Px Code Procedure Description Unit Price 11000001 Room & Board
Total Page：16
File Type：pdf, Size：1020Kb
Load more
Recommended publications
-
Factor XIII and Fibrin Clot Properties in Acute Venous Thromboembolism
International Journal of Molecular Sciences Review Factor XIII and Fibrin Clot Properties in Acute Venous Thromboembolism Michał Z ˛abczyk 1,2 , Joanna Natorska 1,2 and Anetta Undas 1,2,* 1 John Paul II Hospital, 31-202 Kraków, Poland; [email protected] (M.Z.); [email protected] (J.N.) 2 Institute of Cardiology, Jagiellonian University Medical College, 31-202 Kraków, Poland * Correspondence: [email protected]; Tel.: +48-12-614-30-04; Fax: +48-12-614-21-20 Abstract: Coagulation factor XIII (FXIII) is converted by thrombin into its active form, FXIIIa, which crosslinks fibrin fibers, rendering clots more stable and resistant to degradation. FXIII affects fibrin clot structure and function leading to a more prothrombotic phenotype with denser networks, characterizing patients at risk of venous thromboembolism (VTE). Mechanisms regulating FXIII activation and its impact on fibrin structure in patients with acute VTE encompassing pulmonary embolism (PE) or deep vein thrombosis (DVT) are poorly elucidated. Reduced circulating FXIII levels in acute PE were reported over 20 years ago. Similar observations indicating decreased FXIII plasma activity and antigen levels have been made in acute PE and DVT with their subsequent increase after several weeks since the index event. Plasma fibrin clot proteome analysis confirms that clot-bound FXIII amounts associated with plasma FXIII activity are decreased in acute VTE. Reduced FXIII activity has been associated with impaired clot permeability and hypofibrinolysis in acute PE. The current review presents available studies on the role of FXIII in the modulation of fibrin clot properties during acute PE or DVT and following these events. -
Comparative Proteomic Analysis Revealed Complex Responses To
www.nature.com/scientificreports OPEN Comparative proteomic analysis revealed complex responses to classical/novel duck reovirus Received: 12 January 2018 Accepted: 20 June 2018 infections in Cairna moschata Published: xx xx xxxx Tao Yun, Jionggang Hua, Weicheng Ye, Bin Yu, Liu Chen, Zheng Ni & Cun Zhang Duck reovirus (DRV) is an typical aquatic bird pathogen belonging to the Orthoreovirus genus of the Reoviridae family. Reovirus causes huge economic losses to the duck industry. Although DRV has been identifed and isolated long ago, the responses of Cairna moschata to classical/novel duck reovirus (CDRV/NDRV) infections are largely unknown. To investigate the relationship of pathogenesis and immune response, proteomes of C. moschata liver cells under the C/NDRV infections were analyzed, respectively. In total, 5571 proteins were identifed, among which 5015 proteins were quantifed. The diferential expressed proteins (DEPs) between the control and infected liver cells displayed diverse biological functions and subcellular localizations. Among the DEPs, most of the metabolism-related proteins were down-regulated, suggesting a decrease in the basal metabolisms under C/NDRV infections. Several important factors in the complement, coagulation and fbrinolytic systems were signifcantly up-regulated by the C/NDRV infections, indicating that the serine protease-mediated innate immune system might play roles in the responses to the C/NDRV infections. Moreover, a number of molecular chaperones were identifed, and no signifcantly changes in their abundances were observed in the liver cells. Our data may give a comprehensive resource for investigating the regulation mechanism involved in the responses of C. moschata to the C/NDRV infections. Duck reovirus (DRV), a member of the genus Orthoreovirus in the family Reoviridae, is a fatal aquatic bird patho- gen1. -
What Is Optical Imaging?
