Biomedical subjects
Publications and source records attributed to V Sharma.
Lack of a conduit of adequate length or quality poses a dilemma in the occasional patient. We report such a case in whom we applied a modified anastomotic technique using the normal right coronary artery for the proximal anastomotic site of a free right internal mammary artery graft.
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This study examined whether children who initiate physical fights are impulsive as measured by a continuous performance test. A series of 111 7-13-year-old psychiatric patients were diagnosed using DSM-III-R criteria and divided according to whether they showed a persistent pattern of initiating physical fights. Children who initiated fights were impulsive irrespective of whether ADHD was present or not, although ADHD was also associated with increased impulsivity. Oppositional-defiant disorder and conduct disorder diagnoses were not associated with impulsivity. These findings are discussed in terms of an underlying impulsive personality trait and its possible relationship to outcome in children with disruptive behavior disorders.
A total of 1070 men and women aged 65 years and over living in the community in Liverpool were interviewed using the Geriatric Mental State. Diagnoses of depression at case and subcase level were made using the GMS-AGECAT package from an initial interview and at follow-up three years later. Data relating to blood pressure at year 0 was available on 748 subjects. Men not taking anti-hypertensives or antidepressants with diastolic blood pressure greater than 85 mmHg were significantly less likely to be subcases than men with low or normal diastolic pressure. People in this group were also significantly less likely to be cases 3 years later. There were no other significant findings. These results do not support an association between low blood pressure and coincidental or future subcase- or case-level depressive illness.
Murine macrophage inflammatory protein 1 alpha (MIP-1 alpha) and its human equivalent (GOS19, LD78, or AT464) are members of the -C-C family of low-molecular-weight chemokines. Secreted from activated T cells and macrophages, bone marrow-derived MIP-1 alpha/GOS19 inhibits primitive hematopoietic stem cells and appears to be involved in the homeostatic control of stem cell proliferation. It also induces chemotaxis and inflammatory responses in mature cell types. Therefore, it is important to understand the mechanisms which control the expression of MIP-1 alpha/GOS19. Previous work has shown that in Jurkat T cells, a set of widely expressed transcription factors (the ICK-1 family) affect the GOS19 promoter. One member, ICK-1A, behaves as a strong negative regulator. In this communication, we provide evidence that the pathway of induction in the macrophage cell line U937 is different from that in Jurkat cells. Furthermore, we show that the ICK-1 binding site does not confer negative regulation in U937 cells. We provide evidence for an additional binding site, the MIP-1 alpha nuclear protein (MNP) site, which overlaps the ICK-1 site. Interaction of nuclear extracts from various cell lines and tissue with the MNP site leads to the formation of fast-migrating protein-DNA complexes with similar but distinct electrophoretic mobilities. A mutation of the MNP site which does not abrogate ICK-1 binding inactivates the GOS19.1 promoter in U937 cells and reduces its activity by fourfold in Jurkat cells. We propose that the MNP protein(s) binding at the MNP site constitutes a novel transcription factor(s) expressed in hematopoietic cells.
OBJECTIVE: To examine the occurrence of concomitant psychiatric disorders in patients with treatment-resistant unipolar and bipolar depression. METHOD: Forty-nine patients participated as subjects. Twenty-four (49%) had unipolar depression and 25 (51%) had bipolar depression using DSM-III-R criteria. Structured clinical interviews were conducted with all patients. Chart reviews and interviews with family members were also carried out. Information relating to both current and lifetime diagnoses was obtained. RESULTS: Of the entire sample, 75.5% were found to have at least one other Axis I diagnosis and 46.9% had at least two additional Axis I diagnoses. The unipolar group had significantly more current comorbid diagnoses. When type of diagnoses was examined, unipolar patients had significantly more anxiety diagnoses at the time of the index episode, and over their entire lifetime. Bipolar patients had significantly more lifetime substance abuse diagnoses. CONCLUSIONS: Axis I comorbidity appears to be differentially associated with treatment resistance in unipolar and bipolar depression.
