Vessel tractography using an intensity based tensor model with branch detection

In this paper, we present a tubular structure seg- mentation method that utilizes a second order tensor constructed from directional intensity measurements, which is inspired from diffusion tensor image (DTI) modeling. The constructed anisotropic tensor which is fit inside a vessel drives the segmen- tation analogously to a tractography approach in DTI. Our model is initialized at a single seed point and is capable of capturing whole vessel trees by an automatic branch detection algorithm developed in the same framework. The centerline of the vessel as well as its thickness is extracted. Performance results within the Rotterdam Coronary Artery Algorithm Evaluation framework are provided for comparison with existing techniques. 96.4% average overlap with ground truth delineated by experts is obtained in addition to other measures reported in the paper. Moreover, we demonstrate further quantitative results over synthetic vascular datasets, and we provide quantitative experiments for branch detection on patient Computed Tomography Angiography (CTA) volumes, as well as qualitative evaluations on the same CTA datasets, from visual scores by a cardiologist expert

Vessel tractography using an intensity based tensor model

In this paper, we propose a novel tubular structure segmen- tation method, which is based on an intensity-based tensor that fits to a vessel. Our model is initialized with a single seed point and it is ca- pable of capturing whole vessel tree by an automatic branch detection algorithm. The centerline of the vessel as well as its thickness is extracted. We demonstrated the performance of our algorithm on 3 complex contrast varying tubular structured synthetic datasets for quantitative validation. Additionally, extracted arteries from 10 CTA (Computed Tomography An- giography) volumes are qualitatively evaluated by a cardiologist expert’s visual scores

Prothrombin Complex Concentrates in Life-Threatening Bleeding

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Tip 2 diyabetik hastaların birinci derece yakınlarında total homosistein ve asimetrik dimetilargininin plazma düzeyleri

Amaç: Tip 2 diyabetik hastaların birinci derece yakınlarında, ailesinde diyabet öyküsü olmayan sağlıklı olgulara göre kardiyovasküler hastalıklar daha sık görülmektedir. Asimetrik dimetilarginin (ADMA) ve homosistein (Hcy) plazma düzeyleri kardiyovasküler hastalıklar ve endotel disfonksiyonuyla ilişkili göstergelerdir. Bu çalışmada, tip 2 diyabetik hastaların birinci derece yakınlarında ADMA ve Hcy plazma düzeyleri ile bu göstergelerle kardiyovasküler risk faktörleri arasındaki ilişkilerin incelenmesi amaçlandı. Hastalar ve Yöntemler: Dolaşımdaki ADMA ve Hcy düzeyleri 15 tip 2 diyabet hastasının birinci derece yakınında ve ailesinde diyabet öyküsü olmayan 15 kontrol olgusunda ölçüldü. Bulgular: Her iki grup arasında ADMA ve Hcy plazma düzeyleri açısından anlamlı farklılık saptanmadı (p>0.05). Asimetrik dimetilarginin plazma düzeyi tip 2 diyabetik olguların birinci derece yakınlarında, bel çevresi (p=0.02), açlık insülin düzeyi (p=0.03), insülin direnci (p=0.01), total kolesterol (p=0.04) ve HDL kolesterol (p=0.03) ile ilişkiliydi. Sonuç: Bu sonuçlara göre, kardiyovasküler risk faktörlerine sahip olan tip 2 diyabetik olguların birinci derece yakınlarında, ADMA plazma düzeylerinin doğrudan endotel disfonksiyonunun gelişimine katkıda bulunmadığını düşünmekteyiz.Objectives: Cardiovascular diseases are more common among first degree relatives of type 2 diabetic patients than healthy subjects without a family history of diabetes. Plasma asymmetric dimethylarginine (ADMA) and homocysteine (Hcy) levels are markers of endothelial dysfunction and cardiovascular disease. The objective of this study was to evaluate levels of ADMA, Hcy and their association with cardiovascular risk factors in first degree relatives of type 2 diabetic patients. Patients and Methods: The circulating ADMA and Hcy levels were measured in 15 first degree relatives of type 2 diabetic patients and 15 control subjects without a known family history of diabetes. Results: No statistically significant differences were found in plasma levels of ADMA and Hcy between the two groups (p>0.05). Plasma ADMA levels correlated significantly with waist circumference (p=0.02), fasting insulin levels (p=0.03), insulin resistance (p=0.01), total cholesterol (p=0.04) and HDL-cholesterol (p=0.03) levels in the first degree relatives of type 2 diabetic patients. Conclusion: These results suggest that plasma ADMA levels do not directly contribute to the development of endothelial dysfunction in first degree relatives of type 2 diabetic patients with cardiovascular risk factors

