Total Carbon Dioxide (TCO2) Concentrations in Thoroughbred and Quarter Racehorses in Louisiana.

The TCO2 (total carbon dioxide) test is performed on the blood of racehorses as a means of combatting the practice of administering alkalizing agents. This study evaluated serum TCO2 concentrations and factors influencing concentration of TCO2 in Thoroughbred and Quarter Horses. The normality of data were evaluated with a Shapiro-Wilk test. Mann-Whitney tests and Kruskal-Wallis tests were used against different effects. When a fixed effect was detected, Dunn's post-hoc comparisons were performed. The median pre-race serum TCO2 concentration (32.20 mmol/L (interquartile range (IQR): 30.80-33.50)) was higher than that of post-race samples (26.70 mmol/L (IQR: 24.55-29.25)) (P < .0001). The median TCO2 concentrations in pre-race samples were different between Thoroughbred (32.40 mmol/L (IQR: 30.90-33.60)) and Quarter Horses (31.30 mmol/L (IQR: 30.00-32.50)) (P < .0001). The median pre-race TCO2 concentrations were 32.75 (IQR: 31.40-33.90), 31.40 (IQR: 29.80-32.80), 32.50 (IQR: 31.20-33.88), and 31.60 (IQR 30.00-32.70) mmol/L in racehorses at Fair Grounds, Louisiana Downs, Delta Downs, and Evangeline Downs racetracks, respectively (P < .0001). The total serum TCO2 concentrations in Thoroughbred and Quarter Horse racehorses were affected by seasonal temperature variation (P < .0001). A smaller sample size was available for post-race samples (n = 205) and Quarter Horse pre-race samples (n = 351). The results of this study indicated that the breed, seasonal temperature variation, pre-race or post-race sampling, and track location are strongly correlated to total TCO2 concentrations. It was not clear whether the statistically significant differences in TCO2 levels among racetracks in Louisiana were due to location of racetracks and/or seasonal temperature variation.

Right to health: Pediatric nurses' views on the hospitalized child.

OBJECTIVES: This study aimed (a) to determine the views of pediatric nurses regarding their roles and responsibilities in the implementation of child rights in healthcare services and children's right to participate in implementations related to their treatment and care, and (b) to examine the relation between these views and sociodemographic features. METHOD: This cross-sectional study included 335 pediatric nurses recruited in public hospitals in a province located in the Eastern Black Sea Region of Turkey. The data were collected using a digital questionnaire that included variables to determine the sociodemographic features of the participants and their views on the implementation of child rights in healthcare services and children's right to participate in decision-making about their health and care. The final number of the participants in this study was 321 nurses (96% of the population). RESULTS: Most of the participants stated that they agreed with the implementation of child rights in healthcare services adopted by UNICEF. However, the participants' views on the implementation of child rights in healthcare services were affected by variables such as age, gender, marital status, level of education, the state of having children, and the number of years in the profession. Overall, 87.9% of the participants stated that children had the right to participate in the decision-making about their own health and care at an early age. the variables of marital status, educational level, the state of having children, and number of years in the profession affected the participants' views about children's right to actively participate in their health care. CONCLUSION: The majority of pediatric nurses agreed with the implementation of child rights in healthcare services. Moreover, the variables of age, gender, marital status, educational level, the state of having children, and the number of years in the profession were significantly relevant to the views of pediatric nurses regarding child rights.

Reference Intervals of Thyroid Function Tests in First Trimester Vietnamese Pregnant Women.

