tbuckley/cabot-search huggingface dataset:
Expression of a cut-related homeobox gene in developing and polycystic mouse kidney
Authors: Gregory B. Vanden Heuvel, Rolf Bodmer, Kevin R. McConnell, Glenn T. Nagami, Peter Igarashi
Journal: Kidney International (1996)

Cut is a diverged homeobox gene that is essential for normal development of the Malpighian tubules in Drosophila melanogaster. Homologues of Drosophila cut that encode transcriptional repressors have been identified in several mammalian species and cell lineages. We examined the expression of a murine cut homologue (named Cux-1) in the developing mouse using Northern blot analysis and in situ hybridization. At 12.5 d.p.c. and 13.5 d.p.c., Cux-1 was highly expressed in a subset of embryonic tissues, including the developing metanephros. Within the metanephros, Cux-1 was expressed in the nephrogenic zone including both mesenchymal cells (uninduced and condensed mesenchyme) and epithelial cells (ureteric buds, renal vesicles, S-shaped bodies). During later stages of nephrogenesis, Cux-1 was down-regulated such that there was minimal expression in mature glomeruli and tubules. In addition, Cux-1 was detected in the mesonephros, mesonephric duct, and bladder. Expression of Cux-1 was also examined in polycystic kidneys from C57BL/6J-cpk/ cpk mice. At 21 days of age, Cux-1 was highly expressed in cyst epithelium of polycystic kidneys but was minimally expressed in kidneys from phenotypically normal littermates. These results demonstrate that a cut-related homeobox gene is expressed in the developing kidney and urinary tract of the mouse. Expression of Cux-1 in the kidney is inversely related to degree of cellular differentiation. Cux-1 may encode a transcriptional repressor that inhibits terminally differentiated gene expression during early stages of nephrogenesis.
Luteinizing Hormone Releasing Hormone Analogue Therapy for Central Precocious Puberty
Authors: Florence Comite
Journal: JAMA (1986)

The long-acting analogue of luteinizing hormone releasing hormone, D-Trp6-Pro9-NEt-LHRH (LHRHa), is effective in the short-term treatment of central precocious puberty. We report the results of two to four years of LHRHa therapy in 27 children with this disorder. Secondary sex characteristics regressed in most patients. Sex steroid levels and basal and LHRH-stimulated gonadotropin levels remained suppressed compared with pretreatment values. Linear growth rates decreased from 11.0 +/- 0.8 (SEM) cm/yr before treatment to 5.7 +/- 0.4 cm/yr at two years of treatment and 3.7 +/- 0.7 cm/yr at four years of treatment. Predicted heights by the Bayley-Pinneau method increased from 156.4 +/- 2.0 cm before treatment to 162.3 +/- 2.3 cm at two years and 163.4 +/- 2.4 cm at three years. Five patients treated for four years had a mean increase in predicted height of 5.5 cm. To date no adverse effects have been observed. However, the ultimate safety of this analogue is not known. We conclude that LHRHa appears to be an effective long-term therapy for central precocious puberty.
Neuropathy in latent hereditary hepatic porphyria.
Authors: P Mustajoki, A M Seppalainen
Journal: BMJ (1975)

Peripheral nerve conduction velocoties were measured in 20 patients with acute intermittent porphyria and five with variegate porphyria and in 25 controls matched for age and sex. None of the porphyric patients had acute symptoms on examination, and nine had never had symptoms. Compared with the controls, patients had a significantly slower conduction velocity of the slower motor fibres of the ulnar nerve (P less than 0-001) and a slower sensory conduction velocity of the ulnar and median nerves (P less than 0-05). There was no significant difference between the patients and controls in the maximum motor conductionvelocity of the median, ulnar, deep peroneal, or posterior tibial nerves. Slight peripheral neuropathy seems to be associated with latent hereditary hepatic porphyria, even in patients who have never had symptoms.
Efficacy and Safety of Inhaled Insulin Therapy
Authors: Lorraine Tosiello, Priya Ravi
Journal: Annals of Internal Medicine (2006)

