tbuckley/cabot-search huggingface dataset:
Whole-brain circuit dissection in free-moving animals reveals cell-specific mesocorticolimbic networks
Authors: Michael Michaelides, Sarah Ann R. Anderson, Mala Ananth, Denis Smirnov, Panayotis K. Thanos, John F. Neumaier, Gene-Jack Wang, Nora D. Volkow, Yasmin L. Hurd
Journal: Journal of Clinical Investigation (2013)

The ability to map the functional connectivity of discrete cell types in the intact mammalian brain during behavior is crucial for advancing our understanding of brain function in normal and disease states. We combined designer receptor exclusively activated by designer drug (DREADD) technology and behavioral imaging with μPET and [18F]fluorodeoxyglucose (FDG) to generate whole-brain metabolic maps of cell-specific functional circuits during the awake, freely moving state. We have termed this approach DREADD-assisted metabolic mapping (DREAMM) and documented its ability in rats to map whole-brain functional anatomy. We applied this strategy to evaluating changes in the brain associated with inhibition of prodynorphin-expressing (Pdyn-expressing) and of proenkephalin-expressing (Penk-expressing) medium spiny neurons (MSNs) of the nucleus accumbens shell (NAcSh), which have been implicated in neuropsychiatric disorders. DREAMM revealed discrete behavioral manifestations and concurrent engagement of distinct corticolimbic networks associated with dysregulation of Pdyn and Penk in MSNs of the NAcSh. Furthermore, distinct neuronal networks were recruited in awake versus anesthetized conditions. These data demonstrate that DREAMM is a highly sensitive, molecular, high-resolution quantitative imaging approach.
The carrier frequency of the BRCA2 6174delT mutation among Ashkenazi Jewish individuals is approximately 1%
Authors: Carole Oddoux, Jeffery P. Struewing, C. Mark Clayton, Susan Neuhausen, Lawrence C. Brody, Michael Kaback, Bruce Haas, Larry Norton, Patrick Borgen, Suresh Jhanwar, David Goldgar, Harry Ostrer, Kenneth Offit
Journal: Nature Genetics (1996)
LEGISLATION FOR THE PREVENTION OF BLINDNESS.Read before the Chicago Medical Society, April 15, 1894.
Authors: BOERNE BETTMAN
Journal: JAMA (1894)

The object of this paper is to call the attention of the Society to the need of legislation for the prevention of blindness. The necessity for adopting such a measure can only then be advocated when sufficient data have been collected, indicating the cause and increase of blindness, and then demonstrating that legal restrictions would decrease to a large percentage this awful calamity. A thorough elucidation of these facts would tend towards elaboration. I will content myself, therefore, by bringing to your attention in a concise form, the main features only. If we consult the United States census from the year 1850 to date, we learn that the number of blind enumerated during the various decades is as follows: 1850, 9,794; 1860, 12,658; 1870, 20,320; 1880, 48,928; 1890, 50,411.  If compared with the population, which increased from 23,191,876 in 1850 to 62,622,250 in 1890, we obtain the following ratios:  Number
Sodium Restriction and Reserpine Administration in Experimental Renal Hypertension
Authors: PAUL D. REDLEAF, LOUIS TOBIAN
Journal: Circulation Research (1958)

An increase of intracellular potassium and sodium content in the wall of the aorta occurs in experimental renal hypertension. The elevated potassium tends to revert toward normal when blood pressure is again lowered with reserpine. The efficacy of rigid restriction of dietary sodium intake in decreasing blood pressure proved quite limited. The development of renal hypertension in the face of rigid sodium restriction further demonstrates that dietary sodium plays no more than an enhancing role in the pathogenesis of renal "isehemic" hypertension.
FDA Warns Claims for Pharmacy-Made “Bio-identical” Hormones Are Misleading
Authors: Bridget M. Kuehn
Journal: JAMA (2008)

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 HomeNew OnlineCurrent IssueFor Authors 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Host Responses and Persistence of Vector Genome Following Intrabronchial Administration of an E1−E3− Adenovirus Gene Transfer Vector to Normal Individuals
Authors: Ben-Gary Harvey, Neil R. Hackett, Scott Ely, Ronald G. Crystal
Journal: Molecular Therapy (2001)