BACKGROUND: Although TSH suppression by elevated ß-hCG is essentially seen during first trimester, differences in TSH reference ranges between various countries have been reported. Physiologic changes during pregnancy may also influence FT4 assays. This study aims to establish method-specific reference intervals (RIs) of TSH, FT4, and FT3 in Vietnamese, first trimester pregnant women. METHODS: This cross-sectional study was conducted at My Duc Hospital, Ho Chi Minh, Vietnam. Women with singleton pregnancies in the first trimester and conceived naturally were included. Those with a history of thyroid disease, positive thyroid-specific autoantibodies, diffuse goiter or one thyroid nodule > 10 mm in size or ≥ 2 nodules detected by ultrasound, and taking medications affecting thyroid function were excluded. Serum TSH, FT4, and FT3 were measured by chemiluminescent detection technology on the Access 2 Immunoassay System (Beckman Coulter, Inc., USA). Intra- and interassay coefficients of variations (CV) were 3.6% and 4.4% for TSH, 5.4% and 6.1% for FT4, 6.6%, and 6.0% for FT3, respectively. The 2.5th and 97.5th percentiles were used to determine RIs. RESULTS: Between August 1, 2017, to December 1, 2018, there were 876 pregnant women who fulfilled inclusion and exclusion criteria. They had a mean age of 30.1 years, an average BMI of 21.3 kg/m2, and 77.3% of them were primigravida. The RIs for TSH, FT4 and FT3 were 0.17 - 2.35 mIU/L, 0.67 - 1.11 ng/dL and 2.82 - 3.90 pg/mL, respectively. CONCLUSIONS: Established RIs for TSH, FT4, and FT3 in Vietnamese women would help to reduce the misdiagnosis of gestational thyroid disorders.

Trends in CD4 and viral load testing 2005 to 2018: multi-cohort study of people living with HIV in Southern Africa.

INTRODUCTION: The World Health Organization (WHO) recommends a CD4 cell count before starting antiretroviral therapy (ART) to detect advanced HIV disease, and routine viral load (VL) testing following ART initiation to detect treatment failure. Donor support for CD4 testing has declined to prioritize access to VL monitoring. We examined trends in CD4 and VL testing among adults (≥15 years of age) starting ART in Southern Africa. METHODS: We analysed data from 14 HIV treatment programmes in Lesotho, Malawi, Mozambique, South Africa, Zambia and Zimbabwe in 2005 to 2018. We examined the frequency of CD4 and VL testing, the percentage of adults with CD4 or VL tests, and among those having a test, the percentage starting ART with advanced HIV disease (CD4 count <200 cells/mm3 ) or failing to suppress viral replication (>1000 HIV-RNA copies/mL) after ART initiation. We used mixed effect logistic regression to assess time trends adjusted for age and sex. RESULTS: Among 502,456 adults, the percentage with CD4 testing at ART initiation decreased from a high of 78.1% in 2008 to a low of 38.0% in 2017; the probability declined by 14% each year (odds ratio (OR) 0.86; 95% CI 0.86 to 0.86). Frequency of CD4 testing also declined. The percentage starting ART with advanced HIV disease declined from 83.3% in 2005 to 23.5% in 2018; each year the probability declined by 20% (OR 0.80; 95% CI 0.80 to 0.81). VL testing after starting ART varied; 61.0% of adults in South Africa and 10.7% in Malawi were tested, but fewer than 2% were tested in the other four countries. The probability of VL testing after ART start increased only modestly each year (OR 1.06; 95% CI 1.05 to 1.06). The percentage with unsuppressed VL was 8.6%. There was no evidence of a decrease in unsuppressed VL over time (OR 1.00; 95% CI 0.99 to 1.01). CONCLUSIONS: CD4 cell counting declined over time, including testing at the start of ART, despite the fact that many patients still initiated ART with advanced HIV disease. Without CD4 testing and expanded VL testing many patients with advanced HIV disease and treatment failure may go undetected, threatening the effectiveness of ART in sub-Saharan Africa.

Effectiveness of cervical pessary compared to cervical cerclage with or without vaginal progesterone for the prevention of preterm birth in women with twin pregnancies and a short cervix: study protocol for a two-by-two factorial randomised clinical trial.

