tbuckley/cabot-search huggingface dataset:
Strangulated diaphragmatic hernia
Authors: E. Hoffman
Journal: Thorax (1968)

Seventy-six cases of strangulated diaphragmatic hernia were reported up to 1953. An additional 64 cases reported between 1953 and 1966 are reviewed in this paper. The incidence of strangulation in various types of congenital/traumatic, hiatal, and incisional herniae is discussed. Four further cases of strangulated diaphragmatic hernia are presented. The mechanism of strangulation, its diagnosis, complications, and treatment are discussed.
Effects of Maternal Diabetes on Visual Evoked Potentials and Early Psychomotor Development of the Offspring
Authors: Mario Brinciotti, Maria Matricardi, Antonietta Colatrella, Francesco Torcia, Francesco Fallucca, Angela Napoli
Journal: Diabetes Care (2007)

Planning and intensive treatment of diabetes in pregnancy has resulted in dramatic improvements in outcomes in terms of congenital malformations or perinatal morbidity (1), but it is still not clear to what extent maternal diabetes affects cognitive development of newborns. In infants of diabetic mothers (IDMs), significant relations have been reported between poor maternal metabolic regulation during pregnancy and poor child intellectual performance, despite an achievement of overall healthy neuropsychological functioning …
SLIT2 Attenuation during Lung Cancer Progression Deregulates β-Catenin and E-Cadherin and Associates with Poor Prognosis
Authors: Ruo-Chia Tseng, Shih-Hua Lee, Han-Shui Hsu, Ben-Han Chen, Wan-Ching Tsai, Ching Tzao, Yi-Ching Wang
Journal: Cancer Research (2010)

Abstract Chromosome 4p15.3 is frequently deleted in late-stage lung cancer. We investigated the significance of the SLIT2 gene located in this region to lung cancer progression. SLIT2 encodes an extracellular glycoprotein that can suppress breast cancer by regulating β-catenin. In this study, we examined alterations in the structure or expression of SLIT2, its receptor ROBO1, and β-catenin, along with the AKT/glycogen synthase kinase 3β (GSK3β)/β-transducin repeat-containing protein (βTrCP) pathway in lung cancer cell lines and patients. Low SLIT2 expression correlated with an upward trend of pathological stage and poorer survival in lung cancer patients. Importantly, SLIT2, βTrCP, and β-catenin expression levels predicted postoperative recurrence of lung cancer in patients. Stimulating SLIT2 expression by various methods increased the level of E-cadherin caused by attenuation of its transcriptional repressor SNAI1. Conversely, knocking down SLIT2 expression increased cell migration and reduced cell adhesion through coordinated deregulation of β-catenin and E-cadherin/SNAI1 in the AKT/GSK3β/βTrCP pathway. Our findings indicate that SLIT2 suppresses lung cancer progression, defining it as a novel “theranostic” factor with potential as a therapeutic target and prognostic predictor in lung cancer. Cancer Res; 70(2); 543–51
The use of maximum SOFA score to quantify organ dysfunction/failure in intensive care. Results of a prospective, multicentre study
Authors: R. Moreno, J.-L. Vincent, R. Matos, A. Mendonça, F. Cantraine, L. Thijs, J. Takala, C. Sprung, M. Antonelli, H. Bruining, S. Willatts
Journal: Intensive Care Medicine (1999)
Treatment of Chronic Illness— Home or Nursing Home?
Authors: F. P. McKegney
Journal: JAMA (1967)

A member of my family has Parkinson's disease and has been in a nursing home for the past few years. Even though I am a physician, I did not fully realize the difficulties inherent in the management of the chronically ill patient until this personal experience occurred. I note with chagrin that clergymen consider visits to a nursing home to be a rather onerous task, and therefore these patients receive less emotional support than I had imagined. It is apparent to me, also, that physicians share this attitude. The care of the chronically ill patient in all age groups is certainly a major concern in this country, and consideration of the emotional needs of patients in nursing homes will become even more important in the next few years. How does care of these patients, both physical and emotional, differ from care of the patient who is acutely ill? What problems are introduced when the patient is cared for in a nursing home rather than his own home?
Kaolin dust concentrations and pneumoconiosis at a kaolin mine.
Authors: E B Altekruse, B A Chaudhary, M G Pearson, W K Morgan
Journal: Thorax (1984)

