tbuckley/cabot-search huggingface dataset:
The Study of Trauma-Reply
Authors: Francis D. Moore
Journal: JAMA (1979)

<h3>In Reply.—</h3> Emergency care physicians, anesthesiologists, physiologists, physical therapists, and even psychiatrists can all be helpful in improving the care of the severely injured. Despite all that assistance, the final "buck stops here"—with the surgeon. The more groups that can be involved in regional appraisals, the better.
The American Social Security Program
Authors: Robert M. Ball
Journal: New England Journal of Medicine (1964)

IN a modern industrial society almost everyone is dependent upon income from work for his support, and large numbers are threatened with destitution if this income is cut off. For this reason countries throughout the world have adopted measures designed to provide security for working people and their families against income loss owing to an interruption in, or termination of, productive work. The United States uses two distinct, but complementary, methods of assuring a continuing income to people who have had their normal source of support cut off — social insurance and public assistance.Social insurance is intended to provide . . .
Treatment of Hereditary Angioedema
Authors: Chandra M. Kumar
Journal: JAMA (1979)

<h3>To the Editor.—</h3> In his letter "Hereditary Angioedema" (240:2155, 1978), Dr Reimann does not mention the use of androgenic steroids for prophylaxis of attacks. Methyltestosterone was first effectively used by Spaulding<sup>1</sup>in 1960. This was followed by reports of effectiveness of less virilizing analogues, fluoxymesterone, oxymetholone,<sup>2</sup>and danazol.<sup>3</sup>The latter is a synthetic androgen derivative with mild masculanizing effects<sup>4</sup>and is currently the drug of choice for prophylactic management of hereditary angioedema.<sup>5</sup>It is not only highly effective in preventing attacks but has been shown to raise Cl esterase inhibitor function, as well as its levels and that of C4, often to within normal range.
899 RECOMBINANT MAMMALIAN CELL DERIVED HCV VIRUS LIKE PARTICLES TO INDUCE NEUTRALISING ANTIBODY RESPONSES TO HCV
Authors: D. Johnson, R. Chin, L. Earnest-Silveira, H. Zentgraf, C.-T. Bock, B. Chua, D. Jackson, J. Torresi
Journal: Journal of Hepatology (2009)
Remarks of the President
Authors: Donovan F. Ward
Journal: JAMA (1965)

In my last hour of stewardship of the office of President of the American Medical Association, it becomes necessary for me to describe to you, the elected representatives of American medicine, our present status in our legislative struggle. Perhaps a brief review of the highlights will suffice.  You will recall that the first national attempt to socialize health care occurred in 1937-1938 shortly after the social security system was established. Mr. Roosevelt resisted because of his conviction that the idea was too radical to warrant his support.  Then, Mr. Truman in 1949 proposed such legislation, but his proposal never reached a vote in either the House or the Senate. No popular support could be engendered. In 1950, there was a sweep of both House and Senate by conservative candidates, which reflected, in part, the anti-medicare sentiment of the time.  Then Congressman Aime Forand in 1957 introduced the first medicare bill
The Interrenicular Septum A Normal Anatomical Variant Seen on DMSA SPECT
Authors: MONICA A. ROSSLEIGH
Journal: Clinical Nuclear Medicine (1994)

SPECT imaging has been shown to identify additional defects when applied to Tc-99m DMSA scintigraphy. However, the nature of these defects is uncertain. They may be because of small scars or anatomical variants. The interrenicular septum (IRS) is a normal finding that may mimic a scar on ultrasound examination or tomography. In this study, it was found that the IRS may be identified on Tc-99m DMSA SPECT and that it was present in 32% of patients. Its characteristic appearance is a linear area of absent tracer uptake extending from the renal hilum into the parenchyma, usually anterosuperiorly. The preservation of renal cortical uptake differentiates it from a scar, which results in a defect in the rim of cortical Tc-99m DMSA accumulation.
The effects of organic nitrates on prostacyclin biosynthesis and platelet function in humans.
Authors: D J Fitzgerald, L Roy, R M Robertson, G A FitzGerald
Journal: Circulation (1984)