What is Optical Imaging? Optical imaging uses light to interrogate cellular and molecular function in the living body, as well as in animal and plant tissue. The information is ultimately derived from tissue composition and biomolecular processes. Images are generated by using photons of light in the wavelength range from ultraviolet to near infrared. Contrast is derived through the use of: exogenous agents (i.e., dyes or probes) that provide a signal endogenous molecules with optical signatures (i.e., NADH, hemoglobin, collagens, etc.) reporter genes. Florescence Imaging Fluorescence protein imaging uses endogenous or exogenous molecules or materials that emit light when activated by an external light source such as a laser. An external light of appropriate wavelength is used to excite a target molecule, which then fluoresces by releasing longer-wavelength, lower-energy light. Fluorescence imaging provides the ability to localize and measure gene expression including normally expressed and aberrant genes, proteins and other pathophysiologic processes. Other potential uses include cell trafficking, tagging superficial structures, detecting lesions and for monitoring tumor growth and response to therapy. Bioluminescent Imaging (BLI) Bioluminescent imaging uses a natural light-emitting protein such as luciferase to trace the movement of certain cells or to identify the location of specific chemical reactions within the body. Bioluminescent imaging is being applied to both gene expression and therapeutic monitoring. Optical Imaging Technologies Near-infrared fluorescence imaging involves imaging fluorescence photons in the near-infrared range (typically 600– 900 nm). A fluorochrome is excited by a lower wavelength, light source and the emitted excitation is recorded as a slightly higher wavelength with a high sensitivity charge-coupled-device (CCD) camera. -
Treatment of Equine Gastric Impaction by Gastrotomy R
EQUINE VETERINARY EDUCATION / AE / april 2011 169 Case Reporteve_165 169..173 Treatment of equine gastric impaction by gastrotomy R. A. Parker*, E. D. Barr† and P. M. Dixon Dick Vet Equine Hospital, University of Edinburgh, Easter Bush Veterinary Centre, Midlothian; and †Bell Equine Veterinary Clinic, Mereworth, UK. Keywords: horse; colic; gastric impaction; gastrotomy Summary Edinburgh with a deep traumatic shoulder wound of 24 h duration. Examination showed a mildly contaminated, A 6-year-old Warmblood gelding was referred for treatment of 15 cm long wound over the cranial aspect of the left a traumatic shoulder wound and while hospitalised developed scapula that transected the brachiocephalicus muscle a large gastric impaction which was unresponsive to and extended to the jugular groove. The horse was sound medical management. Gastrotomy as a treatment for gastric at the walk and ultrasonography showed no abnormalities impactions is rarely attempted in adult horses due to the of the bicipital bursa. limited surgical access to the stomach. This report describes The wound was debrided and lavaged under standing the successful surgical treatment of the impaction by sedation and partially closed with 2 layers of 3 metric gastrotomy and management of the post operative polyglactin 910 (Vicryl)1 sutures in the musculature and complications encountered. simple interrupted polypropylene (Prolene)1 skin sutures, leaving some ventral wound drainage. Sodium benzyl Introduction penicillin/Crystapen)2 (6 g i.v. q. 8 h), gentamicin (Gentaject)3 (6.6 mg/kg bwt i.v. q. 24 h), flunixin 4 Gastric impactions are rare in horses but, when meglumine (Flunixin) (1.1 mg/kg bwt i.v. -
15-Coned-Ccrn-Cardiovascular.Pdf
1 Cardiovascular Introduction A. Anatomy & Physiology B. Cardiac Assessment 1. Cardiac Risk Factors Non Modifiable Age Gender Family History Race Modifiable Smoking Hypertension Diabetes Obesity Stress Exercise Hyperlipidemia 2. Medical & Surgical History 3. Social History 4. Medication History 5. Physical Exam 2 Color Pulses Rate & Rhythm PMI Location Extremity Temperature Dyspnea Fatigue Level Fluid Retention Palpitations Dizziness 6. Chest Pain Exam PQRST Assessment P: Pain, Placement, Provocation Q: Quality (sharp, stabbing, pressure) , Quantity R: Radiation, Relief S: Severity, Systems (nausea, sweaty, dizziness) T: Timing (when it started, how long did it last, what makes it better or worse) C. Diagnostic Tests & Procedures 1. 12 Lead ECG 2. Echocardiography (Transthoracic and Transesepheal) 3. Stress Test 4. Cardiac Catheterization 5. Doppler Ultrasound 6. Blood Work Acute Coronary Syndrome Cardiac Enzymes: CK-MB, Amino Acids: Troponins Heme Proteins: Myoglobin Lipid Profile Triglycerides Cholesterol Low Density Lipoproteins High Density Lipoprotein Coagulation Profile PT/INR aPTT ACT 3 Misc B Type Naturetic Peptide – BNP C Reactive Protein Homocysteine Hemodynamic Monitoring/Assessment CARDIAC OUTPUT HEART RATE X STROKE VOLUME PRELOAD + AFTERLOAD + CONTRACTILITY + The volume of blood in the The pressure or resistance the LV must contract The ability of the against or overcome to eject the blood or create ventricle at end diastole. systole. myocardium to contract. Total Blood Volume -
