tbuckley/cabot-search huggingface dataset:
THE SIGNIFICANCE OF CANCER CELLS IN THE BLOOD
Authors: Warren H. Cole
Journal: JAMA (1962)

It has come to our attention that some groups studying the blood of cancer patients for cancer cells are using the presence of cancer cells in the peripheral blood as a serious prognostic sign, even to the point of calling these patients inoperable. This editorial is written to warn against premature interpretation of this type. Although we know that the vascular spread of cancer cells is the mechanism which kills most patients with cancer, we are also convinced that most of these cells circulating in the blood stream do not survive. True enough, it is obvious that ultimately many of these cells survive and form metastases which result in the death of the patient. Lymphatic spread of cancer is of much less importance in the lethal outcome. It is assumed that this question of survival or death of the cell is related to the resistance of the patient; as the
Observations on THE MECHANISM OF ABDOMINAL PAIN
Authors: C. H. Mayo
Journal: BMJ (1929)

THE subject of abdominal paini is a most interesting and extensive one, an1d one1w wihichi nmav be discussed fom mnanY points of view.T'he wtoik on the n-ervous svstem is onle of thle glories of British physiology.Of late we haave come, to hear more anid more about.the inv-olunitary nervous system, so that noow the prize-fighter is niot the only one wiho appreciates the inmportance of the solar ple-xus.In America our interest in the sy,impatlhetic nervous ssystem -as greatly stimiiulated a few years ago by the visit of ]Rovle anid Hunter of Australia.Encouraged by theirvwork
S100B Expression Modulates Left Ventricular Remodeling After Myocardial Infarction in Mice
Authors: James N. Tsoporis, Alexander Marks, Abraham Haddad, Fayez Dawood, Peter P. Liu, Thomas G. Parker
Journal: Circulation (2005)

Background— S100B, a 20-kDa, Ca 2+ -binding dimer, is a putative intrinsic negative regulator of myocardial hypertrophy expressed after myocardial infarction. S100B-overexpressing transgenic (TG) and S100B-knockout (KO) mice have been generated to assess the consequences of S100B expression and altered hypertrophy after infarction. Methods and Results— We compared 21 wild-type (WT), 20 TG, and 24 KO mice over 35 days after experimental myocardial infarction with sham-operated controls (n=56). Of those, 4 WT-infarcted mice, 7 TG-infarcted mice, and 1 KO-infarcted mouse and no sham-operated mice died during the observation period. Among survivors, echocardiography, hemodynamic studies, and postmortem examination indicated that the WT and KO groups of infarcted mice mounted a hypertrophic response that was augmented in KO mice. The S100B-overexpressing TG group did not develop hypertrophy but demonstrated increased apoptosis. The postinfarct end-diastolic pressure was lower in KO mice than in WT mice, in accordance with other structural, hemodynamic, and functional parameters, which suggests that abrogation of S100B expression augmented hypertrophy, decreased apoptosis, and was beneficial to preservation of cardiac function within this time frame. Conclusions— S100B regulates the hypertrophic response and remodeling in the early postinfarct period and represents a potential novel therapeutic target.
Regulatable Acetylcholine-Producing Fibroblasts Enhance Cognitive Performance
Authors: Donald P. Pizzo, Nicole G. Coufal, Mark J. Lortie, Fred H. Gage, Leon J. Thal
Journal: Molecular Therapy (2005)

