tbuckley/cabot-search huggingface dataset:
Effects of captopril on the left ventricular compliance and fibrosis after nontransmural infarction in rat
Authors: Byung-Hee Oh, Se-Il Oh, Ki-Hoon Han, Hyo-Soo Kim, Cheol-Ho Kim, Myoung-Mook Lee, Young-Bae Park, Yun-Shik Choi, Jung-Don Seo, Young-Woo Lee, Hee-Chan Kim
Journal: Journal of the American College of Cardiology (1996)
Disappearance of Cystinuria After Renal Transplantation
Authors: A. J. Hoitsma, R. A. P. Koene, F. J. M. Trijbels, L. A. H. Monnens
Journal: JAMA (1983)

<h3>To the Editor.—</h3> Cystinuria is a hereditary disease frequently associated with kidney stones and occasionally with end-stage renal failure. Information on the course of the disease after renal transplantation is available for two patients, both of whom experienced a normal excretion of cystine after renal transplantation.<sup>1-3</sup>Recently, we corroborated these findings in a third cystinuric patient during the brief period his kidney graft functioned. <h3>Report of a Case.—</h3> A 38-year-old man at the time of our study had passed morethan 100 renal stones since the age of 16 years. The diagnosis was based on chemical analysis of a stone and on the demonstration of cystinuria (&gt;75 μmole of cystine per millimole of creatinine). Hypertension and renal impairment caused by chronic pyelonephritis were noted at age 31 years. Renal function declined and treatment with hemodialysis was begun at age 37 years. He received a kidney from a cadaveric donor
Hinman Syndrome
Authors: ALAN E. HARRIS, MORAKINYO A. O. TONEY
Journal: Clinical Nuclear Medicine (1994)

Hinman syndrome is a condition representing urinary voiding dysfunction in the neurologically intact child. The syndrome is probably caused by acquired behavioral and psychosocial disorders manifested by bladder and/or bowel dysfunction mimicking neurologic disease. Clinically, the symptom complex may include day and nighttime enuresis, encopresls, constipation, and recurrent urinary tract infections. Cystoscopy frequently demonstrates normal vesicourethral anatomy (a key finding). Laboratory analysis often demonstrates infected urine. With respect to imaging characteristics, hydronephrosis is found in 66–70% of patients and is generally bilateral. Vesicoureteral reflux occurs in 50–60% of patients, and voiding films will usually demonstrate a carrot-shaped proximal urethra with a persistent narrowing at the external sphincter. The bladder is large and often appears trabeculated with a thickened wall and significant post-void residual.
Proangiogenic Action of Thyroid Hormone Is Fibroblast Growth Factor–Dependent and Is Initiated at the Cell Surface
Authors: Faith B. Davis, Shaker A. Mousa, Laura O’Connor, Seema Mohamed, Hung-Yun Lin, H. James Cao, Paul J. Davis
Journal: Circulation Research (2004)

The effects of thyroid hormone analogues on modulation of angiogenesis have been studied in the chick chorioallantoic membrane model. Generation of new blood vessels from existing vessels was increased 3-fold by either l-thyroxine (T4; 10(-7) mol/L) or 3,5,3'-triiodo-l-thyronine (10(-9) mol/L). T4-agarose reproduced the effects of T4, and tetraiodothyroacetic acid (tetrac) inhibited the effects of both T4 and T4-agarose. Tetrac itself was inactive and is known to block actions of T4 on signal transduction that are initiated at the plasma membrane. T4 and basic fibroblast growth factor (FGF2) were comparably effective as inducers of angiogenesis. Low concentrations of FGF2 combined with submaximal concentrations of T4 produced an additive angiogenic response. Anti-FGF2 inhibited the angiogenic effect of T4. The proangiogenic effects of T4 and FGF2 were blocked by PD 98059, a mitogen-activated protein kinase (MAPK) pathway inhibitor. Endothelial cells (ECV304) treated with T4 or FGF2 for 15 minutes demonstrated activation of MAPK, an effect inhibited by PD 98059 and the protein kinase C inhibitor CGP41251. Reverse transcription-polymerase chain reaction of RNA extracted from endothelial cells treated with T4 revealed increased abundance of FGF2 transcript at 6 to 48 hours, and after 72 hours, the medium of treated cells showed increased FGF2 content, an effect inhibited by PD 98059. Thus, thyroid hormone is shown to be a proangiogenic factor. This action, initiated at the plasma membrane, is MAPK dependent and mediated by FGF2.
Effect of a nitric oxide synthase inhibitor and a glucocorticosteroid on exhaled nitric oxide.
Authors: D H Yates, S A Kharitonov, R A Robbins, P S Thomas, P J Barnes
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