New York Chapter American College of Physicians Annual
New York Chapter American College of Physicians Annual Scientific Meeting Poster Presentations Saturday, October 12, 2019 Westchester Hilton Hotel 699 Westchester Avenue Rye Brook, NY New York Chapter American College of Physicians Annual Scientific Meeting Medical Student Clinical Vignette 1 Medical Student Clinical Vignette Adina Amin Medical Student Jessy Epstein, Miguel Lacayo, Emmanuel Morakinyo Touro College of Osteopathic Medicine A Series of Unfortunate Events - A Rare Presentation of Thoracic Outlet Syndrome Venous thoracic outlet syndrome, formerly known as Paget-Schroetter Syndrome, is a condition characterized by spontaneous deep vein thrombosis of the upper extremity. It is a very rare syndrome resulting from anatomical abnormalities of the thoracic outlet, causing thrombosis of the deep veins draining the upper extremity. This disease is also called “effort thrombosis― because of increased association with vigorous and repetitive upper extremity activities. Symptoms include severe upper extremity pain and swelling after strenuous activity. A 31-year-old female with a history of vascular thoracic outlet syndrome, two prior thrombectomies, and right first rib resection presented with symptoms of loss of blood sensation, dull pain in the area, and sharp pain when coughing/sneezing. When the patient had her first blood clot, physical exam was notable for swelling, venous distension, and skin discoloration. The patient had her first thrombectomy in her right upper extremity a couple weeks after the first clot was discovered. Thrombolysis with TPA was initiated, and percutaneous mechanical thrombectomy with angioplasty of the axillary and subclavian veins was performed. Almost immediately after the thrombectomy, the patient had a rethrombosis which was confirmed by ultrasound. -
Colorectal Cancer Screening
CLINICAL MEDICAL POLICY Policy Name: Colorectal Cancer Screening Policy Number: MP-059-MD-PA Responsible Department(s): Medical Management Provider Notice Date: 03/19/2021 Issue Date: 03/19/2021 Effective Date: 04/19/2021 Next Annual Review: 02/2022 Revision Date: 02/17/2021 Products: Gateway Health℠ Medicaid Application: All participating hospitals and providers Page Number(s): 1 of 10 DISCLAIMER Gateway Health℠ (Gateway) medical policy is intended to serve only as a general reference resource regarding coverage for the services described. This policy does not constitute medical advice and is not intended to govern or otherwise influence medical decisions. POLICY STATEMENT Gateway Health℠ may provide coverage under the medical-surgical benefits of the Company’s Medicaid products for medically necessary colorectal cancer screening procedures. This policy is designed to address medical necessity guidelines that are appropriate for the majority of individuals with a particular disease, illness or condition. Each person’s unique clinical circumstances warrant individual consideration, based upon review of applicable medical records. (Current applicable Pennsylvania HealthChoices Agreement Section V. Program Requirements, B. Prior Authorization of Services, 1. General Prior Authorization Requirements.) Policy No. MP-059-MD-PA Page 1 of 10 DEFINITIONS Average-Risk Population – Patient population defined as having no personal history of adenomatous polyps, colorectal cancer, or inflammatory bowel disease (Crohn’s disease and Ulcerative Colitis); no family history of colorectal cancer or adenomatous polyps, familial adenomatous polyposis, or hereditary nonpolyposis colorectal cancer. High-Risk Population – Patient population defined as having a first-degree relative (sibling, parent, or child) who has had colorectal cancer or adenomatous polyps; OR family history of familial adenomatous polyposis; OR family history of hereditary non-polyposis colorectal cancer; OR family history of MYH- associated polyposis in siblings; OR diagnosis of Cowden syndrome. -
Role of Cornification and Triglyceride Synthesis Genes
