tbuckley/cabot-search huggingface dataset:
Characterisation of the rat oesophagus epithelium antigens defined by the so-called 'antikeratin antibodies', specific for rheumatoid arthritis.
Authors: E Girbal, M Sebbag, V Gomes-Daudrix, M Simon, C Vincent, G Serre
Journal: Annals of the Rheumatic Diseases (1993)

OBJECTIVES--An attempt was made to characterise the antigens recognised by serum IgG antibodies directed to the stratum corneum of rat oesophagus epithelium, the so-called 9antikeratin antibodies9, which were shown to be highly specific for rheumatoid arthritis (RA) and thus to have an actual diagnostic value. METHODS--Immunoblotting was performed with RA serum samples on different extracts of rat oesophagus epithelium separated by various monodimensional and two dimensional electrophoreses. RESULTS--Three low-salt-soluble antigens sensitive to proteinase K and, therefore, of protein nature were identified. Two proteins, with apparent molecular masses of 210 and 120-90 kilodaltons, shared isoelectric points ranging from 5.8 to 8.5; the third protein exhibited isoelectric points from 4.5 to 7.2 while its molecular mass ranged from 130 to 60 kilodaltons. Immunoadsorption of RA serum samples onto cytokeratins extracted from the stratum corneum of rat oesophagus epithelium did not change their immunoreactivity towards the three antigenic proteins. Widely used deglycosylation and dephosphorylation methods failed to modify either the electrophoretic migration of the proteins or their immunoreactivity with RA serum samples. CONCLUSION--The so-called 9antikeratin antibodies9 do not react with cytokeratins. They specifically recognise three late epithelial differentiation proteins which had not been previously described. These proteins may be related to (pro)filaggrin.
THE TOTAL BODY WATER AND THE WATER TURNOVER IN PREGNANCY STUDIED WITH DEUTERIUM OXIDE AS ISOTOPIC TRACER 1
Authors: Donald L. Hutchinson, Albert A. Plentl, Howard C. Taylor
Journal: Journal of Clinical Investigation (1954)

The status of pregnancy profoundly affects the maternal metabolism. By means of isotopic tracers over-all changes in metabolic rates of specific substances can, with certain limitations, be studied. This investigation is concerned with the demonstration of water turnover rates during various stages of pregnancy and an effort is made to define their physiologic and pathologic variations. Based upon clinical evidence, appreciable variations in the state of hydration are expected as pregnancy progresses and even greater variations may be anticipated under certain pathologic conditions. For this reason the water economy of the pregnant woman is of considerable interest to the clinician. Numerous investigations have been carried out to determine changes in specific fluid
d-Tubocurarine in Caesarean Section
Authors: T. C. Gray
Journal: BMJ (1947)

STAPHYLOCOCCAL FOOD-POISONING MBRcITJouISat each of them and no correlation between the storage temperature and the number of cases could be made out.The butcher who was the source of the staphylococcus causing the outbreak had local treatment for the lesion in his hand, which soon healed.He also had a course of sulphathiazole, and swabs from his nose, throat, and hand are now negative.This experience has shown the value and importance in such outbreaks of close liaison between all interested parties and the necessity for thorough and prompt investigation by a bacteriologist with up-to-date services at his disposal. SummaryAn outbreak of toxic food-poisoning following the consump- tion of pressed pickled beef sandwiches is described.The evidence showed Staph.pyogenes aureus (phage type 47/47C) to be the cause.Personnel handling food should pay scrupulous attention to personal hygiene and especially to lesions, however slight.Close liaison between all interested parties was an important factor in finding the cause.Our thanks are due to Drs.Hall, Brothwood, and Carroll and the staff of 'the Lancashire County Council Public Health Depart- ment, especially Mr.
Metabolism of lactose by intestinal mucosa from normal and lactase-deficient subjects.
Authors: D. R. London, P. Cuatrecasas, S. J. Birge, S. Segal
Journal: BMJ (1967)

