tbuckley/cabot-search huggingface dataset:
Dermatoglyphics in Congenital Heart Disease
Authors: MILTON ALTER, ROBERT SCHULENBERG
Journal: Circulation (1970)

Dermatoglyphics form in utero during early gestation and may be influenced by genetic or environmental factors operating at that time. Since cardiac embryogenesis also occurs during early gestation, an analysis of dermatoglyphics in congenital heart disease (CHD) might reveal some types which are associated with aberrant dermatoglyphics. Ten dermatoglyphic traits were analyzed in 225 individuals with CHD proved, in most instances, by extensive radiologic studies and at surgery. These traits were compared with dermatoglyphics in 200 normal control subjects. The analysis revealed that the atd angle was significantly increased in CHD. Except for endocardial fibroelastosis and atrioventricular canal, all subtypes of CHD had a wider atd angle than controls. In ventricular septal defect, patent ductus arteriosus, tetralogy of Fallot, and multiple cardiac defects, the increase was statistically significant. The present study confirms previous reports that the atd angle may be increased in CHD.
Assessment of rebound and relapse following ecallantide treatment for acute attacks of hereditary angioedema
Authors: J. A. Bernstein, E. P. Shea, J. Koester, R. Iarrobino, W. E. Pullman
Journal: Allergy (2012)

Abstract Background Hereditary angioedema ( HAE ) is a rare genetic disease characterized by unpredictable and recurring attacks of angioedema. This study assessed potential attack rebound and relapse following treatment with ecallantide, a plasma kallikrein inhibitor approved for HAE attack treatment. Methods Results were integrated from 2 double‐blind, placebo‐controlled studies of ecallantide treatment for HAE : EDEMA 3‐ DB and EDEMA 4. Symptoms were assessed by treatment outcome score ( TOS ), mean symptom complex severity ( MSCS ) score, and global response. Patients with improvement at 4 h post‐dosing in all three measures followed by any sign of worsening at 24 h were considered to show potential rebound if worsening was beyond baseline or potential relapse if not beyond baseline. Likeliness of rebound or relapse was determined by the number of measures showing worsening and the magnitude of worsening. Patients receiving placebo who met the criteria for rebound/relapse were evaluated for descriptive comparison only. Results Significantly more ecallantide‐treated patients (42 of 70) compared to placebo (26 of 71) showed improvement in three measures at 4 h and were thus eligible for rebound/relapse ( P = 0.006). Of the nine ecallantide‐treated patients with signs of worsening at 24 h, none were likely rebound, one was assessed as possible rebound, one as likely relapse, and two as possible relapse. No patient with potential rebound/relapse experienced new symptoms after dosing. Medical intervention was required in one ecallantide‐treated patient. Conclusion Ecallantide was efficacious for treating acute HAE attacks. Relapse was observed in a small proportion of patients, and there was little evidence of rebound.
Real-Time Monitoring of Rare Circulating Hepatocellular Carcinoma Cells in an Orthotopic Model by<i>In Vivo</i>Flow Cytometry Assesses Resection on Metastasis
Authors: Zhi-Chao Fan, Jun Yan, Guang-Da Liu, Xiao-Ying Tan, Xiao-Fu Weng, Wei-Zhong Wu, Jian Zhou, Xun-Bin Wei
Journal: Cancer Research (2012)

The fate of circulating tumor cells (CTC) is an important determinant of metastasis and recurrence, which leads to most deaths in hepatocellular carcinoma (HCC). Therefore, quantification of CTCs proves to be an emerging tool for diagnosing, stratifying, and monitoring patients with metastatic diseases. In vivo flow cytometry has the capability to monitor the dynamics of fluorescently labeled CTCs continuously and noninvasively. Here, we combine in vivo flow cytometry technique and a GFP-transfected HCC orthotopic metastatic tumor model to monitor CTC dynamics. Our in vivo flow cytometry has approximately 1.8-fold higher sensitivity than whole blood analysis by conventional flow cytometry. We found a significant difference in CTC dynamics between orthotopic and subcutaneous tumor models. We also investigated whether liver resection promotes or restricts hematogenous metastasis in advanced HCC. Our results show that the number of CTCs and early metastases decreases significantly after the resection. The resection prominently restricts hematogenous metastasis and distant metastases. CTC dynamics is correlated with tumor growth in our orthotopic tumor model. The number and size of distant metastases correspond to CTC dynamics. The novel in vivo flow cytometry technique combined with orthotopic tumor models might provide insights to tumor hematogenous metastasis and guidance to cancer therapy.
Government to take health seriously?
Authors: N D Olsen, N Tewson
Journal: BMJ (1987)

