tbuckley/cabot-search huggingface dataset:
Active sodium-urea counter-transport is inducible in the basolateral membrane of rat renal initial inner medullary collecting ducts.
Authors: A Kato, J M Sands
Journal: Journal of Clinical Investigation (1998)

Rat inner medullary collecting ducts (IMCD3s) possess a luminal Na+-dependent, active urea secretory transport process, which is upregulated by water diuresis. In this study of perfused IMCDs microdissected from base (IMCD1), middle (IMCD2), or tip (IMCD3) of the inner medulla, we tested whether furosemide diuresis alters active urea transport. Rats received furosemide (10 mg/d s.c. for 3-4 d) and were compared with pair-fed control rats. Furosemide significantly decreased urine osmolality and urea clearance, and increased blood urea nitrogen. IMCD3s from furosemide-treated rats had significantly lower rates of active urea secretion than IMCD3s from control rats. IMCD2s showed no active urea transport in control or furosemide-treated rats. IMCD1s from control rats had no active urea transport, but IMCD1s from furosemide-treated rats expressed significant rates of active urea reabsorption. In IMCD1s, this active urea reabsorptive transport process was inhibited by: (i) 0. 25 mM phloretin (bath); (ii) 1 mM ouabain (bath); and (iii) replacing bath Na+ with NMDG+; it was stimulated by 10 nM bumetanide (bath). In summary, we found that furosemide decreased active urea secretion in IMCD3s and induced active urea reabsorption in IMCD1s. The new Na+- dependent, active urea reabsorptive transport process may be a basolateral Na+-urea antiporter.
LXR promotes the maximal egress of monocyte-derived cells from mouse aortic plaques during atherosclerosis regression
Authors: Jonathan E. Feig, Ines Pineda-Torra, Marie Sanson, Michelle N. Bradley, Yuliya Vengrenyuk, Dusan Bogunovic, Emmanuel L. Gautier, Daniel Rubinstein, Cynthia Hong, Jianhua Liu, Chaowei Wu, Nico van Rooijen, Nina Bhardwaj, Michael J. Garabedian, Peter Tontonoz, Edward A. Fisher
Journal: Journal of Clinical Investigation (2010)

We have previously shown that mouse atherosclerosis regression involves monocyte-derived (CD68+) cell emigration from plaques and is dependent on the chemokine receptor CCR7. Concurrent with regression, mRNA levels of the gene encoding LXRalpha are increased in plaque CD68+ cells, suggestive of a functional relationship between LXR and CCR7. To extend these results, atherosclerotic Apoe-/- mice sufficient or deficient in CCR7 were treated with an LXR agonist, resulting in a CCR7-dependent decrease in plaque CD68+ cells. To test the requirement for LXR for CCR7-dependent regression, we transplanted aortic arches from atherosclerotic Apoe-/- mice, or from Apoe-/- mice with BM deficiency of LXRalpha or LXRbeta, into WT recipients. Plaques from both LXRalpha and LXRbeta-deficient Apoe-/- mice exhibited impaired regression. In addition, the CD68+ cells displayed reduced emigration and CCR7 expression. Using an immature DC line, we found that LXR agonist treatment increased Ccr7 mRNA levels. This increase was blunted when LXRalpha and LXRbeta levels were reduced by siRNAs. Moreover, LXR agonist treatment of primary human immature DCs resulted in functionally significant upregulation of CCR7. We conclude that LXR is required for maximal effects on plaque CD68+ cell expression of CCR7 and monocyte-derived cell egress during atherosclerosis regression in mice.
Sudden cardiac death screening in adolescent athletes: an evaluation of compliance with national guidelines
Authors: Nicolas L Madsen, Jonathan A Drezner, Jack C Salerno
Journal: British Journal of Sports Medicine (2012)