Adenovirus (Ad)-mediated gene transfer to the respiratory epithelium of experimental animals and to nasal and airway epithelium of individuals with cystic fibrosis is followed by transient gene expression. Extensive studies in experimental animals are consistent with the concept that local cellular host anti-vector immune responses account for this short-term expression, and systemic and local [lung epithelial lining fluid (ELF)] anti-Ad neutralizing antibodies are generated following Ad vector administration to the respiratory epithelial surface. To determine if this paradigm holds in normal humans, a first-generation Ad vector (Ad(GV)CD.10, an E1(-)E3(-) Ad serotype 5-based vector coding for the Escherichia coli cytosine deaminase gene) was sprayed locally in escalating doses (8 x 10(8)-8 x 10(10) particle units (pu), n = 2/group) into the lung airway epithelium of six normal individuals. Serum, ELF, and endobronchial biopsies were obtained at baseline and at various time points following vector administration. In contrast to the observations in experimental animals in which lung administration of first-generation Ad vectors is followed by strong systemic and local host response, bronchial spray administration of the Ad vector to normal humans showed: (1) minimal inflammation in bronchial biopsies, bronchial brushing, and bronchoalveolar lavage fluid; (2) no blood lymphocyte proliferation in five of six individuals in response to in vitro stimulation with Ad antigens; and (3) no significant increase from baseline in blood or lung ELF anti-Ad neutralizing antibodies. Despite this minimal normal human anti-Ad host response, dose-dependent levels of vector DNA in the airway epithelium were transient. Vector DNA in the targeted airway epithelial cells peaked in a dose-dependent fashion at 0.007 to 1.1 copies/cell at day 7 and declined thereafter, reducing to <10% of peak levels by 2 weeks. These observations demonstrate both the strengths and the limits of using experimental animals to predict human responses to gene transfer vectors. While the transient nature of Ad vector persistence in the airway epithelium is predicted by most experimental animal studies, respiratory epithelial administration of first-generation Ad vectors at doses up to 10(10) pu to airway epithelium of healthy individuals elicits minimal to no detectable systemic and mucosal humoral and cellular immune responses, an observation diametrically opposed to the host responses measured in experimental animals. These findings suggest that, while adaptive anti-Ad immune responses likely play some role in the disappearance of the vector DNA following vector administration to the human lung, other mechanisms may also be involved in the response of humans to Ad gene transfer vectors.
Genetic analysis of MRL-lpr mice: relationship of the Fas apoptosis gene to disease manifestations and renal disease-modifying loci.
Authors: M L Watson, J K Rao, G S Gilkeson, P Ruiz, E M Eicher, D S Pisetsky, A Matsuzawa, J M Rochelle, M F Seldin
Journal: The Journal of Experimental Medicine (1992)

In MRL mice, the mostly recessive lpr mutation results in both the accumulation of CD4-, CD8-, CD3+ T cells in lymphoid tissue and many features of generalized autoimmune disease, including immune complex glomerulonephritis. To positionally clone the lpr mutation and analyze the effects of background genes, backcross offspring were examined from the cross: (MRL/MpJ-lpr x CAST/Ei)F1 x MRL/MpJ-lpr. The lpr gene was found to be closely linked to a mouse chromosome 19 marker defined by a variation of a Fas gene restriction fragment. Our results identified differences in RNA expression and differences in the genomic organization of the Fas gene between normal and lpr mice, and confirm the recent report that a mutation in the Fas apoptosis gene is the lpr mutation. However, our results also indicate that the Fas gene is expressed in spleen cells from normal mice, and spleen and lymph node cells from mice with a second mutation at the lpr locus (lprcg). Together these results suggest that altered Fas transcription results in the failure of lymphocytes to undergo programmed cell death and may lead to an altered immune cell repertoire. This mechanism may explain certain central and peripheral defects in tolerance that are present in autoimmune disease. The current study also demonstrates the profound effect of background genes on the degree of nephritis, lymphadenopathy, and anti-DNA antibody production. Of major note, our studies suggest the identification of chromosomal positions for genes that modify nephritis. Analysis of the backcross mice for markers covering most of the mouse genome suggests that over 50% of the variance in renal disease is attributable to quantitative trait loci on mouse chromosomes 7 and 12. Moreover, this study provides a model for dissecting the complex genetic interactions that result in manifestations of autoimmune disease.
Ureteric Stricture with Analgesic Nephropathy
Authors: G. A. MacGregor, N. F. Jones, M. A. Barraclough, A. J. Wing, W. I. Cranston
Journal: BMJ (1973)

