tbuckley/cabot-search huggingface dataset:
Effects of leukotriene B4 in the human lung. Recruitment of neutrophils into the alveolar spaces without a change in protein permeability.
Authors: T R Martin, B P Pistorese, E Y Chi, R B Goodman, M A Matthay
Journal: Journal of Clinical Investigation (1989)

Leukotriene B4 (LTB4) is a major product of human alveolar macrophages and has potent chemotactic activity for neutrophils (PMN) in vitro. To evaluate the effects of LTB4 in the normal human lung, we instilled LTB4 (5 X 10(-7)M, 10 ml) into a subsegment of the right middle lobe and 0.9% NaCl (10 ml) into a subsegment of the lingula using a fiberoptic bronchoscope in 12 healthy human volunteers. 4 h later, we performed bronchoalveolar lavage of the same subsegments. Compared with the NaCl instillation, LTB4 caused a large increase in lavage total cells (NaCl = 6.8 +/- 1.0 X 10(6) vs. LTB4 = 26.4 +/- 5.0 X 10(6), P less than 0.01), most of which were PMN (NaCl = 12.2 +/- 4.6% vs. LTB4 = 55.7 +/- 6.0%, P less than 0.001). In contrast, there was only a small increase in lavage total protein, and the lavage total protein correlated weakly with lavage total cells and PMN. The production of superoxide anion by the lavage PMN in response to phorbol myristate acetate was similar to that of peripheral blood PMN. The migration of lavage PMN was normal toward the chemotactic peptide FMLP, but reduced toward LTB4 and zymosan-activated human serum. Morphometric analysis using transmission electron microscopy indicated a selective loss of small granules in the lung neutrophils as compared with peripheral blood neutrophils. The data indicate that in the normal human lung, LTB4 can recruit active PMN into the airspaces without causing a significant change in the protein permeability of the epithelial barrier.
Dialectical repression theory
Authors: David H. Gleaves
Journal: Behavioral and Brain Sciences (2006)

Erdelyi's dialectical repression theory attempts to reconcile what appear to be incompatible perspectives in the contentious area of memory for trauma. He partially succeeds and makes a strong case that repression is “an empirical fact,” but makes a weaker case that distortions and omissions are due to the same mechanism and that recovered memories are necessarily unreliable. Available data do not suggest that the return of the repressed is any less accurate than the return of the non-repressed.
Unraveling the Role of Podocyte Turnover in Glomerular Aging and Injury
Authors: Nicola Wanner, Björn Hartleben, Nadja Herbach, Markus Goedel, Natalie Stickel, Robert Zeiser, Gerd Walz, Marcus J. Moeller, Florian Grahammer, Tobias B. Huber
Journal: Journal of the American Society of Nephrology (2014)

Podocyte loss is a major determinant of progressive CKD. Although recent studies showed that a subset of parietal epithelial cells can serve as podocyte progenitors, the role of podocyte turnover and regeneration in repair, aging, and nephron loss remains unclear. Here, we combined genetic fate mapping with highly efficient podocyte isolation protocols to precisely quantify podocyte turnover and regeneration. We demonstrate that parietal epithelial cells can give rise to fully differentiated visceral epithelial cells indistinguishable from resident podocytes and that limited podocyte renewal occurs in a diphtheria toxin model of acute podocyte ablation. In contrast, the compensatory programs initiated in response to nephron loss evoke glomerular hypertrophy, but not de novo podocyte generation. In addition, no turnover of podocytes could be detected in aging mice under physiologic conditions. In the absence of podocyte replacement, characteristic features of aging mouse kidneys included progressive accumulation of oxidized proteins, deposits of protein aggregates, loss of podocytes, and glomerulosclerosis. In summary, quantitative investigation of podocyte regeneration in vivo provides novel insights into the mechanism and capacity of podocyte turnover and regeneration in mice. Our data reveal that podocyte generation is mainly confined to glomerular development and may occur after acute glomerular injury, but it fails to regenerate podocytes in aging kidneys or in response to nephron loss.
Inspiratory fraction and exercise impairment in COPD patients GOLD stages II-III
Authors: A. L. P. Albuquerque, L. E. Nery, D. S. Villaça, T. Y. S. Machado, C. C. Oliveira, Â. T. Paes, J. A. Neder
Journal: European Respiratory Journal (2006)