Objective In the USA, the preparticipation physical evaluation (PPE) is the standard of care for screening eight million high-school athletes for their risk of sudden cardiac death (SCD). Our aim was to evaluate both physician and school compliance with national guidelines for SCD screening. Methods We conducted a confidential survey of the Washington Chapter of the American Academy of Pediatrics (AAP), the Washington Academy of Family Physicians (WAFP) and Washington State high-school athletic directors. Responses were evaluated for compliance with the American Heart Association (AHA) guidelines for SCD screening. Results We received a response rate of 72% (559/776) from the AAP, 56% (554/990) from the WAFP and 78% (317/409) from the athletic directors. Only 6% of all providers and 0% of schools were in compliance with AHA guidelines. In addition, 47% of the physicians and 6% of athletic directors reported awareness of the guidelines. There was no difference in compliance between physician specialties (p=0.20). Physician location, years of experience and exposure to SCD were not significantly associated with compliance. Provider knowledge of the guidelines, number of PPE/month and frequency of referrals to cardiology were all positively associated with improved overall compliance (p&lt;0.05). Conclusions Despite the unaltered presence of the AHA SCD screening guidelines for the past 15 years, compliance with the recommendations is poor. Lack of compliance does not reflect clinical experience, but rather lack of knowledge of the guidelines themselves. New directions for provider education and policy requirements are needed to improve this implementation gap.
AN INTRACELLULAR DEFECT IN PROTEIN SYNTHESIS INDUCED BY CARBON TETRACHLORIDE
Authors: Edward A. Smuckler, Oscar A. Iseri, Earl P. Benditt
Journal: The Journal of Experimental Medicine (1962)

The morphological and certain metabolic effects of carbon tetrachloride intoxication were studied in the rat with emphasis on liver alterations. Morphological changes were investigated by histological and electron microscopical means. Functional changes were investigated using histochemical and amino acid incorporation, techniques. The liver constituents were examined chemically. Plasma volume alterations were measured using dye and homologous protein dilution techniques. The histological appearance of the liver of treated animals included cellular swelling, dispersal of the cytoplasmic basophilia, and necrosis. Electron micrographs showed an early (3 hours following carbon tetrachloride administration) and widespread dislocation of the ribonucleoprotein particles from the membranes of the rough endoplasmic reticulum, but no apparent alteration in the mitochondrial structure. Histochemical examination of two mitochondrial enzyme systems, alpha-ketoglutarate dehydrogenase and succinic dehydrogenase, revealed no alterations in activities until a later time (6 to 12 hours following carbon tetrachloride administration). ATPase showed a gross quantitative decrease in activity at 6 and 12 hours, but not earlier. There was a decreased amino acid incorporation into two liver-produced proteins, viz., albumin and fibrinogen. This decrease is not explicable on the basis of the inability of the liver to take up the amino acid, an altered dilution volume into which the amino acid or formed protein is placed, or an impaired capacity of the liver to excrete protein once formed. It is concluded that the decreased amino acid incorporation rate reflects depressed synthesis of protein by the liver. Other pathological changes in the liver, including necrosis, fatty change, and mitochondrial alterations may be dependent upon severe impairment of protein synthesis.
Event-Free Survival of Patients With High-Risk Neuroblastoma Treated With an N6-Like Induction Treatment
Authors: Dominique Valteau-Couanet
Journal: Journal of Clinical Oncology (2005)

In their letter, Akhtar and Maghfor diligently highlight important pitfalls related to retrospective database analyses.Most, if not all, points raised in their comments were already addressed in the Discussion section of our article. 1Indeed, far from drawing a cause-effect relationship, our article simply describes associations between the pretransplant administration of rituximab and outcomes of autologous stemcell transplantation in a group of chemosensitive relapsed non-Hodgkin's lymphoma (primary induction failure and refractory relapses are not autografted at our center).This question is practically unanswerable in a prospective randomized trial, due to the increasing use of rituximab in non-Hodgkin's lymphoma patients.Figure 1 in the article summarizes trends in the administration of rituximab before referral to our center for autografting (including 2003 patients); however, only patients with at least 6 months of follow-up (transplantation before June 2003) were included in the analysis.Additionally, only commonly accepted prognostic indicators (age, time from diagnosis to relapse/transplant, 2 number of prior chemotherapy regimens) with the exception of the IPI score at relapse 3 (information not available in our database) were included in multivariate analyses.To our knowledge, neither pretransplantation therapy (induction 4 or salvage) nor conditioning 5 affects the outcomes of autografting for NHL.Finally, we agree with Akhtar and Maghfor that our article provides no explanation for the delay in platelets recovery in patients who received rituximab pretransplantation.As mentioned in the Results section, this observation is independent of age, time from diagnosis to transplantation, number of chemotherapy courses pretransplantation, number of CD34 ϩ cells infused, and timing of administration of rituximab (Ͻ 3 or Ͼ 3 months).Interestingly, no significant bleeding was observed among our 273 transplantation patients, regardless of prior administration of rituximab, confirming the commonly accepted notion that bleeding after state-ofthe-art autologous transplantation is a rather uncommon complication.
THE CHEMISTRY OF THE LIVER IN ACUTE YELLOW ATROPHY
Authors: H. Gideon Wells
Journal: The Journal of Experimental Medicine (1907)

