Motivations and barriers to implementing electronic health records and ED information systems in Japan

Background

Although electronic health record systems (EHRs) and emergency department information systems (EDISs) enable safe, efficient, and high-quality care, these systems have not yet been studied well. Here, we assessed (1) the prevalence of EHRs and EDISs, (2) changes in efficiency in emergency medical practices after introducing EHR and EDIS, and (3) barriers to and expectations from the EHR-EDIS transition in EDs of medical facilities with EHRs in Japan.

Materials and methods

A survey regarding EHR (basic or comprehensive) and EDIS implementation was mailed to 466 hospitals. We examined the efficiency after EHR implementation and perceived barriers and expectations regarding the use of EDIS with existing EHRs. The survey was completed anonymously.

Results

Totally, 215 hospitals completed the survey (response rate, 46.1%), of which, 76.3% had basic EHRs, 4.2% had comprehensive EHRs, and 1.9% had EDISs. After introducing EHRs and EDISs, a reduction in the time required to access previous patient information and share patient information was noted, but no change was observed in the time required to produce medical records and the overall time for each medical care. For hospitals with EHRs, the most commonly cited barriers to EDIS implementation were inadequate funding for adoption and maintenance and potential adverse effects on workflow. The most desired function in the EHR-EDIS transition was establishing appropriate clinical guidelines for residents within their system.

Conclusion

To attract EDs to EDIS from EHR, systems focusing on decreasing the time required to produce medical records and establishing appropriate clinical guidelines for residents are required.     

Suppression of IFN-gamma production in atopic group at the acute phase of RSV infection

Several studies have suggested that respiratory syncytial virus (RSV) bronchiolitis induced the change of cytokine production profile in childhood. We sought to determine whether the RSV-induced cytokine production was affected by the patient's atopic background. We quantified interferon-gamma (IFN-gamma) and interleukin (IL)-4 in the supernatant of peripheral blood mononuclear cells (PBMCs) cultured for 24 h and in the presence of phytohemaglutinin (PHA), IL-12, or IL-18, from 14 infants who were divided into two groups, those who are non-atopic and an atopic group. In RSV-infected infants with atopic diseases, IFN-gamma production from IL-12- or especially IL-18-stimulated PBMCs was subtotally suppressed in the acute phase, whereas in RSV-infected infants without atopic diseases IFN-gamma production was not suppressed on acute phase. The IFN-gamma suppression observed in the atopic group is not caused by the immaturity of an infant's immune system since reduced IFN-gamma production to RSV is not observed in the infants of non-atopic group. IFN-gamma suppression in regard to RSV infection might be caused by some genetic factor involved in the development of atopic disease such as IL-18 signal cascade.     

Composite implantation of mesenchymal stem cells with endothelial progenitor cells enhances tissue-engineered bone formation

For successful tissue engineering, neovascularization of the implanted tissue is critical. Factors generated by endothelial cells are also considered crucial for the process of osteogenesis. The direct effects of supplementing tissue engineered constructs with cultured endothelial progenitor cells (EPCs) for enhancing bone regeneration have not been reported. In this study, we investigated the potential of EPCs to facilitate neovascularization in implants and evaluated their influence on bone regeneration. The influence of EPC soluble factors on osteogenic differentiation of mesenchymal stem cells (MSCs) was tested by adding EPC culture supernatant to MSC culture medium. To evaluate the influence of EPCs on MSC osteogenesis, canine MSCs-derived osteogenic cells and EPCs were seeded independently onto collagen fiber mesh scaffolds and co-transplanted to nude mice subcutaneously. Results from coimplant experiments were compared to implanted cells absent of EPCs 12 weeks after implantation. Factors from the culture supernatant of EPCs did not influence MSC differentiation. Coimplanted EPCs increased neovascularization and the capillary score was 1.6-fold higher as compared to the MSC only group (p < 0.05). Bone area was also greater in the MSC + EPC group (p < 0.05) and the bone thickness was 1.3-fold greater in the MSC + EPC group than the MSC only group (p < 0.05). These results suggest that soluble factors generated by EPCs may not facilitate the osteogenic differentiation of MSCs; however, newly formed vasculature may enhance regeneration of tissue-engineered bone.     

Clinical evaluation of coronary lesion characteristics in acute myocardial infarction

Coronary lesion instability at the onset of acute myocardial infarction (AMI) was evaluated. The mechanism of AMI has been considered to be coronary lesion instability with occlusive thrombus, although more than one half of AMI occurs in clinically stable patients. A total of 313 AMI patients treated by primary percutaneous transluminal coronary angioplasty with provisional stenting (rate, 41%) were studied. They were divided into 2 groups: group 1A (n = 211), without unstable angina before AMI onset, and group 1B (n = 102), with unstable angina before onset. Moreover, angina patients treated similarly were studied: group 2A (n = 180), with stable angina, and group 2B (n = 204), with unstable angina. Coronary lesion instability at AMI onset was also predicted by C-reactive protein (CRP) levels within 6 hours after onset, before they were affected by myocardial damage. The incidence of repeated AMI and/or target vessel revascularization was 1.9% in group 1A, 7.8% in 1B (p=0.035), 1.7% in 2A, and 5.9% in 2B (p=0.043). Event-free survival curves were consistent with each other in groups 1A and 2A and in groups 1B and 2B. CRP levels on admission were 2.0 +/- 1.7 mg/L in group 1A, 3.3 +/- 4.8 mg/L in group 1B (p<0.001), 2.1 +/- 1.7 mg/L in group 2A, and 3.4 +/- 4.7 mg/L in group 2B (p<0.001). Thus coronary lesion characteristics at AMI onset appeared to be similar in groups 1A and 2A and in groups 1B and 2B. A substantial number of patients have stable culprit lesions at the onset of AMI.     

