tbuckley/cabot-search huggingface dataset:
Clinical Characteristics of Attention Deficit Hyperactivity Disorder in African American Children
Authors: V J Samuel, J Biederman, S V Faraone, P George, E Mick, A Thornell, S Curtis, A Taylor, D Brome
Journal: American Journal of Psychiatry (1998)

OBJECTIVE: The authors' goal was to explore the nature of attention deficit hyperactivity disorder (ADHD) in African American children, which has received scant attention by psychiatric researchers. METHOD: Subjects were 19 African American children with DSM-III-R ADHD and 24 African American children without ADHD. Ethnically sensitive methods were used to evaluate the children comprehensively. The findings were compared with those from an earlier study of Caucasian children with ADHD. RESULTS: African American children with ADHD had higher levels of psychiatric disorders other than ADHD than did African American children who did not have ADHD. CONCLUSIONS: Among African American children, ADHD may be characterized by a narrower pattern of psychiatric comorbidity and dysfunction than has been observed in Caucasians. Given the small number of subjects studied, these findings are preliminary and must be replicated to confirm their validity.
Reactivity of routine HIV antibody tests in children who initiated antiretroviral therapy in early infancy as part of the Children with HIV Early Antiretroviral Therapy (CHER) trial: a retrospective analysis
Authors: Helen Payne, Nonhlanhla Mkhize, Kennedy Otwombe, Joanna Lewis, Ravindre Panchia, Robin Callard, Lynn Morris, Abdel Babiker, Avy Violari, Mark F Cotton, Nigel J Klein, Diana M Gibb
Journal: The Lancet Infectious Diseases (2015)
656 OUTCOME OF PATIENTS WITH CHILD-PUGH C LIVER CIRRHOSIS AND HEPATOCELLULAR CARCINOMA AFTER LIVER TRANSPLANTATION
Authors: W. Sieghart, M. Pinter, I. Graziadei, F. Hucke, S. Rasoul-Rockenschaub, R. Stauber, D. Wagner, W. Vogel, M. Peck-Radosavljevic
Journal: Journal of Hepatology (2011)
The use of aggregates of purified cardiomyocytes derived from human ESCs for functional engraftment after myocardial infarction
Authors: Sung-Hwan Moon, Sun-Woong Kang, Soon-Jung Park, Daekyeong Bae, Sung Joon Kim, Hyang-Ae Lee, Kyung Soo Kim, Ki-Sung Hong, Jong Soo Kim, Jeong Tae Do, Ki Hyun Byun, Hyung-Min Chung
Journal: Biomaterials (2013)
SGLT2 Inhibitors: The Latest “New Kids on the Block”!
Authors: William T. Cefalu, Matthew C. Riddle
Journal: Diabetes Care (2015)

Everything in the world of diabetes is moving fast these days. Over the last few months, we have received extensive new information regarding the burden of diabetes and suggested changes in treatment strategies. Specifically, in the December 2014 issue of Diabetes Care , we reported startling new statistics about the rising costs associated with diabetes and prediabetes (1). The economic burden associated with diagnosed and undiagnosed diabetes, gestational diabetes mellitus, and prediabetes was estimated to be 48% higher than that reported in 2007. For 2012, the estimated total burden exceeded $322 billion, comprising $244 billion in excess medical costs and $78 billion in reduced productivity (1). Following the release of these economic statistics there came further proposals regarding strategies for managing diabetes. In the January 2015 issue of Diabetes Care , and coordinated with a release in Diabetologia , there was an update to the 2012 position statement of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) on the management of hyperglycemia (2).

A prominent change with respect to treatment options since publication of the 2012 statement concerned the sodium–glucose cotransporter (SGLT) 2 inhibitors. Metformin remains the preferred drug for monotherapy, but based on a rapid accumulation of new information about SGLT2 inhibitors, this new class of agents is included as a reasonable choice for second-line or third-line therapy in the updated statement. Because Diabetes Care has recently received many submissions reporting new data and evolving clinical strategies for SGLT2 blockers, our editorial team has elected to feature this class of agents in this issue of Diabetes Care . The articles presented in this issue describe research related to novel combinations with a dipeptidyl peptidase-4 inhibitor or with insulin, favorable effects on blood pressure and weight as well as glycemic control, and …
Maternal Complications and Procedures in Pregnancy and at Birth and Wheezing Phenotypes in Children
Authors: Franca Rusconi, Claudia Galassi, Francesco Forastiere, Marta Bellasio, Manuela De Sario, Giovannino Ciccone, Luigia Brunetti, Elisabetta Chellini, Giuseppe Corbo, Stefania La Grutta, Enrico Lombardi, Silvano Piffer, Fiorella Talassi, Annibale Biggeri, Neil Pearce
Journal: American Journal of Respiratory and Critical Care Medicine (2006)

