bluuebunny/crossref_metadata_2025_split huggingface dataset:
Three Versus Seven-Day Treatment of Asymptomatic Bacteriuria in Pregnant Women: A Pilot Investigation
Authors: Mittal Pooja , Pan Vivien , Wing Deborah A. 
Published: November 2009

Objective:
To compare 3-day vs 7-day antimicrobial treatment for asymptomatic bacteriuria in pregnant women
in a pilot study.

Methods:
Pregnant women with asymptomatic bacteriuria (100,000 cfu/mL) were randomized to 3-day or 7-day
nitrofurantoin treatment. Exclusion criteria included symptomatic bacteriuria at enrollment, previously treated bacteriuria
in the current pregnancy, underlying renal disorders, antibiotic use within one week prior to initial culture or treatment,
bacterial resistance to nitrofurantoin, or other contraindications to nitrofurantoin. Urine test of cure (TOC) was performed
2-4 weeks after initiation of treatment. Subjects with persistent bacteriuria received an additional 7-day treatment course
with an antimicrobial agent based on uropathogen sensitivities and selected at the physician’s discretion. Following
delivery, antenatal, perinatal, and neonatal data were reviewed. Statistical analyses were performed using t-test, Chisquare,
and Fisher exact where appropriate. Analysis was based on intent-to-treat.

Results:
Forty-four of 60 patients had complete prenatal and delivery records. Twenty-four patients (54.5%) were
randomized to 3-day treatment and 20 patients (45.5%) to 7-day treatment. Six (25%) patients in the 3-day group had
persistent bacteriuria at TOC, compared to 2 (10%) patients in the 7-day group (p=0.19). There were no statistical
differences between the groups in maternal age, gestational age at enrollment, mode of delivery, birth weight, NICU
admissions, or the incidence of recurrent urinary tract infections or pyelonephritis.

Conclusion:
Based on our small sample group, 3-day nitrofurantoin treatment had statistically comparable outcomes to 7-
day treatment for asymptomatic bacteriuria in pregnant patients, yet 3-day-treated women were 2.5 times more likely to
have persistent bacteriuria than 7-day-treated women. The possibility of a beta error exists. In light of recent data which
indicates that 1-day nitrofurantoin therapy is less effective than 7-day treatment in pregnant women, we recommend 7-day
treatment for ASB.
Ventromedial Hypothalamic Nitric Oxide Production Is Necessary for Hypoglycemia Detection and Counterregulation
Authors: Fioramonti Xavier , Marsollier Nicolas , Song Zhentao , Fakira Kurt A. , Patel Reema M. , Brown Stacey , Duparc Thibaut , Pica-Mendez Arnaldo , Sanders Nicole M. , Knauf Claude , Valet Philippe , McCrimmon Rory J. , Beuve Annie , Magnan Christophe , Routh Vanessa H. 
Published: November 2009

OBJECTIVEThe response of ventromedial hypothalamic (VMH) glucose-inhibited neurons to decreased glucose is impaired under conditions where the counterregulatory response (CRR) to hypoglycemia is impaired (e.g., recurrent hypoglycemia). This suggests a role for glucose-inhibited neurons in the CRR. We recently showed that decreased glucose increases nitric oxide (NO) production in cultured VMH glucose-inhibited neurons. These in vitro data led us to hypothesize that NO release from VMH glucose-inhibited neurons is critical for the CRR.RESEARCH DESIGN AND METHODSThe CRR was evaluated in rats and mice in response to acute insulin-induced hypoglycemia and hypoglycemic clamps after modulation of brain NO signaling. The glucose sensitivity of ventromedial nucleus glucose-inhibited neurons was also assessed.RESULTSHypoglycemia increased hypothalamic constitutive NO synthase (NOS) activity and neuronal NOS (nNOS) but not endothelial NOS (eNOS) phosphorylation in rats. Intracerebroventricular and VMH injection of the nonselective NOS inhibitor NG-monomethyl-l-arginine (l-NMMA) slowed the recovery to euglycemia after hypoglycemia. VMH l-NMMA injection also increased the glucose infusion rate (GIR) and decreased epinephrine secretion during hyperinsulinemic/hypoglycemic clamp in rats. The GIR required to maintain the hypoglycemic plateau was higher in nNOS knockout than wild-type or eNOS knockout mice. Finally, VMH glucose-inhibited neurons were virtually absent in nNOS knockout mice.CONCLUSIONSWe conclude that VMH NO production is necessary for glucose sensing in glucose-inhibited neurons and full generation of the CRR to hypoglycemia. These data suggest that potentiating NO signaling may improve the defective CRR resulting from recurrent hypoglycemia in patients using intensive insulin therapy.
Regulation of MAP Kinase–Directed Mitogenic and Protein Kinase B–Mediated Signaling by Cannabinoid Receptor Type 1 in Skeletal Muscle Cells
Authors: Lipina Christopher , Stretton Clare , Hastings Simon , Hundal Jonathan S. , Mackie Ken , Irving Andrew J. , Hundal Harinder S. 
Published: November 2009

