tbuckley/cabot-search huggingface dataset:
Rapid accumulation of elastin and collagen in the aortas of sheep in the immediate perinatal period.
Authors: M P Bendeck, B L Langille
Journal: Circulation Research (1991)

While characterizing developmental changes in aortic wall composition in sheep, we observed very rapid accumulation of elastin and collagen in the immediate perinatal period. Thoracic aortic elastin content increased by 41%, and collagen content increased by 49% in approximately 1 week, between 140 days gestation and 3 days postpartum (term = 145 days). Even larger changes were observed in the abdominal aorta. Elastin content increased by 66%, and collagen increased by 57%. The pronounced increase in wall tissue accumulation near birth preceded a marked postnatal increase in arterial pressure. We propose that this elastin and collagen accumulation is a preadaptive response in preparation for the later increase in pressure. The prenatal and postnatal events that initiate this synthesis and accumulation are not known. We also found that, in the 3 weeks after this initial rapid increase, accumulation of elastin and collagen was markedly reduced in the abdominal, but not the thoracic, aorta. This latter finding may be linked to the dramatic decrease in flow through this vessel that results from the loss of the placental circulation. Finally, we observed that relatively high smooth muscle cell replication rates in the abdominal aorta postpartum resulted in no net DNA accumulation. This finding indicates that cell turnover plays an important role in postnatal arterial growth and development.
Localization of Intracranial Tumours
Authors: C. Gleadhill
Journal: BMJ (1968)

PointersCarcinoma of Lung: Low incidence of tumour produced in mice exposed to cigarette smoke and air mixture (p. 637).Spread of Staphylococci: General-practice sur- vey in Edinburgh and North-east England showed that newborn babies acquired Staph.aureus more frequently in hospital than at home, but hospital strains were no more likely to spread within the family or to cause septic lesions than "domestic" strains (p.642).
Reflections on a Century of Excellence
Authors: Morton A. Madoff
Journal: JAMA (1993)

In many ways, Tufts University School of Medicine, Boston, Mass, has never gotten over the manner in which it was founded a century ago. For a multitude of reasons, I hope it never does. By 1893, the College of Physicians and Surgeons, a Boston medical school of unsteady reputation, had settled into a kind of terminal complacency. Its outmoded facilities and undemanding curriculum were a growing source of discontent, perhaps of embarrassment, to its leading faculty members. Administratively unwieldy and academically staid, it hardly seemed the sort of institution capable of competing with the widening ranks of university-affiliated medical schools. Seven of the college's most esteemed faculty members, prominent Boston physicians, petitioned the trustees of Tufts College for permission to incorporate a new medical school under Tufts' aegis. "We propose to furnish a building, equipment, and everything necessary to carry on the work of a first-class medical school without any
[649] CPG 10101 (ACTILON) IN COMBINATION WITH PEGYLATED INTERFERON AND/OR RIBAVIRIN IN CHRONIC HCV GENOTYPE 1 INFECTED PATIENTS WITH PRIOR RELAPSED RESPONSE: WEEK 48 DATA
Authors: M.L. Shiftman, R. Ghalib, E. Lawitz, B. Freilich, S.C. Gordon, P.Y. Kwo, T.R. Riley, E. Schiff, S. Flamm, I.M. Jacobson, N.N. Zein, A. Reuben, M. Swaim, D. Bright, M. Al-Adhami, J. Lekstrom-Himes, F.E. Massari, J.G. McHutchison
Journal: Journal of Hepatology (2007)
Graft–Vs.–Host Disease After Liver Transplantation
Authors: Graeme Alexander, Bernard Portmann
Journal: Hepatology (1990)

Clinically evident, generalized graft–vs.–host disease is not thought to occur as a consequence of transplantation of most solid organs. The large inoculum of donor lymphoid cells required and the inability of the recipient to destroy these passenger cells are apparently rarely produced by solid–organ transplantation. However, there is a risk of graft–vs.–host disease when normal spleens are included in vascularized pancreas transplants. We report on a case of severe, generalized acute graft–vs.–host disease in a recipient of a liver tranplant, involving documented transient chimerism of donor origin. This life–threatening complication was treated successfully with increase in the corticosteroid dosage and administration of anti–thymocyte globulin.
Mechanism of production of intestinal secretion by elevated venous pressure.
Authors: M E Yablonski, N Lifson
Journal: Journal of Clinical Investigation (1976)