There is increasing interest in the potential influence of fetal and early life conditions on childhood wheezing.To investigate the associations between maternal complications and procedures in pregnancy and at birth and the risk of various wheezing phenotypes in young children.We studied 15,609 children, aged 6-7 yr, enrolled in a population-based study. Standardized questionnaires were completed by the children's mothers.Of the children, 9.5% (1,478) had transient early wheezing, 5.4% (884) had persistent wheezing, and 6.1% (948) had late-onset wheezing. Maternal hypertension or preeclampsia was associated with an increased risk of all three wheezing phenotypes (for transient early wheezing: odds ratio [OR], 1.40; 95% confidence interval [95% CI], 1.08-1.82; for persistent wheezing: OR, 1.59; 95% CI, 1.15-2.19; and for late-onset wheezing: OR, 1.47; 95% CI, 1.06-2.01). Use of antibiotics for urinary tract infections was associated with transient early wheezing (OR, 1.52; 95% CI, 1.16-2.00), whereas antibiotic administration at delivery was associated with both transient early wheezing (OR, 1.21; 95% CI, 1.01-1.46) and persistent wheezing (OR, 1.39; 95% CI, 1.10-1.75). Children who had a mother with diabetes were also more likely to have persistent wheezing (OR, 1.72; 95% CI, 0.99-3.00). Neither amniocentesis/chorionic villus sampling, nor weight gain in pregnancy, nor cesarean section was associated with the subsequent development of wheezing. Maternal asthma or atopy was not an effect modifier of the associations found.Some maternal complications during pregnancy and at delivery may increase the risk of developing different phenotypes of wheezing in childhood.
CELLULAR REACTIONS IN THE MENINGES OF RABBITS TO TUBERCULO-LIPOID, PROTEIN, AND POLYSACCHARIDE, COMPARED WITH THE EFFECTS OF TUBERCLE BACILLI
Authors: J. Van Allen Bickford
Journal: The Journal of Experimental Medicine (1932)

1. Both living and dead tubercle bacilli, as well as tuberculophosphatide, give rise to lesions in which the same type of cell is found, a cell which may prove characteristic of the meningeal reaction. After the phosphatide this cell is produced by the phagocytosis of lipoidal material. The vacuoles of these cells are slowly broken into smaller and smaller size until they correspond to the type found in the epithelioid cells with coarse vacuoles. This change is much slower in the cells of the meninges than in the cells of the omentum and subcutaneous tissue. 2. Intrathecal injections of tuberculo-protein produce a characteristic rise in temperature in normal and tuberculous rabbits. Both normal and tuberculous rabbits, after repeated intrameningeal injections of a given dose of tuberculo-protein, may fail to give a rise in temperature and later react to a larger dose.
The lymphatic system controls intestinal inflammation and inflammation-associated colon cancer through the chemokine decoy receptor D6
Authors: Stefania Vetrano, Elena M Borroni, Adelaida Sarukhan, Benedetta Savino, Raffaella Bonecchi, Carmen Correale, Vincenzo Arena, Massimo Fantini, Massimo Roncalli, Alberto Malesci, Alberto Mantovani, Massimo Locati, Silvio Danese
Journal: Gut (2009)

