The impact of managers' perceptions of learning organizations on innovation in healthcare: sample of Turkey

Organizational learning is the process of increasing effective organizational activities through knowledge and understanding. Innovation is the creation of any product, service or process, which is new to a business unit. Significant amount of research on organizational learning place a central meaning on the fact that there is a positive relationship between organizational learning and innovation. Both organizational learning and innovation are essential for organizations to prepare for change. The aim of this study is to determine to what extent the identified learning organization dimensions are associated with innovation. The study used a quantitative non‐experimental design employing statistical analysis via multiple regression and correlation methods to identify the relationships between the variables examined. Because the research was conducted in a non‐experimental way, learning organization dimensions are referred to as predictor variables, and innovation is referred to as the criterion variable. Watkins and Marsick's Dimensions of the Learning Organization Questionnaire was used in the study. Questionnaires were distributed to 498 hospital managers and, 243 valid responses were used in this study. Therefore, 243 hospital managers working at 250 Ministry of Health (public) hospitals across Turkey participated in the study. Results demonstrate that there are significant and positive correlations between learning organization dimensions and innovation. Intercorrelations between learning organization dimensions and correlations between learning organization dimensions and innovation were average and high, respectively. Results further indicate that the dimensions of the learning organizations explained 66.5% of the variance for the innovation. Copyright © 2012 John Wiley & Sons, Ltd.     

Acute liver failure due to non-exertional heatstroke after sauna

Acute liver failure is defined as rapid loss of liver function that patients without previously recognized liver disease sustain a liver damage. Acute liver failure due to non-exertional heatstroke has rarely been reported. We reported here an unusual case of heat stroke induced acute liver failure (ALF) after sauna. A 63 year old man without previously recognized liver and other systemic disease was admitted for loss of consciousness and impaired liver function after sauna. Despite intensive supportive care, ALF developed. Liver transplantation was planned but the patient died on the sixth day of hospitalization. Non-exertional heatstroke induced ALF is a rare and serious condition. ALF caused by non-exertional heatstroke which requires liver transplantation for definitive solution should be kept in mind in early period.     

Molecular determinants of Ca2+ potentiation of diltiazem block and Ca2+-dependent inactivation in the pore region of cav1.2

Diltiazem block of Cav1.2 is frequency-dependent and potentiated by Ca2+. We examined the molecular determinants of these characteristics using mutations that affect Ca2+ interactions with Cav1.2. Mutant and wild-type (WT) Cav1.2 channels were transiently expressed in tsA 201 cells with beta1b and alpha2delta subunits. The four conserved glutamates that compose the Ca2+ selectivity filter in Cav1.2 were mutated to Gln (E363Q, E709Q, E1118Q, E1419Q), and each single mutant was assayed for block by diltiazem using whole-cell voltage-clamp recordings in either 10 mM Ba2+ or 10 mM Ca2+. In Ba2+, none of the mutations affected the potency of diltiazem block of closed channels (0.05 Hz stimulation). However, frequency-dependent block (1Hz stimulation) was eliminated in the mutant E1419Q (domain IV), which recovered more rapidly than WT channels from inactivated channel block. Potentiation of diltiazem block of closed Cav1.2 channels in Ca2+ was abolished in the E1118Q, F1117G (domain III), and E1419Q mutants. Frequency-dependent block in Ca2+ was reduced compared with WT Cav1.2 in the F1117G, E1118Q, and E1419Q mutants. The C-terminal tail IQ domain mutation I1627A, which disrupts Ca2+ dependent inactivation, enhanced diltiazem block of closed channels in Ba2+. We conclude that, in Ba2+, E1419 slows recovery from diltiazem block of depolarized Cav1.2 channels, but in Ca2+, E1118, E1419, and F1117 form a Ca2+ binding site that mediates the potentiation of diltiazem block of both closed and inactivated Cav1.2 channels. Furthermore, Ca2+-dependent inactivation, which is impaired in E709Q, E1118Q, E1419Q, and I1627A, is not required for Ca2+ potentiation of diltiazem block.     

Tauroursodeoxycholic acid and secondary damage after spinal cord injury in rats.

Greater clinical understanding of the pivotal role of apoptosis in spinal cord injury (SCI) has led to new and innovative apoptosis-based therapies for patients with an SCI. Tauroursodeoxycholic acid (TUDCA) is a biliary acid with antiapoptotic properties. To our knowledge, this is the first study in the English language to evaluate the therapeutic efficacy of TUDCA in an experimental model of SCI. Thirty rats were randomized into three groups (sham-operated, trauma only, and trauma plus TUDCA treatment) of 10 each. In groups 2 and 3, spinal cord trauma was produced at the T8-T10 level via the Allen weight drop technique. Rats in group 3 were treated with TUDCA (200 mg/kg intraperitoneal) 1 min after trauma. The rats were killed either 24 h or 5 days after injury. The neuroprotective effect of TUDCA on injured spinal cord tissue and the effects of that agent on the recovery of hind-limb function were assessed. The efficacy of treatment was evaluated with histopathologic examination and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) analysis. Histopathologic characteristics were analyzed by comparison of hematoxylin-and-eosin stained specimens. Neurologic evaluations were performed 24 h, 3 days, and 5 days after trauma. Hind-limb function was assessed with the inclined plane technique of Rivlin and Tator and the modified version of Tarlov's grading scale. Twenty-four hours after injury, there was a significantly higher number of apoptotic cells in the lesioned spinal cord group than in the sham-operated control group. Treatment of the rats with TUDCA significantly reduced the number of apoptotic cells (4.52+/-0.30 vs. 2.31+/-0.24 in group 2) and the degree of tissue injury. Histopathologic examination showed that group 3 rats had better spinal cord architecture compared with group 2 rats. Five days after injury, the mean inclined plane angles in groups 1, 2, and 3 were 65.50 degrees +/- 2.09, 42.00 degrees +/- 2.74, and 53.50 degrees +/- 1.36. Motor grading of the rats revealed a similar trend. These differences were statistically significant (p<0.05). The mechanism of neuroprotection in the treated rats, although not yet elucidated, may be related to the marked antiapoptotic properties of TUDCA. A therapeutic strategy using TUDCA may eventually lead to effective treatment of SCI without toxic effects in humans.     

