tbuckley/cabot-search huggingface dataset:
Up-regulation of heme-binding protein 23 (HBP23) gene expression by lipopolysaccharide is mediated via a nitric oxide-dependent signaling pathway in rat Kupffer cells
Authors: Stephan Immenschuh, Janina Stritzke, Shin-ichiro Iwahara, Giuliano Ramadori
Journal: Hepatology (1999)

Heme-binding protein 23 (HBP23) is a cytosolic protein that binds the prooxidant heme with high affinity and has been implicated in the cellular protection against reactive oxygen species (ROS). Because lipopolysaccharide (LPS) stimulates macrophages to produce large amounts of ROS the gene expression of HBP23 was analyzed during treatment with LPS in cultured rat Kupffer cells (KC). HBP23 was constitutively expressed in KC and up-regulated on the protein and messenger RNA (mRNA) level by LPS with a time response distinct from that of TNFα, but in coordination with that of heme oxygenase-1 (HO-1), which is the inducible isoform of the rate-limiting enzyme of heme degradation. A parallel up-regulation of HBP23 and HO-1 mRNA by LPS was also observed in cultured peritoneal macrophages and peripheral blood monocytes. HBP23 mRNA induction by LPS occurred on the transcriptional level as indicated by blocking with actinomycin D. The induction of HBP23 mRNA expression by LPS was preceded by that of the inducible nitric oxide synthase (iNOS) and the production of nitrite in KC. Treatment with the NOS inhibitor N G -monomethyl l -arginine prevented HBP23 mRNA induction by LPS, which was reversed by an excess of l -arginine. Both the nitric oxide (NO)-donor S-nitroso-N-acetylpenicillamine and the peroxynitrite donor SIN-1 increased HBP23 mRNA expression. HBP23 mRNA induction by LPS was down-regulated by interleukin 10 and transforming growth factor β 1 with a NO-independent mechanism. LPS-stimulated KC exhibited marked protection against the cytotoxicity mediated by H 2 O 2 . The data suggest that NO and peroxynitrite are major mediators of the LPS-dependent up-regulation of HBP23 in KC.
Nursing Homes After Nuclear War: Neglected Medical Resources-Reply
Authors: Herbert L. Abrams
Journal: JAMA (1985)

In Reply.—  Dr Sherman believes that my discussion of available beds for casualties of a massive nuclear exchange neglected an important resource—nursing homes. Using an analytic approach derived from that on which my article was based, he suggests that 280,000 additional beds might by available for the 2 million injured.  I deliberately excluded nursing homes from consideration because the great majority of them are incapable of providing acute care to the blast-, burn-, and radiation-injured patient. They are, in fact, largely a custodial resource rather than an acute medical resource.  Furthermore, Dr Sherman points out that there will be few nursing home survivors. That is surely true of the occupants of the large number of nursing homes destroyed in the exchange; the survivors will, of course, occupy the available beds in the nursing homes that remain. Dr Sherman describes one scenario in which all nursing home patients could be moved
Depletion of γδ T Cells Exacerbates Murine Adriamycin Nephropathy
Authors: Huiling Wu, Yuan Min Wang, Yiping Wang, Min Hu, Geoff Yu Zhang, John F. Knight, David C.H. Harris, Stephen I. Alexander
Journal: Journal of the American Society of Nephrology (2007)

It has been reported that the presence of γδ T cells in kidney is associated with kidney damage in human IgA nephropathy and in rat models of chronic renal injury, including Adriamycin nephropathy (AN), but the functional role of γδ T cells in this setting is unknown. This study examined the functional role of γδ T cells in tissue injury in a murine model of AN. Murine AN was induced in BALB/c mice by a single injection of Adriamycin. γδ T cells as a proportion of CD3+ T cells were significantly increased in AN kidneys (16.8 ± 3.9%) but not in lymph nodes (1.3 ± 0.8%; P < 0.001). The proportion of γδ T cells in AN kidney correlated positively with serum creatinine and glomerular sclerosis. The Vγδ T cell receptor (TCR) repertoire in kidney showed expansion of a subset of cells that expressed Vγ6/Vδ1 genes and that used canonical TCR Vγ6/Vδ1 sequences in the CDR3 region of the TCR. γδ T cells that were sorted from the kidneys expressed TGF-β but not IL-4, IL-10, or IFN-γ. γδ T cells also expressed the activating receptor NKG2D and the NKG2D adaptor molecule DAP12. RAE-1, a ligand of NKG2D, was upregulated in AN kidney. Depletion of γδ T cells using anti–TCR γδ antibod y resulted in worsening of serum creatinine, glomerulosclerosis, and interstitial inflammation. These studies indicate the involvement of the γδ T cell in innate recognition and regulation of inflammation in AN.
Tricyclic Antidepressants
Authors: Duane G. Spiker
Journal: JAMA (1976)

