tbuckley/cabot-search huggingface dataset:
Immune guided missiles.
Authors: T J Hamblin
Journal: BMJ (1982)

Transsexualism observed "Vive la difference" might well be the mating call of the lusty, masculine male, a male, that is, who is not only biologically masculine but whose gender identity is the same.A very few biological males exist, however, whose gender identity is decidedly feminine and who regard "la difference" as an abomination.They see themselves unequivocally as women, a belief which reaches near-delusional proportions-and one which may be reinforced by narrowing the gap between fantasy and reality by the surgical removal of the offending male sexual organs and the substitution of simulated female ones.Such grossly aberrant men are true transsexuals (the condition occurs less often in women) and are to be differen- tiated from transvestites, who obtain a degree of sexual excitement from cross-dressing, or homosexuals, who know themselves to be men but obtain sexual gratification mainly or exclusively from other men.The three conditions can, however, overlap to some extent.With modern hormonal procedures coupled with advances in the technique of plastic surgery the operation demanded by male transsexuals is now available-sex reassignment surgery.From time to time the names of alleged successes hit the head- lines as, for example, those of Christine Jorgensen, Roberta Cowell, Jan Morris, and, a relatively recent addition to the list, that of the six-feet-tall top model Tula.Of particular importance is the case of April Ashley, n'e George Jamieson, not so much because George Jamieson was transformed into what Judge Ormrod had occasion subse- quently to term "a convincing feminine pastiche" but because of the autobiographical account1 of her case just published.Marred as it is by a good deal of literary candyfloss and unnecessary revelations of the goings on among the somewhat rancid social creme de la creme with whom she mixed, the book is, nevertheless, an excellent account of male trans- sexualism and one which should commend itself to anyone interested in this intriguing but sad human condition.April Ashley fulfils almost all the criteria needed to establish a diagnosis of the syndrome.The environmental setting was right.She despised her father, who was a cook in the Royal Navy and not often at home and whom she describes in no uncertain terms as a scoundrel and a boozer.She was, therefore, driven into a dependence on and preference for her mother.Her psychosexual development was right; at the age of 15 she said of herself: "I was taunted for being like a girl and, yes, I wanted to be one."This preoccupation with her gender identity grew: "I was convinced a monstrous mistake had been made and only my being a woman would correct it."After one of several suicide attempts she was admitted to a mental hospital, where heroic attempts were made to alter her determination.She was subjected to ether and thiopentone abreactions and to electric convulsion therapy and given male hormones.It all ended in dismal failure.She told her doctor, "No matter what you do you'll never be able to change my mind."
Arteriovenous Malformations of the Brain
Authors: C. G. Drake
Journal: New England Journal of Medicine (1983)

The report on proton-beam therapy in this issue1 has been awaited by neurologists, neurosurgeons, and other physicians who care for patients with an intracranial arteriovenous malformation. The results of this treatment are complex.In this study, performed by Kjellberg et al., no protection from rebleeding was conferred in the first year or so after treatment. Furthermore, the rate of total obliteration of the lesions ("wipe-out") thereafter was low (20 per cent). However, paradoxically and in contrast to incomplete surgical excision, in which any residual arteriovenous malformation remains dangerous, proton therapy may have conferred some protection from rebleeding even in the . . .
Dysphagia in Parkinsonism
Authors: Jeri A. Logemann
Journal: JAMA (1975)

Eddy D. Palmer, MD,<sup>1</sup>described dysphagia in patients with parkinsonism as restricted to cricopharyngeal achalasia and attributed all swallowing problems in this patient population to this single motility dysfunction. The number of patients studied and the extent of his examination of their neuromuscular control for deglutition was not mentioned. In the Department of Neurology, Northwestern University Medical Center, Chicago, we have examined the neuromuscular control of swallowing in more than 100 patients with Parkinson disease as well as in a population of normal age-matched subjects, by means of cinefluoroscopy and videofluoroscopy. Oral, pharyngeal, and esophageal transit times for each patient have been measured to tenths of a second. The motility patterns of lingual, pharyngeal, and esophageal musculature have been examined in detail by means of frame-by-frame analysis of the films and slow-motion analysis of videotapes. Confirming the reports of numerous other researchers,<sup>2-4</sup>we have found cinefluorography to be highly
Making (anti-) sense out of huntingtin levels in Huntington disease
Authors: Melvin M Evers, Menno H Schut, Barry A Pepers, Melek Atalar, Martine J van Belzen, Richard LM Faull, Raymund AC Roos, Willeke MC van Roon-Mom
Journal: Molecular Neurodegeneration (2015)