Three patients with analgesic nephropathy are reported who, in addition to the accepted features of this syndrome, had dilatation of one or both upper urinary tracts due to ureteric or periureteric fibrosis without intraluminal obstruction. We attribute this lesion to analgesic abuse and suggest that any patient with unexplained ureteric fibrosis should be questioned about analgesic consumption. This association also suggests a possible role for analgesic abuse in the pathogenesis of retroperitoneal fibrosis.
Hypertonicity, but not hypothermia, elicits substance P release from rat C-fiber neurons in primary culture.
Authors: A Garland, J E Jordan, J Necheles, L E Alger, M M Scully, R J Miller, D W Ray, S R White, J Solway
Journal: Journal of Clinical Investigation (1995)

Isocapnic dry gas hyperventilation provokes hyperpnea-induced bronchoconstriction in guinea pigs by releasing tachykinins from airway sensory C-fiber neurons. It is unknown whether dry gas hyperpnea directly stimulates C-fibers to release tachykinins, or whether this physical stimulus initiates a mediator cascade that indirectly stimulates C-fiber tachykinin release. We tested the hypotheses that mucosal hypothermia and/or hyperosmolarity--physical consequences of airway heat and water loss imposed by dry gas hyperpnea--can directly stimulate C-fiber tachykinin release. Neurons isolated from neonatal rat dorsal root ganglia were maintained in primary culture for 1 wk. Cells were then exposed for 30 min at 37 degrees C to graded concentrations of NaCl, mannitol, sucrose, or glycerol (0-600 mOsm) added to isotonic medium, or to isotonic medium at 25 degrees C without or with 462 mOsm mannitol added. Fractional release of substance P (SP) was calculated from supernatant and intracellular SP contents following exposure. Hyperosmolar solutions containing excess NaCl, mannitol, or sucrose all increased fractional SP release equivalently, in an osmolarity-dependent fashion. In marked contrast, hypothermia had no effect on fractional SP release under isotonic or hypertonic conditions. Thus, hyperosmolarity, but not hypothermia, can directly stimulate tachykinin release from cultured rat sensory C-fibers. The lack of effect of glycerol, a solute which quickly crosses cell membranes, suggests that neuronal volume change represents the physical stimulus transduced by C-fibers during hyperosmolar exposure.
Surgical Wound Infection and Closure Technique
Authors: H. Taylor Caswell
Journal: JAMA (1963)

To the Editor:—  In the article entitled Wound Infections Following Potentially Contaminated Operations in the April 27 issue ofThe Journal( 184 : 290), Drs. Bernard and Cole report a 42% infection rate in gastrectomy, appendectomy, biliary-tract surgery, colon surgery, etc., using primary closure. When delayed primary closure was used in these particular operations, a wound-infection rate of 8% resulted.  A wound-infection rate of 42% in the particular operations reported, using a primary closure technique, is totally unacceptable and should initiate a thorough investigation of operating room methods to rule out defects in sterilizing procedures, autoclaves, etc.  In our studies at Temple University Hospital, over a 6-year period, in 3,244 operative procedures similar to those reported by the authors, the wound-infection rate for both staphylococcal and nonstaphylococcal organisms is less than 4%. If colon surgery is eliminated, the figure falls below 2%. In all of these patients primary closure with interrupted
Gangrene and Dopamine
Authors: STEVEN L. BARRIERE
Journal: Annals of Internal Medicine (1977)