Kaolin is removed from underground seams in the mining area to a processing area, where it is sliced, dried, and pulverised to make the finished product. A study was undertaken to determine the dust concentrations in various work areas and to assess the prevalence of radiographic and pulmonary function abnormalities in 65 workers at a Georgia kaolin mine. Respirable dust concentrations were higher in the processing area than in the mine or maintenance areas for all determinations from 1977 to 1981. The mean respirable dust level in the processing area in 1981 was 1.74 mg/m3 and 0.14 mg/m3 in the mine area. Five workers, all of whom had worked at the processing area, had radiographic evidence of kaolin pneumoconiosis. The mean values of forced vital capacity (FVC) and FEV1 of the entire group were within the normal range. When the spirometric values were expressed as a percentage of the predicted values, the FVC and FEV1 were significantly lower in the workers with kaolinosis than in other workers in the processing area. The FVC and FEV1 also declined significantly with increasing years of work in the processing area. The FEV1/FVC%, however, was not significantly altered either by the presence of kaolinosis or by an increasing number of years of work, indicating that the impairment was restrictive and hence likely to be a consequence of dust inhalation rather than smoking. In this study the highest dust concentrations occurred in the processing area, and kaolin pneumoconiosis was limited to those who had worked there. Kaolin exposure appeared to have a small but significant effect on ventilatory capacity in those with kaolin pneumoconiosis and in workers with a longer exposure. There was no association between the radiographic appearances of kaolinosis and cigarette smoking or between the presence of radiographic abnormalities and reduced arterial blood gas tensions.
Proteomic Analysis of Human Acute Leukemia Cells
Authors: Jiu-Wei Cui, Jie Wang, Kun He, Bao-Feng Jin, Hong-Xia Wang, Wei Li, Li-Hua Kang, Mei-Ru Hu, Hui-Yan Li, Ming Yu, Bei-fen Shen, Guan-Jun Wang, Xue-Min Zhang
Journal: Clinical Cancer Research (2004)

Abstract Purpose: French-American-British (FAB) classification of acute leukemia with genetic heterogeneity is important for treatment and prognosis. However, the distinct protein profiles that contribute to the subtypes and facilitate molecular definition of acute leukemia classification are still unclear. Experimental Design: The proteins of leukemic cells from 61 cases of acute leukemia characterized by FAB classification were separated by two-dimensional electrophoresis, and the differentially expressed protein spots were identified by both matrix-assisted laser desorption/ionization–time-of-flight–mass spectrometry (MALDI-TOF-MS) and tandem electrospray ionization MS (ESI-MS/MS). Results: The distinct protein profiles of acute leukemia FAB types or subtypes were successfully explored, including acute myeloid leukemia (AML), its subtypes (M2, M3, and M5) and acute lymphoid leukemia (ALL), which were homogeneous within substantial samples of the respective subgroups but clearly differed from all other subgroups. We found a group of proteins that were highly expressed in M2 and M3, rather than other subtypes. Among them, myeloid-related proteins 8 and 14 were first reported to mark AML differentiation and to differentiate AML from ALL. Heat shock 27 kDa protein 1 and other proteins that are highly expressed in ALL may play important roles in clinically distinguishing AML from ALL. Another set of proteins up-regulated was restricted to granulocytic lineage leukemia. High-level expression of NM23-H1 was found in all but the M3a subtype, with favorable prognosis. Conclusions: These data have implications in delineating the pathways of aberrant gene expression underlying the pathogenesis of acute leukemia and could facilitate molecular definition of FAB classification. The extension of the present analysis to currently less well-defined acute leukemias will identify additional subgroups.
Beta-adrenergic stimulation with isoproterenol enhances left ventricular diastolic performance in hypertrophic cardiomyopathy despite potentiation of myocardial ischemia. Comparison to rapid atrial pacing.
Authors: J E Udelson, R O Cannon, S L Bacharach, T F Rumble, R O Bonow
Journal: Circulation (1989)