A study was carried out to elucidate the physiological mechanisms responsible for the intestinal secretion produced by venous pressure elevation. In dogs, measurements were made of the rate and composition of small intestinal secretion, rate of flow and composition of intestinal lymph, plasma composition, and mucosal water content, all in response to elevations of intestinal venous pressure. Venous pressure elevations above a threshold value of 30-35 cm H2O produce secretion at a rate of approximately proportional to the value of the pressure minus the threshold value. Above the threshold value, there were large increases in the rates of lymph flow and net sustained transcapillary filtration. These rates were also roughly proportional to the incremental venous pressure. It is concluded that intestinal secretion produced by elevated venous pressure is almost surely secretory filtration, a passive process with the driving force for secretion an increase in mucosal tissue fluid pressures to values of only some 4-6 cm H2O. The increased tissue fluid pressure not only provides the driving force but also produces an increase in the hydraulic permeability of the epithelium without which the driving force would be ineffective. The transepithelial channels are large enough to permit insulin to pass freely and even plasma protein to pass in large amounts, and hence are most probably intercellular. Secretory filtration probably represents a general pathophysiological response of transporting epithelia to elevated tissue fluid pressure. It is proposed that the threshold value for secretion and associated changes is explained by dilution of the tissue fluid protein colloid osmotic pressure in a small subepithelial, juxtacapillary compartment.
ADDITIVE EFFECTS OF CERTAIN TRANSFORMING AGENTS FROM SOME VARIANTS OF PNEUMOCOCCUS
Authors: Harriett E. Taylor
Journal: The Journal of Experimental Medicine (1949)

It has proved possible to transform an extreme rough variant of pneumococcus back to the rough state by the action of the desoxyribonucleate fractions of either rough or Type III smooth pneumococci. In a second step, the rough pneumococci produced by this transformation were further changed to the Type III smooth state by means of the desoxyribonucleate fraction of Type III smooth organisms. With use of the Type III desoxyribonucleate, the two steps could be accomplished successively, but not simultaneously, during the growth of a single inoculum of the extreme rough form. These findings have been interpreted as indicating that the desoxyribonucleic acid fraction of Type III smooth pneumococci contains two transforming principles of differing specificity, while the same fraction of rough pneumococci contains but one of these principles. Two distinct spontaneous variants of Type III smooth pneumococci have been isolated which seem to differ from normal Type III smooth pneumococci in synthesizing smaller amounts of the specific polysaccharide. Tests have indicated that these variant Type III races differ from the normal in possessing altered Type III transforming principles. Each of the new transforming agents when influencing rough bacteria, is strictly specific in its action, inducing as it does the formation of the corresponding variant Type III pneumococci. Interaction between the two new transforming principles and rough pneumococci can lead to the production of normal Type III organisms, although neither principle alone can do it. This is interpreted as indicating that the two mutated Type III transforming principles are qualitatively different from each other. Another kind of two-step transformation was accomplished by converting rough pneumococci first into the variant Type III pneumococci which produced very little specific polysaccharide, and then by transforming these latter into normal Type III organisms. After the two-step transformation of the extreme rough pneumococcus, both transforming principles used to effect this can be recognized in the Type III smooth pneumococci finally recovered. By contrast, in the two-step transformation of the rough pneumococcus by way of an intermediate smooth form, only the second transforming principle can be obtained from the resulting fully smooth organisms. The meaning of these facts is discussed.
Diseases of the Homeless
Authors: L. S. Wolfe
Journal: JAMA (1985)

To the Editor.—  This letter is not intended to reduce Dr Gary Rapaport's 1 compassion or anyone else's for our homeless population. He writes that 10% of these people were hypertensive, 5% were arthritic, and 2% were diabetic when seen in a Los Angeles medical center emergency room.  At my general practice office, 30% of my patients are hypertensive, 25% complain of arthritis, and 20% are diabetic. Many are all three. I am advising my patients to leave their houses and take to the road.
Colonic Changes in Patients with Cirrhosis and in Patients with Extrahepatic Portal Vein Obstruction
Authors: S. Misra, M. Dwivedi, V. Misra, S. Dharmani, B. Kunwar, J. Arora
Journal: Endoscopy (2005)