Comments and Corrections1 March 1977Gangrene and DopamineSTEVEN L. BARRIERE, PHARM.D.STEVEN L. BARRIERE, PHARM.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-86-3-366_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In the recent paper by Huseby and Hudson (Ann Intern Med 85:609-611, 1976) discussing adult respiratory distress syndrome in patients with miliary tuberculosis, one of their patients (Patient 1) developed gangrene of both hands and feet, which may or may not have been attributable to the multiple underlying disorders. These included disseminated intravascular coagulation (DIC), possible Gram-negative sepsis and shock; and hypoxemia. The authors did not intend to discuss the etiology of all of these reactions, but it may be worth pointing out that the gangrenous reaction is a well-described side-effect of dopamine administration.Two instances (1, 2)...References1. ALEXANDER C: Pedal gangrene associated with the use of dopamine. N Engl J Med 293:591, 1975 CrossrefMedlineGoogle Scholar2. GREENESMITH SJ: Dopamine gangrene. N Engl J Med 294: 114, 1976 CrossrefMedlineGoogle Scholar1. BONEFRANCISPIERCE RPA: Intravascular coagulation associated with the adult respiratory distress syndrome. Am J Med 61:585-589, 1976 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByRisk Factors of Vasopressor-Induced Symmetrical Peripheral GangreneDopamine-Induced GangreneDopamine gangrene 1 March 1977Volume 86, Issue 3Page: 366-367KeywordsAcute respiratory distress syndromeDisseminated intravascular coagulationDopamineEtiologyHypoxiaMiliary tuberculosisSepsisShock Issue Published: 1 March 1977 PDF DownloadLoading ...
VEGF/SDF-1 promotes cardiac stem cell mobilization and myocardial repair in the infarcted heart
Authors: Jun-Ming Tang, Jia-Ning Wang, Lei Zhang, Fei Zheng, Jian-Ye Yang, Xia Kong, Lin-Yun Guo, Long Chen, Yong-Zhang Huang, Yu Wan, Shi-You Chen
Journal: Cardiovascular Research (2011)

The objective of this study was to investigate whether vascular endothelial growth factor (VEGF) secreted by mesenchymal stem cells (MSC) improves myocardial survival and the engraftment of implanted MSC in infarcted hearts and promotes recruitment of stem cells through paracrine release of myocardial stromal cell-derived factor-1α (SDF-1α). VEGF-expressing MSC (VEGFMSC)-conditioned medium enhanced SDF-1α expression in heart slices and H9C2 cardiomyoblast cells via VEGF and the vascular endothelial growth factor receptor (VEGFR). The VEGFMSC-conditioned medium markedly promoted cardiac stem cell (CSC) migration at least in part via the SDF-1α/CXCR4 pathway and involved binding to VEGFR-1 and VEGFR-3. In vivo, VEGFMSC-stimulated SDF-1α expression in infarcted hearts resulted in massive mobilization and homing of bone marrow stem cells and CSC. Moreover, VEGF-induced SDF-1α guided the exogenously introduced CSC in the atrioventricular groove to migrate to the infarcted area, leading to a reduction in infarct size. Functional studies showed that VEGFMSC transplantation stimulated extensive angiomyogenesis in infarcted hearts as indicated by the expression of cardiac troponin T, CD31, and von Willebrand factor and improved the left ventricular performance, whereas blockade of SDF-1α or its receptor by RNAi or antagonist significantly diminished the beneficial effects of VEGFMSC. Exogenously expressed VEGF promotes myocardial repair at least in part through SDF-1α/CXCR4-mediated recruitment of CSC.
Cranial Hyperostosis (Hyperostosis Cranii or H.C.)
Authors: Oscar Sugar
Journal: JAMA (1964)

Perou has blended his own observations with those of many predecessors to emphasize the importance of the various cranial hyperostoses. A section on classification is followed by chapters on racial and hereditary pathological conditions associated with hyperostosis. Among congenital types discussed are the tori, oxycephalia and other forms of craniosynostosis, macro- and microcephalia, and so-called hyperostosis ex vacuo, which Perou considers really to be a degenerative change. Hyperostosis may be associated with viral infections, parasites, blood dyscrasias, physical and mechanical agents, dietary factors, and known endocrine disturbances. The most profusely illustrated chapter deals with dysplastic and hyperplastic hyperostoses. The familiar "hyperostosis frontalis interna" is included in the more generalized hyperostosis calvariae interna (HCI), a dysplastic process associated with an endocrine imbalance. Fibrous dysplasia, Paget's disease, and even otosclerosis, are considered to be primary osseous dysplasias. A slow, degenerative dystrophic process involving all or part of the calvaria is termed "hyperostosis
Fetal Alcohol Clues
Authors: Mike Mitka
Journal: JAMA (2009)

A study on frog embryos by researchers from Hebrew University in Israel suggests how exposure to ethanol can result in the teratogenic effects of fetal alcohol spectrum disorder (FASD) (Kot-Leibovich H and Fainsod A. Dis Model Mech. 2009;2[5-6]:295-305).
Effect of Acetylcholine on the Pulmonary Circulation in Patients with Chronic Pulmonary Disease
Authors: BERNARD L. CHARMS, BERNARD GIVERTZ, INOUE TOSHIHIKO
Journal: Circulation (1962)