From the liver of a young man who died of typical, " idiopathic" acute yellow atrophy of the liver, after an illness of six weeks, there were isolated and identified the following amino acids: Histidin, lysin, tyrosin, leucin, glycocoll, alanin, prolin, glutaminic acid, aspartic acid. These were found free in extracts of the liver, and presumably represent products of the autolysis of liver cells, although the amount of soluble non-protein nitrogen present in the extracts was so large as to suggest that there must be some other source for these substances. Small quantities of free proteoses and peptones, and of xanthin and hypoxanthin, were also found in the extracts. In the insoluble proteins of the liver the proportion of diamino acids was decreased slightly as compared with normal livers. The proportion of protein phosphorus was increased, probably because of active regenerative proliferation, while the sulphur was normal in amount. Iron was increased because of the large quantity of blood in the liver and the hematogenous pigmentation of the liver cells. Gelatigenous material was increased both absolutely and relatively, because of the loss of parenchyma and the proliferation of the stroma. The proportion of water to solids was much increased, there having been a loss of over two-thirds of the entire parenchymatous elements of the liver. The amount of fat, lecithin and cholesterin was not far from that normal for the liver.
ADMINISTRATION OF 3'-AZIDO-3'-DEOXYTHYMIDINE, AN INHIBITOR OF HTLV-III/LAV REPLICATION, TO PATIENTS WITH AIDS OR AIDS-RELATED COMPLEX
Authors: Robert Yarchoan, KentJ. Weinhold, H.Kim Lyerly, Edward Gelmann, RobertM. Blum, GeneM. Shearer, Hiroaki Mitsuya, JerryM. Collins, CharlesE. Myers, RaymondW. Klecker, PhillipD. Markham, DavidT. Durack, S.Nusinoff Lehrman, DavidW. Barry, MargaretA. Fischl, RobertC. Gallo, DaniP. Bolognesi, Samuel Broder
Journal: The Lancet (1986)
Anemia may influence the outcome of patients undergoing neo-adjuvant treatment of rectal cancer
Authors: R. Berardi, C. Braconi, G. Mantello, M. Scartozzi, S. Del Prete, G. Luppi, R. Martinelli, M. Fumagalli, G. Valeri, I. Bearzi, C. Marmovale, F. Grillö-Ruggieri, S. Cascinu
Journal: Annals of Oncology (2006)
Baby P doctor is allowed to remove herself from medical register
Authors: C. Dyer
Journal: BMJ (2011)

The paediatrician accused of missing Baby P’s broken back two days before he was found dead has been allowed to avoid a public misconduct hearing by removing herself voluntarily from the UK medical register.

A General Medical Council fitness to practise panel accepted that Sabah Al-Zayyat was too ill to attend a hearing, that her absence was “genuine and involuntary,” and that in the “exceptional” circumstances of the case she should be permitted to take her name off the register.

Dr Al-Zayyat was working as a locum consultant paediatrician at the child development clinic at St Ann’s Hospital in north London …
Insulin resistance and vasodilation in essential hypertension. Studies with adenosine.
Authors: A Natali, R Bonadonna, D Santoro, A Q Galvan, S Baldi, S Frascerra, C Palombo, S Ghione, E Ferrannini
Journal: Journal of Clinical Investigation (1994)

