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Biomedical subjects

H S Weiss

Publications and source records attributed to H S Weiss.

At least 19 recordsLinked to original sources
PubMed1992

Argon laser gonioplasty in the treatment of angle-closure glaucoma.

We used argon laser gonioplasty to treat angle-closure glaucoma unrelieved by patent iridectomy. Laser energy (mean; 30 spots, 723 mW, and 0.2 second) was applied to the peripheral iris stroma to open the anterior chamber angle. Twenty of 32 eyes were successfully treated. After a median follow-up period of 18 months, 17 of these 20 successfully treated eyes (85%) had an intraocular pressure less than or equal to 19 mm Hg, and 19 of these 20 successfully treated eyes (95%) had an intraocular pressure less than or equal to 21 mm Hg. The 20 successfully treated eyes had a median duration of angle closure of 12 days. Twelve unsuccessfully treated eyes had a median duration of angle closure of 90 days. All successfully treated eyes had more than 50% of the treated angle opened by argon laser gonioplasty and all but three successfully treated eyes had more than three clock hours opened by argon laser gonioplasty. Argon laser gonioplasty may be successful in treating angle-closure glaucoma unrelieved by iridectomy, especially in cases that are recognized and treated soon after onset.

Acute Disease↗
PubMed1992

Periodic alternating gaze deviation in infancy.

Periodic alternating gaze is a rarely reported phenomenon. We have observed two cases that are unique in their early onset at birth and infancy. Multiple congenital defects of the posterior cranial fossa were present on MRI in both cases. A prominent abnormality shared by both was absence of normal structures in the region of the inferior cerebellar vermis. Periodic alternating gaze appears to be associated with pathologic changes in the hindbrain in these and other reported cases.

Brain↗
PubMed1989

Effects of sodium valproate and oxygen on the craniofacial skeletal pattern in the CD-1 mouse embryo.

Growth retardation is a consistent finding in animal studies on the effect of sodium valproate (NaVP) in the embryo. Apart from fetal weight, the state of ossification in the embryo may be regarded as an indication of growth. The present study was to determine what effect sodium valproate at human therapeutic drug plasma levels had on the craniofacial skeletal pattern in the CD-1 mouse embryo relative to oxygen conditions, drug treatment or the interaction of the two. Two NaVP-filled Alzet osmotic minipumps were implanted subcutaneously on day 5 of gestation for continuous delivery of a total daily dosage of 850 mg/kg for 7 days. During this same time period the dams were also exposed to either normoxic (21% oxygen), hyperoxic (50% oxygen), or hypoxic (12% oxygen) controlled environments. Dams were removed from the oxygen chambers on day 12 and killed on day 18 of gestation. The fetuses were then processed for skeletal evaluation of the craniofacial region. Ossification centers were present in all but six of the skeletal elements studied. The primary ossification delay was in the tympanic bony labyrinth. In addition, there was a decrease in maxillary and mandibular length and cranial base measurements. The greatest toxic effect on the fetus for all skeletal components studied was in the NaVP/hypoxia treated group. This finding suggests that fetal skeletal maturation may be affected by a combination of intrauterine as well as external factors.

Animals↗
PubMed1988

Effects of sodium valproate and oxygen on the CD-1 mouse fetus.

This study reports the effects of valproic acid (VA) on the CD-1 mouse fetus when the drug is administered continuously via osmotic minipumps at human therapeutic drug plasma levels. Two VA-filled Alzet osmotic minipumps were implanted subcutaneously on gestation day 5 for continuous exposure of a total daily dosage of 850 mg/kg on gestation days 5-12. Dams were then exposed continuously to either normoxic (21% oxygen), hyperoxic (50% oxygen), or hypoxic (12% oxygen) controlled environments during gestation days 5-12, in order to determine if hyperoxic maternal conditions offered a protective environment for the fetus, and conversely, if hypoxia exacerbated teratogenicity. Dams were sacrificed on gestation day 18, and litter and fetal data were collected. It was determined in separate groups under normoxic conditions that the osmotic minipump system maintained VA plasma levels corresponding to human therapeutic levels. Sodium valproate was found to induce developmental toxicity in the CD-1 mouse fetus at human therapeutic drug plasma levels. Fetal weights were reduced, and the number of resorptions, deaths, and hematomas was increased. While hypoxia exacerbated the toxic effect on the fetus, hyperoxia failed to ameliorate the outcome.

Animals↗
PubMed1987

Carbon disulfide axonopathy. Another experimental model characterized by acceleration of neurofilament transport and distinct changes of axonal size.

