tbuckley/cabot-search huggingface dataset:
Preconditioning of Isolated Rat Heart Is Mediated by Protein Kinase C
Authors: Max B. Mitchell, Xianzhong Meng, Lihua Ao, James M. Brown, Alden H. Harken, Anirban Banerjee
Journal: Circulation Research (1995)

Abstract Catecholamines have been implicated in the phenomenon of ischemic preconditioning. We have previously demonstrated that ischemic preconditioning against postischemic mechanical dysfunction in the isolated rat heart is mediated by the α 1 -adrenergic receptor. The purpose of this study was to delineate the signal transduction of preconditioning distal to the α 1 -adrenergic receptor. Our results suggest that (1) transient ischemia and α 1 -adrenergic receptor–induced preconditioning is inhibited by protein kinase C (PKC) antagonists, (2) functional protection against global ischemia/reperfusion injury can be induced by infusion of diacylglycerol, the second messenger of the α 1 -adrenergic pathway, and (3) transient ischemia and α 1 -adrenergic preconditioning are both characterized by similar translocation of PKC-δ to the sarcolemma of myocardium. These findings suggest that PKC is an effector of preconditioning in the isolated rat heart.
Prehospital initiation of tirofiban in patients with ST-elevation myocardial infarction undergoing primary angioplasty (On-TIME 2): a multicentre, double-blind, randomised controlled trial
Authors: Arnoud WJ van't Hof, Jurriën ten Berg, Ton Heestermans, Thorsten Dill, Reinhard C Funck, Wouter van Werkum, Jan-Henk E Dambrink, Harry Suryapranata, Gert van Houwelingen, Jan Paul Ottervanger, Pieter Stella, Evangelos Giannitsis, Christian Hamm
Journal: The Lancet (2008)
"PLACEBO" (SIMULATION) ELECTROCONVULSIVE THERAPY
Authors: J. A. GUIDO, J. JONES
Journal: American Journal of Psychiatry (1961)

Nine placebo electroconvulsive tratments produced a definitive symptomatic remission of psychogenic amnesia in a patient diagnosed as Dissociative Reaction. The patient's closeness with the doctor, ward personnel, and ancillary therapies intensified the element of suggestibility and the "placebo effect"(2) of electroconvulsive treatment. This was apparent despite the exclusion of "hysterical components" by psychometric examinations. At no time was the patient fearful or undesiring; as a matter of fact, he was overly willing and frequently requested electroconvulsive treatments. Unlike the use of simulation ECT in chronic schizophrenic patients, this report dismisses the utilization of fear and the loss of consciousness as important therapeutic factors(3, 4). This article also demonstrates the need for more extensive studies to encourage recognition of underlying "neurotic and hysterical factors" when describing the therapeusis of electroconvulsive treatments.
Human conscious response to thermal input is adjusted to changes in mean body temperature
Authors: A D Flouris, S S Cheung
Journal: British Journal of Sports Medicine (2008)

Objective and Design: To detect the dependable criteria of behavioural thermoregulation through modelling temperature fluctuations of individuals allowed to freely manipulate inlet water temperature of a liquid conditioning garment (LCG) during 130 min of passive exposure to −20°C interspersed with a 10 min period of moderate exercise at the 65th minute using a double-blind experiment. Participants: Eleven volunteers (5 women; 23.40 (SD 2.09) years; BMI: 23.24 (SD 2.19)) who lacked previous experience with LCG and cold exposure experiments. Results: Despite variations in core and skin temperatures, thermal comfort, thermal sensation, and mean body temperature did not fluctuate significantly over time. Participants were able to find a desired level of LCG inlet temperature within 25 minutes which was maintained at similar levels until the 65th minute of the cold exposure. During exercise, LCG inlet water temperature decreased significantly. Regression models demonstrated that mean skin temperature and change in mean body temperature were significantly associated with thermal comfort and thermal sensation. Subsequent models revealed that, although all temperature variables were associated with LCG inlet water temperature, the coefficient of determination mainly depended on mean skin temperature and change in mean body temperature. The involvement of skin temperature was anticipated as the liquid conditioning garment was in contact with the skin. Conclusions: Humans generate conscious thermoregulatory responses in resting and exercise conditions during exposures to cold environments that are aimed towards maintaining a threshold mean body temperature, rather than temperature changes in individual body regions.
Glial cells in the mouse enteric nervous system can undergo neurogenesis in response to injury
Authors: Catia Laranjeira, Katarina Sandgren, Nicoletta Kessaris, William Richardson, Alexandre Potocnik, Pieter Vanden Berghe, Vassilis Pachnis
Journal: Journal of Clinical Investigation (2011)