Genetic Diagnosis of Hereditary Hemorrhagic Telangiectasia: Four Novel Pathogenic Variations in Turkish Patients

Aims: Hereditary hemorrhagic telangiectasia is an autosomal dominant disorder characterized by telangiectasia, epistaxis, and vascular malformations. Pathogenic mutations were found in ENG, AVCRL1, SMAD4, and GDF genes. In this study, we present our database of patients with hereditary hemorrhagic telangiectasia regarding the phenotype-genotype relations and discuss two novel ENG gene pathogenic variations in two unrelated families. Methods: Next Generation Sequencing analysis was performed on the peripheral blood of nine patients with hereditary hemorrhagic telangiectasia in four unrelated families. All patients were diagnosed with hereditary hemorrhagic telangiectasia according to the Curaçao criteria. Data on treatment and screenings of visceral involvement were recorded from files. Results: We have found a pathogenic variation in either the ENG or ACVRL1 gene in each family. Two novel pathogenic variations in the ENG gene, including NM_000118.3 (ENG): c.416delC (p.P139fs*24) and NM_000118.3(ENG): c.1139dupT (p.Leu380PhefsTer16), were found in the same family. The NM_000020.2(ACVRL1): c.1298C>T (p.Pro433Leu) pathogenic variation in the ACVRL1 gene in our first family and a novel heterozygous likely pathogenic NM_000020.2(ACVRL1): c.95T>C (p.Val32Ala) variation was found in our second family. Seven of the nine patients were treated with thalidomide for controlling bleeding episodes. All patients responded to thalidomide. In one patient, the response to thalidomide was lost and switched to bevacizumab. Conclusion: In hereditary hemorrhagic telangiectasia, certain types of mutations correlate with disease phenotypes and with next generation sequencing methods. New pathogenic variations can be revealed, which might help manage patients with hereditary hemorrhagic telangiectasi

Obez hastalarda proinflamatuvar sitokinler ile fibrinolitik sistem arasındaki ilişki

Amaç: Obez kişilerde proinflamatuar sitokinlerden TNF-? ve IL-6, fibrinolitik sistem parametrelerinden t-PA ve PAI-1 ve insülin direnci arasındaki ilişki araştırıldı. Hastalar ve Yöntemler: Çalışmaya obez (VKİ ?30 kg/m2) olarak değerlendirilen 54 kişi (41 kadın, 13 erkek; ort. yaş 33.5) ve obezite sorunu olmayan (VKİ <25 kg/m2) 30 kişi (19 kadın, 11 erkek; ort. yaş 22.3) alındı. Fibrinojen düzeyleri koagülometrik olarak ve TNF-?, IL-6, t-PA, PAI-1 düzeyleri ELISA yöntemiyle ölçüldü. Bulgular: Kontrol grubuyla karşılaştırıldığında, obez kişilerde fibrinojen (p<0.01), PAI-1 (p<0.001), TNF-? (p<0.01) ve IL-6 düzeyleri (p<0.001) anlamlı derecede yüksek, t-PA düzeyi (p<0.001) ve t-PA/PAI-1 oranı (p<0.001) anlamlı derecede düşük bulundu. Obezlerde TNF-? ile t-PA (p=0.007) ve t-PA/PAI-1 oranı (p=0.016) arasında ters ilişki saptandı. İnsülin direnci olan ve olmayan obez kişilerde parametreler arasında fark yoktu. Sonuç: Obezitede adipoz dokudan salgılanan özellikle TNF-? gibi inflamatuar sitokinlerin artması fibrinolizde azalmaya yol açar. Obez kişilerde görülen bu değişiklikler, insülin direncinden bağımsız olarak ateroskleroza neden olabilir.Objectives: The aim of this study was to investigate the relationship between proinflammatory cytokines (TNF-&amp;#945; and IL-6), and fibrinolytic system parameters (t-PA, and PAI-1) and insulin resistance in obese individuals. Patients and Methods: The study included 54 obese subjects (BMI &amp;#8805;30 kg/m2; 41 females, 13 males; mean age 33.5 years) and 30 non-obese healthy individuals (BMI &lt;25 kg/m2; 19 females, 11 males; mean age 22.3 years). Fibrinogen levels were measured by the coagulometric method and the measurements of TNF-&amp;#945;, IL-6, t-PA and PAI-1 were carried out by the ELISA method. Results: Compared with non-obese subjects, obese individuals had significantly higher fibrinogen (p&lt;0.01), PAI-1 (p&lt;0.001), TNF-&amp;#945; (p&lt;0.01), and IL-6 (p&lt;0.001) levels, and significantly lower t-PA level (p&lt;0.001) and t-PA/PAI-1 ratio (p&lt;0.001). We also found an inverse relationship between TNF-&amp;#945; and t-PA levels (p=0.007) and t-PA/PAI-1 ratio (p=0.016) in obese individuals. The presence or absence of insulin resistance did not affect proinflammatory cytokines and fibrinolytic system parameters in obese individuals. Conclusion: Our findings indicate increased inflammatory cytokine levels especially in TNF-&amp;#945; level, and decreased fibrinolysis in obese individuals. These changes may contribute to atherosclerotic process independent from insulin resistance in obesity