INTRODUCTION: Women with twin pregnancies and a short cervix are at increased risk for preterm birth (PTB). Given the burden of prematurity and its attendant risks, the quest for effective interventions in twins has been an area of considerable research. Studies investigating the effectiveness of cervical cerclage, cervical pessary and vaginal progesterone in preventing PTB have yielded conflicting results. The aim of this study is to compare the effectiveness of cervical pessary and cervical cerclage with or without vaginal progesterone to prevent PTB in women with twin pregnancies and a cervical length (CL) ≤ 28 mm. METHODS AND ANALYSIS: This multicentre, randomised clinical trial will be conducted at My Duc Hospital and My Duc Phu Nhuan Hospital, Vietnam. Asymptomatic women with twin pregnancies and a CL ≤28 mm, measured at 16-22 weeks' gestation, will be randomised in a 1:1:1:1 ratio to receive a cerclage, pessary, cerclage plus progesterone or pessary plus progesterone. Primary outcome will be PTB <34 weeks. Secondary outcomes will be maternal and neonatal complications. We preplanned a subgroup analysis according to CL from all women after randomisation and divided into four quartiles. Analysis will be conducted on an intention-to-treat basis. The rate of PTB <34 weeks' gestation in women with twin pregnancies and a cervix ≤28 mm and treated with pessary in our previous study at My Duc Hospital was 24.2%. A sample size of 340 women will be required to show or refute that cervical cerclage decreases the rate of PTB <34 weeks by 50% compared with pessary (from 24.2% to 12.1%, α level 0.05, power 80%, 5% lost to follow-up and protocol deviation). This study is not to be powered to assess interactions between interventions. ETHICS AND DISSEMINATION: Ethical approval was obtained from the Institutional Ethics Committee of My Duc Hospital and informed patient consent was obtained before study enrolment. Results of the study will be submitted for publication in a peer-reviewed journal. TRIAL REGISTRATION NUMBER: NCT03863613 (date of registration: 4 March 2019).

Pessary Compared With Vaginal Progesterone for the Prevention of Preterm Birth in Women With Twin Pregnancies and Cervical Length Less Than 38 mm: A Randomized Controlled Trial.

OBJECTIVE: To compare the effectiveness of cervical pessary to vaginal progesterone for the prevention of preterm birth in women with twin pregnancies and short cervix. METHODS: This randomized controlled trial was conducted at My Duc Hospital, Vietnam. Asymptomatic women with twin pregnancies and cervical length less than 38 mm were randomized to Arabin pessary or vaginal progesterone (400 mg once a day) group. The primary outcome was preterm birth at less than 34 weeks of gestation. Secondary outcomes were adverse maternal and perinatal complications. We planned a subgroup analysis according to quartile of cervical length. Analysis was conducted on an intention-to-treat basis. We estimated that the primary outcome would occur in 28.4% of women treated with progesterone. Thus a total sample size of 290 women divided equally into two groups was required to detect a 14% absolute risk difference in the primary outcome between the two groups (power 80%, alpha-error 5%, 10% loss to follow-up). RESULTS: Between March 2016 and June 2017, we randomized 300 women, 150 women in each group. Preterm birth at less than 34 weeks of gestation occurred in 24 (16%) women in the pessary group and 33 (22%) women in the progesterone group (relative risk [RR] 0.73, 95% CI 0.46-1.18). The use of pessary significantly reduced the composite of poor perinatal outcomes (19% vs 27%; RR 0.70, 95% CI 0.43-0.93). In women with cervical length of 28 mm or less (25th percentile), pessary significantly reduced the preterm birth rate at less than 34 weeks of gestation from 46% (16/35) to 21% (10/47) (RR 0.47, 95% CI 0.24-0.90) and significantly improved the composite of poor perinatal outcomes. CONCLUSION: Cervical pessary and 400 mg vaginal progesterone resulted in similar rates of preterm birth at less than 34 weeks of gestation in women with twin pregnancies and cervical length less than 38 mm. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov, NCT02623881.

CaMKII and at least two unidentified kinases phosphorylate regulatory light chain in non-contracting cardiomyocytes.

