tbuckley/cabot-search huggingface dataset:
An Exchange of Ophthalmologists With the People's Republic of China
Authors: Pin C. Wan
Journal: JAMA (1983)

From 1978 through 1981, three teams of ophthalmologists from the United States have traveled to the People's Republic of China under the auspices of the World Eye Foundation. The purpose of these visits has been to open an avenue of exchange between American and Chinese ophthalmologists. The US ophthalmologists delivered lectures and participated in discussion groups with the Chinese ophthalmologists. They had the opportunity to participate in surgical teaching cases, including some using acupuncture anesthesia. They also had the opportunity to develop ongoing working and research relationships with many Chinese ophthalmologists. As a result of these working relationships, some of these Chinese ophthalmologists have had the opportunity to visit and study in the United States. (<i>JAMA</i>1983;249:916-920)
P3-107: Safety of gemcitabine and carboplatin plus bevacizumab for advanced stage non–small cell lung cancer (NSCLC): pooled preliminary safety data from two ongoing studies
Authors: Michael J. Kraut, Atul Kumar, Melanie San-Pedro-Salcedo, Howard Terebelo, Heather Wakelee
Journal: Journal of Thoracic Oncology (2007)
Delayed Hemolytic Transfusion Reactions
Authors: E. Stephen Kurtides
Journal: JAMA (1978)

<h3>To the Editor.—</h3> Solanki and McCurdy did a service to the profession by focusing recently on the phenomenon of delayed hemolytic transfusion reactions (239:729, 1978). They report that all their eight patients were black, had multiple alloantibodies, and survived without major untoward results. They quote only one case from the literature (204:1007, 1968) of "renal failure with delayed transfusion reactions" and consider this "unusual." In 1963 del Greco and I<sup>1</sup>reported an acute hemolytic transfusion reaction due to an anti-K antibody in a patient who was transfused ten years earlier and in whom cross matching was negative just prior to the transfusion in question. Acute renal failure developed in that patient, but he ultimately recovered after repeated hemodialysis. A 1:16 anti-K antibody titer became detectable 72 hours after the transfusion. Such reactions can be fatal<sup>2</sup>(167:1736, 1958). In 1966 we again reported a delayed hemolytic transfusion reaction due
Intracellular pathways mediating estrogen-induced cholangiocyte proliferation in the rat
Authors: Domenico Alvaro, Paolo Onori, Veronica Drudi Metalli, Gianluca Svegliati-Baroni, Franco Folli, Antonio Franchitto, Gianfranco Alpini, Maria Grazia Mancino, Adolfo Francesco Attili, Eugenio Gaudio
Journal: Hepatology (2002)

The aim of this study was to explore the intracellular signaling pathways involved in the stimulatory effects of estrogens on cholangiocyte proliferation. We investigated the tyrosine kinase-receptor pathway by evaluating the protein expression of total and phosphorylated mitogen-activated protein kinase (MAPK) isoform p44/p42 ( e.g. , extracellular signal-regulated kinase [ERK]1/2), the steroid-receptor coactivator Src and Shc (Src-homology/collagen protein). The study was performed in 3-week-old bile duct-ligated (BDL) rats, BDL rats treated with the antiestrogens, tamoxifen or Ici 182,780, and normal control rats. Proliferation was also evaluated in normal purified cholangiocytes treated with 17β estradiol in the presence or absence of tamoxifen, Ici 182,780, ERK, or Src inhibitors. After bile duct ligation, cholangiocyte proliferation was associated with a marked immunohistochemical nuclear positivity for phosphorylated (p)-ERK1/2, which was inhibited by in vivo treatment with tamoxifen or Ici 182,780. Protein expression of total and p-ERK1/2, and Shc in cholangiocytes isolated from BDL rats was markedly increased compared with controls and was inhibited by in vivo treatment with antiestrogens. In vitro , 17β estradiol-induced proliferation of isolated normal cholangiocyte was associated with increased ( P &lt; .01) protein expression of p-ERK1/2, Src, and Shc. Specific inhibitors of ER (Ici 182,780), ERK (U0125), and Src (PP2) inhibited in vitro 17β estradiol-induced cholangiocyte proliferation. In conclusion, this study showed that estrogens induced cholangiocyte proliferation by activating the Src/Shc/ERK pathway. This might suggest that pharmacologic modulation of ER, ERK, and/or Src could be proposed for the treatment of human pathology characterized by dysregulation of cholangiocyte proliferation.
EFFECT OF UNNATURAL NORADRENALINE PRECURSOR ON SYMPATHETIC CONTROL AND ORTHOSTATIC HYPOTENSION IN DOPAMINE-BETA-HYDROXYLASE DEFICIENCY
Authors: A.J.Man In't Veld, A.H. van den Meiracker, F. Boomsma, M.A.D.H. Schalekamp
Journal: The Lancet (1987)
Cure or care?
Authors: Fiona Godlee
Journal: BMJ (2005)