Letters4 April 2006Efficacy and Safety of Inhaled Insulin TherapyLorraine Tosiello, MD and Priya Ravi, MDLorraine Tosiello, MDFrom Overlook Hospital, Summit, NJ 07902.Search for more papers by this author and Priya Ravi, MDFrom Overlook Hospital, Summit, NJ 07902.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-144-7-200604040-00017 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Like many general internists, we have had our interest piqued about inhaled insulin therapy for several years. Because data have eked out slowly, generally through endocrinologic publications and meetings, we were delighted to see the issue addressed recently in “our journal” (1). However, after reading the article, we were disappointed by the design of the study and wonder about the editors' decision to publish it at this particular time.We have 3 concerns about the authors' methods. First, the study was unblinded, which could have introduced conscious and unconscious biases. This shortcoming could have been avoided if ...Reference1. Rosenstock J, Zinman B, Murphy LJ, Clement SC, Moore P, Bowering CK, et al. Inhaled insulin improves glycemic control when substituted for or added to oral combination therapy in type 2 diabetes: a randomized, controlled trial. Ann Intern Med. 2005;143:549-58. [PMID: 16230721] LinkGoogle Scholar Author, Article, and Disclosure InformationAffiliations: From Overlook Hospital, Summit, NJ 07902.Disclosures: None disclosed. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoInhaled Insulin Improves Glycemic Control When Substituted for or Added to Oral Combination Therapy in Type 2 Diabetes Julio Rosenstock , Bernard Zinman , Liam J. Murphy , Stephen C. Clement , Paul Moore , C. Keith Bowering , Rosa Hendler , Shu-Ping Lan , and William T. Cefalu Efficacy and Safety of Inhaled Insulin Therapy Harold Sox Efficacy and Safety of Inhaled Insulin Therapy Julio Rosenstock , Bernard Zinman , Liam J. Murphy , Stephen C. Clement , Paul Moore , C. Keith Bowering , Rosa Hendler , Shu-Ping Lan , and William T. Cefalu Efficacy and Safety of Inhaled Insulin Therapy Balavenkatesh Kanna and Neeti Mishra Metrics Cited byCurrent awareness: Pharmacoepidemiology and drug safety 4 April 2006Volume 144, Issue 7Page: 533KeywordsConflicts of interestHyperinsulinemiaHypoglycemicsInsulinSafetyWeight gain ePublished: 4 April 2006 Issue Published: 4 April 2006 Copyright & PermissionsCopyright © 2006 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Nana’s Words
Authors: Tariq Ahmad
Journal: JAMA (2010)

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
The role of ATP-sensitive potassium channels on DMT1-mediated ferrous iron uptake in SK-N-SH cells
Authors: Xixun Du, Huamin Xu, Ning Song, Hong Jiang, Junxia Xie
Journal: Molecular Neurodegeneration (2012)

Background Elevated iron accumulation has been reported in the substantia nigra (SN) in Parkinson’s disease (PD). Our previous study observed that increased levels of the iron importer divalent metal transporter 1 (DMT1) were involved in this nigral iron accumulation and dopaminergic neurons loss in PD. The iron transport function of DMT1 is also related to the membrane potential level, which increases with hyperpolarization of the cell membrane. Activation of ATP-sensitive potassium (KATP) channels, which could induce hyperpolarization of nigral dopaminergic neurons, is reported to be involved in the selective loss of these neurons in PD. The present study is to investigate whether activation of KATP channels could change the iron uptake function of DMT1. Methods DiBAC4(3) and calcein were used to detect membrane potential and ferrous iron influx. Intracellular iron concentration was measured using an inductively coupled plasma (ICP-2) detector. Mitochondrial transmembrane potential (ΔΨm) and reactive oxygen species (ROS) were measured by flow cytometry using rhodamine123 and H2DCF-DA. Results (1) When treated with diazoxide, a novel KATP channel opener, the membrane potential of SK-N-SH cells showed hyperpolarization. (2) The influx of ferrous iron and the intracellular iron levels were observed dramatically increased when the cells were co-incubated with diazoxide and ferrous iron, resulting in a decreased ΔΨm and an elevated level of ROS production. (3) When treated with diazoxide, cells with DMT1 knockdown showed decreased ferrous iron influx compared with the vector control. (4) When treated with diazoxide, cells overexpressed of SUR1 and Kir6.2 showed increased ferrous iron influx compared with the vector control, which induced a decrease in ΔΨ ma nd an increase in ROS production. Conclusion These results suggest that the activation of the KATP channels could enhance DMT1-mediated ferrous iron uptake, leading to increase intracellular oxidative stress.
Long-term results of related myeloablative stem-cell transplantation to cure sickle cell disease
Authors: Françoise Bernaudin, Gérard Socie, Mathieu Kuentz, Sylvie Chevret, Michel Duval, Yves Bertrand, Jean-Pierre Vannier, Karima Yakouben, Isabelle Thuret, Pierre Bordigoni, Alain Fischer, Patrick Lutz, Jean-Louis Stephan, Nathalie Dhedin, Emmanuel Plouvier, Geneviève Margueritte, Dominique Bories, Suzanne Verlhac, Hélène Esperou, Lena Coic, Jean-Paul Vernant, Eliane Gluckman
Journal: Blood (2007)
MUC1 Oncoprotein Blocks Death Receptor–Mediated Apoptosis by Inhibiting Recruitment of Caspase-8
Authors: Naoki Agata, Rehan Ahmad, Takeshi Kawano, Deepak Raina, Surender Kharbanda, Donald Kufe
Journal: Cancer Research (2008)

