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Biomedical subjects

B Weiss

Publications and source records attributed to B Weiss.

At least 379 records · Page 21Linked to original sources
PubMed1976

Defective interfering passages of Sindbis virus: nature of the defective virion RNA.

Defective interfering particles of Sindbis virus contain 20S RNA identical to that found in BHK cells co-infected with standard and defective virions. We have characterized these RNAs by their oligonucleotide fingerprints. Most of the oligonucleotides were identical to those found in the mRNA (26S RNA) that codes for the virion structural proteins. Three oligonucleotides found in 20S RNA were absent from the 26S RNA pattern and may represent sequences from the 5' end of the virion RNA. Previous difficulties in describing the nature of the defective virion RNA were due to the aggregated state of the RNA. Nucleocapsids obtained from standard and defective virions were essentially the same size and had about the same density, suggesting that defective particles contain more than a single molecule of 20S RNA.

Base Sequence↗
PubMed1976

EEG sleep changes as predictors in depression.

The authors conducted a study of 18 depressed patients to see whether EEG sleep measurements might provide a predictive tool for response to antidepressant medication. They found that although the sedative characteristics of amitriptyline did not differentiate good responders from poor responders until the third week of drug treatment, the good responders showed significant increases in REM latency, decreases in REM sleep time, decreases in REM sleep percent, and decreases in REM activity after only 2 nights of drug treatment.

Amitriptyline↗
PubMed1976

Studies in the behavioral toxicology of environmental contaminants.

Behavioral toxicology represents a relatively new research area in the West, and a new source of information pertinent to standard setting. Despite this abbreviated history, however, it can call on a rather advanced technology, largely provided by the rapid and extensive development of behavioral pharmacology during the past two decades. As exemplified by the U.S. contribution to the joint study of carbon disulfide, the approach derived from this background relies on the acquisition of dose--effect data with a preparation yielding stable baseline performance. The first study in this collaborative series employed pigeons trained to peck a response device consisting of a transilluminnated plastic disk. Various relationships between this response and the occasions on which it led to the delivery of food were explored in order to ascertain which behavioral variables were most sensitive to acute exposures. In addition, a central nervous system drug, whose neurochemical mode of action is believed to parallel that of carbon disulfide, was tested in the same preparations. Further research on these questions is being continued with monkeys.

Animals↗
PubMed1975

[Carcinogenesis due to mustard gas exposure in man, important sign for therapy with alkylating agents].

Sulphur-mustard and nitrogen-mustard are known to act as carcinogens in animal experiments. A similar effect in humans was demonstrated in 245 workers previously exposed occupationally to mustard gas and followed for over 20 years. There was a statistically significant increase in malignant tumours, especially bronchial carcinoma, bladder carcinoma and leukaemia. These findings underline the need for using alkylating agents of the mustard type exclusively in the treatment of malignant neoplasms. Immunosuppression with alkylating agents in the treatment of chronic inflammatory diseases associated with a long life expectancy is no longer justified.

Adult↗
PubMed1975

Alkylmercurial encephalopathy in the monkey (Saimiri sciureus and Macaca arctoides): a histopathologic and autoradiographic study.

Histopathologic and autoradiographic studies were performed on monkeys of the genera Saimiri and Macaca after acute and chronic oral exposure to several dosage regimens of methylmercuric chloride (MeHg). Neuropathologic changes were primarily cortical, although subcortical lesions also were observed. Autoradiographic localization of 203-Hg was greatest within glial cells (particularly Nissl-pump astrocytes, subependymal glia and Bergmann's glia) and mast cells. High levels of label within normal appearing large neurons (particularly those within Gasserian and dorsal root ganglia) indicate a lower susceptibility of these neurons to the toxic effects of MeHg. Blood and brain levels of mercury correlated well with the degree of neuropathologic change, but individual variations in susceptibility to intoxication also existed.

Animals↗
PubMed1975

Synthesis of threo-4,5-dihydroxy diastereomers of sphinganine;.

The threo-4,5-dihydroxy diastereomers of sphinganine were prepared by the following sequence of reactions: (a) benzoylation of sphingenine to the tribenzoyl derivative; (b) osmylation followed by resolution of the mixture of threo-4,5-dihydroxy tribenzoyl (DHTBS) diastereomers; and (c) alkaline hydrolysis to yield the threo-4,5-dihydroxysphinganines (DHS). Carbon atoms 4 and 5 of the high and low melting threo-4,5-DHTBS diastereomers and the compounds derived from them were tentatively assigned 4R, 5S and 5R configurations, respectively;

Amino Alcohols↗
PubMed1975

Mutations simultaneously affecting endonuclease II and exonuclease III in Escherichia coli.

