bluuebunny/crossref_metadata_2025_split huggingface dataset:
Spatial analysis of malaria in Anhui province, China
Authors: Zhang Wenyi , Wang Liping , Fang Liqun , Ma Jiaqi , Xu Youfu , Jiang Jiafu , Hui Fengming , Wang Jianjun , Liang Song , Yang Hong , Cao Wuchun 
Published: October 2008

Abstract

Background
Malaria has re-emerged in Anhui Province, China, and this province was the most seriously affected by malaria during 2005–2006. It is necessary to understand the spatial distribution of malaria cases and to identify highly endemic areas for future public health planning and resource allocation in Anhui Province.

Methods
The annual average incidence at the county level was calculated using malaria cases reported between 2000 and 2006 in Anhui Province. GIS-based spatial analyses were conducted to detect spatial distribution and clustering of malaria incidence at the county level.

Results
The spatial distribution of malaria cases in Anhui Province from 2000 to 2006 was mapped at the county level to show crude incidence, excess hazard and spatial smoothed incidence. Spatial cluster analysis suggested 10 and 24 counties were at increased risk for malaria (P < 0.001) with the maximum spatial cluster sizes at < 50% and < 25% of the total population, respectively.

Conclusion
The application of GIS, together with spatial statistical techniques, provide a means to quantify explicit malaria risks and to further identify environmental factors responsible for the re-emerged malaria risks. Future public health planning and resource allocation in Anhui Province should be focused on the maximum spatial cluster region.
Prune belly syndrome in an Egyptian infant with Down syndrome: A case report
Authors: Metwalley Kotb A , Farghalley Hekma S , Abd-Elsayed Alaa A 
Published: October 2008

Abstract

Introduction
Prune belly syndrome is a rare congenital anomaly of uncertain aetiology almost exclusive to males. The association between prune belly syndrome and Down syndrome is very rare.

Case presentation
A 4-month-old Egyptian boy was admitted to our institute for management of acute bronchiolitis. He was born at full term by normal vaginal delivery. His mother, a 42-year-Egyptian villager with six other children, had no antenatal or prenatal care. On examination, the boy was found to be hypotonic. In addition to features of Down syndrome, karyotyping confirmed the diagnosis of trisomy 21. Ultrasound examination of the abdomen showed bilateral gross hydronephrosis with megaureter. Micturating cystourethrography showed grade V vesicoureteric reflux bilaterally with no urethral obstruction. Serum creatinine concentration was 90 μmol/litre, serum sodium was 132 mmol/litre and serum potassium was 5.9 mmol/litre.

Conclusion
We report an Egyptian infant with Down syndrome and prune belly syndrome. The incidence of this association is unknown. Routine antenatal ultrasonography will help in discovering renal anomalies which can be followed postnatally. Postnatal detection of prune belly syndrome necessitates full radiological investigation to detect any renal anomalies. Early diagnosis of this syndrome and determining its optimal treatment are very important in helping to avoid its fatal course.
The molecular basis of genistein-induced mitotic arrest and exit of self-renewal in embryonal carcinoma and primary cancer cell lines
Authors: Regenbrecht Christian RA , Jung Marc , Lehrach Hans , Adjaye James 
Published: October 2008

Abstract

Background
Genistein is an isoflavonoid present in soybeans that exhibits anti-carcinogenic properties. The issue of genistein as a potential anti-cancer drug has been addressed in some papers, but comprehensive genomic analysis to elucidate the molecular mechanisms underlying the effect elicited by genistein on cancer cells have not been performed on primary cancer cells, but rather on transformed cell lines. In the present study, we treated primary glioblastoma, rhabdomyosarcoma, hepatocellular carcinoma and human embryonic carcinoma cells (NCCIT) with μ-molar concentrations of genistein and assessed mitotic index, cell morphology, global gene expression, and specific cell-cycle regulating genes. We compared the expression profiles of NCCIT cells with that of the cancer cell lines in order to identify common genistein-dependent transcriptional changes and accompanying signaling cascades.

Methods
We treated primary cancer cells and NCCIT cells with 50 μM genistein for 48 h. Thereafter, we compared the mitotic index of treated versus untreated cells and investigated the protein expression of key regulatory self renewal factors as OCT4, SOX2 and NANOG. We then used gene expression arrays (Illumina) for genome-wide expression analysis and validated the results for genes of interest by means of Real-Time PCR. Functional annotations were then performed using the DAVID and KEGG online tools.

