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Biomedical subjects

J Kleinerman

Publications and source records attributed to J Kleinerman.

35 records · Page 2Linked to original sources
PubMed1977

Peripheral airways as a determinant of ventilatory function in the human lung.

We have investigated the morphological differences responsible for the variability in two tests of pulmonary function, maximal expiratory flow rates (MEF) and the frequency dependence of dynamic compliance (CDYN ratio). Functional measurements were obtained from 53 normal and minimally diseased postmortem human lungs. Morphological measurements performed on these same lungs included airway diameter at three levels in the bronchial tree, the amount of bronchial gland mass, and the alveolar surface to volume ratio. Multiple regression analysis suggests that the diameter of the peripheral conduction airways (membranous bronchioles) is the major morphological determinant for both MEF and the CDYN ratio in lungs at any particular age. Age-dependent changes in both functional tests were associated primarily with differences in the alveolar surface to volume ratio. Minimal emphysema and a lesion associated with cigarette smoking, respiratory bronchiolitis, have no demonstrable effect on either MEF or the CDYN ratio. These studies provide further evidence that the peripheral conducting airways are a major determinant of ventilatory function in the normal human lung.

Adolescent↗
PubMed1977

Diffuse pulmonary ossification.

Diffuse pulmonary ossification (DPO) was a complication of "shock lung" after aortic valve replacement in a 52-year-old man. The relationship of DPO to shock lung is discussed. A possible mechanism for this complication is based on the development of a fibrin-platelet-fibroblastic interaction that may establish an intraalveolar lattice for collagen deposition by the fibroblast. The development of acidosis and mechanical forcer may potentiate fibroblastic transformation into an osteoblast. The mechanical forcer may influence the shape of the bone in the lung.

Aortic Valve↗
PubMed1977

Some effects of nitrogen dioxide on the lung.

Nitrogen dioxide (NO2) when inhaled in different concentrations and for varying times produces pulmonary injuries which are dependent on the anatomic site in the lung and the duration of exposure. Single exposures to high concentrations of NO2 for 5-6 hr produce an intense cellular proliferation which regresses within 48 hr in all lung regions except the terminal respiratory bronchiole region and the alveoli where the proliferation persists for 4-7 days. This same delayed response is also observed in more chronic exposures. Histologically, the lesion in the terminal and respiratory bronchioles may resemble an obliterative bronchiolitis, but the lesion clears if further exposure is terminated. Prolonged exposure to 2 ppm NO2, 20-22 hr per day for 7 days per wk, produces an increase in total pulmonary upstream resistance in animals killed immediately after exposure; this resistence returns to normal values within 3 mo after removal from exposure. The internal surface area (ISA) is decreased after 12 mo exposure to NO2, but this loss of surface progresses during the recovery period in air, suggesting an autonomous progression of the tissue destructive process. Exposure to 3.64 ppm NO2 with and without fly ash for periods of 12-14 mo causes no increase in pulmonary resistance and no alteration in lung surface. Lung phospholipids and protein synthesis appear to be depressed following exposure to NO2. Lecithin is significantly increased. The synthesis of proteases by alveolar macrophages is increased during NO2 exposure. Pigmented alveolar macrophages present in animals exposed to NO2 simulate those found in human lungs of young cigarette smokers in the terminal and respiratory bronchioles. The mechanism of tissue injury by oxidants such as NO2 may involve free radical formation, and peroxidation of lipids or proteins.

Air Pollutants↗
PubMed1976

Identification of functional tumor vessels by resorcin-crystal violet stain infusion.

A resorcin-crystal violet solution of low viscosity injected into the circulatory plexus supplying a tumor is used to identify and characterize functional tumor vessels. Unstained sections of tumor tissue demonstrate heavily stained vascular endothelium with no leakage of stain to extravascular tissue for intact vessels, and little or no background staining. The method is simple to apply for tumor vessel morphology and morphometry.

Capillaries↗
PubMed1976

The significance of hematogenous tumor cell clumps in the metastatic process.

