tbuckley/cabot-search huggingface dataset:
The ‘stable/unstable’ chronic isolated anterior syndesmotic injury: A presentation of three cases and a new surgical technique
Authors: L Laver, S Massarwa, G Mann, O Mei-Dan, G Maoz, M Nyska
Journal: British Journal of Sports Medicine (2011)

Background Isolated syndesmotic injuries are reported to comprise 1–11% of all ankle sprains. This number may increase to more than 40% in those involved in high contact and collision sports. These injuries are frequently under-diagnosed often being mistaken for the more common lateral ankle sprains and are inadequately treated as a result, leading to chronic syndesmotic instability. When instability can be objectively documented with clinical and radiographic measures it is defined as mechanical instability. When it is only based on clinical symptoms, it is defined as functional. Symptoms vary from long standing pain, stiffness, recurrent swelling and an instability sensation without actual giving way or mechanical correlation. It may lead often to functional disability and substantial activity restriction. Imaging of the instability may be performed by dynamic ultrasound. However if there is no instability proven in imaging, the surgical decision to explore the syndesmosis is problematic. Proven pathology in the syndesmosis in MRI or CT may serve as relative indication for operation. Surgical options for chronic anterior syndesmotic proven instability include combinations of debridement, ligamentoplasty with varying graft options, syndesmotic screw fixation, translation osteotomy of AITFL insertion and arthroscopic debridement with graft reconstruction and screw fixation – with most techniques reporting satisfying results. There are no clear indications of surgical approach to stable syndesmotic injury. Setting, participants and methods We present three cases of chronic anterior syndesmotic instability suffering from chronic pain and instability sensation, all of which were stable upon radiographic evaluation including Dynamic US examination. MRI disclosed pathology in the anterior synsesmosis – with mainly scar tissue present. All three cases were operated and proven unstable upon in-operative mechanical examination after debridement of the scar tissue. The anterior syndesmosis was reconstructed using figure of eight suturing of the Chaput process to the anterior Fibula. In 6–18 months followup the patients recovered from their symptoms and returned to full activity. Results and conclusions In cases of stable symptomatic syndesmosis injuries there is indication for exploration of the anterior syndesmosis and stabilization if proven unstable.
Effects of the stress response in septic rats and LPS-stimulated alveolar macrophages: evidence for TNF-alpha posttranslational regulation.
Authors: S P Ribeiro, J Villar, G P Downey, J D Edelson, A S Slutsky
Journal: American Journal of Respiratory and Critical Care Medicine (1996)

We have previously demonstrated that induction of the stress response, by heat stress or sodium arsenite, administered 18 h before initiation of sepsis in rats, significantly decreased mortality and lung injury. As a possible mechanism underlying this effect, we hypothesized that the induction of the stress response, prior to bacterial endotoxin (lipopolysaccharide, LPS) stimulation, would cause a decrease in synthesis and/or release of tumor necrosis factor-alpha (TNF-alpha), making the animals more resistant to sepsis. Rats exposed to Salmonella typhosa LPS demonstrated a rise in plasma TNF-alpha. In contrast, rats exposed to heat stress or to sodium arsenite 18 h prior to LPS had significantly lower levels of plasma TNF-alpha. To examine the mechanisms by which the stress response mediates this decrease, we studied cultured alveolar macrophages. Similar to in vivo studies, TNF released into supernatants of alveolar macrophages treated with LPS was significantly higher than from cells exposed to the stress response prior to LPS. The decrease in TNF-alpha protein release was not accompanied by a similar decrease in TNF-alpha mRNA levels or by a decrease in cell-associated TNF-alpha, suggesting possible posttranslational regulation of TNF-alpha. To determine whether the decrease in TNF-alpha release was due to binding and sequestration by heat shock proteins (HSP), TNF-alpha was purified by immunoprecipitation. Under these conditions, TNF-alpha and HSP72kDa coprecipitated from cells that had received stress treatment prior to LPS. These data implicate HSP in posttranslational control of TNF-alpha release in LPS-stimulated alveolar macrophages exposed to the stress response.
Review: Contemporary oral contraceptives are associated with venous thromboembolism and stroke
Authors: Thomas DeLoughery
Journal: Annals of Internal Medicine (2013)

