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1.  Self-monitoring of oral anticoagulation: does it work outside trial conditions? 
Journal of Clinical Pathology  2009;62(2):168-171.
Patient self-monitoring (PSM) of oral anticoagulation therapy (OAT) can improve anticoagulant control, but poor uptake and high dropout rates have prompted suggestions that PSM is suitable for only a minority of patients in the UK.
To determine whether PSM could be a viable alternative to regular hospital anticoagulant clinic attendance, if offered from the start of treatment.
318 consecutive patients referred, for the first time, to an anticoagulation clinic were assessed for eligibility using established criteria. Patients electing for PSM attended training and, following successful assessment, performed a capillary blood INR every two weeks or more frequently if directed to do so by the anticoagulation clinic. Primary outcome measures were uptake of PSM and the percentage time in target therapeutic INR range (TIR) compared to patients electing for routine clinic care.
Of 318 patients referred for OAT, 188 were eligible for PSM. 84 (26%) elected to self-monitor, of whom 72 (23%) remained self-monitoring or had completed their course of treatment at the end of the audit. Self-monitoring patients had significantly better anticoagulant control than those receiving routine hospital anticoagulation clinic care (TIR 71% vs 60%, p = 0.003) and significantly less time outside critical limits, ie, INR <1.5 or >5.0 (0.45% vs 2.04%, p = 0.008).
Patients offered PSM from the start of treatment show increased uptake compared to previous UK studies and a level of oral anticoagulation control comparable to that reported in previous clinical trials.
PMCID: PMC2629005  PMID: 19181634
2.  GABA immunoreactivity and 3H-GABA uptake in mucosal epithelial cells of the rat stomach. 
Gut  1988;29(11):1549-1556.
GABA, best known as a neurotransmitter in the central nervous system, is also present in various peripheral tissues including the gastrointestinal tract, where there is strong evidence that GABA acts as a transmitter in some intrinsic myenteric neurones. Several studies indicate that the gastric mucosa is one of the sites of action of GABA in the gut. Highly specific anti-GABA antibodies have been used to detect endogenous GABA in the mucosa of the rat gastrointestinal tract, and 3H-GABA uptake followed by autoradiography has been used to localise cells with uptake sites for exogenous GABA. It was found that although GABA immunoreactive nerve fibres are essentially absent from this site, some mucosal cells are strongly GABA-immunoreactive. These cells are common in the pyloric stomach and upper part of the small intestine. The autoradiographic experiments provide evidence that these cells also possess high-affinity GABA uptake sites. These observations raise the possibility that in the gastrointestinal tract GABA acts as a gut hormone in a subpopulation of mucosal endocrine cells, in addition to its role as an enteric neurotransmitter.
PMCID: PMC1433825  PMID: 3209112
Pyrogenic tolerance following 7 daily intravenous injections of 2.0 µg/kg E. coli endotoxin in albino rabbits was associated with significant increases in RES phagocytic activity as measured with colloidal carbon. Nevertheless, 4 hours after RES blockade with thorotrast (3 ml/kg), the tolerant rabbits exhibited significantly lower fever indices following intravenous endotoxin challenge than did non-tolerant control animals despite comparably depressed capacities to clear carbon from the blood. Moreover, plasma from rabbits tolerant to endotoxin induced significant tolerance in normal rabbits prepared by thorotrast blockade without enhancing the depressed carbon clearance. This passive protection extended to heterologous endotoxins. Analysis of the data indicates that RES blockade does not abolish tolerance; rather blockade resets the reactivity to endotoxin in the normal and tolerant animal, rendering both exquisitely reactive, but permitting retention of the major portion of tolerance. Apparently the tolerant animal possesses a dual endotoxin defense system. One system is abolished by thorotrast; the other is in part humoral, accounts for the greater portion of tolerance, and is thorotrast-resistant. The nature of the humoral component is not defined but is consistent with that of an opsonin with high endotoxin specificity.
PMCID: PMC2137619  PMID: 13950296

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