tbuckley/cabot-search huggingface dataset:
Histamine release from basophil leukocytes induced by microbial antigen preparations in patients with AIDS
Authors: M. Pedersen, H. Permin, C. Jensen, P. Stahl Skov, S. Norn, V. Faber
Journal: Allergy (1987)

Type I allergy against some common microorganisms was investigated in 14 patients with AIDS and 11 human immunodeficiency virus (HIV) antibody‐positive homosexual men, and in a control group consisting of 13 heterosexual men without HIV antibodies. Basophil histamine release technique was used as a sensitive method to detect type I allergy against Candida albicans (CA), Herpes simplex virus type I (HSV‐I) and cytomegalovirus (CMV). Of the 14 AIDS patients 11 (78%) showed significant histamine release when stimulated with CA, and HSV‐I caused release in 10 (71 %), whereas no response was obtained by CMV. In the group of HIV antibody‐positive men only one released histamine when stimulated with CA and HSV‐I and this patient also had lymphadenopathia. In contrast to these results, no release of histamine was obtained in the control group consisting of 13 heterosexual men. The histamine release caused by CA and HSV‐I is mediated by an immunological reaction, since the release was abolished and regained by removal from and refixation to the cell surface of the cell‐bound immunoglobulins. These results suggest an involvement of type I allergy as a pathogenetic co‐factor in some infections in AIDS, and allergic type I reactions to CA and HSV‐I might be an indicator for the presence of manifest AIDS.
TCT-539 The longitudinal elongation of the contemporary drug eluting stent in a tapered bench-top model
Authors: Masaki Takenaka, Haruo Hirayama, Kenji Hurusawa, Mamoru Nanasato, Takamitu Nin, Yukihiko Yoshida, Ruka Yoshida, Hiroki Kamiya
Journal: Journal of the American College of Cardiology (2012)
Elimination of central sleep apnoea by mitral valvuloplasty: the role of feedback delay in periodic breathing
Authors: A E Rubin
Journal: Thorax (2004)

Central sleep apnoea is a form of periodic breathing which resembles Cheyne-Stokes respiration but occurs only during sleep. One mechanism in the pathogenesis is a delay in chemical feedback from the lungs to the medullary respiratory centre. We explored the relationship between circulatory feedback delay in a patient with central sleep apnoea and Cheyne-Stokes respiration before and after mitral valve repair. Preoperatively the patient had severe central sleep apnoea and an increased circulation time. Following mitral valvuloplasty the circulation time was decreased with resolution of central sleep apnoea. This case demonstrates the role of feedback delay in central sleep apnoea and suggests that similar haemodynamic mechanisms may lead to central sleep apnoea and Cheyne-Stokes respiration.
Cost of teaching medical students
Authors: B. K. Ambati
Journal: JAMA (1995)

To the Editor.  —Dr Weinberg and colleagues 1 couple an exaggeration of the cost of third-year medical student clerkships with a cursory dismissal of the role students play in patient care, painting a false portrait of medical education as a black hole for hospital finances.  The authors state, if two students and two residents had a 1-hour conference with a faculty member, each student... had 0.25 hours of teaching expense, yielding the incorrect conclusion that without students the conference would last 30 minutes. Their calculation that 17.2% of faculty instruction occurs in a mixed setting (with residents) is erroneous. The relevant comparison is time faculty spend with students exclusively vs time with mixed audiences, which occurs even without students; 66.1% of instruction is with mixed audiences.  Considering voluntary faculty time, a cost is inappropriate and insulting. It is sad that we place dollar values on traditions like teaching rounds and
Hepatocyte-specific expression of the humanMDR3P-glycoprotein gene restores the biliary phosphatidylcholine excretion absent inMdr2 (?/?) mice
Authors: Alexander J. Smith, Marleen J. de Vree, Roelof Ottenhoff, Ronald P. Elferink, Alfred H. Schinkel, Piet Borst
Journal: Hepatology (1998)