The enteric nervous system (ENS) in mammals forms from neural crest cells during embryogenesis and early postnatal life. Nevertheless, multipotent progenitors of the ENS can be identified in the adult intestine using clonal cultures and in vivo transplantation assays. The identity of these neurogenic precursors in the adult gut and their relationship to the embryonic progenitors of the ENS are currently unknown. Using genetic fate mapping, we here demonstrate that mouse neural crest cells marked by SRY box-containing gene 10 (Sox10) generate the neuronal and glial lineages of enteric ganglia. Most neurons originated from progenitors residing in the gut during mid-gestation. Afterward, enteric neurogenesis was reduced, and it ceased between 1 and 3 months of postnatal life. Sox10-expressing cells present in the myenteric plexus of adult mice expressed glial markers, and we found no evidence that these cells participated in neurogenesis under steady-state conditions. However, they retained neurogenic potential, as they were capable of generating neurons with characteristics of enteric neurons in culture. Furthermore, enteric glia gave rise to neurons in vivo in response to chemical injury to the enteric ganglia. Our results indicate that despite the absence of constitutive neurogenesis in the adult gut, enteric glia maintain limited neurogenic potential, which can be activated by tissue dissociation or injury.
Diagnostic Performance of Random Urine Samples Using Albumin Concentration vs Ratio of Albumin to Creatinine for Microalbuminuria Screening in Patients With Diabetes Mellitus
Authors: Hon-Yen Wu, Yu-Sen Peng, Chih-Kang Chiang, Jenq-Wen Huang, Kuan-Yu Hung, Kwan-Dun Wu, Yu-Kang Tu, Kuo-Liong Chien
Journal: JAMA Internal Medicine (2014)

A random urine sample measuring the albumin concentration (UAC) without simultaneously measuring the urinary creatinine is less expensive than measuring the ratio of albumin to creatinine (ACR), but comparisons of their diagnostic performance for microalbuminuria screening among patients with diabetes mellitus (DM) have not been undertaken in previous meta-analyses.To compare the diagnostic performance of the UAC vs the ACR in random urine samples for microalbuminuria screening among patients with DM.Electronic literature searches of PubMed, MEDLINE, and Scopus for English-language publications from the earliest available date of indexing through July 31, 2012.Clinical studies assessing the UAC or the ACR of random urine samples in detecting the presence of microalbuminuria among patients with DM using a urinary albumin excretion rate of 30 to 300 mg/d in 24-hour timed urine collections as the criterion standard.Bivariate random-effects models for analysis and pooling of the diagnostic performance measures across studies, as well as comparisons between different screening tests.The primary end point was the diagnostic performance measures of the UAC or the ACR in random urine samples, as well as comparisons between them.We identified 14 studies, with a total of 2078 patients; 9 studies reported on the UAC, and 12 studies reported on the ACR. Meta-analysis showed pooled sensitivities of 0.85 and 0.87 for the UAC and the ACR, respectively, and pooled specificities of 0.88 and 0.88, respectively. No differences in sensitivity (P = .70), specificity (P = .63), or diagnostic odds ratios (P = .59) between the UAC and the ACR were found. The time point of urine collection did not affect the diagnostic performance of either test.The UAC and the ACR yielded high sensitivity and specificity for the detection of microalbuminuria. Because the diagnostic performance of the UAC is comparable to that of the ACR, our findings indicate that the UAC of random urine samples may become the screening tool of choice for the population with DM, considering the rising incidence of DM and the constrained health care resources in many countries.
HTLV-I p30 inhibits multiple S phase entry checkpoints, decreases cyclin E-CDK2 interactions and delays cell cycle progression
Authors: Hicham H Baydoun, Joanna Pancewicz, XueTao Bai, Christophe Nicot
Journal: Molecular Cancer (2010)