Twenty-four patients hospitalized for overdose of a tricyclic antidepressant were monitored clinically, and serial plasma-drug measurements were taken for up to 144 hours. Six of 24 patients had maximum antidepressant plasma levels ≥ 1,000 ng/ml, and their plasma levels at 96 hours ranged from 170 to 1,280 ng/ml. Patients ingesting substantial tricyclic overdoses may remain medically unstable for days. When high tricyclic levels persist, accurate psychiatric assessment is often impossible. (<i>JAMA</i>236:1711-1712, 1976)
An Assessment of Surgical and Anesthesia Staff at 10 Government Hospitals in Sierra Leone
Authors: Emily Vaughan, Frances Sesay, Adaora Chima, Mira Mehes, Benjamin Lee, Dzifa Dordunoo, Alice Sitch, Gilles de Wildt, Thaim B. Kamara, Bailah Leigh, Fizan Abdullah, John Sampson
Journal: JAMA Surgery (2015)

Strengthening workforce capacity to deliver essential surgical and anesthesia care has been identified as a strategy for addressing the unmet burden of morbidity and mortality in under-resourced countries. Sierra Leone is one of the poorest countries in the world and faces the challenge of stretching limited resources to provide appropriate health care for a population of 6 million.To investigate the training of surgical and anesthesia staff in Sierra Leone and to build an evidence base for future health care policy and training programs tailored to local needs.Health care professionals who conduct surgery or deliver anesthesia at 10 of the 23 government hospitals in Sierra Leone were surveyed regarding training and clinical practices. This study surveyed 36 of 70 surgical staff (51%) and 38 of 68 nurse specialists (56%) nationally.Descriptive analysis of demographic details, training levels, and reported needs for future development.Thirty-six surgeons were surveyed in study hospitals, of whom the majority had limited surgical specialization training, whereas most anesthesia was provided by 47 nurse specialists. All consultants had postgraduate qualifications, but 4 of 6 medical superintendents (67%) and all medical officers lacked postgraduate surgical qualifications or formal surgical specialist training. The number of trained anesthesia staff increased after the introduction of the Nurse Anesthesia Training Program in 2008, funded by the United Nations Fund for Population Activities, increasing the number from 2 to 47 anesthesia staff based at the study hospitals. Although 32 of 37 nurse anesthetists (86%) reported having attended training workshops, 30 of 37 (>80%) described anesthesia resources as "poor," reporting a critical need for anesthesia machines and continual oxygen supply. Of the 37, 25 specifically mentioned the need for a better-functioning anesthesia machine and 16 mentioned the need for oxygen.To address unmet surgical need in the long term, accredited local surgical specialization programs are required; training of nonphysician surgical practitioners may offer a short-term solution. To develop safe anesthesia care, governments and donors should focus on providing health care professionals with essential equipment and resources.
Dissociation of termination and prevention of inducibility of sustained ventricular tachycardia with infusion of procainamide: Evidence for distinct mechanisms
Authors: David J. Callans, Francis E. Marchlinski
Journal: Journal of the American College of Cardiology (1992)

