bluuebunny/crossref_metadata_2025_split huggingface dataset:
Guidelines for Adolescent Depression in Primary Care (GLAD-PC): I. Identification, Assessment, and Initial Management
Authors: Zuckerbrot Rachel A. , Cheung Amy H. , Jensen Peter S. , Stein Ruth E.K. , Laraque Danielle ,   and the GLAD-PC Steering Group
Published: November 2007

OBJECTIVES. To develop clinical practice guidelines to assist primary care clinicians in the management of adolescent depression. This first part of the guidelines addresses identification, assessment, and initial management of adolescent depression in primary care settings.
METHODS. By using a combination of evidence- and consensus-based methodologies, guidelines were developed by an expert steering committee in 5 phases, as informed by (1) current scientific evidence (published and unpublished), (2) a series of focus groups, (3) a formal survey, (4) an expert consensus workshop, and (5) draft revision and iteration among members of the steering committee.
RESULTS. Guidelines were developed for youth aged 10 to 21 years and correspond to initial phases of adolescent depression management in primary care, including identification of at-risk youth, assessment and diagnosis, and initial management. The strength of each recommendation and its evidence base are summarized. The identification, assessment, and initial management section of the guidelines includes recommendations for (1) identification of depression in youth at high risk, (2) systematic assessment procedures using reliable depression scales, patient and caregiver interviews, and Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria, (3) patient and family psychoeducation, (4) establishing relevant links in the community, and (5) the establishment of a safety plan.
CONCLUSIONS. This part of the guidelines is intended to assist primary care clinicians in the identification and initial management of depressed adolescents in an era of great clinical need and a shortage of mental health specialists but cannot replace clinical judgment; these guidelines are not meant to be the sole source of guidance for adolescent depression management. Additional research that addresses the identification and initial management of depressed youth in primary care is needed, including empirical testing of these guidelines.
Isolation and Molecular Characterization of Cancer Stem Cells in MMTV-Wnt-1 Murine Breast Tumors
Authors: Cho Robert W. , Wang Xinhao , Diehn Maximilian , Shedden Kerby , Chen Grace Y. , Sherlock Gavin , Gurney Austin , Lewicki John , Clarke Michael F. 
Published: November 2007

Abstract
In human breast cancers, a phenotypically distinct minority population of tumorigenic (TG) cancer cells (sometimes referred to as cancer stem cells) drives tumor growth when transplanted into immunodeficient mice. Our objective was to identify a mouse model of breast cancer stem cells that could have relevance to the study of human breast cancer. To do so, we used breast tumors of the mouse mammary tumor virus (MMTV)-Wnt-1 mice. MMTV-Wnt-1 breast tumors were harvested, dissociated into single-cell suspensions, and sorted by flow cytometry on Thy1, CD24, and CD45. Sorted cells were then injected into recipient background FVB/NJ female syngeneic mice. In six of seven tumors examined, Thy1+CD24+ cancer cells, which constituted approximately 1%–4% of tumor cells, were highly enriched for cells capable of regenerating new tumors compared with cells of the tumor that did not fit this profile (“not-Thy1+CD24+”). Resultant tumors had a phenotypic diversity similar to that of the original tumor and behaved in a similar manner when passaged. Microarray analysis comparing Thy1+CD24+ tumor cells to not-Thy1+CD24+ cells identified a list of differentially expressed genes. Orthologs of these differentially expressed genes predicted survival of human breast cancer patients from two different study groups. These studies suggest that there is a cancer stem cell compartment in the MMTV-Wnt-1 murine breast tumor and that there is a clinical utility of this model for the study of cancer stem cells.
Disclosure of potential conflicts of interest is found at the end of this article.
Ex Vivo Culture of Human Cord Blood Hematopoietic Stem/Progenitor Cells Adversely Influences Their Distribution to Other Bone Marrow Compartments After Intra-Bone Marrow Transplantation
Authors: Yamamura Kentaro , Ohishi Kohshi , Masuya Masahiro , Miyata Eri , Sugimoto Yuka , Nakamura Shiho , Fujieda Atsushi , Araki Hiroto , Katayama Naoyuki 
Published: November 2007