IJGovernment to take health seriously?Next week parliament will debate health promotion.Mini- sters will seek to show that the public health is as "safe in their hands" as the health care service.They will be judged not by their rhetoric but by their actions, and when the Parliamentary Public Accounts Committee judged the per- formance of the Department of Health and Social Security last year it found it wanting.'The department was severely criticised for its organisation and evaluation of preventive services.By chance two days before the parliamentary debate the DHSS will be funding a conference on health promotion.A range of international experts will describe what can be achieved, often from a poor start, by combining political commitment, clear objectives, adequate long term funding, and coordinated public health measures.Ironically the speakers will include Mike Daube, director ofhealth promo- tion in Western Australia and consultant to the World Health Organisation.Four years ago he was prevented by ministers from obtaining a senior post at the Health Education Council.The grounds for the veto were that he had offended commercial interests, initially as director of Action on Smoking and Health and later as honorary secretary of Action on Alcohol Abuse.His effectiveness worried those who put commercial profitability from tobacco, alcohol, and advertising above the public health.Public health has faced great problems since the NHS was formed.Pragmatic political decisions biased the newborn NHS towards domination by hospital specialists, and not until the general practice charter of 1966 was priority given to primary care.The decline ofthe medical officer ofhealth and
TOXICITY OF ARSPHENAMIN (SALVARSAN): REPORT OF CASES
Authors: J. D. Willis
Journal: JAMA (1918)

To the Editor:  —Having read a report by Dr. James C.. Sargent of Milwaukee on five cases of unusual toxicity resulting from administration of the new American made salvarsan, I am constrained to report three cases, believing that this information should be given to the medical profession.  A man, aged 38, suffering from the secondary stage of syphilis, who had had three weekly 0.6 gm. doses of diarsenol with no toxic reactions following, reported for his fourth treatment. The first obtainable American made salvarsan had just reached us, and a dose of this was given after being mixed in the following manner: First the ampule was dissolved in 90 c.c. of hot sterile freshly distilled water, and sufficient cool freshly distilled water was added to bring the amount up to a 200 c.c. bulk. Freshly prepared 15 per cent. sodium hydroxid was added drop by drop, the solution being stirred
Short-term interferon-alfa therapy for acute hepatitis C: A randomized controlled trial
Authors: Hideyuki Nomura, Suketo Sou, Hironori Tanimoto, Takashi Nagahama, Yoichi Kimura, Jun Hayashi, Hiromi Ishibashi, Seizaburo Kashiwagi
Journal: Hepatology (2004)

Acute hepatitis C often progresses to chronic infection. We undertook a randomized controlled trial to determine whether short-term therapy with interferon (IFN) during acute hepatitis C is effective in preventing the development of chronic hepatitis. Thirty patients with acute hepatitis C were randomized into 1 of 2 treatment groups. IFN therapy was initiated 8 weeks after the onset of acute hepatitis in the early-intervention group and after 1 year of observation in the late-intervention group. Short-term therapy consisted of natural IFN-alfa (6 million units) administered on consecutive days for a period of 4 weeks. Any signs of recrudescence of disease were immediately followed by interval IFN therapy (3 times weekly for 20 weeks). In the early-intervention group, short-term therapy was associated with a sustained virological response in 13 of 15 patients (87%). Follow-up treatment was associated with a sustained virological response in both of the remaining 2 patients (100%). The sustained virological response rate was significantly higher in the early-intervention group (87%, 13 of 15 patients after short-term therapy alone, and 100%, 15 of 15 patients after short-term with or without follow-up therapy) than in the late-intervention group (40%, 6 of 15 patients after short-term therapy alone, and 53%, 8 of 15 patients after short-term therapy with or without follow-up therapy, P = .021 and P = .006, respectively). In conclusion, short-term (4 weeks) IFN treatment of patients with acute hepatitis C may be associated with satisfactory results, if initiated at an early stage of the disease. (Hepatology 2004;39:1213-1219.)
Multiple Sclerosis History
Authors: Xavier Bosch
Journal: JAMA (2005)