To determine if termination of hemodynamically tolerated, sustained ventricular tachycardia during intravenous infusion of procainamide predicts the success of procainamide therapy in preventing induction of tachycardia, 15 patients with inducible, sustained ventricular tachycardia in the setting of chronic coronary artery disease were studied. Procainamide was infuse ot a rate of 50 mg/min during ventricular tachycardia until the arrhythmia terminated spontaneously or a total dose of 15 mg/kg was administered. An infusion (2 to 10 mg/min) was given after the loading dose to maintain constant serum drug concentrations after termination of the tachycardia. The infusion of procainamide was well tolerated and resulted in termination of ventricular tachycardia in 14 (93%) of 15 patients after administration of 100 to 1,080 mg (median dose 600 mg). In all patients, programmed ventricular stimulation was repeated immediately after termination of the arrhythmia until ventricular tachycardia was reinitiated or until the stimulation protocol was completed. Of the 14 patients whose ventricular tachycardia terminated during the infusion of procainamide, 1 patient had no inducible sustained tachycardia with repeated programmed stimulation. In the remaining 13 patients, programmed stimulation resulted in initiation of sustained ventricular tachycardia of the same configuration in 7 patients and of a different configuration in 6. In the former 7 patients, the serum procainamide concentration (7.7 ± 4 vs. 7.4 ± 3.3 mg/liter, p = NS) and the observed drug effects on the tachycardia cycle length (449 ± 78 vs. 450 ± 81 ms, p = NS) and QRS duration (184 ± 38 vs. 185 ± 38 ms, p = NS) were similar at the times of termination and reinitiation of ventricular tachycardia. In summary, infusion of procsinamide with use of the described dosing regimen terminated 93% of sustained, nemodynamically tolerated ventricular tachycardia episodes without causing hypotension. The ability to terminate ventricular tachycardia with an infusion of procainamide did not reliably predict subsequent success in preventing inducible ventricular tachycardia. Finally, the reinitiation of ventricular tachycardia with an identical configuration and similar cycle length and at constant serum procainamide concentrations suggests that, at least in some patients (7 of 13; 54%), the electrophysiologic mechanism of drug-induced ventricular tachycardia termination is different from that of arrhythmia prevention.
Congenital Heart Disease: Morphologic Echocardiographic Correlations
Authors: Roger B. Cole
Journal: JAMA (1984)

Drs Gussenhoven and Becker have written a clear and relatively concise text on congenital heart disease, correlating what is morphologically seen at autopsy with the appearances on single and two-dimensional echocardiography. The photographic reproductions of the autopsy material and the echocardiograms are of high quality, although in general the morphological specimens are considerably clearer than their ultrasonic counterparts. A third of the total text deals with the authors' views on proper sequential chamber analysis, and the authors should be commended for a clear explanation of a segmental approach to congenital heart disease, in which the position of the atria, ventricles, and great vessels are first viewed independently, and then in their relationships to each other, such as concordant (normal relationship) or discordant. The remaining two thirds of the book is divided equally between those congenital malformations with normal, and those malformations with abnormal, segmental architecture. This text is not meant
Apolipoprotein C-III-1 activates lysosomal sphingomyelinase in vitro.
Authors: A J Alpert, A L Beaudet
Journal: Journal of Clinical Investigation (1981)

Apolipoprotein (apo)C-III-1 from human very low density lipoprotein stimulates 14-fold the activity of lysosomal sphingomyelinase from human fibroblasts. At the sphingomyelin concentrations tested, maximal stimulation was obtained with 5 microM apoC-III-1 or apoC mixture. Apolipoproteins A-I, A-II, B, and C-I conferred little or no stimulation. Sphingomyelinase was stimulated 20-fold by lysophosphatidylcholine with an optimum concentration of 70 microM using 0.3 mM substrate. Sphingomyelinase activity was inhibited by concentrations of apoC-III-1 and lysophosphatidylcholine three- to fivefold above stimulatory levels. Triton X-100 activated sphingomyelinase 300-fold with a pH optimum of 5.0, while the pH optimum with the biological activators was 4.0. These results raise the possibility of an in vivo activity for the biological activators. The proteins that enter lysosomes as part of a lipoprotein complex may activate lysosomal enzymes that degrade the lipid components.
Nicotine Does Not Influence Arterial Lipid Deposits in Rabbits Exposed to Second-Hand Smoke
Authors: Yi-ping Sun, Bo-qing Zhu, Amanda E. Browne, Richard E. Sievers, Janine M. Bekker, Kanu Chatterjee, William W. Parmley, Stanton A. Glantz
Journal: Circulation (2001)