Mice homozygous for a disruption in the Mdr2 gene ( Mdr2 (−/−) mice) lack the Mdr2 P -glycoprotein ( P -gp) in the canalicular membrane of the hepatocyte and are unable to excrete phosphatidylcholine into the bile. These mice develop a nonsuppurative cholestatic liver disease, presumably caused by the high concentrations of free cytotoxic bile acids in bile. We generated transgenic mice that express the human homolog of Mdr2, MDR3, specifically in the liver by the use of an albumin promoter. In these mice the MDR3 P -gp is exclusively located in the canalicular membrane of hepatocytes and phospholipid excretion into bile is restored. Mice that contain the same amount of MDR3 P -gp as that of Mdr2 P -gp in wild-type mice, also excrete the same amount of phospholipids. No histopathological abnormalities were observed in the livers of these mice. In mice that express MDR3 at a higher or lower level, the phospholipid excretion correlated with the amount of MDR3 P -gp. We conclude that the human MDR3 P -gp is functionally homologous to the murine Mdr2 P -gp and that it can fully replace this P -gp in Mdr2 (−/−) mice, restoring the excretion of phospholipids into the bile. The phospholipid excretion is limited by the amount of MDR3 or Mdr2 P -gp. The excretion of cholesterol is not tightly coupled to the excretion of phospholipids in these mice, because a very low phospholipid excretion level is sufficient to give almost wild-type cholesterol excretion into the bile.
COMPARISON OF THE IMMUNE RESPONSIVENESS OF NZB AND NZB x NZW F1 HYBRID MICE WITH THAT OF OTHER STRAINS OF MICE
Authors: Jean-Charles Cerottini, Paul-Henri Lambert, Frank J. Dixon
Journal: The Journal of Experimental Medicine (1969)

The immune responsiveness of (NZB x NZW) F1 hybrid mice (NZB/W) has been compared with that of three other strains of mice, A/J, BALB/c, and CBA/J. The antigens used included sheep red blood cells (SRBC), keyhole limpet hemocyanin (KLH), bovine serum albumin (BSA), and human γ-globulin (HGG). It was found that important strain differences existed in the amount of antibody produced, but the relative immune responsiveness depended very much upon the nature of antigen. By comparison with the other strains tested, NZB/W mice had a higher antibody production to some antigens (SRBC and BSA) but were low responders to others (KLH). Induction of unresponsiveness to HGG by treatment with ultracentrifuged HGG was studied in the strains cited above. NZB/W mice became tolerant after injection of HGG ultracentrifuged at 100,000 g for 2 hr. Similar experiments carried out with another preparation of HGG (centrifuged at 20,000 g for 30 min) failed to reveal any abnormal behavior of NZB/W mice as compared to BALB/c or A/J mice. These results do not support the concept that NZB/W mice possess a general immune hyperreactivity or a relative inability to be made tolerant to protein antigens. However, they do not rule out the possibility that these mice have a genetically determined hyperresponsiveness to some antigens, in particular to nuclear antigens.
The Effect of Evening Alcohol Consumption on Next-Morning Glucose Control in Type 1 Diabetes
Authors: Benjamin C. Turner, Emma Jenkins, David Kerr, Robert S. Sherwin, David A. Cavan
Journal: Diabetes Care (2001)