In cardiac tissue, regulatory light chain (RLC, myosin light chain 2) phosphorylation (Ser(15)) leads to modulation of muscle contraction through Ca(2+)-sensitization. To elucidate which kinases that are involved in the basal (diastolic phase) RLC phosphorylation, we studied non-contracting adult rat cardiomyocytes. RLC kinase activities in situ were unmasked by maximally inhibiting myosin light chain phosphatase (MLCP) by calyculin A in the absence and presence of various protein kinase inhibitors. Surprisingly MLCK did not contribute to the phosphorylation of RLC in the non-contracting cardiomyocytes. Two kinase activity groups were revealed by different sensitivities to staurosporine. The fraction with the highest sensitivity to staurosporine was inhibited by KN-93, a selective CaMKII inhibitor, producing a 23% ± 7% reduction in RLC phosphorylation. Calmodulin antagonism (W7) and reduction in Ca(2+) (EGTA) combined with low concentration of staurosporine caused a larger decrease in RLC phosphorylation than staurosporine alone. These data strongly suggest that in addition to CaMKII, there is another Ca(2+)/calmodulin-dependent kinase and a Ca(2+)/calmodulin-independent kinase phosphorylating RLC. Thus the RLC phosphorylation seems to be ensured by redundant kinase activities.

CaMKII in addition to MLCK contributes to phosphorylation of regulatory light chain in cardiomyocytes.

The aim was to identify kinase activities involved in the phosphorylation of regulatory light chain (RLC) in situ in cardiomyocytes. In electrically stimulated rat cardiomyocytes, phosphatase inhibition by calyculin A unmasked kinase activities evoking an increase of phosphorylated RLC (P-RLC) from about 16% to about 80% after 80 min. The phosphorylation rate in cardiomyocytes was reduced by about 40% by the myosin light chain kinase (MLCK) inhibitor, ML-7. In rat ventricular muscle strips, calyculin A induced a positive inotropic effect that correlated with P-RLC levels. The inotropic effect and P-RLC elevation were abolished by ML-7 treatment. The kinase activities phosphorylating RLC in cardiomyocytes were reduced by about 60% by the non-selective kinase inhibitor staurosporine and by about 50% by the calmodulin antagonist W7. W7 eliminated the inhibitory effect of ML-7, suggesting that the cardiac MLCK is Ca(2+)/calmodulin (CaM)-dependent. The CaM-dependent kinase II (CaMKII) inhibitor KN-93 attenuated the calyculin A-induced RLC phosphorylation by about 40%, indicating a contribution from CaMKII. The residual phosphorylation in the presence of W7 indicated that also CaM-independent kinase activities might contribute. RLC phosphorylation was insensitive to protein kinase C inhibition. In conclusion, in addition to MLCK, CaMKII phosphorylates RLC in cardiomyocytes. Involvement of other kinases cannot be excluded.

Synthesis and pharmacological properties of a new hydrophilic and orally bioavailable 5-HT4 antagonist.

5-HT4 receptor antagonists have been suggested to have clinical potential in treatment of atrial fibrillation, diarrhea-prone irritable bowel syndrome and urinary incontinence. Recently, the use of 5-HT4 antagonists has been suggested to have a therapeutic benefit in heart failure. Affinity for the hERG potassium ion channel and increased risk for prolonged QT intervals and arrhythmias has been observed for several 5-HT4 ligands. Serotonin may also have beneficial effects in the central nervous system (CNS) through stimulation of the 5-HT4 receptor, and reduced distribution of 5-HT4 antagonists to the CNS may therefore be an advantage. Replacing the amide and N-butyl side chain of the 5-HT4 receptor antagonist SB207266 with an ester and a benzyl dimethyl acetic acid group led to compound 9; a hydrophilic 5-HT4 antagonist with excellent receptor binding and low affinity for the hERG potassium ion channel. To increase oral bioavailability of carboxylic acid 9, two different prodrug approaches were applied. The tert-butyl prodrug 11 did not improve bioavailability, and LC-MS analysis revealed unmetabolized prodrug in the systemic circulation. The medoxomil ester prodrug 10 showed complete conversion and sufficient bioavailability of 9 to advance into further preclinical testing for treatment of heart failure.

Role of microprojections in myoendothelial feedback--a theoretical study.

