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While obesity is widely recognized as a risk factor for cancer, survival among patients with cancer is often higher for obese than for lean individuals. Several hypotheses have been proposed to explain this “obesity paradox,” but no consensus has yet emerged. Here, we propose a novel hypothesis to add to this emerging debate which suggests that lean healthy persons present conditions unfavorable to malignant transformation, due to powerful natural defenses, whereby only rare but aggressive neoplasms can emerge and develop. In contrast, obese persons present more favorable conditions for malignant transformation, because of several weight‐associated factors and less efficient natural defenses, leading to a larger quantity of neoplasms comprising both nonaggressive and aggressive ones to regularly emerge and progress. If our hypothesis is correct, testing would require the consideration of the raw quantity, not the relative frequency, of aggressive cancers in obese patients compared with lean ones. We also discuss the possibility that in obese persons, nonaggressive malignancies may prevent the subsequent progression of aggressive cancers through negative competitive interactions between tumors.

We report the surgical management of a case of Zenker's diverticulum in a 64 year old man, complicated by metallic nail penetration and surgical scarring due to previous surgery for cervical vertebral trauma.

Large cystic renal tumours can be confused with hepatic lesions even on crosssectional imaging. Careful clinical, sonographic and imaging analysis is needed for establishing correct diagnosis. We report a case of papillary cystic renal carcinoma in a 60 year old man, which was confused with amoebic liver abcess and was initially drained. Subsequent recurrence of symptoms prompted us to re-evaluate the case and repeat sonography confirmed the extrahepatic origin of mass based on simple observation that the liver and mass were moving separately on inspiration. Later guided aspiration from solid component of the mass confirmed the diagnosis as renal cell carcinoma. He was successfully treated with radical nephrectomy with uneventful post-operative recovery.

Ganglioneuromas are one of the frequent retroperitoneal tumors arising from extraadrenal sympathetic ganglia or chromaffin tissue. The commonest extraadrenal site is periadrenal region near renal hilum. We present a case of ganglioneuroma in a narrow quadrangular space near right renal hilum, treated laparoscopically.

We present a case of Graves' disease with a image of plain radiograph of neck showing bilateral carotid calcifications and briefly discuss the pathophysiology of vascular calcification in Graves' disease. Keywords Carotid calcifications . Graves' diseaseA 21 year old lady presented with history of goiter, palpitations, weight loss and tremors for 3 years. She was on treatment with carbimazole 30 mg/day and propranolol 30 mg/day since 1 year, with partial relief of symptoms. She is still hyperthyroid with pulse rate of 110/ minute, blood pressure of 130/90 mmHg and moist skin. Clinical examination revealed diffuse large goiter with bruit and bilateral exophthalmos. Cardiac evaluation with revealed no serious abnormality like cardiomyopathy, heart failure or arrhythmias. Plain X-ray neck showed linear calcification of both common carotid arteries (Fig. 1). Thyroid profile (thyroxine, triiodothyronine, thyrotrophin levels) were suggestive of persistent thyrotoxicosis. She was rapidly prepared with 45 mg/day of carbimazole, 120 mg/day of propranolol, 2 mg/day of dexamethasone for 6 days and operated with total thyroidectomy. Post operative period was uneventful except for transient hypocalcemia for 48 hours.Carotid and other vascular calcifications most frequently occurs in atherosclerosis, diabetes, old age, chronic renal failure and vasculitis. They are mostly implicated in atheroma plaque, disturbed mineral metabolism, vasculopathy and Monckeberg's medial calcification [1].In the present case, none of the above factors were operating except for hyperdynamic circulation due to uncontrolled hyperthyroidism. Still, bilateral linear calcifications massive enough to be visible on plain radiograph occurred in a young lady with hyperthyroidism of 3 years duration, in the absence of hyperlipidemia and hypertension. Though exact cause is intriguing, past studies show that elevated thyroid hormone levels can cause vascular smooth muscle calcification by direct triggering of Gla matrix protein related gene [2]. Few studies show increased vascular injury marker titers and arterial wall