Regulatable gene therapy systems provide a method to alter neurotransmitter levels in vivo. We developed a rodent fibroblast cell line expressing the choline acetyltransferase (ChAT) cDNA that is silenced by doxycycline (DOX) administration. The ability of the cell line to improve cognition was tested by grafting after cholinergic lesions. Ibotenic acid was injected bilaterally into the nucleus basalis of rats, which were distributed into three groups. One group received no treatment, while the second group received cortical transplants (Graft). The third group received identical grafts but was treated with DOX to turn off ChAT expression (Graft/DOX). An unlesioned group served as control. Water maze acquisition was significantly better in the Graft group compared to the Graft/DOX group, an effect also seen in the retention and spatial probe trials. However, cognitive enhancement was restricted to spatial tasks, as inhibitory avoidance or open-field activity measures were unchanged. Molecular and biochemical analyses confirmed that DOX regulated transgene transcription and ACh levels. This study demonstrates that regulatable gene therapy has therapeutic value for single-gene disorders and also provides a mechanism to deliver small molecules in a spatiotemporal pattern to delineate the role of these compounds in discrete behavioral tasks.
Inverted formin 2 mutations with variable expression in patients with sporadic and hereditary focal and segmental glomerulosclerosis
Authors: Rasheed A. Gbadegesin, Peter J. Lavin, Gentzon Hall, Bartlomiej Bartkowiak, Alison Homstad, Ruiji Jiang, Guanghong Wu, Alison Byrd, Kelvin Lynn, Norman Wolfish, Carolina Ottati, Paul Stevens, David Howell, Peter Conlon, Michelle P. Winn
Journal: Kidney International (2011)
CAN TYPHOID FEVER BE ABORTED?Third paper read before the Mahoning County, Ohio, Medical Society, March 12,1894, with the Records of the Reported Cases Continued to Date of Recovery; also of three other Members of the Family who were attacked after the Reading of this Paper.
Authors: J. E. WOODBRIDGE
Journal: JAMA (1894)

As a preface to my paper, I wish to acknowledge my indebtedness to the President of this Society, to our last ex-President, to the ex-President of the Ohio State Medical Society present, to Dr. Thomas, Dr. Barnes, Dr. Dickson and all others who have confirmed my diagnoses, watched the results of treatment, or in any way have aided me in my work; and to thank them for their very complimentary remarks in the discussion of my previous papers. Having my work characterized as the greatest discovery of the age by one member, my name associated with that of Jenner by another, and another give expression to his pride that a member of this Society had done what I have; would be exceedingly gratifying to me at any time, but especially just now when I am promulgating ideas which must arouse the indignation of every great medical professor in the world,
Ebola diagnosed in doctor in New York City
Authors: M. McCarthy
Journal: BMJ (2014)

A physician who recently returned to New York City after caring for people in west Africa with Ebola virus disease has tested positive for the virus, city health officials said 23 October.

“We were hoping that it didn’t happen, but we were also realistic,” New York’s governor, Andrew M Cuomo, said in a news conference. “This is New York. People come through New York. People come through New York’s airports, so we can’t say this is an unexpected circumstance.”

Mary Travis Bassett, the city’s health commissioner, said that the physician, 33 year old Craig Spencer, had been working in an Ebola treatment unit with the international relief group Doctors Without Borders in Guinea until 12 October. He left the country for New York two days later, 14 October, traveling by way of Europe and arriving in the United States on 17 October through John …
Endogenous nitric oxide (NO) protects against ischaemia-reperfusion injury in the rabbit
Authors: M. W. Williams, C.S. Taft, S. Ramnauth, Z.-q. Zhao, J. Vinten-Johansen
Journal: Cardiovascular Research (1995)

Objectives: Recent studies suggest that nitric oxide (NO) is deleterious in models of shock and hypoxia-reoxygenation However, the role of endogenous NO in ischaemia-reperfusion injury in vivo remains controversial. We tested the hypothesis that blockade of endogenous NO produced during myocardial ischaemia-reperfusion or during reperfusion alone in vivo increases infarct size after coronary occlusion in the rabbit, and conversely, supplementation with L-arginine would reduce infarct size. Methods: Ketamine-xylazine anaesthetised New Zealand white rabbits were subjected to left coronary artery occlusion for 30 min and reperfusion for 120 min. The rabbits were divided into five groups: (1) saline (VEH); (2) L-nitro arginine (L-NA), a NO-synthase inhibitor, was infused intravenously (15 mg/kg bolus followed by 7.5 mg/kg h−1) before coronary occlusion to block NO synthase activity during ischaemia and reperfusion (IR); (3) L-NA was administered during reperfusion only (R) at the same dose as in the IR group; (4) D-arginine (D-ARG) (25 mg/kg bolus followed by 4 mg/kg min−1), the non-metabolised enantiomer of L-arginine was infused intravenously during reperfusion only; (5) L-arginine (L-ARG) (25 mg/kg bolus followed by 4 mg/kg min−1), the physiological precursor of NO, was infused intravenously during reperfusion only. Results: L-NA infusion in the IR and R groups caused an increase in mean arterial pressure and a decrease in heart rate; however, no significant change in pressure rate product (PRP) occurred immediately after drug infusion. PRP did not change significantly during the experiment across groups except at the end of reperfusion. The area at risk was comparable in all groups, averaging 29(1)%. The infarct size (triphenyltetrazolium chloride) expressed as a percent of area at risk was 27(2)% for the untreated vehicle group. In contrast, L-NA significantly (P < 0.05) increased infarct size in the IR group, 51(2)%; this augmented infarct size persisted when NO synthase activity was blocked during reperfusion only in the R group, 50(2)%. There was no significant (P < 0.05) difference in infarct size between the IR and the R groups. D-ARG-treated group showed a comparable increase in infarct size 48(2)% versus the IR and R groups. However, supplementation of NO with L-arginine (L-ARG) showed no reduction in infarct size, 24(3)%, over vehicle group (VEH). Conclusions: We conclude that (1) blockade of NO synthase activity with L-NA increases infarct size, (2) this effect was expressed primarily during reperfusion, (3) D-arginine mimicked the infarct augmentation of L-NA, while (4) L-arginine supplementation did not reduce infarct size. These data imply that endogenous NO production exerts a tonic cardioprotective effect on myocardial infarct following coronary reperfusion.
A Developmentally Staged Curriculum for Teaching Self-Care to the Child with Insulin-dependent Diabetes Mellitus
Authors: Elaine Kohler, Linda S Hurwitz, Deborah Milan
Journal: Diabetes Care (1982)