Huntington disease (HD) is an autosomal dominant neurodegenerative disorder, characterized by motor, psychiatric and cognitive symptoms. HD is caused by a CAG repeat expansion in the first exon of the HTT gene, resulting in an expanded polyglutamine tract at the N-terminus of the huntingtin protein. Typical disease onset is around mid-life (adult-onset HD) whereas onset below 21 years is classified as juvenile HD. While much research has been done on the underlying HD disease mechanisms, little is known about regulation and expression levels of huntingtin RNA and protein.In this study we used 15 human post-mortem HD brain samples to investigate the expression of wild-type and mutant huntingtin mRNA and protein. In adult-onset HD brain samples, there was a small but significantly lower expression of mutant huntingtin mRNA compared to wild-type huntingtin mRNA, while wild-type and mutant huntingtin protein expression levels did not differ significantly. Juvenile HD subjects did show a lower expression of mutant huntingtin protein compared to wild-type huntingtin protein. Our results in HD brain and fibroblasts suggest that protein aggregation does not affect levels of huntingtin RNA and protein. Additionally, we did not find any evidence for a reduced expression of huntingtin antisense in fibroblasts derived from a homozygous HD patient.We found small differences in allelic huntingtin mRNA levels in adult-onset HD brain, with significantly lower mutant huntingtin mRNA levels. Wild-type and mutant huntingtin protein were not significantly different in adult-onset HD brain samples. Conversely, in juvenile HD brain samples mutant huntingtin protein levels were lower compared with wild-type huntingtin, showing subtle differences between juvenile HD and adult-onset HD. Since most HD model systems harbor juvenile repeat expansions, our results suggest caution with the interpretation of huntingtin mRNA and protein studies using HD cell and animal models with such long repeats. Furthermore, our huntingtin antisense results in homozygous HD cells do not support reduced huntingtin antisense expression due to an expanded CAG repeat.
Environmental, occupational, and genetic risk factors for alpha-1 antitrypsin deficiency.
Authors: Richard R Sharp, Frederick de Serres, Lee Newman, Robert A Sandhaus, John W Walsh, Ernie Hood, G Jean Harry
Journal: Environmental Health Perspectives (2003)

Alpha-1 antitrypsin (AAT) deficiency is an inherited genetic disorder currently diagnosed in approximately 5,000 people in the United States. Although some individuals with AAT deficiency are asymptomatic, the condition often leads to deterioration of lung function in adults and is associated with emphysema, asthma, chronic obstructive pulmonary disease, and other respiratory diseases. In children, AAT deficiency can result in severe liver disease, including fatal cirrhosis in newborn infants. Although much is known about the clinical pathology of AAT deficiency, researchers are just beginning to characterize environmental, occupational, and genetic modifiers affecting the onset and progression of diseases related to AAT deficiency. On 19 August 2002, a group of basic scientists, clinicians, environmental health researchers, and public interest groups gathered at the National Institute of Environmental Health Sciences in Research Triangle Park, North Carolina, to discuss ongoing research on these topics. The goals of this workshop were to a) assess the present state of knowledge regarding environmental and occupational risk factors contributing to AAT deficiency morbidity and mortality, b) define future research needs in this area, and c) explore collaborative opportunities to advance understanding of risk factors affecting the progression of AAT deficiency-related disease. Participants agreed that new research initiatives in these areas represent an opportunity to benefit both basic science, through enhanced understanding of gene-environment interaction, and the AAT deficiency patient community, through innovative new approaches to disease management and treatment.
Comparison of effects of aprikalim and of hypoxic and ischaemic preconditioning on extracellular potassium accumulation, metabolism, and functional recovery of the globally ischaemic rat heart
Authors: A. C. Guo, J. Diacono, D. Feuvray
Journal: Cardiovascular Research (1994)