Impaired left ventricular relaxation and filling is an important pathophysiologic mechanism in hypertrophic cardiomyopathy. To determine whether isoproterenol, known to improve relaxation in isolated cardiac muscle, could favorably modify this effect, we assessed simultaneous left ventricular volume and regional systolic asynchrony (by radionuclide angiography), left ventricular pressure (by micromanometer catheters), and lactate metabolism in 12 patients with hypertrophic cardiomyopathy. Pressure-volume relations were studied during atrial pacing stress to induce myocardial ischemia and during isoproterenol infusion to similar heart rates. Angina occurred in 10 patients with pacing and in 11 patients during isoproterenol infusion; lactate consumption was reduced in nine patients during isoproterenol compared with pacing, including five patients who produced lactate with isoproterenol. During isoproterenol compared with pacing, peak left ventricular pressure was higher (205 +/- 33 vs. 142 +/- 21 mm Hg, p less than 0.001), ejection fraction was higher (77 +/- 10% vs. 71 +/- 12%, p less than 0.02), and regional systolic nonuniformity was diminished. Despite ischemia, these changes in load and nonuniformity during isoproterenol were associated with enhanced diastolic function compared with pacing tachycardia: isoproterenol reduced T 1/2, the half-time of pressure decline after peak negative dP/dt (from 46 +/- 10 to 33 +/- 6 msec, p less than 0.001), shifted the diastolic pressure-volume curve downward and rightward in 10 of 12 patients, and increased end-diastolic volume (from 77 +/- 18% to 100 +/- 11% of control values, p less than 0.001) with no change in end-diastolic pressure (19 +/- 7 to 19 +/- 5 mm Hg, p = NS). Thus, despite ischemia, isoproterenol improved left ventricular relaxation and filling compared with tachycardia in the absence of beta-adrenergic stimulation. Although isoproterenol is detrimental in hypertrophic cardiomyopathy by provoking ischemia, these data suggest that the adverse effects of ischemia on ventricular relaxation and distensibility may be alleviated by beta-adrenergic stimulation, possibly as a result of enhanced inactivation and restored load sensitivity.
William Bryan Davies
Journal: BMJ (2006)

​FormerFormer Welsh secretary BMA (b 1933; q Leeds 1956; KStJ, OBE), d 21 June 2006.



Figure 1



William Bryan Davies (“Bryan”) did his national service with the Royal Irish Fusiliers and was awarded the green hackle. A member of the BMA since his student days, he was made a fellow of the association and became a national leader. Bryan was chairman of the Welsh General Medical Services Committee before becoming Welsh secretary from 1984 to 1992. From 1994 to 1999 he was chairman of the Rhondda NHS Trust. He was made OBE in 1999. He was prominent in St John Ambulance, and his other commitments to his community included being a rotarian, president of Pendyrus Male Voice Choir and of the local bowls and soccer clubs, and medical officer to the Welsh Amateur Boxing Association. Predeceased by his wife, Betty, in 1999, he leaves a daughter and a granddaughter.
Effects of epinephrine on firing characteristics of two functionally different types of carotid baroreceptors.
Authors: J L Seagard, J F van Brederode, C Dan, F A Hopp, E O Elegbe, L A Gallenberg, J P Kampine
Journal: Circulation Research (1991)