Optical properties of the eye contribute to the reduced visibility of spatial patterns at low luminance. To study the limits of spatial vision when optical factors are minimized, we measured contrast-sensitivity functions (CSF's) for 543.5-nm laser interference fringes imaged directly on the retina. Measurements were made in the fovea at four luminance levels, ranging from 0.3 to 300 photopic trolands (Td). At each luminance the fraction of coherent light in the stimulus pattern was varied to assess the masking effects of laser speckle, which is visible as spatial noise in fields of coherent light. Compared with published CSF's obtained under natural viewing conditions, interferometric CSF's were similar in height but broader, with the range of visibility being extended to higher spatial frequencies. The masking effects of speckle were greatest at the highest luminance and were negligible at the lowest luminance. For low coherent fractions, contrast sensitivity improved over the entire luminance range at a rate consistent with a square-root law; with purely coherent light, sensitivity tended to level off at approximately 30 Td because of speckle masking. The results indicate that the optical quality of the eye reduces the spatial bandwidth of vision even at luminances near the foveal threshold. The change in interference fringe visibility with luminance is consistent with noise-limited behavior, and the masking effects of speckle noise diminish as luminance decreases.
Case histories of three bipolar II disorder patients who had periods of sustained euthymia during all their pregnancies are described. The clinical and research implications of these observations are discussed.
One hundred and seventy two strains of beta haemolytic streptococci were isolated from various clinical specimens over a period of one year. Group A was isolated in 69.70% and group C in 16.80 percent. Majority of the strains were isolated during winter season and only 21.00 percent in summer 93.30 percent strains were bacitracin sensitive and all were sensitive to penicillin. The most common T pattern among group A was found to be 5/11/12/27/44 followed by 3/13/B 3264.
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Early appearance of clinical jaundice is rare presentation in enteric fever. Although abnormal biochemical tests suggestive of hepatic involvement has already been suggested in 23-60 per cent of cases. The early hepatic changes have been attributed to generalised bacteraemia, persistence of hepatomegaly and hepatic lesion during pyrexial stage. But the typhoid hepatitis has been ignored as a clinical entity. In this report the importance of typhoid hepatitis and its clinical significance for the diagnosis of enteric fever is highlighted, particularly at places where viral hepatitis and hepatic amoebiasis are usually common and enteric fever is endemic.
Using the polymerase chain reaction, the coding sequence for peanut agglutinin (PNA) was cloned and expressed in Escherichia coli. Amplified PNA is identical to previously reported cDNA, suggesting the absence of any introns in PNA gene. Recombinant (re-) PNA forms inclusion bodies in E. coli. Production of PNA was confirmed by probing Western blots with polyclonal anti-PNA immunoglobulin G. Inclusion bodies were solubilized with 6 M guanidine-HCl and renatured by rapid dilution in the presence of metal ions. The renatured lectin was then purified by affinity chromatography. The re-lectin shows carbohydrate-binding properties similar to the natural PNA. This expression system provides a model for future mutagenesis studies of the carbohydrate-binding site and thus facilitates ongoing efforts to explore the molecular basis for the specificity of lectin-carbohydrate interaction.
IL-7 was originally reported as a cytokine produced by stromal cells which supports pre-B cell proliferation in vitro. To determine whether human B cells secrete IL-7 and express IL-7R we studied a wide panel of B cell lines (CLS). In Northern blot analysis we detected 2.4 kb IL-7 mRNA and by quantitative PCR we demonstrated IL-7 expression in 5 of 6 B CLS derived from patients with AIDS-associated Burkitt's lymphoma (AABCL), 3 of 3 CLS derived from patients with American Burkitt's lymphoma and 5 of 6 normal lymphoblastoid CLS. Only 1 of 5 African Burkitt's lymphoma CLS and 2 of 7 EBV- CLS expressed IL-7. A total of 484-bp amplicons was cloned and sequenced and found to correspond to the original IL-7 sequence. Constitutive IL-7 secretion was detected in 5 of 6 AABCL and in 6 of 7 normal lymphoblastoid CLS but in none of the 7 EBV- CLS. IL-7R expression was demonstrated in 8 of 26 CLS, none of which secreted IL-7. Our data suggest that 1) IL-7 mRNA is expressed in malignant B cell phenotypes, which correspond to a narrow window in the B cell differentiation pathway (pre-B, early B, intermediate B), as well as in normal lymphoblastoid B CLS. 2) IL-7 mRNA is expressed in both EBV+ and EBV- CLS, but only the EBV+ CLS secrete IL-7. 3) B cells activated by both EBV and HIV-1 (AABCL) secrete the greatest amount of IL-7. 4) IL-7 autocrine loops are not evident since IL-7R were detected on on CLS, which do not secrete IL-7. Our data provide the first direct evidence of IL-7 secretion by human cells and it is yet to be determined whether IL-7 is secreted by other cell types.
