we evaluated the lung function of professional cooks exposed to NO2 in hospital kitchens. We performed spirometry in 37 cooks working in four hospital kitchens and estimated the predicted FVC, FEV1 and FEF25-75, based on age, sex, race, weight, and height, according to Knudson standards. NO2 measurements were obtained for 4 consecutive days during 4 different periods at 20-day intervals in each kitchen. Measurements were performed inside and outside the kitchens, simultaneously using Palm diffusion tubes. A time/exposure indicator was defined as representative of the cumulative exposure of each cook. No statistically significant effect of NO2 exposure on FVC was found. Each year of work as a cook corresponded to a decrease in predicted FEV1 of 2.5% (P = 0.046) for the group as a whole. When smoking status and asthma were included in the analysis the effect of time/exposure decreased about 10% and lost statistical significance. on predicted FEF25-75, a decrease of 3.5% (P = 0.035) was observed for the same group and the inclusion of controllers for smoking status and asthma did not affect the effects of time/exposure on pulmonary function parameter. After a 10-year period of work as cooks the participants of the study may present decreases in both predicted FEV1 and FEF25-75 that can reach 20 and 30%, respectively. The present study showed small but statistically significant adverse effects of gas stove exposure on the lung function of professional cooks.

COMPENSATORY LUNG GROWTH: LUNG PROTEIN,DNA and RNA CONTENTS IN TRILOBECTOMIZED RATS

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Compensatory lung growth: protein, DNA and RNA lung contents in undernourished trilobectomized rats

OBJETIVO: demonstrar se ocorre crescimento pulmonar compensatório (CPC) representado pelos conteúdos de proteínas, DNA e RNA no rato adulto jovem, subnutrido, submetido à trilobectomia pulmonar. MÉTODOS: Utilizamos 137 ratos Wistar, machos, distribuídos por sorteio, em 9 grupos, submetidos a três tratamentos (controle, toracotomia, trilobectomia), sacrificados em três momentos (7, 30 e 90 dias). Na trilobectomia foram extirpados os lobos médio, acessório e caudal direitos. Variáveis estudadas: conteúdos pulmonares de proteínas, DNA e RNA. RESULTADOS: No lobo cranial e pulmão esquerdo o conteúdo protéico foi maior nos trilobectomizados. Ocorreu CPC insuficiente para suprir a perda desta variável, sendo menor nos pulmões dos trilobectomizados. O incremento nos conteúdos de DNA do lobo cranial e pulmão esquerdo dos trilobectomizados foram suficientes para compensar a perda desta variável, resultando num conteúdo de DNA dos pulmões semelhante aos controle. O conteúdo de RNA, nos trilobectomizados, foi maior no lobo cranial e pulmão esquerdo, com maior eficiência no primeiro, insuficiente para que se aproximassem aos obtidos nos demais grupos, ficando menores. CONCLUSÃO: Nos trilobectomizados ocorreu CPC, provavelmente com hiperplasia celular e pouca hipertrofia, devido a grande compensação do DNA e pequena do RNA. Esta foi a grande diferença quando comparamos este resultado ao obtido com animais nutridos, que apresentavam hipertrofia pronunciada.

Compensatory lung growth in autologus lobar implant after pneumonectomy in dogs

OBJETIVO: Avaliar se existe crescimento compensatório pulmonar em transplante lobar e verificar se este crescimento é semelhante ao que ocorre após lobectomia. MÉTODOS: Foram utilizados 48 cães, distribuídos em 3 grupos (G1=controle, G2=lobectomia cranial esquerda e G3=pneumonectomia com reimplante do lobo caudal esquerdo). Após 5 meses da cirurgia, os animais foram submetidos à cintilografia pulmonar e a seguir sacrificados para estudo morfométrico pulmonar. RESULTADOS: Os resultados mostraram que não existe correlação da cintilografia nem com a massa nem com o volume do pulmão. Houve crescimento compensatório em massa e volume residual nos dois grupos operados, tanto no pulmão contralateral como no ipsilateral à cirurgia, não existindo até os 5 meses de estudo compensação em capacidade pulmonar total, nem em complacência pulmonar no lobo caudal remanescente do G2 e no lobo caudal reimplantado do G3, havendo maior prejuízo para o lobo reimplantado. Como estudos prévios mostram que o crescimento compensatório pulmonar se inicia com aumento da massa e do volume residual, e que a complacência é compensada posteriormente, este estudo parece ter documentado o início do crescimento compensatório, sendo a complacência pulmonar o fator limitante do crescimento compensatório após 5 meses de estudo. CONCLUSÃO: Conclui-se que existe crescimento compensatório tanto no lobo reimplantado como no pulmão contralateral, mas a complacência ainda encontra-se reduzida. O crescimento compensatório foi semelhante nos dois grupos, mas a complacência do lobo implantado está mais prejudicada.

