bluuebunny/crossref_metadata_2025_split huggingface dataset:
Household catastrophic health expenditure: evidence from Georgia and its policy implications
Authors: Gotsadze George , Zoidze Akaki , Rukhadze Natia 
Published: June 2009

Abstract

Background
To quantify extent of catastrophic household health expenditures, determine factors influencing it and estimate Fairness in Financial Contribution (FFC) index in Georgia to establish the baseline for expected reforms and contribute to the design and fine-tuning of the major reforms in health care financing initiated by the government mid-2007.

Methods
The research is based on the nationally representative Health Care Utilization and Expenditure survey conducted during May-June 2007, prior to preparing for new phase of implementation for the health care financing reforms. Households' catastrophic health expenditures were estimated according to the methodology proposed by WHO – Ke Xu [1]. A logistic regression (logit) model was used to predict probability of catastrophic health expenditure occurrence.

Results
In Georgia between 2000 and 2007 access to care for poor has improved slightly and the share of households facing catastrophic health expenditures have seemingly increased from 2.8% in 1999 to 11.7% in 2007. However, this variance may be associated with the methodological differences of the respective surveys from which the analysis were derived. The high level of the catastrophic health expenditure may be associated with the low share of prepayment in national health expenditure, adequate availability of services and a high level of poverty in the country. Major factors determining the financial catastrophe related to ill health were hospitalization, household members with chronic illness and poverty status of the household. The FFC for Georgia appears to have improved since 2004.

Conclusion
Reducing the prevalence of catastrophic health expenditure is a policy objective of the government, which can be achieved by focusing on increased financial protection offered to poor and expanding government financed benefits for poor and chronically ill by including and expanding inpatient coverage and adding drug benefits. This policy recommendation may also be relevant for other Low and Middle Income countries with similar levels of out of pocket payments and catastrophic health expenditures.
Molecular cloning and expression of a novel trehalose synthase gene from Enterobacter hormaechei
Authors: Yue Ming , Wu Xiu Li , Gong Wei Na , Ding Hong Biao 
Published: June 2009

Abstract

Background
Trehalose synthase (TreS) which converts maltose to trehalose is considered to be a potential biocatalyst for trehalose production. This enzymatic process has the advantage of simple reaction and employs an inexpensive substrate. Therefore, new TreS producing bacteria with suitable enzyme properties are expected to be isolated from extreme environment.

Results
Six TreS producing strains were isolated from a specimen obtained from soil of the Tibetan Plateau using degenerate PCR. A novel treS gene from Enterobacter hormaechei was amplified using thermal asymmetric interlaced PCR. The gene contained a 1626 bp open reading frame encoding 541 amino acids. The gene was expressed in Escherichia coli, and the recombinant TreS was purified and characterized. The purified TreS had a molecular mass of 65 kDa and an activity of 18.5 U/mg. The optimum temperature and pH for the converting reaction were 37°C and 6, respectively. Hg2+, Zn2+, Cu2+and SDS inhibited the enzyme activity at different levels whereas Mn2+ showed an enhancing effect by 10%.

Conclusion
In this study, several TreS producing strains were screened from a source of soil bacteria. The characterization of the recombinant TreS of Enterobacter hormaechei suggested its potential application. Consequently, a strategy for isolation of TreS producing strains and cloning of novel treS genes from natural sources was demonstrated.
Evaluation of the SD FK70 Malaria Ag Plasmodium vivax rapid diagnostic test in a non-endemic setting
Authors: Gillet Philippe , Bosselaers Katrien , Cnops Lieselotte , Bottieau Emmanuel , Van Esbroeck Marjan , Jacobs Jan 
Published: June 2009

Abstract

Background
For clinical and epidemiological reasons, it is interesting to diagnose non-falciparum malaria to the species level. This retrospective study assessed the performance of the SD BIOLINE Malaria Antigen Pv test (FK70), a two-band immunochromatographic test detecting Plasmodium vivax-specific lactate dehydrogenase, on samples of international travellers in a non-endemic setting.