Dogmatism is something we try to avoid at the BMJ , whether our own or other people's. How far we succeed may be open to question. Our predecessors, however, suffered no such qualms, if an editorial published in 1880 is anything to go by. “The nurse,” it says “must be a person who pays blind obedience to [doctors'] orders.” Admirably clear cut, but as Nick Black points out in his article on the rise and demise of the hospital (p 1394), the apparent confidence of these words hides layers of antagonism and insecurity.

At the end of the 19th century, medicine …
Diagnosis of coronary artery anatomy by two-dimensional echocardiography in patients with transposition of the great arteries.
Authors: L Pasquini, S P Sanders, I A Parness, S D Colan
Journal: Circulation (1987)

With the increasing popularity of the Jatene procedure for the treatment of common or D-transposition of the great arteries (D-TGA), the preoperative definition of coronary artery anatomy in D-TGA has assumed great importance. Consequently, the reliability of two-dimensional echocardiography for determining the coronary artery anatomy was studied in 32 infants with D-TGA. Surgical observation of the coronary anatomy was used to assess the accuracy of the echocardiographic diagnosis. The coronary arteries were visualized in 29 of 32 patients (90%), predominantly with the use of parasternal and apical views. In the three remaining patients visualization of the coronary arteries was inadequate to allow determination of their anatomy. The coronary artery anatomy was correctly predicted in 25 of the 29 patients in whom the coronary arteries were visualized. The anatomic patterns included usual coronary anatomy for D-TGA (n = 16), left circumflex coronary from the right coronary artery (n = 6), single right coronary artery (n = 1), single left coronary artery (n = 1), and inverted origin of the coronary arteries (n = 1). The errors in the remaining four patients were (1) false-negative diagnosis of origin of the left circumflex coronary from the right coronary artery (n = 1); (2) false-positive diagnosis of origin of the left circumflex coronary from the right coronary artery (n = 1), and (3) diagnosis of origin of the left circumflex coronary from the right coronary artery when the correct diagnosis was single right coronary artery (n = 2).(ABSTRACT TRUNCATED AT 250 WORDS)
Does one size fit all? Hurley on shared circuits
Authors: Alvin I. Goldman
Journal: Behavioral and Brain Sciences (2008)

Abstract Hurley's high level of generality suggests that a control-theoretic framework underpins all of the phenomena in question, but this is problematic. In contrast to the action-perception domain, where the control-theoretic framework certainly applies, there is no evidence that this framework equally applies to feelings and emotions, such as pain, touch, and disgust, where mirroring and simulational mindreading are also found.
Foods rich in antioxidants may reduce risk of Alzheimer's disease
Authors: D. Josefson
Journal: BMJ (2002)

Dietary intake of antioxidants from food sources may reduce the risk of developing Alzheimer's disease, two new studies have suggested ( JAMA 2002;287:3223-9, 3230-7).

Both studies found that the benefit was present when the intake was from food sources rather than from supplements.

The studies were conducted because it has been suggested that oxidative stress has a mechanistic role in the development of Alzheimer's dementia. Several lines of evidence previously implied that oxidative damage to lipid membranes could disrupt normal neuronal and glial cell functioning, leading to the formation of amyloid plaques and to neuronal cell death.

