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At least 55 records · Page 3Linked to original sources
PubMed1994

Peripheral blood immune responses to surgically induced lung tissue injury.

Surgically induced lung tissue trauma reveals an immune response in peripheral blood, the degree of which could depend on extent and severity of the organ trauma and the presence of lung malignancies. The study included 34 patients who underwent elective thoracic surgery because of benign and malignant lung tissue diseases. Flow-cytometric phenotyping of lymphocyte subsets shows a clear shift to reduced immunocompetent cells after lung tissue injury. Patients with lung tumors reveal a postoperative activation of the macrophage system as indicated by increased plasma levels of neopterin. Increased levels of soluble interleukin-2 receptor in the plasma of these patients may be the result of cellular shedding of the receptor. Lung tissue trauma is also followed by reduced immunoglobulin levels which are most pronounced in the presence of lung malignancies. These results suggest that lung tissue injury leads to postoperative immunosuppression especially in tumor patients.

Adult↗
PubMed1992

Lung tissue resistance during contractile stimulation: structural damping decomposition.

Research in the mechanics of soft tissue, and lung tissue in particular, has emphasized that dissipative processes depend predominantly on the viscous stress. A corollary is that dissipative losses may be expressed as a tissue viscous resistance, (Rti). An alternative approach is offered by the structural damping hypothesis, which holds that dissipative processes within soft tissue depend directly more on the elastic stress than on the viscous stress. This implies that dissipative and elastic processes within lung tissues are coupled at a fundamental level. We induced alterations of Rti by exposing canines to aerosols of the constrictors prostaglandin F2 alpha, histamine, and methacholine and by changing volume history. Using the structural damping paradigm, we could separate those alterations in Rti into the product of two distinct contributions: change in the coefficient of coupling of dissipation to elastance (eta) and change in the elastance itself (Edyn). Response of Edyn accounted for most of the response of resistance associated with contractile stimulation; it accounted for almost all the response associated with differences in volume history. The eta changed appreciably with constriction but accounted for little of the response of Rti with volume history. According to the structural damping hypothesis, induced changes in eta with constriction must reflect changes in the kinetics of the stress-bearing process, i.e., differences in cross-bridge kinetics within the target contractile cell and/or differences in the influence of the target cell on other stress-bearing systems. We conclude that, regardless of underlying processes, the structural damping analysis demonstrates a fundamental phenomenological simplification: when Edyn responds, Rti is obligated to respond to a similar degree.

Airway Resistance↗
PubMed2000

Asbestos content of lung tissue and carcinoma of the lung: a clinicopathologic correlation and mineral fiber analysis of 234 cases.

The aim of this study was to investigate the asbestos content of lung tissue in a series of patients with lung cancer and some history of asbestos exposure. This information was then correlated with demographic information, occupational and smoking history, presence or absence of pathologic asbestosis or pleural plaques, and pathologic features of the cancer. The pulmonary concentration of asbestos fibers in 234 cases of primary carcinoma of the lung was determined by means of a tissue digestion technique. Asbestos body counts were performed in 229 cases and fiber analysis by scanning electron microscopy in 221 cases. Asbestos content was recorded as total asbestos fibers, commercial amphibole fibers, noncommercial amphibole fibers, and chrysotile fibers 5 microm or greater in length per gram of wet lung tissue. The study group included 70 patients with asbestosis (Group I), 44 patients with parietal pleural plaques but without asbestosis (Group II), and 120 patients with neither (Group III). The median asbestos body content of Group I was more than 35 times greater than Group II and more than 300 times greater than Group III. The total asbestos fiber count for Group I was nearly 20 times greater than Group II and more than 50 times greater than Group III. The difference was due almost entirely to commercial amphiboles. In a series of primary lung cancer cases with some history of asbestos exposure, a markedly elevated asbestos content was identified among those with pathologic asbestosis as compared with patients with pleural plaques alone or with neither plaques nor asbestosis.

Aged↗
PubMed1999

Cyclooxygenase-2 (COX-2) mRNA expression levels in normal lung tissues and non-small cell lung cancers.