OBJECTIVE
The endogenous cannabinoid (or endocannabinoid) system (ECS) is part of a central neuromodulatory system thought to play a key role in the regulation of feeding behavior and energy balance. However, increasing evidence suggests that modulation of the ECS may also act to regulate peripheral mechanisms involved in these processes, including lipogenesis in adipose tissue and liver, insulin release from pancreatic β-cells, and glucose uptake into skeletal muscle. It was recently shown that cannabinoid receptor type 1 (CB1) and type 2 (CB2), both key components of the ECS, are expressed in human and rodent skeletal muscle. However, their role in modulating insulin sensitivity in this metabolically active tissue has yet to be determined. Our aim was to establish the role, if any, of these receptors in modulating insulin sensitivity in skeletal muscle cells.

RESEARCH DESIGN AND METHODS
Cultured skeletal muscle cells were exposed to CB1 and/or CB2 pharmacological agonists/antagonists/inverse agonists, and the resulting effects on insulin-regulated phosphatidylinositol 3 kinase (PI 3-kinase)–protein kinase B (PKB) and extracellular signal–related kinases 1/2 (ERK1/2)-directed signaling were determined.

RESULTS
Here, we report that modulating the activity of the ECS in skeletal muscle regulates both insulin-dependent mitogen-activated protein (MAP) kinase (ERK1/2) and the canonical PI 3-kinase/PKB signaling pathways. We show that pharmacological activation or inhibition of CB1 receptor activity exerts a differential effect with regard to MAP kinase– and PKB-directed signaling.

CONCLUSIONS
Our study provides evidence that signaling via cannabinoid receptors can significantly modulate mitogenic and metabolic signaling in skeletal muscle with important implications for muscle growth and differentiation as well as the regulation of glucose and lipid metabolism.
Human Recombinant ACE2 Reduces the Progression of Diabetic Nephropathy
Authors: Oudit Gavin Y. , Liu George C. , Zhong JiuChang , Basu Ratnadeep , Chow Fung L. , Zhou Joyce , Loibner Hans , Janzek Evelyne , Schuster Manfred , Penninger Josef M. , Herzenberg Andrew M. , Kassiri Zamaneh , Scholey James W. 
Published: November 2009

OBJECTIVE
Diabetic nephropathy is one of the most common causes of end-stage renal failure. Inhibition of ACE2 function accelerates diabetic kidney injury, whereas renal ACE2 is downregulated in diabetic nephropathy. We examined the ability of human recombinant ACE2 (hrACE2) to slow the progression of diabetic kidney injury.

RESEARCH DESIGN AND METHODS
Male 12-week-old diabetic Akita mice (Ins2WT/C96Y) and control C57BL/6J mice (Ins2WT/WT) were injected daily with placebo or with rhACE2 (2 mg/kg, i.p.) for 4 weeks. Albumin excretion, gene expression, histomorphometry, NADPH oxidase activity, and peptide levels were examined. The effect of hrACE2 on high glucose and angiotensin II (ANG II)–induced changes was also examined in cultured mesangial cells.

RESULTS
Treatment with hrACE2 increased plasma ACE2 activity, normalized blood pressure, and reduced the urinary albumin excretion in Akita Ins2WT/C96Y mice in association with a decreased glomerular mesangial matrix expansion and normalization of increased α-smooth muscle actin and collagen III expression. Human recombinant ACE2 increased ANG 1–7 levels, lowered ANG II levels, and reduced NADPH oxidase activity. mRNA levels for p47phox and NOX2 and protein levels for protein kinase Cα (PKCα) and PKCβ1 were also normalized by treatment with hrACE2. In vitro, hrACE2 attenuated both high glucose and ANG II–induced oxidative stress and NADPH oxidase activity.