Source Citation Peragallo Urrutia R, Coeytaux RR, McBroom AJ, et al. Risk of acute thromboembolic events with oral contraceptive use: a systematic review and meta-analysis. Obstet Gynecol. 2013;122:380-9. 23969809
Antibody to human follicle-stimulating hormone: cross-reactivity with three other hormones
Authors: Sheldon Schlaff, Saul W. Rosen, Jesse Roth
Journal: Journal of Clinical Investigation (1968)

Antibodies directed against human follicle-stimulating hormone (FSH) were demonstrated in rabbit serum by neutralization of biological activity. Antibodies that bound FSH-(131)I were produced in rabbits and guinea pigs by repeated injections of FSH. By (131)I immunochemical methods, we found that at least 90% of the FSH-(131)I-binding antibody failed to distinguish the four human glycoprotein hormones: FSH, luteinizing hormone, chorionic gonadotropin, and thyrotropin, purified as well as endogenous hormone in plasma. Neither growth hormone, adrenocorticotropin, nor a variety of glycoproteins or animal plasmas were able to react with these antibodies.
The Small GTPase Rac2 Controls Phagosomal Alkalinization and Antigen Crosspresentation Selectively in CD8+ Dendritic Cells
Authors: Ariel Savina, Audrey Peres, Ignacio Cebrian, Nuno Carmo, Catarina Moita, Nir Hacohen, Luis F. Moita, Sebastian Amigorena
Journal: Immunity (2009)
Dispersion of ventricular repolarization and arrhythmia: study of two consecutive ventricular premature complexes.
Authors: C S Kuo, H Atarashi, C P Reddy, B Surawicz
Journal: Circulation (1985)

The effect of two consecutive ventricular premature stimuli (S1S2) during atrial pacing on dispersion of repolarization and inducibility of ventricular arrhythmias was studied in 16 dogs under control conditions and in four dogs in the presence of an increased dispersion of repolarization during atrial pacing induced by general hypothermia and regional warm blood perfusion via selective cannulation of the distal branch of left anterior decending coronary artery. Dispersion of repolarization was measured as the maximal difference between the ends of six simultaneously recorded monophasic action potentials (MAPs) from anterior ventricular surface, and consisted of MAP duration difference and activation time difference. Dispersion of repolarization during atrial pacing at control was 29 +/- 7 msec (activation time difference 4 +/- 6 msec, MAP duration difference 25 +/- 8 msec), that after S1 at paraseptal the site was 81 +/- 8 msec (activation time difference 73 +/- 12 msec, MAP duration difference 8 +/- 5 msec), and that after S1S2 was 148 +/- 27 msec (activation time difference 103 +/- 21, MAP duration difference 44 +/- 26 msec). Neither S1 nor S1S2 induced ventricular arrhythmia. Hypothermia and regional warm blood reperfusion increased dispersion of repolarization during atrial pacing to 70 +/- 22 msec (activation time difference 9 +/- 3 msec, MAP duration difference 61 +/- 19 msec). During hypothermia and regional warm blood reperfusion, S1 produced a dispersion of repolarization of 149 +/- 29 msec (activation time difference 85 +/- 8 msec, MAP duration difference 64 +/- 23 msec) and did not induce ventricular arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)
Pseudopseudo-Darnell's Sign
Authors: MICHAEL A. LACOMBE
Journal: Annals of Internal Medicine (1976)

Comments1 September 1976Pseudopseudo-Darnell's SignMICHAEL A. LACOMBE, M.D.MICHAEL A. LACOMBE, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-85-3-403_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Always on the lookout for new and exciting eponyms (1), I was overjoyed to read of Darnell's sign, that is, "new blue garment pseudo-acrocyanosis syndrome" in the May issue (Ann Intern Med 84:617, 1976). I had recently seen, without knowing it, a case of Darnell's disease with a negative Darnell's sign. This man had wiped his face, in the heat of day, with his "new, blue T-shirt" while coming to the hospital for a sprain. Fortunately, a perceptive nurse pointed out the noncyanotic hands (negative Darnell's sign) and the shirt while I was busily ordering blood gases, oxygen,...Reference1. LACOMBE M: Conn's last words on Conn's sign. Ann Intern Med 75:976-977, 1971 LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 September 1976Volume 85, Issue 3Page: 403-403KeywordsBloodNursesOxygen Issue Published: 1 September 1976 PDF DownloadLoading ...
Antiproliferative effects on keratinocytes of a range of clinically used drugs with calmodulin antagonist activity
Authors: S. MACNEIL, K.A. DAWSON, G. CROCKER, W.F.G. TUCKER, B. BITTINER, J.G. SINGLETON, T. HUNTER, D.F. TJERNEY
Journal: British Journal of Dermatology (1993)