Drug Induced Thrombotic Microangiopathy with Certolizumab Pegol

Background: Certolizumab pegol is used to treat ankylosing spondylitis, Crohn’s disease, psoriatic arthritis, and rheumatoid arthritis. Unlike other monoclonal antibodies such as infliximab and adalimumab, certolizumab does not contain an Fc fraction and hence does not induce complement activation. In this report, we describe the case of a patient with thrombotic microangiopathy caused due to certolizumab pegol, with a brief description about the pathophysiological approach to thrombotic microangiopathy. Case Report: A-39-year-old man suffering from ankylosing spondylitis for the past 10 years presented with fatigue. He had been on certolizumab pegol treatment for 6 months, starting with 400 and 200 mg every 2 weeks. He had significant nonimmune hemolytic anemia and thrombocytopenia without a disseminated intravascular coagulopathy. Schistocytes were observed in more than 10% of the erythrocytes per field. Plasma exchange along with corticosteroid treatment was started. There was a dramatic improvement within a week, and after 10 sessions of plasma exchange, the patient was discharged on corticosteroids with a tapering plan. ADAMTS13 enzyme activity was determined to be normal. Conclusion: The development of drug-induced thrombotic microangiopathy may be either immune-mediated or dose-dependent toxicity-mediated Anti-drug antibodies and their immunological aspects are still unclear and yet to be elucidated

Fondaparinuks heparinin indüklediği trombositopeni hastalarında etkili bir alternatif antikoagülan mıdır? Olgu sunumu ve literatür derlemesi

Heparine bağlı trombositopeni (HIT) nadir olmasına karşın heparin tedavisinin en çok korkulan komplikasyonlarından biridir. Heparine bağlı trombositopeni heparin ile temas sonrası oluşan, antikor aracılı edinsel ve geçici bir trombotik bozukluktur. Fraksiyone olmayan heparin hemodiyaliz sırasında kullanılan standart antikoagülandır ve heparin ile sürekli temas eden hemodiyaliz hastalarında HIT riski artmıştır. Burada kronik zeminde akut böbrek yetersizliği olan ve hemodiyaliz sonrasında HIT gelişen 75 yaşında bir erkek hastayı bildiriyoruz. Hastada derin ven trombozu saptandı ve fondaparinuks ile başarıyla tedavi edildi. Bu yazımızda ayrıca HIT hastalarında gelişen trombozun profilaksi ve tedavisinde fondaparinuksun endikasyon dışı kullanımını derledik. Fondaparinuks heparin ile reaksiyon veren antikorların çoğunluğunca tanınmayacak kadar küçük olduğundan lepirudin ve danaparoid gibi lisanslı ilaçların bulunmadığı durumlarda, semptomatik HIT hastaları için mantıklı bir alternatif antikoagülan olabilir.Although rare, heparin-induced thrombocytopenia (HIT) is one of the most feared complications of heparin therapy. It is an antibody-mediated, acquired and transient thrombotic disorder following exposure to heparin. Unfractionated heparin is the standard anticoagulation used in hemodialysis sessions and hemodialysis patients who are continually exposed to heparin are at increased risk for HIT. We report a 75-year-old male patient with acute-on-chronic renal failure who subsequently developed HIT while on hemodialysis. The patient was presented with deep vein thrombosis and successfully treated with fondaparinux. In this report we also review the off-label use of fondaparinux for the treatment and prophylaxis of thrombosis in patients with HIT. As fondaparinux is too small to be recognized by the majority of heparin-reactive antibodies it could be a reasonable alternative anticoagulant for symptomatic HIT patients where licensed drugs like lepirudin and danaparoid are not available