Abstract
Intra-bone marrow injection is a novel strategy for hematopoietic stem cell transplantation. Here, we investigated whether ex vivo culture of cord blood hematopoietic stem/progenitor cells influences their reconstitution in bone marrow after intra-bone marrow transplantation. Freshly isolated AC133+ cells or cells derived from AC133+ cells cultured with cytokines (stem cell factor, flt-3 ligand, and thrombopoietin) for 5 days were injected into the bone marrow of the left tibia in irradiated NOD/SCID mice. In the bone marrow of the injected left tibia, the engraftment levels of human CD45+ cells at 6 weeks after transplantation did not differ considerably between transplantation of noncultured and cytokine-cultured cells. However, the migration and distribution of transplanted cells to the bone marrow of other, noninjected bones were extremely reduced for cytokine-treated cells compared with noncultured cells. Similar findings were observed for engraftment of CD34+ cells. Administration of granulocyte colony-stimulating factor to mice after transplantation induced the migration of cytokine-cultured cells to the bone marrow of previously aspirated bone but not to other intact bones. These data suggest that ex vivo manipulation of hematopoietic progenitor/stem cells significantly affects their migration properties to other bone marrow compartments after intra-bone marrow transplantation. Our data raise a caution for future clinical applications of the intra-bone marrow transplantation method using ex vivo-manipulated hematopoietic stem cells.
Disclosure of potential conflicts of interest is found at the end of this article.
Concise Review: Isolation and Characterization of Cells from Human Term Placenta: Outcome of the First International Workshop on Placenta Derived Stem Cells
Authors: Parolini Ornella , Alviano Francesco , Bagnara Gian Paolo , Bilic Grozdana , Bühring Hans-Jörg , Evangelista Marco , Hennerbichler Simone , Liu Bing , Magatti Marta , Mao Ning , Miki Toshio , Marongiu Fabio , Nakajima Hideaki , Nikaido Toshio , Portmann-Lanz C. Bettina , Sankar Venkatachalam , Soncini Maddalena , Stadler Guido , Surbek Daniel , Takahashi Tsuneo A. , Redl Heinz , Sakuragawa Norio , Wolbank Susanne , Zeisberger Steffen , Zisch Andreas , Strom Stephen C. 
Published: November 2007

Abstract
Placental tissue draws great interest as a source of cells for regenerative medicine because of the phenotypic plasticity of many of the cell types isolated from this tissue. Furthermore, placenta, which is involved in maintaining fetal tolerance, contains cells that display immunomodulatory properties. These two features could prove useful for future cell therapy-based clinical applications. Placental tissue is readily available and easily procured without invasive procedures, and its use does not elicit ethical debate. Numerous reports describing stem cells from different parts of the placenta, using nearly as numerous isolation and characterization procedures, have been published. Considering the complexity of the placenta, an urgent need exists to define, as clearly as possible, the region of origin and methods of isolation of cells derived from this tissue. On March 23–24, 2007, the first international Workshop on Placenta Derived Stem Cells was held in Brescia, Italy. Most of the research published in this area focuses on mesenchymal stromal cells isolated from various parts of the placenta or epithelial cells isolated from amniotic membrane. The aim of this review is to summarize and provide the state of the art of research in this field, addressing aspects such as cell isolation protocols and characteristics of these cells, as well as providing preliminary indications of the possibilities for use of these cells in future clinical applications.
Disclosure of potential conflicts of interest is found at the end of this article.
Transforming growth factor-β receptor III downregulation in prostate cancer: is inhibin B a tumor suppressor in prostate?
Authors: Sharifi Nima , Lechleider Robert J , Farrar William L 
Published: November 2007

AbstractThe transforming growth factor-β (TGF-β) pathway plays dual roles in cancer, inhibiting epithelial cell growth under normal physiologic conditions, but promoting invasion and metastasis once growth inhibitory responses are lost. Two recent papers show that TGF-β receptor III is the most common TGF-β pathway component downregulated in prostate cancer. Here, we discuss the implications of these findings and what it may mean about the biology of this disease.
Assessing access to safe water and monitoring progress on MDG7 target 10 (access to safe water and basic sanitation): Lessons from Kazakhstan
Authors: O'Hara Sarah , Hannan Tim , Genina Maria 
Published: November 2007