Hence, it was hoped that dietary intake of antioxidants such …
Frozen Section for the Management of Intraoperatively Detected Palpable Tumor Lesions During Nerve-Sparing Scheduled Radical Prostatectomy
Authors: Christian Eichelberg, Andreas Erbersdobler, Alexander Haese, Thorsten Schlomm, Felix K.H. Chun, Eike Currlin, Jochen Walz, Thomas Steuber, Markus Graefen, Hartwig Huland
Journal: European Urology (2006)
Effects of Hypoxanthine–Xanthine Oxidase on Ca <sup>2+</sup> Stores and Protein Synthesis in Human Endothelial Cells
Authors: D. Dreher, L. Jornot, A. F. Junod
Journal: Circulation Research (1995)

We have investigated the effects of reactive O2 metabolites generated by the hypoxanthine-xanthine oxidase (HX-XO) system on intracellular Ca2+ and its relation with protein synthesis in human umbilical vein endothelial cells (HUVECs). Spectrofluorometry with fura 2 showed that the oxidative stress induced a rapid transient rise in cytosolic [Ca2+], followed by a sustained elevation above the baseline value. In the presence of La3+, which blocks Ca2+ influx from the extracellular medium, a transient [Ca2+] increase was still observed, but the sustained rise was suppressed. The HX-XO-related [Ca2+] changes were completely prevented by pretreatment with thapsigargin, which depletes intracellular Ca2+ stores. Hence, the effects of HX-XO on Ca2+ homeostasis were due to mobilization of Ca2+ from the intracellular stores with subsequent influx of extracellular Ca2+. HX-XO mobilized more of sequestered Ca2+ than did thrombin, a receptor agonist that depletes only a part of the intracellular Ca2+ stores (the hormone-sensitive stores). To determine the relevance of the HX-XO-related depletion of Ca2+ stores for cell function, we investigated the role of Ca2+ mobilization in the regulation of protein synthesis. Overall protein synthesis in HUVECs was markedly reduced by thapsigargin, which depletes both hormone-sensitive and -insensitive stores, but was not substantially affected by thrombin. Manipulation of the refilling of the Ca2+ stores via the availability of extracellular Ca2+ significantly influenced the thapsigargin-related and the HX-XO-related inhibition of overall protein synthesis. A corresponding effect of extracellular [Ca2+] was seen in polyribosome distribution profiles, which reflected an inhibition of translation initiation in both treatments.(ABSTRACT TRUNCATED AT 250 WORDS)
REPORT OF SEVENTY-SIX CASES OF CATARACT EXTRACTION, WITH REMARKS.
Authors: FRANK S. MILBURY
Journal: JAMA (1897)

Although the operation for cataract extraction is the most important in the field of ophthalmology, still it may not require more, and probably not as much skill and judgment as many other eye operations, but the beneficial results of restoring vision to the blind are so great and marvelous to the patient and gratifying to the physician, that the operation takes first rank in surgery and its value can not be overestimated. In this paper I wish to report the results in seventy-six consecutive cataract extractions, including complicated and uncomplicated cases, that have been done by me since November, 1891, in individuals ranging in age from 18 months to 87 years. In all cases where the party has passed the age of 25 or 30 and the opacity interferes with useful vision, whether the cataract is mature or not, it is my praclice to remove it. However, some of the
Polio Eradicated in India
Authors: M. J. Friedrich
Journal: JAMA (2014)

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
Cognitive impairment in primary biliary cirrhosis: Symptom impact and potential etiology
Authors: Julia L. Newton, Kieren G. Hollingsworth, Roy Taylor, Ahmed M. El‐Sharkawy, Zia Uda Khan, Ruth Pearce, Kathryn Sutcliffe, Oke Okonkwo, Adrian Davidson, Jennifer Burt, Andrew M. Blamire, David Jones
Journal: Hepatology (2008)