A developmentally staged curriculum has been designed to teach children with insulin-dependent diabetes mellitus about their disorder and its care within an organized program of ongoing ambulatory medical care. A preliminary evaluation of the teaching program based on this curriculum indicates that self-care skills are mastered but that the implementation of self-monitoring aspects decreases during adolescence. A survey of a sampling of participants indicates that interest in the program also declines with adolescence. However, the majority had positive responses at all ages and all children and adolescents had positive responses to the experience of being with diabetic peers. The curriculum is presented to help organize the appropriate teaching of diabetes care to children and adolescents.
Islet Cell Surface Antibodies from Insulin-dependent Diabetics Bind Specifically to Pancreatic B Cells
Authors: M. Van De Winkel, G. Smets, W. Gepts, D. Pipeleers
Journal: Journal of Clinical Investigation (1982)

Viable rat islet cells were used to detect islet cell surface antibodies (ICSA) in the sera of diabetic and control patients. ICSA were present in almost all recent-onset insulin-dependent diabetics younger than 30 yr (15/16); their incidence in other diabetics (6/22) was also higher than in normal controls (1/18) or in patients with autoimmune thyroiditis (1/12). The varying specificity of the ICSA for the different islet cell types led to the recognition of class I sera, whose ICSA bind exclusively to B cells, class II sera, binding only to A and pancreatic polypeptide (PP) cells and class III sera, reacting with the three islet cell types but not with D cells. Most recent-onset insulin-dependent diabetics younger than 30 contained class I-ICSA, which is consistent with an autoimmune basis of their disease and with an involvement of surface antibodies in the B cell destruction. The presence of class II ICSA in three older diabetics and in one normal control raises the question whether autoimmune reactions against A and PP cells exist and are associated with a distinct entity in islet disease.
369. Development of an Amplifiable Gene Expression System in Lentivirus Vectors
Authors: Kit L. Shaw, Karen Pepper, Denise Petersen, Shundi Ge, Gay Crooks, Donald B. Kohn
Journal: Molecular Therapy (2006)

In certain applications of gene therapy, regulated (rather than constitutive) gene expression will be crucial for proper function or optimal effect of the delivered gene. Therefore, an important goal of gene therapy is to be able to deliver genes so that they express in a pattern that recapitulates the expression of an endogenous cellular gene. Additionally, regulating transgene expression will be an important component of efforts for reducing risks of adverse advents associated with gene therapy with integrating vectors.
Levosulpiride and cisapride in the treatment of dysmotility-like functional dyspepsia: a randomized, double-masked trial
Authors: Fermı́n Mearin, Luis Rodrigo, Arturo Pérez-Mota, Agustín Balboa, Isabel Jiménez, Juan José Sebastián, Caro Patón
Journal: Clinical Gastroenterology and Hepatology (2004)
Essential role of dendritic cell CD80/CD86 costimulation in the induction, but not reactivation, of TH2 effector responses in a mouse model of asthma
Authors: Leonie S van Rijt, Nanda Vos, Monique Willart, Alex KleinJan, Anthony J Coyle, Henk C Hoogsteden, Bart N Lambrecht
Journal: Journal of Allergy and Clinical Immunology (2004)
Polycystic Kidney Disease
Authors: Patricia D. Wilson
Journal: New England Journal of Medicine (2004)