Stimulation of the death receptor superfamily induces the activation of caspase-8 and thereby the apoptotic response. The MUC1 oncoprotein is aberrantly overexpressed by diverse human malignancies and inhibits stress-induced apoptosis. The present results show that MUC1 blocks activation of caspase-8 and apoptosis in the response of malignant cells to tumor necrosis factor alpha, tumor necrosis factor-related apoptosis-inducing ligand, and Fas ligand. The results show that MUC1 associates constitutively with caspase-8. The MUC1 cytoplasmic domain (MUC1-CD) binds directly to the caspase-8 p18 fragment upstream to the catalytic Cys(360) site. The results also show that MUC1-CD binds to Fas-associated death domain (FADD) at the death effector domain. In nonmalignant epithelial cells, MUC1 interacts with caspase-8 and FADD as an induced response to death receptor stimulation. The functional significance of these interactions is supported by the demonstration that MUC1 competes with caspase-8 for binding to FADD and blocks recruitment of caspase-8 to the death-inducing signaling complex. These findings indicate that MUC1 is of importance to the physiologic regulation of caspase-8 activity and that overexpression of MUC1, as found in human malignancies, could contribute to constitutive inhibition of death receptor signaling pathways.
RESUSCITATED OUT-OF-HOSPITAL CARDIAC ARREST WITH NO EVIDENCE OF NONCARDIAC CAUSE: POPULATION CHARACTERISTICS AND 30 DAYS OUTCOMES
Authors: Kracht Julien, Ali Farhat, Matthieu Godin, Eric Durand, Fabienne Tamion, Christophe Tron, Brahim Baala, Helene Eltchaninoff
Journal: Journal of the American College of Cardiology (2015)
Paclitaxel- Versus Sirolimus-Eluting Stents for Unprotected Left Main Coronary Artery Disease
Authors: Julinda Mehilli, Adnan Kastrati, Robert A. Byrne, Olga Bruskina, Raisuke Iijima, Stefanie Schulz, Jürgen Pache, Melchior Seyfarth, Steffen Maßberg, Karl-Ludwig Laugwitz, Josef Dirschinger, Albert Schömig
Journal: Journal of the American College of Cardiology (2009)
Cardiac transplantation does not effect ischaemia-induced arrhythmias in rats
Authors: P Guo
Journal: Cardiovascular Research (1999)

Objective: In many species arrhythmias induced by myocardial ischaemia appear to be in part dependent upon cardiac sympathetic nerves. However, previous experiments in rats did not suggest that myocardial or other catecholamines are involved in ischaemic arrhythmogenesis in this species. The aim of this study was to investigate this further using transplanted hearts. Methods: We transplanted ’donated’ hearts onto the abdominal aorta of recipient rats and, at varying periods after transplantation, subjected donated and recipient hearts to occlusion of the left anterior descending (LAD) coronary artery. Donated and recipient hearts were tested at various times after transplantation for responsiveness to drugs acting upon aspects of the autonomic nervous system. The intention of this latter study was to assess the status of innervation and receptors simultaneously in both donated and recipient hearts. Results: Donated (transplanted) hearts showed responses consistent with denervation and receptor supersensitivity. Changes varied with the duration of the transplant. Over the same period recipient hearts did not change in responsiveness to drugs. When subjected to coronary artery occlusion, transplanted hearts responded to occlusion with the same frequency and severity of arrhythmias as recipient and other control hearts, regardless of the duration of transplant, or sensitivity to drugs. Conclusions: The results of these experiments suggest that cardiac innervation is not an important factor in the genesis of ischaemia-induced arrhythmias in rats.
Reversible Unilateral Pulmonary Hypoperfusion Secondary to Mucus Plugs
Authors: RODNEY G. STINNETT, SVEN-OLA HIETALA, MELVIN J. FRATKIN
Journal: Clinical Nuclear Medicine (1977)