Nitric oxide (NO) is produced by a variety of cells within the respiratory tract, including inflammatory epithelial cells. NO has been detected in the exhaled air of normal human subjects, and its concentration is raised in asthmatic patients. To study whether exhaled NO arises from the respiratory tract, we administered a NO synthase (NOS) inhibitor, NG-monomethyl-L-arginine (L-NMMA), by inhalation (490 mg) in a double-blind randomized manner in nine normal and six asthmatic subjects. Because exhaled NO may arise from an inducible isoform of NO synthase that may be inhibited by glucocorticosteroids, we also studied the effects of oral prednisolone (30 mg orally for 3 d) in seven normal and six asthmatic subjects in a separate double-blind crossover study with matched placebo. After nebulized L-NMMA, there was a significant fall in peak exhaled NO compared with saline control values, with a mean fall of 43.6 +/- 5.6% in normal subjects (p < 0.01) and of 39.7 +/- 6.5% (p < 0.01) in asthmatic subjects, which persisted for 4 h. There were no effects of L-NMMA inhalation on heart rate, blood pressure, or FEV1 in either normal or asthmatic patients. Administration of oral prednisolone (30 mg) resulted in a fall in exhaled NO concentrations in asthmatic subjects by 21.6 +/- 5.0% at 48 h (p < 0.01) but no significant change in normal subjects. These data suggest that NOS inhibitors may be safely given in normal and asthmatic patients and that the increased exhaled NO seen in asthmatic patients is likely to be caused by induction of inducible NOS.
Mechanisms of Tumor Necrosis Factor α Antagonist–Induced Lupus in a Murine Model
Authors: Yuan Xu, Haoyang Zhuang, Shuhong Han, Chao Liu, Hai Wang, Clayton E. Mathews, John Massini, Lijun Yang, Westley H. Reeves
Journal: Arthritis & Rheumatology (2014)

Tumor necrosis factor α (TNFα) antagonists are effective for treating rheumatoid arthritis and other inflammatory diseases, but their use can be complicated by the development of lupus-like phenomena. This study was undertaken to investigate the role of TNFα in a murine model of lupus.Toll-like receptor 7 (TLR-7) ligand-driven lupus was induced by injection of pristane into C57BL/6 (B6) mice deficient in TNFα (TNFα(-/-) ) or TNFα-intact B6 mice as wild-type controls. Autoantibody and type I interferon (IFN) production was measured in each group of mice, and the effects of the presence or absence of TNFα on type I IFN-producing plasmacytoid dendritic cells (PDCs), Ly-6C(high) monocytes, and TNFα-producing neutrophils were determined.TNFα(-/-) mice did not spontaneously develop autoantibodies or clinical manifestations of lupus, suggesting that TNFα deficiency alone is insufficient to cause lupus. Although the levels of type I IFN were comparable between untreated TNFα(-/-) and wild-type control mice, untreated TNFα(-/-) mice had increased circulating levels of PDCs and PDC-like cells, which enhanced the potential for production of type I IFN. When treated with pristane, TNFα(-/-) mice developed more severe lupus compared to pristane-treated controls, characterized by increased levels of anti-Sm/RNP autoantibodies, type I IFN, PDCs, and peritoneal inflammatory (Ly-6C(high) ) monocytes. In pristane-treated TNFα(-/-) mice, the numbers of neutrophils, a cell type that promotes resolution of inflammation, were decreased considerably, whereas the responses of inflammatory monocytes and PDCs and the production of type I IFN were increased and prolonged.Low levels of TNFα will increase the number of circulating PDCs in mice, thereby enhancing the potential to produce type I IFN. However, this does not necessarily lead to type I IFN production or autoimmunity unless there is concomitant exposure to endogenous TLR-7 ligands, which are released from dead cells following pristane treatment. In humans, the rate of clearance of dead cells, along with the levels of TNFα, may influence who will develop lupus following treatment with TNFα inhibitors.
Abstract 4533: Characteristics of HS6ST2 expression in colorectal cancer
Authors: Hideharu Kimura, Shigeru Hatabe, Tokuzo Arao, Hidetoshi Hayashi, Tomoyuki Nagai, Kazuko Matsumoto, Yoshihiko Fujita, Masao Fukushima, Akihiko Ito, Kiyotaka Okuno, Kazuto Nishio
Journal: Cancer Research (2012)