The role of axonal transport in the development of structural changes of axons can be examined using experimental models. Two different compounds, 2,5-hexanedione (2,5-HD) and carbon disulfide (CS2), cause axonopathies characterized by the formation of neurofilaments (NF) containing enlargements in preterminal regions of central and peripheral axons. These axonopathies are excellent experimental models of the giant axonal neuropathies, a group of acquired and inherited human diseases of the central and peripheral nervous system. We previously reported that following administration of 2,5-HD, transport of NF is accelerated while number of NF and cross-sectional area are decreased in regions of the axon proximal to the enlargements. We proposed that acceleration of NF transport leads to a 'longitudinal' redistribution of NF which are decreased proximally and increased distally where they form the NF containing axonal enlargements. We have now carried out morphometric, transport and immunocytochemical studies in primary visual axons of rats exposed to CS2. NF-containing axonal enlargements were observed in optic tract and superior colliculus and they increased in number in a proximodistal direction. There was no detectable axonal degeneration and the cross-sectional area of axons proximal to the enlargements was decreased. Transport of NF was markedly accelerated. Immunostaining showed that all 3 NF subunits and phosphorylated epitopes of the 200-kDa NF subunit were present in the NF-containing axonal enlargements. All these findings were similar to those previously observed in the 2,5-HD axonopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Inhibitory effect of toluene on tumor promotion in mouse skin.

In the two-stage mouse model for skin tumorigenesis with phorbol-12-myristate-13-acetate (PMA) as promoter, topical application of 40 microliters of toluene 2X/week at the initiation/promotion site (the back) reduced the average number of tumors/mouse (ANT/M) to approximately one-fourth that of controls. Control procedure involved initiation of C3H mice with benzo[a]pyrene (BaP) and CD-1 mice with 7,12-dimethylbenz[a]anthracene (DMBA) followed by promotion with from 1 to 5 micrograms PMA in 40 microliters acetone 2X/week. Forty microliters of toluene 2X/week per se was a weak promoter (6-13% of control ANT/M), and produced mild skin irritation at the application site but behavior and body weights were normal. The toluene inhibition of tumorigenesis was not a direct chemical action on PMA since similar effects occurred whether toluene was the vehicle for PMA or whether it was applied up to 1 day before PMA (i.e., prepromotion). Prepromotion with acetone had no effect on tumorigenesis, substantiating its use as control vehicle and suggesting that the toluene inhibition was a specific tissue reaction. The inhibitory effect appeared to be on PMA promotion rather than on initiation since toluene and acetone produced similar numbers of tumors when used as the vehicle for BaP or DMBA in two-stage or BaP in single-stage trials. The inhibition was not permanent since tumorigenesis returned to control rates 2-3 weeks after prepromotion with toluene ceased but promotion with PMA in acetone continued. Toluene may be unique among reported promotion inhibitors in that it is a widely used commercial chemical which sometimes serves as a vehicle in cancer-screening trials. Since its metabolism is reasonably well defined, it may be of value in exploring further the process of tumor promotion.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1986

Inhibition and enhancement of skin tumors in mice by dimethyl sulfoxide depending on method of application.

The role of dimethyl sulfoxide [(DMSO) CAS: 67-68-5] in experimental tumorigenesis was investigated because of conflicting reports in the literature ranging from inhibition to no effect to enhancement. With the use of numbers of skin tumors produced on the back of the mouse following topical applications of carcinogenic agents as the variable and with acetone serving as the control solvent, the following results were obtained: When DMSO was the solvent for benzo[a]pyrene (CAS: 50-32-8) in the single-stage model (C3H mice), tumor numbers doubled. When DMSO was the solvent for 7,12-dimethylbenz[a]anthracene (CAS: 57-97-6) serving as initiator in the two-stage model (CD-1 mice), tumor numbers were unaffected. In the two-stage model, when DMSO was the solvent for the potent promoter phorbol-12-myristate-13-acetate [(PMA) CAS: 16561-29-8] or was applied to skin at the initiation site (the back) before PMA, tumor numbers were reduced to one-third of control. However, when DMSO was applied before PMA to the abdomen, a site remote from initiation, tumor numbers doubled. Enhancement of PMA appears to be unique. Recognition that diverse effects can occur depending on the method of application of DMSO may help to decipher the conflicting literature on its relation to tumorigenesis, could be of value in probing the mechanism of tumor promotion, and might signal further caution in its clinical use.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1979

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↗
PubMed1978

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↗
PubMed1978

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↗
PubMed1977

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↗
PubMed1976

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↗
PubMed1976

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↗
PubMed1975

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↗