Insulin-mediated vasodilation has been proposed as a determinant of in vivo insulin sensitivity. We tested whether sustained vasodilation with adenosine could overcome the muscle insulin resistance present in mildly overweight patients with essential hypertension. Using the forearm technique, we measured the response to a 40-min local intraarterial infusion of adenosine given under fasting conditions (n = 6) or superimposed on a euglycemic insulin clamp (n = 8). In the fasting state, adenosine-induced vasodilation (forearm blood flow from 2.6 +/- 0.6 to 6.0 +/- 1.2 ml min-1dl-1, P < 0.001) was associated with a 45% rise in muscle oxygen consumption (5.9 +/- 1.0 vs 8.6 +/- 1.7 mumol min-1dl-1, P < 0.05), and a doubling of forearm glucose uptake (0.47 +/- 0.15 to 1.01 +/- 0.28 mumol min-1dl-1, P < 0.05). The latter effect remained significant also when expressed as a ratio to concomitant oxygen balance (0.08 +/- 0.03 vs 0.13 +/- 0.04 mumol mumol-1, P < 0.05), whereas for all other metabolites (lactate, pyruvate, FFA, glycerol, citrate, and beta-hydroxybutyrate) this ratio remained unchanged. During euglycemic hyperinsulinemia, whole-body glucose disposal was stimulated (to 19 +/- 3 mumol min-1kg-1), but forearm blood flow did not increase significantly above baseline (2.9 +/- 0.2 vs 3.1 +/- 0.2 ml min-1dl-1, P = NS). Forearm oxygen balance increased (by 30%, P < 0.05) and forearm glucose uptake rose fourfold (from 0.5 to 2.3 mumol min-1dl-1, P < 0.05). Superimposing an adenosine infusion into one forearm resulted in a 100% increase in blood flow (from 2.9 +/- 0.2 to 6.1 +/- 0.9 ml min-1dl-1, P < 0.001); there was, however, no further stimulation of oxygen or glucose uptake compared with the control forearm. During the clamp, the ratio of glucose to oxygen uptake was similar in the control and in the infused forearms (0.27 +/- 0.11 and 0.23 +/- 0.09, respectively), and was not altered by adenosine (0.31 +/- 0.9 and 0.29 +/- 0.10). We conclude that in insulin-re15-76sistant patients with hypertension, adenosine-induced vasodilation recruits oxidative muscle tissues and exerts a modest, direct metabolic effect to promote muscle glucose uptake in the fasting state. Despite these effects, however, adenosine does not overcome muscle insulin resistance.
Oxidized Low-Density Lipoproteins Trigger Endoplasmic Reticulum Stress in Vascular Cells
Authors: Marie Sanson, Nathalie Augé, Cécile Vindis, Carole Muller, Yoshio Bando, Jean-Claude Thiers, Marie-Agnès Marachet, Kamelija Zarkovic, Yoshiki Sawa, Robert Salvayre, Anne Nègre-Salvayre
Journal: Circulation Research (2008)

Oxidized low-density lipoproteins (oxLDLs) trigger various biological responses potentially involved in atherogenesis. Disturbing endoplasmic reticulum (ER) function results in ER stress and unfolded protein response, which tends to restore ER homeostasis but switches to apoptosis when ER stress is prolonged. We aimed to investigate whether ER stress is induced by oxLDLs and can be prevented by the ER-associated chaperone ORP150 (150-kDa oxygen-regulated protein). oxLDLs and the lipid oxidation products 7-ketocholesterol and 4-hydroxynonenal induce ER stress in human endothelial cells (HMEC-1), characterized by the activation of ER stress sensors (phosphorylation of Ire1alpha and PERK, nuclear translocation of ATF6) and of their subsequent pathways (eukaryotic initiation factor 2alpha phosphorylation, expression of XBP1/spliced XBP1, CHOP, and KDEL chaperones GRP78, GRP94, ORP150). ER stress was inhibited by the antioxidant N-acetylcysteine. In advanced atherosclerotic lesions, phospho-Ire1alpha, KDEL, and ORP150 staining were localized in lipid-rich areas with 4-hydroxynonenal adducts and CD68-positive macrophagic cells. By comparison, staining for 4-hydroxynonenal, phospho-Ire1alpha, KDEL, and ORP were faint and more diffuse in intimal hyperplasia. ER stress takes part in the apoptotic effect of oxLDLs, through the Ire1alpha/c-Jun N-terminal kinase pathway, as assessed by the protective effect of specific small interfering RNAs and c-Jun N-terminal kinase inhibitor. Forced expression of the chaperone ORP150 reduced both oxLDL-induced ER stress and apoptosis. ER stress markers and ORP150 chaperone are expressed in areas containing oxLDLs in atherosclerotic lesions and are induced by oxLDLs and oxidized lipids in cultured cells. The forced expression of ORP150 highlights its new protective role against oxLDL-induced ER stress and subsequent apoptosis.
Sleep Quality and Preclinical Alzheimer Disease
Authors: Yo-El S. Ju, Jennifer S. McLeland, Cristina D. Toedebusch, Chengjie Xiong, Anne M. Fagan, Stephen P. Duntley, John C. Morris, David M. Holtzman
Journal: JAMA Neurology (2013)