Therapeutic efficacy of SJA6017, a calpain inhibitor, in rat spinal cord injury

Apoptosis is an important element of the secondary processes that occur after spinal cord injury. Calpain and caspases are key proteases in apoptotic cell death. We evaluated the neuroprotective effects of SJA6017 (a calpain inhibitor) and measured functional recovery in a rat spinal cord injury model. Thirty Wistar albino rats were divided into three groups of 10 animals each: sham-operated (group 1), trauma control (group 2) and trauma-plus-SJA6017 treatment (group 3). Spinal cord trauma was produced in the thoracic region of the animals. Rats in group 3 received SJA6017 1 min after trauma. Treatment efficacy was evaluated after injury using light microscopy and TUNEL staining. Neurological performance was assessed using an inclined plane and a modified version of the Tarlov's grading scale. Group 2 rats showed moderate trauma with widespread edema, hemorrhage, vascular thrombi and necrosis 24 h after injury. Group 3 rats had significantly reduced tissue injury and apoptosis. Tarlov scores revealed that group 3 rats also had ameliorated recovery of limb function. Our results demonstrate that treatment with SJA6017 reduces apoptotic cell death, preserves spinal cord tissue and improves functional outcome. Treating calpain-induced apoptosis with this agent may be a feasible therapeutic strategy for patients with spinal cord injury.     

Ca v 1.3 is preferentially coupled to glucose-stimulated insulin secretion in the pancreatic beta-cell line INS-1

L-Type Ca(2+) channel blockers inhibit glucose and KCl-stimulated insulin secretion by pancreatic beta cells. However, the role of the two distinct L-type channels expressed by beta cells, Ca(v)1.2 and Ca(v)1.3, in this process is not clear. Therefore, we stably transfected INS-1 cells with two mutant channel constructs, Ca(v)1.2DHPi or Ca(v)1.3 DHPi. Whole-cell patch-clamp recordings demonstrated that both mutant channels are insensitive to dihydropyridines (DHPs), but are blocked by diltiazem. INS-1 cells expressing Ca(v)1.3/DHPi maintained glucose- and KCl-stimulated insulin secretion in the presence of DHPs, whereas cells expressing Ca(v)1.2/DHPi demonstrated DHP resistance to only KCl-induced secretion. INS-1 cells were also stably transfected with cDNAs encoding the intracellular loop between domains II and III of either Ca(v)1.2 or Ca(v)1.3 (Ca(v)1.2/II-III or Ca(v)1.3/II-III). Glucose- and KCl-stimulated insulin secretion in Ca(v)1.2/II-III cells were not different from untransfected INS-1 cells. However, glucose-stimulated insulin secretion was completely inhibited and KCl-stimulated secretion was substantially resistant to inhibition by DHPs, but sensitive to omega-agatoxin IVA in Ca(v)1.3/II-III cells. Moreover, the L-type channel agonist FPL 64176 markedly enhanced KCl-stimulated secretion by Ca(v)1.3/II-III cells. Together, our results suggest that Ca(2+) influx via Ca(v)1.3 is preferentially coupled to glucose-stimulated insulin secretion in INS-1 cells.     

Antifungal Activity of Propolis Against Yeasts Isolated From Blood Culture: In Vitro Evaluation

Background: Due to the failure of available antifungal agents in the treatment of candidemia and the toxic activities of these drugs, a lot of researches are being conducted to develop new nontoxic and effective antifungal agents for optimal control of fungal pathogens. The aim of this study is to evaluate the in vitro antifungal activity of propolis against yeasts isolated from the blood cultures of intensive care unit patients. Methods: Seventy‐six strains were included in this study. The in vitro antifungal activity of propolis, fluconazole (FLU), and itraconazole (ITR) was investigated by the microdilution broth methods (CLSI guidelines M27‐A3 for yeast). The propolis sample was collected from Kayseri, Turkey. Results: Of the 76 isolates, 33 were identified as Candida albicans while 37 were C. parapsilosis, three were C. tropicalis, and three were identified as C. glabrata. The geometric mean range for MIC (μg/ml) with regard to all isolates was 0.077 to 3 μg/ml for FLU and ITR, and 0.375 to 0.70 μg/ml for propolis. It was shown that propolis had significant antifungal activity against all Candida strains and the MIC range of propolis was determined as 0185 to 3 μg/ml. Conclusion: This study demonstrated that propolis had significant antifungal activity against yeasts isolated from blood culture compared with FLU and ITR. The propolis MIC in azole‐resistant strains such as C. glabrata was found lower than the FLU MIC.