Methods
Stored blood samples from international travellers suspected of malaria were used, with microscopy corrected by PCR as the reference method. Samples infected by Plasmodium vivax (n = 100), Plasmodium falciparum (n = 75), Plasmodium ovale (n = 75) and Plasmodium malariae (n = 25) were included, as well as 100 malaria-negative samples. End points were sensitivity, specificity, inter-reader reliability and reproducibility.

Results
The overall sensitivity of the FK70 for the diagnosis of P. vivax was 88.0% (95% confidence interval (CI): 83.6% – 90.3%). For parasite densities > 500/μl, a sensitivity of 97.2% (CI: 92.6% – 99.1%) was obtained. Specificity was 98.5%, with 4 out of 75 P. falciparum samples testing positive. None of the P. ovale samples tested positive. Nearly two-thirds (57/88, 64.7%) of positive P. vivax samples showed faint or weak line intensities, with stronger line intensities at higher parasite densities. The test showed excellent reproducibility and reliability for test results and line intensities (kappa values exceeding 0.98 and 0.87 respectively).

Conclusion
The FK70 test performed well in diagnosing P. vivax infections in a non-endemic reference setting. It can be of added value to microscopy in species differentiation of malaria infections, especially at parasite densities > 500/μl.
Spatial and temporal distribution of falciparum malaria in China
Authors: Lin Hualiang , Lu Liang , Tian Linwei , Zhou Shuisen , Wu Haixia , Bi Yan , Ho Suzanne C , Liu Qiyong 
Published: June 2009

Abstract

Background
Falciparum malaria is the most deadly among the four main types of human malaria. Although great success has been achieved since the launch of the National Malaria Control Programme in 1955, malaria remains a serious public health problem in China. This paper aimed to analyse the geographic distribution, demographic patterns and time trends of falciparum malaria in China.

Methods
The annual numbers of falciparum malaria cases during 1992–2003 and the individual case reports of each clinical falciparum malaria during 2004–2005 were extracted from communicable disease information systems in China Center for Diseases Control and Prevention. The annual number of cases and the annual incidence were mapped by matching them to corresponding province- and county-level administrative units in a geographic information system. The distribution of falciparum malaria by age, gender and origin of infection was analysed. Time-series analysis was conducted to investigate the relationship between the falciparum malaria in the endemic provinces and the imported falciparum malaria in non-endemic provinces.

Results
Falciparum malaria was endemic in two provinces of China during 2004–05. Imported malaria was reported in 26 non-endemic provinces. Annual incidence of falciparum malaria was mapped at county level in the two endemic provinces of China: Yunnan and Hainan. The sex ratio (male vs. female) for the number of cases in Yunnan was 1.6 in the children of 0–15 years and it reached 5.7 in the adults over 15 years of age. The number of malaria cases in Yunnan was positively correlated with the imported malaria of concurrent months in the non-endemic provinces.

Conclusion
The endemic area of falciparum malaria in China has remained restricted to two provinces, Yunnan and Hainan. Stable transmission occurs in the bordering region of Yunnan and the hilly-forested south of Hainan. The age and gender distribution in the endemic area is characterized by the predominance of adult men cases. Imported falciparum malaria in the non-endemic area of China, affected mainly by the malaria transmission in Yunnan, has increased both spatially and temporally. Specific intervention measures targeted at the mobile population groups are warranted.
Cadmium induces lung inflammation independent of lung cell proliferation: a molecular approach
Authors: Kundu Subhadip , Sengupta Suman , Chatterjee Soumya , Mitra Soham , Bhattacharyya Arindam 
Published: June 2009

Abstract

Background
Cadmium is one of the inflammation-related xenobiotics and has been regarded as a potent carcinogen. The relationship between inflammation and cell proliferation due to chronic infection has been studied, but the mechanism is not fully clear. Though the mode of cadmium toxicity is well characterized in animal cells, still it requires some further investigations. Previously we reported that cadmium induces immune cell death in Swiss albino mice. In the present study we showed that instead of inducing cell death mechanism, cadmium in low concentration triggers proliferation in mice lung cell and our results reveals that prior to the induction of proliferation it causes severe inflammation.

