tbuckley/cabot-search huggingface dataset:
Cardiogenic shock due to antihistamine overdose. Reversal with intra-aortic balloon counterpulsation
Authors: R. S. Freedberg
Journal: JAMA (1987)

MANY H<sub>1</sub>histaminergic blocking agents have central and peripheral anticholinergic activity that, in sufficient dose, may produce syndromes that mimic atropine toxicity.<sup>1</sup>Most frequently the cardiological manifestations of antihistamine toxicity derive from their quinidinelike effect on the conduction system. This property, shared by anticholinergic agents, may induce a toxic reaction of the heart in the form of conduction disturbance or dysrhythmia<sup>2</sup>but rarely produces clinically significant myocardial pump failure. In the case of a patient with severe myocardial depression secondary to antihistamine overdose, cardiogenic shock was refractory to vasopressor support, and attempted extracorporeal maintenance of the circulation with "partial cardiopulmonary bypass" proved inadequate to sustain life.<sup>3</sup>Herein we report the case of a patient whose antihistamine overdose resulted in cardiogenic shock refractory to pharmacologic intervention but in whom intra-aortic balloon counterpulsation allowed stabilization of her tenuous hemodynamic status. The patient received mechanical support with an intra-aortic balloon
SUMMARY OF BUREAU OF CHEMISTRY INVESTIGATIONS OF POISONING DUE TO RIPE OLIVES
Journal: JAMA (1920)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
A cost-effectiveness analysis of alternative approaches for long-term treatment of proximal venous thrombosis
Authors: R. D. Hull
Journal: JAMA (1984)

Recent data from randomized trials have provided a clear understanding of the effectiveness and safety of differing long-term anticoagulant therapies for proximal vein thrombosis. An issue that has not been addressed is their cost-effectiveness. We have performed a cost-effectiveness analysis to rank alternative approaches for long-term therapy. Less intense oral anticoagulant therapy using warfarin sodium is the most cost-effective approach and is preferred in the majority of patients. (<i>JAMA</i>1984;252:235-239)
Quantitative Aspects of Chemical Carcinogenesis and Tumor Promotion in Liver
Authors: H. W. Kunz, H. A. Tennekes, R. E. Port, M. Schwartz, D. Lorke, G. Schaude
Journal: Environmental Health Perspectives (1983)

Chronic exposure of rodents to high dose levels of drugs, food additives and environmental chemicals frequently results in liver enlargement. Several of these compounds have been found to enhance the incidence of liver tumors in animals briefly exposed previously to hepatocarcinogens. Accordingly, it has been advanced that these agents act as tumor promoters. This contention has remained subject of controversy following reports that these substances may also cause liver tumors in noncarcinogen-treated rodents, particularly in those characterized by a relatively high incidence of "spontaneous" liver tumors. Since many of these chemicals are in common use, a crucial question would seem to be whether such effects are due to facilitation of the expression of pre-existing oncogenic potential, i.e., to tumor promotion, or to the synergistic action of weakly carcinogenic agents. As a result of mechanistic differences tumor promotion and syn-carcinogenesis must exhibit different dose-time-response characteristics, and, accordingly, it should be possible, in principle, to discriminate between these phenomena. However, since tumor manifestation periods in low-dose groups frequently exceed the animals average lifespan, this approach may not always yield conclusive data, unless a sensitive early marker of carcinogenic activity can be employed. There is evidence that enzyme-deficient preneoplastic areas in liver can be used for this purpose. A strong quantitative correlation between carcinogen dose, the extent of ATPase deficient areas, and the subsequent appearance of tumors has now been established for a number of hepatocarcinogens. Experimental data are consistent with the concept that two critical events (hits) are required for induction of ATPase deficiency in hepatocytes. The first hit is carcinogen-dependent, whereas the second hit would seem to be due to time-dependent event(s). Tumor-promoters, such as phenobarbital, were found to accelerate and increase formation of preneoplastic islets. This evidence, together with data indicating that the compound is devoid of carcinogenic potential, suggests that phenobarbital may be operative at relatively early stages of hepatocarcinogenesis by increasing the probability of the occurrence of the time-dependent second hit. Such effects are dose-dependent and appear to be related to the induction of liver enlargement. The changes in hepatocellular ploidy status and atypical nuclear figures observed during phenobarbital treatment and cessation thereof, suggest that this compound might induce abnormal redistributions of genetic material. It is postulated that these cytological changes may result in phenotypical manifestation of recessive oncogenic information.
Current Comment
Journal: JAMA (1925)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Abstract 2941: Combination of hemiasterlin derivative <i>(R)(S)(S)</i>-BF65 and PI3K/mTOR dual inhibitor NVP-BEZ235 as a new strategy to inhibit ovarian cancer growth and metastasis
Authors: Po-Chia Su, Tzu-En Huang, Lih-Ching Hsu
Journal: Cancer Research (2019)