Results
We found that cancer cells treated with genistein undergo cell-cycle arrest at different checkpoints. This arrest was associated with a decrease in the mRNA levels of core regulatory genes, PBK, BUB1, and CDC20 as determined by microarray-analysis and verified by Real-Time PCR. In contrast, human NCCIT cells showed over-expression of GADD45 A and G (growth arrest- and DNA-damage-inducible proteins 45A and G), as well as down-regulation of OCT4, and NANOG protein. Furthermore, genistein induced the expression of apoptotic and anti-migratory proteins p53 and p38 in all cell lines. Genistein also up-regulated steady-state levels of both CYCLIN A and B.

Conclusion
The results of the present study, together with the results of earlier studies show that genistein targets genes involved in the progression of the M-phase of the cell cycle. In this respect it is of particular interest that this conclusion cannot be drawn from comparison of the individual genes found differentially regulated in the datasets, but by the rather global view of the pathways influenced by genistein treatment.
Simultaneous ipsilateral proximal interphalangeal and metacarpophalangeal dislocation of the fifth phalanx: A case report
Authors: Unay Koray , Ozkan Korhan , Ugutmen Ender , Ozkan Feyza Unlu , Eren Abdullah , Bilsel Kerem 
Published: October 2008

Abstract

Introduction
There is no case of simultaneous ipsilateral proximal interphalangeal and metacarpophalangeal dislocation of a finger in the literature.

Case presentation
A 61 years old male patient sustained an ipsilateral dorsal dislocation of the PIP joint of his fifth finger and dorsal dislocation of the metacarpophalangeal joint. Closed reduction of proximal interphalangeal joint was achieved while open reduction of the metacarpophalangeal joint was carried out.

Conclusion
The single most important element preventing reduction of the metacarpophalangeal joint was an interposition of the volar plate between proximal end of the phalanx and the head of the metacarpal.
Acute kidney injury is common, parallels organ dysfunction or failure, and carries appreciable mortality in patients with major burns: a prospective exploratory cohort study
Authors: Steinvall I , Bak Z , Sjoberg F 
Published: October 2008

Abstract
Introduction
The purpose of this study was to determine the incidence, time course, and outcome of acute kidney injury after major burns and to evaluate the impact of possible predisposing factors (age, gender, and depth and extent of injury) and the relation to other dysfunctioning organs and sepsis.

Method
We performed an explorative cohort study on patients with a TBSA% (percentage burned of total body surface area) of 20% or more who were admitted to a national burn centre. Acute kidney injury was classified according to the international consensus classification of RIFLE (Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease). Prospectively collected clinical and laboratory data were used for assessing organ dysfunction, systemic inflammatory response, and sepsis.

Results
The incidence of acute kidney injury among major burns was 0.11 per 100,000 people per year. Of 127 patients, 31 (24%) developed acute kidney injury (12% Risk, 8% Injury, and 5% Failure). Mean age was 40.6 years (95% confidence interval [CI] 36.7 to 44.5), TBSA% was 38.6% (95% CI 35.5% to 41.6%), and 25% were women. Mortality was 14% and increased with increasing RIFLE class (7% normal, 13% Risk, 40% Injury, and 83% Failure). Renal dysfunction occurred within 7 days in 55% of the patients and recovered among all survivors. Age, TBSA%, and extent of full thickness burns were higher among the patients who developed acute kidney injury. Pulmonary dysfunction and systemic inflammatory response syndrome were present in all of the patients with acute kidney injury and developed before the acute kidney injury. Sepsis was a possible aggravating factor in acute kidney injury in 48%. Extensive deep burns (25% or more full thickness burn) increased the risk for developing acute kidney injury early (risk ratio 2.25).

Conclusions
Acute kidney injury is common, develops soon after the burn, and parallels other dysfunctioning organs. Although acute kidney injury recovered in all survivors, in higher acute kidney injury groups, together with cardiovascular dysfunction, it correlated with mortality.
Modeling synthetic lethality
Authors: Le Meur Nolwenn , Gentleman Robert 
Published: October 2008

Abstract
Background
Synthetic lethality defines a genetic interaction where the combination of mutations in two or more genes leads to cell death. The implications of synthetic lethal screens have been discussed in the context of drug development as synthetic lethal pairs could be used to selectively kill cancer cells, but leave normal cells relatively unharmed. A challenge is to assess genome-wide experimental data and integrate the results to better understand the underlying biological processes. We propose statistical and computational tools that can be used to find relationships between synthetic lethality and cellular organizational units.