CONCLUSIONS
Treatment with hrACE2 attenuates diabetic kidney injury in the Akita mouse in association with a reduction in blood pressure and a decrease in NADPH oxidase activity. In vitro studies show that the protective effect of hrACE2 is due to reduction in ANG II and an increase in ANG 1–7 signaling.
Divergent Regulation of Energy Expenditure and Hepatic Glucose Production by Insulin Receptor in Agouti-Related Protein and POMC Neurons
Authors: Lin Hua V. , Plum Leona , Ono Hiraku , Gutiérrez-Juárez Roger , Shanabrough Marya , Borok Erzsebet , Horvath Tamas L. , Rossetti Luciano , Accili Domenico 
Published: November 2009

OBJECTIVE
The sites of insulin action in the central nervous system that regulate glucose metabolism and energy expenditure are incompletely characterized. We have shown that mice with hypothalamic deficiency (L1) of insulin receptors (InsRs) fail to regulate hepatic glucose production (HGP) in response to insulin.

RESEARCH DESIGN AND METHODS
To distinguish neurons that mediate insulin's effects on HGP from those that regulate energy homeostasis, we used targeted knock-ins to express InsRs in agouti-related protein (AgRP) or proopiomelanocortin (POMC) neurons of L1 mice.

RESULTS
Restoration of insulin action in AgRP neurons normalized insulin suppression of HGP. Surprisingly, POMC-specific InsR knock-in increased energy expenditure and locomotor activity, exacerbated insulin resistance and increased HGP, associated with decreased expression of the ATP-sensitive K+ channel (KATP channel) sulfonylurea receptor 1 subunit, and decreased inhibitory synaptic contacts on POMC neurons.

CONCLUSIONS
The contrasting phenotypes of InsR knock-ins in POMC and AgRP neurons suggest a branched-pathway model of hypothalamic insulin signaling in which InsR signaling in AgRP neurons decreases HGP, whereas InsR activation in POMC neurons promotes HGP and activates the melanocortinergic energy expenditure program.
Depression and Advanced Complications of Diabetes
Authors: Lin Elizabeth H.B. , Rutter Carolyn M. , Katon Wayne , Heckbert Susan R. , Ciechanowski Paul , Oliver Malia M. , Ludman Evette J. , Young Bessie A. , Williams Lisa H. , McCulloch David K. , Von Korff Michael 
Published: November 2009

OBJECTIVE
To prospectively examine the association of depression with risks for advanced macrovascular and microvascular complications among patients with type 2 diabetes.

RESEARCH DESIGN AND METHODS
A longitudinal cohort of 4,623 primary care patients with type 2 diabetes was enrolled in 2000–2002 and followed through 2005–2007. Advanced microvascular complications included blindness, end-stage renal disease, amputations, and renal failure deaths. Advanced macrovascular complications included myocardial infarction, stroke, cardiovascular procedures, and deaths. Medical record review, ICD-9 diagnostic and procedural codes, and death certificate data were used to ascertain outcomes in the 5-year follow-up. Proportional hazard models analyzed the association between baseline depression and risks of adverse outcomes.

RESULTS
After adjustment for prior complications and demographic, clinical, and diabetes self-care variables, major depression was associated with significantly higher risks of adverse microvascular outcomes (hazard ratio 1.36 [95% CI 1.05–1.75]) and adverse macrovascular outcomes (1.24 [1.0–1.54]).

CONCLUSIONS
Among people with type 2 diabetes, major depression is associated with an increased risk of clinically significant microvascular and macrovascular complications over the ensuing 5 years, even after adjusting for diabetes severity and self-care activities. Clinical and public health significance of these findings rises as the incidence of type 2 diabetes soars. Further research is needed to clarify the underlying mechanisms for this association and to test interventions to reduce the risk of diabetes complications among patients with comorbid depression.
Declining β-Cell Compensation for Insulin Resistance in Hispanic Women With Recent Gestational Diabetes Mellitus
Authors: Xiang Anny H. , Kawakubo Miwa , Trigo Enrique , Kjos Siri L. , Buchanan Thomas A. 
Published: November 2009

OBJECTIVE
To identify factors associated with declining β-cell compensation for insulin resistance.

RESEARCH DESIGN AND METHODS
In a cohort of Hispanic women with recent gestational diabetes mellitus, oral glucose tolerance tests (OGTTs), intravenous glucose tolerance tests (IVGTTs), and bioelectrical impedance measurements were performed at 15-month intervals for up to 5 years, or until fasting plasma glucose exceeded 140 mg/dl (7.8 mmol/l). Data were analyzed to identify predictors of declining β-cell compensation for insulin resistance (the disposition index [DI]) and to examine the mechanism of weight gain and changes in circulating levels of selected adipokines and inflammatory markers on β-cell compensation decline.

