tbuckley/cabot-search huggingface dataset:
Binding and covalent cross-linking of purified von Willebrand factor to native monomeric collagen.
Authors: P Bockenstedt, J McDonagh, R I Handin
Journal: Journal of Clinical Investigation (1986)

We have analyzed the interaction of the adhesive glycoprotein, von Willebrand factor (vWF), with native monomeric collagen monolayers by adsorbing acid soluble Types I and III collagen derived from calf skin to polystyrene microtiter wells and incubating the wells with purified human 125I-vWF. The binding of 125I-vWF was saturable, reversible, specific, and was abolished by heat denaturation of the collagen monomers. Binding was half-maximal at 5 micrograms/ml, and, at saturation, 7.5 ng 125I-vWF were bound to each microgram of immobilized collagen. 125I-vWF did not bind to wells coated with other extracellular matrix or plasma proteins such as fibronectin, fibrinogen, gelatin, or the q subunit of the first component of complement (C1q). In addition, bound 125I-vWF could not be displaced from collagen by the addition of either fibronectin or fibrinogen. After incubation with Factor XIIIa, plasma transglutaminase, 125I-vWF bound to collagen could no longer be displaced by vWF, which suggests covalent cross-linking of vWF to collagen monomers. Factor XIIIa-dependent covalent cross-linking of vWF to collagen, but not to fibronectin or laminin, was also demonstrated by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate.
The Effect of Priscoline on Peripheral Blood Flow in Normal Subjects and Patients with Peripheral Vascular Disorders
Authors: THEODORE B. VAN ITALLIE, CHARLES W. CLARKE
Journal: Circulation (1951)

Using the venous occlusion plethysmograph the authors have studied the peripheral circulation of normal subjects and persons with peripheral vascular disease. It is demonstrated that the vasodilating agent Priscoline (2-benzyl-4,5-imidazoline hydrochloride) frequently increases peripheral blood flow to a degree comparable to that produced by either sympathectomy or indirect body heating. In addition, the combined use of plethysmography and a vasodilating procedure is shown to be of value in the diagnosis of peripheral vascular disorders.
The Association of HLA-B* 5101 and Phenobarbital-Induced Severe Cutaneous Adverse Drug Reactions in Thai Children
Authors: Plernpit Likkasittipan, Wiparat Manuyakorn, Surakameth Mahasirimongkol, Suwat Benjaponpitak, Anannit Visudtibhan, Nuanjun Wichukchinda, Sukanya Wattanapokayakit
Journal: Journal of Allergy and Clinical Immunology (2015)
PROGNOSTIC VALUE OF 128-CHANNEL CORONARY COMPUTED TOMOGRAPHIC ANGIOGRAPHY FOR ASYMPTOMATIC TYPE II DIABETIC PATIENTS
Authors: Mineok Chang, Ik Jun Choi, Jin Jin Kim, Sungmin Lim, Minkyu Kang, Byung-Hee Hwang, Donggyu Moon, Eun ho Choo, Jae Gyung Kim, Tae-Hun Kim, Yoon Seok Koh, Suk Min Seo, Chan Jun Kim, Pum Joon Kim, Kiyuk Chang, Wook Sung Chung, Ki-Bae Seung
Journal: Journal of the American College of Cardiology (2013)
In-111 Labeled Octreotide Imaging of a Primary Carcinoid Lesion Undetected by Conventional Imaging Studies in a Patient With “Chronic Pancreatitis”
Authors: SHIVAANI KUMMAR, SUZY L. KIM, RAGHUVEER K. HALKAR, JAMES R. GALT
Journal: Clinical Nuclear Medicine (1996)

This is a case report of a patient with an initial diagnosis of chronic pancreatitis who actually had metastatic carcinoid tumor. His symptoms of abdominal pain, weight loss, and diarrhea were manifestations of the large tumor bulk within the liver as well as carcinoid syndrome. Although abdominal CT scans showed multiple liver lesions, the primary lesion was not identified by conventional imaging studies. However, the mid-gut primary lesion was visualized on In-111 labeled octreotide scintigraphy; where the liver lesions were better delineated and seen to be separate from the normal pancreas when the Tc-99m sulfur colloid images were compared to the octreotide images.
Genetic Risk in Childhood Obesity: Implications for Clinical Practice—Reply
Authors: Jose R. Fernandez
Journal: JAMA Pediatrics (2013)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Pediatrics HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Pediatrics journal
Elevated plasma levels of matrix metalloproteinase-9 (92-kd type IV collagenase/gelatinase B) in hepatocellular carcinoma
Authors: A Hayasaka
Journal: Hepatology (1996)