Sympathetic stimulation and catecholamine exposure have been shown to sensitize the arterial baroreceptors, but the extent or importance of this effect is not known. We performed this study to investigate the effects of sympathetic feedback on the carotid sinus baroreceptors, specifically examining the effect of the stimulation on the two different functional types of baroreceptors characterized in an earlier study. The existence of two baroreceptor function-response curves has suggested that the roles of the two functionally different baroreceptors may not be the same. If true, the effects of epinephrine exposure on baroreceptor firing characteristics may contribute to differential roles played by each baroreceptor type in the control of blood pressure. Single-fiber baroreceptor activity from a vascularly isolated carotid sinus was recorded during slow increases in carotid sinus pressure before and during exposure to epinephrine (10(-8) to 10(-6) M). Baroreceptor firing characteristics were determined from function curves plotting carotid sinus pressure versus nerve activity, with curve-fitting analysis of the hyperbolic type I and sigmoidal type II baroreceptor curves used to obtain threshold (Pth) and saturation (Psat) pressures, threshold (Fth) and saturation (Fsat) firing rates, and sensitivity (slope) for each baroreceptor before and during epinephrine exposure. The possible mechanisms of observed changes were examined using our previously published baroreceptor computer model. Epinephrine exposure was found to significantly increase sensitivity, Fth, and Fsat of both types of baroreceptors, with a relatively greater effect on type I sensitivity and on type II Fth and Fsat. Epinephrine also was found to increase the level of spontaneous discharge for type II baroreceptors.(ABSTRACT TRUNCATED AT 250 WORDS)
Myocytes Die by Multiple Mechanisms in Failing Human Hearts
Authors: Sawa Kostin, Lieven Pool, Albrecht Elsässer, Stefan Hein, Hannes C.A. Drexler, Eyal Arnon, Yukihiro Hayakawa, René Zimmermann, Erwin Bauer, Wolf-Peter Klövekorn, Jutta Schaper
Journal: Circulation Research (2003)

We tested the hypothesis that myocyte loss in failing human hearts occurs by different mechanisms: apoptosis, oncosis, and autophagic cell death. Explanted hearts from 19 patients with idiopathic dilated cardiomyopathy (EF≤20%) and 7 control hearts were analyzed. Myocyte apoptosis revealed by caspase-3 activation and TUNEL staining occurred at a rate of 0.002±0.0005% ( P &lt;0.05 versus control) and oncosis assessed by complement 9 labeling at 0.06±0.001% ( P &lt;0.05). Cellular degeneration including appearance of ubiquitin containing autophagic vacuoles and nuclear disintegration was present at the ultrastructural level. Nuclear and cytosolic ubiquitin/protein accumulations occurred at 0.08±0.004% ( P &lt;0.05). The ubiquitin-activating enzyme E1 and the ligase E3 were not different from control. In contrast, ubiquitin mRNA levels were 1.8-fold ( P &lt;0.02) elevated, and the conjugating enzyme E2 was 2.3-fold upregulated ( P &lt;0.005). The most important finding, however, is the 2.3-fold downregulation of the deubiquitination enzyme isopeptidase-T and the 1.5-fold reduction of the ubiquitin-fusion degradation system-1, which in conjunction with unchanged proteasomal subunit levels and proteasomal activity results in massive storage of ubiquitin/protein complexes and in autophagic cell death. A 2-fold decrease of cathepsin D might be an additional factor responsible for the accumulation of ubiquitin/protein conjugates. It is concluded that in human failing hearts apoptosis, oncosis, and autophagy act in parallel to varying degrees. A disturbed balance between a high rate of ubiquitination and inadequate degradation of ubiquitin/protein conjugates may contribute to autophagic cell death. Together, these different types of cell death play a significant role for myocyte disappearance and the development of contractile dysfunction in failing hearts.
Left Atrial Tachycardia Originating From the Mitral Annulus–Aorta Junction
Authors: Mario D. Gonzalez, Leonardo J. Contreras, Monique R.M. Jongbloed, Jaime Rivera, Timothy P. Donahue, Anne B. Curtis, Michael S. Bailey, Jamie B. Conti, Glenn I. Fishman, Martin J. Schalij, Adriana C. Gittenberger–de Groot
Journal: Circulation (2004)

