tbuckley/cabot-search huggingface dataset:
Recovery of neurocognitive functions following sustained abstinence after substance dependence and implications for treatment
Authors: Mieke H.J. Schulte, Janna Cousijn, Tess E. den Uyl, Anna E. Goudriaan, Wim van den Brink, Dick J. Veltman, Thelma Schilt, Reinout W. Wiers
Journal: Clinical Psychology Review (2014)
Human atrial natriuretic peptide and nicorandil as adjuncts to reperfusion treatment for acute myocardial infarction (J-WIND): two randomised trials
Authors: Masafumi Kitakaze, Masanori Asakura, Jiyoong Kim, Yasunori Shintani, Hiroshi Asanuma, Toshimitsu Hamasaki, Osamu Seguchi, Masafumi Myoishi, Tetsuo Minamino, Takahiro Ohara, Yoshiyuki Nagai, Shinsuke Nanto, Kouki Watanabe, Shigeru Fukuzawa, Atsushi Hirayama, Natsuki Nakamura, Kazuo Kimura, Kenshi Fujii, Masaharu Ishihara, Yoshihiko Saito, Hitonobu Tomoike, Soichiro Kitamura
Journal: The Lancet (2007)
Incidence and Diagnostic Features of Macroregenerative Nodules Vs. Small Hepatocellular Carcinoma in Cirrhotic Livers
Authors: Linda Ferrell, Teresa Wright, John Lake, John Roberts, Nancy Ascher
Journal: Hepatology (1992)

In Japan, the presence of a large regenerative nodule within a cirrhotic liver, referred to as a macroregenerative nodule or adenomatous hyperplasia, is thought to play a role in the pathogenesis of hepatocellular carcinoma. These lesions, however, have received little attention outside of Japan. We examined 110 sequentially explanted cirrhotic livers for the presence of such nodules. By gross examination, 19 livers (17.3%) had 40 nodules (10 livers had more than one nodule) between 0.8 and 3.5 cm in diameter. By histological examination, 28 of these were macroregenerative nodules and 12 were hepatocellular carcinomas. Three of these hepatocellular carcinomas, however, appeared to have arisen in association with a macroregenerative nodule. We found that the architectural features of thickened cell plates, formation of trabeculae and loss of reticulin were usually very helpful in differentiating benign macroregenerative nodules from hepatocellular carcinoma. The incidence of macroregenerative nodules in our series was similar to that seen in the Japanese studies, and although we feel that they may play a role in the pathogenesis of carcinoma, we do not believe their presence is necessary for the development of hepatocellular carcinoma.
Melanoma follow-up: protocols and practice
Authors: E. Hormbrey, P. Banwell, P. Gillespie, P. Budny
Journal: British Journal of Dermatology (2000)

S ir, The incidence and mortality of cutaneous malignant melanoma are increasing at the rate of between 3 and 7% in European countries. 1 Ideally, national guidelines should ensure that treatment and follow‐up of melanoma patients are based upon sound scientific data. In creating a more uniform practice, the quality of melanoma management could be optimized. We report an audit of compliance that facilitated the creation of a unified melanoma follow‐up policy within a subregional plastic surgery department. Melanoma follow‐up has been a contentious issue for many years. 2 There has been great debate as to the timing, 3 benefits 4 and cost‐effectiveness 5, 6 of hospital follow‐up, both in the ‘short‐term’ (for 5–10 years) and longer. 7 This has major implications in terms of clinic workload, out‐patient attendance costs, time available for new cases and patient throughput. 7, 8 We performed an audit of melanoma follow‐up in our hospital. Each of the consultants initially had a different preferred follow‐up policy ( Table 1a). We questioned all junior staff and found that only one of the 10 doctors was aware of these policies. A retrospective audit was then conducted of the last 50 out‐patient episodes when attending for melanoma follow‐up. Of the 50 patients, 24 (48%) were not followed up according to the consultant’s preferred policies. Eleven cases (22%) were due to further disease and 13 (26%) were due to incorrect follow‐up. The results of the audit data and a review of the published literature highlighted the need for an agreed, combined and unified follow‐up policy. The revised policy ( Table 1b) was then instituted and distributed to clinics, junior staff and consultants. These changes resulted in an immediate and significant reduction in clinic costs: 9% for thick melanoma (≥ 0·76 mm Breslow thickness).
Clinical relevance of mixed respiratory viral infections in adults with influenza A H1N1
Authors: M.A. Marcos, S. Ramón, A. Antón, E. Martinez, A. Vilella, V. Olivé, C. Cillóniz, A. Moreno, A. Torres, T. Pumarola
Journal: European Respiratory Journal (2011)

