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Biomedical subjects

H S Weiss

Publications and source records attributed to H S Weiss.

At least 37 records · Page 2Linked to original sources

Effect of temperature on benzo[a]pyrene-induced hyperplastic and neoplastic skin lesions in mice.

The time required for tumor development and death in inbred C3H/HeJ mice treated with 1.0 or 0.1 mg benzo(a)pyrene (BP) twice weekly was shortest in mice kept in a cool environment (CE), intermediate in mice kept in a normal temperature environment (NE), and longest in mice kept in a warm environment (WE). Incidence of tumors (predominantly squamous carcinomas) and mortality was 100% by 36 weeks in all environments in the high-dose group. In the low-dose group, by 36 weeks tumor incidence was least in the WE compared with that in the NE and CE. Squamous carcinomas predominated in the NE and CE, but the incidence of fibromas and epithelial hyperplasias exceeded that of squamous carcinomas in the WE. Cutaneous epithelial hyperplasia, considered a preneoplastic change, was evaluated by light and electron microscopy at weekly intervals for 70 days. Increased epidermal thickness was induced by the toluene (T) vehicle alone, was significantly enhanced by BP treatment, and was more severe in mice in the CE and NE than in the WE. Although epithelial hyperplasia induced by BP was interpreted as a preneoplastic lesion, no ultrastructural differences were detected between T- and BP-treated mice in any environment. Results indicated that WE diminished the preneoplastic proliferative response of skin to BP and subsequently delayed the onset of squamous carcinomas induced by high doses of BP and reduced the incidence of squamous carcinomas at low doses of BP.

Animals↗

The interaction of topically applied toluene and ambient temperature on O2 uptake of tissue homogenates.

These studies examined the role of toluene in temperature-cancer experiments where it was used as a solvent for benzo(a)pyrene (BaP). Toluene (0.08 ml/wk topically) and ambient temperature (cool Ta = 16 degrees C, normal Ta = 23 degrees C and warm Ta = 32 degrees C) interacted to affect O2 uptake of tissue homogenates. After 3.5 weeks of acclimation and 2 weeks of toluene (0.16 ml total), O2 uptake of muscle homogenates was elevated 32% for all Ta's; O2 uptake of skin homogenates was elevated 139% for all Ta's; however, O2 uptake of liver homogenates was elevated 665% in cool Ta, elevated 36% in normal Ta but depressed 50% in warm Ta. The pattern of liver homogenate O2 uptake of C greater than N greater than W is similar to that for tumorigenesis when BaP is dissolved in the toluene, although toluene alone is nontumorigenic. Common cellular mechanisms may be involved in the metabolism of toluene, the activation of BaP and in thermogenic acclimation.

Administration, Topical↗

Lecithin changes in murine Mycoplasma pulmonis respiratory infection.

We examined the lipid content of bronchoalveolar (BA) washes from both mice and rats infected with Mycoplasma pulmonis, an etiological agent of murine pneumonia. During a 30-day period after intranasal inoculation, the total lipid content from infected and control rats (in milligrams per animal) remained relatively equal and unchanged. The saturated, unsaturated, and total lecithin contents in infected rats (in milligrams per animal) all increased. The maximum lecithin values were detected at 7 to 10 days after infection; later, the levels fell to control values. There was essentially no change in any lecithin value from uninfected animals. Although in BA washes from infected animals the mass of disaturated lecithins increased, the percentage of this fraction in the total lecithin pool decreased. The fatty acids of the lecithins from BA washes of infected mice had significantly less palmitic and significantly more oleic and linoleic acids than the lecithins isolated from the BA washes of control animals. Both the relative decrease in the mass of disaturated lecithins in the BA washes and the increase in the percentage of esterified unsaturated fatty acids in the lecithins may be directly related to the reduced lung function reported to occur during the course of murine M. pulmonis pneumonia.

Animals↗

Role of shell diffusion area in incubating eggs at simulated high altitude.

Embryonic development is inhibited when eggs are incubated at 9,100 m (0.3 atm) despite a normoxic environment. The problem apparently relates to respiratory gas exchange occurring by diffusion through gas-filled pores in the shell. Gaseous flux is therefore inversely proportional to ambient pressure and is affected by the physical characteristics of the ambient gas (Chapman-Enskog equation). Excess loss of H2O and CO2 occurs in eggs incubating at altitude and could be detrimental. Such increased loss should be correctable by decreasing diffusion area. This was tested by progressively increasing coverage of the shell with paraffin and incubating at simulated 0.3 ATA (225 Torr) in 100% O2. Uncoated eggs failed to hatch, but numbers of chicks increased with increased coverage. Maximum hatch was an extrapolated 90% of controls at 69% shell coverage. With further coverage, hatch size decreased. Egg weight loss, and estimate of H2O diffusion, was around three times controls in uncoated eggs but decreased linearly with paraffin coverage, reaching near normal at maximum hatch. Reduction of diffusion area to 0.3 normal at maximum hatch generally balanced the increased flux predicted for 0.3 ATA.