The inspiratory-to-total lung capacity ratio or "inspiratory fraction" (inspiratory capacity(IC)/total lung capacity (TLC)) may be functionally more representative than traditional indices of resting airflow limitation and lung hyperinflation in patients with chronic obstructive pulmonary disease (COPD). In the present retrospective study, a comparison was made of the individual performance of post-bronchodilator IC, IC/TLC and forced expiratory volume in one second (FEV(1)) in predicting a severely reduced peak oxygen uptake (V'(O(2)); <60% predicted) in 44 COPD patients Global Initiative for Chronic Obstructive Lung Disease stages II-III (post-bronchodilator FEV(1) ranging from 31-79% pred). Patients with lower IC/TLC values (<or=0.28) showed increased lung volumes and reduced exercise capacity as compared with other subjects. Following a multiple linear regression analysis, only IC/TLC and FEV(1) remained as independent predictors of V'(O(2)) (r(2) = 0.33). A receiver operating characteristic (ROC) curve analysis revealed that an IC/TLC <or=0.28 had the highest specificity (89.6%), positive predictive value (80%) and overall accuracy (86.3%) in identifying patients with V'(O(2)) <60% pred. In addition, the area under the ROC curve tended to be higher for IC/TLC than IC. In conclusion, post-bronchodilator total lung capacity-corrected inspiratory fraction provides useful information in addition to forced expiratory volume in one second and inspiratory capacity, to estimate the likelihood of chronic obstructive pulmonary disease patients to present with severely reduced maximal exercise capacity.
Confocal chromoscopic endomicroscopy is superior to chromoscopy alone for the detection and characterisation of intraepithelial neoplasia in chronic ulcerative colitis
Authors: D P Hurlstone, R Kiesslich, M Thomson, R Atkinson, S S Cross
Journal: Gut (2008)

The diagnosis of intraepithelial neoplasia is pivotal for ongoing clinical management decisions in ulcerative colitis. Previous studies have compared the diagnostic yield of endomicroscopy with conventional "white light" endoscopy and hence the overall objective increase of endomicroscopy targeted biopsies as compared to chromoscopy guided alone is not apparent.We performed a prospective randomised controlled study to compare the diagnostic yield of intraepithelial neoplasia and cancer in patients undergoing ulcerative colitis screening using chromoscopy assisted endomicroscopy (group A) versus pan-colonic chromoscopy assisted colonoscopy (group B).Patients were randomised in a 1:1 ratio to undergo screening colonoscopy using either chromoscopic endomicroscopy or chromoscopy alone with targeted biopsies. Circumscribed lesions were characterised using endomicroscopy and chromoscopy with pit pattern analysis. Targeted biopsies in addition to conventional 10 cm quadrantic biopsies were taken. Primary outcome addressed the number of intraepithelial neoplasias detected in each group.Endomicroscopy targeted biopsies significantly increased the yield of intraepithelial neoplasia as compared to pan-chromoscopy and biopsy alone (p<0.001) and also increased the yield of high-grade dysplastic lesions (p<0.001). Endomicroscopy targeted biopsies increased the diagnostic yield of intraepithelial neoplasia as compared to chromoscopy guided biopsies alone by 2.5-fold.This is the first randomised controlled study to show the true clinical benefit of endomicroscopy for the in vivo detection and characterisation of intraepithelial neoplasia in chronic ulcerative colitis surveillance colonoscopy. Endomicroscopy with targeted biopsy may potentially be the "gold standard" for the detection of intraepithelial neoplasia in ulcerative colitis.
Effect of methacholine challenge on cellular composition of sputum induction
Authors: A Spanevello, A M Vignola, A Bonanno, M Confalonieri, E Crimi, V Brusasco
Journal: Thorax (1999)

<h3>BACKGROUND</h3> Induced sputum and methacholine inhalation challenge are routinely used for the assessment of airway inflammation and airway hyperresponsiveness, respectively. This study investigates whether a methacholine challenge performed one hour before sputum induction alters the cellular and biochemical constituents of sputum. <h3>METHODS</h3> Sixteen stable asthmatic patients with lung function within the normal range underwent two sputum inductions within one week. One hour before one of the sputum inductions a methacholine challenge was performed. <h3>RESULTS</h3> There were no significant differences in total cell count, macrophages, neutrophils, eosinophils, lymphocytes, epithelial cells, ECP, and albumin between the two challenges. The repeatability of cell counts was good for all cells, ECP and albumin, but poor for total cells. <h3>CONCLUSIONS</h3> In patients with stable asthma a methacholine challenge carried out one hour before sputum induction does not significantly alter the cellular and biochemical constituents of sputum.
Polyp Guideline: Diagnosis, Treatment, and Surveillance for Patients with Nonfamilial Colorectal Polyps*
Authors: John H. Bond
Journal: Annals of Internal Medicine (1993)

