Is It Useful to Measure Efficiency Indices of a Deceased-Donor Kidney Transplant Program in One Intensive Care Unit?

BACKGROUND: Before 2010, donor detection rate and donor conversion rate at our tertiary level care institution were low. To assess the effectiveness of the implemented organizational changes, an analysis of organizational indicators with the use of the DOPKI (Improving the Knowledge and Practices in Organ Donation) project was conducted. METHODS: Three groups of DOPKI indicators were used: indicators of the potential for deceased organ donation, indicators on areas for improvement in the deceased donation process, and indicators of program effectiveness. We compared the 3-year period before instituting organizational measures with the 3-year period after the changes. RESULTS: Significant differences in almost all DOPKI indicators were found. Most importantly, the number of actual donors has increased significantly, pointing to the effectiveness of the organizational measures that we put in place in 2010. In addition, the study highlights the value of the use of DOPKI indicators in one intensive care unit to improve the transplant program on a hospital level. CONCLUSIONS: We conclude by arguing that despite the lack of a uniform national database, DOPKI indicators could still be useful for improving the quality of donor programs.

Community engagement in US biobanking: multiplicity of meaning and method.

BACKGROUND/AIMS: Efforts to improve individual and population health increasingly rely on large-scale collections of human biological specimens and associated data. Such collections or 'biobanks' are hailed as valuable resources for facilitating translational biomedical research. However, biobanks also raise important ethical considerations, such as whether, how and why biobanks might engage with those who contributed specimens. This paper examines perceptions and practices of community engagement (CE) among individuals who operate 6 diverse biobanks in the US. METHODS: Twenty-four people from a diverse group of 6 biobanks were interviewed in-person or via telephone from March to July 2011. Interview transcripts were coded and analyzed for common themes. RESULTS: Emergent themes include how biobank personnel understand 'community' and CE as it pertains to biobank operations, information regarding the diversity of practices of CE, and the reasons why biobanks conduct CE. CONCLUSION: Despite recommendations from federal agencies to conduct CE, the interpretation of CE varies widely among biobank employees, ultimately affecting how CE is practiced and what goals are achieved.

Smooth muscle contractility after intestinal resection.

Intestinal resection is followed by structural and functional adaptation of the remnant, including motor adaptation. Since changes also occur in intestinal smooth muscle, our aim was to determine whether changes in motor function are related to changes in smooth muscle contractility. Eighteen dogs underwent transection alone (GPI, n=6), 50% distal resection (GP II, n = 6) and 50% distal resection with jejunocolostomy (GP III, n = 6). Histologic measurements and length-tension studies with response to carbachol were made at 12 weeks. Longitudinal muscle (LM) length tended to increase in the resected animals but not significantly (174 +/- 23 and 180 +/- 23 vs 156 +/- 16 cm, GP II, GP III, and GP I, respectively). Circular muscle (CM) length was similar in all three groups (8.2 +/- 0.9 and 7.9 +/- 0.6 vs 7.5 +/- 0.6 cm). Both CM and LM tended to be thicker in the resected groups (CM: 660 +/- 163 and 733 +/- 139 vs 569 +/- 199 micron; LM: 213 +/- 77 and 246 +/- 76 vs 220 +/- 104 micron, GP II, GP III, and GP I, respectively, NS). Length-tension relationships for both CM and LM were similar in all three groups. The length (Lo) at which maximal active tension (To) was achieved was 130-140% initially in both LM and CM. Passive tension at Lo and the response to cholinergic stimulation were similar in all three groups. There were no significant differences in absolute active and total tension generated or force/cm2. The carbachol dose responses were similar with the maximal active tension occurring at 10(-4) M carbachol. The ED50 was greater in CM than in LM (P < 0.05 for transection animals). The ED50 was lower after resection and bypass (P < 0.05 GP III vs Gp I). There were no significant differences in in vitro smooth muscle length tension relationships or the response to cholinergic stimuli of jejunum 12 weeks after resection with or without bypass of the ICJ. Thus, any changes in motor adaptation during this period are related to earlier transient effects or other factors.