Background and aims Inflammatory CC chemokines have long been associated with cancer, but unequivocal evidence of a role in clinically relevant models of carcinogenesis is lacking. D6, a promiscuous decoy receptor that scavenges inflammatory CC chemokines, plays a non-redundant role in reducing the inflammatory response in various organs. As inflammation is a key player in the development of inflammatory bowel disease (IBD) and IBD-associated colorectal cancer, we investigated D6 expression in human colitis and colon cancer, and its role in experimental colitis and inflammation-associated colon cancer. Results In humans, D6 was mainly expressed by lymphatic vessels and leukocytes in the mucosa of individuals with IBD and colon cancer, as well as the mucosa of control individuals. Mice lacking expression of D6 were significantly more susceptible to experimental colitis than wild-type mice and failed to resolve colitis, with significantly higher levels of several pro-inflammatory chemokines. In bone marrow chimeric mice, the ability of D6 to regulate colitis was tracked to the stromal/lymphatic compartment, with no contribution of haemopoietic cells. Finally, after administration of the carcinogen azoxymethane, D6 −/− mice showed increased susceptibility to colitis-associated cancer in the distal segment of the colon compared with wild-type mice. Conclusions D6 expressed on lymphatic vessels plays a key role in the control of intestinal inflammation and the development of inflammation-associated colon cancer. Our results reveal a new unexpected role for the lymphatic system in the pathogenesis of IBD and intestinal cancer, and candidate chemokines as novel players in tumour promotion and progression.
Risk of Bacterial Infection in Patients With Cirrhosis and Acute Variceal Hemorrhage, Based on Child–Pugh Class, and Effects of Antibiotics
Authors: Puneeta Tandon, Juan G Abraldes, Adam Keough, Ravin Bastiampillai, Saumya Jayakumar, Michelle Carbonneau, Eric Wong, Dina Kao, Vince G Bain, Mang Ma
Journal: Clinical Gastroenterology and Hepatology (2014)
Endothelial Vasodilator Function Is Preserved at the Spastic/Inflammatory Coronary Lesions in Pigs
Authors: Kenji Miyata, Hiroaki Shimokawa, Tohru Yamawaki, Ikuko Kunihiro, Xuchen Zhou, Taiki Higo, Eriko Tanaka, Naoki Katsumata, Kensuke Egashira, Akira Takeshita
Journal: Circulation (1999)

Background —The question of whether or not endothelial vasodilator function in the spastic coronary artery is preserved is still controversial. We recently developed a porcine model in which long-term and local treatment with interleukin-1β (IL-1β) from the adventitial site causes coronary arteriosclerotic changes and vasospastic responses to autacoids. The aim of this study was to examine the endothelial vasodilator function in our new porcine model of the spasm both in vivo and in vitro. Methods and Results —A segment of the porcine coronary artery was aseptically wrapped with cotton mesh that held absorbed IL-1β–bound microbeads. Two weeks after the procedure, intracoronary administration of serotonin caused coronary vasospasm at the IL-1β–treated site (n=10). Coronary vasodilatation to bradykinin, substance P, or an increase in coronary blood flow was preserved at the spastic site. Vasodilator responses to 3-morpholinosydnonimine (an NO donor) and nitroglycerin also were comparable between the 2 sites. The vasoconstricting response to N G -monomethyl- l -arginine and the extent of the augmentation of the serotonin-induced vasoconstriction were comparable between the 2 sites. Organ chamber experiments showed that endothelium-dependent relaxations to bradykinin, the calcium ionophore A23187, and even the vasospastic agonist serotonin were preserved at the spastic site, whereas contractions to serotonin were augmented at the spastic site regardless of the presence or absence of the endothelium (n=6). Endothelium-independent relaxations to sodium nitroprusside were also preserved at the spastic site. Conclusions —These results indicate that endothelial vasodilator function is preserved at the spastic site and that the spasm is caused primarily by smooth muscle hypercontraction in our porcine model.
Effect of Age and Coronary Artery Disease on the Postural Adjustment of Peripheral Circulation
Authors: ERNST SIMONSON
Journal: Circulation Research (1959)

Circulatory regulation tends to minimize gravitational effects of postural changes. The changes of the extracranial volume pulse, recorded by means of an impedance plethysmograph, in tilted head-up and head-down position, are significantly greater in older than in younger men, indicating impairment of circulatory postural regulation with age. Surprisingly enough, this impairment is partially compensated in coronary patients, possibly due to hyperactive carotid sinus reflexes.
Regulatory effects of glucose on the catalytic activity and cellular content of glucokinase in the pancreatic beta cell. Study using cultured rat islets.
Authors: C Chen, H Hosokawa, L M Bumbalo, J L Leahy
Journal: Journal of Clinical Investigation (1994)

Glucose regulates the cellular content of glucokinase in the pancreatic beta cell by altering the level of the enzyme. We investigated the existence of a second regulatory pathway, an alteration in the catalytic activity, by comparing Vmax and protein levels of glucokinase in rat islets cultured under high glucose conditions (16.7 mM) for 6, 14, and 24 h. The Vmax was increased by glucose at all time points. In contrast, glucokinase protein levels on Western blots were unchanged from the control value at 6 h but increased 40% at the later time points (P < 0.0002). Further evidence for a dual regulatory system was obtained with a reversal protocol. After a 6-h incubation at high glucose, an additional 3-h incubation at 5.5 mM glucose restored glucokinase Vmax to normal, but failed to change the Vmax after a 24-h incubation at high glucose. Finally, 10 microM cycloheximide partially prevented the increase in glucokinase Vmax induced by 24 h of high glucose, but had no effect at 6 h, suggesting the early increase in enzymatic activity did not require protein synthesis. In summary, glucose regulates both the catalytic activity and cellular content of glucokinase in the beta cell. Glucose-induced increases in glucokinase activity are an important element of the beta cell adaptive response to hyperglycemia.
Renal papillary necrosis in a patient with sickle cell trait.
Authors: G Zadeii, J W Lohr
Journal: Journal of the American Society of Nephrology (1997)