Qualitative studies suggest that patients with primary biliary cirrhosis (PBC) experience significant problems with memory and concentration. Studies of nonhepatic disease have linked hypotension and cognitive impairment. In this study, we determined the prevalence of cognitive symptoms in PBC, examined the relationship between symptoms and overt cognitive impairment and structural brain lesions, and explored the role of autonomic dysfunction. The prevalence of cognitive symptoms was determined in 198 patients with PBC. Twenty-eight representative early-stage female patients with PBC and 11 matched controls underwent formal cognitive testing at baseline and after 2 years of follow-up. Autonomic nervous system function was assessed according to heart rate variability and baroreflex sensitivity. Eleven subjects with PBC had structural brain lesions quantified via magnetic resonance imaging. Cognitive symptoms were frequent in our PBC population, with 53% of patients experiencing moderate or severe problems with concentration and/or memory, which were unrelated in their severity to biochemical and histological makers of liver disease severity, suggesting that this symptom burden is largely or entirely unrelated to hepatic encephalopathy. Perceived cognitive symptoms correlated with objectively assessed cognitive impairment (r2 = 0.2, P < 0.05). Cognitive deficits were seen in the PBC cohort compared with controls, with significant decline detected over 2 years of follow-up. Correlations were seen between cognitive performance (full-scale intelligence quotient) and systolic blood pressure (P = 0.01, r2 = 0.2) with decline in cognitive function associated with autonomic abnormalities. Structural brain lesions were found in PBC, the density of which correlated with degree of cognitive impairment (P = 0.01, r2 = 0.5) and autonomic function (P = 0.03, r2 = 0.2). Conclusion: Cognitive symptoms are prevalent in PBC independent of liver disease severity and are associated with poorer performance on objective cognitive testing. Cognitive impairment is, in turn, associated with structural brain lesions and autonomic dysfunction, which may predict risk of cognitive decline. (HEPATOLOGY 2008.)
Induction of Cytokine Expression in Leukocytes by Binding of Thrombin-Stimulated Platelets
Authors: Franz-Josef Neumann, Nikolaus Marx, Meinrad Gawaz, Korbinian Brand, Ilka Ott, Claudia Rokitta, Christian Sticherling, Christian Meinl, Andreas May, Albert Schömig
Journal: Circulation (1997)

Background Activated platelets tether and activate myeloid leukocytes. To investigate the potential relevance of this mechanism in acute myocardial infarction (AMI), we examined cytokine induction by leukocyte-platelet adhesion and the occurrence of leukocyte-platelet conjugates in patients with AMI. Methods and Results We obtained peripheral venous blood samples in 20 patients with AMI before and daily for 5 days after direct percutaneous transluminal coronary angioplasty (PTCA) and in 20 patients undergoing elective PTCA. Throughout the study period, CD41 immunofluorescence of leukocytes (flow cytometry) revealed increased leukocyte-platelet adhesion in patients with AMI compared with control patients (mean±SE of fluorescence [channels] before PTCA: 77±16 versus 35±9; P equals;.003). In vitro, thrombin-stimulated fixed platelets bound to neutrophils and monocytes. Within 2 hours, this resulted in increased mRNA for interleukin (IL)-1β, IL-8, and monocyte chemoattractant protein (MCP)-1 in unfractionated leukocytes. After 4 hours, IL-1β and IL-8 concentration of the cell-free supernatant had increased by 268±36% and 210±7%, respectively, and cellular MCP-1 content had increased by 170±8%. Addition of activated platelets to adherent monocytes had a similar effect and was associated with nuclear factor-κB activation. Inhibition of binding by anti–P-selectin antibodies reduced the effect of activated platelets on cytokine production. Conclusions In patients with AMI, leukocyte-platelet adhesion is increased. Binding of activated platelets induces IL-1β, IL-8, and MCP-1 in leukocytes. Our findings suggest that leukocyte-platelet adhesion contributes to the regulation of inflammatory responses in AMI.
Microbiological Studies on Sodium 6-(2,6 Dimethoxybenzamido) Penicillanate Monohydrate (BRL 1241) in Vitro and in Patients
Authors: G. T. Stewart
Journal: BMJ (1960)

A report in 1959 by Batchelor et al. on the isolation of 6-aminopenicillanic acid drew attention to the possibility of synthesizing new forms of penicillin by the introduction of side-chains.Derivatives prepared in this way may or may not possess antibacterial activity, but we were particularly impressed by the range and mode of action of one derivative, supplied to us in 1959 as BRL 1241 (" celbenin ").The compound-sodium 6- (2,6 dimethoxybenzamido)penicillanate monohydrate- may be represented by the following structural formula: OCH3 s /CH3
Stimulation of collagen α1(I) gene expression is associated with lipid peroxidation in hepatocellular injury: A link to tissue fibrosis?
Authors: Pierre Bedossa, Karl Houglum, Christian Trautwein, Axel Holstege, Mario Chojkier
Journal: Hepatology (1994)