Abstract Background Human T-cell leukemia virus type I (HTLV-I) has efficiently adapted to its host and establishes a persistent infection characterized by low levels of viral gene expression and slow proliferation of HTLV-I infected cells over decades. We have previously found that HTLV-I p30 is a negative regulator of virus expression. Results In this study we show that p30 targets multiple cell cycle checkpoints resulting in a delayed entry into S phase. We found that p30 binds to cyclin E and CDK2 and prevents the formation of active cyclin E-CDK2 complexes. In turn, this decreases the phosphorylation levels of Rb and prevents the release of E2F and its transcriptional activation of genes required for G1/S transition. Our studies also show that HTLV-II p28 does not bind cyclin E and does not affect cell cycle progression. Conclusions In contrast to HTLV-I, the HTLV-II-related retrovirus is not oncogenic in humans. Here we report that the HTLV-I p30 delays cell cycle progression while its homologue, HTLV-II p28, does not, providing evidence for important differences between these two related retrovirus proteins.
Long-Term Stable Expression of Human Apolipoprotein A-I Mediated by Helper-Dependent Adenovirus Gene Transfer Inhibits Atherosclerosis Progression and Remodels Atherosclerotic Plaques in a Mouse Model of Familial Hypercholesterolemia
Authors: L. Maria Belalcazar, Aksam Merched, Boyd Carr, Kazuhiro Oka, Kuang-Hua Chen, Lucio Pastore, Arthur Beaudet, Lawrence Chan
Journal: Circulation (2003)

Background— Epidemiologic studies and transgenic mouse experiments indicate that high plasma HDL and apolipoprotein (apo) A-I protect against atherosclerosis. We used helper-dependent adenovirus (HD-Ad) gene transfer to examine the effect of long-term hepatic apoA-I expression on atherosclerotic lesion progression and remodeling in a mouse model of familial hypercholesterolemia. Methods and Results— We treated LDL receptor–deficient (LDLR −/− ) mice maintained on a high-cholesterol diet for 6 weeks with either a HD-Ad containing human apoA-I gene (HD-Ad-AI) or saline (control). HD-Ad-AI treatment did not affect plasma liver enzymes but induced the appearance of plasma human apoA-I at or above human levels for the duration of the study. Substantial amounts of human apoA-I existed in lipid-free plasma. Compared with controls, HDLs from treated mice were larger and had a greater inhibitory effect on tumor necrosis factor-α–induced vascular cellular adhesion molecule-1 expression in cultured endothelial cells. Twenty-four weeks after injection, aortic atherosclerotic lesion area in saline-treated mice progressed ≈700%; the rate of progression was reduced by &gt;50% by HD-Ad-AI treatment. The lesions in HD-Ad-AI–treated mice contained human apoA-I that colocalized mainly with macrophages; they also contained less lipid, fewer macrophages, and less vascular cellular adhesion molecule-1 immunostaining but more smooth muscle cells (α-actin staining) and collagen. Conclusions— HD-Ad-AI treatment of LDLR −/− mice leads to long-term overexpression of apoA-I, retards atherosclerosis progression, and remodels the lesions to a more stable-appearing phenotype. HD-Ad–mediated transfer of apoA-I may be a useful clinical approach for protecting against atherosclerosis progression and stabilizing atherosclerotic lesions associated with dyslipidemia in human patients.
Lenalidomide Combined With R-CHOP Overcomes Negative Prognostic Impact of Non–Germinal Center B-Cell Phenotype in Newly Diagnosed Diffuse Large B-Cell Lymphoma: A Phase II Study
Authors: Grzegorz S. Nowakowski, Betsy LaPlant, William R. Macon, Craig B. Reeder, James M. Foran, Garth D. Nelson, Carrie A. Thompson, Candido E. Rivera, David J. Inwards, Ivana N. Micallef, Patrick B. Johnston, Luis F. Porrata, Stephen M. Ansell, Randy D. Gascoyne, Thomas M. Habermann, Thomas E. Witzig
Journal: Journal of Clinical Oncology (2014)

