Bethesda Hospital

About: Bethesda Hospital is a healthcare organization based out in Ambur, Tamil Nadu, India. It is known for research contribution in the topics: Population & Helicobacter pylori. The organization has 386 authors who have published 472 publications receiving 15193 citations.

The use of a rating scale of attentional behaviour

Abstract: In recent years there has been increasing awareness of the limitations of conventional neuropsychological assessment in terms of predicting functional performance in everyday life. In response to the growing recognition of the need for ecological validity in rehabilitation settings, clinicians have begun to develop methods (e.g. rating scales and behaviour checklists) of assessing the impact of neuropsychological impairments on the everyday behaviour of the patient. However, there have been few attempts to investigate the validity or reliability of such scales. The aims of the present study were: (i) to design a rating scale of attentional behaviour, to be completed by therapists treating traumatically head-injured patients who were receiving a remedial intervention for their attentional deficits; (ii) to examine the scale's correlation with neuropsychological measures of attention; (iii) to assess its internal structure and intra-rater reliability; and (iv) to examine the use of the scale by rat...

Evaluation of a remedial programme for attentional deficits following closed-head injury.

Abstract: Although the frequency and implications of disorders of attention in head-injured subjects have been recognised in recent years, there have been few carefully controlled attempts to evaluate remedial interventions. The present study employed a multiple baseline across subjects design to evaluate a computer-mediated programme for the remediation of deficits in speed of information processing in 10 severely head-injured subjects, aged 17-38 years. Following a baseline period, the effectiveness of computer training alone was compared with that combined with therapist feedback and reinforcement in separate training phases, each lasting 3 weeks. The final phase involved a return to baseline conditions. Dependent measures of attention, taken across all phases, included psychometric measures of processing speed, a rating scale completed by the patient's Occupational Therapist, and a video of the patient working in therapy. Results suggested that, once spontaneous recovery and practice effect were controlled, the patients showed little response to the interventions in terms of the dependent measures used.

Effect of Helicobacter pylori eradication on chronic gastritis during omeprazole therapy.

Abstract: BACKGROUND We have previously observed that profound acid suppressive therapy in Helicobacter pylori positive patients with gastro-oesophageal reflux disease is associated with increased corpus inflammation and accelerated development of atrophic gastritis. AIM To investigate if H pylori eradication at the start of acid suppressive therapy prevents the development of these histological changes. PATIENTS/METHODS In a prospective randomised case control study, patients with reflux oesophagitis were treated with omeprazole 40 mg once daily for 12 months. H pylori positive patients were randomised to additional double blind treatment with omeprazole 20 mg, amoxicillin 1000 mg and clarithromycin 500 mg twice daily or placebo for one week. Biopsy sampling for histology, scored according to the updated Sydney classification, and culture were performed at baseline, and at three and 12 months. RESULTS In the persistently H pylori positive group (n=24), active inflammation increased in the corpus and decreased in the antrum during therapy (p=0.032 and p=0.002, respectively). In contrast, in the H pylori positive group that became H pylori negative as a result of treatment (n=33), active and chronic inflammation in both the corpus and antrum decreased (p⩽0.0001). The decrease in active and chronic inflammation in the corpus differed significantly compared with the persistently H pylori positive group (both p=0.001). For atrophy scores, no significant differences were observed between H pylori eradicated and persistently H pylori positive patients within one year of follow up. No changes were observed in the H pylori negative control group (n=26). CONCLUSIONS H pylori eradication prevents the increase in corpus gastritis associated with profound acid suppressive therapy. Longer follow up is needed to determine if H pylori eradication prevents the development of atrophic gastritis.

Genetic factors influencing pyrimidine-antagonist chemotherapy.

Abstract: Pyrimidine antagonists, for example, 5-fluorouracil (5-FU), cytarabine (ara-C) and gemcitabine (dFdC), are widely used in chemotherapy regimes for colorectal, breast, head and neck, non-small-cell lung cancer, pancreatic cancer and leukaemias. Extensive metabolism is a prerequisite for conversion of these pyrimidine prodrugs into active compounds. Interindividual variation in the activity of metabolising enzymes can affect the extent of prodrug activation and, as a result, act on the efficacy of chemotherapy treatment. Genetic factors at least partly explain interindividual variation in antitumour efficacy and toxicity of pyrimidine antagonists. In this review, proteins relevant for the efficacy and toxicity of pyrimidine antagonists will be summarised. In addition, the role of germline polymorphisms, tumour-specific somatic mutations and protein expression levels in the metabolic pathways and clinical pharmacology of these drugs are described. Germline polymorphisms of uridine monophosphate kinase (UMPK), orotate phosphoribosyl transferase (OPRT), thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and methylene tetrahydrofolate reductase (MTHFR) and gene expression levels of OPRT, UMPK, TS, DPD, uridine phosphorylase, uridine kinase, thymidine phosphorylase, thymidine kinase, deoxyuridine triphosphate nucleotide hydrolase are discussed in relation to 5-FU efficacy. Cytidine deaminase (CDD) and 5'-nucleotidase (5NT) gene polymorphisms and CDD, 5NT, deoxycytidine kinase and MRP5 gene expression levels and their potential relation to dFdC and ara-C cytotoxicity are reviewed.