Wpływ dystrybucji tkanki tłuszczowej oraz wybranych adipokin na insulinooporność w stanie przedcukrzycowym

  Introduction: The risk of developing insulin resistance and metabolic syndrome is particularly high in central obesity. In this study we evaluated the effects of fat distribution and some adipokines on insulin resistance in prediabetic patients. Material and methods: Eighty-seven age- and sex-matched patients were divided into three groups according to their 75-gram oral glucose tolerance test results as follows: impaired fasting glucose group, impaired glucose tolerance group, and normal glucose tolerance group. Fasting insulin levels were measured. Homeostatic model assessment of insulin resistance was calculated. Body fat mass measurements were assessed by bioelectric impedance analyser and abdominal fat thicknesses (subcutaneous, visceral, and preperitoneal) by ultrasonography. The fasting serum levels of several adipokines [adiponectin, leptin, resistin, vaspin, visfatin, retinol-binding protein-4 (RBP-4), tumour necrosis factor-alpha (TNF-alpha)] were measured by ELISA method. Results: The mean body mass index, fat mass measurements, and abdominal fat thicknesses of the groups were similar. There were no differences between groups in terms of the mean fasting insulin, vaspin, RBP-4, leptin, resistin, and TNF-alpha. In comparison of the prediabetic and normal groups, the levels of adiponectin (p &lt; 0.001) and visfatin (p &lt; 0.001) were lower in the prediabetic group. Furthermore, we found that high body mass index (p &lt; 0.01) and fat mass (p &lt; 0.01) and low adiponectin (p &lt; 0.05) levels have roles in the development of insulin resistance in the prediabetic group. Conclusions: We suggested that in the prediabetic period not only obesity but also decreased adiponectin levels play some role in the pathogenesis of insulin resistance. (Endokrynol Pol 2016; 67 (3): 277–282)    Wstęp: Ryzyko rozwoju insulinooporności i zespołu metabolicznego zwiększa się zwłaszcza u osób z otyłością centralną. W niniejszym badaniu oceniono wpływ dystrybucji tkanki tłuszczowej i wybranych adipokin na insulinooporność u osób ze stanem przedcukrzycowym. Materiał i metody: Osiemdziesięciu siedmiu chorych dobranych pod względem wieku I płci podzielono na 3 grupy w zależności od wyniku testu doustnego obciążenia 75 g glukozy: osoby z nieprawidłową glikemią na czczo, osoby z nieprawidłową tolerancją glukozy i osoby z prawidłową tolerancją glukozy. Zmierzono stężenie insulin na czczo. Do oszacowania insulinooporności zastosowano model homeostazy. Masę tkanki tłuszczowej oceniono za pomocą analizatora bioimpedancji elektrycznej, a grubość brzusznej tkanki tłuszczowej (podskórnej, trzewnej i przedotrzewnowej) zmierzono metodą ultrasonograficzną. Stężenie na czczo w surowicy kilku adipokin (adiponektyna, leptyna, rezystyna, waspina, wisfatyna, białko wiążące retinol-4 [RBP-4], czynnik martwicy nowotworów alfa [TNF-alfa]) zmierzono, stosując metodę ELISA. Wyniki: Średni wskaźnik masy ciała, masa tkanki tłuszczowej I grubość brzusznej tkanki tłuszczowej były podobne we wszystkich grupach. Nie stwierdzono różnic między grupami pod względem średniego stężenia insuliny na czczo ani stężeń waspiny, RBP-4, leptyny, rezystyny i TNF-alfa. W porównaniu grup ze stanem cukrzycowym i grupy z prawidłową tolerancją glukozy wykazano, że stężenia adiponektyny (p &lt; 0,001) i wisfatyny (p &lt; 0,001) były niższe u osób ze stanem przedcukrzycowym. Ponadto stwierdzono, że wysoki wskaźnik masy ciała (p &lt; 0,01) i duża masa tkanki tłuszczowej (p &lt; 0,01) oraz niskie stężenie adiponektyny (p &lt; 0,05) przyczyniają się do rozwoju insulinooporności u osób ze stanem przedcukrzycowym. Wnioski: Autorzy sugerują, że nie tylko otyłość, ale również obniżenie stężenia adiponektyny odgrywają pewną rolę w patogenezie insulinooporności w okresie przedcukrzycowym. (Endokrynol Pol 2016; 67 (3): 277–282)