RESULTS
A total of 60 nondiabetic women had a median of four sets of OGTT + IVGTT during a median follow-up of 52 months. Fourteen of the women developed diabetes. None of the baseline characteristics were significantly predictive of a decline in DI. There were significant univariate associations between declining DI and weight gain (specifically fat gain), declining adiponectin and rising C-reactive protein. Multivariate analysis showed that the weight gain was the most significant factor associated with declining DI. The amount of association between weight gain and declining DI was explained 31% by changes in adiponectin and C-reactive protein and 40% by changes in insulin resistance.

CONCLUSIONS
These results identify weight gain as the strongest factor associated with declining β-cell compensation for insulin resistance in Hispanic women at high risk for type 2 diabetes. Such effect may be mediated through at least two effects: alterations in adipokine levels and increasing insulin resistance.
Effects of Metformin With or Without Supplementation With Folate on Homocysteine Levels and Vascular Endothelium of Women With Polycystic Ovary Syndrome
Authors: Palomba Stefano , Falbo Angela , Giallauria Francesco , Russo Tiziana , Tolino Achille , Zullo Fulvio , Colao Annamaria , Orio Francesco 
Published: November 2009

OBJECTIVE
To evaluate whether the administration of metformin exerts any effects on serum homocysteine (Hcy) levels in patients with polycystic ovary syndrome (PCOS) and whether supplementation with folate enhances the positive effects of metformin on the structure and function of the vascular endothelium.

RESEARCH DESIGN AND METHODS
A total of 50 patients affected by PCOS, without additional metabolic or cardiovascular diseases, were enrolled in a prospective nonrandomized placebo-controlled double-blind clinical study. They were grouped into two treatment arms that were matched for age and BMI. Patients were treated with a 6-month course of metformin (1,700 mg daily) plus folic acid (400 μg daily; experimental group, n = 25) or placebo (control group, n = 25). Complete hormonal and metabolic patterns, serum Hcy, folate, vitamin B12, endothelin-1 levels, brachial artery diameter at the baseline (BAD-B) and after reactive hyperemia (BAD-RH), flow-mediated dilation, and intima-media thickness in both common carotid arteries were evaluated.

RESULTS
After treatment, a significant increase in serum Hcy levels was observed in the control group compared with the baseline values and the experimental group. A beneficial effect was observed in the concentrations of BAD-B, BAD-RH, flow-mediated dilation, intima-media thickness, and serum endothelin-1 in both groups. However, the results were improved more significantly in the experimental group than in the control subjects.

CONCLUSIONS
Metformin exerts a slight but significant deleterious effect on serum Hcy levels in patients with PCOS, and supplementation with folate is useful to increase the beneficial effect of metformin on the vascular endothelium.
Semantic values in Translating from English to Bangla
Authors: Huq Mohammad Daniul 
Published: November 2009

Translating from other languages to Bangla is confronted with multiple factors. Hindrance seems hidden within the system, or to say, with the applied discipline of this very language, pivot of all may be examined as the transference of semantic values from SL to TL. This paper tries to depict the nature of Bangla while examining the peripheral aspects related to a meaningful and ostensive translated version. Discussion with appropriate examples forms the main burden of the paper. Concerns of translation theories vs. problems will ultimately be taken up exposing Bangla in particular trivial examples. It is expected that, subjectivity and individual traits of an author will find expression in style register. DOI:	10.3329/dujl.v1i2.3716 The Dhaka University Journal of Linguistics: Vol. 1 No. 2 August, 2008 Page: 45-66
Bengali Noun Phrase complex: A minimalist approach
Authors: Bhattacharja Shishir 
Published: November 2009

In this article, we show, following the Minimalist approach, how features like definiteness and specificity are checked either through Probe-Goal or through overt movement to different projections situated in the left periphery of Noun Phrase complex (NPC) constituated of, as we suggest, the NP itself and the traditonal DP split into four different projections: Deixis Phrase, Determiner Phrase, Classifier Phrase and Quantifier Phrase. At the end of this article we point out some of the limitations of this approach and show how they can be handled in the Substantivist or similar approaches. Key words: Definiteness, Specificity, Deixis, Classifier, Quantifier, SubstantiveDOI:	10.3329/dujl.v1i2.3717 The Dhaka University Journal of Linguistics: Vol. 1 No.2 August, 2008 Page: 67-86
An analysis of the sounds and words used in Pali Language
Authors: Barua Shantu 
Published: November 2009