Matrix metalloproteinase 9 (MMP-9), a 92-kd gelatinase/type IV collagenase, has been implicated as playing an important role in cancer invasion and metastasis. A previous study showed that serum type IV collagenase activity correlated with metastasis by hepatocellular carcinoma (HCC). The aims of this study were to determine the plasma levels of immunoreactive MMP-9 in patients with HCC and to compare the levels with the clinical features including vascular invasion.This study included 100 patients with HCC, 21 patients with chronic hepatitis (CH), 24 patients with liver cirrhosis (LC), and 138 healthy control subjects. Plasma MMP-9 levels were measured with a specific one-step sandwich enzyme immunoassay.Plasma MMP-9 levels in HCC (62 [33 to 130 ng/mL] median [25%, 75%], 13 to 660 ng/mL, minimum, maximum) were significantly elevated compared with those in normal controls (36 [25 to 45], range, 2.8-70 ng/mL), in CH (28 [18 to 30], 13 to 66 ng/mL) and in LC (35 [26 to 58], 16 to 86 ng/mL) (P < .0000001; P = .0000003; and P = .00205, respectively). When the cut-off level was defined as 60 ng/mL from a receiver operating characteristic curve, plasma MMP-9 concentrations had a sensitivity of 53% and a specificity of 89% for the detection of HCC from CH and LC. The levels were significantly higher in HCC patients with macroscopic portal venous invasion (79 [36 to 160], 15-660 ng/mL) than those without the invasion (44 [27 to 80], 13 to 210 ng/mL) (P = .00726). Plasma MMP-9 levels in patients with HCC were not correlated with tumor number, size, volume, or serum alpha-fetoprotein levels.The present data suggest that plasma MMP-9 levels can be a candidate for a novel marker for HCC. The levels appear to reflect its potential and ongoing activity of vascular invasion. A long-term follow-up of the patients will be necessary to determine whether increased plasma MMP-9 levels are predictive of more invasive and metastatic HCC.
THE FORMATION OF POISONS BY MICRO-ORGANISMS. CONSIDERED IN RELATION TO THE PRODUCTION OF DISEASE.
Authors: G. V. BLACK
Journal: JAMA (1884)

[Presented in Section of Practical Medicine and Materia Medica of the American Medical Association, May, 1884.] INTRODUCTION. If we review the history of the observation and experiment that has been had, bearing on the relations of micro-organisms to the production of disease, we may formulate the following propositions: 1. Experiment and observation has shown that there are many varieties of micro-organisms that do not produce disease or injury; that the mere presence of these life forms is not sufficient to cause disease. 2. Experiment has, also, shown that there are certain varieties of micro-organisms that do uniformly induce disease when they obtain entrance into the bodies of animals, or men. 3. All through the experimentation on this subject it has been noticed that poisons have appeared in connection with the disease producing organisms. 4. These poisons seem to be a product of the micro-organisms; and while produced only in connection
856 HEPATIC PROGENITOR CELLS OVEREXPRESS SERPINB3 IN A MOUSE MODEL OF FULMINANT HEPATITIS
Authors: S. Quarta, G. Villano, C. Turato, A. Biasiolo, L. Vidalino, M. Ruvoletto, N. Tono, F. Calabrese, L. Nicolosi, P. Bernardi, A. Gatta, P. Pontisso
Journal: Journal of Hepatology (2009)
Scintigraphic Demonstration of Ectopic Thyroid Tissue in a Thyroglossal Duct Cyst in the Presence of a Normal Thyroid
Authors: Sampath Santhosh, Bhagwant Rai Mittal, Koramadai Karuppusamy Kamaleshwaran, Rahul Parghane, Anish Bhattacharya, Baljinder Singh
Journal: Clinical Nuclear Medicine (2011)

The presence of any functioning thyroid tissue in an aberrant location along the embryologic line of descent of the gland is considered as ectopic. Thyroglossal duct cyst (TGDC) may also show presence of thyroid tissue. Presence of thyroid tissue in all the reported TGDC has been demonstrated only after ablation of the orthotopic thyroid. We report a case of TGDC in which presence of the thyroid tissue was observed in the presence of a normal-functioning thyroid.
Name-Based Surveillance and Public Health Interventions for Persons with HIV Infection
Authors: Dennis H. Osmond, Andrew B. Bindman, Karen Vranizan, J. Stan Lehman, Frederick M. Hecht, Dennis Keane, Arthur Reingold
Journal: Annals of Internal Medicine (1999)