families.Therefore, the studied children may have come from communities with inadequate sanitation and living conditions.Regarding macrophage counts, our results were similar to those found in other published studies.Also, CD4+/CD8+ ratio values found in this study were also similar to those described for healthy children [4, 8].These peculiarities found in the BAL of healthy children should be considered when interpreting results from children with lung diseases.Thus, in our setting, the number of eosinophils and lymphocytes found in ''normal'' children's BAL seems to be slightly elevated in relation to the results of studies conducted in developed countries.Therefore, we could accept ,2% eosinophils and ,14% lymphocytes as BAL reference values for our setting.In our view, advancements in understanding cellular and immunological processes in normal children will provide the basis for acquiring greater knowledge of infant and childhood lung diseases, and a better understanding of the way in which, in later phases of life, such respiratory diseases are manifested.
Preexcitation and Tachycardias in Wolff-Parkinson-White Syndrome, Type B
Authors: JOHN W. LISTER, FRANCIS X. WORTHINGTON, THOMAS O. GENTSCH, JOHN A. SWENSON, DAVID A. NATHAN, ARTHUR J. GOSSELIN
Journal: Circulation (1972)

Electrophysiologic events in a 52-year-old man with Wolff-Parkinson-White (W-P-W) syndrome, type B, recurrent supraventricular tachycardias, and coronary artery disease were studied during cardiac catheterization and at open-heart surgery. During cardiac catheterization reciprocal tachycardias were repeatedly initiated by premature atrial beats and terminated by rapid right atrial pacing. Our results confirm that the tachycardia usually seen in the W-P-W syndrome is reciprocal tachycardias with orthograde conduction to the ventricles through the normal atrioventricular conduction system and retrograde conduction to the atria via the Kent bundle. The epicardial surface of the ventricles was "mapped" at surgery. The earliest site of excitation was the posterior base of the left ventricle near the crux of the heart. Kent bundle conduction was temporarily ablated with lidocaine (Xylocaine) hydrochloride. This is the first case of W-P-W syndrome, type B, in which the anomalous A-V bundle entered the left ventricle. Our results indicate that the analysis of the electrocardiogram in localizing an abnormal A-V connection cannot be relied upon completely.
Measurement of Arterial Wall Thickness as a Surrogate Marker for Atherosclerosis
Authors: Eric de Groot, G. Kees Hovingh, Albert Wiegman, Patrick Duriez, Andries J. Smit, Jean-Charles Fruchart, John J.P. Kastelein
Journal: Circulation (2004)

Large observational studies and atherosclerosis regression trials of lipid-modifying pharmacotherapy have established that intima-media thickness of the carotid and femoral arteries, as measured noninvasively by B-mode ultrasound, is a valid surrogate marker for the progression of atherosclerotic disease. To exploit fully the potential of ultrasound imaging in atherosclerosis research, standardized and strictly implemented imaging protocols should be used in both observational studies and applied clinical research. This article describes such a protocol developed at the Academic Medical Center of the University of Amsterdam, the Netherlands. Results are presented from a study that estimated atherosclerosis progression from childhood into old age by measuring intima-media thickness in subjects with familial hypercholesterolemia compared with healthy controls.
Failure of the cholinergic modulation of norepinephrine release during acute myocardial ischemia in the rat.
Authors: X J Du, A M Dart, R A Riemersma, M F Oliver
Journal: Circulation Research (1990)