The relationship between the size distribution of vessels in an implanted tumor, the size distribution of tumor cell clumps collected in the venous effluent of the tumor, and the development of pulmonary metastases have been studied. The purpose is to evaluate the importance of clumps and their site of formation in the metastatic process. The results demonstrate a negative exponential character for both the size distribution of effluent tumor clumps and the tumor vessel population. Tumor trauma or massage increases total tumor cells and clumps released into the effluent. Serial amputation demonstrates that tumor cells are continuously being released on a day-by-day basis in vivo. A linear relationship exists between the proportion of vessels with diameters large enough to pass a tumor clump of a given size and the proportion of clumps of that size within the venous effluent. Injection of tumor cells in clumps of 6 to 7 cells produces a significantly greater number of metaststic foci than does a similar number of single tumor cells; larger clumps produce significantly more metastatic foci than do smaller clumps matched for the number of cells. These studies verify the significance of tumor clumps in the metastatic process. It is suggested that tumor cell clumps arise locally within the vascular bed of the tumor.

Animals↗
PubMed1976

Mechanism of Bacillus Calmette-Guérin-induced suppression of metastases in a poorly immunogenic fibrosarcoma.

Bacillus Calmette-Guérin (BCG) reduces the rate of spontaneous pulmonary metastases from a poorly immunogenic fibrosarcoma. To be effective, BCG (1 X 10(6) organisms) must be given in admixture with (1 X 10(6)) tumor cells at the time of transplantation. Reduction of metastasis at this dosage of BCG occurs without a change in the size of the primarytumor or the extent of necrosis within it. Tumors transplanted in admixture with spleen cells from BCG-exposed donors reduced the number of metastases, while spleen cells from normal or tumor-bearing donors had no effect on metastases. Fewer total tumor cells and clumps are collected from the venous effluent of tumors transplanted with BCG than from control tumors. The BCG-treated tumors have more host macrophages intimately associated with the effluent tumor cells then did controls. These data indicate that BCG can inhibit the metastatic potential of a weakly immunogenic fibrosarcoma. The mechanism of this effect appears to be a depression of entry or tumor cells into the tumor vascular channels which may be related to the interaction of tumor cells with BCG-stimulated macrophages.

Animals↗
PubMed1976

Stochastic model of metastases formation.

A mathematical model is developed to describe the dynamics of the hematogenous metastatic process to the lung from a solid tumor growing in a peripheral body site. The accumulation of tumor cell clumps of various sizes in the pulmonary circulation and the formation of metastatic foci are described by a non-homogeneous, two-dimensional Markov process. An analytical solution is found for the special case of metastases produced by the intravenous injection of tumor cell clumps. The system is decoupled experimentally to determine the time-varying entrance rate of tumor cell clumps into the circulation from a growing fibrosarcoma and the number of metastatic foci produced by the intravenous injection of tumor clumps. Model validation is based on comparisons of model simulations with data for the development of metastatic foci and the probability of cure following tumor excision. The model is used to simulate hypothetical therapy to prevent tumor metastases.

Animals↗
PubMed1975

Serum trypsin inhibitory capacity and Pi phenotypes. I. Methods and control values.

Serum trypsin inhibitory capacity determinations are of considerable value in detecting genetically determined types of obstructive pulmonary disease and hepatic disease. These determinations must frequently be followed by determination of protease inhibitor (Pi) phenotype in order to confirm the diagnosis. Piphenotyping has been a specialized and time-consuming procedure, and suggested improvements in the methodology and technics may make it more generally applicable as a clinical laboratory procedure. The prevalence of phenotypes other than MM in a group of 700 control sera from blood donors is reported as a baseline to evaluate typically American populations of mixed ethnic and racial characteristics. There are suggestive differences in prevalences of S and Z genes relating to ethnic stock and racial groups. It is important when comparing the prevalences of S and Z genes in diseasedpopulations to use control groups of similar ethnic and racial compositions. Pi phenotyping is a necessary laboratory procedure in the diagnosis of certain forms of genetically determined chronic obstructive pulmonary disease and hepatic disease. The distributions of all serum protease inhibitory capacity values and those for S and Z Pi phenotypes are shown.

Adolescent↗
PubMed1975

Serum trypsin inhibitory capacity and pi phenotypes. II. Prevalence of alpha1-antitrypsin deficiency in an allergy population.

