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Biomedical subjects

J Stein

Publications and source records attributed to J Stein.

At least 325 records · Page 18Linked to original sources
PubMed1990

Adherence among children and adolescents with insulin-dependent diabetes mellitus over a four-year longitudinal follow-up: II. Immediate and long-term linkages with the family milieu.

Cross-sectional and longitudinal findings drawn from a 4-year longitudinal study of an onset cohort of preadolescents and early adolescents with insulin-dependent diabetes and their families are presented. Patient and parent perceptions of the family environment near the time of diagnosis are used to examine patterns of adherence in the first year of illness as well as over the four follow-up years. We found that family conflict, cohesion, and organization were strongly associated with independently rated first-year adherence levels. The strongest predictor of longer term adherence was family conflict, as experienced by the patients. In addition, parents' and youngsters' perceptions of family cohesion predicted improved adherence as well as overall higher levels of patient adherence. The findings are discussed with respect to the clinical implications of discovering those family characteristics that can, shortly after diagnosis, predict short- and long-term adherence. In addition, we present planned investigations intended to further clarify paths from family perceptions to individual diabetes behaviors.

Adaptation, Psychological↗
PubMed1989

Down-regulation of histone H3 and H4 gene transcription in differentiated L6 myotubes.

The core histone mRNA levels in terminally differentiated L6 myotubes decrease to less than 5% of the amount present in proliferating myoblasts in parallel with the cessation of DNA synthesis (Bird, RC., Jacobs, F.A., Stein, G., Stein, J. and Sells, B.H. (1985) Biochim. Biophys. Acta 824, 209-217). The role of gene transcription in the down-shift of histone mRNA levels was assessed using a cell-free system. The level of transcription from the differentiation-independent adenovirus major late promoter was directly related to the RNA polymerase II activity of myoblast and myotube nuclear extracts. In addition, both extracts actively transcribed the histone H4 gene template containing only the 5 proximal promoter region (-210 bp). In contrast, inclusion of the distal-proximal promoter region (-410 to -210 bp) in the template resulted in a 60% decrease in transcription by the myotube extract. A similar down-shift in transcription of the histone H3 gene template (containing 900 bp 5 of the initiation site) by myotube nuclear extracts was also observed. The decrease in histone mRNA levels in myotubes may therefore be controlled in part by a transcriptional mechanism involving a negative regulatory factor.

Animals↗
PubMed1989

Origin of leukemic relapse after bone marrow transplantation: comparison of cytogenetic and molecular analyses.

Leukemic relapse following bone marrow transplant (BMT) is generally due to the recurrence in recipient cells, but may rarely occur as a result of donor cell transformation. Donor cell relapse is generally identified using cytogenetic markers such as the sex chromosomes. Recently, molecular techniques have been used to identify the origin of bone marrow cells by their DNA restriction fragment length polymorphisms. We describe the case of a male pediatric patient who had a leukemic relapse 30 months following BMT from his sister. Both cytogenetic and molecular techniques were used to identify the origin of the leukemic relapse. Cytogenetic analyses indicated the absence of the Y chromosome and the presence of a donor cell type 9qh polymorphism, suggesting a donor cell relapse. Molecular analyses also indicated the absence of the Y chromosome but demonstrated the recurrence of recipient DNA markers from three other chromosomes, suggesting a recipient cell relapse. While the leukemic cell lineage cannot be definitively assigned in this case, our results suggest that caution must be exercised when assigning leukemic cell lineage following post-BMT relapse.

Bone Marrow↗
PubMed1989

In vivo protein binding sites and nuclease hypersensitivity in the promoter region of a cell cycle regulated human H3 histone gene.

The chromatin structure and protein-DNA interactions of a cell cycle regulated human H3 histone gene have been examined at different levels of resolution. Using traditional Southern blot analysis we have investigated the accessibility of the H3 coding region and its flanking sequences to DNase I, S1 nuclease and restriction endonuclease digestion. Using the native genomic blotting method recently developed in our laboratory, two sites of protein-DNA interaction in the proximal 240 bp of the promoter region of this H3 gene were established. Further in vivo analysis of protein-DNA binding sites in intact cells by genomic sequencing revealed, with single nucleotide resolution, the guanine contacts and footprints of the proteins bound to the promoter. The relative locations of protein-DNA interactions in this H3 gene are similar to those identified in vivo and in vitro in a cell cycle dependent human H4 histone gene. The proteins complexed with the H3 histone gene promoter can be dissociated between 0.16 and 0.28 M NaCl. The protein-DNA contacts persist throughout the cell cycle and thus may have a functional relationship with the basal level of transcription of this H3 gene that occurs during and outside of S phase.

Base Sequence↗
PubMed1989

Fine mapping of the chromatin structure of a cell cycle-regulated human H4 histone gene.