Abstract Metastasis is a big issue to cancer therapy and is the major cause of therapeutic failure and cancer death. Therefore, inhibiting cancer metastasis is a key challenge in cancer treatment. Ovarian cancer is the most deadly cancer among women and combination treatment strategy is usually used to fight against this disease not only to reduce the toxicity and side effects, but also to enhance the anticancer effect. (R)(S)(S)-BF65 is a hemiasterlin derivative and potent anti-tubulin agent with IC50 values in the low nanomolar range against various cancer cells. Previous studies indicated that (R)(S)(S)-BF65 in combination with an allosteric Akt inhibitor MK-2206 synergistically inhibited the growth of SKOV3 human ovarian cancer cells. Using the MTT assay, we demonstrated that (R)(S)(S)-BF65 could also enhanced the growth inhibitory effect of NVP-BEZ235, a PI3K/mTOR dual inhibitor in SKOV3 cells. The IC50 was 11.6 μM for NVP-BEZ235 and 20.6 nM for (R)(S)(S)-BF65 after 48 h-treatment. With a molar ratio of 1:1000 or 1:500, the combination of (R)(S)(S)-BF65 and NVP-BEZ235 displayed an additive to mild synergistic cytotoxic effect with CI50 values of 0.96 and 0.91, respectively. Interestingly, the combination of (R)(S)(S)-BF65 and NVP-BEZ235, at concentrations much lower than those required for growth inhibition, significantly inhibited cell migration and invasion as demonstrated by wound healing migration, transwell migration and invasion assays. The combinatorial effect was much more effective than single treatments. Epithelial-mesenchymal transition (EMT) plays an important role in cancer metastasis. It has been reported that activation of the PI3K/Akt pathway leads to phosphorylation and inactivation of GSK3β, which may in turn induce EMT. Western blot analysis of EMT markers revealed that NVP-BEZ235 downregulated mesenchymal markers β-catenin and Slug, and upregulated the epithelial marker, E-cadherin. (R)(S)(S)-BF65 also downregulated mesenchymal markers β-catenin and Snail, but had no effect on E-cadherin. The combination of both led to downregulation of more mesenchymal markers including β-catenin, Slug, Snail and ZEB1, and upregulation of E-cadherin, which may at least in part explain why the combination was more effective than single treatments to suppress cell migration and invasion. Taken together, the combination of (R)(S)(S)-BF65 and NVP-BEZ235 may be a promising strategy to inhibit ovarian cancer growth and metastasis. Citation Format: Po-Chia Su, Tzu-En Huang, Lih-Ching Hsu. Combination of hemiasterlin derivative (R)(S)(S)-BF65 and PI3K/mTOR dual inhibitor NVP-BEZ235 as a new strategy to inhibit ovarian cancer growth and metastasis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 2941.
Commentaire du travail de Shun H et al., pp. 398
Authors: Julien Branche, Laurent Heyries, Marine Camus, Emmanuel Coron, Gilles Lesur
Journal: Endoscopy (2015)

See also: Endoscopic radiofrequency ablation for early esophageal squamous cell neoplasia: report of safety and effectiveness from a large prospective trialEndoscopy 2015; 47(05): 398-408DOI: 10.1055/s-0034-1391285
Pregnancy and travel: the risks of hepatitis and scuba diving
Authors: Regina M. Curtis
Journal: JAMA (1989)

<h3>To the Editor. —</h3> The article "Pregnancy and Travel"<sup>1</sup>is a well-presented reference for physicians who practice travel medicine. Precisely because of its potential use as a general reference, comment needs to be made about the recommendations on scuba diving during pregnancy for recreational divers. Current recommendations of most hyperbaric physicians and the general consensus of the Undersea and Hyperbaric Medical Society are that women should not dive during pregnancy.<sup>2,3</sup> The experimental data from animal models are inconclusive and statistically suboptimal. Pregnancy produces dynamic changes in many body systems— cardiovascular, renal, pulmonary, hematologic, and endocrine. The interaction and subsequent effects of hyperbaria and the differential in the partial pressure of gases (molecular nitrogen, molecular oxygen, and carbon dioxide) are not known. Consequently, it is not possible to establish depth/time profiles that are safe for pregnant women. The recompression therapy of a pregnant woman who incurs decompression sickness or
Antibiotic therapy for cat-scratch disease?
Authors: C. W. Bogue
Journal: JAMA (1989)

Cat-scratch disease is usually a benign, self-limited disease that causes regional lymphadenopathy. Occasionally, it may present with systemic symptoms and have a prolonged course. To date, antibiotic therapy has not been proved to be of value. We describe three patients with cat-scratch disease who were treated successfully with gentamicin sulfate. Two patients had extensive hepatic involvement, and one patient had regional lymphadenopathy. All three patients responded within 48 hours to intravenous gentamicin. Extensive follow-up has shown no recurrence of symptoms. These cases suggest that gentamicin may be efficacious in shortening the course of cat-scratch disease. Prospective, randomized trials should be performed to confirm these results. (<i>JAMA</i>. 1989;262:813-816)
Book Review
Journal: British Journal of Dermatology (1975)