Results
In Saccharomyces cerevisiae, we identified multi-protein complexes and pairs of multi-protein complexes that share an unusually high number of synthetic genetic interactions. As previously predicted, we found that synthetic lethality can arise from subunits of an essential multi-protein complex or between pairs of multi-protein complexes. Finally, using multi-protein complexes allowed us to take into account the pleiotropic nature of the gene products.

Conclusions
Modeling synthetic lethality using current estimates of the yeast interactome is an efficient approach to disentangle some of the complex molecular interactions that drive a cell. Our model in conjunction with applied statistical methods and computational methods provides new tools to better characterize synthetic genetic interactions.
Mice with heterozygous deficiency of lipoic acid synthase have an increased sensitivity to lipopolysaccharide-induced tissue injury
Authors: Yi Xianwen , Kim Kuikwon , Yuan Weiping , Xu Longquan , Kim Hyung-Suk , Homeister Jonathon W , Key Nigel S , Maeda Nobuyo 
Published: October 2008

Abstractα-Lipoic acid (1, 2-dithiolane-3-pentanoic acid; LA), synthesized in mitochondria by LA synthase (Lias), is a potent antioxidant and a cofactor for metabolic enzyme complexes. In this study, we examined the effect of genetic reduction of LA synthesis on its antioxidant and anti-inflammatory properties using a model of LPS-induced inflammation in Lias+/– mice. The increase of plasma proinflammatory cytokine, TNF-α, and NF-κB at an early phase following LPS injection was greater in Lias+/– mice compared with Lias+/+ mice. The circulating blood white blood cell (WBC) and platelet counts dropped continuously during the initial 4 h. The counts subsequently recovered partially in Lias+/+ mice, but the recovery was impaired totally in Lias+/– mice. Administration of exogenous LA normalized the recovery of WBC counts in Lias+/– mice but not platelets. Enhanced neutrophil sequestration in the livers of Lias+/– mice was associated with increased hepatocyte injury and increased gene expression of growth-related oncogene, E-selectin, and VCAM-1 in the liver and/or lung. Lias gene expression in tissues was 50% of normal expression in Lias+/– mice and reduced further by LPS treatment. Decreased Lias expression was associated with diminished hepatic LA and tissue oxidative stress. Finally, Lias+/– mice displayed enhanced mortality when exposed to LPS-induced sepsis. These data demonstrate the importance of endogenously produced LA for preventing leukocyte accumulation and tissue injury that result from LPS-induced inflammation.
11β-Hydroxysteroid Dehydrogenase Type II Inhibition Causes Cerebrovascular Remodeling and Increases Infarct Size after Cerebral Ischemia
Authors: Osmond Jessica M. , Dorrance Anne M. 
Published: October 2008

Direct mineralocorticoid receptor (MR) activation with deoxycorticosterone acetate has deleterious effects on the cerebral vasculature. Inhibition of 11β-hydroxysteroid dehydrogenase type II (11βHSD2) mimics the detrimental effects of elevated mineralocorticoids in the heart, but the effect of enzyme inactivation on the cerebral vasculature is unknown. Therefore, we hypothesized that systemic 11βHSD2 inhibition with carbenoxolone (CBX) would cause remodeling of the middle cerebral artery (MCA) and increase the damage caused by cerebral ischemia. Six-week-old male Sprague Dawley rats were divided into control and CBX (2.5 mg/d) + 0.9% NaCl treated. After 4 wk treatment, rats were used to assess either structure and reactivity of the MCA or the response to cerebral ischemia using the MCA occlusion technique. Cerebral damage was assessed by 2,3,5-triphenyltetrazolium chloride staining and expressed as a percentage of the hemisphere infarcted. CBX treatment increased systolic blood pressure (153.2 ± 7.3 vs. 122.1 ± 4.4 mm Hg; P &lt; 0.05) compared with control rats. MCAs from CBX treated rats were smaller and stiffer than control MCAs over a range of intralumenal pressures, indicating inward remodeling of the vessel. CBX treatment significantly increased ischemic cerebral infarct size compared with control rats (27.1 ± 5.4% vs. 14.8 ± 4.2%; P &lt; 0.05). These data indicate that inhibition of 11βHSD2, and, thus, disproportionate glucocorticoid activation of the MR, results in remodeling of the MCA and worsens the outcome of cerebral ischemia, further underscoring the importance of understanding the mechanism by which MR activation leads to cerebrovascular disease.11β-Hydroxysteroid dehydrogenase inhibition increases blood pressure, altering cerebral vessel structure in a manner that increases the damaged caused by focal cerebral ischemia in rats.
Alterations in Hypothalamic KiSS-1 System in Experimental Diabetes: Early Changes and Functional Consequences
Authors: Castellano J. M. , Navarro V. M. , Roa J. , Pineda R. , Sánchez-Garrido M. A. , García-Galiano D. , Vigo E. , Dieguez C. , Aguilar E. , Pinilla L. , Tena-Sempere M. 
Published: October 2008

