'Copying letters to patients is coming to a clinic near you'

Essex, Charles

doi:10.1136/bmj.326.7402.1330

Cited by 11 publications

(6 citation statements)

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“…Clinicians in cardiology (25), respiratory medicine (25), rheumatology (2,26), oncology (1,27) and paediatrics (28) have documented their practice of copying clinical correspondence to patients. The findings have been relatively homogenous: patient participation has been high (4,26–27) (range: 76–90%) and few patients (3%) indicated disapproval (25).…”

Section: Experience In Medical and Surgical Specialtiesmentioning

confidence: 99%

Does copying clinical or sharing correspondence to patients result in better care?

Minhas

2007

International Journal of Clinical Practice

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Section: Experience In Medical and Surgical Specialtiesmentioning

confidence: 99%

Does copying clinical or sharing correspondence to patients result in better care?

Minhas

2007

International Journal of Clinical Practice

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“…EDITOR–Chantler and Johnson proposed action research on the proposal to send patients copies of clinical correspondence, and Essex discussed the issue of copying letters to patients in the patient issue 1 2…”

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confidence: 99%

Copying letters to patients: Most patients want copies of letters from outpatient clinics and find them useful

O’Driscoll

2003

BMJ

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“…Some research studies have shown that heat-labile toxin (LT) secreted by Enterotoxigenic Escherichia coli (ETEC) and Vibrio cholerae , as well as cholera enterotoxin (CT) secreted by Vibrio cholerae , stimulate adenylate cyclase, resulting in an increase in the cAMP level and the activation of cAMP-dependent protein kinase A (PKA), ultimately leading to the phosphorylation of CFTR channels (Sears and Kaper, 1996; Vaandrager et al, 1997; Hug et al, 2003). ETEC also secretes two subtypes of heat-stable toxins (STs), namely, STa and STb (Rasheed et al, 1990; Arriaga et al, 1995). STa activates guanylate cyclase C (GC-C), which leads to cGMP accumulation and the phosphorylation of CFTR channels (Crane and Oh, 1997).…”

Section: Discussionmentioning

confidence: 99%

Plumbagin Prevents Secretory Diarrhea by Inhibiting CaCC and CFTR Channel Activities

Zhu

Yang

et al. 2019

Front. Pharmacol.

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Secretory diarrhea, which primarily originates through intestinal pathogens and viruses, is a health burden in many regions worldwide. Enterocyte Cl− channels, as the final step in enterotoxin-induced fluid secretion, constitute an attractive class of targets for diarrhea therapy. Chloride channel inhibitors have become a new class of candidates for antisecretion and anti-intestinal motility agents. In the present study, we identified plumbagin as a transmembrane protein 16A (TMEM16A) inhibitor in a cell-based fluorescence-quenching assay, and the IC50 value was ∼12.46 µM. Short-circuit current measurements showed that plumbagin reversibly inhibited the Eact-induced Cl− current on the apical side of TMEM16A-transfected Fischer rat thyroid (FRT) cells with no significant effect on cytoplasmic Ca2+ signaling. Notably, plumbagin also inhibited the activity of intestinal epithelial calcium-activated chloride channel (CaCC) and cystic fibrosis transmembrane conductance regulator (CFTR) in both HT-29 cells and mouse colons, but had no effects on the activity of the Na+-K+ ATPase or K+ channels. In in vivo experiments, the administration of plumbagin reduced both Escherichia coli heat-stable enterotoxin (STa)- and cholera toxin (CT)-induced intestinal fluid secretion. In neonatal mouse models of CT- and rotavirus infection-induced diarrhea, 0.4 µg plumbagin inhibited secretory diarrhea by >40% and 50%, respectively, without affecting intestinal epithelial integrity or the rotaviral infection. In addition, plumbagin exerted inhibitory effects on the vasoactive intestinal peptide (VIP)-, prostaglandin E2 (PGE2)-, and 5-hydroxytryptamine (5-HT)-stimulated Cl− currents. In the evaluations of intestinal motility, plumbagin significantly delayed intestinal motility and inhibited intestinal smooth muscle contractility without an evident impact on contractive frequency. Collectively, our results indicate that plumbagin inhibits both Ca2+- and cAMP-activated Cl− channels, accounting for the mechanisms of plumbagin inhibition of chloride secretion and intestinal motility. Thus, plumbagin can be a lead compound in the treatment of CT-induced, Traveler’s, and rotaviral diarrhea, as well as other types of secretory diarrhea that result from excessive intestinal fluid secretion and increased intestinal peristalsis.

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'Copying letters to patients is coming to a clinic near you'

Abstract: Perspectives'Copying letters to patients is coming to a clinic near you'

Cited by 11 publications

References 0 publications

Does copying clinical or sharing correspondence to patients result in better care?

Does copying clinical or sharing correspondence to patients result in better care?

Copying letters to patients: Most patients want copies of letters from outpatient clinics and find them useful

Plumbagin Prevents Secretory Diarrhea by Inhibiting CaCC and CFTR Channel Activities

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