The results of prior studies indicate that nitroglycerin stimulates prostacyclin release by cultured endothelium and by the coronary vasculature in vivo. However, the accuracy of these findings in coronary vasculature relies on plasma samples obtained from the circulation via cardiac catheters, a procedure we have shown to stimulate prostacyclin release, thereby confounding interpretation of drug action. We studied the effects of short-acting (nitroglycerin) and long-acting (isosorbide dinitrate) nitrates on a noninvasive index of prostacyclin synthesis, excretion of urinary 2,3-dinor-6-keto-PGF1 alpha. Nitroglycerin was infused into six subjects to either a maximum of 480 micrograms/min or until mean arterial pressure fell by 20 mm Hg. Urine was collected for negative ion chemical ionization gas chromatographic, mass spectrometric analysis before and during the nitroglycerin infusion and for two 2 hr periods after nitroglycerin. The peak nitroglycerin infusion rate was 387 +/- 67 micrograms/min, which caused a fall in supine blood pressure (systolic/diastolic) of 11 +/- 5/14 +/- 4 mm Hg and a 12 +/- 3 beats/min increase in heart rate. Excretion of 2,3-dinor-6-keto-PGF1 alpha (pg/mg creatinine) was unchanged from control infusion values (106 +/- 19.5) either during (123 +/- 21) or after (134 +/- 14.6; 139 +/- 36) nitroglycerin infusion. Platelet aggregation to arachidonic acid (0.33 to 1.33 microM) and epinephrine (1 to 10 microM) ex vivo was inhibited in only one subject in whom excretion of 2,3-dinor-6-keto-PGF1 alpha was unaltered. Serum thromboxane B2 was not changed by nitroglycerin infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
MOLLUSCUM CONTAGIOSUM AND M. &amp; B. 693.
Authors: JAMES SOMMERVILLE
Journal: British Journal of Dermatology (1941)

Journal Article MOLLUSCUM CONTAGIOSUM AND M. & B. 693. Get access JAMES SOMMERVILLE, M.B., Ch.B.Glasgow. JAMES SOMMERVILLE, M.B., Ch.B.Glasgow. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology and Syphilis, Volume 53, Issue 8-9, 1 August 1941, Pages 255–257, https://doi.org/10.1111/j.1365-2133.1941.tb10925.x Published: 01 August 1941
STIM1 strengthens clotting
Authors: Hema Bashyam
Journal: The Journal of Experimental Medicine (2008)

On page 1583, Varga-Szabo et al. show that platelets missing a calcium channel opener build puny, feeble clots that may actually save lives.






Figure 1

Vessel-blocking clots (top) are avoided when platelets lack STIM1 (bottom).




Platelets require calcium to initiate clotting in response to extracellular cues. When calcium is needed, most cells first deplete their ER stores. This depletion is sensed by an ER protein called STIM1, which sits near enough to the plasma membrane to open up calcium channels on the cell surface. But since platelets have only stunted ER-like tubules, they were thought to rely instead on an activation-induced lipid, which opens surface calcium channels independently of internal stores.

Platelets also have plenty of STIM1, however, which Varga-Szabo et al. now show is needed for slow-but-steady clot formation. Activated STIM1-deficient platelets, the authors found, did not accumulate calcium from external sources.

Internal calcium stores in the mutant platelets were sufficient for rapid clot formation in response to short-lived ligands such as thrombin. But platelets needed STIM1-induced calcium influx to clot in response to collagen on injured vessels, which triggers a slower signaling pathway. In the absence of STIM1, clots were small and disintegrated easily, particularly under conditions that mimicked blood flow. The defective platelets continually broke away from the clots, suggesting that STIM1 helps make platelets stickier.

The results suggest that a quick calcium burst from ER-like tubules might be sufficient to build small clots to patch up a minor tear. The STIM1-driven calcium spike, on the other hand, might be necessary to form larger clots under high shear, as occurs in small or fat-clogged vessels.

Mice lacking STIM1 were protected from injury-induced vessel blockage and strokes, as their feeble clots allowed some blood to flow into injured brain tissues. As the clotting problem didn't prolong bleeding, a small, transient clot might be all that's needed to prevent hemorrhage, with the added bonus of avoiding a complete halt in blood flow.
Cardiac Arrest During Nasotracheal Aspiration
Authors: Charles Fineberg
Journal: JAMA (1960)