The effect of ischemia on cholinergic presynaptic inhibition of exocytotic norepinephrine release was studied in the innervated perfused rat heart. In normoxic hearts, vagal nerve stimulation significantly reduced exocytotic norepinephrine overflow to 75% of control values. This inhibitory effect was not affected by 3 minutes of low-flow ischemia (67% of control overflow values), but was attenuated or abolished by 10-minute low-flow ischemia or by 1-, 3-, and 5-minute stop-flow ischemia (107%, 85%, 101%, and 120% of control overflow values, respectively). The alpha-adrenergic antagonist phentolamine could completely or partly restore the failure of vagally induced inhibition of norepinephrine overflow in hearts with 1-, 3-, and 5-minute stop-flow ischemia (72%, 73%, and 85% of control overflow values, respectively). The muscarinic agonist methacholine substantially inhibited norepinephrine overflow to 18% of control overflow values in normoxic hearts. This effect was also significantly attenuated by 10-minute low-flow ischemia or by 1-, 3-, and 5-minute stop-flow ischemia (46%, 38%, 53%, and 55% of control overflow values, respectively). The cholinesterase inhibitor physostigmine did not restore the methacholine-induced inhibition of norepinephrine overflow after 3-minute stop-flow ischemia to normoxic level (55% vs. 17%). These results indicate that myocardial ischemia interferes with endogenous and exogenous cholinergic presynaptic inhibition of norepinephrine overflow in the rat heart. The extent of this attenuation depends on the severity and duration of ischemia. Reduced exocytotic acetylcholine release, which is at least in part due to an enhanced adrenergic presynaptic modulation, and dysfunction of presynaptic muscarinic receptors are suggested as two possible mechanisms.
Interleukin-HP1, a T cell-derived hybridoma growth factor that supports the in vitro growth of murine plasmacytomas.
Authors: J Van Snick, A Vink, S Cayphas, C Uyttenhove
Journal: The Journal of Experimental Medicine (1987)

We have recently described the purification and NH2-terminal amino acid sequence of a T cell-derived hybridoma growth factor that was provisionally designated interleukin-HP1 (IL-HP1). Here we report that a T cell supernatant containing high titers of this hybridoma growth factor considerably facilitated the establishment of primary cultures of murine plasmacytomas. Most plasmacytoma cell lines derived from such cultures remained permanently dependent on IL-HP1-containing T cell supernatant for both survival and growth in vitro. These cell lines, however, retained their ability to form tumors in irradiated pristane-treated mice. Analytical fractionation of a T cell supernatant rich in IL-HP1 by either gel filtration, isoelectric focusing, or reversed-phase HPLC revealed the existence of only one plasmacytoma growth factor activity that strictly copurified with IL-HP1, strongly suggesting the identity of both factors. This conclusion was further supported by the finding that IL-HP1 purified to homogeneity supported the growth of both B cell hybridomas and plasmacytomas. For half-maximal growth, plasmacytomas, however, required a concentration of IL-HP1 of approximately 30 pM, which is approximately 200 times higher than that required by B cell hybridomas. A clear difference in the specificity of IL-HP1 and B cell stimulatory factor 1 (BSF-1) was demonstrated by the finding that IL-HP1-dependent plasmacytomas did not survive in the presence of BSF-1, whereas helper T cell lines that proliferated in the presence of BSF-1 failed to respond to IL-HP1.
Screening for von Hippel-Lindau Disease by DNA Polymorphism Analysis
Authors: Gladys M. Glenn
Journal: JAMA (1992)

Objective.\p=m-\VonHippel-Lindau (VHL) disease is a rare, inherited multisystem neoplastic disorder.There is no biochemical test available to distinguish VHL dis- ease gene carriers from their healthy siblings.We evaluated DNA polymorphism analysis as a method for identifying disease gene carriers.Design.\p=m-\Prospectivecomparison of the results of DNA analysis with a comprehensive clinical screening examination.Setting.\p=m-\The Clinical Center of the National Institutes of Health.Patients.\p=m-\Bloodwascollected from 182 members of 16 families with VHL disease.Forty-eight asymptomatic individuals, at risk of developing this hereditary ill- ness (with an affected parent or sibling), were examined for occult disease at the Clinical Center of the National Institutes of Health and tested by DNA polymorphism analysis.Results.\p=m-\DNA polymorphism analysis predicted nine disease gene carriers and 33 individuals with the wild-type (normal) allele among the 48 individuals at risk of developing VHL disease; the test was not informative in six individuals.All nine individuals predicted to carry the VHL gene had evidence of occult disease on clinical examination.There was no clinical evidence of VHL disease in 32 of 33 individuals predicted to carry the wild-type allele.Conclusions.\p=m-\DNApolymorphism analysis can identify individuals likely to carry the VHL disease gene among asymptomatic members of disease families.This technique serves to focus attention on those individuals who require periodic medical examination and may help to alleviate the morbidity and mortality associ- ated with this disease.
Clinical and laboratory characteristics of systemic anaplastic large cell lymphoma in Chinese patients
Authors: Yan-Fang Wang, Yan-Li Yang, Zi-Fen Gao, Chun-Ju Zhou, Xylina Gregg, Yun-Fei Shi, Jing Wang, Xiao-Feng Yang, Xiao-Yan Ke
Journal: Journal of Hematology & Oncology (2012)