The Millennium Development Goals (MDGs), designed to combat global poverty and hunger, protect the environment, improve health and sanitation and promote education and gender equality, were agreed at the UN Millennium Summit in September 2000. The importance of access to clean water in the overall MDG process has been highlighted and shown to contribute to all other goals and targets. Goal 7 target 10 aims to “halve, by 2015, the proportion of people without sustainable access to safe drinking water and improved sanitation”, compared with 1990. The aim of this MDG is clear and considered to be achievable in most countries. However, it is argued that the base data upon which the targets are set and against which progress will be measured can be problematic, partly because of reliance on poor government information and also on the apparent need of the UN to have a consistent base year and set of definitions across the world.
In this paper, we report the findings of a major water and sanitation survey conducted in Kazakhstan designed specifically to quantify the current level of access, providing the base upon which to determine implementation priorities and against which to measure progress. As well as providing country-specific information the survey highlighted several important issues that have more general relevance. We raise three major questions associated with Target 10: how to define “access”, how to define “improved source” or “improved sanitation” and whether 1990 is always an appropriate base year. Moreover, we argue that there is need to reconsider the way progress is monitored and that the focus on global comparisons is detrimental to making real progress. In conclusion we argue that improving water supply and sanitation can be done in a way that is (1) appropriate for the country, (2) feasible (and fairly easy) to monitor progress and (3) more likely to be accepted by government as there is a sense of relevance.
Using the Climate Assessment Tool (CAT) in U.S. EPA BASINS integrated modeling system to assess watershed vulnerability to climate change
Authors: Imhoff J.C. , Kittle J.L. , Gray M.R. , Johnson T.E. 
Published: November 2007

During the last century, much of the United States experienced warming temperatures and changes in amount and intensity of precipitation. Changes in future climate conditions present additional risk to water and watershed managers. The most recent release of U.S. EPA's BASINS watershed modeling system includes a Climate Assessment Tool (CAT) that provides new capabilities for assessing impacts of climate change on water resources. The BASINS CAT provides users with the ability to modify historical climate and conduct systematic sensitivity analyses of specific hydrologic and water quality endpoints to changes in climate using the BASINS models (Hydrologic Simulation Program – FORTRAN (HSPF)). These capabilities are well suited for addressing questions about the potential impacts of climate change on key hydrologic and water quality goals using the watershed scale at which most important planning decisions are made.
This paper discusses the concepts that motivated the CAT development effort; the resulting capabilities incorporated into BASINS CAT; and the opportunities that result from integrating climate assessment capabilities into a comprehensive watershed water quality modeling system.
Benchmark simulation model no 2: general protocol and exploratory case studies
Authors: Jeppsson U. , Pons M.-N. , Nopens I. , Alex J. , Copp J.B. , Gernaey K.V. , Rosen C. , Steyer J.-P. , Vanrolleghem P.A. 
Published: November 2007

Over a decade ago, the concept of objectively evaluating the performance of control strategies by simulating them using a standard model implementation was introduced for activated sludge wastewater treatment plants. The resulting Benchmark Simulation Model No 1 (BSM1) has been the basis for a significant new development that is reported on here: Rather than only evaluating control strategies at the level of the activated sludge unit (bioreactors and secondary clarifier) the new BSM2 now allows the evaluation of control strategies at the level of the whole plant, including primary clarifier and sludge treatment with anaerobic sludge digestion.
In this contribution, the decisions that have been made over the past three years regarding the models used within the BSM2 are presented and argued, with particular emphasis on the ADM1 description of the digester, the interfaces between activated sludge and digester models, the included temperature dependencies and the reject water storage. BSM2-implementations are now available in a wide range of simulation platforms and a ring test has verified their proper implementation, consistent with the BSM2 definition. This guarantees that users can focus on the control strategy evaluation rather than on modelling issues. Finally, for illustration, twelve simple operational strategies have been implemented in BSM2 and their performance evaluated. Results show that it is an interesting control engineering challenge to further improve the performance of the BSM2 plant (which is the whole idea behind benchmarking) and that integrated control (i.e. acting at different places in the whole plant) is certainly worthwhile to achieve overall improvement.
Large GLUT4 Vesicles Are Stationary While Locally and Reversibly Depleted During Transient Insulin Stimulation of Skeletal Muscle of Living Mice
Authors: Lauritzen Hans P.M.M. , Galbo Henrik , Brandauer Josef , Goodyear Laurie J. , Ploug Thorkil 
Published: November 2007