At the mitral annulus-aorta (MA-Ao) junction, the left atrium is continuous through the subaortic curtain with the musculature of the anterior mitral leaflet. Under experimental conditions, this region can generate abnormal electrical activity. In patients with left atrial tachycardia, we investigated whether this region could be the source of this arrhythmia.In 10 (28%) of 35 consecutive patients with left atrial tachycardia, the arrhythmia originated from the MA-Ao junction. Sustained, self-limited episodes of atrial tachycardia (cycle length, 340+/-56 ms; duration, 125+/-69 seconds) were repeatedly induced. Prematurity of the extrastimulus and time to first atrial tachycardia complex were directly correlated (R=0.66; P<0.001). During tachycardia, bipolar electrograms at the earliest site preceded onset of the P wave by 44+/-14 ms and were of longer duration and lower amplitude than those recorded from nearby left atrial sites (52+/-8 versus 24+/-4 ms, P<0.001; and 0.53+/-0.08 versus 3.45+/-0.96 mV, respectively; P<0.001). Ablation eliminated the tachycardia with no recurrence after a mean follow-up of 24+/-19 months. A comparative study in mouse embryos demonstrated the presence of the developing specialized conduction system in the MA-Ao region starting at embryonic age 11.5.The MA-Ao junction can be a frequent source of left atrial tachycardia. This previously unrecognized site of origin may explain why catheter ablation has been less successful in eliminating left versus right atrial tachycardias. Remnants of the developing specialized conduction system could be the underlying substrate of this arrhythmia.
Identification of a histamine release inhibitory factor produced by human mononuclear cells in vitro.
Authors: R Alam, J A Grant, M A Lett-Brown
Journal: Journal of Clinical Investigation (1988)

Human mononuclear cells (MNC) secrete histamine-releasing factor(s) (HRF) when cultured in vitro. HRF induces the release of histamine and other mediators from basophils and mast cells. We have shown that MNC also produced a histamine release inhibitory factor (HRIF), and that the synthesis is augmented by culture with physiologic concentrations of histamine (10(-10) to 10(-6) M) and by the mitogen concanavalin A (Con A). HRIF does not affect release initiated by other secretagogues such as allergen, anti-IgE, C5a, Con A, and phorbol myristate acetate. HRIF requires a preincubation with the cells for 5-10 min for maximal inhibition, and this effect is not abolished by washing the cells after the preincubation. The biological activity of HRIF is protease-sensitive, neuraminidase-resistant, and relatively heat-stable. HRIF can be distinguished from HRF by a lower apparent molecular mass (8,000-10,000 D).
Congenital hepatic fibrosis: the long-term prognosis.
Authors: D N Kerr, S Okonkwo, R G Choa
Journal: Gut (1978)

The long-term prognosis in congenital hepatic fibrosis has been assessed in 30 patients, 13 treated at Newcastle and 17 from other British centres. Twenty-four patients had been followed-up for more than five years from diagnosis. Shunt operations, performed in 18 patients, were successful in controlling haemorrhage with a low mortality (1/18), low incidence of recurrent haemorrhage (3/18) and portal-systemic encephalopathy (3/18) but with a higher incidence of postoperative jaundice (7/18). About a third of the survivors had some evidence of hepatic dysfunction but none had chronic portal systemic encephalopathy. Intelligence quotient was close to normal but educational achievement and job status were low. Serum albumin fell after shunt surgery and a few patients developed ascites: anaemia and hypersplenism however, were corrected by surgery. Blood ammonia is raised in survivors with congenital hepatic fibrosis and rises further after a normal meal; further observations are needed on cerebral function after several decades of survival.
Assembly and Regulation of the CD40 Receptor Complex in Human B Cells
Authors: Michelle R. Kuhné, Michael Robbins, John E. Hambor, Matthew F. Mackey, Yoko Kosaka, Toshihide Nishimura, Jason P. Gigley, Randolph J. Noelle, David M. Calderhead
Journal: The Journal of Experimental Medicine (1997)

CD40 is a member of the tumor necrosis factor (TNF) receptor superfamily. Studies with human B cells show that the binding of CD154 (gp39, CD40L) to CD40 recruits TNF receptor– associated factor 2 (TRAF2) and TRAF3 to the receptor complex, induces the downregulation of the nonreceptor-associated TRAFs in the cell and induces an increased expression of Fas on the cell surface. Combined signaling through the interluekin 4 receptor and CD40 induces an increased expression of Fas with a commensurate increase in the level of TRAF2, but not TRAF3, that is recruited to the receptor complex. In contrast, engagement of the membrane immunoglobulin and CD40 limits Fas upregulation and reduces the recruitment of TRAF2, relative to TRAF3, to the CD40 receptor complex. These studies show that the TRAF composition of the CD40 receptor complex can be altered by signals that influence B cell differentiation.