Thirty-two drugs, including some in use for a variety of clinical disorders, were examined for their ability to inhibit calmodulin activity in vitro. From these, 10 drugs were selected for their inhibition of calmodulin activity and examined for their ability to inhibit proliferation of rapidly dividing human keratinocytes. A significant correlation between antiproliferative activity and calmodulin antagonist potency was found. Of these drugs there were several, including miconazole, dequalinium chloride, bromocriptine and tamoxifen, whose use is well established and well documented. The potential use of these drugs (and others identified in this way) as antipsoriatic agents is discussed.
Peptic ulcer in India and Bangladesh.
Authors: F Tovey
Journal: Gut (1979)

Progress reportPeptic ulcer in India and Bangladesh Historical backgroundAlthough gastric ulcer was known in the United Kingdom in the 19th century, duodenal ulcer did not become a clinical problem until the beginning of this century.It is not surprising therefore that earlier medical records in India do not mention duodenal ulcer and it is difficult to know whether it is truly a disease of this century"2 or that previously cases were missed because of lack of diagnostic awareness.In the famine years 1877-78 in Madras, Porter in a series of 381 necropsies reports only one gastric ulcer in an old woman, but in 1905 Niblock3 was reporting operations for pyloric stenosis and said that cases had been seen since 1890.By 1924 Bradfield4,5 was able to report 226 operations for one year for peptic ulcer in Madras.An apparent increase was occurring in Calcutta, where the prevalence of duodenal ulcer in 1000 necropsies in 19146 was 0 4% and in 1925 had risen to 0 9% in 1600 necropsies7.Other reports8-14 confirm the rising recognition of duodenal ulcer in the south and in Bengal.Reports from the Punjab, however, com- mented on its rarity.White in 189215 reported his surprise at finding a perforated duodenal ulcer on necropsy and Hallilay in 192416 commented on the absence of peptic ulcer in Punjabi soldiers. Present situationDuodenal ulceration constitutes the major problem in the high incidence areas and consequently much more information is available about duodenal ulcer than gastric ulcer.As a result, this report concentrates on the occurrence of duodenal ulcer and mostly mentions gastric ulcer as it relates to duodenal ulceration.Prepyloric ulcers are uncommon and are included with duodenal ulcers.Concomitant duodenal and gastric ulcers are discussed separately. Geographical distribution of duodenal ulcerIn a vast, developing country like India it is impossible to obtain exact figures of disease incidence.In determining the distribution of a given disease the picture has to be built up by assessing reports from a variety of sources such as the opinions of experienced workers, necropsy reports, the opinions or figures of radiologists, hospital admission, or operation figures.Weight has to be given to actual figures when available, as distinct from clinical impressions, bearing in mind the fallacies of selection in all hospital figures.However, when information from a certain area points consistently to a high incidence and from another area with equal facilities to a low incidence, it can be regarded as significant.By illustration, in 1973 a rural hospital of 700 beds at Kumudini near Dacca was having 70 positive barium meals a week 329 on July 14,
Moving Ahead With Health Care System Reform
Authors: John D. Rockefeller
Journal: JAMA (1995)

For those of us who are committed to passing health care system reform legislation, the new year and new Congress will bring many changes and challenges. One problem we will confront is a proposal to redirect Medicare and Medicaid spending to help pay down the federal deficit, rather than to pay for health care system reform. Most of the comprehensive health care system reform bills of the last 2 years relied on reductions in projected spending of these two federal health programs. Savings from Medicare were to be used to finance additional Medicare benefits, such as prescription drugs, a home care program for disabled people of all ages, low-income subsidies, and, in some cases, even deficit reduction. Medicaid savings were generally to be used to pay for health care coverage for low-income families. The basic idea was that we could responsibly limit Medicare and Medicaid spending if we also expanded
Intestinal absorption and enterohepatic cycling of biliary iron originating from plasma non-transferrin-bound iron in rats
Authors: P Brissot, U Bolder, C D Schteingart, J Arnaud, A F Hofmann
Journal: Hepatology (1997)

