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Cost analysis has been frequently neglected in program evaluations but is currently of high relevance in policy decisions on quality assurance in medicine. The Ambulatory Care Medical Audit Demonstration (ACMAD) Project implemented and evaluated a program of medical record-based quality assurance in eleven sites for nine medical topics. Total direct costs for the project were $1.22 million over five years; indirect costs, $694,000. A computerized data system enabled disaggregation of the cost data by person, timing, type of work, project phase, health topic, health center, and research or operational nature. Of the costs incurred, 79% were for operational reasons, with 21% incurred for research reasons. Costs per audited case were 31% higher in hospitals than in neighborhood health centers. Audit topics of low per-case costs tended to have automated case findings, straightforward and limited abstracting, little need to examine multiple visits, and a low proportion of case-found patients ineligible for audit. [ABSTRACT FROM AUTHOR]

Fracture fixation using adhesive is a promising alternative in craniofacial surgeries, replacing the plates and screws system. The advantages include the ease of application and avoidance of drilling holes that may weaken the bone and cause fractures. In this study the bond strengths of selected adhesives were evaluated and compared with resorbable plates and screws. Four adhesives, octyl-cyanoacrylate, N-butyl-cyanoacrylate, a novel methyl-methacrylate, and a novel cyanoacrylate derivative, were tested for their microtensile and shear bond strengths. The bone samples were cut into rectangular bars and bonded with selected adhesives for microtensile testing. For the shear bond test, paired bars were bonded at the overlap, while two other sets of bars were attached by a Lactosorb plate using either adhesive or screws. Data were analysed by analysis of variance (ANOVA). The microtensile bond strengths of N-butyl-cyanoacrylate, novel cyanoacrylate derivative, and novel methyl-methacrylate derivative were significantly greater than octyl-cyanoacrylate. When bone sections were fixed with resorbable plates and adhesives, shear bond strength was significantly greater for N-butyl-cyanoacrylate than plate and screws, while the bond strengths of other adhesives were comparable with the plate and screws. N-Butyl cyanoacrylate was shown to have the greatest potential for fixation of fractured bone in craniofacial surgical applications., (Copyright © 2013 International Association of Oral and Maxillofacial Surgeons. Published by Elsevier Ltd. All rights reserved.)

The growth hormone-releasing hormone (GHRH) gene produces a precursor molecule that contains GHRH and a carboxyl-terminal peptide that we have named GHRH-related peptide (GHRH-RP). This peptide, like GHRH, stimulates the expression of stem cell factor (SCF), an important reproductive and hematopoietic cytokine, in vitro and in vivo. In the present study, using primary cultures of rat Sertoli cells, we compared the time course of action and the level of SCF stimulation seen following treatment with GHRH-RP and GHRH. Additionally, we investigated the activity of a truncated peptide, p75-92NH2, whose sequence is contained within GHRH-RP. All three of these peptides were shown to stimulate the steady-state levels of SCF mRNA to a comparable degree. However, the time course of action for GHRH-RP differed markedly from that of GHRH. GHRH-RP and p75-92NH2, similar to GHRH, induce SCF expression, at least in part, via the activation of the protein kinase A/cyclic adenosine monophosphate intracellular signaling pathway.

Growth hormone-releasing hormone (GHRH) belongs to a family of peptides expressed at high levels in the brain and digestive system of mammals. We have identified GHRH mRNA and peptide in rat and human germ cells, and detected a GHRH receptor mRNA in Sertoli cells. GHRH treatment of cultured Sertoli cells results in accumulation of cAMP and increased expression ofc-fos and stem cell factor (SCF), two factors critical for normal germ cell development. The current study was designed to localize within testis the transcription of other members of the GHRH family, and their receptors, and to determine if they also stimulate SCF. RNAs from separated testicular cells were amplified by comparative reverse transcription-polymerase chain reaction (RT-PCR). Southern blot analysis of the PCR products verified the presence of five GHRH family peptide and receptor transcripts in distinct testicular cell types. Transcripts encoding VIP and glucagon, and the receptors for pituitary adenylate cyclase activating peptide (PACAP) and glucagon, were detected predominantly in Leydig cells. In contrast, expression of GHRH, PACAP, secretin, and secretin receptor predominated in germ cells. Receptors for GHRH and VIP were expressed equally in all testicular cell types. To determine if, like GHRH, any of these other peptides activate Sertoli cell expression of SCF, primary Sertoli cell cultures were treated for 4-6 h with 10 or 100 nM of each individual factor. There was no consistent stimulation of SCF mRNA by VIP, PACAP, glucagon, or secretin. Differential expression of these peptides and their receptors suggests that they may each have unique paracrine functions within the testis.