Using long-term streptozotocin (STZ)-treated male rats, we recently proposed that defective function of hypothalamic KiSS-1 system is mechanistically relevant for central hypogonadotropism of uncontrolled diabetes. However, the temporal pattern of such defects and its potential contribution to disturbed gonadotropin secretion in the diabetic female remain so far unexplored. To cover these issues, expression analyses and hormonal tests were conducted in diabetic male (1 wk after STZ; short term) and female (4 wk after STZ; long term) rats. Short-term diabetic males had lower basal testosterone levels and decreased gonadotropin responses to orchidectomy (ORX), which associated with significantly attenuated post-ORX rises of hypothalamic KiSS-1 mRNA. Yet kisspeptin administration to diabetic males was able to acutely elicit supramaximal LH and testosterone responses and normalize post-ORX gonadotropin secretion. Long-term diabetic females showed persistent anestrus and significantly decreased basal gonadotropin levels as well as blunted LH responses to ovariectomy; changes that were linked to lowering of basal and postovariectomy expression of hypothalamic KiSS-1 mRNA. Moreover, despite prevailing gonadotropin suppression, LH responses to acute kisspeptin administration were fully preserved, and even enhanced after its repeated injection, in diabetic females. In sum, our present findings further define the temporal course and mechanistic relevance of altered hypothalamic KiSS-1 system in the hypogonadotropic state of uncontrolled diabetes. Furthermore, our data provide the basis for the potential therapeutic intervention of the KiSS-1 system as adjuvant in the management of disturbed gonadotropin secretion of type 1 diabetes in the female.
The time-course and functional consequences of disturbances of the hypothalamic Kisspeptin-1-system in a rat model of uncontrolled diabetes are reviewed, with findings of potential physiopathologic and therapeutic implications for impaired fertility in type 1 diabetes.
Presence, Actions, and Regulation of Myostatin in Rat Uterus and Myometrial Cells
Authors: Ciarmela Pasquapina , Wiater Ezra , Smith Sean M. , Vale Wylie 
Published: October 2008

Myostatin, a member of the TGF-β superfamily of proteins, is known to suppress skeletal muscle mass and myocyte proliferation. The muscular component of the uterus is the myometrium, a tissue that regulates its mass in response to different physiological conditions under the influence of sex steroids. Recently, our laboratory reported effects of activin-A, another TGF-β family member, on signalling and proliferation of rat uterine explants and human myometrial cell lines in culture. Here, we explore the expression, actions, and regulation of myostatin in uterine smooth muscle. Myostatin mRNA was demonstrated to be expressed in a myometrial cell line, pregnant human myometrial 1 cell line (PHM1). Functional assays showed that myostatin induced phosphorylation of Smad-2 and reduced proliferation of PHM1 number in a time and dose-dependent manner. Furthermore, myostatin activated smad-2 specific signalling pathways in rat uterine explants. To expand on our in vitro findings, we found that myostatin is expressed in rat uterus and determined that myostatin mRNA expression varies as a function of the phase of the estrous cycle. Uterine levels of myostatin peaked during late estrus and were the lowest at proestrus. Ovariectomy increased myostatin expression; estrogen treatment strongly decreased myostatin levels, whereas progesterone weakly decreased myostatin expression. In conclusion, myometrial cells are myostatin sensitive, myostatin mRNA levels are modulated in vivo in rats during the estrous cycle, and in response to steroid deprivation and replacement.
Myometrial cells are myostatin-sensitive; myostatin mRNA levels are modulated in rats during the estrous cycle and in response to steroid deprivation and replacement.
Glucagon-Like Peptide-2 Reduces Intestinal Permeability But Does Not Modify the Onset of Type 1 Diabetes in the Nonobese Diabetic Mouse
Authors: Hadjiyanni Irene , Li Kunmin Karen , Drucker Daniel J. 
Published: October 2008