Polycystic kidney diseases are inherited renal disorders due mainly to mutations in genes that regulate the development and function of cells that line renal tubules. This review outlines the clinical importance of polycystic kidney diseases and discusses the cell biology and molecular mechanisms that cause the formation of hundreds of cystic lesions in the renal parenchyma.
THE INCIDENCE AND PATHOGENESIS OF DEGENERATIVE ARTHRITIS
Authors: CHESTER S. KEEFER
Journal: JAMA (1934)

In determining the incidence of chronic degenerative arthritis, three general methods may be used: 1. The various joints may be examined post mortem. 2. Roentgen examination of the joints may be made. 3. The number of patients having symptoms referable to their joints may be determined. Of these three, the first is by far the most satisfactory. It is generally known that anatomic changes may be present with few symptoms and, unless there are evidences of irregularities at the margin of the joint surfaces or a decrease in the joint space, roentgen examinations of joints may fail to demonstrate changes. In order to gather more precise information regarding the incidence of degenerative arthritis, we have examined approximately 150 knee joints obtained from patients dying of a variety of diseases. Aside from these observations, we have compiled from the literature the results of anatomic studies of the joints as found at
4-g Monofilament Is Clinically Useful for Detecting Diabetic Peripheral Neuropathy
Authors: Yukihiro Nagai, Yu Sugiyama, Toshio Abe, Gakuji Nomura
Journal: Diabetes Care (2001)

The American Diabetes Association recommends the use of the 10-g Semmes-Weinstein monofilament for the early identification of diabetic patients at risk for foot ulceration (1). However, this 10-g monofilament can only detect advanced diabetic peripheral neuropathy (DPN). Thus, we evaluated whether other monofilaments could be useful for the detection of early DPN with high sensitivity and high specificity, and compared the results of monofilament tests with the results of microneurography.

We recruited 65 patients (aged 61.0 ± 1.3 years, diabetes duration 9.8 ± 1.0 years [range 1-35]) with type 2 diabetes to participate in this study. Of these patients, 24 were treated with oral hypoglycemic …
Abstract 320: Investigating the patterns of nuclear factor-kappa B activity in the host-tumor microenvironment during ovarian cancer progression
Authors: Andrew J. Wilson, Hye-Jeong Lee, Whitney Barham, Lianyi Chen, Halina Onishko, Dineo Khabele, Fiona Yull
Journal: Cancer Research (2012)

Abstract Most women diagnosed with ovarian cancer initially present with metastatic disease characterized by peritoneal implants and ascites. Activation of inflammatory processes mediated by nuclear factor-kappa B (NF-κB) is thought to be critical to the distinct clinical pattern of spread of ovarian tumors. However, the relative contribution of NF-κB activity in tumor cells and host inflammatory cells to ovarian cancer progression remains unknown. Therefore, our goal was to develop and characterize model systems to investigate NF-κB activity in these cell populations during ovarian tumorigenesis. To study the host NF-κB response, ID8 mouse ovarian cancer cells were injected intra-peritoneally into C57BL/6 mice carrying an NF-κB-dependent green fluorescent protein (GFP)/luciferase fusion transgene (NGL). In a reciprocal approach, ID8 cells stably expressing the NGL reporter (ID8-NGL) were injected into wild-type C57BL/6 mice to investigate NF-κB activation in the developing tumor. Non-invasive imaging of the mice was performed by bioluminescence imaging (BLI) of the NGL reporter and by positron emission tomography (PET-CT) imaging of abdominal tumor burden. Preliminary experiments confirmed these models were highly reproducible, with peritoneal-wide tumor dissemination accompanied by the onset of late-stage, irreversible ascites. Mice injected with ID8-NGL cells showed greater than 100-fold increase in NF-κB reporter activity during tumor progression. There was a modest overall decrease in abdominal NF-κB activity over time in ID8-injected NGL mice, although the possibility of “masking” effects of the ascites fluid on bioluminescence, and NF-κB activity in specific host cell populations, need to be elaborated. These models will allow us to define the patterns of NF-κB activity in the host-tumor microenvironment during ovarian cancer progression, and will provide a powerful platform for future preclinical investigation of novel therapeutic agents targeting NF-κB in ovarian cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 320. doi:1538-7445.AM2012-320
The dual mTORC1 and mTORC2 inhibitor AZD8055 has anti-tumor activity in acute myeloid leukemia
Authors: L Willems, N Chapuis, A Puissant, T T Maciel, A S Green, N Jacque, C Vignon, S Park, S Guichard, O Herault, A Fricot, O Hermine, I C Moura, P Auberger, N Ifrah, F Dreyfus, D Bonnet, C Lacombe, P Mayeux, D Bouscary, J Tamburini
Journal: Leukemia (2011)
Unusual In Vivo Distribution of 99mTc-Diphosphonate
Authors: GOPAL B. SAHA, DONALD L. HERZBERG, CHARLES M. BOYD
Journal: Clinical Nuclear Medicine (1977)