In iron overload, non-transferrin-bound iron (NTBI) is found in plasma and is rapidly removed by hepatocytes. Some of this NTBI is excreted into bile. Biliary excretion of NTBI, in the form of an iron-deferiprone chelate, is greatly increased by deferiprone, an iron chelator. The aim of this study was to test whether biliary iron as such or as an iron-deferiprone chelate (both originating from plasma NTBI) is absorbed from the intestine and re-secreted into bile. In healthy biliary fistula (donor) rats, biliary 55Fe originating from plasma NTBI was obtained by injecting Fe citrate (to saturate transferrin) followed by 55Fe. This biliary 55Fe was infused into the duodenum of (recipient) rats whose transferrin was saturated or unsaturated. Similar experiments were performed using iron-overloaded (donor) rats given deferiprone, followed by infusion of the biliary 55Fe-deferiprone chelate into iron-overloaded (recipient) rats. The results show that in healthy (recipient) rats, duodenal infusion of 55Fe from NTBI was followed by increased plasma 55Fe when transferrin was unsaturated, or by biliary excretion of 55Fe when transferrin was saturated, indicating intestinal absorption of 55Fe. In iron-overloaded rats, neither plasma nor bile became radioactive, indicating no intestinal absorption of iron from the deferiprone chelate. We conclude that biliary iron, originating from NTBI, is absorbed from the intestine, and undergoes enterohepatic circulation if transferrin is saturated. In iron-overloaded rats, biliary iron originating from plasma NTBI and present as an iron-deferiprone chelate in bile is not absorbed.
Update in Allergy and Immunology
Authors: John J. Condemi
Journal: Annals of Internal Medicine (1996)

Updates from the Annual Session1 November 1996Update in Allergy and ImmunologyJohn J. Condemi, MDJohn J. Condemi, MDFrom Allergy Asthma Immunology of Rochester, Rochester, New York.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-125-9-199611010-00008 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Advances in allergy and immunology have focused on four major areas. First, careful questioning of patients continues to be the best “test” to uncover the cause of idiopathic urticaria and anaphylaxis, but an interesting and previously unsuspected association has been found between chronic urticaria and thyroid disease. Second, research has focused on identifying the relevant antibody of the antiphospholipid antibody syndrome. Third, the use of steroids in asthma may have variable effects, depending on when the steroids are used. Finally, the results of one study may help physicians identify and treat a subgroup of patients with the chronic fatigue syndrome.... References1. Leznoff A, Josse RG, Denburg J, Dolovich J. Association of chronic urticaria and angioedema with thyroid autoimmunity. Arch Dermatol. 1983; 119:636-40. Google Scholar2. Wong S, Dykewicz MS, Patterson R. Idiopathic anaphylaxis. A clinical summary of 175 patients. Arch Intern Med. 1990; 150:1323-8. Google Scholar Author, Article, and Disclosure InformationAffiliations: From Allergy Asthma Immunology of Rochester, Rochester, New York.Corresponding Author: John J. Condemi, MD, Allergy Asthma Immunology of Rochester, 919 Westfall Road, Building B, Rochester, NY 14618.Current Author Addresses: Dr. Condemi: Allergy Asthma Immunology of Rochester, 919 Westfall Road, Building B, Rochester NY 14618. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByChronic Urticaria: Review of the Literature 1 November 1996Volume 125, Issue 9Page: 744-750KeywordsAllergy and immunologyAnaphylaxisAntiphospholipid syndromeChronic fatigue syndromeFoodLatexLupus erythematosusThrombosisThyroidUrticaria Issue Published: 1 November 1996 CopyrightCopyright © 1996 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
THE ACUTE EFFECTS IN MAN OF A RAPID INTRAVENOUS INFUSION OF HYPERTONIC SODIUM BICARBONATE SOLUTION. II. CHANGES IN RESPIRATION AND OUTPUT OF CARBON DIOXIDE 1
Authors: R. B. Singer, R. C. Deering, J. K. Clark
Journal: Journal of Clinical Investigation (1956)