We previously characterized and cloned a unique human hepatic dihydrodiol dehydrogenase (DDH) that exhibits high affinity binding for bile acids (Stolz, A., Hammond, L., Lou, H., Takikawa, H., Ronk, M., and Shively, J. E. (1993) J. Biol. Chem. 268, 10448-10457). This hepatic dihydrodiol dehydrogenase demonstrates significant sequence homology with the cytosolic rat bile acid binder 3 alpha-hydroxysteroid dehydrogenase and other members of the monomeric oxidoreductase gene family. We now report the genomic organization and chromosomal localization of the human hepatic DDH in order to further define its physiological role and provide additional insight into the development of this gene family. The 15-kilobase human hepatic DDH gene was contained in an overlapping cosmid and lambda genomic clones and is composed of nine exons. A major transcriptional start site was determined to be 30 base pairs upstream from the ATG initiation methionine by both primer extension and S1 nuclease mapping studies. The human hepatic DDH gene was mapped by chromosomal in situ hybridization and analysis of human-mouse somatic cell hybrids to the tip of the short arm of chromosome 10 at p14. Strict conservation of the intron-exon junctions in the human hepatic DDH and two other members of the monomeric oxidoreductase gene family, aldose reductase and mouse major vas deferens protein suggests evolution from a common ancestral gene. Human hepatic DDH mRNA was identified in both human hepatoma Hep G2 and human lung carcinoma cell line NCI-H322 by RN'ase protection; thus, these cell lines will be useful in examining the regulation of the gene.
The present study describes some unexpected receptor mediated effects of N-methylcarbamylcholine on mouse M1 muscarinic receptor gene transfected cell line (M1Y1) that were not evident from biochemical studies with mouse and rat brain tissue where N-methylcarbamylcholine exhibited only nicotinic properties. Although N-methylcarbamycholine was devoid of muscarinic properties in mouse and rat brain preparations, as determined by phosphoinositide turnover and inhibition of [3H]QNB binding, it exhibited significant muscarinic characteristics in the transfected M1Y1 cell line. At a concentration of 10(-6) M or greater, N-methylcarbamycholine caused a transient increase in intracellular Ca2+ of 50 s duration that was reversible by atropine or pirezepine. The Ca(2+)-transient was not elicited by other nicotinic agents such as nicotine and N,N-dimethylcarbamylcholine, a close analogue of N-methylcarbamylcholine, with comparable affinity for nicotinic receptors and devoid of muscarinic activity. N-Methylcarbamylcholine also stimulated phosphoinositide turnover in M1Y1 cells with an estimated EC50 value 10 times greater than that of carbachol, and the effect was blocked by atropine. Both carbachol and N-methylcarbamycholine inhibited [3H]QNB binding in a concentration-dependent manner; however, the IC50 for carbachol was over two orders of magnitude greater than that observed in mouse and rat brain membranes. In considering possible explanations for the differential characteristics of N-methylcarbamylcholine in mouse and rat brain as compared to the transfected M1Y1 cells, it was concluded that the difference may be attributable to differences in the receptor-transduction coupling efficiency and the microenvironment of the muscarinic receptors.
In a 6-week double-blind study, 220 patients with major depression (mostly outpatients) were randomly assigned to receive a fixed dose of brofaromine 150 mg daily (n = 111) or placebo (n = 109) after a 1-week single-blind placebo washout. Except for the HAM-D sleep items, brofaromine was superior to placebo on measures of depression as determined by the four methods of assessing drug efficacy: (1) psychiatric symptom rating (HAM-D 17-item less the three sleep items); (2) self-rating scale (Beck Depression Inventory); (3) Clinical Global Assessment of Efficacy; and (4) drop-out rate due to lack of efficacy. Most commonly reported adverse events with brofaromine were: headache, nausea, dizziness and sleep disturbance. Brofaromine was found to be an effective antidepressant, superior to placebo with a good tolerability profile.