Although many studies have been devoted to a delineation of the clinical syndrome of isolated lactase deficiency in the adult (Cuatrecasas et al., 1965 ; Haemmerli et al., 1965 ; McMichael et al., 1965 ; Peternel, 1965 ; Sheehy and Anderson, 1965 ; Cook and Kajubi, 1966), to the in-vivo metabolism of lactose in this syndrome (Durand, 1964 ; Cuatrecasas et al., 1965), and to the characteristics of the enzymes whose absence is respon sible for the disorder (Dahlqvist et al., 1963 ; Semenza et al., 1965 ; Hsia et al., 1966), there have been no investigations of the cellular transport and metabolism of lactose by the small intestine in lactase deficiency. Miller and Crane (1961a, 1961b) have shown that disaccharides, particularly sucrose and maltose, are hydrolysed at the brush border of the hamster intestinal epithelial cell and that the products of hydrolysis are either actively transported into the cell or diffuse into the intracellular compartment. These workers were unable to show that intact disaccharides could be concentrated in the mucosal cell. On the other hand, Escherichia coli possess transport systems which facilitate the entry of unchanged galactosides without the necessity for prior hydrolysis (Rickenberg et al., 1956 ; Cohen and Monod, 1957). It therefore seemed important to study the cellular handling of lactose in isolated lactase deficiency to determine if disaccharide accumulation could occur in the mucosal cell of the human small intestine in the absence of the hydrolytic enzyme.
Feeling unreal: 30 cases of DSM-III-R depersonalization disorder
Authors: Daphne Simeon, Shira Gross, Orna Guralnik, Dan J. Stein, James Schmeidler, Eric Hollander
Journal: American Journal of Psychiatry (1997)

In contrast to the recent surge of interest in other dissociative disorders, DSM-III-R depersonalization disorder has not been thoroughly investigated and characterized. The authors systematically elucidated its phenomenology, comorbidity, traumatic antecedents, and treatment history.Thirty adult subjects (19 women and 11 men) were consecutively recruited and administered various structured and semistructured interviews as well as the self-rated Dissociative Experiences Scale. An age- and sex-matched normal comparison group was also recruited.The mean age at onset of depersonalization disorder was 16.1 years (SD = 5.2). The illness had a chronic course that was usually continuous but sometimes episodic. Severe distress and high levels of interpersonal impairment were characteristic. Unipolar mood and anxiety disorders were common, but none emerged as specifically related to the depersonalization. A wide variety of personality disorders was manifested; avoidant, borderline, and obsessive-compulsive were most common. Although not highly traumatized, the subjects with depersonalization disorder reported significantly more childhood trauma than the normal comparison subjects. Depersonalization had been typically treatment refractory; only serotonin reuptake inhibitors and, to a lesser extent, benzodiazepines had been of any therapeutic benefit.This study supports the conceptualization of depersonalization disorder as a distinct disorder with a characteristic course that is independent of mood, anxiety, and personality symptoms. A subtle relationship may exist between childhood trauma and depersonalization disorder that merits further investigation. The disorder appears to be highly treatment refractory, and prospective treatment trials are warranted.
Protective role of HO-1 and carbon monoxide in ethanol-induced hepatocyte cell death and liver injury in mice
Authors: Bakytzhan Bakhautdin, Dola Das, Palash Mandal, Sanjoy Roychowdhury, Jazmine Danner, Katelyn Bush, Katherine Pollard, James W. Kaspar, Wei Li, Robert G. Salomon, Megan R. McMullen, Laura E. Nagy
Journal: Journal of Hepatology (2014)
X-Linked Ectodermal Dysplasia Receptor Is Downregulated in Breast Cancer via Promoter Methylation
Authors: Vasu Punj, Hittu Matta, Preet M. Chaudhary
Journal: Clinical Cancer Research (2010)