Objective: The aim was to compare the effects of a potassium channel opener, aprikalim, and of hypoxic and ischaemic preconditioning on extracellular K+ concentration change, metabolism, and ventricular function in isolated globally ischaemic rat hearts. Methods: Isovolumetric rat hearts (37°C) were treated with 1 μM (apri 1) or 30 (μM (apri 30) aprikalim. or preconditioned with either 10 min of hypoxia (N2PC) or 5 min of ischaemia followed by 5 min of perfusion (IPC5) or 10 min of ischaemia followed by 3 min of perfusion (IPC10). Control hearts received neither treatment nor preconditioning. All hearts received 30 min of sustained ischaemia followed by 25 min of reperfusion. Extracellular K+ concentration was measured with a potassium sensitive electrode inserted into the extracellular space of the left ventricular wall. Results: Recovery of left ventricular developed pressure after 25 min of reperfusion was only 19.20(SEM 5.09)% of the preischaemic level in the control group. No recovery was obtained for the apri 1 group. In contrast, a very good recovery was obtained for the apri 30 group [96.69(10.92)%]. the N2PC group [104.92(17.40)%], and the IPCI0 group [84.96(9.86)%]. The IPC5 group, however, did not have improved recovery of left ventricular pressure [14.15(5.61)%]; this is likely to be related to differences in the stimulation of anaerobic glycolysis. The protection was also markedly attenuated by pretreatment with 50 μM glibenclamide in the apri 30, N2PC, and IPC10 groups [22.76(9.00), 66.06(6.09), and 46.18(7.06)%, respectively]. Hearts treated with aprikalim before inducing ischaemia showed a concentration dependent increase in [K+]e. Hypoxic (N2PC) and ischaemic preconditioning (IPC5 and IPC10) were also associated with an increase in [K+]e over the 5-10 min period preceding the 30 min of sustained ischaemia. During sustained ischaemia all groups showed a nearly triphasic pattern of extracellular K+ changes with an early rising phase, with the exception of the N2PC group for which the early [K+]e rise was barely detectable. Conclusions: An increase in [K+]ebefore sustained ischaemia is one of the mechanisms involved in the conditions affording protection. Although important, this is not sufficient, and further protection may be accomplished bv decreased stimulation of anaerobic glycolysis during the sustained ischaemia. Cardiovascular Research 1994:28:864-871
Cost-Effectiveness Analysis of Diagnostic Strategies for Suspected Pulmonary Embolism Including Helical Computed Tomography
Authors: Arnaud Perrier, Mathieu R. Nendaz, François P. Sarasin, Nigel Howarth, Henri Bounameaux
Journal: American Journal of Respiratory and Critical Care Medicine (2002)

We performed a formal decision analysis to evaluate the cost-effectiveness of various strategies for pulmonary embolism, including helical computed tomography (CT), and determined the most cost-effective schemes for each clinical probability of pulmonary embolism. Other tests included D-dimer (DD), lower limb venous ultrasound (US), ventilation-perfusion (V/Q) scan, and angiography. Outcome measures were 3-month survival and costs per patient managed. Baseline sensitivity of CT was 70%, corresponding to the performance of single-detector CT, and that figure was raised in sensitivity analysis to account for the expected higher sensitivity of newer multidetector CT scanners. All strategies were compared with a reference strategy, namely the V/Q scan in all patients followed when nondiagnostic by an angiogram. For low clinical probability patients, the most cost-effective strategy was DD, US, and V/Q scan, patients with a nondiagnostic V/Q scan being left untreated. Replacing V/Q scan by CT was also cost-effective. For intermediate and high clinical probability patients, a fourth test must be added, either CT or angiography in patients with nondiagnostic V/Q scan, or angiography in patients with a negative helical CT. When using sensitivity figures above 85% (in the multidetector range), DD, US, and CT became the most cost-effective strategy for all clinical probability categories. Helical CT as a single test was not cost-effective. In summary, including helical CT in diagnostic strategies for pulmonary embolism is cost-effective provided that it is combined with DD and US. In contrast, helical CT as a single test is not cost-effective.
THE PRECIPITIN REACTION OF ANTIPNEUMOCOCCUS SERA
Authors: Harry Sobotka, Mae Friedlander
Journal: The Journal of Experimental Medicine (1928)