OBJECTIVE—Insulin stimulates glucose transport in skeletal muscle by GLUT4 translocation from intracellular compartments to sarcolemma and t-tubules. We studied in living animals the recruitment of GLUT4 vesicles in more detail than previously done and, for the first time, analyzed the steady-state recycling and subsequent re-internalization of GLUT4 on an insulin bolus.
RESEARCH DESIGN AND METHODS—A confocal imaging technique was used in GLUT4-enhanced green fluorescent protein–transfected superficial muscle fibers in living mice.
RESULTS—During the first 30 min of insulin stimulation, very few superficially or deeply located GLUT4 storage vesicles (&gt;1 μm) moved in toto. Rather, big vesicles were stationary in their original position at sarcolemma or t-tubules and were locally depleted of GLUT4 by budding off of smaller vesicles. Photobleaching experiments revealed that during initial translocation and steady-state recycling, GLUT4 microvesicles (&lt;1 μm) move from perinuclear GLUT4 depots out along the plasma membrane. Furthermore, after photobleaching of t-tubule areas, recovery of GLUT4 was slow or absent, indicating no recycling of GLUT4 from perinuclear or adjacent (1 μm) or more distant (20 μm) t-tubule areas. During waning of insulin effect, GLUT4 was re-internalized to basal stores with a delay in t-tubules compared with sarcolemma, probably reflecting delayed disappearance of insulin from t-tubules.
CONCLUSIONS—In skeletal muscle, insulin reversibly stimulates local depletion of GLUT4 storage vesicles at sarcolemma and t-tubules rather than inducing movement of intact storage vesicles. During steady-state stimulation, recycling of GLUT4-containing microvesicles over longer distances (10–20 μm) takes place between perinuclear depots and sarcolemma but not at t-tubules.
Attenuation of Interstitial Fibrosis and Tubular Apoptosis in db/db Transgenic Mice Overexpressing Catalase in Renal Proximal Tubular Cells
Authors: Brezniceanu Marie-Luise , Liu Fang , Wei Chih-Chang , Chénier Isabelle , Godin Nicolas , Zhang Shao-Ling , Filep Janos G. , Ingelfinger Julie R. , Chan John S.D. 
Published: November 2007

OBJECTIVE—The present study investigated the relationships between reactive oxygen species (ROS), interstitial fibrosis, and renal proximal tubular cell (RPTC) apoptosis in type 2 diabetic db/db mice and in db/db transgenic (Tg) mice overexpressing rat catalase (rCAT) in their RPTCs (db/db rCAT-Tg).
RESEARCH DESIGN AND METHODS—Blood pressure, blood glucose, and albuminuria were monitored for up to 5 months. Kidneys were processed for histology and apoptosis studies (terminal transferase-mediated dUTP nick-end labeling or immunostaining for active caspase-3 and Bax). Real-time quantitative PCR assays were used to quantify angiotensinogen (ANG), p53, and Bax mRNA levels.
RESULTS—db/db mice developed obesity, hyperglycemia, hypertension, and albuminuria. In contrast, db/db rCAT-Tg mice became obese and hyperglycemic but had normal blood pressure and attenuated albuminuria compared with db/db mice. Kidneys from db/db mice displayed progressive glomerular hypertrophy, glomerulosclerosis, interstitial fibrosis, and tubular apoptosis and increased expression of collagen type IV, Bax, and active caspase-3, as well as increased ROS production. These changes, except glomerular hypertrophy, were markedly attenuated in kidneys of db/db rCAT-Tg mice. Furthermore, ANG, p53, and Bax mRNA expression was increased in renal proximal tubules of db/db mice but not of db/db rCAT-Tg mice.
CONCLUSIONS—Our results indicate a crucial role for intra-renal ROS in the progression of hypertension, albuminuria, interstitial fibrosis, and tubular apoptosis in type 2 diabetes and demonstrate the beneficial effects of suppressing ROS formation.
Impaired Glucose-Stimulated Insulin Secretion Is Coupled With Exocrine Pancreatic Lesions in the Cohen Diabetic Rat
Authors: Weksler-Zangen Sarah , Raz Itamar , Lenzen Sigurd , Jörns Anne , Ehrenfeld Shira , Amir Gail , Oprescu Andrei , Yagil Yoram , Yagil Chana , Zangen David H. , Kaiser Nurit 
Published: November 2007