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
Current Status of Pharmaceutical and Genetic Therapeutic Approaches to Treat DMD
Authors: Christophe Pichavant, Annemieke Aartsma-Rus, Paula R Clemens, Kay E Davies, George Dickson, Shin'ichi Takeda, Steve D Wilton, Jon A Wolff, Christine I Wooddell, Xiao Xiao, Jacques P Tremblay
Journal: Molecular Therapy (2011)

Duchenne muscular dystrophy (DMD) is a genetic disease affecting about one in every 3,500 boys. This X-linked pathology is due to the absence of dystrophin in muscle fibers. This lack of dystrophin leads to the progressive muscle degeneration that is often responsible for the death of the DMD patients during the third decade of their life. There are currently no curative treatments for this disease but different therapeutic approaches are being studied. Gene therapy consists of introducing a transgene coding for full-length or a truncated version of dystrophin complementary DNA (cDNA) in muscles, whereas pharmaceutical therapy includes the use of chemical/biochemical substances to restore dystrophin expression or alleviate the DMD phenotype. Over the past years, many potential drugs were explored. This led to several clinical trials for gentamicin and ataluren (PTC124) allowing stop codon read-through. An alternative approach is to induce the expression of an internally deleted, partially functional dystrophin protein through exon skipping. The vectors and the methods used in gene therapy have been continually improving in order to obtain greater encapsidation capacity and better transduction efficiency. The most promising experimental approaches using pharmaceutical and gene therapies are reviewed in this article. Duchenne muscular dystrophy (DMD) is a genetic disease affecting about one in every 3,500 boys. This X-linked pathology is due to the absence of dystrophin in muscle fibers. This lack of dystrophin leads to the progressive muscle degeneration that is often responsible for the death of the DMD patients during the third decade of their life. There are currently no curative treatments for this disease but different therapeutic approaches are being studied. Gene therapy consists of introducing a transgene coding for full-length or a truncated version of dystrophin complementary DNA (cDNA) in muscles, whereas pharmaceutical therapy includes the use of chemical/biochemical substances to restore dystrophin expression or alleviate the DMD phenotype. Over the past years, many potential drugs were explored. This led to several clinical trials for gentamicin and ataluren (PTC124) allowing stop codon read-through. An alternative approach is to induce the expression of an internally deleted, partially functional dystrophin protein through exon skipping. The vectors and the methods used in gene therapy have been continually improving in order to obtain greater encapsidation capacity and better transduction efficiency. The most promising experimental approaches using pharmaceutical and gene therapies are reviewed in this article.
MCP-1 protects mice in lethal endotoxemia.
Authors: D A Zisman, S L Kunkel, R M Strieter, W C Tsai, K Bucknell, J Wilkowski, T J Standiford
Journal: Journal of Clinical Investigation (1997)

The overzealous production of proinflammatory cytokines in sepsis can result in shock, multiorgan dysfunction, and even death. In this study, we assessed the role of monocyte chemoattractant protein-1 (MCP-1) as a mediator of sepsis in endotoxin-challenged mice. Intraperitoneal administration of LPS to CD-1 mice induced a substantial time-dependent increase in MCP-1 in plasma, lung, and liver. The passive immunization of mice with rabbit antimurine MCP-1 antiserum 2 h before endotoxin administration resulted in a striking increase in LPS-induced mortality from 10% in control animals to 65% in anti-MCP-1-treated animals. Importantly, the administration of anti-MCP-1 antibodies to endotoxin-challenged mice resulted in increases in peak TNF-alpha and IL-12 levels, and also in a trend toward decreased serum levels of IL-10. Conversely, the administration of recombinant murine MCP-1 intraperitoneally significantly protected mice from endotoxin-induced lethality, and resulted in an increase in IL-10 levels, a decrease in IL-12 levels, and a trend toward decreased levels of TNF. In conclusion, our findings indicate that MCP-1 is a protective cytokine expressed in murine endotoxemia, and does so by shifting the balance in favor of antiinflammatory cytokine expression in endotoxin-challenged animals.
Fine structure and histochemistry of epithelioid cells in sarcoidosis
Authors: E. M. V. James, W. J. Williams
Journal: Thorax (1974)