Abstract Background. We have found that the gene expression of heparin sulfate D-glucosaminyl 6-O-sulfotransferase-2 (HS6ST2) is overexpressed in colorectal cancer in a previous study. Aims of this study are to evaluate the HS6ST2 expression in colorectal cancer tumor samples in relation to the clinicopathological features. Methods. The mRNA expression levels of HS6ST2 were analyzed in various cancer cell lines using real-time RT-PCR. HS6ST2 protein expression was evaluated using immunohistochemistry. Tumor specimens were obtained from 103 colorectal cancer patients operated in Kinki University Hospital. Results. High mRNA expression was observed in 2/15 (13%) of gastric cancer and 3/6 (50%) of colorectal cancer cell lines. In immunohistochemistry analysis, cytoplasm staining was found in cancer cells, not in normal colon cells, and positive staining of HS6ST2 expression was seen in 37 patients (36.3%). There were no relationships between clinicopathological features and HS6ST2 expression in cancer cells. Colon cancer patients with HS6ST2 expression tend to have worse overall survival (p = 0.097, Log-rank test).Conclusion. The cytoplasm expression of HS6ST2 is tumor-specific in colon tissues. HS6ST2 may contribute to be worse outcome. 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 4533. doi:1538-7445.AM2012-4533
Magnesium Deficiency and Digitalis Toxicity-Reply
Authors: L. Cohen
Journal: JAMA (1984)

<h3>In Reply.—</h3> According to several recommendations, the intake of magnesium should be 300 to 500 mg daily. Almost everywhere where it is measured, it is below this value. A state of marginal magnesium deficiency exists. Body stores of magnesium can be depleted by long-term digitalis use or long-term diuretic therapy. Habitual alcohol intake can lead to magnesium depletion. When these various factors are superimposed on the suboptimal magnesium intake, a true magnesium deficiency state develops. It has been calculated that 170 mg/day of supplementary magnesium would probably alleviate the magnesium deficiency. Magnesium supplementation has already begun in Finland, where a specially formulated table salt contains 65% sodium, 25% potassium, and 10% magnesium. The new salt increases magnesium intake and concomitantly reduces the sodium intake.<sup>1</sup>It follows, therefore, that one way to achieve prophylactic administration of magnesium in the patient who has used digitalis is by recourse to dietary magnesium
Bleeding and thrombosis in acute promyelocytic leukemia
Authors: Aditi Choudhry, Thomas G. DeLoughery
Journal: American Journal of Hematology (2012)

Acute promyelocytic leukemia (APL) has evolved from being a deadly to a highly curable disease, due to targeted molecular therapy with all-trans retinoic acid (ATRA). As a result, the incidence of early hemorrhagic deaths for which APL is notorious has reduced to 5-10% as reported in clinical trials. These results are not replicated outside of clinical trials as is evident from recent population-based registries. High incidence of early hemorrhagic deaths remains the greatest contributor to treatment failure in this otherwise curable leukemia. Additionally, thrombosis is now being increasingly recognized in APL patients and may be associated with ATRA usage.
Transformation of human osteoblasts to anchorage-independent growth by insoluble nickel particles.
Authors: X Lin, M Costa
Journal: Environmental Health Perspectives (1994)

Nickel compounds are well established by epidemiologic studies as human carcinogens. Although the carcinogenicity of nickel compounds has been studied in experimental animals and in a variety of cultured mammalian cells, there are only sporadic reports of nickel-induced transformation of human cells. In attempts to study the mechanisms of nickel-induced carcinogenesis in human cells, an immortalized human osteoblastic cell line (HOS) that could not grow in soft agar or form tumors in athymic nude mouse was repeatedly treated with a water-soluble nickel compound (NiCl2) or a less water-soluble nickel compound crystalline (NiS). After three rounds of NiS treatment, there was an increase in anchorage-independent (AI) colony formation. This was not found in untreated or NiCl2-treated cells. Ten AI colonies obtained from NiS-treated cells were isolated. All of these clones showed changes in cell morphology, including the appearance of uniform polygon shape, growth in multilayers, and heavy staining with Giemsa. Most of these clones were retested for their ability to grow in soft agar and showed growth efficiencies of 5 to 50%. It has been shown by other investigators that aggregate growth is well correlated with tumorigenic potential in viral or chemical transformants of HOS cells. Four of seven tested NiS-transformed clones were able to form large aggregates compared to their untransformed counterparts, and continued to proliferate in aggregate form when they were plated on 0.9% agar. Current investigations focus on the molecular and genetic changes induced by nickel compounds in these human cells.
Adult (Not Internal) Medicine
Authors: Edgardo Zavala-Alarcon
Journal: Annals of Internal Medicine (1998)