Second-hand smoke (SHS) accelerates atherogenesis and impairs vascular function. The role of nicotine in this process has not been defined.To examine the potential effects of nicotine on atherogenesis and vascular function, 48 rabbits receiving a 0.5% cholesterol diet were randomized to control (cholesterol diet only), SHS from nicotine-standard research cigarettes (SHS-ST), and SHS from nicotine-free research cigarettes (SHS-NF). The SHS rabbits were exposed to 48 nicotine-standard (12 animals) or nicotine-free (12 animals) cigarettes/d, 5 d/wk for 10 weeks. Air carbon monoxide and particulates and plasma carboxyhemoglobin were significantly higher in the 2 SHS groups than the control group (P<0.001). The SHS-ST group had significant increases in plasma nicotine and cotinine compared with the other groups (P<0.001). There was no difference in serum lipids. Lipid lesions were increased in both SHS groups (54+/-5% [SEM] aorta and 66+/-4% pulmonary artery, 53+/-7% and 69+/-4%, and 39+/-4% and 43+/-3% in the SHS-ST, SHS-NF, and control groups, respectively; P=0.049 aorta and P<0.001 pulmonary artery).SHS exposure increased arterial lipid lesions, but nicotine did not contribute significantly to this effect. This effect is presumably due to other combustion products in the smoke.
BASELINE ANXIETY IMPACTS IMPROVEMENT IN QUALITY OF LIFE IN ATRIAL FIBRILLATION PATIENTS UNDERGOING CATHETER ABLATION
Authors: Sanghamitra Mohanty, Prasant Mohanty, Luigi Di Biase, Chintan Trivedi, Rong Bai, Pasquale Santangeli, John Burkhardt, Rodney Horton, Joe Gallinghouse, Javier Sanchez, Jason Zagrodzky, Shane Bailey, Andrea Natale
Journal: Journal of the American College of Cardiology (2014)
Review of Arthur L. Caplan, Smart Mice, Not-So-Smart People: An Interesting and Amusing Guide to Bioethics<sup>1</sup>
Authors: Jason Behrmann
Journal: The American Journal of Bioethics (2007)

Click to increase image sizeClick to decrease image size Acknowledgment: I would like to thank Dr. Bryn Williams-Jones of the University of Montreal for helpful comments on this review.
IgM bullous disease associated with IgM gammopathy: a report of two cases and review
Authors: C. le Roux-Villet, C. Prost-Squarcioni, B. Sassolas, F. Caux, B. Flageul, N. Lievre, M. Heller, L. Dubertret, P. Musette
Journal: British Journal of Dermatology (2004)

Sir, Several skin disorders have been described in patients with IgM gammopathy.1, 2 We report two patients with benign IgM monoclonal gammopathy associated with an unusual bullous skin disease characterized by deposition of monotypic IgM at the basement membrane zone (BMZ). Patient 1. In 1999, a 64‐year‐old woman was referred to our department with a bullous eruption, which had started in 1992. There were tense blisters on the trunk, without erythema (Fig. 1A). Extreme skin fragility was present. No mucosal lesions were seen. After blister healing, a few milia developed without atrophic scars. A subepidermal blister was observed by histology. Linear deposition of IgM‐κ and C3 along the BMZ was detected by direct immunofluorescence (IF). Immunoelectron microscopy (IEM) showed a cleavage in the lamina lucida and IgM deposition on the lamina densa (Fig. 1B). No amyloid deposits were shown. Indirect IF on normal skin and immunoblot analysis on normal epidermal extracts did not allow detection of any antibodies against the BMZ. Serum immunoelectrophoresis revealed a well‐delineated IgM‐κ monoclonal band. After poor response to several treatments (dapsone, methotrexate, topical steroids and cyclophosphamide), the patient was given systemic steroids (0·5 mg kg−1 daily), with benefit.
TAENIA SAGINATA IN THE GALLBLADDER
Authors: Edward B. Benedict
Journal: JAMA (1926)

J. B., a man, aged 74, entered the Massachusetts Eye and Ear Infirmary to be operated on for cataract of the left eye. Operation was performed for cataract, Feb. 3, 1926. The present illness began during convalescence, ten days after the cataract operation, when the patient began complaining of occasional dull right upper quadrant pain. The pain continued for three days, becoming gradually more severe and radiating to the back and between the scapulae. The afternoon of the fourth day the pain was so severe that it doubled him up. He began vomiting, and continued to vomit practically all night. The next morning he was seen in consultation by a member of the surgical staff at the Massachusetts General Hospital. On physical examination there was very marked tenderness and spasm in the right upper quadrant, so that this whole area was rigit. As the diagnosis seemed clear, and the patient
Crosstalk between the Androgen Receptor and β-Catenin in Castrate-Resistant Prostate Cancer
Authors: Gang Wang, Jun Wang, Marianne D. Sadar
Journal: Cancer Research (2008)