We investigated the role of myoendothelial projections (MPs) in endothelial cell (EC) feedback response to smooth muscle cell (SMC) stimulation using mathematical modelling. A previously developed compartmental EC-SMC model is modified to include MPs as subcellular compartments in the EC. The model is further extended into a 2D continuum model using a finite element method (FEM) approach and electron microscopy images to account for MP geometry. The EC and SMC are coupled via non-selective myoendothelial gap junctions (MEGJs) which are located on MPs and allow exchange of Ca(2+), K(+), Na(+) and Cl(-) ions and inositol 1,4,5-triphosphate (IP3). Models take into consideration recent evidence for co-localization of intermediate-conductance calcium-activated potassium channels (IKCa) and IP3 receptors (IP3Rs) in the MPs. SMC stimulation causes an IP3-mediated Ca(2+) transient in the MPs with limited global spread in the bulk EC. A hyperpolarizing feedback generated by the localized IKCa channels is transmitted to the SMC via MEGJs. MEGJ resistance (Rgj) and the density of IKCa and IP3R in the projection influence the extent of EC response to SMC stimulation. The predicted Ca(2+) transients depend also on the volume and geometry of the MP. We conclude that in the myoendothelial feedback response to SMC stimulation, MPs are required to amplify the SMC initiated signal. Simulations suggest that the signal is mediated by IP3 rather than Ca(2+) diffusion and that a localized rather than a global EC Ca(2+) mobilization is more likely following SMC stimulation.

Could platelet indices be new biomarkers for inflammatory bowel diseases?

BACKGROUND AND AIM: Ulcerative colitis (UC) and Crohn's disease (CD) are chronic inflammatory diseases. Many serum biomarkers have been studied for diagnosis and monitoring of disease activity in inflammatory bowel diseases (IBD). Platelets play an important role in inflammation. The aim of the present study is to determine whether platelet indices; mean platelet volume (MPV), platelet distribution width (PDW) and platelet-crit (PCT) would be useful, cheap, non-invasive biomarkers for following up and determining severity of IBD. MATERIALS AND METHODS: The study group consisted of 175 patients with IBD (UC n: 103 and CD n: 72) and the control group included 40 healthy subjects. Disease activity was evaluated both by endoscope and clinically. Platelet indices and inflammatory parameters were measured for all study participants. Patients were checked in both active and remission phase of the diseases. RESULTS: In patients with active UC and CD, there was a statistically significant decrease in MPV, PDW levels and increase in PCT levels when compared to healthy controls. In remission phase of IBD while MPV levels were lower, PDW and PCT levels were higher than control group. Both PDW (r: -0.271 p: 0.032) and PCT (r: 0.295 p: 0.027) had a significant correlation with UC disease activity. There was statistically significant change in all platelet indices during diseases follow-up. CONCLUSIONS: The present report revealed that changes of platelet indices in IBD are noteworthy. They can be added to other inflammatory markers especially to monitor disease from active phase to remission phase.

Prostanoid-mediated inotropic responses are attenuated in failing human and rat ventricular myocardium.

Prostanoid-modulatory approaches in heart failure patients have displayed effects which may seem to be mutually incompatible. Both treatment with prostanoids and inhibition of prostanoid synthesis have resulted in increased mortality in heart failure patients. Currently, it is unknown if prostanoids mediate contractile effects in failing human heart and if this can explain some of the clinical effects seen after prostanoid modulatory treatments. Therefore, the objectives of this study were to determine if prostanoids could elicit direct inotropic responses in human ventricle, and if so to determine if they are modified in failing ventricle. Contractile force was measured in left ventricular strips from non-failing or failing human and rat hearts. The ratio of phosphorylated to non-phosphorylated myosin light chain 2 (MLC-2) was measured by Western blotting in myocardial strips, and the levels of prostanoid FP receptor mRNA and protein were measured in rat by real-time RT-PCR and receptor binding assays. In non-failing human hearts, prostanoids evoked a positive inotropic effect and an increase of MLC-2 phosphorylation which was absent in failing human hearts. In failing rat heart, the prostanoid FP receptor-mediated inotropic response and prostanoid FP receptor-density was reduced by ~40-50% compared to non-failing rat heart. Prostanoids mediate a sustained positive inotropic response in non-failing heart, which appears to be down regulated in failing heart. The pathophysiological significance of changes in prostanoid-mediated inotropic support in the failing heart remains to be determined.