For the first day or so after a major operation, the patient's cough may be ineffective in clearing the trachea and bronchi of secretions, with resultant pneumonitis and atelectasis. Retained tracheobronchial secretions are often seen after upper abdominal operations,1such as gastrectomy and cholecystectomy, and the condition may be aggravated by the use of an indwelling nasogastric tube.2Atelectasis is probably the most frequent post-operative complication of thoracic operations.3  A high humidity in the inspired air or in oxygen and the control of pain are probably the most important factors in promoting an effective cough. Despite these measures, post-operative patients are frequently unable to clear the tracheobronchial tree of secretions. When this occurs, nasotracheal aspiration4is undoubtedly the most effective method of removing the retained secretions. Moreover, it frequently stimulates an effective cough. It is readily available at the bedside and may be repeated frequently without the need
One Year after a Successful Start of <i>Theranostics</i>
Authors: Xiaoyuan (Shawn) Chen
Journal: Theranostics (2012)

As Theranostics begins its second year of publication, I would like to thank our authors, reviewers, and audience for their outstanding support in 2011. I look forward to working with you in 2012 to continue our mission to distinguish Theranostics as a leader of publishing cutting edge research in this important and emerging field.
Abstract 2643: Regulation of stem cell differentiation by p53.
Authors: Mangmang Li, Yunlong He, Wendy Dubois, Jing Huang
Journal: Cancer Research (2013)

Abstract Differentiation is one of the barriers for tumorigenesis and reprogramming. In addition, embryonic stem (ES) and induced pluripotent stem (iPS) cells utilize differentiation to maintain their genomic stability by removing cells with mutation burden from the population in response to DNA damage. The tumor suppressor p53 is critical for regulating the differentiation of ES and iPS cells. However, the mechanism of how p53 regulates the differentiation of ES and iPS cells is unclear. To systematically study the underlying mechanisms, we employ an integrated genome-wide study in mouse ES cells. Systems analyses reveal that p53-activated genes and p53-repressed genes have distinct regulatory mechanisms and functions in mouse ES cells. Binding of p53 at promoter region significantly correlates with gene activation but not with repression. In addition, we unexpectedly identify a novel regulatory mode for p53-mediated repression through interfering with distal enhancer activity. This regulatory mode explains some but not all of the p53-mediated repressive events. Importantly, many ES cell-enriched core transcription factors are p53-repressed genes. Further analyses demonstrate that p53-repressed genes are functionally associated with ES and iPS cell status while p53-activated genes are linked to differentiation. Genome-wide analyses also show that p53-activated genes and -repressed genes have distinguishable features of expression levels and epigenetic markers, such as H3K4me3, H3K27me3 and H3K79me2. Upon DNA damage, p53 regulates the self-renewal and pluripotency of ES cells. Together, these results support a model that, in response to DNA damage, p53 affects the status of ES cells through activating differentiation-associated genes and repressing ES cell-enriched genes. Because many poorly differentiated tumors express ES-cell gene signature, our results may also have far-reaching implications in how p53 restricts the origin of cancer stem cells in adult tissues. Citation Format: Mangmang Li, Yunlong He, Wendy Dubois, Jing Huang. Regulation of stem cell differentiation by p53. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2643. doi:10.1158/1538-7445.AM2013-2643 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Abstract 3833: Codon-optimized GM-CSF gene as an adjuvant to enhance the immunity of a human papillomavirus 16 E7 DNA vaccine in mice
Authors: Jian-Tai Qiu, Cheng-Tao Lin, Chyong-Huey Lai, Kuo-Shiang Chang, Tzong-Shoon Wu
Journal: Cancer Research (2010)

Abstract Granulocyte macrophage-colony stimulating factor (GM-CSF) is a potent immunomodulatory cytokine. We have generated a novel codon optimized murine GM-CSF sequences as an adjuvant. The codon optimized murine GM-CSF plasmids significantly increased GM-CSF expression levels in all cells tested, including murine, monkey, and human cell lines. Here we show that coadministration of plasmids encoding the codon optimized GM-CSF sequence with the HPV-16 E7 DNA vaccine resulted in complete tumor regression in 100% of the C57BL/6 mice tested. Consistent with these findings, coadministarton of these plasmids elicited E7-specific CTL responses and a protective immune response against challenge of E7- expressing TC-1 tumors in mice. Histological analysis revealed that the tumor destruction occurred at the margins of the tumor, where there was a heavy lymphocytic infiltrate. We also created a TC-1 tumors expressing E7 and GM-CSF genes. Combining a GM-CSF secreting TC-1 vaccine with a systemic DNA vaccination successfully treated &amp;gt;90% of the mice bearing an established tumor but showed no resistance to an unrelated ovarian cancer. This novel codon optimized GM-CSF plasmid may prove a practical molecular strategy for overcoming this limitation of DNA vaccines and potentiating immune responses to vaccines as well as other immunotherapeutic strategies. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3833.
Continuous infusion of monoclonal antibody‐purified factor VIII: Rational approach to serious hemorrhage in patients with allo‐/autoantibodies to factor VIII
Authors: Erlinda M. Gordon, Fatma Al‐Batniji, Jonathan C. Goldsmith
Journal: American Journal of Hematology (1994)