We have shown that lipid peroxidation stimulates collagen alpha 1(I) gene transcription in cultured cells. Because increased lipid peroxidation and collagen production coexist in many hepatic disorders, including experimental carbon tetrachloride intoxication, we investigated whether lipid peroxidation modulates collagen gene expression in rats treated with carbon tetrachloride. In this animal model, we show colocalization of increased collagen alpha 1(I) mRNA with lipid peroxidation by means of in situ hybridization and immunohistochemical study for malondialdehyde and 4-hydroxynonenal protein adducts, respectively. However, allyl alcohol treatment, which induced a similar degree of hepatocellular injury but without aldehyde-protein adducts, did not increase collagen alpha 1(I) gene expression, suggesting that hepatocyte necrosis is not sufficient to induce the expression of collagen type I. Furthermore, in the absence of an inflammatory response, coculture experiments of hepatocytes and Ito cells treated with carbon tetrachloride indicate that hepatocytes exert a "paracrine" stimulation of both lipid peroxidation and collagen gene expression in Ito cells. These experiments suggest that hepatocyte lipid peroxidation plays a major role in the regulation of collagen alpha 1(I) gene expression by Ito cells and that it may be a link between hepatocyte injury and hepatic fibrosis.
The tumour necrosis factor-alpha inhibitor adalimumab rapidly reverses the decrease in epidermal Langerhans cell density in psoriatic plaques
Authors: K.B. Gordon, B.K. Bonish, T. Patel, C.L. Leonardi, B.J. Nickoloff
Journal: British Journal of Dermatology (2005)

The pathophysiology of psoriasis is poorly understood, and the mechanism of action of biological agents interfering with tumour necrosis factor (TNF)-alpha that improve psoriatic plaques is completely unknown.To begin to unravel the mechanism of action, cellular changes occurring in plaques following administration of adalimumab, a humanized monoclonal antibody against TNF-alpha, were investigated.Thirteen different patients underwent sequential biopsies as part of a clinical trial. Each biopsy was immunostained and evaluated to calculate the relative density of epidermal Langerhans cells (LCs) before and after treatment (days 2, 7, 28, 84). To explore the basis for reduced epidermal LC densities in plaques, a SCID-Hu animal model was utilized. Acute psoriatic lesions were created within 2 weeks by injection of superantigen-activated CD4+ T cells into engrafted symptomless skin.Compared with symptomless skin, untreated plaques had a significantly reduced density of epidermal LCs. There was a rapid increase in density of epidermal LCs in plaques following treatment with adalimumab beginning as early as day 7. The paucity of epidermal LCs in plaques was contrasted to the prominent density of LCs in other skin disorders with chronic inflammation and alterations in keratinization, including lichen planus and inflamed seborrhoeic keratosis. Rapid creation of plaques using the SCID-Hu model was accompanied by loss of epidermal LCs, indicating that diminished LC density occurs at an early stage of lesion formation.These data shed light on a new immunopathological perspective highlighting a rapid loss of epidermal LCs in acute psoriatic lesions, with sustained decreased density of LCs in chronic plaques. Furthermore, an unexpected insight into the mechanism of action was uncovered for adalimumab, in which rapid restoration of epidermal LC density was observed.
Authors' reply to Camelford letters
Authors: P. Altmann
Journal: BMJ (2000)

<h3>Summary</h3> Lipid composition is a determinant of organelle identity; however, whether the inner nuclear membrane (INM) domain of the endoplasmic reticulum (ER) harbors a unique lipid chemistry that contributes to its identity is not known. Here, we demonstrate that a unique INM lipid environment enriched in diacylglycerol protects the nucleo-cytoskeletal linker Sun2 from local degradation by the ubiquitin-proteasome system. A membrane binding amphipathic helix in the nucleoplasmic domain of Sun2 senses INM lipids and is essential to its protein stability. We show that the protein phosphatase CTDNEP1 localizes to the INM to maintain a distinct INM lipid environment necessary for Sun2 accumulation through regulation of the phosphatidic acid phosphatase lipin 1. Thus, the INM lipid environment sculpts the INM proteome via direct lipid-protein interactions that regulate protein stability, which has broad implications for mechanisms of diseases associated with the nuclear envelope.