Abstract Background Systemic anaplastic large cell lymphoma (S-ALCL) is a rare disease with a highly variable prognosis and no standard chemotherapy regimen. Anaplastic lymphoma kinase (ALK) has been reported as an important prognostic factor correlated with S-ALCL in many but not all studies. In our study, we retrospectively analyzed 92 patients with S-ALCL from the Peking University Lymphoma Center for clinical and molecular prognostic factors to make clear the role of ALK and other prognostic factors in Han Chinese S-ALCL. Results The majority of Chinese S-ALCL patients were young male patients (median age 26, male/female ratio 1.7) and the median age was younger than previous reports regardless of ALK expression status. The only statistically significant different clinical characteristic in S-ALCL between ALK positive (ALK + ) and ALK negative (ALK - ) was age, with a younger median age of 22 for ALK + compared with 30 for ALK - . However, when pediatric patients (≤18) were excluded, there was no age difference between ALK + and ALK - . The groups did not differ in the proportion of males, those with clinical stage III/IV (49 vs 51%) or those with extranodal disease (53 vs 59%). Of 73 evaluable patients, the 3-year and 5-year survival rates were 60% and 47%, respectively. Univariate analysis showed that three factors: advanced stage III/IV, lack of expression of ALK, and high Ki-67 expression, were associated with treatment failure in patients with S-ALCL. However, ALK expression correlated with improved survival only in patients younger than 14 years, while not in adult patients. In multivariate analysis, only clinical stage was an independent prognostic factor for survival. Expressions of Wilms tumor 1 (WT1) and B-cell lymphoma 2 protein (BCL-2) correlated with the expression of ALK, but they did not have prognostic significance. High Ki-67 expression was also a poor prognostic factor. Conclusions Our results show that ALK expression alone is not sufficient to determine the outcome of ALCL and other prognostic factors must be considered. Clinical stage is an independent prognostic factor. Ki-67 expression is a promising prognostic factor.
Alveolar nitric oxide in adults with asthma: evidence of distal lung inflammation in refractory asthma
Authors: M. Berry, B. Hargadon, A. Morgan, M. Shelley, J. Richter, D. Shaw, R. H. Green, C. Brightling, A. J. Wardlaw, I. D. Pavord
Journal: European Respiratory Journal (2005)

Recent studies have suggested that alveolar nitric oxide (NO) concentration is a noninvasive test of distal lung inflammation. The current study determined whether alveolar NO concentration can be measured in patients with asthma of varying severity, tested the hypothesis that there is an association between alveolar NO and bronchoalveolar lavage (BAL) eosinophil count and determined whether refractory asthma is characterised by a raised alveolar NO concentration. Finally, the present authors assessed the effect of 2 weeks of prednisolone (30 mg q.d. ) on alveolar NO concentration. Alveolar NO concentration was both measurable and repeatable in patients with refractory asthma. A positive correlation was found between alveolar NO concentration and BAL eosinophil count but not with bronchial wash or sputum eosinophil count. Alveolar NO concentration was increased in patients with refractory asthma (7.1 ppb) compared with mild-to-moderate asthma (3.4 ppb) and normal controls (3.4 ppb) and reduced by treatment with prednisolone. In conclusion, these findings support the hypothesis that alveolar nitric oxide is a measure of distal airway inflammation and suggest that distal lung inflammation is present in refractory asthma.
Environmental epigenetic inheritance through gametes and implications for human reproduction
Authors: Yanchang Wei, Heide Schatten, Qing-Yuan Sun
Journal: Human Reproduction Update (2014)