<b>James, E. M. Valerie and Jones Williams, W. (1974).</b><i>Thorax</i>, <b>29</b>, 115-120. <b>Fine structure and histochemistry of epithelioid cells in sarcoidosis.</b> In this fine structure study of epithelioid cells in the granulomata of sarcoidosis we confirm our previous findings that they appear to be synthesizing rather than phagocytosing cells. The numerous characteristic intracytoplasmic vesicles, 0·5 μ in size, are shown to contain mucoglycoprotein and only rarely acid phosphatase activity. Epithelioid cells show varying quantities of extravesicular acid phosphatase activity which is sometimes on the outer surface of the protein-containing vesicles. The possible role of secretory products of epithelioid cells in the formation and persistence of granulomata is discussed. It is suggested that epithelioid cells may be forming lymphokines.
Immune lysis of normal human and paroxysmal nocturnal hemoglobinuria (PNH) red blood cells. II. The role of complement components in the increased sensitivity of PNH red cells to immune lysis.
Authors: W F Rosse, J V Dacie
Journal: Journal of Clinical Investigation (1966)

tions of the components of complement (desig- nated C'1, C'2, C'3, or C'4).These reactions are presently understood to occur as follows (3):EAC', * EAC'ja (4) (addition and activation of C'1).EAC'ia + C'4 ) EAC'la,4 (addition of C'4).
HLA-D region-associated determinants serve as targets for human cell-mediated lysis.
Authors: C Feighery, P Stastny
Journal: The Journal of Experimental Medicine (1979)

Effector cells for cell-mediated lysis (CML) were generated by in vitro culture of lymphocytes from selected donors with X-irradiated cells from unrelated subjects who were HLA-D homozygous and matched to the responders for the antigens of the HLA-A and HLA-B regions. By using chromium labeled monocytes as target cells, cytotoxicity was found to correlate with presence of HLA-D region antigens matching those of the stimulating cells. Such CML reactions apparently directed at products of HLA-D, were inhibited by addition of unlabeled monocytes or B lymphocytes. These unlabeled cells had to be matched for HLA-D with the stimulating cells used to generate the effector populations. The results suggested that products of HLA-D, perhaps the DR antigens, were recognized by cytotoxic lymphocytes.
Valve replacement for aortic regurgitation: long-term follow-up with factors influencing the results.
Authors: D A Samuels, G D Curfman, A L Friedlich, M J Buckley, W G Austen
Journal: Circulation (1979)

One hundred consecutive cases of valve replacement for aortic regurgitation performed between 1967--1971 were analyzed to identify and quantitate factors related to a favorable result. Of 83 perioperative survivors, 78% (n = 65) became asymptomatic and 58% (n = 48) were alive 5--9 years postoperatively. The cause of aortic regurgitation affected both the speed of progression of symptoms and the postoperative result. Death due to myocardial failure may be prevented by optimal timing of operation. Accordingly, we identified variables that discriminated between patients who had an excellent postoperative result and those who died of myocardial failure. The most important discriminators were the severity (p = 0.03) and duration (p = 0.04) of dyspnea, the extent of therapy for heart failure (p = 0.001), physical findings of left ventricular failure (p = 0.002), the cardiothoracic ratio (p = 0.007), the resting pulmonary capillary wedge pressure (p = 0.01), and a cardiac index less than 2.2 1/min/m2 (p = 0.03). The data suggest that evidence of left ventricular failure, even of mild degree, is an indication for operation in patients with severe aortic regurgitation.
Abstract 4904: Mechanisms of cytotoxicity of bifunctional epoxide cross-linking agents
Authors: Christopher Ng, Vanesa L. Silvestri, Morgan T. Lingar, Julie T. Millard
Journal: Cancer Research (2011)