One of the cyclooxygenase (COX) isoforms, COX-2, is overexpressed in various human cancers. In this study, we examined the gene expression levels of COX-2 in primary non-small cell lung cancers (NSCLC), metastatic lymph nodes, and normal lung tissues. The expression levels of the COX-2 gene were assessed by means of the reverse transcription polymerase chain reaction in 76 autopsy samples (29 primary NSCLC, 29 corresponding normal lung tissues, and 9 metastatic lymph nodes). The expression levels in NSCLC (both adenocarcinomas and squamous cell carcinomas) were significantly higher than in normal lung tissues and were significantly higher in adenocarcinomas than in squamous cell carcinomas. Differences between the levels of expression of COX-2 in primary tumors and their corresponding metastatic lymph nodes in 9 adenocarcinoma patients were not significant. Our results indicate that COX-2 may be associated with carcinogenesis of NSCLC, and that it may be a target for the treatment of NSCLC.

Adenocarcinoma↗
PubMed1994

[Quantitative study on DNA-adduct in normal lung tissues of smoking and non-smoking lung cancer patients].

Lung tissues from 32 cases of lung cancer with surgical operation, 22 smokers and 10 nonsmokers, were analyzed with P1-mediated modification of 32P-postlabelling technique. The level of lung DNA-adduct in cigarette smokers was higher that in nonsmokers with significant difference (P < 0.001). Autoradiogram showed a diagonal radioactive zone in smokers' lung tissues. Correlation analysis indicated DNA-adduct in lung tissues increased with the number of cigarettes smoked with a regression equation of Y = 0.411 X + 3.52, r = 0.74, P < 0.001.

Adult↗
PubMedDate not supplied

Changes in lung tissue fibronectin content and synthesis during postnatal lung growth.

We studied changes in lung tissue fibronectin content and synthesis during postnatal lung growth in rats. We reasoned that fibronectin, which is important in cell differentiation, migration, and adhesion, and in the organization of the extracellular matrix, might play a role in the rapid cell proliferation and alveolar septal formation that occurs postnatally in mammalian lungs. Newborn rats were sacrificed at 4, 7, 11, 14, and 21 days after birth. The lungs were perfused and lavaged, tissue fibronectin was extracted using urea and heparin (Bray et al, Science 1981; 214:793) and the extracted fibronectin was measured by enzyme-linked immunoassay. Tissue fibronectin synthesis was measured by the in vivo incorporation of 35S-methionine into fibronectin that was extracted from lung tissue and immunoprecipitated. Lavage fibronectin and albumin content and lung tissue collagen (hydroxyproline) content were also determined. Lung tissue fibronectin content per g dry lung almost doubled between days 4 and 7 after birth, was slightly higher at day 14 than at day 7, and decreased sharply between days 14 and 21. Lung tissue fibronectin synthesis per g dry lung increased steadily between days 4 and 14 to reach a peak value of about 2.5 times the 4-day value; it then decreased sharply between days 14 and 21. The period of increased fibronectin content and synthesis (4 to 14 days) coincided with the period during which lung cell proliferation and secondary alveolar septa formation are known to be the most active, and the sharp decrease in fibronectin content and synthesis (between 14 and 21 days) coincided with the period during which lung growth and remodeling markedly decrease.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Penetration of vancomycin into human lung tissue.

Vancomycin penetration into lung tissue was evaluated in thirty patients following the administration of 1 g of vancomycin as a 1 h i.v. infusion. Mean concentrations (range) of vancomycin in lung tissue were 9.6 (6.3-12.1) mg/kg at 1h, 5.7 (4.7-7.4) mg/kg at 2 h, 4.2 (0.8-6.5) mg/kg at 3-4 h, 2.4 (1.4-4.7) mg/kg at 6 h, and 2.8 (0.9-7.8) mg/kg at 12 h after the end of infusion. Ratios of lung tissue to serum concentration ranged 0.24 to 0.41 at 1 and 12 h, respectively. One of six patients observed at 6 h, and 3 of 7 patients at 12 h did not have detectable levels of vancomycin in lung tissue. A 1 h iv infusion of a 1 g dose of vancomycin does not achieve sustained lung concentrations above the MIC for susceptible staphylococci over a dosing interval of 12 h. Therefore, a more appropriate modality of administration, such as continuous infusion, should be considered.

Aged↗
PubMed2006

Coxsackievirus and adenovirus receptor expression in non-malignant lung tissues and clinical lung cancers.