Lenalidomide has significant single-agent activity in relapsed diffuse large B-cell lymphoma (DLBCL). We demonstrated that lenalidomide can be safely combined with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone); this new combination is known as R2CHOP. The goal of this phase II study was to evaluate the efficacy of this combination in newly diagnosed DLBCL.Eligible patients were adults with newly diagnosed untreated stages II to IV CD20(+) DLBCL. Patients received lenalidomide 25 mg orally per day on days 1 through 10 with standard-dose R-CHOP every 21 days for six cycles. All patients received pegfilgrastim on day 2 of each cycle and aspirin prophylaxis throughout. DLBCL molecular subtype was determined by tumor immunohistochemistry and classified as germinal center B-cell (GCB) versus non-GCB in the R2CHOP patients and 87 control patients with DLBCL from the Lymphoma Database who were treated with conventional R-CHOP.In all, 64 patients with DLBCL were enrolled, and 60 were evaluable for response. The overall response rate was 98% (59 of 60) with 80% (48 of 60) achieving complete response. Event-free survival and overall survival (OS) rates at 24 months were 59% (95% CI, 48% to 74%) and 78% (95% CI, 68% to 90%), respectively. In R-CHOP patients, 24-month progression-free survival (PFS) and OS were 28% versus 64% (P < .001) and 46% versus 78% (P < .001) in non-GCB DLBCL versus GCB DLBCL, respectively. In contrast, there was no difference in 24-month PFS or OS for R2CHOP patients on the basis of non-GCB and GCB subtype (60% v 59% [P = .83] and 83% v 75% [P = .61] at 2 years, respectively).R2CHOP shows promising efficacy in DLBCL. The addition of lenalidomide appears to mitigate a negative impact of non-GCB phenotype on patient outcome.
Reverse-engineering the Arabidopsis thaliana transcriptional network under changing environmental conditions
Authors: Javier Carrera, Guillermo Rodrigo, Alfonso Jaramillo, Santiago F Elena
Journal: Genome biology (2009)

Understanding the molecular mechanisms plants have evolved to adapt their biological activities to a constantly changing environment is an intriguing question and one that requires a systems biology approach. Here we present a network analysis of genome-wide expression data combined with reverse-engineering network modeling to dissect the transcriptional control of Arabidopsis thaliana. The regulatory network is inferred by using an assembly of microarray data containing steady-state RNA expression levels from several growth conditions, developmental stages, biotic and abiotic stresses, and a variety of mutant genotypes. We show that the A. thaliana regulatory network has the characteristic properties of hierarchical networks. We successfully applied our quantitative network model to predict the full transcriptome of the plant for a set of microarray experiments not included in the training dataset. We also used our model to analyze the robustness in expression levels conferred by network motifs such as the coherent feed-forward loop. In addition, the meta-analysis presented here has allowed us to identify regulatory and robust genetic structures. These data suggest that A. thaliana has evolved high connectivity in terms of transcriptional regulation among cellular functions involved in response and adaptation to changing environments, while gene networks constitutively expressed or less related to stress response are characterized by a lower connectivity. Taken together, these findings suggest conserved regulatory strategies that have been selected during the evolutionary history of this eukaryote.
Angiotensin II in arterial and renal venous plasma and renal lymph in the dog
Authors: Michael D. Bailie, Floyd C. Rector, Donald W. Seldin
Journal: Journal of Clinical Investigation (1971)

Angiotensin II was determined by radioimmunoassay in systemic arterial, pulmonary arterial, and renal venous plasma and in renal hilar lymph in dogs. Levels of the peptide were determined prior to and during progressive graded hemorrhage or reduction in renal perfusion pressure. Levels of angiotensin II in plasma consistently rose during transit through the lung indicating pulmonary conversion of angiotensin I to angiotensin II. On the other hand, angiotensin II in the renal vein plasma was less than that in arterial plasma indicating renal extraction of the peptide from plasma. When renal hilar lymph was sampled under similar conditions, angiotensin II in lymph was consistently higher than that in arterial or renal venous plasma. Furthermore, in some experiments angiotensin II in lymph increased at a time when the concentration in plasma was undetectable. No evidence was found to indicate that angiotensin II in plasma entered renal lymph. It was concluded that angiotensin II levels in lymph reflected the concentration of angiotensin II in renal tissue. The data further suggested that angiotensin II is partially removed from arterial plasma by hydrolysis during transit through the kidney.
Molecular definition of a polymorphic antigen (LA45) of free HLA-A and -B heavy chains found on the surfaces of activated B and T cells.
Authors: J A Madrigal, M P Belich, R J Benjamin, A M Little, W H Hildebrand, D L Mann, P Parham
Journal: The Journal of Experimental Medicine (1991)