Abstract Hemorrhage in a patient with factor VIII inhibitor is associated with increased morbidity and mortality. Treatment with factor IX complex concentrates or recombinant factor VIIA (rVIIa) may not control bleeding and may induce thrombosis. In this study, continuous infusion of a monoclonal antibody‐purified factor VII concentrate (Monoclate‐P) was used successfully in two hemophilic patients with factor VIII alloantibodies and one nonhemophilic patient with a factor VIII autoantlbody. In two patients, hemorrhage was life‐threatening, and, in one, bleeding did not stop with repeated infusions of activated factor IX complex concentrates. The patients' ages ranged from 4 to 15 years, and the inhibitor levels from 6 to 300 Bethesda units/ml. Clinical hemostasis was excellent, and In vivo recovery of infused factor VIII was achieved. When an excess of monoclonal factor VIII was added to the inhibitor plasma in vitro, a stable level of residual factor VIII activity was noted after an initial rapid loss. This second‐order reaction occurs in plasmas of patients with type I factor VIII inhibitors. In one patlent, we showed that the saturation dose of the factor VIII inhibitor predicted in vivo recovery of factor VIII:C. These data emphasize the importance of characterizing the kinetic reactions of the factor VIII inhibitor. Furthermore, we confirm previous reports that continuous infusion of monoclonal factor VIII is a safe and effective treatment of patients with factor VIII inhibitors in whom hemorrhage Is either life‐threatening or refractory to standard treatment. © 1994 Wiley‐Liss, Inc.
Mechanisms of hepatocyte protection against hypoxic injury by atrial natriuretic peptide
Authors: Rita Carini, Maria Grazia De Cesaris, Roberta Splendore, Cinzia Domenicotti, Maria Paola Nitti, Maria Adelaide Pronzato, Emanuele Albano
Journal: Hepatology (2003)

Atrial natriuretic peptide (ANP) reduces ischemia and/or reperfusion damage in several organs, but the mechanisms involved are largely unknown. We used freshly isolated rat hepatocytes to investigate the mechanisms by which ANP enhances hepatocyte resistance to hypoxia. The addition of ANP (1 micromol/L) reduced the killing of hypoxic hepatocytes by interfering with intracellular Na(+) accumulation without ameliorating adenosine triphosphate (ATP) depletion and pH decrease caused by hypoxia. The effects of ANP were mimicked by 8-bromo-guanosine 3', 5'-cyclic monophosphate (cGMP) and were associated with the activation of cGMP-dependent kinase (cGK), suggesting the involvement of guanylate cyclase-coupled natriuretic peptide receptor (NPR)-A/B ANP receptors. However, stimulating NPR-C receptor with des-(Gln(18), Ser(19),Gly(20),Leu(21),Gly(22))-ANP fragment 4-23 amide (C-ANP) also increased hepatocyte tolerance to hypoxia. C-ANP protection did not involve cGK activation but was instead linked to the stimulation of protein kinase C (PKC)-delta through G(i) protein- and phospholipase C-mediated signals. PKC-delta activation was also observed in hepatocytes receiving ANP. The inhibition of phospholipase C or PKC by U73122 and chelerythrine, respectively, significantly reduced ANP cytoprotection, indicating that ANP interaction with NPR-C receptors also contributed to cytoprotection. In ANP-treated hepatocytes, the stimulation of both cGK and PKC-delta was coupled with dual phosphorylation of p38 mitogen-activated protein kinase (MAPK). The p38 MAPK inhibitor SB203580 abolished ANP protection by reverting p38 MAPK-mediated regulation of Na(+) influx by the Na(+)/H(+) exchanger. In conclusion, ANP recruits 2 independent signal pathways, one mediated by cGMP and cGK and the other associated with G(i) proteins, phospholipase C, and PKC-delta. Both cGK and PKC-delta further transduce ANP signals to p38 MAPK that, by maintaining Na(+) homeostasis, are responsible for ANP protection against hypoxic injury.
Treatment of Plantar Warts
Authors: Marvin D. Steinberg
Journal: JAMA (1967)