Methods
Swiss albino mice were treated with different concentrations of cadmium to determine the LD50. Mice were subdivided (5 mice each) according to the exposure period (15, 30, 45, 60 days) and were given sub lethal dose (5 mg/Kg body weight) of cadmium chloride and ibuprofen (50 mg/Kg body weight, recommended dose) once in a week. SEM and histology were performed as evidence of changes in cellular morphology. Inflammation was measured by the expression of Cox-2 and MMPs. Expression of proinflammatory cytokines (Cox-2, IL-6), signaling and cell cycle regulatory molecules (STAT3, Akt, CyclinD1) were measured by western blot, ELISA and immunoprecipitation. Mutagenecity was evidenced by comet assay. Cell proliferation was determined by cell count, cell cycle and DNA analysis.

Results
Prolonged exposure of low concentration of cadmium resulted in up regulation of proinflammatory cytokines and cell cycle regulatory molecules. Though NSAIDs like Ibuprofen reduces the expression of inflammatory cytokines, but it did not show any inhibitory effect on cadmium adopted lung cell proliferation.

Conclusion
Our results prove that cadmium causes both inflammation and cell proliferation when applied in a low dose but proliferative changes occur independent of inflammation.
An In Vivo Mouse Model of Long-Term Potentiation at Synapses between Primary Afferent C-Fibers and Spinal Dorsal Horn Neurons: Essential Role of Ephb1 Receptor
Authors: Liu Wen-Tao , Han Yuan , Li Hao-Chuan , Adams Brandt , Zheng Ji-Hong , Wu Yong-Ping , Henkemeyer Mark , Song Xue-Jun 
Published: June 2009

Background Long-term potentiation (LTP), a much studied cellular model of synaptic plasticity, has not been demonstrated at synapses between primary afferent C-fibers and spinal dorsal horn (DH) neurons in mice in vivo. EphrinB-EphB receptor signaling plays important roles in synaptic connection and plasticity in the nervous system, but its role in spinal synaptic plasticity remains unclear. Results This study characterizes properties of LTP at synapses of C-fibers onto neurons in the superficial DH following high-frequency stimulation (HFS) of a peripheral nerve at an intensity that activates C-fibers and examines associated activation of Ca2+/calmodulin-activated protein kinase II (p-CaMKII), extracellular signal-regulated kinase (p-ERK) and the cyclic AMP response element binding protein (p-CREB) and expression of c-Fos, and it investigates further roles for the EphB1 receptor in LTP. HFS induced LTP within 5 min and lasts for 3–8 h during the period of recording and resulted in upregulation of p-CaMKII, p-ERK and p-CREB protein levels in the spinal cord and expression of c-Fos in DH. Intrathecal pretreatment of MK-801 or EphB2-Fc prevented LTP and significantly reduced upregulation of p-CaMKII, p-ERK, p-CREB and c-Fos. Further, targeted mutation of EphB1 receptor prevented induction of LTP and associated increases in phosphorylation of CaMKII, ERK, and CREB. Conclusion This study provides an in vivo mouse model of LTP at synapses of C-fibers onto the superficial DH neurons that will be valuable for studying the DH neuron excitability and their synaptic plasticity and hyperalgesia. It further takes advantage of examining functional implications of a specific gene targeted mice and demonstrates that the EphB1 receptor is essential for development of LTP.
Occurrence and adverse effect on outcome of hyperlactatemia in the critically ill
Authors: Khosravani Houman , Shahpori Reza , Stelfox H Thomas , Kirkpatrick Andrew W , Laupland Kevin B 
Published: June 2009

Abstract
Introduction
Hyperlactatemia is frequent in critically ill patients and is often used as a marker of adverse outcome. However, studies to date have focused on selected intensive care unit (ICU) populations. We sought to determine the occurrence and relation of hyperlactatemia with ICU mortality in all patients admitted to four ICUs in a large regional critical care system.

Methods
All adults ([greater than or equal to] 18 years) admitted to ICUs in the Calgary Health Region (population 1.2 million) during 2003 to 2006 were included retrospectively. Lactate determinations were at the discretion of the attending service and hyperlactatemia was defined by a lactate level > 2 mmol/L.