The mechanism of the precipitin reaction between antipneumococcus sera and the type-specific soluble carbohydrate is investigated. The sensitivity of the reaction is found to be generally constant when expressed by the product of the concentrations of the two reacting substances. Precipitin index (P.I.) is defined as one-millionth of the reciprocal value of this product. See PDF for Structure Zonal phenomena and their bearing on the absolute concentration and the equivalent weight of the antibody are discussed. The greater tendency towards exhibition of a post-zone in Type III is connected with the lower acid equivalent of the homologous specific carbohydrate. The influence of the addition of normal serum and the influence of slight changes in pH are studied. The addition of normal serum as well as the increase in pH promote the pro-zone, whereas decrease in pH promotes the post-zone. The sensitivity of the reaction is accordingly influenced by the pH in different ways depending on the range of concentration. The precipitin index allows the recognition and elimination of zonal irregularities. Thus it offers a method for the standardization of pneumonia antibody.
Pneumatosis cystoides intestinalis of the ascending colon
Authors: A. Casarotto, M. Franceschi, M. Rebonato, F. Contin, A. Cerofolini
Journal: Endoscopy (2010)

Pneumatosis cystoides intestinalis (PCI) is a rare condition in which multiple submucosal or subserosal air-filled cysts develop in the submucosa or in subserosa of the colon [1]. The etiological mechanisms are not clear. PCI is associated with raised intra-abdominal pressure because of ileus surgery, colonoscopy, pulmonary diseases, connective tissue disorders, ingestion of carbohydrates such as lactulose and sorbitol, use of α-glucosidase inhibitors [1], and ulcerative colitis [2]; in rare cases it is asymptomatic [3].
1007. Genetic Strategies to Improve Oncolytic Adenoviruses for Targeted and Efficient Virotherapy of Malignant Melanoma
Authors: Stephan Schierer, Daniela Kosmides, Angel A. Rivera, Andrea Hesse, Astrid Mainka, Andrea L. Volk, Gerold Schuler, David T. Curiel, Dirk M. Nettelbeck
Journal: Molecular Therapy (2005)

Virotherapy with oncolytic adenoviruses constitutes a novel and promising strategy for the treatment of cancer that has been rapidly translated into clinical trials. This strategy combines specific tumor cell killing by viral cell lysis with amplification and spread of the therapeutic agent in the tumor. Initial pre-clinical and clinical investigations have demonstrated that side effects are tolerable even after high titer systemic application, however, therapeutic potency was inadequate. Here we report on the development of a new generation of oncolytic adenoviruses by means of three different strategies of genetic modifications aiming at improved efficacy and specificity.
Hepatitis C virus core protein triggers hepatic angiogenesis by a mechanism including multiple pathways
Authors: Mohamed Hassan, Denis Selimovic, Hanan Ghozlan, Ola Abdel-kader
Journal: Hepatology (2009)

Chronic hepatitis C virus (HCV) infection is associated with the production of serum cytokines, including transforming growth factor (TGF)-beta2. Despite the occurrence of hepatic angiogenesis in liver conditions, the role of HCV proteins in this context is currently unknown. We demonstrated that the development of hepatic neoangiogenesis in patients infected with HCV is associated with the expression of TGF-beta2 and vascular endothelial growth factor (VEGF) and with activation of endothelial cells, as evidenced by CD34 expression. The analysis of liver biopsies of HCV-positive and HCV-negative patients using immunostaining showed significant elevation of TGF-beta2, VEGF, and CD34 expression in patients who were HCV-positive. Using an HCV established culture system, we confirmed further the production of both TGF-beta2 and VEGF proteins, in the hepatoma cell lines HepG2 and Huh7 by transfection with full-length HCV RNA (JFH1) or by the regulated expression of core. In addition, regulated expression of core protein in HepG2 or Huh7 cells was found to induce expression and activation of the transcription factor E2F1 and apoptosis signal-regulating kinase 1 (ASK1), activation of c-jun-N-terminal kinase (JNK) and p38, and extracellular-regulated kinase (ERK), and transcription factors activator protein 1 (AP-1), activating transcription factor 2 (ATF-2), cyclic adenosine monophosphate response element binding (CREB), E2F1, hypoxia inducing factor 1 alpha (HIF-1alpha), and specificity protein 1. Furthermore, data obtained from inhibitor experiments revealed the importance of E2F1 and ASK1 in the modulation of core-induced activation of JNK and p38 pathways and suggested an essential role for JNK, p38, and ERK pathways in the regulation of core-induced production of TGF-beta2 and VEGF proteins. Thus, our data provide insight into the molecular mechanisms whereby core protein mediates the development of hepatic angiogenesis in patients with chronic HCV infection.
CERTAIN ASPECTS OF MOUSE PROTECTION TESTS FOR ANTIBODY IN PNEUMOCOCCUS PNEUMONIA
Authors: Frederick T. Lord, Elbert L. Persons
Journal: The Journal of Experimental Medicine (1931)