We have observed changes in the chromatin structure of a human histone gene promoter that may be functionally related to variations in transcription during the cell cycle. A detailed analysis of the chromatin structure of a cell cycle-dependent human H4 histone gene and its flanking sequences was performed using DNase I, S1 nuclease, and restriction endonucleases. This gene was previously shown to have a DNase I- and S1-sensitive site for which the boundaries varied with the cell cycle, and we have now precisely mapped these modifications. During S phase, the entire coding region of this gene and the 5'-flanking region up to approximately -600 base pairs are sensitive to both DNase I and S1, while during mitosis/G1, accessibility to these enzymes is greatly decreased in regions from -250 to -600 base pairs and downstream of +100 base pairs. DNase I- and S1-hypersensitive sites in the proximal promoter region (which contains two sites of protein-DNA interaction as well as sequence elements necessary for the correct initiation of transcription) are present throughout the cell cycle, as is an additional site sensitive to both DNase I and S1, located at -700 to -800 base pairs. Restriction enzyme analysis confirmed the general openness of the promoter region and relative insensitivity of the 3'-flanking region, while salt wash experiments indicated several discrete sites in the promoter that are candidates for regulatory interactions. The chromatin structure of the proximal promoter region of this H4 gene is different during early S phase when it is maximally transcribed, as indicated by the ability of a high salt wash to render this region inaccessible to the restriction enzyme MspI only at this time of the cell cycle.

Cell Cycle↗
PubMed1989

Specific interactions of histone H1 and a 45 kilodalton nuclear protein with a putative matrix attachment site in the distal promoter region of a cell cycle-regulated human histone gene.

Protein-DNA interactions within the promoter of a cell cycle-regulated human H4 histone gene were examined by binding of 5'-end-labeled DNA segments to Western blots of nuclear protein fractions. Specific protein interactions were observed with DNA segments located between -500 bp and -1,070 bp upstream of the ATG initiation codon and included a histone H1 binding segment flanked on both sides by binding sites for a 45 kD nuclear protein. This region of the gene contains a DNase I-sensitive site in the center (-720 to -820 bp), and sequence analysis revealed the presence of scaffold attachment sequences in the two flanking segments. Topoisomerase II consensus sequences and in vitro topoisomerase II cleavage sites were also detected in the two flanking segments. Our results suggest that the 45 kd nuclear protein may preferentially interact with these two segments of the H4 histone gene to mediate association with the nuclear matrix. The presence of negative regulatory elements in this putative matrix attachment region provides a basis for the speculation that such nuclear proteins are associated with alterations in gene-matrix interaction that are functionally related to gene expression.

Binding Sites↗
PubMed1989

Altered binding of human histone gene transcription factors during the shutdown of proliferation and onset of differentiation in HL-60 cells.

Two sites of protein-DNA interaction have been identified in vivo and in vitro in the proximal promoter regions of an H4 and an H3 human histone gene. In proliferating cells, these genes are transcribed throughout the cell cycle, and both the more distal site I and the proximal site II are occupied by promoter-binding factors. In this report we demonstrate that during the shutdown of proliferation and onset of differentiation of the human promyelocytic leukemia cell line HL-60 into cells that exhibit phenotypic properties of monocytes, histone gene expression is down-regulated at the level of transcription. In vivo occupancy of site I by promoter factors persists in the differentiated HL-60 cells, but protein-DNA interactions at site II are selectively lost. Furthermore, in vitro binding activity of the site II promoter factor HiNF-D is lost in differentiated cells, and nuclear extracts from differentiated cells do not support in vitro transcription of these histone genes. Our results suggest that the interaction of HiNF-D with proximal promoter site II sequences plays a primary role in rendering cell growth-regulated histone genes transcribable in proliferating cells. It appears that while cell-cycle control of histone gene expression is mediated by both transcription and mRNA stability, with the shutdown of proliferation and onset mRNA stability, with the shutdown of proliferation and onset of differentiation, histone gene expression is regulated at the transcriptional level.

Base Sequence↗
PubMed1989

A neuroanatomical hypothesis for panic disorder.

Anxiety disorders, the most common psychiatric conditions in the United States, have generated a great deal of research and scientific debate. Panic disorder, the best-studied anxiety disorder, is often believed to be either a biological disease or a psychological disease. The authors present a neuroanatomical model of panic disorder that attempts to reconcile these views. The model locates the three components of the disease--the acute panic attack, anticipatory anxiety, and phobic avoidance--in three specific sites of the CNS: the brainstem, limbic system, and prefrontal cortex, respectively. The authors suggest experiments to test their model.

Acute Disease↗
PubMed1989

Mania and nondominant hemisphere function.