Pulmonary arteriolar vasoconstriction and diminished blood flow occurs in response to regional pulmonary hypoxia. Radionuclide perfusion lung scanning may demonstrate the induced ischemia with images that are indistinguishable from those of pulmonary emboli. Our case report of mucus plug bronchial obstruction dramatically illustrates the marked reduction in pulmonary blood flow that may occur with regional hypoxia.
THE BACTERICIDAL VALUES OF SOME WIDELY ADVERTISED ANTISEPTICS.
Authors: F. H. VERHOEFF
Journal: JAMA (1907)

In a brief communication to this journal it was pointed out<sup>1</sup>that if hydrocele fluid is added in sufficient amount to a solution of sodium aurate, protargol or argyrol, although no visible reaction takes place, the bactericidal power of the antiseptic is immediately destroyed. Following a suggestion that this inhibitory action of serum in all probability also held true for all other non-irritating antiseptics, G. S. Derby<sup>2</sup>tested its action on the following silver preparations: Collargol, albargin, ichthargan, argentamin, largin and argonin. In each case he found, as was anticipated, that the antiseptic was rendered ineffective. The importance of this action of serum on an antiseptic will be apparent when it is considered that in penetrating the tissues the antiseptic at once meets with an excess of serum, and hence loses its bactericidal power. In view of the great claims made by manufacturers and others in regard to
Endotoxin Augments Myeloid Dendritic Cell Influx into the Airways in Patients with Allergic Asthma
Authors: Frank Schaumann, Meike Müller, Armin Braun, Birgit Luettig, David B. Peden, Jens M. Hohlfeld, Norbert Krug
Journal: American Journal of Respiratory and Critical Care Medicine (2008)

Epidemiologic studies have shown that exacerbation of asthma is modulated by environmental endotoxin. High levels of endotoxin are associated with asthma symptoms and the current use of asthma medication. However, the underlying mechanisms by which endotoxin modulates asthma are not completely understood.The aim of the study was to test whether endotoxin enhances the response of individuals with allergic asthma to allergen, and to determine if this interaction is associated with increased numbers of antigen-presenting cells in the airways.Seventeen subjects with mild allergic asthma underwent segmental challenge with allergen, endotoxin, and the combination of both in three different lung segments via bronchoscopy. The cellular influx including monocytes, myeloid dendritic cells (mDCs), and plasmacytoid dendritic cells (pDCs), as well as the level of cytokines, were assessed in bronchoalveolar lavage fluid obtained 24 hours after segmental challenge. Monocytes, mDCs, and pDCs were isolated and their capacity to induce T cell proliferation was determined.Endotoxin enhanced the cellular response to allergen. The combination of allergen and endotoxin resulted in increased numbers of total cells, lymphocytes, neutrophils, eosinophils, monocytes, and mDCs, as well as increased levels of lipopolysaccharide-binding protein, IL-1alpha, IL-6, and tumor necrosis factor-alpha in the bronchoalveolar lavage fluid compared with allergen alone. Isolated mDCs but not pDCs induced a strong T cell proliferation in vitro.Endotoxin augments the allergic inflammation in the lungs of individuals with asthma, and induces an enhanced influx of monocytes and functionally active antigen-presenting mDCs into the respiratory tract.
Mortality Associated With Use of IUDs
Authors: Henry S. Kahn
Journal: JAMA (1975)

Five deaths associated with the use of an intrauterine contraceptive device (IUD) were reported during the first half of 1973 through a nationwide mail survey of physicians whose practices were likely to be involved with intrauterine contraception. Four of the five reported deaths involved serious infections, and two of these four occurred in relation to a pregnancy. Use of an IUD prior to death ranged from seven months to 3 1/2 years. The mortality attributable to IUDs is estimated to be lower than that attributable to combination oral contraceptives.
Detrimental effect of fractalkine on myocardial ischaemia and heart failure
Authors: Wanling Xuan, Yulin Liao, Baihe Chen, Qiaobing Huang, Dingli Xu, Yili Liu, Jianping Bin, Masafumi Kitakaze
Journal: Cardiovascular Research (2011)

