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R Tomar

Publications and source records attributed to R Tomar.

10 recordsLinked to original sources
PubMed2005

Is there a case for a specialist forensic psychiatry service for the elderly?

BACKGROUND: The number of elderly offenders in England and Wales is increasing. There is, therefore, a concern that their needs may not be met by existing forensic services. However, there is a paucity of information on elderly patients referred to existing forensic psychiatric units. METHOD: Data on patients over the age of 65 years referred to a large medium secure forensic psychiatric unit in London were collected for a 13-year period using a retrospective design. The sample was divided into those who had first offended before the age of 65 and those who had offended after the age of 65. Data was also collected on victims of the offences. RESULTS: 5477 referrals were made during the study period. Those aged over 65 years accounted for 78 (1.4%) of all referrals. These 78 referrals were for 55 patients. Forty-five of these had offended. Case notes of 42 patients from this group were screened. Sexual and violent offences accounted respectively for 20 (47%) and 15 (36%) of offences. 31% had no psychiatric disorder but organic disorders accounted for 21% of cases. Only eight (19%) required admission to the medium secure unit. Fourteen (33%) had first offended after the age of 65 while others were known to either the forensic services or criminal justice system before the age of 65. The two groups did not differ from each other. CONCLUSIONS: The elderly accounted for very few referrals to the medium secure forensic service, yet there is a high prevalence of psychiatric morbidity in both remand and sentenced elderly prisoners. Therefore, elderly offenders with psychiatric morbidity may benefit from specialist old age psychiatric forensic services, perhaps at a supraregional level.

Age Distribution↗
PubMed2000

Guidelines for clinical use of the antinuclear antibody test and tests for specific autoantibodies to nuclear antigens. American College of Pathologists.

The following guideline presents a series of recommendations based on published medical literature for use of the antinuclear antibody (ANA) test and tests for specific autoantibodies to nuclear antigens in the diagnostic evaluation, prognostic assessment, and monitoring of patients with systemic rheumatic diseases. The guideline emphasizes the need for clinical evaluation to improve the usefulness of test results in patient management. Consideration is given to appropriate use of the generic ANA test in the initial evaluation of patients with signs and symptoms of a systemic rheumatic disease, the evaluation of patients suspected of having lupus erythematosus, use in clinical situations in which the ANA test is required to establish a disease diagnosis, and identification of clinical situations in which the ANA test has little value. Sections are also devoted to recommendations aimed at improving the analytic methods used to detect and measure ANA and specific autoantibodies to nuclear antigens and to the appropriate use of tests for specific autoantibodies in several disease situations that commonly occur in patients with suspected or documented systemic rheumatic diseases. Emphasis is placed on the use of these tests only in situations in which the test results can be expected to provide information necessary for clinical decision making. Those tests of limited medical usefulness and situations in which test results are likely to be misleading are also identified.

Antibodies, Antinuclear↗
PubMed1994

Chromosomal loss and breakage in mouse bone marrow and spleen cells exposed to benzene in vivo.

Benzene is a widely recognized human and animal carcinogen. In spite of considerable research, relatively little is known about the genotoxic events that accompany benzene exposure in vivo. To gain insights into the mechanisms underlying the genotoxic effects of benzene, we have characterized the origin of the micronuclei that are formed in bone marrow erythrocytes and splenic lymphocytes of benzene-treated mice using two molecular cytogenetic approaches: (a) fluorescence in situ hybridization with a centromeric DNA probe; and (b) staining with the calcinosis-Raynaud's phenomenon-esophageal dismobility-sclerodactyly-telangiectasia syndrome of scleroderma (CREST) antibody, an antibody recognizing a centromeric protein. Following the p.o. administration of benzene (220 or 440 mg/kg) to male CD-1 mice, a significant increase in micronuclei was observed in the bone marrow erythrocytes. In situ hybridization with a centromeric DNA probe and immunofluorescent staining with the CREST antibody indicated that the micronuclei in bone marrow erythrocytes were formed from both chromosome loss and breakage. The majority of the micronuclei originated from chromosome breakage. A dose-related increase in micronucleated cells was also observed in splenocyte cultures established from these benzene-treated animals. In contrast to the bone marrow erythrocyte results, the majority of benzene-induced micronuclei in the cytokinesis-blocked splenocytes labeled with the CREST antibody indicating that these micronuclei were the result of whole chromosome loss. These data demonstrate that both aneuploidy and chromosomal breakage are early genotoxic events induced by benzene or its metabolites in vivo and also indicate that the nature of the chromosomal alterations may vary depending on the target organ or cell type.

Aneuploidy↗
PubMed1994

Detection of hydroquinone-induced nonrandom breakage in the centromeric heterochromatin of mouse bone marrow cells using multicolor fluorescence in situ hybridization with the mouse major and minor satellite probes.