Natriuretic peptides increase beta1-adrenoceptor signalling in failing hearts through phosphodiesterase 3 inhibition.

AIMS: Whereas natriuretic peptides increase cGMP levels with beneficial cardiovascular effects through protein kinase G, we found an unexpected cardio-excitatory effect of C-type natriuretic peptide (CNP) through natriuretic peptide receptor B (NPR-B) stimulation in failing cardiac muscle and explored the mechanism. METHODS AND RESULTS: Heart failure was induced in male Wistar rats by coronary artery ligation. Contraction studies were performed in left ventricular muscle strips. Cyclic nucleotides were measured by radio- and enzyme immunoassay. Apoptosis was determined in isolated cardiomyocytes by Annexin-V/propidium iodide staining and phosphorylation of phospholamban (PLB) and troponin I was measured by western blotting. Stimulation of NPR-B enhanced beta1-adrenoceptor (beta1-AR)-evoked contractile responses through cGMP-mediated inhibition of phosphodiesterase 3 (PDE3). CNP enhanced beta1-AR-mediated increase of cAMP levels to the same extent as the selective PDE3 inhibitor cilostamide and increased beta1-AR-stimulated protein kinase A activity, as demonstrated by increased PLB and troponin I phosphorylation. CNP promoted cardiomyocyte apoptosis similar to inhibition of PDE3 by cilostamide, indicative of adverse effects of NPR-B signalling in failing hearts. CONCLUSION: An NPR-B-cGMP-PDE3 inhibitory pathway enhances beta(1)-AR-mediated responses and may in the long term be detrimental to the failing heart through mechanisms similar to those operating during treatment with PDE3 inhibitors or during chronic beta-adrenergic stimulation.

Caffeic acid phenethyl ester modulates methotrexate-induced oxidative stress in testes of rat.

The aim of this study was to investigate the possible protective role of caffeic acid phenethyl ester on testicular toxicity of methotrexate in rats. Nineteen male rats were divided into three groups as follows: group I, control; group II, methotrexate-treated; group III, methotrexate + caffeic acid phenethyl ester-treated. In the second day of experiment, a single dose of methotrexate was intraperitoneally administered to groups II and III, although a daily single dose of caffeic acid phenethyl ester was intraperitoneally administered to group III for 7 days. At the end of the experiment, the testes of the animals were removed and weighed. In the tissue, the level of lipid peroxidation as malondialdehyde and activities of superoxide dismutase were higher in the methotrexate group than in the control group. Lipid peroxidation levels and superoxide dismutase activities were decreased in caffeic acid phenethyl ester + methotrexate group compared with methotrexate group. The activities of catalase in the methotrexate group decreased insignificantly although its activities were significantly increased by caffeic acid phenethyl ester administration. The activity of glutathione peroxidase did not change in the groups. There was significant difference in body weight between control and methotrexate-induced groups. In conclusion, the administration of methotrexate causes elevation of oxidative stress although treatment with caffeic acid phenethyl ester has protective effects on the oxidative stress in testes.

Prostanoid F receptors elicit an inotropic effect in rat left ventricle by enhancing myosin light chain phosphorylation.