Introduction Sickle cell disease (SCD) is the most prevalent and severe monogenic disorder due to a mutation in the b-globin gene, responsible for the production of an abnormal hemoglobin (HbS) which polymerizes under hypoxia. Cerebral vasculopathy (CV) generally appearing during childhood, is responsible for ischemic stroke, making SCD the first etiology of stroke in children and young adults. To date, several biological and hemodynamical determinants have been identified in CV development such as severe anemia and/or high intracranial vascular flow velocities (> 200 cm/s). Chronic blood exchange transfusion decreases the risk of stroke in children having a pathological Doppler. However some patients still have a progressive impairment despite conventional treatment highlighting the need for new therapeutic strategies and a better understanding of the physiopathology. Therefore, by developing a 3D carotid model reproducing exactly vascular parameters of a SCD patient, we aim to: (i) determine the mechanisms of CV development in SCD, (ii) find new therapeutic approaches and (iii) predict the risk of progression of CV. Materials and methods Three-dimensional reconstructions of the internal carotid, middle cerebral and anterior cerebral artery from SCD patients were generated from magnetic resonance angiograms (MIMICS & 3Matics software, Materialise). We performed 3D simulations of the Navier-Stokes equations in patient specific geometries, including the state-of-the-art techniques of Computational Hemodynamics (multiscale coupling, backflow stabilization - FeLiSCe software) and other factors - such as the increase of the ejection fraction or the drop of peripheral resistances). Blood viscosity was based on a SCD cohort. Hemodynamic properties such as flow velocities (TMMV) and wall shear stress (WSS) in different areas of modelled carotid were then computed according to flow variations. Modelled carotid was obtained by 3D printing according to computer design (CATIA software). The next steps will consist in 1/importing doppler parameters from patients in a programmable pump for flow assays with blood mimicking fluid to measure TMMV and WSS at different areas in carotid, 2/incorporating resting or activated platelets in BMF to evaluate impact of high WSS on platelets degranulation, 3/developing a flow co-culture of smooth muscle cells (SMCs) and human umbilical vein endothelial cells (HUVECs) on carotid wall. HUVECs and SMCs at different zones of the carotid undergoing high/low WSS and oscillatory flow will be analysed Preliminary results Our preliminary results suggest that the carotid inlet flow but not blood viscosity is responsible for the pathological intra cranial velocities (Figure 1A). At high carotid inlet flow, areas of high and low WSS appeared in children (Figure 1B), suggesting the existence of turbulent flow that could lead to arterial wall damages. Figure 2A shows a 3D printed carotid reproducing the exact SCD child's one. The material of artificial carotid is compatible with HUVECs culture (Figure 2B) and fluidic experiment at high inlet flow (Figure 2C). On Doppler ultrasonography, the velocities measured in different sections of carotid were comparable to patient's data and these velocities were modified according to variations of inlet flow values. Conclusions and perspectives By modification of input conditions, our 3D personalized model can predict high or low vascular velocities areas and will allow a better understanding of the pathophysiological processes involved at the interface between abnormal flow and cells on carotid wall. This innovative model could be a pertinent tool to evaluate individually effectiveness of new therapeutic strategies in SCD patients. Furthermore, this work may constitute a proof of concept that can be transposed to other diseases. Disclosures Verlhac: Addmedica, Paris: Other: Financial Support; Bluebird Bio: Consultancy. Bartolucci:AddMedica: Honoraria, Membership on an entity's Board of Directors or advisory committees; Roche: Membership on an entity's Board of Directors or advisory committees; HEMANEXT: Membership on an entity's Board of Directors or advisory committees; Global Blood Therapeutics: Membership on an entity's Board of Directors or advisory committees; Agios: Membership on an entity's Board of Directors or advisory committees; Novartis: Membership on an entity's Board of Directors or advisory committees.

Hashimoto's thyroiditis (HT) is the commonest cause of hypothyroidism, especially in iodine replete areas. The clinical presentation of HT is usually insidious with mild goiter and progressive hypothyroidism. But, HT presents with large goiter and compressive symptoms in some cases. The treatment of HT is mostly conservative with thyroxine treatment sooner or later. Occasionally, surgery is indicated for large goiters with persistent pressure symptoms or associated nodules. We report a rare case of unusually large goiter with compressive symptoms, hitherto unreported in literature. Fig. 3: Ex vivo specimen of large diffuse goiter on grossing chart