tbuckley/cabot-search huggingface dataset:
Life hangs on chance and the generosity of others
Authors: A. K. Webb
Journal: BMJ (2001)

Laura came to us from the paediatric cystic fibrosis centre when she was 16 years old. She had severe lung disease and been placed on the transplant list in January 1997. She had just completed her GCSEs and had got top marks. She had just started her A levels and wanted to study theatre and drama at university. Her disease progressed; we put her on to overnight ventilation and permanent intravenous antibiotics.

Our patients listed for transplantation continued to die on the waiting list because of the shortage of donors. Laura's activities became more limited at school, and she needed help with mobility and portable oxygen. Characteristically, despite her limitations and against advice, she …
A Successful Program to Lower Cesarean-Section Rates
Authors: Stephen A. Myers, Norbert Gleicher
Journal: New England Journal of Medicine (1988)

Despite the consensus that national cesarean-section rates are excessive, they continue to rise. Currently, approximately one of every four deliveries is by cesarean section. We developed an initiative to reduce the number of cesarean deliveries to a rate of 11 percent of all deliveries at our inner-city hospital. Participation by attending physicians was voluntary and not linked to any sanction. The program included a stringent requirement for a second opinion, objective criteria for the four most common indications for cesarean section, and a detailed review of all cesarean sections and of individual physicians' rates of performing them. During the first two years of the program, the cesarean-section rate fell from 17.5 percent of 1697 deliveries in 1985 to 11.5 percent of 2301 deliveries in 1987 (P less than 0.05). The proportion of infants with five-minute Apgar scores lower than 7 increased from 3 percent in 1985 to 4.9 percent in 1987 (P less than 0.05), but neither the fetal mortality rate (11.9 per 1000) nor the neonatal mortality rate (11.2 per 1000) in 1987 differed significantly from the rates in 1985. A single maternal death, unrelated to cesarean delivery, occurred during the study. Rates of both primary and repeat cesarean sections decreased, although only the decline in the rate of primary cesarean sections, from 12 to 6.8 percent, was statistically significant (P less than 0.05). During the same period, operative vaginal deliveries (i.e., forceps deliveries and midpelvic procedures) declined from 10.4 to 4.3 percent (P less than 0.05) of total deliveries. We conclude that an initiative within an obstetrics department can reduce cesarean-section rates substantially without adverse effects on the outcome for mother or infant.
Manifestations of Copper Deficiency in a Patient with Systemic Sclerosis on Intravenous Hyperalimentation
Authors: Richard W. Vilter, Richard C. Bozian, Evelyn V. Hess, David C. Zellner, Harold G. Petering
Journal: New England Journal of Medicine (1974)

COPPER deficiency is very rare in human beings. In 1931, Josephs suggested that it might account for iron-resistant anemia in milk-fed infants.1 It has been reported in a thriving premature infant,2 in severely malnourished infants with chronic diarrhea,3 , 4 and in several children5 and two adult patients6 whose nutrition was dependent on intravenous hyperalimentation. Anemia, leukopenia and neutropenia have been noted in all groups. Severe demineralization of bone was described in the infants. There are reports of infants with anemia, hypoproteinemia, hypoferremia and hypocupremia, possibly of dietary origin7 , 8 or caused by protein-losing enteropathy, abnormal loss of ceruloplasmin and impaired copper retention. . . .
Interaction between cytochalasin B-treated malarial parasites and erythrocytes. Attachment and junction formation.
Authors: L H Miller, M Aikawa, J G Johnson, T Shiroishi
Journal: The Journal of Experimental Medicine (1979)

We have previously demonstrated that invasion of erythrocytes (RBCs) by malaria merozoites follows a sequence: recognition and attachment in an apical orientation associated with widespread deformation of the RBC, junction formation, movement of the junction around the merozoite that brings the merozoite into the invaginated RBC membrane, and sealing of the membrane. In the present paper, we describe a method for blocking invasion at an early stage in the sequence. Cytochalasin-treated merozoites attach specifically to host RBCs, most frequently by the apical region that contains specialized organelles (rhoptries) associated with invasion. The parasite then forms a junction between the apical region and the RBC. Cytochalasin blocks movement of this junction, a later step in invasion. Cytochalasin-treated (Plasmodium knowlesi) merozoites attach to Duffy-negative human RBCs, although these RBCs are resistant to invasion by the parasite. The attachment with these RBCs, however, differs from susceptible RBCs in that there is no junction formation. Therefore the Duffy associated antigen appears to be involved in junction formation, not initial attachment.
Antiprostaglandin synthetase activity of nonsteroidal anti-inflammatory drugs and gastrointestinal micro-bleeding: a comparison of flurbiprofen with benoxaprofen.
Authors: A C Yeung Laiwah, T E Hilditch, P W Horton, J A Hunter
Journal: Annals of the Rheumatic Diseases (1981)

