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Biomedical subjects

R White

Publications and source records attributed to R White.

At least 721 records · Page 40Linked to original sources
PubMed1979

Tyrosinase maturation and pigment expression in B16 melanoma: relation to theophylline treatment and intracellular cyclic AMP.

We have studied the effects of theophylline treatment on pigmentation characteristics and growth of two B16 melanoma cell lines, HFH-18 and P/140. Cell counts of control and theophylline-treated cultures confirmed that the drug inhibits cell growth. Light and electron microscope cytochemistry with the L-dopa reaction indicated that the two cell lines differ in their ability to transfer Golgi-associated tyrosinase to developing premelanosomes. The results of these experiments, considered with results of electrophoretic analyses and activity measurements by the Pomerantz method, also provide evidence that increased tyrosinase synthesis occurs in response to theophylline treatment. In addition, results indicate that theophylline induces changes in the rate of synthetic or degradative posttranslational modification of tyrosinase. Measurements of intracellular cyclic AMP levels by radioimmunoassay in control cultures and in theophylline- and alpha-MSH-treated cultures were made. Although the hormone induced spectacular increases in cyclic AMP levels, theophylline produced no detectable change. These results indicate that theophylline differs from alpha-MSH because theophylline-induced changes in pigmentation may not require the participation of intracellular cyclic AMP.

Animals↗
PubMed1979

Laboratory-based surveillance of influenza virus in the United States during the winter of 1977-1978. I. Periods of prevalence of H1N1 and H3N2 influenza A strains, their relative rates of isolation in different age groups, and detection of antigenic variants.

Influenza A (H3N2) viruses were isolated from outbreaks and epidemics of disease during the period December 1977 to March 1978. For the last two months of this period, H1N1 strains of influenza A were also responsible for epidemics. In some regions (e.g., Hawaii) co-circulation of H1N1 AND H3N2 strains occurred, whereas in other regions (e.g., Wisconsin) isolation of H3N2 strains had almost ceased prior to isolation of H1N1 strains. Few influenza B isolates were reported. Analysis of the ages of patients from whom specimens were submitted for influenza virus isolation confirmed that, whereas H3N2 strains were isolated from persons of all ages, greater than 97 per cent of H1N1 isolates in six states analyzed were recovered from patients less than 26 years old, although specimens were tested from older persons who were ill during the period of prevalence of H1N1 influenza. The majority of H3N2 isolates tested by hemagglutinin-inhibition reaction were similar to A/Texas/1/77, and the majority of H1N1 isolates were similar to A/USSR/90/77. Antigenic analysis of isolates, however, identified a small number of variants of H3N2 and H1N1 strains.

Adolescent↗
PubMed1979

Effects of cigarette smoke on elastase secretion by murine macrophages.

Mice were chronically exposed to cigarette smoke for various time periods up to 4 weeks. As a consequence of the exposure, there was an increase in the number of alveolar macrophages obtained from the lungs of these mice. Light microscopic examination of cultured cells revealed increased numbers of highly pleomorphic cells filled with pigmented residues of cigarette smoke. These cells were more mitotically active, with a five fold increase in the number of alveolar colony-forming cells compared to the controls. When macrophages derived from mice exposed to cigarette smoke were cultured at high density in the absence of serum, they secreted significantly greater amounts of elastase than did the same number of control macrophages. At concentrations as low as 0.50 micrograms/ml, cycloheximide reversibly inhibited elastase secretion from both the control and experimental cultures. The effects of cigarette smoke inhalation on elastase secretion by alveolar macrophages do not appear to be a direct effect of cigarette smoke on these cells. Exposure of normal mouse macrophages in vitro to pulses of aqueous extracts of cigarette smoke, while significantly increasing secretion of elastase by peritoneal exudative macrophages, did not augment that of resident or exudative alveolar macrophages. These results suggest that the increased elastase secretion observed with the use of cultured macrophages derived from mice exposed to cigarette smoke is the result of either indirect activation of resident macrophages or the recruitment of a highly activated exudative population into the lungs of the exposed animals.

Animals↗
PubMed1979

Lung injury induced by leukocytic proteases.

Human polymorphonuclear neutrophilic leukocytes (PMNs) contain large amounts of neutral proteases that can degrade elastin, collagen, proteoglycan, and basement membrane. The instillation of one of the purified enzymes (elastase) into dog lungs in vivo causes degradation of elastic fibers and other alveolar septal components and results in anatomic changes similar to those of human pulmonary emphysema. Cigarette smoking is a major risk factor associated with pulmonary emphysema in man. One mechanism for this association may be interference with the regulation of PMN elastase activity by alveolar antiproteases. This possibility is supported by the observation that the oxidizing activity of tobacco smoke inactivates alpha 1-proteinase inhibitor in vitro. Macrophages also secrete an elastolytic protease, albeit at low levels. The short-term exposure of cultured mouse macrophages to cigarette smoke augments the rate of elastase secretion by these cells. Mouse macrophage elastase is not inhibited by alpha 1-proteinase inhibitor or alpha 2-macroglobulin. This unusual property of macrophage elastase may facilitate its attack upon elastin over prolonged intervals despite very low levels of macrophage elastase production. A unified hypothesis of lung injury in pulmonary emphysema is presented, involving both PMN and macrophage elastases and the actions of cigarette smoke. (Am J Pathol 97:111--136, 1979).

Animals↗
PubMed1979

Prlonged bubble production by transient isobaric counter-equilibration of helium against nitrogen.