Abstract Book reviewed in this article: Atopic Dermatitis. G. Rajka (1975). Dermatology—Diagnosis and treatment of cutaneous disorders W.D.Stewart, Julius L.Danto and Stuart Maddin (1974). Haut-veranderungen by inneren Krankheiten. I.Pastinszky and I.Racz (1974).
In This Issue
Journal: Journal of Clinical Investigation (2011)

Insight into how to design safer glucocorticoidsGlucocorticoids (GCs) and their synthetic analogs are used widely to treat transplant recipients and patients with numerous other conditions, including rheumatoid arthritis, asthma, and some forms of cancer.The beneficial effects of these drugs (e.g., dexamethasone) are a result of their potent antiinflammatory and immunosuppressive properties.However, their long-term use is limited by severe side effects, including hyperglycemia, hepatic steatosis (fatty liver), and type 2 diabetes.Several lines of previously published data led Patel and colleagues to hypothesize that the metabolic effects of GC drugs require the presence of nuclear receptors known as liver x receptors (LXRs) (431-441).Using mice lacking either LXRα or LXRβ or lacking both LXRs, it was shown that LXRβ is required to mediate many of the negative side effects of GC drugs.Specifically, LXRβ was required for dexamethasone-induced hyperglycemia, hyperinsulinemia, and hepatic steatosis.Importantly, it was not required for the immunosuppressive effects of dexamethasone.The authors therefore suggest that GC drugs designed to selectively activate the GC receptor and to not elicit involvement of LXRβ should cause fewer severe metabolic side effects than those currently in clinical use.
Human DIIIA Erythrocytes: RhD protein is associated with multiple dispersed amino acid variations
Authors: Cheng‐Han Huang, Ying Chen, Marion Reid
Journal: American Journal of Hematology (1997)

As a partial D antigen of the Rh blood group system, the D category IIIa phenotype occurs mainly in Blacks, but its molecular basis has not been defined. Here we describe studies of the D category DIIIa and VS+ red blood cells (RBC) from two unrelated probands by Southern blot, cDNA PCR, and nucleotide sequencing. Rh haplotyping by Sph I restriction fragment length polymorphisms indicated that the two probands carried Dce/dCe and Dce/DcE genotypes, respectively. Sequence analysis of Rh cDNAs showed that their erythroid cells expressed both D and CE transcripts. Nevertheless, the D transcripts were found to contain four nucleotide changes scattered in three exons: nt455 A-to-C (exon 3), nt602 C-to-G (exon 4), nt 654 C-to-G (exon 5), and nt667 T-to-G (exon 5). These variations resulted in the following amino acid substitutions characteristic of RhCE polypeptides: 152 Asn-to-Thr, 201 Thr-to-Arg, 218 Ile-to-Met, and 223 Phe-to-Val. The 152Thr and 223Val residues were predicted to reside in proximity to the third and fourth extracellular loops, respectively. Together, these results establish a correlation of the four amino acid changes in the RhD protein with the expression of DIIIa as a partial D antigen on the RBC membrane. Since the varied nucleotides identified in DIIIa all pre-exist in CE, they are likely to have originated from CE by templated micro-conversion event(s). The identification of a specific nt736 C-to-G transversion in CE in the two probands suggests that 245Val may involve the expression of VS antigen. Am. J. Hematol. 55:139–145, 1997. © 1997 Wiley-Liss, Inc.
Block randomisation
Authors: P. Sedgwick
Journal: BMJ (2011)

Researchers evaluated the effectiveness of a newly developed integrated care programme to help patients with chronic low back pain return to work. The programme was a combined patient and workplace directed intervention, delivered in the outpatient setting. A randomised controlled study design was used, with usual care being the control treatment. The study period was one year.1 Trial participants were recruited from primary and secondary care if aged between 18 and 65 years and they had had low back pain for more than 12 weeks. In total 134 participants were allocated to the integrated care programme or to control treatment by block randomisation, with a block size of four. The researchers reported that the duration of time until a fully sustained return to work was significantly shorter for patients receiving integrated care than for those undergoing usual care. Which of the following statements, if any, are true?
Acid and the larynx.
Journal: BMJ (1972)

differing circumstances.Having designed the machine and watched it in motion for five years the working party now feels that it can be steered effectively into the new relationships which will arise when the N.H.S. is reorganized in 1974.At the same time Sir George Godber and his col- leagues wish to withdraw from the scene in favour of a new team.They deserve the thanks of all Health Service staff for their several efforts to find a flexible administrative struc- ture-linking medicine and management-in which the energies and ideas of hospital doctors can be harnessed to make the best use of our limited N.H.S. resources.
Lumleian Lectures on the Convulsive Diseases of Women
Authors: R. Barnes
Journal: BMJ (1873)