Fluorescence in situ hybridization with a mouse major satellite probe and CREST staining were used to characterize the origin of micronuclei occurring in mouse bone marrow erythrocytes following administration of the benzene metabolite hydroquinone. Hydroquinone was administered to male CD-1 mice by i.p. injection on three consecutive days and the bone marrow cells were harvested 24 h later. A pronounced difference in the results was observed using the two approaches: 63% of the micronuclei induced by hydroquinone labeled with the major satellite probe whereas only 28% labeled with the CREST antibody. To determine whether the observed difference was due to a disruption of the kinetochore or a result of breakage within centromeric heterochromatin, we developed a tandem label multicolor hybridization assay, which requires the presence of both the mouse major and minor satellite probes in a micronucleus for a classification of chromosomal loss. The minor probe targets a centromeric region physically linked to the short arm of mouse chromosomes, whereas the major probe hybridizes to the centromeric heterochromatin adjacent to the long arm. Using this approach, 29% of the micronuclei induced by hydroquinone hybridized with both the major and minor satellite probes, indicating chromosome loss; an additional 37% labeled with only the major satellite probe indicating breakage within the centromeric heterochromatin. Although the region targeted by the major satellite probe comprises only 5-10% of the mouse genome, these major-probe containing micronuclei represent 53% of the micronuclei formed as the result of chromosome breakage.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Efficient transformation of previously activated and dividing T lymphocytes by human T cell leukemia-lymphoma virus.

Modifying previously reported techniques, we attempted to increase the efficiency of human T cell leukemia-lymphoma virus (HTLV) transformation of human T lymphocytes. Lethally irradiated donor cells (DCs) were cultured with target mononuclear cells (TMCs). DCs included ten HTLV+ T cell lines with varying degrees of virus expression or seven cell lines that do not express HTLV. TMCs were prepared from 20 cord and 16 adult peripheral blood samples, including eight patients with acquired immunodeficiency syndrome (AIDS). TMCs were either added directly to the DCs or were first stimulated with phytohemagglutinin (PHA) (5 micrograms/mL) and grown in T cell growth factor (TCGF) prior to exposure to DCs. The presence of integrated HTLV proviral DNA in the transformed cells was determined by dot blot hybridization, utilizing a cloned probe to the HTLV-I genome. HTLV production by transformed TMCs was assessed for HTLV p19, reverse transcriptase, and virus particles. No transformation occurred with T cell donor lines that do not express HTLV. Low virus expressor DCs could only, with rare exception, transform preactivated TMCs. High-titer virus-producing DCs could transform activated and nonactivated cord blood cells and activated adult TMCs. Only MT-2 could routinely transform nonactivated normal adult and activated AIDS TMCs. HUT 102 B2 could transform only one activated AIDS sample, the cells of which initially expressed HTLV-like proteins and virions. Transformed cell lines contained subsets of mature T lymphocytes with variable HTLV expression. Prior activation and culture of the T lymphocytes increases the probability and rate of transformation by HTLV, allowing for biologic detection of low HTLV-producing cells and for in vitro expansion of T lymphocyte subsets from selected patients.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

The combination of insulin and metformin in treatment of non-insulin-dependent diabetes mellitus.

OBJECTIVE: To assess whether, in the treatment of non-insulin-dependent diabetes mellitus (NIDDM), (1) metformin in conjunction with insulin can safely cause a decrease in glycosylated hemoglobin (HbA1c) to 7% or less and (2) this combination therapy may result in weight loss and lower insulin dose in comparison with insulin treatment alone. METHODS: Forty patients with NIDDM being treated with insulin on their first visit to the Diabetes Center were identified by retrospective review of medical records of all patients encountered during a 1-year period. These patients were classified into groups who were receiving insulin only (group 1) or insulin + metformin (group 2) at the most recent visit. Group 2 was subdivided into those with a body mass index of either =30 kg/m 2 (group 2A) or >30 kg/m 2 (group 2B). Blood glucose, HbA1c, insulin dose, and weights were analyzed from their initial and most recent visits. RESULTS: HbA1c decreased from 10 +/- 2.7% to 7 +/- 1.1% (P<0.01) in group 1 and from 9.8 +/- 2.1% to 7.2 +/- 1.4% (P<0.01) in group 2. The magnitude of decrease in HbA1c, however, was not different between the two groups. Total insulin dose increased from 40 (33 to 50) U/day to 58 (41 to 67) U/day (P<0.05) in group 1 and from 63 (42 to 118) U/day to 67 (50 to 96) U/day in group 2 (not significantly different). The median increase in insulin dose was 8 U in group 1, whereas the median decrease was 3 U in group 2 (P<0.05). Similar decreases were noted in group 2A. The decrease in insulin dose was inversely related to the initial insulin dose per kilogram of body weight in group 2 (r = -0.5; P<0.01). Patients in group 1 had an increase in weight from 75.0 +/- 8.6 kg to 77.7 +/- 9.0 kg (P<0.01), whereas weight decreased from 100.4 +/- 24.2 kg to 98.5 +/- 22.3 kg in group 2 (P<0.05). A decrease in weight was seen even in group 2A. The increase in weight was 3 +/- 3.3 kg in group 1, whereas weight decreased by 1.9 +/- 3.9 kg in group 2 (P<0.01). CONCLUSION: Insulin + metformin is safe and is as effective as insulin alone in improving glycemic control in obese and nonobese patients with NIDDM. This combination therapy, however, lowers insulin dose and promotes weight loss, which may be of importance in decreasing the cardiovascular risk factors in these subjects.

Journal Article↗