OBJECTIVE—Alcohol is associated with acute hypoglycemia in patients with type 1 diabetes. After drinking alcohol in the evening, delayed hypoglycemia has also been described, although its cause is unknown. We performed a controlled study to investigate this phenomenon. RESEARCH DESIGN AND METHODS—We admitted six men with type 1 diabetes (aged 19–51 years, HbA1c 7.0–10.3%) on two occasions, from 5:00 p.m. to 12:00 noon the following day. They received regular insulin injections before standardized meals, at 6:00 p.m. and 8:00 a.m., and a basal insulin infusion (0.15 mU · kg−1 · min−1) from 11:00 p.m. They drank either dry white wine (0.75 g/kg alcohol) or mineral water at 9:00 p.m. over 90 min. Blood glucose, alcohol, insulin, cortisol, growth hormone, and glucagon levels were measured. RESULTS—Blood ethanol reached a mean (SEM) peak of 19.1 (1.2) mmol/l and was undetectable by 8:00 a.m. There were no significant differences in evening or overnight blood glucose levels between the studies. In the morning, fasting and postprandial blood glucose levels were significantly lower after consumption of wine (postprandial peak 8.9 [1.7] vs. 15 [1.5] mmol/l, P &amp;lt; 0.01), and from 10:00 a.m., five subjects required treatment for hypoglycemia (nadir 1.9–2.9 mmol/l). None of the subjects had hypoglycemia after consumption of water. After consumption of wine, growth hormone secretion was significantly reduced between midnight and 4:00 a.m. (area under the curve 2.1 [1.1] vs. 6.5 [2.1] μg · l–1 · h–1, P = 0.04). There were no differences in insulin or other hormone levels. CONCLUSIONS—In type 1 diabetes, moderate consumption of alcohol in the evening may predispose patients to hypoglycemia after breakfast the next morning. This is associated with reduced nocturnal growth hormone secretion. Patients should be informed of this risk and advised regarding appropriate preventative measures.
Low-Level Expression of Proapoptotic Bcl-2–Interacting Mediator in Leukemic Cells in Patients with Chronic Myeloid Leukemia: Role of BCR/ABL, Characterization of Underlying Signaling Pathways, and Reexpression by Novel Pharmacologic Compounds
Authors: Karl J. Aichberger, Matthias Mayerhofer, Maria-Theresa Krauth, Anja Vales, Rudin Kondo, Sophia Derdak, Winfried F. Pickl, Edgar Selzer, Michael Deininger, Brian J. Druker, Christian Sillaber, Harald Esterbauer, Peter Valent
Journal: Cancer Research (2005)

Abstract Chronic myeloid leukemia (CML) is a myeloproliferative disease in which BCR/ABL enhances survival of leukemic cells through modulation of proapoptotic and antiapoptotic molecules. Recent data suggest that proapoptotic Bcl-2–interacting mediator (Bim) plays a role as a tumor suppressor in myeloid cells, and that leukemic cells express only low amounts of this cell death activator. We here show that primary CML cells express significantly lower amounts of bim mRNA and Bim protein compared with normal cells. The BCR/ABL inhibitors imatinib and AMN107 were found to promote expression of Bim in CML cells. To provide direct evidence for the role of BCR/ABL in Bim modulation, we employed Ba/F3 cells with doxycycline-inducible expression of BCR/ABL and found that BCR/ABL decreases expression of bim mRNA and Bim protein in these cells. The BCR/ABL-induced decrease in expression of Bim was found to be a posttranscriptional event that depended on signaling through the mitogen-activated protein kinase pathway and was abrogated by the proteasome inhibitor MG132. Interestingly, MG132 up-regulated the expression of bim mRNA and Bim protein and suppressed the growth of Ba/F3 cells containing wild-type BCR/ABL or imatinib-resistant mutants of BCR/ABL. To show functional significance of “Bim reexpression,” a Bim-specific small interfering RNA was applied and found to rescue BCR/ABL-transformed leukemic cells from imatinib-induced cell death. In summary, our data identify BCR/ABL as a Bim suppressor in CML cells and suggest that reexpression of Bim by novel tyrosine kinase inhibitors, proteasome inhibition, or by targeting signaling pathways downstream of BCR/ABL may be an attractive therapeutic approach in imatinib-resistant CML.
Remarks ON THE TREATMENT OF THE WOUNDED KNEE-JOINT: Made at the Opening of a Discussion at Rouen
Authors: H. G. Barling
Journal: BMJ (1917)