Abstract Purpose: The X-linked ectodermal dysplasia receptor (XEDAR) is a novel receptor of the tumor necrosis factor receptor family that binds to ectodysplasin-A2 (EDA-A2) and induces cell death. The purpose of this study was to determine the tumor-suppressive potential of XEDAR in the development of breast cancer. Experimental Design: We analyzed the expression of XEDAR in breast cancer cell lines and tumor samples using quantitative real-time PCR analysis and immunoblotting. We analyzed the human XEDAR gene promoter for the presence of any CpG island and examined its methylation status using methylation-specific real-time PCR. We examined the effect of 5-aza-2′-deoxycytidine on the expression of XEDAR and sensitivity to EDA-A2–induced apoptosis in breast cancer cell lines. Results: Expression of XEDAR, but not EDA-A2, was downregulated in most tumorigenic breast cancer cell lines and tumor samples. Loss of XEDAR expression correlated with the hypermethylation of its promoter. Ectopic expression of XEDAR in MDA-MB-231 cells resulted in significant induction of apoptosis and reduction in colony formation. Treatment with 5-aza-2′-deoxycytidine restored XEDAR expression in breast cancer cell lines with methylated XEDAR promoter and sensitized them to EDA-A2–induced cell death. Conclusions: Our results suggest that XEDAR expression is downregulated in most breast cancers via promoter methylation, which may contribute to accelerated tumor development by blocking EDA-A2–induced cell death. XEDAR may represent a novel breast tumor suppressor gene, and restoration of its expression by treatment with DNA demethylating agents may represent an attractive approach for the treatment of breast cancer. Clin Cancer Res; 16(4); 1140–8
Angiogenesis and Tumor Proliferation/Metastasis of Human Colorectal Cancer Cell Line SW620 Transfected with Endocrine Glands-Derived-Vascular Endothelial Growth Factor, As a New Angiogenic Factor
Authors: Takanori Goi, Masako Fujioka, Yoshiki Satoh, Shinsuke Tabata, Kenji Koneri, Hideki Nagano, Yasuo Hirono, Kanji Katayama, Kazuo Hirose, Akio Yamaguchi
Journal: Cancer Research (2004)

Abstract Endocrine glands-derived-vascular endothelial growth factor (EG-VEGF) was recently cloned as a new angiogenic factor that selectively acts on the endothelium of endocrine gland cells. We evaluated the involvement of EG-VEGF in colorectal cancer. The expression of EG-VEGF was confirmed in all of the colorectal cancer cell lines. (On the other hand, the expression of EG-VEGF mRNA was not detected in colorectal normal mucosae.) Stable EG-VEGF infectors of colorectal cancer cell line SW620 were produced, EG-VEGF transfectants were implanted into cecum and s.c., and cell proliferation was evaluated. Angiogenesis was evaluated by dorsal air sac method. Liver metastasis was evaluated after the implantation of EG-VEGF transfectants into the mouse spleen. Tumor proliferation (cecum, s.c.) was significantly higher in the EG-VEGF transfectants than in the control cells. The small vessels were significantly increased in EG-VEGF transfectants as compared with those in control cells. Also, liver metastatic ratio was higher in the EG-VEGF transfectants than in the control cells. In this study, EG-VEGF, a new angiogenic factor, may lead to angiogenesis, promoting cell proliferation and liver metastasis in colorectal cancers. When the EG-VEGF gene-overexpressing colorectal cancer cell line that had been treated with phosphorothioate antisense EG-VEGF oligonucleotides was injected s.c. into mice, angiogenesis and tumor growth were inhibited. Although the novel angiogenesis factor EG-VEGF was not expressed in the normal colorectal mucosa, it was expressed in colorectal cancer cells, which indicates that it is a cancer-specific and possibly tissue-specific angiogenesis factor in the large intestine, and which suggests that it can be targeted by a novel antiangiogenesis therapy.
Chronic obstructive pancreatitis due to a pancreatic cyst in a patient with autosomal dominant polycystic kidney disease
Authors: D Malka, P Hammel, V Vilgrain, J-F Fléjou, J Belghiti, P Bernades
Journal: Gut (1998)

Background —Autosomal dominant polycystic kidney disease, the most frequent inherited polycystic disease, is a systemic disorder characterised by the development of numerous and bilateral kidney cysts leading to chronic renal failure. Extrarenal cysts are located mainly in the liver but also in various organs including the pancreas. To our knowledge, complications of pancreatic cysts in this disease have never been reported. Patient —The first case of painful chronic obstructive pancreatitis due to a true pancreatic cyst in a patient with autosomal dominant polycystic kidney disease is reported. Abdominal transparietal and endoscopic ultrasonography, computed tomography, and endoscopic retrograde cholangiopancreatography showed a cystic lesion in the body of the pancreas associated with upstream dilatation of the main pancreatic duct. Intraoperative ultrasonography before and after cyst fluid aspiration, and pancreatography and pathological examination of the resected distal pancreas confirmed that both main pancreatic duct enlargement and chronic pancreatitis were caused by a benign cyst. Conclusion —Chronic obstructive pancreatitis should be added to the extrarenal complications of autosomal dominant polycystic kidney disease.
Mechanism of increased amplitude and duration of the plateau with sudden shortening of diastolic intervals in rabbit ventricular cells.
Authors: M Hiraoka, S Kawano
Journal: Circulation Research (1987)