Pali is the name of the language of Theravada Buddhist literature. It belongs to Indo-European language family, especially to Middle Indo-Aryan. Tripitaka, the sacred text of the Buddhist, was first handed down in this language, and from then Pali was recognized as the language of literature. After the Tripitaka many religious and secular books were written in this language and thus, Pali became the language of a vast literature. It was originated in India, however, with the spread of Buddhism, it was accrosed the boundary of India and practiced in Sri Lanka, Thailand, Myanmar (Burma), Cambodia, Vietnam and Bangladesh; and a noteworthy number of books were written in those countries in this language. Pali contains many elements or characteristics of other languages, such as Vedic, Classical Sanskrit, Shinhalese, Dravidan etc. Hence, scholars termed it as compromising speech'. The main objective of this article is to present a clear conception of the phonological and morphological characteristics of Pali language.DOI:	10.3329/dujl.v1i2.3720 The Dhaka University Journal of Linguistics: Vol. 1 No.2 August: 2008 Page: 125-146
Bengali Upasarga: A morphological analysis
Authors: Khairunnahar Khondokar 
Published: November 2009

In Bengali an upasarga- a special kind of prefx- is a vibrant element which is determined as bound morpheme in a morphological consideration. If words are analyzed structurally, the result is outnumbered words, which are mainly constructed by such a prefix. More specifically, most of the terms in Bengali are created with the help of these prefixes. Thus, the main goal of this paper is to provide a structural interpretation of such bound morphemes enriching the words in Bengali. Key words: prefix, bound morpheme, class changing, class maintaining, morphologyDOI:	10.3329/dujl.v1i2.3722 The Dhaka University Journal of Linguistics: Vol.1 No.2 August, 2008 Page: 157-168
Developing Professionally
Authors: Khan Rubina 
Published: November 2009

Teaching is a challenging job and teachers need to perform well in order to deliver their lessons effectively. One major prerequisite for effective performance is the need for teachers to engage in continuous professional development (CPD). Professional development (PD) includes a cluster of activities related to the enhancement of career growth and refinement of the skills of the practitioner. It may range from activities like attending pre-service and in-service training, participating in conferences, seminars, workshops, joining teacher associations, reading books and articles etc. This article briefly highlights the key ingredients of professional development, outlines the sources of PD and argues that professional development is essential for promoting individual and professional growth. Keywords: Professional Development (PD), Continuous Professional Development (CPD), Teacher Development (TD), knowledge base, ELT professional, facets of Continuous Professional Development.DOI:	10.3329/dujl.v1i2.3723 The Dhaka University Journal of Linguistics: Vol. 1 No .2 August, 2008 Page: 169-180
Caspase-1, Caspase-8, and Calpain Are Dispensable for IL-33 Release by Macrophages
Authors: Ohno Tatsukuni , Oboki Keisuke , Kajiwara Naoki , Morii Eiichi , Aozasa Katsuyuki , Flavell Richard A. , Okumura Ko , Saito Hirohisa , Nakae Susumu 
Published: November 2009

AbstractIn addition to IL-1 and IL-18, IL-33 was recently identified as a member of the IL-1 cytokine family. rIL-33 can promote production of Th2-type cytokines by Th2 cells and mast cells in vitro. Administration of rIL-33 to mice results in increases in IgE secretion and eosinophilic inflammation. However, the precise immune cell source of IL-33 remains unclear. Moreover, although recombinant pro-IL-33 is cleaved by recombinant caspase-1 in vitro, as are pro-IL-1β and pro-IL-18, the involvement of caspase-1 in pro-IL-33 cleavage remains controversial. In this study, we show that mouse peritoneal macrophages, but not splenic dendritic cells, produced IL-33 upon stimulation with LPS. Likewise, mouse bone marrow cell-derived cultured mast cells also produced a small, but significant amount of IL-33 via FcεRI cross-linking, but not in response to stimulation with LPS. To our surprise, IL-33 release was found even in caspase-1-deficient, caspase-8 inhibitor-treated, and calpain inhibitor-treated macrophages. These observations suggest that caspase-1-, caspase-8-, and calpain-independent IL-33 production by macrophages and/or mast cells may contribute to the pathogenesis of Th2-type allergic inflammation.