Name-based surveillance of HIV infection is the law in 31 U.S. states but remains controversial. This policy can be advocated solely to support surveillance of the epidemic, but a frequent argument is that it also provides a public health benefit by allowing follow-up of HIV-infected persons. These persons can then receive timely medical care and can be assisted with notifying sex and needle-sharing partners. Few comparative data are available to evaluate the outcomes of these interventions. In five states with name-based surveillance of HIV infection, the Multistate Evaluation of Surveillance for HIV Study Group surveyed a cross-sectional probability sample of persons with AIDS who tested positive for HIV before the date of their AIDS diagnosis. Health department follow-up of a reported HIV infection was not associated with more timely receipt of medical care after a positive HIV test result. Only 8.6% of persons who delayed medical care after their first positive HIV test result gave concern about being reported by name as a reason; no person gave it as the main reason. Persons who were tested anonymously and those who were tested confidentially did not differ in the mean number of sex and needle-sharing partners notified: Those tested anonymously reported personally notifying 3.85 sex and needle-sharing partners, and those tested confidentially reported notifying-personally and through the health department-3.80 partners. Many researchers and policymakers believe that name-based surveillance of HIV infection will have positive or negative effects on partner notification and access to health care. These results suggest that the potential for such effects has been exaggerated.
Globotriaosylceramide leads to KCa3.1 channel dysfunction: a new insight into endothelial dysfunction in Fabry disease
Authors: S. Park, J. A. Kim, K. Y. Joo, S. Choi, E.-N. Choi, J.-A. Shin, K.-H. Han, S.-C. Jung, S. H. Suh
Journal: Cardiovascular Research (2010)

Excessive endothelial globotriaosylceramide (Gb3) accumulation is associated with endothelial dysfunction and impaired endothelium-dependent relaxation in Fabry disease. In endothelial cells, K(Ca)3.1 channels contribute to endothelium-dependent relaxation. However, the effect of Gb3 on K(Ca)3.1 channels and the underlying mechanisms of Gb3-induced dysfunction are unknown. Herein, we hypothesized that Gb3 accumulation induces K(Ca)3.1 channel dysfunction and aimed to clarify the underlying mechanisms.The animal model of Fabry disease, α-galactosidase A (Gla) knockout mice, displayed age-dependent K(Ca)3.1 channel dysfunction. K(Ca)3.1 current and the channel expression were significantly reduced in mouse aortic endothelial cells (MAECs) of aged Gla knockout mice, whereas they were not changed in MAECs of wild-type and young Gla knockout mice. In addition, K(Ca)3.1 current and the channel expression were concentration-dependently reduced in Gb3-treated MAECs. In both Gb3-treated and aged Gla knockout MAECs, extracellular signal-regulated kinase (ERK) and activator protein-1 (AP-1) were down-regulated and repressor element-1 silencing transcription factor (REST) was up-regulated. Gb3 inhibited class III phosphoinositide 3-kinase and decreased intracellular levels of phosphatidylinositol 3-phosphate [PI(3)P]. In addition, endothelium-dependent relaxation was significantly attenuated in Gb3-treated mouse aortic rings.Gb3 accumulation reduces K(Ca)3.1 channel expression by down-regulating ERK and AP-1 and up-regulating REST and the channel activity by decreasing intracellular levels of PI(3)P. Gb3 thereby evokes K(Ca)3.1 channel dysfunction, and the channel dysfunction in vascular endothelial cells may contribute to vasculopathy in Fabry disease.
ENDOTHELIAL COLONY-FORMING CELLS ARE ASSOCIATED WITH INFARCT SIZE REDUCTION THROUGH REDUCTION OF MICROVASCULAR OBSTRUCTION
Authors: Nicolas F. Meneveau, Frederic Deschaseaux, Vincent Descotes-Genon, Francois Schiele, Pierre Tiberghien, Jean-Pierre Bassand, Siamak Davani
Journal: Journal of the American College of Cardiology (2010)
Memo suggests Upjohn concealed Halcion side effects
Authors: C Dyer
Journal: BMJ (1994)

An investigation by the United States Food and Drug Administration (FDA) into possible misconduct by Upjohn, makers of the sleeping pill Halcion (triazolam), “strongly suggested” that the company knowingly concealed side effects in an early clinical trial, according to an FDA memorandum. Subjects in protocol 321, a study of 28 healthy prisoners for 42 days in 1972, experienced more adverse reactions than were shown in the summary that the pharmaceutical giant submitted to the FDA in its application for approval. The true incidence of side effects emerged only in 1991, when the original data came to light during a court case in the US over Halcion.