A monomoprhic monoclonal antibody (LA45 antibody) reactive with "a new activation-induced surface structure on human T lymphocytes" (LA45 antigen) that resembled free class I heavy chains has recently been described (Schnabl, E., H. Stockinger, O. Majdic, H. Gaugitsch, I.J.D. Lindley, D. Maurer, A. Hajek-Rosenmayr, and W. Knapp. 1990. J. Exp. Med. 171:1431). This antibody was used to clone a class I-like heavy chain (LA45 gene) from the HUT 102 tumor cell, which paradoxically did not give rise to the LA45 antigen on transfection into monkey COS cells. We show here that the LA45 gene is HLA-Aw66.2, a previously uncharacterized allele of the HLA-A locus. The previously determined LA45 sequence differs from that of HLA-Aw66.2, from HUT 102, and the CR-B B cell line derived from the same individual as HUT 102 by substitution of tryptophan for serine at position 4 in the alpha 1 domain. Transfection of HLA-Aw66.2, and of a mutant of this gene with serine 4 substituted for tryptophan, into a human B cell line (C1R) both resulted in expression of the LA45 epitope. Furthermore, we find expression of the LA45 epitope on Epstein Barr virus-transformed B cell lines as well as lectin-activated T cells, but not on long-term T cell lines or unstimulated peripheral blood T cells. The specificity of the LA45 antibody is polymorphic and the presence of the LA45 epitope is precisely correlated with the sequence arginine, asparagine (RN) at residues 62 and 63 of the helix of the alpha 1 domain. The LA45 epitope is broadly distributed, being associated with half the alleles of both HLA-A and -B loci but none of the HLA-C locus. All the results are consistent with the presence of pools of free HLA-A and -B heavy chains at the surfaces of certain cell types but not others. Such molecules are probably responsible for the HLA-associated class I alloantigens of lectin-activated T cells. We hypothesize the free heavy chains result from dissociation of beta 2-microglobulin from subpopulations of empty HLA-A,B molecules, or molecules with weakly bound peptides, that vary in size depending on cellular activation and peptide supply.
The Immediate vs the Important
Authors: J. Michael McGinnis
Journal: JAMA (2004)

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REGULATION OF T CELL FATE BY NOTCH
Authors: Ellen Robey
Journal: Annual Review of Immunology (1999)

▪ Abstract The transmembrane receptor Notch participates in diverse cell fate decisions throughout embryonic development. Notch receptors and their ligands are expressed in the mammalian thymus, raising the possibility that Notch could regulate T cell fate decisions. Expression of a constitutively activated form of Notch in developing thymocytes causes thymocytes normally destined for the CD4 lineage to adopt the CD8 lineage instead. This suggests that Notch activity normally acts to direct CD4 + CD8 + precursors to the CD8 lineage. The choice between CD4 and CD8 T cell fates is also controlled by MHC recognition during positive selection, implying that recognition of class I or II MHC might regulate Notch signaling. Possible models for the regulation of Notch by MHC recognition during CD4 versus CD8 lineage determination are discussed.
In B-cell chronic lymphocytic leukemias, 7q21 translocations lead to overexpression of the CDK6 gene
Authors: Sandrine Hayette, Isabelle Tigaud, Evelyne Callet-Bauchu, Martine Ffrench, Sophie Gazzo, Kamal Wahbi, Mary Callanan, Pascale Felman, Charles Dumontet, Jean-Pierre Magaud, Ruth Rimokh
Journal: Blood (2003)
First report of effective and feasible treatment of multifocal lymphangiomatosis (Gorham–Stout) with bevacizumab in a child
Authors: T.G.P. Grunewald, L. Damke, M. Maschan, U. Petrova, O. Surianinova, A. Esipenko, D. Konovalov, U. Behrends, J. Schiessl, K. Wörtler, S. Burdach, I. von Luettichau
Journal: Annals of Oncology (2010)
Minimum amount of physical activity for reduced mortality and extended life expectancy: a prospective cohort study
Authors: Chi Pang Wen, Jackson Pui Man Wai, Min Kuang Tsai, Yi Chen Yang, Ting Yuan David Cheng, Meng-Chih Lee, Hui Ting Chan, Chwen Keng Tsao, Shan Pou Tsai, Xifeng Wu
Journal: The Lancet (2011)