By using 51Cr-labelled erythrocytes and 141Ce-labelled microspheres to correct for daily variations in faecal output, gastrointestinal microbleeding was measured in hospital patients with rheumatoid arthritis before and after administration of 2 propionic acid derivatives. These were flurbiprofen and benoxaprofen, respectively a potent and a weak prostaglandin synthetase inhibitor. Increased faecal blood loss occurred consistently with flurbiprofen and not with benoxaprofen. Our results provide indirect evidence for the cytoprotective effect of prostaglandins on the gastrointestinal mucosa in man. The quantitative correlation between faecal occult blood loss as measured by the above techniques and the Haemoccult slide test is also discussed.
Alcohol and Alpha-Lipoprotein Cholesterol
Authors: M. A. MISHKEL
Journal: Annals of Internal Medicine (1974)

Comments and Correction1 October 1974Alcohol and Alpha-Lipoprotein CholesterolM. A. MISHKEL, M.D.M. A. MISHKEL, M.D.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-81-4-564_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The paper of Ginsberg and associates (1) describes the effect of moderate quantities of alcohol on plasma lipoproteins in normolipemic and hyperlipemic patients. The pathogenesis of the hyperlipidemia is complex, for alcohol, in moderate or excessive amounts, may produce or aggravate type IV, type V, and even type I hyperlipoproteinemia. Also, in the recovery phase of severe type V hyperlipoproteinemia, the lipoprotein electrophoretic pattern and ultracentrifugation frequently mimics type III hyperlipoproteinemia.I wish to report a related finding that I have not seen described before: an elevation of alpha-lipoprotein cholesterol that appeared to be related to heavy...References1. GINSBERGOLEFSKYFARQUHAR DJJ: Moderate ethanol ingestion and plasma triglyceride levels. A study in normal and hypertriglyceridemic persons. Ann Intern Med 80:143-149, 1974 LinkGoogle Scholar2. WILLEAARSETH LS: Demonstration of hyper-α-lipoproteinemia in three diabetic patients. Clin Genet 4:281-285, 1973 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: McMaster Clinic Hamilton General Hospital Hamilton, Ontario L8L 2X2 Canada PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByAlcohol Consumption and Cardiovascular Risk FactorsA pedigree of homozygous familial hyperalphalipoproteinemiaA genetic study of hyper-alpha-lipoproteinemiaMyocardial infarction in familial hyper-alpha and hypo-beta-lipoproteinaemia.The relationship between lipoprotein levels and xanthomas during progression and regression of atherosclerosisFamilial hyper-alpha-lipoproteinemia in 26 kindredsElevation of High-Density Lipoprotein in Epileptic Patients Treated with PhenytoinAlcohol Consumption and Coronary-Artery DiseaseComposition of HDL-2 and HDL-3 in familial hyperalphalipoproteinemiaFamilial hyper-alpha-lipoproteinemia: Studies in eighteen kindreds 1 October 1974Volume 81, Issue 4Page: 564-565KeywordsAlcoholsBlood plasmaCholesterolHyperlipidemiaLipoproteinsPathogenesisUltracentrifugation Issue Published: 1 October 1974 PDF DownloadLoading ...
Echocardiographic observations on the mechanism of production of the second heart sound.
Authors: P A Chandraratna, J M Lopez, L S Cohen
Journal: Circulation (1975)

This investigation was designed to determine the echocardiographic correlates of the aortic and pulmonary components of the second heart sound. Simultaneous recordings of the ECG, phonocardiogram, carotid pulse tracing and the echocardiogram of the aortic valve were made in 54 patients. The tracings were recorded at a paper speed of 100 mm/sec, with 20 msec time lines. Aortic valve closure (AVC) on the echocardiogram occurred before the onset of the aortic component of the second heart sound (A2) in all but two patients. The mean AVC-to-A2 interval was 12 msec with a range of 5 to 25 msec. Simultaneous recordings of the pulmonary valve echocardiogram, ECG, phonocardiogram and carotid pulse tracing were made in 14 patients. Pulmonary valve closure (PVC) on the echocardiogram preceded the pulmonary component of the second sound (P2) in all patients. The mean PVC-2 interval was 60 msec with a range of 30 to 75 msec. We conclude that aortic valve closure and pulmonary valve closure are not directly responsible for the genesis of the second heart sound (S2). These observations are consonant with the theory that S2 is caused by deceleration of columns of blood resulting from semilunar valve closure, throwing the cardiohemic system into vibration.
Who Shall Study Medicine?
Authors: Bruce Cooley
Journal: JAMA (1981)