The memo of December 1992, obtainable under the US Freedom of Information Act, shows that the FDA considered referring the case to the US Department of Justice for an investigation by a grand jury. But it decided not to go …
A comparison of the effects of inhaled furosemide and ethacrynic acid on sodium-metabisulfite-induced bronchoconstriction in subjects with asthma.
Authors: S Pye, I Pavord, P Wilding, J Bennett, A Knox, A Tattersfield
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

Inhaled furosemide prevents bronchoconstriction induced by a number of challenges in asthma. One approach to determine the mechanism underlying this protection has been to examine the effects of diuretics with different or overlapping pharmacologic effects. We have compared the effects of furosemide on sodium metabisulfite-induced bronchoconstriction with those of equivalent diuretic doses of ethacrynic acid, a loop diuretic that, unlike furosemide, does not interact directly with the membrane Na/K/Cl cotransporter protein or inhibit carbonic anhydrase. Eight subjects with mild asthma were studied on five occasions, receiving nebulized furosemide (20 and 40 mg), ethacrynic acid (25 and 50 mg), or placebo (normal saline) in random order and double-blind 10 min before a cumulative dose challenge with inhaled sodium metabisulfite. After placebo the geometric mean sodium metabisulfite PD20 was 7.9 mumol. Furosemide 20 mg and 40 mg increased the PD20 by a mean 1.1 (95% confidence interval, -0.2-2.4; p > 0.05) and 1.6 (0.4-2.9; p < 0.02) doubling doses to 17.1 and 24.7 mumol, respectively. After inhaled ethacrynic acid 25 mg and 50 mg, the geometric mean PD20 was increased by 0.9 (-0.4-2.2; p > 0.05) and 1.5 (0.2-2.8; p < 0.05) doubling doses to 14.5 and 22.4 mumol, respectively. Thus, equivalent diuretic doses of furosemide and ethacrynic acid have a similar inhibitory effect on sodium metabisulfite-induced bronchoconstriction in asthma. This suggests that interaction with the Na/K/Cl cotransporter protein, or carbonic anhydrase inhibition, is not relevant to the effects of furosemide in asthma.
Passenger Leukocytes, Cytokines, and Transfusion Reactions
Authors: Anneke Brand
Journal: New England Journal of Medicine (1994)

Febrile, nonhemolytic reactions have been a clinical problem since the beginning of transfusion therapy. In the 1960s, antileukocyte antibodies were identified as a cause of these reactions, an observation that led to the discovery of the HLA antigens. The importance of antileukocyte antibodies has been shown by the Italian transfusion program for children with thalassemia, in which the use of leukocyte-depleted red cells virtually abolished febrile, nonhemolytic reactions1. However, febrile transfusion reactions to red cells are not always due to antileukocyte antibodies. Therefore, it is still reasonable to allow two or three reactions to occur before a costly regimen . . .
A PLEA FOR A STANDARD MEDICAL CURRICULUM.
Authors: GEORGE M. KOBER
Journal: JAMA (1904)

My experience as dean during the last few years impels me to make a strong plea for the unification of curricula in medical schools. You, with other representatives of medical colleges, will recall the fact that the state medical examining and licensing boards differ widely in the minimum standard requirements for license to practice medicine, and no sooner have we adapted our curricula to the requirements of one state when we are confronted with another adjustment of studies to meet the demands of another state, and failure to do so means refusal of recognition of the school, and "the holder of our diploma is not even permitted to appear for examination. I venture to say that nearly every school had to make changes last year in order to comply with the requirements of the state of Michigan. We all admit that the problem of the medical university is to supply
Induction of antigen-specific human cytotoxic T cells by Toxoplasma gondii.
Authors: I A Khan, K A Smith, L H Kasper
Journal: Journal of Clinical Investigation (1990)