OBJECTIVE—The Cohen diabetes–sensitive rat develops postprandial hyperglycemia when fed a high-sucrose, copper-poor diet, whereas the Cohen diabetes–resistant rat maintains normoglycemia. The pathophysiological basis of diabetes was studied in the Cohen diabetic rat centering on the interplay between the exocrine and endocrine compartments of the pancreas.
RESEARCH DESIGN AND METHODS—Studies used male Cohen diabetes–sensitive and Cohen diabetes–resistant rats fed 1-month high-sucrose, copper-poor diet. Serum insulin and glucose levels were measured during glucose and insulin tolerance tests. The pancreas was evaluated for weight, insulin content, macrophage, and fat infiltration. Glucose-stimulated insulin secretion (GSIS) was determined in isolated perfused pancreas and in islets.
RESULTS—Hyperglycemic Cohen diabetes–sensitive rats exhibited reduced pancreatic weight with lipid deposits and interleukin-1β–positive macrophage infiltration in the exocrine pancreas. Islet morphology was preserved, and total pancreatic insulin content did not differ from that of Cohen diabetes–resistant rats. Lipids did not accumulate in skeletal muscle, nor was insulin resistance observed in hyperglycemic Cohen diabetes–sensitive rats. Intravenous glucose-tolerance test revealed markedly elevated glucose levels associated with diminished insulin output. Insulin release was induced in vivo by the non-nutrient secretagogues arginine and tolbutamide, suggesting a selective unresponsiveness to glucose. Decreased GSIS was observed in the isolated perfused pancreas of the hyperglycemic Cohen diabetes–sensitive rat, whereas islets isolated from these rats exhibited glucose-dependent insulin secretion and proinsulin biosynthesis.
CONCLUSIONS—The association of the in vivo insulin secretory defect with lipid accumulation and activated macrophage infiltration in the exocrine pancreas suggests that changes in the islet microenvironment are the culprit in the insulin secretory malfunction observed in vivo.
Impact of Common Type 2 Diabetes Risk Polymorphisms in the DESIR Prospective Study
Authors: Vaxillaire Martine , Veslot Jacques , Dina Christian , Proença Christine , Cauchi Stéphane , Charpentier Guillaume , Tichet Jean , Fumeron Frédéric , Marre Michel , Meyre David , Balkau Beverley , Froguel Philippe ,   for the DESIR Study Group
Published: November 2007

OBJECTIVE— The emerging picture of type 2 diabetes genetics involves differently assembled gene variants, each modestly increasing risk with environmental exposure. However, the relevance of these genes for disease prediction has not been extensively tested.
RESEARCH DESIGN AND METHODS— We analyzed 19 common polymorphisms of 14 known candidate genes for their contribution to prevalence and incidence of glucose intolerance in the DESIR (Data from an Epidemiological Study on the Insulin Resistance syndrome) prospective study of middle-aged Caucasian subjects, including 3,877 participants (16.8% with hyperglycemia and 7.9% with diabetes after the 9-year study).
RESULTS— The GCK (Glucokinase) −30A allele was associated with increased type 2 diabetes risk at the end of the follow-up study (adjusted OR 1.34 [95% CI 1.07–1.69]) under an additive model, as supported in independent French diabetic case subjects (OR 1.22, P = 0.007), with increased fasting glycemia (0.85% per A allele, P = 6 × 10−5) and decreased homeostasis model assessment of β-cell function (4%, P = 0.0009). IL6 (Interleukin- 6) −174 G/C interacts with age in disease risk and modulates fasting glycemia according to age (1.36% decrease over 56 years, P = 5 × 10−5). These polymorphisms together with KCNJ11 (Kir6.2)-E23K and TCF7L2-rs7903146 may predict diabetes incidence in the DESIR cohort. Each additional risk allele at GCK, TCF7L2, and IL6 increased risk by 1.34 (P = 2 × 10−6), with an OR of 2.48 (95% CI 1.59–3.86), in carriers of at least four at-risk alleles compared with those with none or one risk allele.
CONCLUSIONS— Our data confirm several at-risk polymorphisms for type 2 diabetes in a general population and demonstrate that prospective studies are valuable designs to complement classical genetic approaches.