Letters1 June 1998Adult (Not Internal) MedicineEdgardo Zavala-Alarcon, MD and Mauricio Pineda-Roman, MDEdgardo Zavala-Alarcon, MDMaricopa Medical Center; Phoenix, AZ 85008Search for more papers by this author and Mauricio Pineda-Roman, MDMaricopa Medical Center; Phoenix, AZ 85008Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-128-11-199806010-00026 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:We certainly agree with the concepts expressed in Dr. Goldman's editorial [1]. Accordingly, we would like to suggest another self-explanatory name for the internist that emphasizes the character of the discipline and the fact that it is a defined specialty: adult care specialist. This name clearly identifies the internist as adult-focused, clinically oriented, and possessing the scientific and academic strengths that have been historically identified with our specialty. It also serves the marketing and educational purposes sought with a name change and correlates the specialty adult medicine with its practitioners.A similar denomination was proposed by Kurtz ...References1. Goldman L. Adult (not internal) medicine [Editorial]. Ann Intern Med. 1997; 127:835-6. Google Scholar2. Kurtz KJ, Goodman PH. The adult medicine specialist. Am J Med. 1985; 78:725-6. Google Scholar Author, Article, and Disclosure InformationAffiliations: Maricopa Medical Center; Phoenix, AZ 85008 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 June 1998Volume 128, Issue 11Page: 958KeywordsPrimary care physicians Issue Published: 1 June 1998 CopyrightCopyright © 1998 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Minister defends immunisation campaign
Authors: C. Court
Journal: BMJ (1995)

Junior health minister Mr Tom Sackville has responded to criticism of the British government's campaign last autumn to vaccinate eight million schoolchildren against measles. He described the results of the campaign as “excellent.”

Mr Sackville said that it would have been “indefensible not to implement this campaign” and added: “Since the campaign, the only two cases of measles that have occurred in the age groups covered have been in children who were not immunised in the campaign. A predicted epidemic has been …
Simultaneous onset of primary cutaneous B-cell lymphoma and human herpesvirus 8-associated Kaposi's sarcoma
Authors: E. BERTI, A.V MARZANO, I. DECLEVA, G. BESTETTI, M. PIZZUTO, L. POIREL, M. CAPRA, C. PARRAVICINI, M. CORBELLINO
Journal: British Journal of Dermatology (1997)

We report the simultaneous occurrence of Kaposi's sarcoma (KS) and primary cutaneous B-cell lymphoma (CBCL) of the leg in a 79-year-old woman, seronegative for HIV-1, HTLV-1 and HTLV-2. The CBCL underwent complete clinical remission after local radiotherapy, whilst the KS became disseminated within a year following diagnosis. However, 2 years after the diagnosis of KS, the patient died with neurological symptoms. These were presumed to be due to involvement of the central nervous system by lymphoma, although in the absence of an autopsy, this could not be proven. Skin biopsies from the original KS and CBCL lesions, as well as short-term culture of spindle cells from the KS lesion and peripheral blood mononuclear cells (PBMC), were studied by semiquantitative polymerase chain reaction (PCR) using primers specific for DNA sequences of a novel gamma-herpesvirus-8 (HHV-8). PCR studies were strongly positive for the virus on KS cells and PBMC; conversely, a low viral load was found on CBCL cells. A high titre of serum IgG antibodies reacting with the nuclei of the HHV-8 positive cell line BCP-1 was found. These data suggest that reactivation of latent infection with HHV-8 had occurred in this patient, and that HHV-8 is directly involved in KS, but not in CBCL of the leg, an aggressive variant of CBCL.
Hepatic Veno-occlusive Disease Associated with Renal Transplantation and Azathioprine Therapy
Authors: ALEXANDRA E. READ
Journal: Annals of Internal Medicine (1986)

Four patients with renal transplants developed hepatic veno-occlusive disease after immunosuppressive therapy with azathioprine. Severe progressive portal hypertension developed in all patients, with the clinical presentation varying from a mild viral-like syndrome to rapidly fulminant liver failure and death. The disease was associated with cytomegalovirus infection but not with the dose of azathioprine, the type or duration of transplant, or the type of underlying kidney disease. In view of the high mortality rate associated with veno-occlusive disease (a combined 55% in our four patients and in five reported in the literature) and wide spectrum of clinical presentation in patients with renal transplants, a high index of suspicion is required and aggressive intervention indicated.
Heparin-enhanced plasma phospholipase A2 activity and prostacyclin synthesis in patients undergoing cardiac surgery.
Authors: H Nakamura, D K Kim, D M Philbin, M B Peterson, F Debros, G Koski, J V Bonventre
Journal: Journal of Clinical Investigation (1995)