AIMS: The aims of this study were to determine if the prostanoid F receptor (FPR)-mediated inotropic effect in rat ventricle is mediated by increased phosphorylation of myosin light chain-2 (MLC-2) and to elucidate the signalling pathway(s) activated by FPRs to regulate MLC-2 phosphorylation. METHODS AND RESULTS: Contractility was measured in left ventricular strips from adult male rats. Strips were also snap-frozen, and changes in the phosphorylation level of both MLC-2 and myosin phosphatase targeting subunit-2 (MYPT-2) were quantified. FPR stimulation with fluprostenol increased contractility by approximately 100% above basal and increased phosphorylation of both MLC-2 (by approximately 30%) and MYPT-2 (by approximately 50%). The FPR-mediated inotropic effect and MLC-2 phosphorylation were reduced by a similar magnitude in the presence of the myosin light chain kinase (MLCK) inhibitor ML-7 (approximately 60-70%) and an inhibitor of Ca(2+)/calmodulin, W-7 (approximately 35%). Inhibition of Rho-associated kinase by Y-27632 reduced the FPR-mediated inotropic effect and MLC-2 phosphorylation by approximately 40-45% and MYPT-2 phosphorylation by approximately 70%. ML-7 and Y-27632 together reduced contractility and MLC-2 phosphorylation by approximately 70-80%. The FPR-mediated inotropic effect was only modestly affected by high concentrations of the inositol tris-phosphate (IP(3)) receptor blocker 2-APB, but not by the protein kinase C (PKC) inhibitor bisindolylmaleimide. CONCLUSION: The FPR-evoked inotropic effect is mediated by increasing the phosphorylation of MLC-2 through regulation of both MLCK and myosin light chain phosphatase activities. The second messenger IP(3) and PKC are unlikely to be involved in the signalling cascade of the FPR-mediated positive inotropic effect. Therefore, FPR signalling mechanism(s) regulating MLC-2 phosphorylation likely extend beyond those classically established for G(q/11)-coupled receptors.

Real-time and secure wireless health monitoring.

We present a framework for a wireless health monitoring system using wireless networks such as ZigBee. Vital signals are collected and processed using a 3-tiered architecture. The first stage is the mobile device carried on the body that runs a number of wired and wireless probes. This device is also designed to perform some basic processing such as the heart rate and fatal failure detection. At the second stage, further processing is performed by a local server using the raw data transmitted by the mobile device continuously. The raw data is also stored at this server. The processed data as well as the analysis results are then transmitted to the service provider center for diagnostic reviews as well as storage. The main advantages of the proposed framework are (1) the ability to detect signals wirelessly within a body sensor network (BSN), (2) low-power and reliable data transmission through ZigBee network nodes, (3) secure transmission of medical data over BSN, (4) efficient channel allocation for medical data transmission over wireless networks, and (5) optimized analysis of data using an adaptive architecture that maximizes the utility of processing and computational capacity at each platform.

Hepatitis B vaccination in children with juvenile idiopathic arthritis.

OBJECTIVES: To evaluate the responsiveness of children with juvenile idiopathic arthritis (JIA) to hepatitis B vaccination and to determine the most useful vaccination schedule. METHODS: 39 children with JIA were enrolled in the study; all were in remission and negative to serological testing for hepatitis B surface antigen (HbsAg). The control group consisted of 41 healthy children. There were two different vaccination schedules: group I was vaccinated at 0, 1, and 3 months; group II was vaccinated at 0, 1, and 6 months. Positive responsiveness to the vaccine was defined as an anti-hepatitis B antibody titre above 10 mIU/ml. RESULTS: All the children except one with systemic JIA developed an antibody response. None of the JIA patients experienced a flare up or clinical deterioration related to the vaccination. The antibody levels in children with JIA were significantly lower than in the healthy controls. Comparison of the antibody levels between the two vaccination schedules showed no statistical difference in the controls; in the JIA subjects the group II schedule resulted in a trend to a greater response than the group I schedule (p<0.07). Vaccine responsiveness was not influenced by either methotrexate or prednisolone treatment. CONCLUSIONS: Children with JIA had an adequate response to hepatitis B vaccination and the response was not affected by immunosuppressive treatment. A vaccination schedule at 0, 1, and 6 months seems to be preferable to 0, 1, and 3 months.

Congenital syphilis presenting with nephrotic syndrome and leucocytoclastic vasculitis.

Nephrotic syndrome is a well-recognized entity in congenital syphilis but leucocytoclastic vasculitis has not yet been described. We report a case of nephrotic syndrome and leucocytoclastic vasculitis associated with congenital syphilis in a 45-day-old male infant who did well after treatment with intravenous penicillin.