IF any apology is needed for discussing wounds of the knee-joint it will be found in the number of such cases occurring during tlle -war, and in tlle deaths, the amputa- tions, the loss of function in thle joints resulting therefrom, which have been and still are a matter of constant anxiety to us all.If we had attained tlle acme of success, or if we were agreed on the lines of treatment to be adopted, tlle dis- cussion to-day would be unnecessary.BuLt neither of these conditions can be claimed; success suchi as we desire is still far from us, and whilst there is agreement as to treat- ment up to a certain point, then comnes divergence.
An autoimmune disease with multiple molecular targets abrogated by the transgenic expression of a single autoantigen in the thymus.
Authors: F Alderuccio, B H Toh, S S Tan, P A Gleeson, I R van Driel
Journal: The Journal of Experimental Medicine (1993)

Many autoimmune diseases are characterized by autoantibody reactivities to multiple cellular antigens. Autoantigens are commonly defined as targets of the autoimmune B cell response, but the role, if any, of these autoantigens in T cell-mediated autoimmune diseases is generally unknown. Murine experimental autoimmune gastritis is a CD4+ T cell-mediated organ-specific autoimmune disease induced by neonatal thymectomy of BALB/c mice. The murine disease is similar to human autoimmune gastritis and pernicious anemia, and is characterized by parietal and chief cell loss, submucosal mononuclear cell infiltrates, and autoantibodies to the alpha and beta subunits of the gastric H/K ATPase. However, the specificity of T cells that cause the disease is not known. To examine the role of the H/K ATPase in this T cell-mediated disease, transgenic mice were generated that express the beta subunit of the H/K ATPase under the control of the major histocompatibility complex class II I-Ek alpha promoter. We show that transgenic expression of the gastric H/K ATPase beta subunit specifically prevents the onset of autoimmune gastritis after neonatal thymectomy. In addition, thymocyte transfer experiments suggest that tolerance of pathogenic autoreactive T cells is induced within the thymus of the transgenic mice. We conclude that the beta subunit of the gastric H/K ATPase is a major T cell target in autoimmune gastritis and that thymic expression of a single autoantigen can abrogate an autoimmune response to multiple autoantigens.
Ubiquitous Healthcare Service Has the Persistent Benefit on Glycemic Control and Body Weight in Older Adults With Diabetes
Authors: Seon Mee Kang, Min Joo Kim, Hwa Young Ahn, Ji Won Yoon, Min Kyong Moon, Hye Seung Jung, Sung Hee Choi, Soo Lim, Kyong Soo Park, Hak C. Jang
Journal: Diabetes Care (2012)

The use of information technology such as the Internet and mobile communication devices in medicine is known as telemedicine or ubiquitous healthcare (u-healthcare). U-healthcare can help improve glycemic control (1–3), and we have reported that a u-healthcare service for older adults with type 2 diabetes resulted in better glycemic control with less hypoglycemia than conventional care (1). In the current study, we investigated whether the beneficial effects of this u-healthcare service on glycemic control and BMI persist after completion of the service.

This was a prospective follow-up study of our previous study (1). Briefly, 144 subjects with type 2 diabetes older than 60 years of age were randomized to one of three groups: a u-healthcare group, a self-monitored blood glucose (SMBG) group, or a routine care group (control group). After completion of the study, …
PARalyzer: definition of RNA binding sites from PAR-CLIP short-read sequence data
Authors: David L Corcoran, Stoyan Georgiev, Neelanjan Mukherjee, Eva Gottwein, Rebecca L Skalsky, Jack D Keene, Uwe Ohler
Journal: Genome biology (2011)