Sleep and circadian problems are very common in Alzheimer disease (AD). Recent animal studies suggest a bidirectional relationship between sleep and β-amyloid (Aβ), a key molecule involved in AD pathogenesis.To test whether Aβ deposition in preclinical AD, prior to the appearance of cognitive impairment, is associated with changes in quality or quantity of sleep.Cross-sectional study conducted from October 2010 to June 2012.General community volunteers at the Washington University Knight Alzheimer's Disease Research Center.Cognitively normal individuals (n = 145) 45 years and older were recruited from longitudinal studies of memory and aging at the Washington University Knight Alzheimer's Disease Research Center. Valid actigraphy data were recorded in 142. The majority (124 of 142) were recruited from the Adult Children Study, in which all were aged 45 to 75 years at baseline and 50% have a parental history of late-onset AD. The rest were recruited from a community volunteer cohort in which all were older than 60 years and healthy at baseline.Sleep was objectively measured using actigraphy for 2 weeks. Sleep efficiency, which is the percentage of time in bed spent asleep, was the primary measure of sleep quality. Total sleep time was the primary measure of sleep quantity. Cerebrospinal fluid Aβ42 levels were used to determine whether amyloid deposition was present or absent. Concurrent sleep diaries provided nap information.Amyloid deposition, as assessed by Aβ42 levels, was present in 32 participants (22.5%). This group had worse sleep quality, as measured by sleep efficiency (80.4% vs 83.7%), compared with those without amyloid deposition, after correction for age, sex, and APOEε4 allele carrier status (P = .04). In contrast, quantity of sleep was not significantly different between groups, as measured by total sleep time. Frequent napping, 3 or more days per week, was associated with amyloid deposition (31.2% vs 14.7%; P = .03).Amyloid deposition in the preclinical stage of AD appears to be associated with worse sleep quality but not with changes in sleep quantity.
High-level expression of the T-cell chemokines CCL3 and CCL4 by chronic lymphocytic leukemia B cells in nurselike cell cocultures and after BCR stimulation
Authors: Jan A. Burger, Maite P. Quiroga, Elena Hartmann, Andrea Bürkle, William G. Wierda, Michael J. Keating, Andreas Rosenwald
Journal: Blood (2008)
THE CLINICAL ASPECTS OF TRAUMATIC EPILEPSY
Authors: D. DENNY-BROWN
Journal: American Journal of Psychiatry (1944)

Epilepsy is an infrequent complication of injury to the head in general. All present information indicates that laceration of the brain is an essential factor, whether or not accompanied by injury to the skull or dura, though accompanying laceration of the dura and especially sepsis greatly increase the liability. It is considered important from the point of view of prognosis to separate early conclusions (within for example the first eight weeks) from epilepsy of later onset. There are also indications that it is advantageous to grade different severities of convulsions, of which the only index we have at present is degree of generalization. Intellectual impairment is an unsatisfactory clinical index of prognosis for the type of head injury which it most frequently follows is one that does not have high liability to convulsive disorder.
Shoulder joint kinetics of the elite wheelchair tennis serve
Authors: Machar Reid, Bruce Elliott, Jacque Alderson
Journal: British Journal of Sports Medicine (2007)

The shoulder is a key joint in wheelchair locomotion and commonly implicated in injury among virtually all wheelchair populations. In tennis, quantification of the shoulder joint kinetics that characterise the wheelchair serve could enhance injury prevention and rehabilitation practices as well as assist coaches evaluate the efficacy of their current technical instruction.A 12-camera, 250 Hz Vicon motion analysis system (Oxford Metrics Inc., UK) recorded the 3D flat (WFS) and kick serve (WKS) motions of two male top 30-ranked international wheelchair players. Mechanical comparisons between wheelchair players, as well as to the previously captured data of 12 high-performance able-bodied players executing the same types of serves, were undertaken.Without the benefit of a propulsive leg action, wheelchair players developed lower peak absolute (approximately 32 m/s) and horizontal (approximately 28 m/s) pre-impact racquet velocities than able-bodied players (approximately 42 m/s, approximately 38 m/s). Wheelchair serve tactics nevertheless necessitated that higher pre-impact horizontal and right lateral racquet velocities characterised the WFS (approximately 29 m/s, WKS: approximately 26 m/s) and WKS (approximately 4 m/s, WFS: approximately 11 m/s) respectively. The shoulder joint kinetics that contributed to the differential racquet velocity profiles were mostly developed independent of wheelchair serve type, but varied with and were likely related to the level and severity of spinal cord injury of the individual players.Compared with able-bodied players, wheelchair players experienced matching pre- and post-impact shoulder joint loads, such that wheelchair and able-bodied playing populations appear subject to similar shoulder joint injury risk.