Objective: To outline the preferable approach to the management of patients with nonfamilial colorectal polyps. Data Sources: The human subject English language literature for the past 15 years, searched using MEDLINE and the terms polyp-, adenoma-, and polypectomy-colorectal. Study Selection: The titles and abstracts of all pertinent articles were reviewed. All randomized, controlled trials and large case–control and cohort studies related to colorectal polyps were reviewed in depth. Data Synthesis: Evidence was evaluated along a hierarchy with randomized, controlled trials receiving the greatest weight. Conclusions and recommendations were reviewed by a large group of experts in gastroenterology, radiology, and pathology and were circulated for comment to primary care medical societies. Conclusions: Most patients with polyps should undergo colonoscopy to excise the polyp and search for synchronous neoplasms. Small polyps (<0.5 cm) require individualization. A hyperplastic polyp found during proctosigmoidoscopy is not an indication for colonoscopy. Large sessile polyps require careful follow-up to ensure complete resection. The need for further treatment of a resected polyp with invasive carcinoma depends on several well-defined clinical and pathologic criteria. Follow-up surveillance after polypectomy should be tailored to the individual risk assessment for each patient. Initial follow-up should be performed at 3 years for most postpolypectomy patients. After one negative result of a 3-year examination, the interval can be increased to 5 years. Patients with one small tubular adenoma do not have an increased risk for cancer, and therefore follow-up surveillance may not be indicated. Adoption of these recommendations should substantially reduce the cost of postpolypectomy surveillance and of screening for colorectal cancer. * This guideline has been officially endorsed by the American Society for Gastrointestinal Endoscopy and the American Gastroenterological Association. It is an official statement of the American College of Gastroenterology. For a list of the members of the Practice Parameters Committee of the American College of Gastroenterology, see end of text.
Ammonia and related amino acids in the pathogenesis of brain edema in acute ischemic liver failure in rats
Authors: Margaret Swain, Roger F. Butterworth, Andres T. Blei
Journal: Hepatology (1992)

The pathogenesis of brain edema in acute liver failure is poorly understood. We have previously shown that rats with ischemic acute liver failure (portacaval anastomosis followed by hepatic artery ligation) exhibit brain edema and intracranial hypertension, with swelling of cortical astrocytes as the most prominent neuropathological abnormality. Because ammonia has been shown to induce swelling of astrocytes in vivo and in vitro , we examined the relationship between brain ammonia, amino acids generated from ammonia metabolism and brain water content in this model. Four groups of animals were studied: rats subjected to two sham operations, rats subjected to portacaval anastomosis and a sham operation, rats subjected to a sham operation and hepatic artery ligation and rats subjected to portacaval anastomosis and hepatic artery ligation. The last group of animals was studied at three progressive stages of encephalopathy. Cortical gray matter water increased from 80.26% ± 0.22% (sham + sham) to 82.46% ± 0.06% (last stage of devascularization). In cerebral cortex, brain ammonia increased to a maximum of 5.4 mmol/L. Glutamine, generated in glial cells from ammonia and glutamate, increased sixfold to 24 mmol/L and remained at this level throughout all stages of encephalopathy. Alanine, which may be generated from the transamination of glutamine, increased in parallel to the increase in water (r = 0.80, n = 15). In this model of fulminant liver failure and associated brain edema, brain ammonia increases to levels associated with in vitro swelling of brain slices and glial cells. The accumulation of osmogenic aminoacids such as glutamine and alanine may contribute to the selective astrocyte swelling seen in this condition. Ammonia, by its metabolically related amino acids, may play a role in the pathogenesis of brain edema in acute liver failure. (Hepatology 1992;15:449-453).
Lipoid proteinosis: an inherited disorder of collagen metabolism?
Authors: J.I. HARPER, V.C. DUANCE, T.J. SIMS, N.D. LIGHT
Journal: British Journal of Dermatology (1985)