Region-Dependent Role of the Mucous/Glycocalyx Layers in Insulin Permeation Across Rat Small Intestinal Membrane

The regional difference in the contribution of the mucous/glycocalyx layers in rat small intestine, as a diffusional or enzymatic barrier, to the absorption of insulin was investigated by in vitro studies. The mucous/glycocalyx layers from the duodenum, the jejunum, and the ileum in rat were successfully removed without damaging membrane integrity, by exposing them to a hyaluronidase solution in situ. In an in vitro transport experiment, the apparent permeability coefficient (P_app) of insulin for the hyaluronidase-pretreated group was significantly increased compared to the PBS-pretreated (control) group in all small intestinal regions, and the P_app of insulin in both PBS- and hyaluronidase-pretreated groups increased in the following order: duodenum < jejunum < ileum. On the other hand, irrespective of small intestinal regions, the P_app of FD-4 and of antipyrine, respectively the passive para- and transcellular permeation marker, exhibited no significant differences between PBS- and hyaluronidase-pretreated group. In addition, a significant amount of insulin was degraded in the mucous/glycocalyx layers compartment removed by hyaluronidase pretreatment, and the degradation activity in the mucous/glycocalyx layers showed regional differences in the following order: duodenum > jejunum > ileum. These findings suggest that, irrespective of small intestinal regions, the mucous/glycocalyx layers contributed to insulin permeation predominantly as an enzymatic barrier, and not as a diffusional barrier. Furthermore, the variation of the enzymatic activities in the mucous/glycocalyx layers and in the brush-border membrane would be one factor that accounts for the regional differences in the transport of insulin.     

In Vivo Evaluation of Acyclovir Prodrug Penetration and Metabolism Through Rat Skin Using a Diffusion/Bioconversion Model

Purpose. In order to evaluate the in vivo penetration of prodrugs which undergo metabolism in skin, we analyzed thein vivo penetration profiles of acyclovir prodrugs based on a two-layer skin diffusion model in consideration of metabolic process. Methods. Acyclovir prodrugs (e.g., valerate, isovalerate and pivarate) were used as model prodrugs and the amounts excreted in urine were measured after percutaneous application. In vivo penetration profiles were then estimated by employing a deconvolution method and the penetration of acyclovir prodrugs was analyzed using a diffusion model. Subsequently, diffusion, partitioning and metabolic parameters were compared under in vitro and in vivo conditions. Results. Although total penetration amounts at the end of the experiment were similar for the three prodrugs, the ratio of intact prodrug to total penetration amount differed significantly. Moreover, the excretion and absorption profiles were also very different for each prodrug. Enzymatic hydrolysis rate constants calculated under in vivo conditions were considerably larger than those obtained in the skin homogenate and in vitro penetration experiments. Conclusions. The present skin diffusion/bioconversion model combined with computer analysis enables us to comprehensively account for diffusion, partitioning and metabolism during in vivo percutaneous absorption. Nevertheless, different enzymatic hydrolysis rate constants obtained under bothin vivo and in vitro conditions demonstrate the difficulty of obtaining accurate values for in vivo enzymatic activity from related in vitro experiments.     

Neurological deterioration in small vessel disease may be associated with increase of infarct volume

BACKGROUND AND PURPOSE: The mechanism of neurological deterioration in small vessel disease is unclear. We examined the relationship between neurological deterioration and change of infarct volume in acute small vessel disease. METHODS: We studied consecutive patients with acute supratentorial small vessel disease. Patients were classified into two groups (D: group with deterioration, N: group with no deterioration). We performed serial MRI studies, measured infarct volumes using NIH Image, and calculated the changes in infarct volume (Delta volume) between initial and follow-up diffusion-weighted imaging (DWI). RESULTS: Seventy-two patients (44 males, 68+/-11 years of age) were enrolled. Fifteen patients exhibited neurological deterioration (group D) and 57 patients did not (group N). Initial infarct volume was 0.66 cm3 in group D and 0.45 cm3 in group N (p=0.025). Infarct volumes on follow-up DWI were 1.41 cm3 and 0.72 cm3, respectively (p=0.001). The Delta volume in group D was larger than that in group N (0.76 cm3 vs 0.27 cm3, p=0.001). In order to differentiate D from N group, sensitivity specificity analysis yielded a cut-off value of Delta volume of 0.5 cm3 for differentiation of the two groups, which exhibited a sensitivity of 80% and specificity of 84%. Multivariate logistic regression analysis demonstrated that increase in infarct volume of over 0.5 cm3 (odds ratio; 18.0, 95% CI; 1.4 to 270, p=0.027) was independently associated with neurological deterioration in patients with acute small vessel disease. CONCLUSIONS: Enlargement of infarct volume may contribute to neurological deterioration in acute small vessel disease.     