Abstract Crosslinking and immunoprecipitation (CLIP) protocols have made it possible to identify transcriptome-wide RNA-protein interaction sites. In particular, PAR-CLIP utilizes a photoactivatable nucleoside for more efficient crosslinking. We present an approach, centered on the novel PARalyzer tool, for mapping high-confidence sites from PAR-CLIP deep-sequencing data. We show that PARalyzer delineates sites with a high signal-to-noise ratio. Motif finding identifies the sequence preferences of RNA-binding proteins, as well as seed-matches for highly expressed microRNAs when profiling Argonaute proteins. Our study describes tailored analytical methods and provides guidelines for future efforts to utilize high-throughput sequencing in RNA biology. PARalyzer is available at http://www.genome.duke.edu/labs/ohler/research/PARalyzer/ .
Keratinocyte growth factor-induced hyperplasia of rat alveolar type II cells in vivo is resolved by differentiation into type I cells and by apoptosis
Authors: H. Fehrenbach, M. Kasper, T. Tschernig, T Pan, D. Schuh, J.m Shannon, M. Müller, R.j Mason
Journal: European Respiratory Journal (1999)

Keratinocyte growth factor (KGF) is a potent mitogen of alveolar epithelial type II cells (AEII). AEII hyperplasia is resolved within several days following intratracheal instillation of KGF by unknown mechanism(s). AEII hyperplasia was induced in rat lungs by intrabronchial instillation of 5 mg recombinant human (rh)KGF x kg body weight(-1) or an equivalent amount of diluent. Epithelial architecture, cell proliferation, transformation of AEII into type I cells (AEI) and apoptosis were investigated by means of immunohistochemistry, stereology, double immunofluorescence microscopy, electron microscopy and the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labelling (TUNEL) technique in lungs fixed 1, 2, 3 and 7 days after treatment. After 1 day of rhKGF instillation, an increase was observed in the nuclear antigen Ki-67, a proliferation marker detected by the antibody MIB-5-expressing surfactant protein (SP)-B, -C, -D-positive AEII. The incidence of mitosis was increased by day 2, resulting in AEII micropapillae with intense basolateral expression of the exon 6 containing isoform (v6) of CD446 (CD44v6), a marker for AEII. By day 3, monolayers of AEII exhibiting lateral CD44v6 covered 45% of the alveolar surface. After 7 days, there were numerous intermediate AEII/AEI cells characterized by a flat elongated shape, staining for SP-D, apical appearance of AEI marker Lycopersicon esculentum lectin and lateral staining for AEII marker CD44v6. Increased numbers of TUNEL-positive epithelial cells were seen at days 2-7. In conclusion, restoration of normal alveolar epithelium after instillation of recombinant human keratinocyte growth factor is accomplished by terminal differentiation and apoptosis of hyperplastic alveolar epithelial type II cells in vivo.
THE PATHOGENIC ROLE OF COAGULASE-NEGATIVE STAPHYLOCOCCI
Authors: R.J. HOLT
Journal: British Journal of Dermatology (1972)

Summary.— Coagulase‐negative staphylococci are now recognized as colonizers of internal artificial prostheses and as primary pathogens of the urinary tract, in addition to their more traditional role in causing bacteraemia associated with cardiac lesions. Bacteriological investigations into the colonization of ventriculo‐atrial shunts are described; they revealed that nearly all the cocci responsible for this complication belonged to one subgroup, S. II, within the general staphylococci and micrococci. Tests for lysozyme and de‐oxyribonuclease activity were made on staphylococci and micrococci recovered from the urinary tract and from colonized prostheses to see whether production of these enzymes gave better indications of pathogenicity than the well‐established coagulase test. Many strains from the urinary tract produced both lysozyme and de‐oxyribonuclease, while almost all strains from prostheses produced neither.
Aristolochic Acids Induce Chronic Renal Failure with Interstitial Fibrosis in Salt-Depleted Rats
Authors: Fre[Combining Acute Accent]de[Combining Acute Accent]ric D. Debelle, Joe[Combining Diaeresis]lle L. Nortier, Eric G. De Prez, Christian H. Garbar, Anne R. Vienne, Isabelle J. Salmon, Monique M. Deschodt-Lanckman, Jean-Louis Vanherweghem
Journal: Journal of the American Society of Nephrology (2002)