A series of 138 patients seen consecutively in an adult allergy clinic were studied to determine serum alpha1-antitrypsin (alpha1-AT) levels and protease inhibitor (Pi) phenotypes. These were compared with a control group of 700 healthy young adult blood donors. Both total serum trypsin inhibitory capacity (STIC) and alpha1-AT levels as determined by immunoelectrophoresis (IEP) were measured. Phenotypes were determined by antigen-antibody-crossed IEP. Alpha1-AT levels in the allergy group were not significantly different from control values. STIC in the allergy group was 1.34 +/- 0.28 mg. trypsin inhibited per ml. serum and in the controls, 1.32 +/- 0.28 mg. IEP values were 205 +/- vs. 200 +/- 36 mg. per dl. Similarly, no increase in Pi phenotypes known to be related to any disease state was observed. Since Pi phenotypes other than the most common MM are rare in Negro populations, phenotype data were corrected to include only Caucasian subjects. In the allergy group adjusted for racial composition we found 2.86% MZ, 5.72% MS; no SZ, SS or ZZ was detected. A comparable control group contained 3.68% MZ, 6.23% MS, 0.71% SZ-SS, but no ZZ Pi phenotype.

Adolescent↗
PubMed1975

Elastic behavior of postmortem human lungs: effects of aging and mild emphysema.

The elastic behavior of postmortem human lungs has been studied in an effort to differentiate the effects of normal aging from those of mild emphysema. Static pressure-volume (P-V) curves were measured in 50 lungs obtained from men 15-85 yr of age, including 12 lungs with mild-to-moderate emphysema. The emphysema was quantitatively assessed by gross and microscopic methods. The P-V relationship in all lungs is accurately described by the empirically fitted equation, P = alpha1ea2v. This expression is useful because the two parameters separate the effects of elastic behavior (alpha1) from size (alpha2) on the P-V curve. There is a close negative correlation (R = -0.94) Between age and alpha1 in normal lungs but no significant age dependence of alpha2. Further decreases in alpha1 are found in most emphysematous lungs. Alpha1 is more than 2 SEE below the age-predicted mean in five of nine lungs with minimal emphysema (1-10% by point count) and more than 5 SEE below the mean in the three more severely affected lungs. There is a close correlation (R = +0.90) between alpha1 and the alveolar surface-to-volume ratio in both normal and emphysematous lungs.

Adolescent↗
PubMedDate not supplied

Lung proteolytic activity and serum protease inhibition after NO2 exposure.

Proteolytic activity (PA) of lung extracts was measured in control hamsters and in those exposed to 20 ppm NO2 for 24 hours (acute) and 30 days (chronic). Total PA of these lungs as measured by pH 7.4 caseinolysis was slightly increased after the 24-hour, but normal following the 30-day exposure. Lung extract fractions from NO2-exposed animals display an increased PA at pH 3.0 and 9.0, but are near control levels at pH 7.0. Serum protease inhibitor (PI) activity is significantly increased after short NO2 exposure as compared with control conditions. No significant increase is observed in PI after chronic exposure. Increase in 24-hr NO2 lung extract PA is associated with increase in PI, which may neutralize the augmented proteolysis. These studies are consistent with previous observations that indicate prolonged NO2 exposure does not produce significant emphysema in the hamster lung.

Animals↗
PubMedDate not supplied

Effects of nitrogen dioxide on elastin and collagen contents of lung.

Male Syrian hamsters were exposed to 30 +/- 5 ppm nitrogen dioxide for 22 hr daily for 3 wk. Nitrogen dioxide-exposed hamsters sacrificed at various times during the 3 wk exposure showed a general loss of body weight and an increased dry lung weight when compared with the controls, which were housed in a similar, but nitrogen dioxide-free environment. Analysis of total lung collagen and total lung elastin revealed a net decrease in the moieties within 4 and 10 days, respectively, following commencement of nitrogen dioxide exposure. Total lung collagen returned toward pre-exposure levels by the 14th day of nitrogen dioxide exposure. Total lung elastin did not return toward normal until termination of nitrogen dioxide exposure. Recovery in room air for 3 wk following 21 days of nitrogen dioxide exposure restored the total pulmonary collagen and elastin to valutin and collagen degradation and synthesis differ during and after nitrogen dioxide exposure. Lung collagen loss was observed earlier and was restored to normal values during the continuation of nitrogen dioxide exposure. Lung elastin loss occurred later and persisted during the entire period of exposure but returned to normal after exposure was terminated.

Animals↗