Abstract The discovery that bifunctional alkylating agents have antitumor activity led to the development of cancer chemotherapy over 50 years ago. While these compounds form a variety of cellular lesions, DNA interstrand cross-links are believed to be the most lethal, impeding both replication and expression of the genetic material. We are characterizing the mechanisms by which diepoxybutane (DEB) and the structurally related compound epichlorohydrin (ECH) exert their cytotoxic effects in cultured cells. Our first goal is to determine the relationship between interstrand cross-linking and cytotoxicity. We are assaying cross-linking ability in cultured cells using Hoechst 33258 to determine the amount of duplex DNA following alkaline denaturation. Only cross-linked DNA reanneals rapidly and interacts with the dye, which is highly fluorescent when bound to duplex DNA. Preliminary results in chicken 6C2 and human HL60 cells suggest a correlation between cross-linking and LD50 values for these compounds. Our second goal is to characterize the pathways by which these compounds induce apoptosis. Reverse-transcriptase real-time PCR analysis of HL-60 cells treated with DEB and ECH under conditions determined to induce apoptosis suggests up-regulation of several key genes involved in the mitochondrial apoptotic pathway, including BAK1, BAX, DIABLO, PUMA and APAF1. Finally, we are identifying the covalent structure of the ECH-cross-linked lesion via electrospray LC/MS. Characterization of the DNA modifications induced by these agents is an important step in understanding how these compounds exert their cytotoxic effects. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4904. doi:10.1158/1538-7445.AM2011-4904
International Medical Care: A Comparison and Evaluation of Medical Care Services Throughout the World
Authors: Norman B. Roberg
Journal: JAMA (1972)

This excellent volume explains the changing concept of medical care, the systems of care in 23 countries, and the medical and administrative problems encountered by all nations. The contributors include both physicians and administrators; they recognize the obligation to make medical care available to all people; and all make critical and realistic judgments born of experience and free of polemic, utopianism, and political oversimplification. Fry describes the inevitable involvement of the state in medical care: medical care must be coordinated with all other aspects of the nation's welfare, aside from the problem of financing. He and Robinson describe how progress increases demand, how resources will remain inadequate to meet the public's "insatiable wants and total needs," and how, with growing governmental involvement, the relationship between the medical profession and government inevitably becomes strained. Cohen explains the problems of insurance (no panacea) and, with others, emphasizes the need for professional participation
Abstract 4665: Sensitization of head and neck cancer cells toward cisplatin by inhibition of autophagy
Authors: Changxiong Guo, Krishna Rao, Thomas Robbins, Daotai Nie
Journal: Cancer Research (2012)

Abstract Cisplatin is a commonly used chemotherapeutics but its efficacy is limited by the resistance presented by some tumor cells. Autophagy is a form of cell death by self-digesting organelles. The present study was undertaken to examine whether cisplatin can induce autophagy and whether autophagy modulates the efficacy of cisplatin against head and neck squamous cancer cells (HNSCC). In responses to increasing doses of cisplatin, there was a steady increase in autophagy, as indicated by LC3 punctate staining, in a cisplatin resistant UMSCC-15S cell line, whereas induction of autophagy was rapidly peaked at low doses of cisplatin in the UMSCC-10B cell line which was more sensitive toward cisplatin. Further studies found that there were increased autophagic fluxes at basal level in the cisplatin sensitive UMSCC-10B cells when compared to cisplatin resistant UMSCC-15S cells. Inhibition of autophagy by chloroquine significantly reduced colony formation of both cell lines, and sensitized UMSCC-15S cells toward cisplatin treatment. Our studies suggest that autophagy responses can be modulated to augment the efficacy of cisplatin against HNSCCs. 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 4665. doi:1538-7445.AM2012-4665