Results
A total of 13,932 ICU admissions occurred among 11,581 patients. The median age was 63 years (37% female), the mean APACHE II score was 25 ± 9 (n = 13,922). At presentation (within first day of admission), 12,246 patients had at least one lactate determination and the median peak lactate was 1.8 (IQR 1.2 to 2.9) mmol/L. The cumulative incidence of at least one documented episode of hyperlactatemia was 5578/13,932 (40%); 5058 (36%) patients had hyperlactatemia at presentation, and a further 520 (4%) developed hyperlactatemia subsequently. The incidence of hyperlactatemia varied significantly by major admitting diagnostic category (P < 0.001) and was highest among neuro/trauma patients 1053/2328 (45%), followed by medical 2047/4935 (41%), other surgical 900/2274 (40%), and cardiac surgical 1578/4395 (36%). Among a cohort of 9107 first admissions with ICU stay of at least one day, both hyperlactatemia at presentation (712/3634 (20%) vs. 289/5473 (5%); P < 0.001) and its later development (101/379 (27%) vs. 188/5094 (4%); P < 0.001) were associated with significantly increased case fatality rates as compared with patients without elevated lactate. After controlling for confounding effects in multivariable logistic regression analysis, hyperlactatemia was an independent risk factor for death.

Conclusions
Hyperlactatemia is common among the critically ill and predicts risk for death.
Timing of the Ovarian Circadian Clock Is Regulated by Gonadotropins
Authors: Yoshikawa Tomoko , Sellix Michael , Pezuk Pinar , Menaker Michael 
Published: June 2009

Abstract
The timing of ovulation is critically important to the success of reproduction. Current thinking attributes the timing of ovulation to LH secretion by the pituitary, itself timed by signals from the hypothalamus. The discovery of an internal circadian timer in the ovary raises the possibility that ovulation is in fact timed by an interaction between clocks in the hypothalamus/pituitary and those in the ovary. We asked whether ovarian clocks were influenced by signals from the brain and pituitary. Ovaries of Period1-luciferase transgenic rats display circadian rhythms in vitro. To determine whether the phase of these rhythms is set by neural or endocrine signals, we surgically denervated or heterotopically transplanted ovaries with or without encapsulation in dialysis membranes. Animals’ light-dark cycles were phase advanced or delayed 6 h, and the resetting of the ovarian clock was tracked by culturing ovaries at intervals over the next 12 d. Resetting trajectories of control, surgically denervated, and encapsulated ovaries were similar, demonstrating that endocrine signals are sufficient to transmit phase information to the ovary. We next evaluated LH and FSH as potential endocrine signals. Using the phase of Per1-luc expression in granulosa cell cultures, we demonstrated that both of these pituitary hormones caused large phase shifts when applied to the cultured cells. We hypothesize that the ovarian circadian clock is entrained by hormonal signals from the pituitary and that ovulation depends, in part, on the phase in the ovarian circadian cycle at which these signals occur.
The Uterine Placental Bed Renin-Angiotensin System in Normal and Preeclamptic Pregnancy
Authors: Anton Lauren , Merrill David C. , Neves Liomar A. A. , Diz Debra I. , Corthorn Jenny , Valdes Gloria , Stovall Kathryn , Gallagher Patricia E. , Moorefield Cheryl , Gruver Courtney , Brosnihan K. Bridget 
Published: June 2009

Abstract
Previously, we demonstrated activation of the renin-angiotensin system in the fetal placental chorionic villi, but it is unknown whether the immediately adjacent area of the maternal uterine placental bed is regulated similarly. This study measured angiotensin peptides, renin-angiotensin system component mRNAs, and receptor binding in the fundus from nonpregnant subjects (n = 19) and in the uterine placental bed from normal (n = 20) and preeclamptic (n = 14) subjects. In the uterine placental bed from normal pregnant women, angiotensin II peptide levels and angiotensinogen, angiotensin-converting enzyme, angiotensin receptor type 1 (AT1), AT2, and Mas mRNA expression were lower as compared with the nonpregnant subjects. In preeclamptic uterine placental bed, angiotensin II peptide levels and renin and angiotensin-converting enzyme mRNA expression were significantly higher than normal pregnant subjects. The AT2 receptor was the predominant receptor subtype in the nonpregnant fundus, whereas all angiotensin receptor binding was undetectable in normal and preeclamptic pregnant uterine placental bed compared with nonpregnant fundus. These findings suggest that the maternal uterine placental bed may play an endocrine role by producing angiotensin II, which acts in the adjacent placenta to vasoconstrict fetal chorionic villi vessels where we have shown previously that AT1 receptors predominate. This would lead to decreased maternal-fetal oxygen exchange and fetal nutrition, a known characteristic of preeclampsia.
Soluble Corticotropin-Releasing Hormone Receptor 2α Splice Variant Is Efficiently Translated But Not Trafficked for Secretion
Authors: Evans Ryan T. , Seasholtz Audrey F. 
Published: June 2009