<h3>To the Editor.—</h3> In his recent COMMENTARY Dr Blum argues for medical school admissions committees using outside community service as a "most important" criteria for choosing candidates instead of minor variations in grade-point average or MCAT scores. Although I agree that there are many important nonquantifiable factors that contribute to making a good physician, including improving the health and welfare of the community, community service is not the physician's raison d'être. Most physicians' primary responsibility is the care of individual patients. The vast majority of a physician's time is spent taking care of patients or related work. Why should schools select candidates on the basis of directing a neighborhood clean-up project or a dance program for the elderly, neither of which points out specific medical or social skills other than organization abilities and interest? What is there about "civic-minded" persons that makes them better able to function as physicians? In
Effects of intranasal cocaine on sympathetic nerve discharge in humans.
Authors: T N Jacobsen, P A Grayburn, R W Snyder, J Hansen, B Chavoshan, C Landau, R A Lange, L D Hillis, R G Victor
Journal: Journal of Clinical Investigation (1997)

Cocaine-induced cardiovascular emergencies are mediated by excessive adrenergic stimulation. Animal studies suggest that cocaine not only blocks norepinephrine reuptake peripherally but also inhibits the baroreceptors, thereby reflexively increasing sympathetic nerve discharge. However, the effect of cocaine on sympathetic nerve discharge in humans is unknown. In 12 healthy volunteers, we recorded blood pressure and sympathetic nerve discharge to the skeletal muscle vasculature using intraneural microelectrodes (peroneal nerve) during intranasal cocaine (2 mg/kg, n = 8) or lidocaine (2%, n = 4), an internal local anesthetic control, or intravenous phenylephrine (0.5-2.0 microg/kg, n = 4), an internal sympathomimetic control. Experiments were repeated while minimizing the cocaine-induced rise in blood pressure with intravenous nitroprusside to negate sinoaortic baroreceptor stimulation. After lidocaine, blood pressure and sympathetic nerve discharge were unchanged. After cocaine, blood pressure increased abruptly and remained elevated for 60 min while sympathetic nerve discharge initially was unchanged and then decreased progressively over 60 min to a nadir that was only 2+/-1% of baseline (P < 0.05); however, plasma venous norepinephrine concentrations (n = 5) were unchanged up to 60 min after cocaine. Sympathetic nerve discharge fell more rapidly but to the same nadir when blood pressure was increased similarly with phenylephrine. When the cocaine-induced increase in blood pressure was minimized (nitroprusside), sympathetic nerve discharge did not decrease but rather increased by 2.9 times over baseline (P < 0.05). Baroreflex gain was comparable before and after cocaine. We conclude that in conscious humans the primary effect of intranasal cocaine is to increase sympathetic nerve discharge to the skeletal muscle bed. Furthermore, sinoaortic baroreflexes play a pivotal role in modulating the cocaine-induced sympathetic excitation. The interplay between these excitatory and inhibitory neural influences determines the net effect of cocaine on sympathetic discharge targeted to the human skeletal muscle circulation.
Response to Peer Commentaries on Mechanisms Underlying an Ability to Behave Ethically—Neuroscience Addresses Ethical Behaviors: Transitioning From Philosophical Dialogues to Testable Scientific Theories of Brain and Behavior
Authors: Donald W. Pfaff, Martin Kavaliers, Elena Choleris
Journal: The American Journal of Bioethics (2008)

It is a pleasure to respond to several of the comments on our article “Mechanisms underlying an ability to behavior ethically” (Pfaff et al. 2008). Summarizing the main point of that article in a p...
IMMUNOPROTECTION OF RATS AGAINST HAEMOPHILUS INFLUENZAE TYPE B DISEASE MEDIATED BY MONOCLONAL ANTIBODY AGAINST A HAEMOPHILUS OUTER-MEMBRANE PROTEIN
Authors: EricJ. Hansen, PaulA. Gulig, StellaM. Robertson, CarolynF. Frisch, ElizabethJ. Haanes
Journal: The Lancet (1982)
Brain function theories, EEG sources, and dynamic states
Authors: Mark E. Pflieger
Journal: Behavioral and Brain Sciences (2000)