Although eicosanoid production contributes to physiological and pathophysiological consequences of cardiopulmonary bypass (CPB), the mechanisms accounting for the enhanced eicosanoid production have not been defined. Plasma phospholipase A2 (PLA2) activity, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), and thromboxane B2 (TXB2) levels were measured at various times during cardiac surgery. Plasma PLA2 activity increased after systemic heparinization, before CPB. This was highly correlated with concurrent increases in plasma 6-keto-PGF1 alpha, TXB2 concentrations did not increase with heparin administration but did increase significantly after initiation of CPB. High plasma PLA2 activity, 6-keto-PGF1 alpha, and TXB2 concentrations were measured throughout the CPB period. Protamine, administered to neutralize the heparin, caused an acute reduction of both plasma PLA2 activity and plasma 6-keto-PGF1 alpha, but no change in plasma TXB2 concentrations. Thus the ratio of TXB2 to 6-keto-PGF1 alpha increased significantly after protamine administration. Enhanced plasma PLA2 activity was also measured in patients with lower doses of heparin used clinically for nonsurgical applications. Human plasma PLA2 was identified as group II PLA2 by its sensitivity to deoxycholate and dithiothreitol, its substrate specificity, and its elution characteristics on heparin affinity chromatography. Heparin addition to PMNs in vitro resulted in dose-dependent increases in cellular PLA2 activity and release of PLA2. The PLA2 released from the PMN had characteristics similar to those of post-heparin plasma PLA2. In conclusion, plasma PLA2 activity and 6-keto-PGF1 alpha concentrations are markedly enhanced with systemic heparinization. Part of the anticoagulant and vasodilating effects of heparin may be due to increased plasma prostacyclin (PGI2) levels. In addition the pulmonary vasoconstriction sometimes associated with protamine infusion during cardiac surgery might be due to decreased plasma PLA2 activity, with an associated increased TXB2/6-keto-PGF1 alpha ratio.
Personalised chemotherapy based on tumour marker decline in poor prognosis germ-cell tumours (GETUG 13): a phase 3, multicentre, randomised trial
Authors: Karim Fizazi, Lance Pagliaro, Agnes Laplanche, Aude Fléchon, Josef Mardiak, Lionnel Geoffrois, Pierre Kerbrat, Christine Chevreau, Remy Delva, Frederic Rolland, Christine Theodore, Guilhem Roubaud, Gwenaëlle Gravis, Jean-Christophe Eymard, Jean-Pierre Malhaire, Claude Linassier, Muriel Habibian, Anne-Laure Martin, Florence Journeau, Maria Reckova, Christopher Logothetis, Stephane Culine
Journal: The Lancet Oncology (2014)
Coagulation activation induced by fibrinolytic therapy is blunted by the combination of a low-dose fibrinolytic and a platelet glycoprotein IIb/IIIa inhibitor: The GUSTO V Italian hematologic substudy
Authors: Piera Angelica Merlini, Diego Ardissino, Annamaria Andreoli, Silvio Ricci, Alessandra Repetto, Alessandro Lombardi, Ospedale Niguarda
Journal: Journal of the American College of Cardiology (2003)
Medical Student Abuse
Authors: Ralph D. Caldroney
Journal: JAMA (1984)

<h3>To the Editor.—</h3> Drs Rosenberg and Silver<sup>1</sup>in their COMMENTARY on medical student abuse have brought to an open forum a problem that has long been an embarrassment to those of us ensconced in academia. It is difficult to take issue with any of their central points. The problem does exist and doubtless occurs in each and every medical school. While the hair on the backs of the neck of many an academician was undoubtedly raised while reading this article, a vituperative response offers no hope for a balanced reply. Therefore, as my mother taught me, I have counted to ten and my gastrin level has returned to baseline. I feel I can safely proceed and respond to this gauntlet tossed down. Two points disturb me about this article. The first is quite simple. What is the scope of the problem? Is this a rare occurrence, as I suspect, or
Evaluation of Amniotic Membrane Transplantation as an Adjunct to Medical Therapy as Compared with Medical Therapy Alone in Acute Ocular Burns
Authors: Amol Tamhane, Rasik B. Vajpayee, Nihar R. Biswas, Ravindra M. Pandey, Namrata Sharma, Jeewan S. Titiyal, Radhika Tandon
Journal: Ophthalmology (2005)