AbstractCRH directs the physiological and behavioral responses to stress. Its activity is mediated by CRH receptors (CRH-R) 1 and 2 and modulated by the CRH-binding protein. Aberrant regulation of this system has been associated with anxiety disorders and major depression, demonstrating the importance of understanding the regulation of CRH activity. An mRNA splice variant of CRH-R2α (sCRH-R2α) was recently identified that encodes the receptor’s ligand-binding extracellular domain but terminates before the transmembrane domains. It was therefore predicted to serve as a secreted decoy receptor, mimicking the ability of CRH-binding protein to sequester free CRH. Although the splice variant contains a premature termination codon, predicting its degradation by nonsense-mediated RNA decay, cycloheximide experiments and polysome profiles demonstrated that sCRH-R2α mRNA escaped this regulation and was efficiently translated. However, the resulting protein was unable to serve as a decoy receptor because it failed to traffic for secretion because of an ineffective signal peptide and was ultimately subjected to proteosomal degradation. Several other truncated splice variants of G protein-coupled transmembrane receptors regulate the amount of full-length receptor expression through dimerization and misrouting; however, receptor binding assays and immunofluorescence of cells cotransfected with sCRH-R2α and CRH-R2α or CRH-R1 indicated that sCRH-R2α protein does not alter trafficking or binding of full-length CRH-R. Although sCRH-R2α protein does not appear to function as an intracellular or extracellular decoy receptor, the regulated unproductive splicing of CRH-R2α pre-mRNA to sCRH-R2α may selectively alter the cellular levels of full-length CRH-R2α mRNA and hence functional CRH-R2α receptor levels.
24-Dehydrocholesterol Reductase/Seladin-1: A Key Protein Differentially Involved in Adrenocorticotropin Effects Observed in Human and Rat Adrenal Cortex
Authors: Battista Marie-Claude , Roberge Claude , Martinez Antoine , Gallo-Payet Nicole 
Published: June 2009

Abstract
DHCR24 (24-dehydrocholesterol reductase), or seladin-1, is one of the most expressed genes in the adrenal gland. Because the rat and human adult adrenal cortex differ in their respective functional properties, the aim of the present study was to verify whether seladin-1 may be differentially involved in basal and ACTH-stimulated steroidogenesis and oxidative stress management. Seladin-1 expression was predominantly observed in both human and rat zona fasciculata, with a predominant cytoplasmic localization in human cells and a nucleo-cytoplasmic distribution in rat cells. In human fasciculata cells, localization of the protein was primarily associated with the endoplasmic reticulum. Although its expression was increased by ACTH, its intracellular localization was not altered by ACTH treatment (10 nm) or by the seladin-1 inhibitor U18666A (75 nm). Preincubation with U18666A did not modify the ACTH-induced increase in cortisol secretion but abolished the ACTH-induced increase in dehydroepiandrosterone secretion. In rat fasciculata cells, ACTH induced a massive redistribution of seladin-1 from the cytoplasm (cis-Golgi apparatus) to the nucleus, which was inhibited by preincubation with U18666A. Preincubation with U18666A also decreased ACTH-induced seladin-1 and 11β-hydroxylase protein expression as well as corticosterone production, increased ACTH-induced ROS production but decreased ACTH-induced expression of the detoxifying protein aldo-ketoreductase 1b7. Thus, protection against acutely elevated ACTH-induced oxidative stress in rat fasciculata cells is correlated with nuclear relocalization of seladin-1 and its effects on cellular detoxifying machinery. Altogether, these results indicate that seladin-1 expression and intracellular localization are correlated with both the intensity and nature of ACTH-induced steroidogenesis and resultant oxidative stress.