This commentary discusses three features of the general theoretical framework proposed by Nunez: (1) Functional concepts, such as computation and control, are not foundational. (2) A mismatch between the concept of subcortical input and EEG output is problematic for the input/output operator concept of cortical dynamics. (3) The concept of brain state is relatively static.
Metasma: a mask of stress
Authors: Ronni Wolf, D. Wolf, A. Tamir, Y. Politi
Journal: British Journal of Dermatology (1991)

Journal Article Metasma: a mask of stress Get access Ronni Wolf, Ronni Wolf Department of Dermatology. Tel‐Aviv Sourasky Medical Center, Ichilov Hospital and Sackler FacuJty of Medicine Tel‐Aviv University, Tel‐Aviv, Israel Search for other works by this author on: Oxford Academic Google Scholar D. Wolf, D. Wolf Department of Dermatology. Tel‐Aviv Sourasky Medical Center, Ichilov Hospital and Sackler FacuJty of Medicine Tel‐Aviv University, Tel‐Aviv, Israel Search for other works by this author on: Oxford Academic Google Scholar A. Tamir, A. Tamir Department of Dermatology. Tel‐Aviv Sourasky Medical Center, Ichilov Hospital and Sackler FacuJty of Medicine Tel‐Aviv University, Tel‐Aviv, Israel Search for other works by this author on: Oxford Academic Google Scholar Y. Politi Y. Politi Department of Dermatology. Tel‐Aviv Sourasky Medical Center, Ichilov Hospital and Sackler FacuJty of Medicine Tel‐Aviv University, Tel‐Aviv, Israel Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 125, Issue 2, 1 August 1991, Page 192, https://doi.org/10.1111/j.1365-2133.1991.tb06075.x Published: 01 August 1991
New Exposure Biomarkers as Tools for Breast Cancer Epidemiology, Biomonitoring, and Prevention: A Systematic Approach Based on Animal Evidence
Authors: Ruthann A. Rudel, Janet M. Ackerman, Kathleen R. Attfield, Julia Green Brody
Journal: Environmental Health Perspectives (2014)

Exposure to chemicals that cause rodent mammary gland tumors is common, but few studies have evaluated potential breast cancer risks of these chemicals in humans.The goal of this review was to identify and bring together the needed tools to facilitate the measurement of biomarkers of exposure to potential breast carcinogens in breast cancer studies and biomonitoring.We conducted a structured literature search to identify measurement methods for exposure biomarkers for 102 chemicals that cause rodent mammary tumors. To evaluate concordance, we compared human and animal evidence for agents identified as plausibly linked to breast cancer in major reviews. To facilitate future application of exposure biomarkers, we compiled information about relevant cohort studies.Exposure biomarkers have been developed for nearly three-quarters of these rodent mammary carcinogens. Analytical methods have been published for 73 of the chemicals. Some of the remaining chemicals could be measured using modified versions of existing methods for related chemicals. In humans, biomarkers of exposure have been measured for 62 chemicals, and for 45 in a nonoccupationally exposed population. The Centers for Disease Control and Prevention has measured 23 in the U.S. population. Seventy-five of the rodent mammary carcinogens fall into 17 groups, based on exposure potential, carcinogenicity, and structural similarity. Carcinogenicity in humans and rodents is generally consistent, although comparisons are limited because few agents have been studied in humans. We identified 44 cohort studies, with a total of > 3.5 million women enrolled, that have recorded breast cancer incidence and stored biological samples.Exposure measurement methods and cohort study resources are available to expand biomonitoring and epidemiology related to breast cancer etiology and prevention.
How Reliable Is Estimation of Glomerular Filtration Rate at Diagnosis of Type 2 Diabetes?
Authors: Richard A. Chudleigh, Gareth Dunseath, William Evans, John N. Harvey, Philip Evans, Richard Ollerton, David R. Owens
Journal: Diabetes Care (2007)