The dermal collagen of a patient with lipoid proteinosis was investigated by immunohistochemistry and biochemical analysis. The affected skin was found to contain significantly less collagen per unit dry weight than normal dermis but showed elevated levels of type 3 collagen with respect to type I. Purification of collagen types from affected skin after pepsin digestion showed no novel forms, but a doubling in the yield of type 5 collagen. These results correlated well with those of immunohistochemistry which showed a patchy, diffuse, widely distributed type 3 collagen and an increase in types 4 and 5 collagens associated with 'onion skin' endothelial basement membrane thickening. Estimation of collagen cross-links showed an abnormal pattern with a preponderance of the keto-imine form not normally associated with skin. These results strongly suggest that lipoid proteinosis involves a primary perturbation of collagen metabolism.
Pulmonary surfactant in cystic fibrosis
Authors: M Griese, P Birrer, A Demirsoy
Journal: European Respiratory Journal (1997)

Cystic fibrosis (CF) leads to a chronic inflammation of the airways with significant air flow limitations developing early in the course of the disease. As a well-functioning pulmonary surfactant is necessary to keep the alveoli and the small conducting airways open during expiration, we hypothesized that the biochemical and biophysical properties of surfactant may be impaired in CF. Bronchoalveolar lavage fluid obtained during a clinically stable period was analysed from 20 CF patients (5.9-20 yrs) and 17 healthy children and adults. CF patients had significantly elevated total and polymorphonuclear neutrophil cell counts, whereas the concentrations of total protein and phospholipids did not differ from controls. The percentage of surface active phospholipids, phosphatidylcholine and phosphatidylglycerol, and the concentration of surfactant protein A were significantly reduced in CF patients. Surfactant protein B was unchanged. Although the relative proportion of large aggregates was higher in CF, their surface active properties were inferior, as assessed in the pulsating bubble surfactometer. Because the capacity of CF lavage fractions to inhibit surfactant function was the same as that of controls, impaired minimal surface tension was more likely to be due to the biochemical alterations detected, than to inhibition of a well-functioning surfactant. The impaired pulmonary surfactant system in clinically stable patients with cystic fibrosis is in agreement with the view that surfactant dysfunction may contribute to lung disease in cystic fibrosis.
Impacting tumor cell-fate by targeting the inhibitor of apoptosis protein survivin
Authors: Ronan J Kelly, Ariel Lopez-Chavez, Deborah Citrin, John E Janik, John C Morris
Journal: Molecular Cancer (2011)

Abstract Survivin ( BIRC5 ), a member of the inhibitor of apoptosis protein (IAP) family that inhibits caspases and blocks cell death is highly expressed in cancer and is associated with a poorer clinical outcome. Functioning simultaneously during cell division and apoptosis inhibition, survivin plays a pivotal role in determining cell survival. Survivin has consistently been identified by molecular profiling analysis to be associated with higher tumor grade, more advanced disease, abbreviated survival, accelerated rates of recurrence, and chemotherapy and radiation resistance. Survivin's differential expression in cancer compared to normal tissue and its role as a nodal protein in a number of cellular pathways make it a highly flexible therapeutic target, suitable for small-molecule inhibitiors, molecular antagonists, and vaccination-based therapies. By targeting survivin it is hoped that multiple tumor signaling circuitries may be simultaneously disabled. This effect may be applicable to many tumor histologies irrespective of specific genetic makeup. To date, survivin inhibitors have shown modest activity as single agents, but it is anticipated that when given in combination with cytotoxic chemotherapy or monoclonal antibodies they may exhibit enhanced efficacy. This review discusses the complex circuitry of survivin in human cancers and highlights clinical trials involving novel agents that target this important protein.
Evaluation of the addition of rituximab to CODOX-M/IVAC for Burkitt's lymphoma: a retrospective analysis
Authors: J.A. Barnes, A.S. LaCasce, Y. Feng, C.E. Toomey, D. Neuberg, J.S. Michaelson, E.P. Hochberg, J.S. Abramson
Journal: Annals of Oncology (2011)
Nerve conduction studies of upper extremities in tennis players
Authors: T Çolak, B Bamaç, A Özbek, F Budak, Y S Bamaç
Journal: British Journal of Sports Medicine (2004)