Action potentials and membrane currents were recorded from isolated single ventricular cells from rabbit hearts using the suction pipette whole-cell clamp method. Action potentials elicited after short diastolic intervals of less than 2 seconds showed an increase and prolongation of the plateau compared to those elicited after a 10-second rest period. The recovery of the tetrodotoxin-insensitive secondary inward current revealed a transient increase at short diastolic intervals above the level of full recovery (after 10 seconds). The increased secondary inward current recovery, however, was voltage-dependent, and the period of its increase did not cover the entire diastolic intervals of the action potential overshoots, suggesting the contribution of another ionic current to the changes in potential. During depolarizing voltage steps, from + to -20 mV, a rapid activating and then inactivating outward current was elicited, which overlapped the calcium current. This outward current exhibited time- and voltage-dependent properties similar to those of the transient outward current in Purkinje and other cardiac preparations. The recovery of the transient outward current was slow, achieving only 75% of its full level at 2 seconds, whereas the same level of calcium current recovery was achieved at 200 milliseconds. The application of 4-aminopyridine suppressed most of the transient outward current, and the rest of the current was abolished by caffeine or Co2+. The 4-aminopyridine sensitive transient outward current exhibited slow recovery kinetics compared to those of the other or calcium current, and its inhibition caused elimination of the augmented plateau during electrical restitution. The application of verapamil or Co2+ for inhibition of secondary inward current also abolished the action potential overshoot. These results indicate that an increase and prolongation of the plateau at short diastolic intervals are produced by the slower recovery from inactivation in the 4-aminopyridine-sensitive transient outward current than that in the calcium current.
Points from Letters: Rats Today
Authors: J. G. Wilson
Journal: BMJ (1975)

vogue in the future should Parliament as at present constituted beconme too unwieldy to function effectively.Moreover, the medical profession would be freer to set up and supervise what mtust surely come, and that is a body of aware persons to interview at regular intervals all persons in paid authority above a certain level of responsibility, in- cluding doctors, lawyers, M.P.s, teachers, etc., regairding their continuing suitability to hold such authority.Under the pro- fession's present subservience to politics this would be difficult to implement, if at all."What shall it profit a man if he shall gain the whole world and lose his own soul?"And as a profession we are in grave danger of doing just that.-I am, etc.,
Temporal Events Underlying Arterial Remodeling After Chronic Flow Reduction in Mice
Authors: Radu Daniel Rudic, Mariarosaria Bucci, David Fulton, Steven S. Segal, William C. Sessa
Journal: Circulation Research (2000)

Abstract —To define the cellular events of vascular remodeling in mice, we measured blood flow and analyzed the morphology of remodeled vessels at defined points after a flow-reducing remodeling stimulus for 3, 7, 14, and 35 days. Acute ligation of the left external carotid artery reduced blood flow in the left common carotid artery (LC) compared with sham and contralateral right common carotid arteries (RCs). In morphometric analyses, the decrease in diameter in LCs was reversible by vasodilator perfusion 3 days after ligation, whereas ligation for 7 days or greater resulted in a permanent diameter reduction. Coincident with structural remodeling at day 7 was an increase in cell death in remodeled LCs. Functionally, rings from remodeled LCs contracted to prostaglandin F 2α and relaxed to acetylcholine in a manner identical to that of control arteries. However, remodeled LCs were hypersensitive to the nitrovasodilator sodium nitroprusside (at day 7) and exhibited a marked reduction in basal NO synthesis at 7 and 14 days after ligation. The impairment of endothelial NO synthase function was likely due to post-translational mechanisms, given that endothelial NO synthase mRNA and protein levels did not change in remodeled LCs. These data define the ontogeny of flow-triggered luminal remodeling in adult mice and suggest that endothelial dysfunction occurs during reorganization of the vessel wall.
A study of the association of HLA DR, DQ, and complement C4 alleles with systemic lupus erythematosus in Iceland
Authors: K Steinsson, S Jonsdottir, G J Arason, H Kristjansdottir, R Fossdal, I Skaftadottir, A Arnason
Journal: Annals of the Rheumatic Diseases (1998)