The Cockcroft-Gault (CG) and Modification of Diet in Renal Disease (MDRD) equations previously have been recommended to estimate glomerular filtration rate (GFR). We compared both estimates with true GFR, measured by the isotopic (51)Cr-EDTA method, in newly diagnosed, treatment-naïve subjects with type 2 diabetes.A total of 292 mainly normoalbuminuric (241 of 292) subjects were recruited. Subjects were classified as having mild renal impairment (group 1, GFR <90 ml/min per 1.73 m(2)) or normal renal function (group 2, GFR >/=90 ml/min per 1.73 m(2)). Estimated GFR (eGFR) was calculated by the CG and MDRD equations. Blood samples drawn at 44, 120, 180, and 240 min after administration of 1 MBq of (51)Cr-EDTA were used to measure isotopic GFR (iGFR).For subjects in group 1, mean (+/-SD) iGFR was 83.8 +/- 4.3 ml/min per 1.73 m(2). eGFR was 78.0 +/- 16.5 or 73.7 +/- 12.0 ml/min per 1.73 m(2) using CG and MDRD equations, respectively. Ninety-five percent CIs for method bias were -11.1 to -0.6 using CG and -14.4 to -7.0 using MDRD. Ninety-five percent limits of agreement (mean bias +/- 2 SD) were -37.2 to 25.6 and -33.1 to 11.7, respectively. In group 2, iGFR was 119.4 +/- 20.3 ml/min per 1.73 m(2). eGFR was 104.4 +/- 26.3 or 92.3 +/- 18.7 ml/min per 1.73 m(2) using CG and MDRD equations, respectively. Ninety-five percent CIs for method bias were -17.4 to -12.5 using CG and -29.1 to -25.1 using MDRD. Ninety-five percent limits of agreement were -54.4 to 24.4 and -59.5 to 5.3, respectively.In newly diagnosed type 2 diabetic patients, particularly those with a GFR >/=90 ml/min per 1.73 m(2), both CG and MDRD equations significantly underestimate iGFR. This highlights a limitation in the use of eGFR in the majority of diabetic subjects outside the setting of chronic kidney disease.
Abstract 4441: Ube2e inhibits the ubiquitination and degradation of EGFR mediated by Cbl and Ube2d
Authors: Ke Ma, Stanley Lipkowitz, Rachel Klevit, Mariya Sergeyevna Liyasova
Journal: Cancer Research (2014)

Abstract Receptor tyrosine kinases (RTKs) have a demonstrated role as drivers of malignant transformation. Many RTKs (e.g., EGFR, MET, FLT3) are negatively regulated by ubiquitination and degradation mediated by Cbl proteins a family of RING finger (RF) ubiquitin ligases (E3s). There are three mammalian family members Cbl, Cbl-b and Cbl-c. All Cbl proteins have a highly conserved N-terminal tyrosine kinase binding domain and a C3HC4 (RF) domain. Loss of Cbl protein function has be associated with malignant transformation drive by increased RTK activity. E3s such as the Cbl proteins confer specificity to the ubiquitination process and direct the conjugation of ubiquitin to one or more lysines on the specific target proteins in collaboration with ubiquitin-conjugating enzymes (E2s). The E2s bind to the E3 and together they mediate ubiquitination of specific substrates. There are approximately 30 human E2s. All of the E2s have a highly conserved catalytic domain (UBC domain). In this study, we characterized the interaction of Cbl with E2s. Using an in vitro E3 assay, we found that only the Ube2d family (Ube2d1, Ube2d2, and Ube2d3) of E2s mediates autoubiquitination of the three Cbl proteins. Subsequently, using the yeast two-hybrid system, we found that Ube2e1, Ube2e2, Ube2e3, Ube2L3, Ube2u, Ube2w and Ube2z can interact with Cbl even though they do not support autoubiquitination of Cbl in vitro E3 assay. Among these E2s, three Ube2e family members and Ube2w bind to the RF domain of Cbl as demonstrated by the loss of interaction when the RF domain is disrupted. Further, we demonstrated that Ube2e family members are involved in regulation of EGFR activity mediated by Cbl in HeLa cells. Knockdown of Ube2e increases down-regulation and ubiquitination of EGFR in HeLa cells. We further showed that three Ube2e inhibit autoubiquitination of Cbl mediated by Ube2d2 in vitro. Together these data suggest that RTK degradation can be modulated by competition between E2s for the Cbl E3s. Citation Format: Ke Ma, Stanley Lipkowitz, Rachel Klevit, Mariya Sergeyevna Liyasova. Ube2e inhibits the ubiquitination and degradation of EGFR mediated by Cbl and Ube2d. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4441. doi:10.1158/1538-7445.AM2014-4441
NARRATION
Authors: F. R. C. Johnstone
Journal: JAMA (1967)

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