The influence of regular and intense practice of an asymmetric sport such as tennis on nerves in the elbow region was examined.The study included 21 male elite tennis players with a mean (SD) age of 27.5 (1.7) years and 21 male non-active controls aged 26.4 (1.9) years. Anthropometric measurements (height, weight, limb length, and perimeters of arm and forearm) were determined for each subject, and range of motion assessment and radiographic examination carried out. Standard nerve conduction techniques using constant measured distances were applied to evaluate the median, ulnar, and radial nerves in the dominant and non-dominant limb of each individual.The sensory and motor conduction velocities of the radial nerve and the sensory conduction velocity of the ulnar nerve were significantly delayed in the dominant arms of tennis players compared with their non-dominant arms and normal subjects. There were no statistical differences in the latencies, conduction velocities, or amplitudes of the median motor and sensory nerves between controls and tennis players in either the dominant or non-dominant arms. However, the range of motion of the upper extremity was significantly increased in tennis players when compared with control subjects. Tennis players were taller and heavier than control subjects and their dominant upper limb lengths were longer, and arm and forearm circumferences greater, than those of the control subjects.Many of the asymptomatic tennis players with abnormal nerve conduction tests in the present study may have presymptomatic or asymptomatic neuropathy similar to subclinical entrapment nerve neuropathy.
The Unfolded Protein Response: A Pathway That Links Insulin Demand with β-Cell Failure and Diabetes
Authors: Donalyn Scheuner, Randal J. Kaufman
Journal: Endocrine Reviews (2008)

Abstract The endoplasmic reticulum (ER) is the entry site into the secretory pathway for newly synthesized proteins destined for the cell surface or released into the extracellular milieu. The study of protein folding and trafficking within the ER is an extremely active area of research that has provided novel insights into many disease processes. Cells have evolved mechanisms to modulate the capacity and quality of the ER protein-folding machinery to prevent the accumulation of unfolded or misfolded proteins. These signaling pathways are collectively termed the unfolded protein response (UPR). The UPR sensors signal a transcriptional response to expand the ER folding capacity, increase degredation of malfolded proteins, and limit the rate of mRNA translation to reduce the client protein load. Recent genetic and biochemical evidence in both humans and mice supports a requirement for the UPR to preserve ER homeostasis and prevent the β-cell failure that may be fundamental in the etiology of diabetes. Chronic or overwhelming ER stress stimuli associated with metabolic syndrome can disrupt protein folding in the ER, reduce insulin secretion, invoke oxidative stress, and activate cell death pathways. Therapeutic interventions to prevent polypeptide-misfolding, oxidative damage, and/or UPR-induced cell death have the potential to improve β-cell function and/or survival in the treatment of diabetes.
Germinal Center B Cells Regulate Their Capability to Present Antigen by Modulation of HLA-DO
Authors: Kim S. Glazier, Sandra B. Hake, Helen M. Tobin, Amy Chadburn, Elaine J. Schattner, Lisa K. Denzin
Journal: The Journal of Experimental Medicine (2002)

Peptide acquisition by MHC class II molecules is catalyzed by HLA-DM (DM). In B cells, HLA-DO (DO) inhibits or modifies the peptide exchange activity of DM. We show here that DO protein levels are modulated during B cell differentiation. Remarkably, germinal center (GC) B cells, which have low levels of DO relative to naive and memory B cells, are shown to have enhanced antigen presentation capabilities. DM protein levels also were somewhat reduced in GC B cells; however, the ratio of DM to DO in GC B cells was substantially increased, resulting in more free DM in GC B cells. We conclude that modulation of DM and DO in distinct stages of B cell differentiation represents a mechanism by which B cells regulate their capacity to function as antigen-presenting cells. Efficient antigen presentation in GC B cells would promote GC B cell–T cell interactions that are essential for B cells to survive positive selection in the GC.
RGS2 Determines Short-Term Synaptic Plasticity in Hippocampal Neurons by Regulating Gi/o- Mediated Inhibition of Presynaptic Ca2+ Channels
Authors: Jing Han, Melanie D. Mark, Xiang Li, Mian Xie, Sayumi Waka, Jens Rettig, Stefan Herlitze
Journal: Neuron (2006)
Bilateral pulmonary varicosities associated with coarctation of the aorta
Authors: G. Rizk, R. Melhem, I. Dagher
Journal: Thorax (1970)

Varicosities of the pulmonary vein are rare. Twenty-eight cases confirmed anatomically or by angiography have been reported. In this paper the authors report a rather unique patient who had bilateral varices of the lungs in conjunction with coarctation of the aorta. The plain film and angiographic features of pulmonary varices are discussed. A brief review of the cases reported previously is also presented.
PEGylated NaHoF4 nanoparticles as contrast agents for both X-ray computed tomography and ultra-high field magnetic resonance imaging
Authors: Dalong Ni, Jiawen Zhang, Wenbo Bu, Chen Zhang, Zhenwei Yao, Huaiyong Xing, Jing Wang, Fei Duan, Yanyan Liu, Wenpei Fan, Xiaoyuan Feng, Jianlin Shi
Journal: Biomaterials (2015)