Twenty-seven patients with various forms of chronic pulmonary disease have been studied with constant infusion of acetylcholine directly into the pulmonary artery. Although many showed a slight decrease in pulmonary artery pressure, this was not great and those with the highest pressures showed the least response. Pulmonary resistances showed similar small changes, if any. Arterial oxygen saturations did not fall uniformly and in those with the lowest levels, an actual increase was observed. It is suggested that vasomotor activity is only one of several factors determining pulmonary artery pressure in patients with chronic pulmonary disease and that anatomic or extravascular factors may become primary. Vasomotor activity seems to be relatively unimportant in the regulation of ventilation/perfusion relationships in patients with far-advanced disease.
* Outcomes following acute variceal bleeding in the 2007 UK national audit
Authors: V. Jairath, R. Logan, S. Hearnshaw, B. Kahan, S. Travis, M. Murphy, K. Palmer
Journal: Gut (2011)

<h3>Introduction</h3> Most outcome data following acute variceal haemorrhage (AVH) come from centres of expertise which may not reflect ‘real-life’ outcomes. <h3>Methods</h3> To describe clinical characteristics and outcomes of patients presenting with AVH throughout the UK. The authors analysed data from the 2007 UK Comparative Audit of Upper Gastrointestinal Bleeding<sup>1</sup>. In this study prospective data were collected on consecutive patients presenting to 208 UK hospitals with all cause AUGIB between 1 May and 30 June 2007. Here the authors describe patients who presented with AVH. <h3>Results</h3> 599/6750 (8.9%) presenting with AUGIB had known cirrhosis. 88% (526/599) of these presented with variceal bleeding and 12% (73/599) with non-variceal bleeding. 86% (452/526) of those with AVH were acute admissions (median age 53 years; IQR 46–63, 68% male). Before admission 8% (43/526) were taking aspirin, 4% (19/526) warfarin and 4% (22/526) NSAIDS. Median MELD score on admission was 15 (IQR 11–20). Prior to endoscopy 57% (299/526) received an intravenous PPI, 44% (232/526) vasopressin (or analogue), 27% (144/526) antibiotics and 2% (11/526) tranexamic acid. 62% (328/526) presented outside normal working hours (OOH). For endoscopy, 30% (157/526) were performed OOH and 66% (346/526) within 24 h of presentation, with 12% (65/526) under general anaesthetic. 80% (418/526) had oesophageal varices and 11% (59/426) gastric varices as the source of bleeding, but just 64% (339/526) had a therapeutic procedure at the index endoscopy. 30% (162/526) underwent a repeat endoscopy. 5% (30/526) had a Sengstaken-Blakemore tube inserted and 4/526 (0.8%) patients underwent TIPSS. 26% (135/526) had rebleeding during admission and 15% (80/526) died. The median length of stay was 9 days (IQR 5–21 days). AUROC analysis showed that the admission MELD score usefully predicted mortality (AUROC 0.78), but poorly predicted the need for therapeutic endoscopy or rebleeding risk. The clinical Rockall score was a poor predictor of mortality, need for therapeutic intervention at endoscopy or rebleeding risk (AUROC 0.64, 0.52 and 0.61 respectively). <h3>Conclusion</h3> Mortality following AVH may have improved in recent years, but notable deficiencies in the timeliness and use of endoscopic intervention for AVH persist. The admission MELD best predicted mortality. The Rockall score was not a useful predictor of clinically important outcomes following AVH.
PREFRONTAL LOBOTOMY AND TRANSORBITAL LEUCOTOMY: A COMPARATIVE STUDY OF 175 PATIENTS
Authors: F. A. FREYHAN
Journal: American Journal of Psychiatry (1954)

1. Favorable results with transorbital leucotomy approximate those with lobotomy. 2. Death, undesirable personality changes, and postoperative convulsions were minimal with transorbital leucotomy in contrast with lobotomy. 3. Psychosurgery should be of a type which causes the least cerebral damage. 4. The high rate of psychosurgical failures, the absence of valid prognostic criteria, and the frequency of relapses preclude clear concepts on the specificity of therapeutic effectiveness as well as on the role of the frontal lobes in the psychopathology. 5. Course and pattern of the schizophrenic psychoses seem to be of great prognostic significance. 6. The therapeutic benefits can be dramatic in individual cases but are rather limited on the whole. It seems desirable to narrow the range of applicability still further in order to obtain more satisfactory results.