A patient with sickle cell trait who presented with gross hematuria and was subsequently found to have renal papillary necrosis is presented. The hematuria resolved with conservative therapy consisting of bed rest and hydration with hypotonic intravenous fluids. The pathophysiology of renal abnormalities associated with sickle cell trait is described. The management of the primary clinical manifestations of this disorder, hematuria and papillary necrosis, are discussed.
The High-Affinity IgG Receptor, FcγRI, Plays a Central Role in Antibody Therapy of Experimental Melanoma
Authors: Lisette Bevaart, Marco J.H. Jansen, Martine J. van Vugt, J. Sjef Verbeek, Jan G.J. van de Winkel, Jeanette H.W. Leusen
Journal: Cancer Research (2006)

We examined the role of FcgammaR in antibody therapy of metastatic melanoma in wild-type and different FcgammaR knock-out mice. Treatment of B16F10-challenged wild-type mice with TA99 antibody specific for the gp75 tumor antigen resulted in a marked decrease in numbers of lung metastases. Treatment of individual FcgammaR knock-out mice revealed the high-affinity IgG receptor, FcgammaRI (CD64), to represent the central FcgammaR for TA99-induced antitumor effects. The potential of immune-modulating agents to further enhance the protective effect induced by monoclonal antibody (mAb) TA99 was examined in combination treatments consisting of mAb TA99 and a TLR-4 agonist, monophosphoryl lipid A (MPL). MPL did potently boost TA99 antibody-induced effects, and combination therapy was, again, found to be dependent on the presence of FcgammaRI.
Soluble Interleukin-2 Receptor Levels in Patients With Dilated Cardiomyopathy
Authors: Constantinos J. Limas, Irvin F. Goldenberg, Catherine Limas
Journal: Circulation (1995)

Background There is evidence that autoimmunity plays an important role in the initiation and progression of myocardial injury in dilated cardiomyopathy. Abnormalities of both cellular and humoral immunity have been described in this disease. Soluble interleukin-2 receptor (sIL-2R) levels in the serum reflect activation of T lymphocytes in the periphery or in tissues. The present study explored the possibility that activation of cellular immunity is frequent in patients with idiopathic dilated cardiomyopathy and may have functional consequences. Methods and Results Serum sIL-2R levels were determined with an enzyme-linked immunosorbent assay in 50 dilated cardiomyopathy patients, 30 patients with ischemic heart disease, and 22 normal control subjects. In addition, the presence of anti–β-receptor and antimyosin antibodies was sought in the serum of cardiomyopathy patients. High sIL-2R levels (&gt;1400 pg/mL) were found in 38% of the dilated cardiomyopathy patients but only 6% of the ischemic heart disease patients. The group of sIL-2R–positive patients was characterized by higher average age, a higher percentage of women, and more severe disease (lower ejection fraction, higher left ventricular filling pressures, and lower cardiac output). Although the prevalence of cardiac autoantibodies did not correlate with the presence of high sIL-2R levels, higher titers of autoantibodies were found predominantly in the sIL-2R–positive group. Conclusions T-lymphocyte activation, as reflected in elevated sIL-2R levels, is frequent in patients with dilated cardiomyopathy and is associated with more severe disease. Cellular and humoral immune activation may correlate with progression of the disease process.
Diagnosis of pulmonary complications of the acquired immune deficiency syndrome.
Authors: M J Rosen, T W Tow, A S Teirstein, M T Chuang, A Marchevsky, E J Bottone
Journal: Thorax (1985)