Neurotrophin-3 levels in cerebrospinal fluid from children with bacterial meningitis, viral meningitis, or encephalitis

Neurotrophin-3 levels were measured in the cerebrospinal fluid of 35 patients with bacterial meningitis, viral meningitis, or encephalitis by two-site enzyme immunoassay. Elevated cerebrospinal fluid levels of neurotrophin-3 were demonstrated in 8 of 18 patients with bacterial meningitis. Follow-up examination of the eight patients at the convalescent stage showed diminished cerebrospinal fluid levels of neurotrophin-3. In contrast, none of the 17 patients with viral meningitis or encephalitis showed an elevation of neurotrophin-3 levels in cerebrospinal fluid. No relationships were observed between neurotrophin-3 levels and cerebrospinal fluid cell numbers, cerebrospinal fluid protein levels, serum C-reactive protein concentrations, or outcome in bacterial meningitis. Since neurotrophin-3 is involved in the survival of neurons and the modulation of the immune system, neurotrophin-3 could play a neuroprotective or immunomodulatory role in bacterial meningitis.     

Effects of Repeated Administration of Pilocarpine and Isoproterenol on Aquaporin-5 Expression in Rat Salivary Glands

Aquaporins are water channel proteins which enable rapid water movement across the plasma membrane. Aquaporin-5 (AQP5) is the major aquaporin and is expressed on the apical membrane of salivary gland acinar cells. We examined the effects of repeated administration of pilocarpine, a clinically useful stimulant for salivary fluid secretion, and isoproterenol (IPR), a stimulant for salivary protein secretion, on the abundance of AQP5 protein in rat salivary glands by immunofluorescence microscopy and semi-quantitative immunoblotting. Unexpectedly AQP5 was decreased in pilocarpine-administered salivary glands, in which fluid secretion must be highly stimulated, implying that AQP5 might not be required for fluid secretion at least in pilocarpine-administered state. The abundance of AQP5, on the other hand, was found to be significantly increased in IPR-administered submandibular and parotid glands. To address the possible mechanism of the elevation of AQP5 abundance in IPR-administered animals, changes of AQP5 level in fasting animals, in which the exocytotic events are reduced, were examined. AQP5 was found to be decreased in fasting animals as expected. These results suggested that the elevation of cAMP and/or frequent exocytotic events could increase AQP5 protein. AQP5 expression seems to be easily changed by salivary stimulants, although these changes do not always reflect the ability in salivary fluid secretion.     

Time course of endothelial dysfunction and myocardial injury during myocardial ischemia and reperfusion in the cat

Myocardial ischemia and reperfusion have been shown to impair coronary vasorelaxation to endothelium-dependent vasodilators. To examine the time course of this dysfunction, occlusion of the left anterior descending (LAD) coronary artery (90 minutes) was followed by reperfusion for 0, 2.5, 5, 20, 180, or 270 minutes. Coronary arterial rings from the ischemic LAD and control left circumflex (LCx) arteries were tested for responsiveness to the endothelium-dependent receptor-mediated vasodilator, acetylcholine (ACh), and the endothelium-dependent nonreceptor-mediated vasodilator, A23187, as well as the endothelium-independent vasodilator, NaNO2. ACh relaxation was not impaired after 90 minutes of ischemia without reperfusion. However, 2.5 minutes of reperfusion resulted in depressed ACh responses (36 +/- 10% of control) that was further reduced to 16 +/- 6% at 20 minutes, and remained comparably depressed at every time thereafter. A23187 vasodilator responses were also attenuated after reperfusion, although the reduced response occurred later (that is, at 20 minutes). There was no significant decrease in response to NaNO2 in the LAD at any time or to any vasodilator in LCx control rings. Treatment with recombinant human superoxide dismutase (hSOD, 5 mg/kg/hr, that is, 15,545 SOD units/kg/hr), starting 10 minutes before reperfusion, preserved the vasodilator response to ACh (82 +/- 6%) and A23187, but treatment with the hydroxyl ion scavenger N-(2-mercapto proprionyl)-glycine (MPG) (8 mg/kg/hr) only protected the A23187 response. No damage to the surface of the endothelium was observed by scanning electron microscopy at any time point. Myocardial cell damage increased with time of reperfusion as assessed by increasing plasma CK activities and amounts of necrotic tissue indexed to area at risk. Significant myocardial injury occurred at 3 hours after reperfusion. These findings suggest that endothelial dysfunction resulting in reduced endothelium-derived relaxing factor release occurs before the development of myocardial cell necrosis and may be due to oxygen-derived free radicals produced rapidly on reperfusion.