Gillespie et al. BMC Genomics 2013, 14:169 http://www.biomedcentral.com/1471-2164/14/169 RESEARCH ARTICLE Open Access Transcriptome analysis of pigeon milk production – role of cornification and triglyceride synthesis genes Meagan J Gillespie1,2*, Tamsyn M Crowley1,3, Volker R Haring1, Susanne L Wilson1, Jennifer A Harper1, Jean S Payne1, Diane Green1, Paul Monaghan1, John A Donald2, Kevin R Nicholas3 and Robert J Moore1 Abstract Background: The pigeon crop is specially adapted to produce milk that is fed to newly hatched young. The process of pigeon milk production begins when the germinal cell layer of the crop rapidly proliferates in response to prolactin, which results in a mass of epithelial cells that are sloughed from the crop and regurgitated to the young. We proposed that the evolution of pigeon milk built upon the ability of avian keratinocytes to accumulate intracellular neutral lipids during the cornification of the epidermis. However, this cornification process in the pigeon crop has not been characterised. Results: We identified the epidermal differentiation complex in the draft pigeon genome scaffold and found that, like the chicken, it contained beta-keratin genes. These beta-keratin genes can be classified, based on sequence similarity, into several clusters including feather, scale and claw keratins. The cornified cells of the pigeon crop express several cornification-associated genes including cornulin, S100-A9 and A16-like, transglutaminase 6-like and the pigeon ‘lactating’ crop-specific annexin cp35. Beta-keratins play an important role in ‘lactating’ crop, with several claw and scale keratins up-regulated. Additionally, transglutaminase 5 and differential splice variants of transglutaminase 4 are up-regulated along with S100-A10. -
Identification of Intracellular Factor XIII in Human Monocytes and Macrophages
Identification of Intracellular Factor XIII in Human Monocytes and Macrophages Per Henriksson, Susanne Becker, Garry Lynch, and Jan McDonagh Department of Pediatrics, and Blood Coagulation Laboratory, University of Lund, General Hospital, Malmd, Sweden; Department of Obstetrics and Gynecology, University ofNorth Carolina, Chapel Hill, North Carolina 27514; Department ofPathology, Beth Israel Hospital and Harvard Medical School, and Charles A. Dana Research Institute, Boston, Massachusetts 02215 Abstract transglutaminases have been identified, of which the most well characterized are tissue transglutaminase and Factor XIIIa. A Factor XIII is a blood protransglutaminase that is distributed tissue transglutaminase, which may be present in many cell in plasma and platelets. The extracellular and intracellular types, is usually isolated from liver or erythrocytes (1). It is a zymogenic forms differ in that the plasma zymogen contains A monomeric protein (relative molecular weight [Mn' - 75,000- and B subunits, while the platelet zymogen has A subunits 80,000) which has only been detected as an active enzyme; no only. Both zymogens form the same enzyme. Erythrocytes, in zymogen has been found (2-4). Factor XIIIa, the blood contrast, contain a tissue transglutaminase that is distinct from coagulation enzyme that was first found to catalyze the covalent Factor XIII. In this study other bone marrow-derived cells stabilization of fibrin, exists in two zymogenic forms. Extra- were examined for transglutaminase activity. Criteria that were cellular or plasma Factor XIII is a noncovalently associated used to differentiate Factor XIII proteins from erythrocyte tetramer (MW- 320,000), consisting of two A and two B transglutaminase included: (a) immunochemical and immuno- subunits; intracellular Factor XIII is a dimer (Mr - 150,000) histochemical identification with monospecific polyclonal and of A subunits. -
Factor XIII Deficiency
Haemophilia (2008), 14, 1190–1200 DOI: 10.1111/j.1365-2516.2008.01857.x ORIGINAL ARTICLE Factor XIII deficiency L. HSIEH and D. NUGENT Division of Hematology, ChildrenÕs Hospital of Orange County, Orange, CA, USA Summary. Inherited factor XIII (FXIII) deficiency is been more than 60 FXIII mutations identified in the a rare bleeding disorder that can present with current literature. In addition, single nucleotide umbilical bleeding during the neonatal period, polymorphisms have been described, some of which delayed soft tissue bruising, mucosal bleeding and have been shown to affect FXIII activity, contribut- life-threatening intracranial haemorrhage. FXIII defi- ing further to the heterogeneity in patient presenta- ciency has also been associated with poor wound tion and severity of clinical symptoms. Although healing and recurrent miscarriages. FXIII plays an there is a