Unlike schizophrenics, actively disturbed manic and hypomanic patients perceived intensely affective musical stimuli without configurational errors or exacerbation of symptoms. The result disagrees with the prevailing hypothesis of manic affect-related cognitive defect in nondominant hemisphere function.

Adolescent↗
PubMed1989

[Mutagenicity testing in the sperm head test/mouse and mutagenic potency of 2 disinfectants on the basis of peracetic acid and phenols, respectively].

For the improvement of the registration of data by assessment of mutagenic risk the analysis of sperm-head abnormalities have been rendered as a suitable at indirect evidence of mutagenic potency. The reproduction of the results is well. The sensitivity of the test is high. The quantitative evaluation of genotoxic effects is possible. By reason of comparatively low methodical expense the screening investigations of species mouse are suitable, before more expensive tests will be accomplished for the elucidation of the mutation type. At 35 day-long intraperitoneal application the double number of sperm head abnormalities was approximately induced through Wofasteril (dose refer to main agent peracetic acid 2.6 mg/kg bw/d) and about 1/3 through cyclophosphamide (dose 25 mg/kg bw/d). With a 50% reduction of Wofasteril dose the mutagenic threshold-concentration was too low. The phenolic disinfectant Wofasept caused only slight no significant increase of the rate of sperm-head abnormalities (doses refer to the content of compounds, for Chlorocresol 1.6 mg/kg bw/d, for Clorofen 0.7 mg/kg bw/d and for detergent 4.8 mg/kg bw/d).

Acetates↗
PubMed1988

Dyslexia.

Explore the source record for details and available documents.

Dyslexia↗
PubMed1988

Effect of photoreactivation on mutagenesis of lambda phage by ultraviolet light.

There is disagreement in the literature as to whether the major mutagenic photoproduct induced in DNA by ultraviolet light is the cyclobutane dipyrimidine dimer, the most common product, or the [6-4] photoproduct, the next most frequent. In the experiments reported here, cyclobutane dimers were removed from irradiated lambda phage DNA by enzymatic photoreactivation, a process thought to affect no other photoproduct. Photoreactivation of lambda phage in host cells and of lambda DNA in solution reduced clear plaque mutants per plaque-forming unit by two-thirds, in host cells with a constant and near-maximal expression of the SOS functions required for mutagenesis. This result is interpreted to mean that removal of cyclobutane dimers in or near the mutated gene reduces mutation induced by ultraviolet light by two-thirds; therefore, cyclobutane dimers in the phage DNA are responsible for most observed mutations. DNA sequences of mutations in photoreactivated phage showed a smaller fraction of G.C to A.T transitions and a larger fraction of A.T to G.C transitions, compared to phage that were not photoreactivated. This suggests that cyclobutane dimers at TC and CC sites are particularly mutagenic.

Bacteriophage lambda↗
PubMed1988

Inducible DNA-protein interactions of the murine kappa immunoglobulin enhancer in intact cells: comparison with in vitro interactions.

The large intron of the kappa immunoglobulin gene contains a cis-acting enhancer element, which is important in the tissue-specific expression of the gene. We have confirmed the binding activity of a sequence-specific factor present in lymphoid extracts derived from cell lines expressing, or induced to express, the kappa gene. We have extended these studies to show the binding activity is present in normal activated splenic B cells as well as lambda producing cells, and have demonstrated by DNAse footprint analysis full protection of a sequence containing the 11 bp homology to the SV-40 core enhancer. We have compared these in vitro binding studies with an analysis of protein-DNA interactions in intact murine cell lines using genomic sequencing techniques. We demonstrate significant alterations in DMS reactivity of DNA in the murine 70Z/3 cell line after it is induced to kappa expression. These alterations occur at guanine residues which are part of the the 11 bp core sequence, and are identical to those observed in cells constitutively expressing kappa. This provides direct evidence for the induced binding of the tissue specific factor to intact chromatin. In intact chromatin we also observed significant alteration in the reactivity of a guanine, 3' of the core sequence, which is part of a potential secondary DNA structure, and protection of four residues that are part of a region homologous to the heavy chain enhancer.

Animals↗
PubMed1988

Rezsö Bálint and his most celebrated case.

In 1907, Rezsö Bálint (1874-1929), a young Hungarian physician, recorded observations he had made on a patient who suffered from a remarkable constellation of symptoms--fixation of gaze, neglect of objects in the visual surround, and misreaching--following damage to the posterior parietal lobes. Although Bálint's syndrome, the name now given to these disorders of attention and visuomotor control, is well established in the neurologic literature, there remain problems of interpretation. Bálint's own attempts to understand exactly what was wrong with his patient offer a unique insight into the nature of neurologic thought at the beginning of this century.

Brain Diseases↗