The Lung

Husain, Aliya N.

doi:10.1016/b978-1-4377-0792-2.50020-1

Cited by 58 publications

(89 citation statements)

References 138 publications

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“…Clinically, chronic bronchitis and emphysema present in the same patient are referred to as COPD. The main etiological factor for COPD is smoking (Husein 2010).…”

Section: Introductionmentioning

confidence: 99%

Claudin-3 and Clara Cell 10 kDa Protein as Early Signals of Cigarette Smoke–Induced Epithelial Injury along Alveolar Ducts

et al. 2012

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Smoking-associated chronic obstructive pulmonary disease is characterized by inflammation, changes affecting small airways, and development of emphysema. Various short-and long-term models have been introduced to investigate these processes. The aim of the present study was to identify markers of early epithelial injury/adaptation in a short-term animal model of cigarette smoke exposure. Initially, male BALB/c mice were exposed to smoke from one to five cigarettes and lung changes were assessed 4 and 24 hr after smoking cessation. Subsequently, animals were exposed to smoke from five cigarettes for 2 consecutive days and lungs investigated daily until the seventh postexposure day. Lung homogenates cytokines were determined, bronchioloalveolar fluid cells were counted, and lung tissue was analyzed by immunohistochemistry. Exposure to smoke from a single cigarette induced slight pulmonary neutrophilia. Smoke from two cigarettes additionally induced de novo expression of tight junction protein, claudin-3, by alveolar duct (AD) epithelial cells. Further increases in smoke exposure induced epithelial changes in airway progenitor regions. During the recovery period, the severity/frequency of epithelial reactions slowly decreased, coinciding with the switch from acute to a chronic inflammatory reaction. Claudin-3 and Clara cell 10 kDa protein were identified as possible markers of early tobacco smoke-induced epithelial injury along ADs.

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“…Clinically, chronic bronchitis and emphysema present in the same patient are referred to as COPD. The main etiological factor for COPD is smoking (Husein 2010).…”

Section: Introductionmentioning

confidence: 99%

Claudin-3 and Clara Cell 10 kDa Protein as Early Signals of Cigarette Smoke–Induced Epithelial Injury along Alveolar Ducts

et al. 2012

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“…[3][4][5] Most of the asthma patients are allergic to inhaled and chemical antigens which lead to their sensitization and a hyper-responsive airway. 6,7 These antigens stimulate the induction of TH2 type T cells and other immune cells, which produce proallergic, proinflammatory cytokines (interleukin IL-4, IL-5, IL-13), and chemokines (eotaxins) which mediate the inflammatory process.…”

mentioning

confidence: 99%

Study of serum IgE levels in childhood asthma in Barabanki region, India

Rathoria¹,

Bansal²,

Gupta³

et al. 2018

Int J Contemp Pediatr

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Background: Elevated Serum Immunoglobulin E (IgE) levels are characteristic of most of the allergic diseases including asthma. Most of the asthma patients are allergic to inhaled antigens and chemical antigens, which lead to their sensitization and induce a state of hypersensitivity that is IgE mediated hypersensitivity reaction. The aim of this study was to estimate and compare serum IgE levels in childhood asthmatics and in normal subjects and to obtain the relationship between serum IgE levels and severity of asthma.Methods: A stratified sample of 58 patients within the age group of 5-15 years including 36 male and 22 female asthmatic patients and 58 healthy controls within the same age group were included in this study and classified according to GINA classification 2016. Serum IgE levels were estimated by using ELISA kit.Results: Mean IgE levels ranged from 163.82 IU/mL in normal subjects to 881.81 IU/mL in asthmatics. The mean values of Serum IgE levels in mild, moderate and severe asthmatic children were 625.25 IU/mL, 871.77 IU/mL, 1225.05 IU/mL respectively.Conclusions: High Serum Immunoglobulin E levels were found in childhood asthmatics as compared to normal subjects. Serum IgE levels were found to increase as the severity of asthma increased. The variability in each grade of asthma was very large so we could not find any statistically significant correlation.

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“…It is now the second most common malignant disease diagnosed among both men and women in the United States [1]. A variety of benign and malignant tumors develop in the lung; 90-95% are carcinomas, about 5% are bronchial carcinoids, and 2-5% are mesenchymal and other miscellaneous tumors [2]. Non-small cell lung carcinoma (NSCLC) is less often metastatic and is less responsive to chemotherapy than small cell carcinomas.…”

Section: Introductionmentioning

confidence: 99%

EMMPRIN and fascin expression in non-small cell lung carcinoma

et al. 2010

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AbstractFascin and EMMPRIN (CD 147) have a demonstrated relationship with the invasion and progression of many tumors. The aim of this study was to analyze fascin and EMMPRIN expression in non-small cell lung carcinoma and their relationship with clinicopathologic features. Fascin and EMMPRIN expression levels were investigated via the immunohistochemistry of paraffin-embedded tissues of 64 patients with non-small cell lung carcinoma, including 46 squamous cell carcinoma and 18 adenocarcinoma patients. The patients were scored on the basis of staining extent and intensity, and were then assigned a combined score. Fascin expression was present in 44 of 46 (95.6%) patients with SCC and 16 of 18 (88.8%) patients with adenocarcinoma. There was a significant correlation between fascin expression and tumor stage in the SCC and adenocarcinoma groups. EMMPRIN expression was observed in all patients with SCC (46 of 46, 100%) and 16 of 18 (88.8%) patients with adenocarcinoma. There was significant correlation between EMMPRIN expression and both tumor stage and diameter in the SCC group, but not in the adenocarcinoma group. This study revealed that high levels of fascin and EMMPRIN expression may indicate the importance of their roles in the progression of non-small cell lung carcinoma and they could be used as prognostic marker for these tumors.

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The Lung

Cited by 58 publications

References 138 publications

Claudin-3 and Clara Cell 10 kDa Protein as Early Signals of Cigarette Smoke–Induced Epithelial Injury along Alveolar Ducts

Claudin-3 and Clara Cell 10 kDa Protein as Early Signals of Cigarette Smoke–Induced Epithelial Injury along Alveolar Ducts

Study of serum IgE levels in childhood asthma in Barabanki region, India

EMMPRIN and fascin expression in non-small cell lung carcinoma

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