Adaptation, Physiological↗

Oxygen uptake and lung function in mice infected with Streptococcus pneumoniae, influenza virus, or Mycoplasma pulmonis.

Model systems of respiratory infection in mice were established with Streptococcus pneumoniae, influenza virus, and Mycoplasma pulmonis. The LT50 for S. pneumoniae was 2 1/2 days, for lethal influenza 6 days, and for M. pulmonis 5 days. Morbidity in sublethal influenza infections reached a peak during days 5 to 10, with recovery indicated by the third week. The course of each pulmonary infection was followed by use of the animal's maximal ability to consume oxygen (VO2max by determining the weight, compliance, and stability of the excised lung, and in some cases by following O2 consumption of minced tissue. Depression of VO2max began early in each infection; reductions ranged from 9% at the peak of sublethal influenza infection to 50% 12 to 48 hr before the LT50 of fatal infections. The depressions were not relieved by 100% O2. The noninvasive VO2max test, evoked by cold air, was simple, rapid, and reproducible and appeared to serve as a quantitative measure of over-all function during infection. Each type of infection caused an increase in lung weight, with the largest noted during fatal Mycoplasma illness and lethal influenza. The effects on lungs by influenza and M. pulmonis infections were similar but could be differentiated from those with S. pneumoniae. With sublethal influenza, CL was reduced 30% between days 5 to 10, with recovery by the third week. Ctis was not affected. M. pulmonis infections and lethal influenza caused depressions in CL of over 60% by day 4 but only a 30% decrease in Ctis. The data suggest that the decreased compliance in influenza and M. pulmonis infections was due primarily to increased surface tension. In contrast, S. pneumoniae did not affect compliance.

Animals↗

Alterations of fast axoplasmic transport in experimental methyl n-butyl ketone neuropathy.

Methyl n-butyl ketone (MBK) is known to produce a giant axonal neuropathy in man and experimental animals characterized pathologically by a gradual increase in the number of neurofilaments which become associated with focal areas of axonal swelling and thinning of the myelin sheath. Fast axoplasmic transport was studied in rats exposed to MBK. In 10 severely paralyzed rats exposed to MBK there was a significant impediment of fast axoplasmic transport following dorsal root ganglion injections (x +/- S.D. = 283.2 +/- 20.34 mm/day) compared to normal controls (417.6 +/- 23.78 mm/day). In rats undergoing injections into the ventral horn of the spinal cord there was a gradual impairment of the mean down flow rate for transport of [3H]leucine which correlated with the severity of the MBK induced neuropathy. Quantitative morphological determinations showed that the total number of neurotubules per unit cross-sectional myelin area and the number of neurotubules associated with mitochondria in swollen axons was unchanged from normal. The total number of mitochondria in randomly sampled axons varied significantly from controls but the absolute number of mitochondria associated with neurotubules was unchanged from normal. The results of these studies suggest that the impediment of fast axoplasmic transport may be related to the increased neurofilaments producing focal areas of axonal blockage.

Animals↗

Peripheral nerve changes induced by methyl n-butyl ketone and potentiation by methyl ethyl ketone.

A study of the sequential morphological changes in the peripheral nerve induced by experimental inhalation exposure of methyl n-butyl ketone (MBK) revealed that the earliest change was an increase in the number of neurofilaments in the large myelinated nerve fibers. This change occurred prior to axonal swelling or myelin thinning. As the duration of exposure lengthened the number of neurofilaments gradually increased and ultimately produced axonal swelling with secondary thinning of the myelin sheath. This appears to be the pathogenesis of the "giant axonal" neuropathy. Another change observed early in this neuropathy was the presence of inpouchings of the myelin sheath, which also increased in number in parallel to the duration of exposure. A careful study of the sequential changes in the entire motor unit did not show a predilection for early morphological changes at the axon terminal. Abnormalities at the neuromuscular junction occurred only after a full spectrum of changes were seen in the main nerve trunk, nerve roots and intramuscular nerves. An important observation was the marked potentiation of peripheral neurotoxicity observed when animals were exposed to MBK in combination with methyl ethyl ketone (MEK) at a ratio of 1:5, MBK:MEK. The latter solvent showed no neurotoxic effect alone. This might help explain a recent outbreak of a polyneuropathy affecting many workers. One further observation was that the sural nerve of a patient with prolonged exposure to MBK showed changes similar to those induced experimentally.

