Frequency and clinical expression of cardiac troponin I mutations in 748 consecutive families with hypertrophic cardiomyopathy.

Objectives: The aim of this study was to evaluate the potential utility of genetic diagnosis in clinical management of families with hypertrophic cardiomyopathy (HCM) caused by mutations in the gene for cardiac troponin I (TNNI3).

Background: Knowledge about the clinical disease expression of sarcomeric gene mutations in HCM has predominantly been obtained by investigations of single individuals (probands) or selected families. To establish the role of genetic diagnosis in HCM families, systematic investigations of probands and their relatives are needed.

Severe disease expression of cardiac troponin C and T mutations in patients with idiopathic dilated cardiomyopathy.

Objectives: We performed genetic investigations of cardiac troponin T (TNNT2) and troponin C (TNNC1) in 235 consecutive patients with idiopathic dilated cardiomyopathy (DCM) to evaluate prevalence of mutations and associated disease expression in affected families.

Background: Recently, mutations in sarcomeric genes have been reported in DCM. However, the prevalence, penetrance, and clinical significance of sarcomere gene mutations in large consecutive cohorts of DCM patients are poorly defined.

PlasmoDB: the Plasmodium genome resource. A database integrating experimental and computational data.

PlasmoDB (http://PlasmoDB.org) is the official database of the Plasmodium falciparum genome sequencing consortium. This resource incorporates the recently completed P.

PlasmoDB: the Plasmodium genome resource. An integrated database providing tools for accessing, analyzing and mapping expression and sequence data (both finished and unfinished).

PlasmoDB (http://PlasmoDB.org) is the official database of the Plasmodium falciparum genome sequencing consortium. This resource incorporates finished and draft genome sequence data and annotation emerging from Plasmodium sequencing projects.

Systematic investigation of physiological correlates of motion sickness induced by viewing an optokinetic rotating drum.

Purpose: This study investigated the physiological correlates of motion sickness provoked by viewing an optokinetic rotating drum.

Method: A total of 52 subjects viewed an optokinetic rotating drum for 16 min. Subjective symptoms of motion sickness (SSMS) and ratings of over-all sickness were measured during the drum rotation.

MANAGEMENT OF KALA AZAR - AN UPDATE.

Kala azar continues to be a medical problem in India and with the increase in incidence of HIV Infection it is likely that kala azar will be encountered more frequently and in its atypical forms. To aid diagnosis, several immunological tests are now available and they are more sensitive and specific than the aldehyde test. Like many other diseases today, the treatment of kala azar is hampered by drug resistance.

The beta 3-adrenoceptor agonist CL316243 prevents indomethacin-induced jejunal ulceration in the rat by reversing early villous shortening.

Jejunal villi undergo early histological shortening and vascular injury in indomethacin-induced ulcerative enteropathy in the rat. The protective effects of the beta 3-adrenoceptor agonist CL316243 on this rat model and the mechanism of action were examined using histological techniques. Groups of rats received oral indomethacin (15 mg/kg) and oral CL316243 (0, 0.

Comparison of the profiles of agonists as stimulants of the beta 3-adrenoceptor in vitro with their gastroprotective effects in the conscious rat.

1. This paper compares the activity of a range of agonists as stimulants of the beta 3-adrenoceptor in rat isolated oesophagus with their ability to afford protection against indomethacin-induced gastric damage in the conscious rat. 2.

Air pollutant stress changes the steady-state transcript levels of three photosynthesis genes.

Six-week-old tobacco plants (Nicotiana tabacum L., cv. SR-1) were fumigated with different, but defined and realistic combinations of NO(2), automobile exhaust and ozone for two days.

Transcriptional activation of plant defence genes by short-term air pollutant stress.

The expression of defence genes was monitored by RNA blot analyses in tobacco plants (Nicotiana tabacum cv. SR-1) treated with various air pollutants at realistic concentrations that prevail in urban areas. Six-week-old plants responded with an increase in the steady-state mRNA levels of phenylalanine ammonia-lyase (PAL), chalcone synthase (CHS), chitinase and beta-1,3-glucanase, when exposed to defined and subnecrotic concentrations of automobile exhaust and/or ozone over a period of 48 h.

The effect of non-steroidal anti-inflammatory drugs on the accumulation and release of interleukin-1-like activity by peritoneal macrophages from the mouse.

1. The non-steroidal anti-inflammatory drugs (NSAIDs) indomethacin, 10 and 100 microM, piroxicam, 100 microM, and sodium meclofenamate, 1 and 100 microM, potentiated the lipopolysaccharide (LPS)-stimulated release of interleukin-1 (IL-1)-like activity from mouse peritoneal macrophages. Aspirin up to 100 microM was without effect.

Neutrophil infiltration does not contribute to the ulcerogenic effects of indomethacin in the rat gastric antrum.

We have previously suggested (Trevethick et al., Gut 34, 156-160) that indomethacin-induced ulceration of the rat gastric antrum may be a neutrophil-dependent process. Accordingly, in this study we have used an anti-neutrophil serum (ANS) to investigate the effects of neutrophil depletion on this pathology.

Stimulation and release of interleukin-1 from peritoneal macrophages of the mouse.

Lipopolysaccharide (LPS) caused a concentration-dependent increase of released and cell-associated interleukin-1 (IL-1) in resident peritoneal macrophages from the mouse. LPS was about 30 times more potent at stimulating the level of cell-associated IL-1 than it was at stimulating the release of IL-1. Human recombinant tumour necrosis factor-alpha (TNF-alpha) and the calcium ionophores A23187 and ionomycin induced a concentration-dependent increase of cell-associated IL-1 but failed to cause release of IL-1 at concentrations producing maximal stimulation of cell-associated IL-1.

Leukotrienes do not contribute to the pathogenesis of indomethacin-induced ulceration of the gastric antrum in the re-fed rat.

The potential involvement of leukotrienes in the pathogenesis of indomethacin-induced ulceration of the rat gastric antrum has been studied. Pretreatment with the leukotriene biosynthesis inhibitor, MK886 (30 mg/kg p.o.