It is generally agreed that in metabolic acidosis respiration is stimulated, with consequent reduc- tion of alveolar and arterial CO2 pressure, Pco2; in metabolic alkalosis, however, there has been disagreement as to whether or not there is a cor- responding respiratory inhibition, with elevation of Pco2.Evidence that such inhibition does oc- cur has been presented in several reports (1-4); on the other hand, some investigators have found no significant change in Pco2 (5).Opportunity for the collection of further evidence on this ques- tion was afforded by a series of studies on the ef- fects of acute metabolic alkalosis induced in hu- man subjects by the infusion of hypertonic sodium bicarbonate solution, approximately 2.3 mEq.per kilogram of body weight.The first paper of this series (6) described the ionic transfers as observed in arterial or cutaneous blood, and calculated for extracellular and other body fluid compartments, including the volume of distribution of the excess sodium bicarbonate.The plasma acid-base data from these experiments readily permit the calcu- lation of arterial Pco2, before, during, and for two hours following the infusion.We consider the changes in calculated arterial Pco2 to repre- sent the most reliable index of respiratory changes, because this sampling method produced the least disturbance to respiration.However, we are also reporting in this, the second paper of the series, results of additional experiments in which alveolar Pco2, total pulmonary ventilation, and respiratory
Production and cytokine-mediated regulation of monocyte chemoattractant protein-1 by human proximal tubular epithelial cells
Authors: Wiguno Prodjosudjadi, Jort S.J. Gerritsma, Ngaisah Klar-Mohamad, Arnout F. Gerritsen, Jan A. Bruijn, Mohamed R. Daha, Leendert A. van ES
Journal: Kidney International (1995)
Plasma miRNA (miR: microribonucleic acid) Levels in Patients with Decompensated Heart Failure: Can miRNA Be an Indicator of the Effectiveness of the Treatment?
Authors: Ahmet Sayın, Murat Bilgin, Burcu Zihni, Mustafa Beyazıt Alkan, Hatice Soner Kemal, İlker Gül, Bekir Serhat Yıldız, İsmihan Merve Tekin, Cumhur Gündüz, Mehdi Zoghi
Journal: Journal of the American College of Cardiology (2013)
Poorly Controlled Cardiovascular Risk Factors and ICD-9-CM Codes
Authors: James S. Kennedy
Journal: Annals of Internal Medicine (2006)

Letters5 September 2006Poorly Controlled Cardiovascular Risk Factors and ICD-9-CM CodesJames S. Kennedy, MDJames S. Kennedy, MDFrom FTI Cambio Health Solutions, Brentwood, TN 37027.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-145-5-200609050-00019 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR: The article by Rodondi and colleagues (1) on therapy modification in response to poorly controlled cardiovascular risk factors ignores the reality that the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) classifies patients with “poorly controlled” cardiovascular risk factors as “well controlled.” Accordingly, physicians using such terms as poorly controlled to describe their uncontrolled, diabetic, hypertensive, and hyperlipidemic patients must have their records coded as “well controlled,” since ICD-9-CM requires strict interpretation of physician diagnosis assignment. Similarly, patients with “hypertensive emergency” and “hypertensive crisis” will be coded as having well-controlled hypertension by ICD-9-CM unless the physician ...Reference1. Rodondi N, Peng T, Karter AJ, Bauer DC, Vittinghoff E, Tang S, et al. Therapy modifications in response to poorly controlled hypertension, dyslipidemia, and diabetes mellitus. Ann Intern Med. 2006;144:475-84. [PMID: 16585661] LinkGoogle Scholar Author, Article, and Disclosure InformationAuthors: James S. Kennedy, MDAffiliations: From FTI Cambio Health Solutions, Brentwood, TN 37027.Disclosures: None disclosed. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoTherapy Modifications in Response to Poorly Controlled Hypertension, Dyslipidemia, and Diabetes Mellitus Nicolas Rodondi , Tiffany Peng , Andrew J. Karter , Douglas C. Bauer , Eric Vittinghoff , Simon Tang , Daniel Pettitt , Eve A. Kerr , and Joe V. Selby Poorly Controlled Cardiovascular Risk Factors and ICD-9-CM Codes Nicolas Rodondi , Eve A. Kerr , and Joe V. Selby Metrics 5 September 2006Volume 145, Issue 5Page: 394KeywordsCardiovascular therapyConflicts of interestDatabasesHypertensionMedical risk factorsMedicare ePublished: 5 September 2006 Issue Published: 5 September 2006 Copyright & PermissionsCopyright © 2006 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Ornithine Transcarbamylase Deficiency: Adult Onset of Severe Symptoms
Authors: James M. Gilchrist, Rosalind A. Coleman
Journal: Annals of Internal Medicine (1987)

Deficiency of ornithine transcarbamylase, an enzyme in the urea cycle, results in hyperammonemia. The X-linked recessive inheritance results in neonatal death of affected males but a variable symptomatic pattern in females, with onset of symptoms in childhood. We report the cases of two heterozygous women with onset of severe symptoms (encephalopathy and focal neurologic deficits) in adulthood.