Abstract The androgen-signaling pathway plays an important role in the development and hormonal progression of prostate cancer to the castrate-resistant stage (also called androgen-independent or hormone refractory). The Wnt pathway and β-catenin contribute to prostate biology and pathology. Here application of Affymetrix GeneChip analysis revealed the genomic similarity of the LNCaP hollow fiber model to clinical samples and identified genes with differential expression during hormonal progression. The fiber model samples clustered according to the expression profile of androgen-regulated genes to provide genomic evidence for the reactivation of the AR signaling pathway in castrate-resistant prostate cancer. Pathway-based characterization of gene expression identified activation of the Wnt pathway. Together with the increased expression of AR and β-catenin, there was increased nuclear colocalization and interaction of endogenous AR and β-catenin in castrate-resistant prostate cancer from castrated mice. Surprisingly, no interaction or colocalization of AR and β-catenin could be detected in xenografts from noncastrated mice. These studies provide the first in vivo evidence to support aberrant activation of the AR through the Wnt/β-catenin signaling pathway during progression of prostate cancer to the terminal castrate-resistant stage. [Cancer Res 2008;68(23):9918–27]
Bilateral renal carcinoma.
Authors: C P Newman, D M Essenhigh
Journal: BMJ (1982)

nephrotoxic effect of paracetamol or its metabolites has also been suggested.4Histology is compatible with either hypothesis.As in previous reports' 4 5 all patients in this series had evidence of liver damage, although in at least one (case 6) the changes were slight, and in nearly all patients the prothrombin time was near normal or at least improving when renal failure became fully established.There is clearly a poor correlation between the severity of liver damage and the development of renal failure.Thus, although liver failure remains the major cause of death from paracetamol overdose, this study emphasises that acute renal failure may occur in the absence of fulminant liver failure and is a source of considerable morbidity in these patients.'Wilkinson SP, Moodie H, Arroyo VA, Williams R. Frequency of renal impairment in paracetamol overdose compared with other causes of acute liver failure.
The Mode of Action and Use of Chlorothiazide and Related Compounds
Authors: JOHN H. LARAGH
Journal: Circulation (1962)

Chlorothiazide acts to inhibit renal tubular reabsorption of electrolytes. Experimental data are presented which indicate that, under various conditions, anion reabsorption is depressed unselectively so that the pre-existing ratio (Cl/HCO 3 ) is not changed during chlorothiazide diuresis. The data suggest that chlorothiazide acts primarily to block sodium ion reabsorption. Chlorothiazide diuresis is potentiated experimentally by KHCO 3 and clinically by acetazoleamide, organomercurials, or spirolactone. The latter two can also operate to block the potassium wastage of chlorothiazide. Increased potassium excretion caused by chlorothiazide is viewed as a consequence of the activity of the drug in blocking sodium reabsorption proximal to the site of potassium secretion. According to this concept, all chlorothiazide-type compounds will cause potassium depletion in proportion to their capacity to block proximal sodium reabsorption by diverting more sodium distally to the site of potassium secretion. Unlike mercurial agents, chlorothiazide either depresser or does not change excretion of free water during a water diuresis. These data suggest that chlorothiazide acts both in the proximal and distal portions of the nephron, while mercurial agents may act largely in the proximal tubule. The different mode of action of chlorothiazide on tubular reabsorption of electrolytes, as compared with other diuretic agents (acetazoleamide, organomercurials, spirolactone), affords evidence that a number of discrete tubular transport mechanisms participate in the regulation of electrolyte and water balance and provide a rational basis for combined use of various types of diuretic agents in treating edematous patients. The nature of the antihypertensive action of chlorothiazide has not yet been elucidated. The effect may be related to electrolyte and fluid depletion, but evidence for a more direct action on the circulation is reviewed. Other aspects of the pharmacology of chlorothiazide and its derivatives are considered, and the application of this information in treatment of states of edema or hypertension is discussed.
Cosmetic Facial Surgery
Authors: Robert Kotler
Journal: JAMA (1983)

COSMETIC surgery of the face has been performed in this country since the turn of the century, but until recently, most of it had been done surreptitiously and had frequently been considered an indulgence of only the wealthy or the vain. Cosmetic facial surgery has burgeoned in the past decade. The reasons are many, including our continuing affluence, job competition, the fitness boom, and, of course, the publicity given public figures who have openly discussed their cosmetic facial surgery. Some of the types of cosmetic facial surgery generally available are discussed in the following sections.  Cosmetic Nasal Surgery  Rhinoplasty continues to be the most frequently performed cosmetic facial surgical procedure. Today's operation is a perfection of the technique originally developed in the 1920s by Jacques Joseph, a Berlin orthopedic surgeon. Rhinoplasty surgery, now performed entirely through incisions within the nose, has undergone the maturation and sophistication capable of yielding results