We studied mutants of E. coli originally identified as being deficient in either endonuclease II (deoxyribonucleate oligonucleotidohydrolase, EC 3.1.4.30) or exonuclease III [deoxyribonucleate (double-stranded) 5'-nucleotidohydrolase, EC 3.1.4.27] activity. Twelve independently derived mutants were tested, including three new endonuclease II mutants. Deficiency of one enzyme was always accompanied by deficiency of the other. Furthermore, temperature-sensitivity of one activity was always accompanied by temperature-sensitivity of the other, and the enzymes were co-purified. The results suggested a physical association between exonuclease III and endonuclease II, which may be of advantage in the excision-repair of DNA. A thermolabile endonuclease II was purified from one of the new mutants, indicating that it had an altered structural gene. This mutation, and all similar ones mapped by genetic transduction, was located between the pncA and aroD genes on the E. coli chromosome. One mutant had a prolonged generation time, an increased sensitivity to the alkylating agents methyl-methanesulfonate and mitomycin C, and a decreased plating efficiency for bacteriophage lambda, but no marked sensitivity to ultraviolet or gamma-irradiation. Its enzymatic and biological abnormalities were simultaneously revertible, suggesting they were caused by a single mutation. These results suggested a role for these enzymes in normal cell growth processes and in the repair of alkylation damage.

Chromosome Mapping↗
PubMed1975

Newborn blood levels of lidocaine and mepivacaine in the first postnatal day following maternal epidural anesthesia.

Distribution and elimination of lidocaine and mepivacaine were studies in 114 subjects after obstetric epidural anesthesia, Epinephrine significantly lowered the concentrations of lidocaine in the mothers' circulations by about 33 per cent, and the concentrations of mepivacaine by about 22 per cent. It also significantly altered their concentrations in the newborns' circulations at delivery and in the first 4 hours after birth. More mepivacaine than lidocaine crossed the placenta. The mepivacaine concentration in the cord blood was 36 to 47 per cent higher, and the mean fetal to maternal ratio for mepivacaine without epinephrine was 0.64, in contrast to 0.52 for the equivalent lidocaine group. Of importance was the long persistance of either drug in the newborns' circulation. Detectable levels of lidocaine and mepivacaine were present until 8 and 24 hours after birth, respectively. Pharmacokinetic models revealed that the long-term rate of disappearance of lidocaine was approximately three times as fast as that of mepivacaine. Computed half-times averaged 3 hours for lidocaine and 9 hours for mepivacaine.

Adult↗
PubMed1975

Behavioral effects of mercury and methylmercury.

Intoxication by elemental mercury or by methylmercury is revealed primarily by changes in behavior and by neurological signs. Disorders of movement and posture have been most widely reported, both in animal experiments and in cases of human exposure. Specific sensory symptoms are also prominent in human methylmercury poisoning. Recent data indicate similar symptoms in monkeys during long-term exposure to methylmercury. Similar sensory impairment has not been described in experiments with subprimates. Variations in the profile of behavioral and neurological effects are discussed in terms of differences in species and differences between acute and long-term exposure. The latter condition poses the most difficult questions for human health, yet has been less frequently studied. Procedures are suggested that may help to revolve these problems. In particular, tests of learned behavior hold great promise toward identifying specific symptoms and toward understanding how mercury compounds affect behavior.

Air Pollutants↗
PubMed1975

Defective particles in alphavirus infections.

This article summarizes our studies with defective-interfering particles of Sindbis virus obtained by high multiplicity passaging of the virus in BHK cells. Cells infected with these defective passages accumulate a species of RNA (20S) at the expense of 26S RNA--the mRNA coding for the viral structural proteins. Although the structure of the RNA in defective particles remains undefined, our studies of replicative forms and replicative intermediates suggest that it is larger than the intracellular 20S RNA. The defective particles are unable to synthesize detectable amounts of viral structural proteins when they infect a cell in the absence of standard virus and they do not contribute to the stimulation of intracellular viral RNA synthesis. We have proposed a model for the mechanism of interference by these defective particles in which standard and defective RNAs compete for a limited amount of viral-specific replicase.

Cell Line↗
PubMed1975

Differential activation and inhibition of the multiple forms of cyclic nucleotide phosphodiesterase.

The brain as well as other mammalian tissues contains several different forms of cyclic nucleotide phosphodiesterase separable by polyacrylamide gel electrophoresis. Each tissue and each individual type of cell has its own distinctive pattern and ratio of these multiple forms of phosphodiesterase. The different forms have several distinguishing properties and characteristics, and their activities may be differentially regulated both acutely and chronically. The enzyme forms have different stabilities, kinetic properties, substrate specificities, and sensitivities to an endogenous activator and to several inhibitors of phosphodiesterase. The phosphodiesterase inhibitors studied not only inhibit the different forms of phosphodiesterase to different degrees but apparently do so by different mechanisms. Thus whereas theophylline, cyclic GMP, and low concentrations of papaverine inhibit the phosphodiesterases by competing with the substrate (cyclic AMP), trifluoperazine apparently inhibits phosphodiesterase by interfering with the phosphodiesterase activator. This confers a great deal of specificity to this drug, since only one form of phosphodiesterase is markedly activated by the activator. Chronically, a specific form of phosphodiesterase appears to be inducible. This induction is probably controlled by the intracellular cyclic AMP concentration. The phosphodiesterase activator also appears to be regulatable, the age of the animal being one of the factors controlling its activity. Finally, since different types of cells have different relative amounts of the phosphodiesterases and since these forms of the enzyme can be differentially inhibited by drugs, it may be possible to develop drugs which will selectively increase the cyclic AMP concentration in discrete cell types. Evidence that cyclic AMP is involved in certain disease states suggests further that by selectively altering the concentration of cyclic AMP in these cells, one might be able to alter the course of the disease.

Adenylyl Cyclases↗