Interactions between genetic predisposition and environmental toxicants for development of lung cancer

Significant interindividual variations in health outcome may be caused by the inheritance of variant polymorphic genes, such as CYP2D6 and CYP2E1 for activation, and GSTM1 and GSTT1 for detoxification of chemicals. However. mechanistic studies linking the inheritance of predisposing genes with genotoxic effects towards cancer have yet to be systematically conducted. We have studied 54 lung cancer patients and 50 matched normal controls, who have been cigarette smokers, to elucidate the role of polymorphic genes in cancer. Our data indicates that the inheritance of unfavorable CYP2D6, CYP2E1, and GSTT1 genes is strongly correlated with the smoking-related lung cancer. For heavy cigarette smokers (> 30 pack-years), the smoking habit is the strongest predictor of lung cancer risk irrespective of the inheritance of unfavorable metabolizing genes. For moderate to light smokers (< 30 pack-years), the genetic predisposition plays on important role For the risk (odds ratio = 3.46; 95% CL = 0.46-40.2). Using a subgroup of the study population, we observed that cigarette smokers having the defective GST genes have significantly more chromosome aberrations as determined by the fluorescence-in-situ-hybridization (FISH) technique than smokers with the normal GST genes (P < 0.001). In conclusion, our study provides data to indicate that individuals who have inherited unfavorable metabolizing genes have increased body burden of toxicants to cause increased genetic damage and to have increased risk for cancer. Studies like ours can be used to understand the basis for interindividual variations in cancer outcome, to identify high risk individuals and to assess health risk. (C) 1997 Wiley Liss, Inc.

Predisposing genes and increased chromosome aberrations in lung cancer cigarette smokers

Genotoxic effects linking cigarette smoking with lung cancer have not been consistently demonstrated, therefore claims for the cause-effect relationships are vigorously contested. Using matched populations of 22 lung cancer patients who have been cigarette smokers (LCP), 22 non-cancerous cigarette smokers (SC) and 13 non-smokers (NSC), we have applied the fluorescence in situ hybridization (FISH) tandem probe assay to elucidate the frequency of chromosome breakage among the participants. Two probes were used, a classical satellite probe which hybridizes to the large heterochromatin region of chromosome 1, and an alpha-satellite probe which targets a small region adjacent to the heterochromatin probe. The highest frequency of structural aberrations was observed in LCP (1.4 +/- 0.1) followed by SC (1.25 +/- 0.1) and NSC (0.4 +/- 0.1). Aberration frequencies were not significantly different between LCP and SC (p > 0.05), however, a statistically significant difference was detected between the smoker populations combined (LCP and SC) and the NSC (p < 0.001). The breakage frequencies showed a positive correlation with duration of smoking for LCP (r = 0.5; p < 0.01), but not for SC (P > 0.05). In addition, the aberration frequencies were influenced by the inheritance of polymorphic glutathione S-transferase (GST) genes. LCPs missing one or the other GST (GSTM1 or GSTT1) genes were found to have significantly higher chromosome breaks compared to LCPs with both genes present (p < 0.05), Our data indicate that genetic predisposition and chromosome aberrations may be mechanistically related to the initiation of lung carcinogenesis; therefore, they may be useful biomarkers for lung cancer among cigarette smokers. (C) 1997 Elsevier B.V. B.V.