Background and Study Aims: Figures for the prevalence of anorectal varices and portal hypertensive colopathy have varied considerably in the available studies of patients with cirrhosis, and few studies have observed these changes in patients with extrahepatic portal vein obstruction (EHPVO). Our aim was to investigate the colonic changes, if any, in patients with EHPVO and to compare them with those seen in patients with cirrhosis of the liver. Patients and Methods: A total of 50 patients with cirrhosis and 35 patients with EHPVO, all of whom had a history of at least one episode of bleeding from esophageal varices, underwent both upper gastrointestinal endoscopy and colonoscopy. Results: Anorectal varices were seen more commonly in patients with EHPVO than in patients with cirrhosis (63 % vs. 38 %, P < 0.03). Of the patients with anorectal varices, large anorectal varices were also more common in patients with EHPVO than in patients with cirrhosis (73 % vs. 32 %, P < 0.01). Colopathy was noted in 40 % of patients with EHPVO and in 62 % of patients with cirrhosis (P < 0.05). Of the patients with EHPVO, colopathy was noted in 27 % of patients who also had anorectal varices and in 61.5 % of patients without anorectal varices (P < 0.05). Similarly, patients with both cirrhosis and anorectal varices were found to have a lower prevalence of colopathy than cirrhotic patients without anorectal varices (42 % vs. 74 %, P < 0.03). Conclusions: Anorectal varices are more common in patients with EHPVO, while portal hypertensive colopathy is more common in patients with cirrhosis. Large anorectal varices are also more common in patients with EHPVO than in patients with cirrhosis and there is an inverse relationship between anorectal varices and colopathy in both cirrhotic patients and patients with EHPVO.
VENEREAL CLINICS: A LAY POINT OF VIEW
Authors: H. W. Bayly
Journal: BMJ (1921)

<h3>Objective</h3> To examine the length of time between receiving funding and publishing the protocol and main paper for randomised controlled trials. <h3>Design</h3> An observational study using survival analysis. <h3>Setting</h3> Publicly funded health and medical research in Australia. <h3>Participants</h3> Randomised controlled trials funded by the National Health and Medical Research Council of Australia between 2008 and 2010. <h3>Main outcome measures</h3> Time from funding to the protocol paper and main results paper. Multiple variable survival models examining whether study characteristics predicted publication times. <h3>Results</h3> We found 77 studies with a total funding of $A59 million. The median time to publication of the protocol paper was 6.4 years after funding (95% CI 4.1 to 8.1). The proportion with a published protocol paper 8 years after funding was 0.61 (95% CI 0.48 to 0.74). The median time to publication of the main results paper was 7.1 years after funding (95% CI 6.3 to 7.6). The proportion with a published main results paper 8 years after funding was 0.72 (95% CI 0.56 to 0.87). The HRs for how study characteristics might influence timing were generally close to one with narrow CIs, the notable exception was that a longer study length lengthened the time to the main paper (HR=0.62 per extra study year, 95% CI 0.43 to 0.89). <h3>Conclusions</h3> Despite the widespread registration of clinical trials, there remain serious concerns of trial results not being published or being published with a long delay. We have found that these same concerns apply to protocol papers, which should be publishable soon after funding. Funding agencies could set a target of publishing the protocol paper within 18 months of funding.
Diagnostic Patient Studies in Surgery
Authors: Edwin A. Deitch
Journal: JAMA (1987)

The first question I asked myself after receiving this text to review was: Is there a true need for a book devoted entirely to diagnostic studies, especially since there are entire texts available devoted to material presented in each chapter? The answer is "yes." This textbook provides a foundation for the surgical clinician to become literate in the field of diagnostic patient studies. After reading this text, the reader will have a better understanding of the principles and pitfalls of most diagnostic tests and will be able to put the "surprising" test result into clinical perspective. For example, after reading the chapters on imaging (ultrasound, radionuclide scanning, and computed tomography), the reader will have an appreciation of the relative efficiencies and limitations of each of these techniques, and can decide which of these imaging tests should be ordered first on a particular patient. The format of this textbook is straightforward
The Varying Clinical Spectrum of the Systolic Click-Late Systolic Murmur Syndrome
Authors: MARY E. FONTANA, HOBERT L. PENCE, RICHARD F. LEIGHTON, CHARLES F. WOOLEY
Journal: Circulation (1970)