Traditional studies focused on DNA as the heritable information carrier that passes the phenotype from parents to offspring. However, increasing evidence suggests that information, that is independent of the DNA sequence, termed epigenetic information, can be inherited between generations. Recently, in our lab, we found that prediabetes in fathers increases the susceptibility to diabetes in offspring through gametic cytosine methylation changes. Paternal prediabetes changed overall methylation patterns in sperm, and a large portion of differentially methylated loci can be transmitted to pancreatic islets of offspring up to the second generation. In this review, we survey the extensive examples of environmentally induced epigenetic inheritance in various species, ranging from Caenorhabditis elegans to humans. We focus mainly on elucidating the molecular basis of environmental epigenetic inheritance through gametes, which is an emerging theme and has important implications for explaining the prevalence of obesity, type 2 diabetes and other chronic non-genetic diseases, which is also important for understanding the influence of environmental exposures on reproductive and overall health in offspring. For this review, we included relevant data and information obtained through a PubMed database search for all English language articles published up to August 2014 which included the term 'environmental epigenetic inheritance' and 'transgenerational epigenetic inheritance'. We focused on research papers using animal models including Drosophila, C. elegans, mouse and rat. Human data were also included. Evidence from animal models suggests that environmental epigenetic inheritance through gametes exists in various species. Extensive molecular evidence suggests that epigenetic information carriers including DNA methylation, non-coding RNAs and chromatin proteins in gametes play important roles in the transmission of phenotypes from parents to offspring. Given the large number of experimental evidence from various organisms, it is clear that parental environmental alterations can affect the phenotypes of offspring through gametic epigenetic alterations. This more recent thinking based on new data may have implications in explaining the prevalence of obesity, type 2 diabetes and other chronic non-genetic diseases. This also implies that, in the near future, epigenetic factors which are heritable should be regarded important in determining the risk of certain diseases. Moreover, identification of epigenetic markers in gametes (polar body or sperm) may hold great promise for predicting susceptibility to and preventing certain non-genetic diseases in offspring, as well as providing indications on parental environmental exposures.
Allogenicity of Human Cardiac Stem/Progenitor Cells Orchestrated by Programmed Death Ligand 1
Authors: Laura Lauden, Wahid Boukouaci, Luis R. Borlado, Itziar Palacios López, Pilar Sepúlveda, Ryad Tamouza, Dominique Charron, Reem Al-Daccak
Journal: Circulation Research (2012)

Rationale: Transplantation of allogeneic cardiac stem/progenitor cells (CPC) in experimental myocardial infarction promoted cardiac regeneration and improved heart function. Although this has enhanced prospects of using allogeneic CPC for cardiac repair, the mechanisms regulating the behavior of these allogeneic cells, which are central to clinical applications, remain poorly understood. Objective: T cells orchestrate the allogeneic adaptive immune response. Therefore, to provide insight into the mechanisms regulating the immunologic behavior of human CPC (hCPC), we investigated the allogeneic T-cell response elicited by cryopreserved c-kit–selected hCPC. Methods and Results: By using an experimental model of allogeneic stimulation, we demonstrate that, whether under inflammatory conditions or not, hCPC do not trigger conventional allogeneic Th1 or Th2 type responses but instead induce proliferation and selective expansion of suppressive CD25 high CD127 low human leukocyte antigen-DR + FoxP3 high effector regulatory T cells. The regulatory T-cell proliferation and amplification were dependent on the interaction with the B7 family member programmed death ligand 1 (PD-L1), which is substantially expressed on hCPC and increased under inflammatory conditions. Thus, hCPC in allogeneic settings acquire the capacity to downregulate an ongoing immune response, which was dependent on PD-L1. Conclusions: Collectively, these data reveal that hCPC in allogeneic settings have a tolerogenic immune behavior, promoting a contact PD-L1–dependent regulatory response and a PD-L1–dependent allogeneic-driven immunomodulation. Our study attributes an important role for PD-L1 in the immune behavior of allogeneic hCPC and raises the possibility of using PD-L1 expression as a marker to identify and select low-risk high-benefit allogeneic cardiac repair cells.
Primary follicular lymphoma of the gastrointestinal tract: a study of 25 cases and a literature review
Authors: G. Damaj, V. Verkarre, A. Delmer, P. Solal-Celigny, I. Yakoub-Agha, C. Cellier, F. Maurschhauser, R. Bouabdallah, V. Leblond, F. Lefrère, D. Bouscary, J. Audouin, B. Coiffier, B. Varet, T. Molina, N. Brousse, O. Hermine
Journal: Annals of Oncology (2003)
P59. Depleting the suppressors for the benefit of immunotherapy against cervical cancer
Authors: O Draghiciu, BN Hoogeboom, T Meijerhof, HW Nijman, CAHH Daemen
Journal: Journal for ImmunoTherapy of Cancer (2014)

Meeting abstracts Cancer vaccines aim at inducing tumour-specific immune responses. However, in clinical studies so far these approaches have limited antitumour effect. Evidence is accumulating that MDSC (myeloid-derived suppressor cells) can suppress the antitumour immune response. Reversal of