Forty eight patients with the acquired immunedeficiency syndrome (AIDS) presented to the Mount Sinai Hospital in New York with persistent cough and dyspnoea or an abnormal chest radiograph, or both. Thirty two (67%) were found to have Pneumocystis carinii pneumonia, either alone or in combination with another pathogen. Of these patients, eight (25%) had a normal chest radiograph. Abnormalities in the single breath carbon monoxide diffusing capacity and alveolar-arterial oxygen gradient [A-a) DO2) suggested infection with Pneumocystis carinii. Fibreoptic bronchoscopy with transbronchial biopsy was 100% sensitive in the diagnosis of pneumocytis pneumonia. Fibreoptic bronchoscopy should be undertaken in patients suspected of having a pulmonary complication of AIDS, even if the chest radiograph is normal.
Angiopoietin-1 Regulates Endothelial Cell Survival Through the Phosphatidylinositol 3′-Kinase/Akt Signal Transduction Pathway
Authors: Injune Kim, Hwan Gyu Kim, June-No So, Joo Heon Kim, Hee Jin Kwak, Gou Young Koh
Journal: Circulation Research (2000)

Abstract —Angiopoietin-1 (Ang1) is a strong apoptosis survival factor for endothelial cells. In this study, the receptor/second messenger signal transduction pathway for the antiapoptotic effect of Ang1 on human umbilical vein endothelial cells was examined. Pretreatment with soluble Tie2 receptor, but not Tie1 receptor, blocked the Ang1-induced antiapoptotic effect. Ang1 induced phosphorylation of Tie2 and the p85 subunit of phosphatidylinositol 3′-kinase (PI 3′-kinase) and increased PI 3′-kinase activity in a dose-dependent manner. The PI 3′-kinase–specific inhibitors wortmannin and LY294002 blocked the Ang1-induced antiapoptotic effect. Ang1 induced phosphorylation of the serine-threonine kinase Akt at Ser473 in a PI 3′-kinase–dependent manner. Expression of a dominant-negative form of Akt reversed the Ang1-induced antiapoptotic effect. Ang1 mRNA and protein were present in vascular smooth muscle cells but not in endothelial cells. Cultured vascular smooth muscle cells, but not human umbilical vein endothelial cells, secreted Ang1. These findings indicate that the Tie2 receptor, PI 3′-kinase, and Akt are crucial elements in the signal transduction pathway leading to endothelial cell survival induced by the paracrine activity of Ang1.
Mycobacterium avium subspecies paratuberculosis and Crohn's disease: a systematic review and meta-analysis
Authors: Martin Feller, Karin Huwiler, Roger Stephan, Ekkehardt Altpeter, Aijing Shang, Hansjakob Furrer, Gaby E Pfyffer, Thomas Jemmi, Andreas Baumgartner, Matthias Egger
Journal: The Lancet Infectious Diseases (2007)
Local Tenomodulin Absence, Angiogenesis, and Matrix Metalloproteinase Activation Are Associated With the Rupture of the Chordae Tendineae Cordis
Authors: Naritaka Kimura, Chisa Shukunami, Daihiko Hakuno, Masatoyo Yoshioka, Shigenori Miura, Denitsa Docheva, Tokuhiro Kimura, Yasunori Okada, Goki Matsumura, Toshiharu Shin'oka, Ryohei Yozu, Junjiro Kobayashi, Hatsue Ishibashi-Ueda, Yuji Hiraki, Keiichi Fukuda
Journal: Circulation (2008)

Rupture of the chordae tendineae cordis (CTC) is a well-known cause of mitral regurgitation. Despite its importance, the mechanisms by which the CTC is protected and the cause of its rupture remain unknown. CTC is an avascular tissue. We investigated the molecular mechanisms underlying the avascularity of CTC and the correlation between avascularity and CTC rupture.We found that tenomodulin, which is a recently isolated antiangiogenic factor, was expressed abundantly in the elastin-rich subendothelial outer layer of normal rodent, porcine, canine, and human CTC. Conditioned medium from cultured CTC interstitial cells strongly inhibited tube formation and mobilization of endothelial cells; these effects were partially inhibited by small-interfering RNA against tenomodulin. The immunohistochemical analysis was performed on 12 normal and 16 ruptured CTC obtained from the autopsy or surgical specimen. Interestingly, tenomodulin was locally absent in the ruptured areas of CTC, where abnormal vessel formation, strong expression of vascular endothelial growth factor-A and matrix metalloproteinases, and infiltration of inflammatory cells were observed, but not in the normal or nonruptured area. In anesthetized open-chest dogs, the tenomodulin layer of tricuspid CTC was surgically filed, and immunohistological analysis was performed after several months. This intervention gradually caused angiogenesis and expression of vascular endothelial growth factor-A and matrix metalloproteinases in the core collagen layer in a time-dependent manner.These findings provide evidence that tenomodulin is expressed universally in normal CTC in a concentric pattern and that local absence of tenomodulin, angiogenesis, and matrix metalloproteinase activation are associated with CTC rupture.