An unusual accumulation of 99mTc diphosphonate appeared within the stomach, thyroid and lungs of a patient along with minimal uptake in the bone. Many factors involving the patient's disease processes and medications might result in in vivo radiopharmaceutical changes producing the observed atypical bone scans.
211 EFFECTS OF RADIOFREQUENCY ABLATION (RFA) IN COMBINATION WITH SORAFENIB IN A 2-TUMOR RAT MODEL OF HEPATOCELLULAR CARCINOMA
Authors: C. Hora, J. Mertens, B. Saar, J. Kettenbach, M. Ledermann, A.-C. Piguet, S. Mertens, J. Schmitt, J.-F. Dufour, A. Geier
Journal: Journal of Hepatology (2011)
Patients with chronic idiopathic neutropenia of adults have increased serum concentrations of inflammatory cytokines and chemokines
Authors: Helen A. Papadaki, Stavroula Coulocheri, George D. Eliopoulos
Journal: American Journal of Hematology (2000)

Serum levels of inflammatory cytokines and chemokines were measured in 132 patients with chronic idiopathic neutropenia of adults (CINA) and 34 healthy volunteers (controls) using commercially available micro-ELISA determination kits. We found that serum interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), transforming growth factor-β1 (TGF-β1), and soluble tumor necrosis factor receptor p55 (sTNF-RI) were all significantly increased in CINA patients compared to controls. Individual cytokine values inversely correlated with the number of circulating neutrophils. Serum levels of interleukin-8 (IL-8) and RANTES, two potent chemokines for neutrophils and lymphocytes, respectively, were also significantly increased in the group of patients and they inversely correlated with the number of circulating neutrophils. Contrarily, serum levels of interleukin-4 (IL-4), interferon-γ (IFN-γ), soluble CD23 (sCD23), and soluble interleukin-2 receptor (sIL-2R) did not show any significant change in the patients studied. We assume that CINA patients have increased serum concentrations of inflammatory cytokines and chemokines mainly produced by activated macrophages, while they disclose normal levels of inflammatory molecules mainly released from activated lymphocytes. These findings provide further evidence for an underlying low-grade chronic inflammatory process in CINA patients, as we previously have suggested. If this chronic inflammation is really the cause of the disorder or it simply represents the result of neutropenia remains to be elucidated. Am. J. Hematol. 65:271–277. © 2000 Wiley-Liss, Inc.
Influence of Nutrition and Genetics on Morphology and Caries Susceptibility
Authors: Kenneth J. Paynter
Journal: JAMA (1961)

GENETIC inheritance is probably the most important determinant of dentition. Severe local or metabolic disturbances during tooth formation can upset predetermined development patterns, and cause pathological changes such as hypoplasia of enamel, or alteration in eruption pattern. Until lately, little had been done to determine whether more subtle alterations in tooth development could be produced by less traumatic alterations in the environment, and if so, whether such changes were related to dental disease. In this paper the relation of genetics to dentition, the recent attempts to vary developmental environment through nutrition, and the effect of these variations on developing teeth in terms of tooth morphology and caries susceptibility will be reviewed. The relation of this experimental work to human disease also will be discussed. <h3>Relation of Genetics to Dentition</h3> Genetic inheritance determines many of our dental characteristics, including such broad aspects as general arrangement of teeth in the arch