Fractalkine (FKN) is a newly identified membrane-bound chemokine; its role in myocardial ischaemia and heart failure is largely unknown. We attempted to investigate the role of FKN in myocardial ischaemia and ischaemia or pressure overload-induced ventricular remodelling and heart failure. FKN-induced changes of heart failure-related genes in cultured rat cardiac cells and the effect of FKN on cultured cardiomyocyte injury during anoxia/reoxygenation (A/R) were examined. The direct influence of FKN neutralization on heart failure and the potential mechanism was also investigated. In mice with failing hearts, myocardial FKN expression was correlated with the lung weight/body weight ratio, left ventricular fractional shortening, and brain natriuretic peptide expression. In cultured rat cells, exposure to FKN increased natriuretic peptide A expression in cardiomyocytes, matrix metalloproteinase-9 expression in fibroblasts, and intercellular adhesion molecule-1 expression in microvascular endothelial cells. FKN also promoted cardiomyocyte damage during A/R and neutralizing FKN antibody treatment improved heart failure induced by myocardial infarction or pressure overload. Neutralizing FKN or its receptor inhibited the activation of mitogen-activated protein kinases (MAPKs) in hypoxic cardiomyocytes or ischaemic myocardium. FKN promotes myocardial injury and accelerates the progress of heart failure, which is associated with the activation of MAPKs.
Sterol Balance in Man as Plasma Cholesterol Concentrations Are Altered by Exchanges of Dietary Fats*
Authors: Norton Spritz, E. H. Ahrens, Scott Grundy
Journal: Journal of Clinical Investigation (1965)

The term fecal steroid is used in preference to sterol because of the significant amounts of ketonic metabolites of cholesterol that invariably are present in neutral and acidic fractions.
The growth of acute kidney injury: a rising tide or just closer attention to detail?
Authors: Edward D. Siew, Andrew Davenport
Journal: Kidney International (2014)

Acute kidney injury (AKI), previously termed acute renal failure, is associated with increased mortality, prolonged hospital stay, and accelerated chronic kidney disease (CKD). Over the past 2 decades, dramatic rises in the incidences of AKI have been reported, particularly within the United States. The question arises as to whether these changes reflect actual increases in disease incidence, or are potentially explained by the introduction of consensus definitions that rely on small standardized changes in serum creatinine, changes in coding and reimbursement, or increasingly available and more liberal use of dialysis. In this review, we explore the secular trends in AKI incidence in North America and Western Europe and its potential contributors.
Optical Coherence Tomography for the Monitoring of Neovascular Age-Related Macular Degeneration
Authors: Mayret M. Castillo, Graham Mowatt, Andrew Elders, Noemi Lois, Cynthia Fraser, Rodolfo Hernández, Winfried Amoaku, Jennifer M. Burr, Andrew Lotery, Craig R. Ramsay, Augusto Azuara-Blanco
Journal: Ophthalmology (2014)
Myocardial Infarction in the Third Trimester of Pregnancy
Authors: Eli Shapiro
Journal: JAMA (1962)

MYOCARDIAL INFARCTION in pregnancy is a rare phenomenon. At least 12 well-documented cases can be found in the literature. Ten others have been reported, and probably a good number of these were diagnosed correctly, but the proof in these instances seems somewhat less convincing. Other reports discuss 8 patients who have become pregnant after having sustained a myocardial infarction. Of the above-mentioned 30 patients, 8 died and 22 survived (table). In all instances when the patient survived the first 2 days after a myocardial a myocardial infarction, the patient survived the delivery. A patient recently treated at the Massachusetts Memorial Hospitals illustrates this principle.    Report of a Case  A 33-year-old pregnant woman was admitted to this hospital on April 25, 1960, immediately after the onset of vise-like substernal chest pain radiating down the left arm. The pain occurred at the start of a lukewarm shower bath. It was associated with
O33 SVR AND SAFETY OF LOWER DOSES OF MK-5172 25 mg AND 50 mg DAILY FOR 12 WEEKS IN HCV GENOTYPE (G)1 TREATMENT-NAIVE NON-CIRRHOTIC PATIENTS
Authors: M. Lagging, A. Brown, O.R. Weiland, P. Mantry, A. Ramji, F. Weilert, J.M. Vierling, J. Talaty, I.N. Gendrano, P. Hwang, B. Zhang, J. Wahl, M. Robertson, N. Mobashery
Journal: Journal of Hepatology (2014)