Calcitonin gene-related peptide mediates capsaicin-induced neuroendocrine responses in rat antrum.

BACKGROUND: Calcitonin gene-related peptide (CGRP) is a 37-amino acid peptide localized to primary sensory afferent nerves in the rat stomach. The actions of CGRP in regulating antral neuroendocrine function were examined in vitro through the use of capsaicin, an agent capable of evoking neuropeptide release from peripheral sensory nerve endings. These results were compared with the effects of exogenous CGRP and CGRP antagonist, CGRP8-37. METHODS: Rat antral mucosal/submucosal fragments were incubated in either static or dynamic perifusion experiments. Media were assayed for gastrin, somatostatin, CGRP, and acetylcholine. RESULTS: Capsaicin, like exogenous CGRP, stimulated antral somatostatin release and inhibited both gastrin release and acetylcholine discharge. Low dose capsaicin (1 x 10(-5) mol/L) caused significant stimulation of CGRP release: 33 +/- 0.2 vs. 14 +/- 1 pg/mL protein; P < 0.001. Tetrodotoxin blocked capsaicin-induced inhibition of acetylcholine release and prevented partially capsaicin-mediated stimulation of CGRP release. The CGRP receptor antagonist CGRP8-37 prevented capsaicin-induced D-cell stimulation and inhibition of G-cell secretion and cholinergic discharge. CONCLUSIONS: The effects of capsaicin-induced changes in antral D- and G-cell secretion and acetylcholine discharge are due primarily to release of CGRP. Antral CGRP release from primary sensory afferent nerve terminals may act as a local effector substance to regulate antral neuroendocrine function.

Calcitonin gene-related peptide: mechanisms of modulation of antral endocrine cells and cholinergic neurons.

Actions of human calcitonin-gene related peptide (hCGRP) on acetylcholine (ACh) discharge and gastrin and somatostatin release from rat antral mucosal-submucosal fragments were examined in both dynamic perifusion experiments and short-term static incubation studies. The principal findings of the dynamic perifusion experiments were that hCGRP exerted a dual or biphasic effect on ACh discharge and gastrin release. Initial exposure of antral tissues to hCGRP (1 x 10(-8) M) resulted in stimulation of both ACh and gastrin release that was of brief duration. Continued hCGRP perifusion caused subsequent inhibition of ACh and gastrin release that was substantially greater in duration and magnitude than the initial stimulatory responses. Static incubation studies indicated that hCGRP (10(-10) to 10(-7) M) stimulated somatostatin and inhibited gastrin release in a dose-dependent manner. Inhibition of gastrin and ACh release by hCGRP appeared to be an indirect effect that was mediated by somatostatin as suggested by studies with pertussis toxin (200 ng/ml). Furthermore, studies with atropine (1 x 10(-6) M) and tetrodotoxin (1 x 10(-6) M) indicated that CGRP-induced stimulation of somatostatin release and inhibition of ACh discharge occurred independent of muscarinic receptor activation and nerve excitation. In conclusion, results of these studies indicate that CGRP is capable of exerting both stimulatory and inhibitory effects on ACh release from mucosal-submucosal neurons and gastrin release from antral mucosal G cells in in vitro studies. These data suggest that the inhibitory effects of CGRP on cholinergic discharge and gastrin release are due to the paracrine effects of somatostatin released from antral D cells by direct action of CGRP.

gamma-Aminobutyric acid localization and function as modulator of cholinergic neurotransmission in rat antral mucosal/submucosal fragments.