In the renal proximal tubule, external Ca2+ ([Ca2+]o) is required for parathyroid hormone to elevate cytosolic Ca2+ ([Ca2+]i). However, other hormones increase [Ca2+]i in the absence of [Ca2+]o. These differences may arise from a diversity of signal transduction pathways acting on external and internal Ca2+ pools. However, Ca2+ influx may be necessary to expedite and maintain the rise of [Ca2+]i for a period after the initial surge. In this study, F- was used to probe the roles of intracellular Ca2+ mobilization, Ca2+ influx, and phosphoinositide (PI) hydrolysis on the surge of [Ca2+]i in rat proximal tubules. In the presence of external Ca2+; 1-20 mM F- evoked incremental rises of [Ca2+]i in tubules loaded with aequorin. Whereas 10 mM F- increased [Ca2+]i in the absence of [Ca2+]o, the time constant for the [Ca2+]i surge was increased. These findings are consistent with a role of Ca2+ influx on the effect of F- on [Ca2+]i. Indeed, 10 mM F- also enhanced the uptake of 45Ca2+, and promoted Ca2+ influx in aequorin- and fura-2-loaded, Ca(2+)-deprived tubules. In tubules, F- also activated PI hydrolysis with a time course that paralleled Ca2+ mobilization. The effect of F- on [Ca2+]i was not altered when the 39-kDa pertussis toxin substrate was inactivated with the toxin. This G protein was most likely Gi, because prostaglandin E2, an activator of Gi in tubules, dissociated the pertussis toxin-sensitive protein. The results support the notion that activation of a signal-transduction complex, the F- substrate, causes Ca2+ influx, mobilizes internal Ca2+, and activates PI hydrolysis in rat proximal tubules.(ABSTRACT TRUNCATED AT 250 WORDS)

Medical decision analysts are interested in the changes in health benefits from inappropriate ordering of tests, imperfect information from tests, and imperfect results of treatments. Operational failures in the decision-making sequence, caused by human and system factors, may also alter health benefits. An evaluation of operational failures in follow-up of positive urine cultures in pediatric patients is reported. Branching criteria were developed by physician representatives from each of eight pediatric group practices to evaluate the care of patients aged 6 months to 16 years, inclusive. Of 858 cases evaluated, 52 percent failed at one or more nodes in the criteria sequence. Rates of failure at individual nodes among cases reaching these nodes varied from 2 percent to 48 percent. Like those of other researchers, our findings suggest that decision analyses that do not take operational failures into consideration may inaccurately predict the yield of health benefits achieved in actual practice.

Angiotensin-II (AII) and potassium (K+) as stimuli of aldosterone secretion enhance each other's stimulatory potential. In the present study we looked for evidence that AII and K+ act through a common mechanism of signal transduction to affect secretion. Bovine adrenal glomerulosa cells were loaded with the calcium (Ca2+) probe aequorin to permit detection over prolonged time periods of the changes in cytosolic Ca2+ that occur in response to AII and K+. Perfusion fractions were collected for simultaneous measurement of aldosterone production rates. AII (10(-7) M) produced an immediate and transient increase in Ca2+, followed by a Ca2+ plateau that remained above baseline for as long as AII was present. An increase in K+ concentration (from 5 to 12 mM) produced a slow and eventually sustained increase in cytosolic Ca2+, which resembled the plateau produced by AII. Nitrendipine (10(-5) M) completely inhibited the secretory response to AII and K+ (during 60-min incubations) and inhibited the typical K+-induced increase in Ca2+. The sustained increase in Ca2+ with AII (the plateau) required extracellular Ca2+ and was proportional to the prevailing extracellular K+ concentration. When glomerulosa cells were incubated with AII, the aldosterone secretory response to K+ was substantially enhanced (P less than 0.001). In summary, stimulation by both AII and K+ resulted in a sustained increase in Ca2+ influx. AII-induced Ca2+ influx was dependent on the ambient K+ concentration. These results indicate that AII and K+ act together to determine the optimal rate of Ca2+ entry, which may then lead to the appropriate secretory rate of aldosterone.