Striking auscultatory variations with changes in posture were observed in 30 individuals with either mid-late systolic clicks, late systolic murmurs, or both, particularly in the upright position. Twenty-seven patients had late systolic murmurs; in nine, however, the murmur was not heard until assumption of the sitting position. Mid-late systolic clicks were heard in 20 patients while supine and in three only on sitting. Click movement (usually toward the first sound) was common during sitting or standing. Late systolic murmurs became holosystolic in 25 patients. In 20, the murmur did not become holosystolic until standing. Systolic whoops, not heard in the supine position, developed on assumption of the sitting position (three patients) or standing (three patients). With prompt squatting, the auscultatory findings reverted to those heard in the supine position in eight of nine patients. All observations were confirmed with phonocardiograms. Structural alterations in the mitral valve complex resulting in systolic prolapse of leaflets into the left atrium occur in these patients. Posture related changes in mitral valve function most likely explain the auscultatory phenomena.
THE EFFICACY OF THE TREATMENT OF ACUTE PURULENT OTITIS BY ASEPTIC DRAINAGE.
Authors: H. GRADLE
Journal: JAMA (1904)

The object of this paper is to show the superiority of the treatment of acute purulent otitis by aseptic drainage. The method itself is the familiar one which has gradually gained in popularity. Its principles are paracentesis as soon as the diagnosis is made, and continuous absorption of the discharge by an aseptic gauze drain in the meatus and a large dressing over the auricle. After sterilization of the meatus and auricle by means of carbolic acid solution the sterility of the gauze is further assured by the liberal use of powdered boric acid in the dressing. The external gauze pad is changed as soon as moisture shows, while the tampon in the meatus may be left 24 to 48 hours at a time. Notwithstanding its simplicity and efficacy, the superiority of this treatment is not universally acknowledged. In illustration I might quote two recent publications by acknowledged authorities. Politzer
Transglutaminase 1 deficiency and corneocyte collapse: an indication for targeted molecular screening in autosomal recessive congenital ichthyosis
Authors: G. Esposito, G. Tadini, F. Paparo, A. Viola, L. Ieno, W. Pennacchia, F. Messina, L. Giordano, A. Piccirillo, L. Auricchio
Journal: British Journal of Dermatology (2007)

Conflicts of interest: none declared. Sir, Autosomal recessive congenital ichthyosis (ARCI) is a rare clinically and genetically heterogeneous skin disease.1 In childhood, ARCI phenotypes range from severe nonerythrodermic lamellar ichthyosis (NELI) to mild congenital ichthyosiform erythroderma (CIE).1 ARCI‐related genes are TGM1 on 14q11.2,2,ABCA12 on 2q33–35,3,FLJ39501 on 19p12–q12,4,ALOXE3/ALOX12B on 17p13,3 and ichthyn on 5q33.3 This genetic heterogeneity makes genetic counselling and prenatal diagnosis of ARCI difficult. However, about 35–40% of patients with ARCI have complete or partial transglutaminase 1 (TGase1) deficiency.5 Because clinical manifestations may differ among TGase1‐deficient patients,5 it is difficult to identify candidates for TGM1 mutation screening. At present, TGase1 deficiency is detected by electron microscopy and/or TGase1 assay of a skin punch biopsy, which is an invasive procedure.6 However, although the epidermis of patients with NELI or CEI and TGase1 deficiency is usually characterized by a specific ultrastructure, patients with the same TGM1 genotype may have different ultrastructures and/or phenotypes.5, 6 Therefore, ultrastructure alone does not invariably discriminate TGase1‐deficient patients.
Is a High Glycogen Content Beneficial or Detrimental to the Ischemic Rat Heart?
Authors: Heather R. Cross, Lionel H. Opie, George K. Radda, Kieran Clarke
Journal: Circulation Research (1996)