lifelong risk of bleeding, the prognosis is integral role in haemostasis by catalysing the cross- excellent when current prophylactic treatment is linking of fibrin, platelet membrane and matrix available using cryoprecipitate or plasma-derived proteins throughout thrombus formation, thus sta- FXIII concentrate. bilizing the blood clot. The molecular basis of FXIII deficiency is characterized by a high degree of Keywords: bleeding disorders, coagulation, factor heterogeneity, which contributes to the different XIII, factor XIII deficiency, fibrin stabilizing factor, clinical manifestations of the disease. There have protransglutaminase clear that intracellular FXIII, especially in platelet Introduction and vascular bed may play an equally important role Prior to delving into the clinical and biochemical in haemostasis. details which characterize this fascinating clotting In plasma, FXIII circulates as a pro-transglutamin- factor, it is worth taking a moment to consider this ase (FXIII-A2B2) composed of two catalytic A important fact: factor XIII (FXIII) is not just another subunits (FXIII-A2) and two non-catalytic B subunits plasma protein in the clotting cascade. -
Anti-Inflammatory Role of Curcumin in LPS Treated A549 Cells at Global Proteome Level and on Mycobacterial Infection
Anti-inflammatory Role of Curcumin in LPS Treated A549 cells at Global Proteome level and on Mycobacterial infection. Suchita Singh1,+, Rakesh Arya2,3,+, Rhishikesh R Bargaje1, Mrinal Kumar Das2,4, Subia Akram2, Hossain Md. Faruquee2,5, Rajendra Kumar Behera3, Ranjan Kumar Nanda2,*, Anurag Agrawal1 1Center of Excellence for Translational Research in Asthma and Lung Disease, CSIR- Institute of Genomics and Integrative Biology, New Delhi, 110025, India. 2Translational Health Group, International Centre for Genetic Engineering and Biotechnology, New Delhi, 110067, India. 3School of Life Sciences, Sambalpur University, Jyoti Vihar, Sambalpur, Orissa, 768019, India. 4Department of Respiratory Sciences, #211, Maurice Shock Building, University of Leicester, LE1 9HN 5Department of Biotechnology and Genetic Engineering, Islamic University, Kushtia- 7003, Bangladesh. +Contributed equally for this work. S-1 70 G1 S 60 G2/M 50 40 30 % of cells 20 10 0 CURI LPSI LPSCUR Figure S1: Effect of curcumin and/or LPS treatment on A549 cell viability A549 cells were treated with curcumin (10 µM) and/or LPS or 1 µg/ml for the indicated times and after fixation were stained with propidium iodide and Annexin V-FITC. The DNA contents were determined by flow cytometry to calculate percentage of cells present in each phase of the cell cycle (G1, S and G2/M) using Flowing analysis software. S-2 Figure S2: Total proteins identified in all the three experiments and their distribution betwee curcumin and/or LPS treated conditions. The proteins showing differential expressions (log2 fold change≥2) in these experiments were presented in the venn diagram and certain number of proteins are common in all three experiments. -
Geisinger Lewistown Hospital Published: March 25, 2019
Geisinger Lewistown Hospital Published: March 25, 2019 DESCRIPTION CHARGE Fine needle aspiration; without imaging guidance $ 607.00 Fine needle aspiration; without imaging guidance $ 286.00 Fine needle aspiration; with imaging guidance $ 2,218.00 Fine needle aspiration; with imaging guidance $ 1,691.00 Placement of soft tissue localization device(s) (eg, clip, metallic pellet, wire/needle, radioactive seeds), percutaneous, including imaging guidance; first lesion $ 1,979.00 Placement of soft tissue localization device(s) (eg, clip, metallic pellet, wire/needle, radioactive seeds), percutaneous, including imaging guidance; each $ 1,385.00 additional lesion (List separately in addition to code for primary procedure) Incision and drainage of abscess (eg, carbuncle, suppurative hidradenitis, cutaneous or subcutaneous abscess, cyst, furuncle, or paronychia); simple or single $ 657.00 Incision and drainage of abscess (eg, carbuncle, suppurative hidradenitis, cutaneous or subcutaneous abscess, cyst, furuncle, or paronychia); complicated or $ 986.00 multiple Incision and drainage of pilonidal cyst; simple $ 657.00 Incision and drainage of pilonidal cyst; complicated $ 3,726.00 Incision and removal of foreign body, subcutaneous tissues; simple $ 1,694.00 Incision and removal of foreign body, subcutaneous tissues; complicated $ 4,710.00 Incision and drainage of hematoma, seroma or fluid collection $ 3,470.00 Puncture aspiration of abscess, hematoma, bulla, or cyst $ 1,272.00 Puncture aspiration of abscess, hematoma, bulla, or cyst $ 657.00 Incision