gamma-Aminobutyric acid, a neurotransmitter in the central nervous system, has been shown to be present in and synthesized and secreted by rodent and feline myenteric plexus neurons. The aims of the present studies were to measure gamma-aminobutyric acid concentrations and synthesis and to establish cellular localization and uptake of gamma-aminobutyric acid by immunocytochemistry and autoradiography, respectively, within mucosal and submucosal tissues of the rat antrum. Direct demonstration of [3H]gamma-aminobutyric acid release and the effects of exogenous gamma-aminobutyric acid and muscimol, a GABA alpha agonist, on [3H]acetylcholine release from antral mucosal/submucosal fragments were examined in perifusion experiments. gamma-Aminobutyric acid content and synthesis, as reflected by glutamic acid decarboxylase activity, were present within antral mucosa at levels two to three times that of the body and muscular layers of both the gastric body and antrum. gamma-Aminobutyric acid was identified immunocytochemically, principally in mucosal epithelial cells of the antrum. Exogenous gamma-aminobutyric acid and muscimol were capable of stimulating acetylcholine release through a GABA alpha receptor-mediated mechanism that was abolished by tetrodotoxin. These results indicate that gamma-aminobutyric acid is present in and taken up by epithelial cells of the gastric antrum and that gamma-aminobutyric acid is capable of being synthesized by antral mucosal/submucosal tissues. Furthermore, these studies suggest that a peripheral gamma-aminobutyric acid mechanism that may modulate cholinergic neurotransmission and endocrine cell function exists within the antrum.

Occupational injury and illness in the semiconductor manufacturing industry.

Two thousand nine hundred and ninety-four reports of OSHA-reportable occupational injury or illness cases in 1984 from member companies of a national trade association of semiconductor manufacturing firms were analyzed. The 37 participating manufacturing facilities represented 16 companies employing over 95,000 persons, or approximately one-third of the U.S. work force for this industry in 1984. The annual incidence rate for all reportable injuries and illnesses was 2.7 per 100 full-time employees (FTE) for men and 3.7 per 100 FTE for women. Strains, sprains, or dislocations were the most frequently reported incidents (N = 956 [31.9%]), followed by cuts, lacerations, punctures, scratches, and abrasions (N = 445 [14.9%]), and chemical burns (N = 401 [13.4%]). Increased work-loss days per case were associated with manufacturing sites that did not have an employee health clinic on the premises, with custodial occupations, and with female gender.

Evidence for presynaptic inhibitory histamine (H2) receptors in the rat hindquarter vasculature.

Histamine released within walls of resistance blood vessels is suggested to mediate an active portion of baroreceptor-mediated neurogenic vasodilatation in skeletal muscle vasculature. Studies were undertaken to examine the possibility that histamine-mediated active vasodilatation could be effected, in part, by an inhibitory presynaptic action of histamine on vascular sympathetic varicosities. All experiments were conducted in constant-flow autoperfused rat hindquarters in which vasoconstrictor responses were evoked by sympathetic chain (L2-4) stimulation at varying frequencies or intraarterial norepinephrine (0.5 microgram) administration. Intraarterial histamine infusion resulted in a significant inhibition of nerve-stimulated hindquarter vasoconstriction, with the greatest reduction (20%) occurring at the 82.5-ng/ml/min dose. The inhibitory effect of histamine was not stimulation frequency dependent, and occurred when the vasoconstrictor responses to intraarterial norepinephrine and dilator responses to intraarterial nitroglycerin (1 microgram) were unaltered by the histamine infusions. The H2 agonist impromidine produced a significant inhibition of nerve-stimulated hindquarter vasoconstrictor responses without altering perfusion pressure responsiveness to either intraarterial norepinephrine or nitroglycerin. The magnitude of this inhibition of nerve-stimulated vasoconstrictor response was equivalent to or greater than that produced by histamine. The alpha 2-agonist clonidine produced a significant inhibitory effect on neurogenic vasoconstrictor responses with a maximum of 54%. Cimetidine infusion (10 mg/kg i.a.) essentially abolished the inhibitory effect of histamine on nerve-stimulated hindquarter vasoconstriction. These results are consistent with the existence of inhibitory presynaptic histamine receptors on sympathetic varicosities in the hindquarter vascular bed. Furthermore, evidence supports these inhibitory receptors being of the H2 class and the possibility that histamine-mediated active vasodilatation in rat hindquarters involves inhibitory presynaptic histamine receptors.