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Biomedical subjects

S D Solomon

Publications and source records attributed to S D Solomon.

12 recordsLinked to original sources
PubMed1992

SDH1, the gene encoding the succinate dehydrogenase flavoprotein subunit from Saccharomyces cerevisiae.

We describe the isolation, sequence and construction of a disruption of the yeast SDH1 gene, encoding the flavoprotein subunit of succinate dehydrogenase. This is the first eukaryotic flavoprotein subunit-encoding gene to be fully sequenced. The deduced amino acid (aa) sequence is 50% identical to the Escherichia coli enzyme sequence. The yeast gene encodes an N-terminal extension of 45 aa relative to the E. coli sequence which may act as a mitochondrial targeting signal. Disruption of the gene results in the inability to respire, assayed as the inability to utilize the nonfermentable carbon source, glycerol. This is the expected phenotype for disruption of an essential component of the yeast citric acid cycle.

Amino Acid Sequence↗
PubMed1992

Efficacy of treatments for posttraumatic stress disorder. An empirical review.

OBJECTIVE--The purpose of this article is to review the empirical evidence for the efficacy of a range of treatments for posttraumatic stress disorder (PTSD). Reviewed studies focused on rape victims, combat veterans, the tragically bereaved, torture victims, accident victims, of physical assault, and child abuse victims. DATA SOURCES--Peer-reviewed journals (Psych-Info, MEDLINE), book chapters (PILOTS database), active investigators, abstracts from the 1990 and 1991 International Society for Traumatic Stress Studies. STUDY SELECTION--We identified 255 English-language reports of treatment for PTSD. We restricted our focus to randomized, clinical trials that included a systematic assessment of PTSD using DSM-III or DSM-III-R criteria (N = 11). DATA EXTRACTION--Studies were assessed according to methodological strength: random assignment to the treatment of interest, and either an alternative treatment or control group; sample selection; and inclusion of statistical tests of significance. DATA SYNTHESIS--Drug studies show a modest but clinically meaningful effect on PTSD. Stronger effects were found for behavioral techniques involving direct therapeutic exposure, particularly in terms of reducing PTSD intrusive symptoms. However, severe complications have also been reported from the use of these techniques in patients suffering from other psychiatric disorders. Studies of cognitive therapy, psychodynamic therapy, and hypnosis suggest that these approaches may also hold promise. However, further research is needed before any of these approaches can be pronounced effective as lasting treatment of PTSD. CONCLUSIONS--Further studies should specifically address combined treatment approaches, optimal treatment length and timing, effects of comorbidity, and unstudied traumatized populations.

Combined Modality Therapy↗
PubMed1991

Methotrexate in rheumatoid arthritis: effects on disease activity in a multicenter prospective study.

One hundred and twenty-three patients with rheumatoid arthritis (RA) who successfully completed a randomized trial comparing oral methotrexate (MTX) to auranofin enrolled in a longterm prospective study of oral MTX. Of the 91 patients who completed 24 months of therapy, a significant (p = 0.0001) improvement was noted compared to baseline in all clinical disease variables and the Westergren erythrocyte sedimentation rate (ESR). Marked improvement occurred in 94 (76%) and 98 (80%) of the patients in the joint pain/tenderness index and joint swelling index at the last evaluable visit (mean 26 months). Of the 77 patients with an elevated ESR at baseline, 29 (38%) patients normalized it (less than 20 mm/h) while receiving therapy (p less than 0.01). A significant reduction in prednisone dose was also seen. Adverse events occurred frequently but were generally mild in severity. Twenty-seven patients (22%) withdrew during the study. Four (3%) withdrew due to lack of efficacy, and 6 (5%) because of adverse experiences. The overall probability of continuing therapy in the study for 48 months was projected at 72%. This large prospective study supports the observation of earlier smaller studies that MTX is an effective drug in the treatment of RA.

Administration, Oral↗
PubMed1990

A molecular basis for familial hypertrophic cardiomyopathy: an alpha/beta cardiac myosin heavy chain hybrid gene.

An alpha/beta cardiac myosin heavy chain (MHC) hybrid gene is coinherited with familial hypertrophic cardiomyopathy (FHC) in one kindred. FHC is a disease of the heart muscle characterized by a thickening of the left ventricular wall with myocyte and myofibrillar disarray that is inherited as an autosomal dominant trait. We demonstrate here and in the accompanying article that the cardiac MHC genes, which encode integral myofibrillar components, are mutated in all affected individuals from two unrelated families with FHC. In one kindred, an unequal crossover event during meiosis may have produced the alpha/beta cardiac MHC hybrid gene that is present in affected individuals. We conclude that mutations in the cardiac MHC genes can cause FHC.

Amino Acid Sequence↗
PubMed1990

Familial hypertrophic cardiomyopathy is a genetically heterogeneous disease.

We demonstrate that familial hypertrophic cardiomyopathy (FHC), an autosomal dominant disorder of heart muscle, is a genetically heterogeneous disease. The locus responsible for FHC in members of one large kindred was recently mapped to chromosome 14q11-12 (FHC-1). We have characterized three additional unrelated families in which the gene for FHC segregates as an autosomal dominant trait to determine if these disease loci also map to FHC-1. All family members were clinically studied by physical examination, electrocardiogram, and two-dimensional echocardiography. Genetic studies were performed using DNA probes which are derived from loci that are closely linked to FHC-1. In one family the genetic defect maps to the previously identified FHC-1 locus. However, the loci responsible for FHC in two other families were not linked to FHC-1. We conclude that FHC can be caused by defects in at least two loci and is a genetically heterogeneous disorder.

Cardiomyopathy, Hypertrophic↗
PubMed1990

A locus for familial hypertrophic cardiomyopathy is closely linked to the cardiac myosin heavy chain genes, CRI-L436, and CRI-L329 on chromosome 14 at q11-q12.

We report that a gene responsible for familial hypertrophic cardiomyopathy (HC) is closely linked to the cardiac alpha and beta myosin heavy chain (MHC) genes on chromosome 14q11. We have recently shown that probe CRI-L436, derived from the anonymous DNA locus D14S26, detects a polymorphic restriction fragment that segregates with familial HC in affected members of a large Canadian family. Using chromosomal in situ hybridization, we have mapped CRI-L436 to chromosome 14 at q11-q12. Because the cardiac MHC genes also map to this chromosomal band, we have determined the genetic distances between the cardiac beta MHC gene, D14S26, and the familial HC locus. Data presented here show that these three loci are linked within 5 centimorgans on chromosome 14 at q11-q12. The possibility that defects in either the cardiac alpha or beta MHC genes are responsible for familial HC is discussed.

Cardiomyopathy, Hypertrophic↗