The It~fuene of Ovarian Nists.-Vomiting in Pregnancy; Three Groups of Cases; Comptication with Poisoned Blood.-Tetanus.-Whooping-Cough.-7heRise of Convulsive Diseases in Pregnancy puts to test the various 7heories of the Genesis of these Diseascs.-Inftuence of the Shock of Convulsion in inducing Stnrctural Change in Nervous Centres; in altering Ptriodicity or Susceptibility.MR. PRESIDENT AND GENTLEMEN,-Since our last meeting, one of the two women whom I described as suffering during pregnancy from uncontrollable spasmodic twitchings or "jumpings" of the legs, has been delivered, labour having come on prematurely.The fact is inter- esting, in illustration of the law of augmented centric nervous irritability.The immediate provoking cause of the labour seemed to be a distress- ing cough which the patient caught a week before at Hastings.The commotion caused by the cough destroyed the harnony or balance of nerve-supply and demand; and the irritation, beginning under its influ- ence, was propagated to the part of the cord which rules over the dynamics of parturition.When the nervous centres are in a state of exalted tension, irritation telling upon any part of the brain through the emotions, or of the cord through reflex action, seems liable to spread and involve the whole cord.And if one part, as in pregnancy, be especially irritable, this part will be excited to its special action.Or we might express it in another way.We may imagine the spinal cord to be a conductor along which an impression made at any point is transmitted rapidly to the rest, testing and calling into action any part which is in an especially excitable condition.Thus, as in the present case, cough excites labour; but under other conditions of special influence, as of blood-poisoning, or of proclivity from hereditary disposition, a cough might set up convulsion.This law of the propagation of excitation from one part of the spinal cord to another part in a state of peculiar susceptibility, is admirably illustrated in a remarkable clinical experiment recorded by Harvey."It seems to me," says our immortal physiologist, "on deep investigation, that the throes of childbirth, just as sneezing, proceed from the motion and agitation of the whole body.I am acquainted with a young woman who, during labour, fell into so profound a state of coma that no remedies had power to rouse her; nor was she,'in fact, able to swallow.When called to her, finding that injections and other remedies had been employed in vain, I dipped a feather in a powerful sternu- tatory, and passed it up the nostrils.Although the stupor was so pro.found that she could not sneeze, or be roused in any way, the effect was to excite convulsions throughout the body, beginning at the shoulders, and gradually descending to the lower extremities.As
Abstract 2791: RelB upregulates PD-L1 in advanced prostate cancer: An insight into tumor immunoescape
Authors: Yanyan Zhang, Shuyi Zhu, Peipei Qian, Xiumei Wang, Zhi Xu, Wenbo Sun, Yong Xu
Journal: Cancer Research (2019)

Abstract Interaction between programmed death (PD)-1 receptor and its ligand (PD-L1) is essential for suppression of activated T-lymphocytes. Thus, the high level of PD-L1 in tumors is critical for triggering the inhibitory effect on T cell responses leading to immunoescape. However, the mechanism underlying PD-L1 overexpression in cancers remains fully elucidated. Hence, we demonstrate that PD-L1 is uniquely expressed at a high level in advanced prostate cancer with high constitutive RelB, a member to drive the NF-κB alternative pathway. Clinical investigation indicated that the high levels of RelB/PD-L1 are correlated to the patient’s Gleason scores, which was confirmed by quantification of their levels in several prostate cancer cell lines vs. normal prostate epithelial cell. Knocked out RelB in androgen-independent PC-3 cells resulted in reducing PD-L1 expression. Consistently, ectopic expression of RelB in androgen-dependent 22Rv1 cells led to increasing PD-L1 level, implicating that RelB participates in PD-L1 regulation in prostate cancer. Cytokine IFN-γ is able to induce PD-L1 expression through promoting RelB nuclear translocation, revealing that RelB may directly regulate PD-L1 transcription. Accordingly, an NF-κB enhancer element was identified in the promoter region, which is responsible for RelB-mediated PD-L1 transcriptional activation. These results suggest that overexpression of PD-L1 in advanced prostate cancer is, at least in part, through RelB activation. The finding from this study provides a potential approach for enhancing immunotherapeutic efficiency by targeting RelB-activated NF-κB alternative pathway. Note: This abstract was not presented at the meeting. Citation Format: Yanyan Zhang, Shuyi Zhu, Peipei Qian, Xiumei Wang, Zhi Xu, Wenbo Sun, Yong Xu. RelB upregulates PD-L1 in advanced prostate cancer: An insight into tumor immunoescape [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 2791.