Primary healthcare information needs

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Primary Care Sharing the Evidence (PRISE) Project Executive summary

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The rivermead assessment of somatosensory performance (RASP): standardization and reliability data. Clin. Rehabil. 16, 523–533. doi:10.1191/ 0269215502cr522oa

Objective: To develop a standardized, clinically relevant, quantitative assessment of somatosensory performance in patients with stroke. Design: Prospective observational study and test evaluation. Setting: Local Oxford hospitals and a regional neurological rehabilitation centre. Subjects: Stroke patients with a rst, lateralized acute stroke in hospital, and age-matched control subjects. Method: Each patient was assessed in a structured way using a new battery of formal tests of somatosensory performance. Results: A total of 100 patients and 50 controls were fully investigated. Control subjects performed at or near ceiling on all tests, but patients showed impaired performance on all tests. The Rivermead Assessment of Somatosensory Performance (RASP) showed good intra-rater and inter-rater reliability for all subtests. There were however only weak relationships between scores of sensory impairment and scores of motor impairment or mobility and dependence. Conclusions: The RASP provides a practical and reliable assessment of sensory loss, which provides the clinician with a comprehensive picture of the patient's performance and can be used to inform and monitor rehabilitation and recovery. in uence on everyday activities and rehabilitation outcome. 2-4 Patients with both sensory and motor loss show a worse prognosis than patients with motor loss only. 5 Accurate and reliable diagnostic instruments may help in establishing the effectiveness of clinical treatments

The molecular basis of spinal muscular atrophy

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A study visit to the United States July 24 - August 21, 1982

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Somatostatin Analogs Modulate AIP in Somatotroph Adenomas: The Role of the ZAC1 Pathway

CONTEXT: Somatotroph adenomas harboring aryl hydrocarbon receptor interacting protein (AIP) mutations respond less well to somatostatin analogs, suggesting that the effects of somatostatin analogs may be mediated by AIP. OBJECTIVE: The objective of the investigation was to study the involvement of AIP in the mechanism of effect of somatostatin analogs. DESIGN: In the human study, a 16-wk somatostatin analog pretreatment compared with no pretreatment. In the in vitro cell line study, the effect of somatostatin analog treatment or small interfering RNA (siRNA)/plasmid transfection were studied. SETTING: The study was conducted at a university hospital. PATIENTS: Thirty-nine sporadic and 10 familial acromegaly patients participated in the study. INTERVENTION: Interventions included preoperative lanreotide treatment and pituitary surgery. OUTCOME: For the human study, GH and IGF-I levels, AIP, and somatostatin receptor staining were measured. For the cell line, AIP and ZAC1 (zinc finger regulator of apoptosis and cell cycle arrest) expression, metabolic activity, and clone formation were measured. RESULTS: Lanreotide pretreatment reduced GH and IGF-I levels and tumor volume (all P < 0.0001). AIP immunostaining was stronger in the lanreotide-pretreated group vs. the surgery-only group (P < 0.001). After lanreotide pretreatment, the AIP score correlated to IGF-I changes in females (R = 0.68, P < 0.05). Somatostatin receptor staining was not reduced in samples with AIP mutations. In GH3 cells, 1 nm octreotide increased AIP mRNA and protein (both P < 0.01) and ZAC1 mRNA expression (P < 0.05). Overexpression of wild-type (but not mutant) AIP increased ZAC1 mRNA expression, whereas AIP siRNA knockdown reduced ZAC1 mRNA (both P < 0.05). The siRNA-mediated knockdown of AIP led to an increased metabolic activity and clonogenic ability of GH3 cells compared with cells transfected with a nontargeting control (both P < 0.001). CONCLUSION: These results suggest that AIP may play a role in the mechanism of action of somatostatin analogs via ZAC1 in sporadic somatotroph tumors and may explain their lack of effectiveness in patients with AIP mutations

Adult stem cell activity in naked mole rats for long-term tissue maintenance

The naked mole rat (NMR), Heterocephalus glaber, the longest-living rodent, provides a unique opportunity to explore how evolution has shaped adult stem cell (ASC) activity and tissue function with increasing lifespan. Using cumulative BrdU labelling and a quantitative imaging approach to track intestinal ASCs (Lgr5+) in their native in vivo state, we find an expanded pool of Lgr5+ cells in NMRs, and these cells specifically at the crypt base (Lgr5+CBC) exhibit slower division rates compared to those in short-lived mice but have a similar turnover as human LGR5+CBC cells. Instead of entering quiescence (G0), NMR Lgr5+CBC cells reduce their division rates by prolonging arrest in the G1 and/or G2 phases of the cell cycle. Moreover, we also observe a higher proportion of differentiated cells in NMRs that confer enhanced protection and function to the intestinal mucosa which is able to detect any chemical imbalance in the luminal environment efficiently, triggering a robust pro-apoptotic, anti-proliferative response within the stem/progenitor cell zone

European Guideline on IgG4-related digestive disease – UEG and SGF evidence-based recommendations

The overall objective of these guidelines is to provide evidence-based recommendations for the diagnosis and management of immunoglobulin G4 (IgG4)-related digestive disease in adults and children. IgG4-related digestive disease can be diagnosed only with a comprehensive work-up that includes histology, organ morphology at imaging, serology, search for other organ involvement, and response to glucocorticoid treatment. Indications for treatment are symptomatic patients with obstructive jaundice, abdominal pain, posterior pancreatic pain, and involvement of extra-pancreatic digestive organs, including IgG4-related cholangitis. Treatment with glucocorticoids should be weight-based and initiated at a dose of 0.6–0.8 mg/kg body weight/day orally (typical starting dose 30-40 mg/day prednisone equivalent) for 1 month to induce remission and then be tapered within two additional months. Response to initial treatment should be assessed at week 2–4 with clinical, biochemical and morphological markers. Maintenance treatment with glucocorticoids should be considered in multi-organ disease or history of relapse. If there is no change in disease activity and burden within 3 months, the diagnosis should be reconsidered. If the disease relapsed during the 3 months of treatment, immunosuppressive drugs should be added