1. Though in general in pneumococcus pneumonia the appearance of protective substance coincides rather sharply with the fall in the temperature, antibody may appear spontaneously in the blood serum as early as the 3rd or 4th day and crisis and recovery may be delayed until the 6th to the 10th day. 2. Recovery at times occurs without demonstrable protective substance in the blood in patients who later develop protection. 3. The amount of antibody developed in the course of pneumococcus pneumonia is small and in the majority of cases tested was insufficient to protect against more than 100 lethal doses of homologous pneurnococci and never against more than 10,000 lethal doses. 4. Treatment with Felton's antibody late in the course of the disease materially increases the amount of protective substances in the blood. A high degree of protection may be established by treatment in fatal cases. After the 3rd day doses of more than 200,000 Felton units are usually necessary to produce a greater degree of protection than might otherwise be expected. 5. The formation of protective substances by the patient himself is not an assurance against progress of the infection to a fatal termination. 6. Protective substance in the blood and pneumococcic septicemia may occur simultaneously.
Care of the Trauma Patient
Authors: Robert M. Kradjian
Journal: JAMA (1966)

World-wide attention focused on Parkland Memorial Hospital in Dallas when fatally injured John F. Kennedy was taken there Nov 22, 1963. Now, from this center comes a valuable book on care of the injured patient. With 120,000 emergency patients and 2,500 operative procedures for treatment of trauma each year, Parkland Hospital may well be, as stated on the jacket, "the busiest trauma center in the world." Of the book's three major divisions, the first is devoted to general principles. The reader will find discussions of shock, wound management, infections, the metabolic response to trauma, anesthesia for injured patients, and intravenous therapy. In a second section, specific types of injuries are considered. Appropriate specialists discuss trauma to the abdomen, chest, nervous system, hand, eye, and other sites. A third division deals with complications that follow trauma or surgery for trauma. Topics include fluid management, pulmonary disorders, renal failure, embolism, stress ulcers,
Dr Alexis Carrel and Tissue Culture
Authors: Leonard Hayflick
Journal: JAMA (1984)

<h3>To the Editor.—</h3> In his LANDMARK PERSPECTIVE entitled "Dr Alexis Carrel and Tissue Culture," Dr Hassan Najafi perpetuates the myth of Carrel's chick heart cell strain that allegedly "lived and multiplied for more than 34 years and retained original characteristics throughout the entire period of cultivation." The scientific method demands confirmation of experimental results before acceptance. Despite attempts made in many laboratories, no one has ever succeeded in serially propagating chick fibroblasts beyond one year.<sup>1</sup>Perpetuation of the myth of Carrel's alleged immortal culture does a disservice to cell biologists and gerontologists who for 50 years have repeatedly failed to confirm Carrel's claim. Dr Najafi implies that this failure is due to the almost universal use of enzymes and chelating agents. The effect of these materials or any other chemical or mechanical influence on the finitude of normal cell proliferation was ruled out rigorously by us more than 20
Treatment of Injuries to the Knee Joint
Authors: Clay R. Murray
Journal: New England Journal of Medicine (1947)

INJURIES to the knee joint may be discussed under the following three headings: diagnosis, treatment of surrounding structures and treatment of the joint itself. The third consideration, which is the most important, is the aspect of treatment that is usually neglected.The basis of all treatment of the knee joint is an appreciation of the physiology of the knee and of how it is disturbed by injury to the joint. There is a mistaken idea that various ligaments stabilize the knee joint. The only two positions in which the ligaments stabilize the joints in living human beings are complete extension . . .
Spontaneous seroconversion from HBeAg to anti-HBe is preceded and heralded by a progressive. Increase of 2′,5′-oligoadenylate (2′,5′-OAS) activity
Authors: G. Saracco, S. Macagno, G. Actis, F. Rosina, M. Martorelli, G. Verme, M. Rizzetto
Journal: Journal of Hepatology (1989)