Adenoviral vector mediated gene delivery has been applied in clinical trials and mechanistic studies to explore new treatment approaches for lung cancers. The expression of coxsackievirus adenovirus receptor (CAR), the primary receptor for the most commonly used adenovirus serotype 5 (Ad5)-based vectors, predominantly determines the permissiveness of lung cancer cells. CAR expression is also suggested to modulate tumor cell proliferation capacity. Here, we studied CAR expression in archival lung cancer specimens by using well-characterized CAR 72 antibodies. High levels of CAR expression were observed in most of the 32 cases of squamous cell carcinoma lung cancers and in all the five cases of small cell lung cancers investigated. In contrast, high levels of CAR expression were detected only in 6 of 22 adenocarcinoma lung cancers. The relative levels of CAR expression did not correlate with the pathologic grade in lung cancers, and was thus inconsistent with a role of modulating cancer cell proliferation. Of note, CAR expression was not detected in non-malignant alveolar cells. Our data suggest a preferred utility of Ad5 vector mediated gene delivery to squamous cell carcinoma lung cancers, small cell lung cancers, but not to the majority of adenocarcinoma lung cancers.

Adult↗
PubMed2000

Wet-to-dry ratio of lung tissue and surfactant outwash after one-lung flooding.

Unilateral flooding of the lung after intubation with a double-lumen tube enables intraoperative sonography of the lung tissue. The flooding restricts the pulmonary blood stream of the flooded lung in a relevant degree and thus reduces the right-to-left shunt volume. The deficient perfusion of the lung tissue during the flooded phase might cause capillary permeability disorders and secondary oedema development. This can be determined by examination of extravascular lung water (EVLW) after draining and reventilation of the flooded lung. Although one-time unilateral lung flooding must be distinguished from bronchopulmonary lavage, it is interesting to study the effects of flooding on the surfactant system. The wet-to-dry ratio of the lung tissues of 13 female pigs was ascertained at different times following one-lung flooding (1 to 11 weeks). A trend towards an increased wet-to-dry ratio in the previously flooded lung was found only in the tissue samples taken 1 h after reventilation. After only 24 h, the two lungs no longer differed in their wet-to-dry ratio. In six pigs, the phospholipid content of the drained flooding liquid was determined. It was shown that the surfactant loss caused by flooding was maximally 47% of the calculated surfactant pool of the respective lung.

Animals↗
PubMed1997

[Steroid resistance and lung-tissue cytokines in experimental bleomycin-induced lung fibrosis].

To examine the mechanism of steroid resistance in lung fibrosis, cytokines expressed in the lung tissue of mice with bleomycin-induced lung fibrosis were studied. 1. Glucocorticoid administration (1 mg/kg/day) did not affect the grade of lung fibrosis induced by intratracheal injection of bleomycin (3.76 micrograms/g). 2. Cytokines expressed in the lung tissue were studied with the reverse-transcriptase polymerase chain reaction. Levels of promotor cytokines, such as TNF alpha, TGF beta, INF gamma, and IL-2, were significantly higher in lung tissue from the bleomycin group. The expression of these cytokines in the glucocorticoid group was low, especially the peak value. Expression of IL-4 was high in the bleomycin group, and was not inhibited in the glucocorticoid group. Expression of the down-regulator cytokine IL-10 was also high in the bleomycin group and very low in the glucocorticoid group. 3. The non-selectivity of glucocorticoids with respect to promotor and suppressive cytokines may account in part for steroid resistance in bleomycin-induced pulmonary fibrosis.

Animals↗
PubMed2003

[Levels and distribution of 15 rare earth elements in tumor and normal lung tissue from the patients with lung cancer].