Adult↗

Increased lung compliance in mice exposed to sulfur dioxide.

Mice exposed 6-9 days to 40 ppm. SO2 lost 21% of body weight, but static lung compliance increased 37% (P less than or equal to 0.01). Slopes of saline volume-pressure curves increased 8% (non-sig) pointing to a decrease in surface tension rather than tissue elasticity. Alveolar stability, lung weight and lung wet/dry ratio decreased 2 to 6%, whereas trapped gas in-increased 17%, but none were statistically significant.

Animals↗

Surface-active agent in Eustachian Tube Function.

Using 15 fresh guinea pig temporal bones, Eustachian tubal function was tested repeatedly before and after saline washing to demonstrate the effect of surface-active agent. Although tubal opening pressures for the 15 ears varied considerably, in each ear tested, a higher pressure was required to open the Eustachian tube after saline washing (P less than .001). A significant statistical difference in Eustachian tube opening pressure was also found between consecutive trials before washing the Eustachian tube with saline (P less than .001). This phenomenon disappeared after saline washing. It is possible that these phenomena occurred as a result of surface-active agent (surfactant) functioning in the Eustachian tube.

Air Pressure↗

Pituitary-thyroid function of rats in hypobaric oxygen-inert gas environments.

Rats (200-260 g) were exposed in sealed, recycling chambers continuously for 2-30 days to gas mixtures designed to maintain the same alveolar PO2 in the presence or absence of inert gas. Mixtures with inert gas (N2, He, or Ne) were at ground level; those without inert gas (100 percent O2) were in an altitude chamber. The O2 categories were: I-100 percent O2 at 747 torr; II-74 percent O2 + 26 percent inert and 566 torr 100 percent O2; III-47 percent O2 + 53 percent inert and 381 torr 100 percent O2; IV-21 percent O2 + 79 percent inert and 197 torr 100 percent O2. One of the two room-air controls was "restricted-fed" to the level of the lowest intake group. Measurements included body, pituitary, and thyroid weight, food and water intake, plasma volume and hematocrit, pituitary and plasma TSH, and plasma PBI. Severe depression in all variables and over 50 percent mortality was seen in I by day 4. All variables were depressed in II, but there was no mortality to 20 days. Pituitary-thyroid function appeared to be particularly sensitive to depression by hyperoxia, with plasma TSH levels reduced between 42 and 60 percent in II and III. No effect was attributable to the inert gas, whether it was N2, He, or Ne, nor was any specific effect traceable to the presence or absence of inert gas.

Animals↗

Improved hatch rate in helium-oxygen by reducing shell diffusion area.

For eggs incubating in a He atmosphere (79% He/21% O2), covering approximately 50% of the shell with melted paraffin improves hatch rate to control values (from 20% to 74%) and decreases egg weight loss to control values (from 17% to 9%). In air (79% N2/21% O2) the same paraffin treatment depresses hatch rate. The role of the inert gases in incubation appears to be an indirect one related to their modification of the rate of gaseous flux across the shell with the adverse effects of He due to excessively rapid diffusion.

Air↗

Effects of age and magnesium ions on oxygen toxicity in the neonate chicken.

White Leghorn male chicks, 2-6 days and 4 weeks old, were injected with MgCl2 (2 mM Mg/kg body weight) and exposed to 100% O2 at 75 lb/in2 (approximately 5 atm). Compared to saline-injected controls, average time to onset of convulsions was delayed 37% in the younger group with no significant difference in the protective effect during days 2-6. The delay in onset of convulsions was 66% in the 4-week-old group. The protective action of Mg++ in the chick agrees closely with that reported for the mature rat. Chicks treated with Mg++ did not appear depressed. Susceptibility to hyperbaric O2 convulsions increased uniformly between the 2nd and 6th day, with time to onset of convulsions decreasing by 1.4 min/day from the 19.3 +/- 1.01 (SE) min observed at day 2 for saline controls. Between the 6th and 28th day, susceptibility was relatively stable with time to onset decreasing by about 0.2 min/day in controls.

Animals↗