<h3>OBJECTIVE</h3> To perform an exploratory analysis of the relative contribution of single MHC genes to the pathogenesis of systemic lupus erythematosus (SLE) in a homogenous white population. <h3>METHODS</h3> MHC class II alleles and C4 allotypes were determined in 64 SLE patients and in ethnically matched controls. HLA-DR and DQ typing was performed by polymerase chain reaction amplification with sequence specific primers. C4 allotypes were determined by agarose gel electrophoresis. <h3>RESULTS</h3> The frequency of C4A*Q0 was significantly higher in patients than in controls (46.9%<i>v</i> 25.3%, p=0.002). HLA-DRB1, DQA1, and DQB1 alleles in the whole group of SLE patients were not significantly different from those of controls. On the other hand increase in DRB1*03 was observed in the group of patients with C4A*Q0, as compared with patients with other C4A allotypes (p=0.047). There was no significant correlation between severe and mild disease, as judged by the SLEDAI, and HLADR, DQ alleles and comparing the patients with C4A*Q0 with those with other C4A allotypes there was no significant difference regarding clinical manifestations. <h3>CONCLUSION</h3> The results are consistent with the argument that C4A deficiency contributes independently to susceptibility and the pathogenesis of SLE. C4A*Q0 in SLE patients in Iceland shows weaker linkage disequilibrium with DR3 genes than reported in most other white populations and emphasises the role of ethnicity.
Fructosamine and glycated albumin for risk stratification and prediction of incident diabetes and microvascular complications: a prospective cohort analysis of the Atherosclerosis Risk in Communities (ARIC) study
Authors: Elizabeth Selvin, Andreea M Rawlings, Morgan Grams, Ronald Klein, A Richey Sharrett, Michael Steffes, Josef Coresh
Journal: The Lancet Diabetes & Endocrinology (2014)
Salvage treatment of advanced non-small-cell lung cancer previously treated with docetaxel-based front-line chemotherapy with irinotecan (CPT-11) in combination with cisplatin
Authors: S. Kakolyris, C. Kouroussis, K. Kalbakis, D. Mavroudis, J. Souglakos, N. Vardakis, S. Kremos, V. Georgoulias
Journal: Annals of Oncology (2000)
Effect of 7,8-Dihydroxyflavone, a Small-Molecule TrkB Agonist, on Emotional Learning
Authors: Raul Andero, Scott A. Heldt, Keqiang Ye, Xia Liu, Antonio Armario, Kerry J. Ressler
Journal: American Journal of Psychiatry (2010)

Objective: Despite increasing awareness of the many important roles played by brain-derived neurotrophic factor (BDNF) activation of TrkB, a fuller understanding of this system and the use of potential TrkB-acting therapeutic agents has been limited by the lack of any identified small-molecule TrkB agonists that fully mimic the actions of BDNF at brain TrkB receptors in vivo. However, 7,8-dihydroxyflavone (7,8-DHF) has recently been identified as a specific TrkB agonist that crosses the blood-brain barrier after oral or intraperitoneal administration. The authors combined pharmacological, biochemical, and behavioral approaches in a preclinical study examining the role of 7,8-DHF in modulating emotional memory in mice. Method: The authors first examined the ability of systemic 7,8-DHF to activate TrkB receptors in the amygdala. They then examined the effects of systemic 7,8-DHF on acquisition and extinction of conditioned fear, using specific and well-characterized BDNF-dependent learning paradigms in several models using naive mice and mice with prior traumatic stress exposure. Results: Amygdala TrkB receptors, which have previously been shown to be required for emotional learning, were activated by systemic 7,8-DHF (at 5 mg/kg i.p.). 7,8-DHF enhanced both the acquisition of fear and its extinction. It also appeared to rescue an extinction deficit in mice with a history of immobilization stress. Conclusions: These data suggest that 7,8-DHF may be an excellent agent for use in understanding the effects of TrkB activation in learning and memory paradigms and may be attractive for use in reversing learning and extinction deficits associated with psychopathology.