Ten tumor tissue and normal tissue around tumors were collected from the patients with lung cancer. After digested by mixed acids(HNO3:HClO4 = 10:1), 15 rare-earth elements (REEs) in the tissue were measured directly by ELAN 5000 ICP-MS. Tissue levels and distribution of 15 REEs were analyzed and compared with those in healthy human lung tissue measured in the same condition. Re (rhenium) was used as an internal standard element to compensate for matrit inhibition and sensitivity drift. Recoveries of standard addition for REEs was 92.9%-111.3% and the precision was 0.96%-3.07%. Results showed that levels of 15 REEs in normal tissues around the tumor was as 2.07-2.51 times high as those in the tumor tissue, while the REE distribution curves of them was similar. There were positive abnormalities of Ce and negative abnormalities of Eu in REE curves of both tissue after chondrite-normalized. Compared REE level and distribution pattern in normal tissue with those in tumor tissue from patients with lung cancer, it was found that contents of light REE in lung tissue of health human were much higher while the contents of media and heavy REE were much lower. LREE/HREE in the tumor tissue and normal tissue with lung cancer and health human lung tissue were 12.99, 13.72 and 44.11 respectively. This study suggested that there might be light REEs accumulation in human lung tissue compared with REE distribution in the air particulates and soil. Light REEs accumulation in the lung of healthy people was more obviously than that in patients with lung cancer.

Adult↗
PubMed1982

Antigen-induced release of histamine from rat tissues in vitro: dissociation in development of serosal mast cell, lung tissue, and tracheal tissue response capacity.

We examined the temporal development and the fading in Sprague Dawley rats, actively sensitized to ovalbumin (OA), of the capacity of serosal mast cells, chopped lung tissue, and occasionally chopped tracheal tissue, to respond at antigen challenge in vitro with histamine release. Response capacity of both serosal mast cells and lung tissue developed within 2-3 weeks after injection of 1 microgram OA or more together with 100 mg of alum. Maximum response capacity was observed in cells and tissue from animals injected with 10 micrograms OA, part of the response capacity then remained until 3 months after immunization. Development of serosal mast cell reactivity was occasionally dissociated from that of lung tissue. When low amounts of alum (1 or 10 mg) were employed as adjuvant, lung tissue reactivity could be induced in the virtual absence of serosal mast cell response capacity. Silica gel was less efficient than alum as an adjuvant for induction of a primary response, but 'secondary' tissue responses could be induced when silica gel was used as an adjuvant. Pretreatment of the animals with cyclophosphamide before the booster injection enhanced and prolonged the response capacity of lung tissue. Animals injected with OA together with Freund's complete adjuvant did not provide responding serosal mast cells; response capacity of lung tissue varied with immunization dose of antigen. Antigen-induced histamine release from chopped tracheal tissue did not correlate to response capacity of lung tissue. Thus, the development in the rat of response capacity with respect to antigen-induced histamine release dissociates from serosal mast cells, lung tissue, and tracheal tissue.

Adjuvants, Immunologic↗
PubMed1995

Expression of tumor necrosis factor receptors in human lung cancer cells and normal lung tissues.

The purpose of this study was to investigate the expression of tumor necrosis factor (TNF) receptors for the control of the biologic action of TNF-alpha in lung cancer cells and normal lung tissues. Lung cancer specimens and normal lung tissues were freshly obtained in pairs from 15 patients who underwent surgery for lung cancer. Thirteen lung cancer specimens expressed the 55 kDa TNF receptor messenger RNA (mRNA), whereas only six lung cancer specimens expressed the 75 kDa TNF receptor mRNA by Northern blot analysis. The 55 kDa and 75 kDa TNF receptors mRNA were detected in all and 11 normal lung tissues, respectively. All four lung carcinoma cell lines examined expressed the 55 kDa TNF receptor mRNA, but only RERF-LC-MS (MS) expressed both the 55 kDa and 75 kDa TNF receptors mRNA. Immunohistochemical examination revealed that lung cancer cells expressed the 55 kDa TNF receptor, but not the 75 kDa TNF receptor at the protein level. In normal lung tissues, the 55 kDa TNF receptor was detected in alveolar macrophages, bronchioles, and some small vessels. The 75 kDa TNF receptor was detected in alveolar macrophages. All four lung carcinoma cell lines examined exhibited the only 55 kDa TNF receptor. TNF-mediated tumor cell lysis was observed in all lung carcinoma cell lines that exhibited the 55 kDa TNF receptor except A549, which is a TNF-insensitive cell line. In surface binding assays, specific surface binding of TNF-alpha to TNF-insensitive cell line A549 was observed to be about half that of TNF-sensitive cell lines. We demonstrated the expression of two distinct TNF receptors in human lung cancer and normal lung tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