The production of systemic gas bubbles by isobaric counter-equilibration of helium against 5 atmospheres saturated nitrox (0.3 ATA O2 in both mixes) in awake goats was demonstrated. Sixteen animal exposures (8 dives, 2 animals per dive) to a sudden isobaric gas switch from saturation on N2 to He were conducted; 8 saturations occurred at 132 fsw and 8 at 198 fsw. Central venous bubbles were detected acoustically by means of a Doppler ultrasonic cuff surgically implanted around the inferior vena cava of each animal. Bubbles occurred from 20 to 60 min after the switch in both the 132 fsw and 198 fsw exposures, but were not always present in the 132 fsw exposure, and did not persist for as long. Bubbles or other Doppler events were often detected for the entire isobaric period-12 h-following the gas switch in the 198 fsw exposures. Decompressions were conducted according to the USN saturation tables and were uneventful, with only occasional bubbles. Supersaturation ratios calculated to have occurred for a considerable period after the gas switch were approximately 1.15 (tissue gas tension pi, divided by ambient hydrostatic pressure, P) with maxima at 1.26 for the faster tissues. These values are limiting ones in USN decompression only for the slower tissues. In general, therefore, these results argue for reducing the permissible ascent criteria for the faster tissues-assuming bubbles are to be avoided-and allowing more time at stops for non-saturation decompression. Gas switches from a more soluble to a less soluble and/or more rapidly diffusing gas should therefore be avoided until physiological limits are well worked out.

Animals↗
PubMed1978

Plasma clearance of glycoproteins with terminal mannose and N-acetylglucosamine by liver non-parenchymal cells. Studies with beta-glucuronidase, N-acetyl-beta-D-glucosaminidase, ribonuclease B and agalacto-orosomucoid.

Glycoproteins having mannose and/or N-acetylglucosamine in the terminal non-reducing position [Stockert, Morell & Scheinberg (1976) Biochem. Biophys. Res. Commun. 68, 988--993], and various lysosomal enzymes [Stahl, Schlesinger, Rodman & Doebber (1976) Nature (London) 264, 86--8] are rapidly cleared from plasma by the liver after intravenous administration. A liver cell-separation technique was used to determine the cellular localization of 125I-labelled beta-glucuronidase, ribonuclease B, agalacto-orosomucoid and asialo-orosomucoid. On a specific readioactivity basis, all ligands except 125I-labelled asialo-orosomucoid were enriched in the non-parenchymal cell fraction. Isolated cells, fixed and stained for beta-glucuronidase or N-acetyl-beta-D-glucosaminidase activity after intravenous injection of the enzymes, showed enrichment in the non-parenchymal cell fraction (probably Kupffer cells). After uptake by the non-parenchymal cells, liver lysosomal beta-glucuronidase and N-acetyl-beta-D-glucosaminidase showed degradation half-times of 2.2 and 0.4 days respectively.

Acetylglucosamine↗
PubMed1978

Infection of mouse liver by human adenovirus type 5.

CBA mice, inoculated intravenously with large doses of adenovirus type 5, showed raised levels of serum aspartate aminotransferase (SAAT; EC 2.6.I.I) and died within a few days from histologically demonstrable hepatic necrosis. After inoculation of I LD50, virus was rapidly taken up by the tissues where infectivity then declined greatly. Organ titres then increased about 100-fold by 48 h p.i. but, in the liver, which showed intranuclear inclusion bodies, and by electron microscopy, scattered intranuclear and intracytoplasmic adenovirions, the increase was 10000- to 100000-fold. P antigen was detected by single radial diffusion in liver extracts, and by immunofluorescence in 80% of liver cells at 36 h p.i. Hexon, penton base and fibre antigens appeared later and in fewer cells. The maximum amount of hexon, of demonstrable type 5 specificity, was shown by radioimmunoassay to be equivalent to up to 5 x 1011 whole adenovirions/g liver. It is concluded that human adenovirus type 5 undergoes an abortive but lytic infection in most liver cells but that replication may proceed to completion in a few.

Adenoviridae Infections↗
PubMed1978

Role of cardiac output in the pressor responses to graded muscle ischemia in man.

Ten men repeatedly performed leg exercise (100-150 W) for 7 min with 30-min recovery periods interspersed. Both legs were made ischemic by total occlusion (OCCL), first for 3 min immediately after exercise and second for 30 s before exercise ended and 3 min into recovery. In addition legs were occluded for 3 min at rest (seated). OCCL at rest increased mean arterial pressure (MAP) by 9 Torr but did not affect cardiac output (CO) or heart rate (HR). OCCL at the end of exercise significantly raised MAP and HR above control values during 3-min recovery but CO was unaffected. OCCL 30 s before the end of exercise further increased MAP and HR significantly during recovery; MAP, CO, and HR were significantly increased above control values (CO by 2.1 1-min-1) during the 3rd min of recovery. We conclude that a strong reflex from ischemic legs maintains normal or elevated CO during leg OCCL. Thus CO was too high relative to total vascular conductance so that MAP was elevated.

Blood Pressure↗
PubMed1978

Indigenous labor supply, sustenance organization, and population redistribution in nonmetropolitan America: an extension of the ecological theory of migration.

The ecological theory of migration asserts that change in sustenance organization, to the extent that it produces changes in the opportunities for living, necessitates a change in population size. Migration may thus be viewed as a demographic response to the populations's need to reestablish a balance between its size and sustenance organization, thus attaining its best possible living standard. However, the levels of net in- or out-migration needed to restore the balance should be affected by the degree of positive or negative growth of the indigenous labor force population. We thus test the hypothesis that changes in opportunities for living will be balanced by net changes in the number of persons in the labor force, where this is a function of both indigenous labor supply and net migration.

Ecology↗