Chinese-herb nephropathy (CHN) is a rapidly progressive renal fibrosis associated with the intake of a Chinese herb (Aristolochia fangchi) containing nephrotoxic and carcinogenic aristolochic acids (AA). This study attempted to reproduce the main features of human CHN (renal failure, tubular atrophy, and interstitial fibrosis) in a rat model similar to that of cyclosporin-induced nephropathy. Salt-depleted male Wistar rats received daily subcutaneous injections of either 1 mg/kg body wt AA (low-dose AA group), 10 mg/kg body wt AA (high-dose AA group), or vehicle (control group) for 35 d. On days 10 and 35, assessment of renal function, measurements of urinary excretion of glucose, protein, and leucine aminopeptidase, and histologic analyses were performed (six rats euthanized/group). High-dose AA induced glucosuria, proteinuria, and elevated serum creatinine levels and reduced leucine aminopeptidase enzymuria on days 10 and 35, whereas low-dose AA had no significant effect. Tubular necrosis associated with lymphocytic infiltrates (day 10) and tubular atrophy surrounded by interstitial fibrosis (day 35) were the histologic findings for the high-dose AA-treated rats. In both AA groups, urothelial dysplasia was also observed, as well as fibrohistiocytic sarcoma at the injection site. A short-term model of AA-induced renal fibrosis was established in salt-depleted Wistar rats. These results support the role of AA in human CHN and provide a useful model for examination of the pathophysiologic pathways of renal fibrosis.
Trends in hospital admission rates for whooping cough in England across five decades: database studies
Authors: Nick Haslam, Uy Hoang, Michael J Goldacre
Journal: Journal of the Royal Society of Medicine (2014)

Objectives Our aim was to report on trends in hospitalisation rates for pertussis in England from the 1960s to 2011; and to provide context for the recent unexpected activity of Bordetella pertussis in the UK. Design A retrospective analysis of English national Hospital Episode Statistics (HES, 1968–2011) and the Oxford Record Linkage Study (ORLS, 1963–2011) for people admitted to hospital with whooping cough. Setting England and the Oxford Record Linkage Study area. Main outcome measures Age- and gender-specific hospital admission rates, and summary age- and sex-standardised rates, for people aged under 25 years per 100,000 population in each age group. Results Admission rates declined from the 1960s to the early 1970s. For example, the standardised rates were 12.8 (95% confidence interval 11.2–14.5) per 100,000 in England in 1968 and 4.0 (3.0–4.9) per 100,000 in 1973. They then increased to reach 45.0 (41.4–48.6) per 100,000 in 1978 and 47.4 (43.7–51.1) in 1982. From the late 1980s, admission rates continued to decline, falling to between 1 and 4 per 100,000 in each of the years between 2003 and 2011. While the trend in hospital admissions closely followed that in notifications, the annual ratio between these two measures was not consistent ranging from 1.07 (95% confidence interval 1.00–1.14) to 4.03 (3.79–4.27) notifications per admission over the last 10 years. Conclusions Epidemics of whooping cough in the late 1970s and early 1980s were associated with a significant rise in hospital admission rates. Current admission rates are low, by historical comparison. Vaccine programmes must continue to be fully implemented in order to improve control of pertussis activity.
P<scp>AIN</scp> M<scp>ECHANISMS</scp>: Labeled Lines Versus Convergence in Central Processing
Authors: A.D. (Bud) Craig
Journal: Annual Review of Neuroscience (2003)

▪ Abstract The issue of whether pain is represented by specific neural elements or by patterned activity within a convergent somatosensory subsystem has been debated for over a century. The gate control theory introduced in 1965 denied central specificity, and since then most authors have endorsed convergent wide-dynamic-range neurons. Recent functional and anatomical findings provide compelling support for a new perspective that views pain in humans as a homeostatic emotion that integrates both specific labeled lines and convergent somatic activity.