The development of type 1 diabetes (T1D) has been linked to environmental factors and dietary components. Increasing evidence indicates that the integrity of the gut mucosa plays a role in the development of autoimmune diseases, and evidence from both preclinical and clinical studies demonstrates that increased leakiness of the intestinal epithelium precedes the development of type 1 diabetes. However, there is limited information on modulation of gut barrier function and its relationship to diabetes development. Here we show that the nonobese diabetic (NOD) mouse, a model of T1D, exhibits enhanced intestinal transcellular permeability before the development of autoimmune diabetes. Treatment of NOD mice with a glucagon-like peptide 2 (GLP-2) analog, synthetic human [Gly2] glucagon-like peptide-2 (h[Gly2]GLP-2, increased the length and weight of the small bowel and significantly improved jejunal transepithelial resistance. However, chronic administration of once daily h[Gly2]GLP-2 failed to delay or reverse the onset of T1D when treatment was initiated in young, normoglycemic female NOD mice. Furthermore, h[Gly2]GLP-2 administration had no significant effect on lymphocyte subpopulations in NOD mice. These findings demonstrate that h[Gly2]GLP-2-mediated enhancement of gut barrier function in normoglycemic NOD mice disease is not sufficient to prevent or delay the development of experimental T1D.
Increased intestinal permeability often precedes the clinical appearance of autoimmune disorders such as celiac disease or type 1 diabetes. These studies show that glucagon-like peptide 2 reduces gut permeability, but not the onset of diabetes in NOD mice.
Commentary: Introduction to The Year in Basic Science Series
Authors: Shupnik Margaret A. 
Published: October 2008

Abstract
This year, in response to member input and suggestions to highlight the vibrant basic science of endocrinology, The Endocrine Society Annual Meeting (ENDO 08) introduced a new feature, The Year in Basic Science series. Among the many interests and strengths of our members, three broad areas were chosen for initial consideration: nuclear receptors, kinase signaling, and hormones and cancer. Speakers were invited to present and discuss important publications during the past year between annual meetings (roughly June to June), and to put these findings into broad perspective for the endocrine community. Three distinguished researchers, Bert O'Malley, Tony Means, and Kate Horwitz, graciously agreed to participate in the inaugural venture, and this series of articles is based on their presentations at ENDO 08. Each individual approached this somewhat daunting task slightly differently. However, all three observed important and often common themes that ultimately link current basic molecular findings to broad translational and clinical problems, including metabolism and energy balance, neuronal migration and synapse formation, long-term memory formation, and endocrine pathology in cancer, reproduction and osteoporosis.
Heterogeneous Asymmetric Catalysis in Water with Amphiphilic Polymer-Supported Homochiral Palladium Complexes
Authors: Uozumi Yasuhiro 
Published: October 2008

Abstract
Heterogeneous aquacatalytic highly selective organic transformations are what may be considered ideal chemical processes of the next generation, where the advantages of both aqueous- and heterogeneous-switching are combined in one system to meet green sustainable chemical requirements. Heterogeneous aquacatalytic asymmetric reactions were achieved with palladium complexes of homochiral phosphine ligands which were immobilized onto amphiphilic polystyrene–poly(ethylene glycol) (PS–PEG) resin beads via chemical bonding. The catalyst was recovered by simple filtration and was reused without any loss of catalytic activity and stereoselectivity. In particular, a novel chiral P,N-ligand, (3R,9aS)-2-aryl-3-[2-(diphenylphosphino)phenyl]tetrahydro-1H-imidazo[1,5-a]indole-1-one, was designed and prepared on PS–PEG to realize palladium-catalyzed π-allylic substitution of both cyclic and acyclic substrates with carbon, nitrogen, and oxygen nucleophiles in water with enantioselectivity of up to 99% ee.