Abstract A high glycogen level may be beneficial to the ischemic heart by providing glycolytic ATP or detrimental by increasing intracellular lactate and protons. To determine the effects of high glycogen on the ischemic myocardium, the glycogen content of Langendorff-perfused rat hearts was either depleted or elevated before 32 minutes of low-flow (0.5 mL/min) ischemia with Krebs-Henseleit buffer with or without 11 mmol/L glucose, followed by 32 minutes of reperfusion with buffer containing 11 mmol/L glucose. 31 P nuclear magnetic resonance spectra were acquired sequentially throughout. Further experiments involved early reperfusion or the addition of HOE 694, a Na + -H + exchange inhibitor, during reperfusion. When glucose was supplied throughout ischemia, no ischemic contracture occurred, and postischemic recovery of contractile function was highest, at 88% of preischemic function. In the absence of glucose, normal-glycogen hearts underwent ischemic contracture at 5 minutes, had an end-ischemic pH of 6.87, and recovered to 54%, whereas in high-glycogen hearts, contracture was delayed to 13 minutes, the end-ischemic pH was 6.61, and functional recovery decreased to 13%. Contracture onset coincided with the decrease in glycolysis, which occurred as glycogen became fully depleted. Functional recovery in the high-glycogen hearts increased to 89% when reperfused before contracture and to 56% when reperfused in the presence of HOE 694. Thus, during brief ischemia in the high-glycogen hearts, ischemic glycogen depletion and contracture were avoided, and the hearts were protected from injury. In contrast, during prolonged ischemia in the high-glycogen hearts, glycogen became fully depleted, and myocardial injury occurred; the injury was exacerbated by the lower ischemic pH in these hearts, leading to increased Na + -H + exchange during reperfusion. The contradictory findings of past studies concerning the effect of high glycogen on the ischemic myocardium may thus be due to differences in the extent of glycogen depletion during ischemia.
Successful Two-Week Treatment Schedules for Subacute Endocarditis Caused by Penicillin-Sensitive Streptococcus Viridans.
Authors: Charles A. Terhune
Journal: Annals of Internal Medicine (1970)

Meeting Abstracts1 May 1970Successful Two-Week Treatment Schedules for Subacute Endocarditis Caused by Penicillin-Sensitive Streptococcus Viridans.Charles A. Terhune, M.D., James S. Tan, M.D., Samuel Kaplan, M.D., Morton Hamburger, M.D., F.A.C.P.Charles A. Terhune, M.D.Search for more papers by this author, James S. Tan, M.D.Search for more papers by this author, Samuel Kaplan, M.D.Search for more papers by this author, Morton Hamburger, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-72-5-784_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe treatment ofStreptococcus viridansinfection has not been standardized. During the past 2 decades restriction of the treatment period to 2 weeks has been explored at our Medical Center. Fifty patients received a 2-week course of treatment, as follows:Group 1 (1947-52)—parenteral penicillin G alone: 13.Group 2 (1954-67)—penicillin G + streptomycin: 9 (some of this group received oral penicillin V for 4 or more days).Group 3 (1955-69)—penicillin V orally + streptomycin: 24 (7 of these received 1 to 3 days of parenteral penicillin G initially).Group 4 (1965-69)—other PNC related antibiotics (cephaloridine, ampicillin, nafcillin) with or without... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Charles A. Terhune, M.D.; James S. Tan, M.D.; Samuel Kaplan, M.D.; Morton Hamburger, M.D., F.A.C.P.Affiliations: Cincinnati, Ohio PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1970Volume 72, Issue 5Page: 784-784KeywordsAntibioticsEndocarditisPenicillinStreptococcal infectionsStreptococcusStreptomycin ePublished: 1 December 2008 Issue Published: 1 May 1970 PDF downloadLoading ...
In-vivo confocal real-time mini-microscopy in animal models of human inflammatory and neoplastic diseases
Authors: M. Goetz, C. Fottner, E. Schirrmacher, P. Delaney, S. Gregor, C. Schneider, D. Strand, S. Kanzler, B. Memadathil, E. Weyand, M. Holtmann, R. Schirrmacher, M. Weber, M. Anlauf, G. Klöppel, M. Vieth, P. Galle, P. Bartenstein, M. Neurath, R. Kiesslich
Journal: Endoscopy (2007)

Background and study aims: Although various improvements in tissue imaging modalities have recently been achieved, in-vivo molecular and subsurface imaging in the field of gastroenterology remains a technical challenge. In this study we evaluated a newly developed, handheld, miniaturized confocal laser microscopy probe for real-time in-vivo molecular and subsurface imaging in rodent models of human disease.