To further the understanding of the role of T cells in immunity to the parasite Toxoplasma gondii, antigen-specific T cell clones were generated using peripheral blood mononuclear cells from seropositive individuals. Whole parasites were used to stimulate a proliferative expansion of antigen-reactive cells, followed by limiting dilution cloning in the presence of irradiated, autologous PBMC and rIL-2. Three parasite antigen-specific T cell clones expressing the CD3+ phenotype were selected for further characterization. Phenotypic analysis with monoclonal antibodies revealed two clones reactive with CD8 (RTg1 and RTg3) while the other (RTg2) phenotyped as CD4+, CD8-. When tested in a proliferation assay using a panel of different T. gondii proteins, clone RTg1 reacted with a single large protein (Mr greater than 180,000) as well as smaller components (less than 12,000), clone RTg2 reacted with a protein of Mr = 28,000 and clone RTg3 reacted with a protein of 116,000 plus smaller components (less than 12,000). Only the 28,000 = Mr antigen recognized by RTg2 was reactive on Western blot with autologous donor antisera. All three clones produced IFN-gamma and IL-2 in varying amounts upon antigenic stimulation in the presence of irradiated APC. Moreover, one clone RTg1, exhibited direct parasite cytotoxicity, inhibiting extracellular T. gondii by greater than 70% when incubated at an effector/target ratio of 40:1. This clone was alpha, beta TCR heterodimer positive and exerted its cytotoxic parasiticidal activity in the apparent absence of MHC restriction. The results provide evidence for the existence of circulating antigen-specific cytotoxic T cells in normal humans who are toxoplasma antibody seropositive.
Dilemmas in distinguishing between dominant and recessive forms of dystrophic epidermolysis bullosa
Authors: R. Mallipeddi, O. Bleck, J.E. Mellerio, G.H.S. Ashton, R.A.J. Eady, J.A. Mcgrath
Journal: British Journal of Dermatology (2003)

Background Dystrophic epidermolysis bullosa (DEB) is a heterogeneous inherited blistering skin disorder. The mode of inheritance may be autosomal dominant or recessive but all forms of DEB result from mutations in the gene encoding the anchoring fibril protein, type VII collagen, COL7A1. Consequently, in spite of careful clinical and skin biopsy examination, it may be difficult to distinguish mild recessive cases from de novo dominant disease in families with clinically normal parents and no other affected siblings; this distinction has significant implications for the accuracy of genetic counselling. Objectives To assess whether COL7A1 mutation analysis might help determine mode of inheritance in mild to moderate DEB. Methods We performed COL7A1 screening using heteroduplex analysis and direct nucleotide sequencing in four individuals with mild to moderate 'sporadic' DEB and clinically unaffected parents. Results In each patient, we identified a heterozygous glycine substitution within the type VII collagen triple helix. However, in two cases these mutations had been inherited in trans with a non‐sense mutation on the other allele (i.e. autosomal recessive DEB). In the other two cases, no additional mutation was identified and neither mutation was present in parental DNA (i.e. de novo dominant disease). Conclusions This study highlights the usefulness of DNA sequencing in determining the inherited basis of some sporadic cases of DEB. However, delineation of glycine substitutions should prompt comprehensive COL7A1 gene sequencing in the affected individual, as well as clinical assessment of parents and mutation screening in parental DNA, if the true mode of inheritance is to be established correctly.
A Critique of Gastroscopy
Authors: N. C. Tanner
Journal: BMJ (1944)

CARBON TETRACHLORIDE POISONING MEDICALIJOURNAL 49 was not gregter than 0.006 g./hour (the excretion of 0.01 in Period V is probably due to the fact that the patient was given further methionine on this day) and during the.secondinvestigation was not less than 0.012 g./hour.Calculating from these figures, we can determine the percentage of methionine sulphur recovered as neutral sulphur after the two infusions.These figures are given in Table III.
Centrilobular distribution of acetaldehyde and collagen in the ethanol-fed micropig
Authors: Charles H. Halsted, Jesús Villanueva, Carol J. Chandler, Boris Ruebner, Robert J. Munn, Seppo Parkkila, Onni Niemelä
Journal: Hepatology (1993)

We established a new animal model of alcoholic liver disease in the micropig, a species that consumes ethanol voluntarily in the diet. Ten micropigs were pair-fed diets containing 40% of calories as ethanol or cornstarch with identical amounts of fat, protein and micronutrients for 12 mo. Liver histopathology in the ethanol-fed pigs included steatonecrosis in all five and interstitial and perivenous fibrosis in three. Electron microscopy showed Ito-cell transformation with perisinusoidal collagen accumulation. Acetaldehyde adducts were found by immunofluorescence in the centrilobular region and were focused in perivenous zone 3 of all ethanol-fed animals. Protein and triglyceride levels were increased, whereas vitamin A and iron levels were decreased in liver homogenates from ethanol-fed animals. Thus, in this new animal model of alcoholism, ethanol feeding produced the features of alcoholic liver disease concurrent with hepatic deficiency of selected nutrients. Histological and immunofluorescent studies provide in vivo evidence that perivenous collagen deposition is linked to ethanol metabolism and acetaldehyde production. (HEPATOLOGY 1993;18:954-960).