To the Editor:—  Please permit me to add to the already excellent answer given to the question on Recurrent Plantar Warts ( 201 :1059, 1967).  The four areas which blanch and are very tender are most probably porokeratotic. Recent studies done on well over 100 similar cases by Dr. Jacob Taub and myself show a relationship between these exquisitely sensitive lesions and underlying sweat gland hypertrophy. Clinically the lesion is pink and depressed somewhat centrally, and it is surrounded by a whitish areola. This white areola is histologically composed of compact parakeratotic epithelium. The bulbous central portion resembles a coronoid lamella. Neither structure shows normal passage of glandular elements.  The lesions occur under weight-bearing areas especially when a metatarsal head is depressed, or arthritic, or when a sesamoid bone is enlarged and displaced. These painful lesions or areas are discrete and not confluent as are verrucae. They may occur under any
Recurrent infections, pericarditis and renal disease in a patient with total C2 deficiency and decreased NK cell function consistent with acute rheumatic fever and systemic lupus erythematosus.
Authors: D B Bittleman, K K Maves, J A Bertolatus, S M Bonsib, P Densen, Z K Ballas, J M Weiler
Journal: Annals of the Rheumatic Diseases (1994)

Recurrent infections, pericarditis and renal disease in a patient with total C2 deficiency and
Abstract 2517: Potent antitumor activity of AbGn-ADC, a humanized monoclonal antibody conjugated with dolastatin analogue, to gastric and pancreatic cancers expressing AbGn carbohydrate epitope
Authors: Chiu-Chen Huang, Yu-Chi Hsieh, Yu-Ying Tsai, Shu-Hua Lee, Evelyn Chiang, Meng-Ru Liu, Shih-Yao Lin
Journal: Cancer Research (2012)

Abstract AbGn is a glycotope-specific humanized monoclonal antibody recognizing Lewisa- like carbohydrate expressed in gastric and pancreatic cancer cells. While AbGn binding to normal tissues is restricted to only luminal surface of the epithelium in gastro-intestinal track and secretory glands, about 50% of gastric and pancreatic cancer samples tested express AbGn epitope and can be recognized by AbGn antibody. FACS analysis and confocal microscopic studies demonstrated extensive internalization of AbGn after binding to the cell surface. The internalized AbGn co-localized with lysosomal marker LAMP1, suggesting that AbGn-mediated internalization followed the lysosomal pathway. A novel antibody-drug conjugate (AbGn-ADC) was generated by linking AbGn to a dolastatin analogue, a potent inhibitor of microtubulin polymerization, through a dipeptide-based cleavable linker. This AbGn-ADC was evaluated for antitumor activity in vitro and in mouse xenograft models. AbGn-ADC eliminated cancer cell lines with nanomolar potency in vitro. No cell death could be detected in SW480 cells, a gastric cell line with no AbGn epitope expression, suggesting high selectivity of AbGn-ADC. When used to treat mice with established human gastric (SNU-16) or pancreatic (Panc.02.03B) cancer xenografts, AbGn-ADC significantly reduced the size of the established tumors (p&amp;lt;0.01). No body weight loss or signs of toxicity was observed in AbGn-ADC treated mice. These findings support the potential of further development of AbGn-ADC for treating gastric and pancreatic cancers. Data from pre-clinical AbGn-ADC tolerability study in relevant non-human primate will be presented. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2517. doi:1538-7445.AM2012-2517
WHICH PATIENTS ARE MORE LIKELY TO EXPERIENCE ADVERSE CHANGES ON IMAGING FOLLOWING ACUTE AORTIC DISSECTION?
Authors: Troy LaBounty, Reed Pyeritz, Linda Pape, Santi Trimarchi, Lori D. Conklin, Jehangir Appoo, Blaz Mrevlje, Dinesh Mittal, Patroklos Pappas, Mark A. Groh, Jean Bismuth, Daniel Montgomery, Alberto Forteza, Christoph Nienaber, Kim Eagle, Eric Isselbacher
Journal: Journal of the American College of Cardiology (2015)
Microendoscopic Features of the Surface Epithelium in Patients with Colonic Tumors
Authors: V. P. Strekalovsky, S. L. Khankin, L. L. Kapuller
Journal: Endoscopy (1989)

Vital studies of the colonic mucosa in 127 patients using the method of colonomicroscopy have allowed us to establish that the surface epithelium has a heterogeneous structure. It was possible to single out three main types of cell organization. Correlation has also been detected between types of cell organization of surface epithelium and morphological structure of the most common neoplasms of the colon.