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Acta Veterinaria Hungarica
Authors: Yonca B. Kabak, Mahmut Sozmen, Alparslan K. Devrim, Mert Sudagidan, Funda Yildirim, Tolga Guvenc, Murat Yarim, Yavuz M. Gulbahar, Ishtiaq Ahmed, Efe Karaca, and Sinem Inal

VEGF expression indicates aggressive biological behaviour in human cutaneous SCCs. Similarly, VEGF-C expression was correlated with the depth of tumour invasion, tumour stage and lymph node metastasis in human oesophageal cancers ( Kitadai et al., 2001

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Orvosi Hetilap
Authors: Nikolett Wohner, Gergely Varga, Péter Szloboda, Péter Farkas, András Masszi, Laura Horváth, Gergely Szombath, Judit Várkonyi, Szabolcs Benedek, and Tamás Masszi

. 12 Wiernik PH, Lossos IS, Tuscano JM, et al. Lenalidomide monotherapy in relapsed or refractory aggressive non-Hodgkin’s lymphoma. J Clin Oncol. 2008; 26: 4952–4957. 13

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Hematológia–Transzfuziológia
Authors: Viktória Fésüs, Ediz Eyupoglu, Richárd Kiss, Emma Ádám, András Kozma, Zoltán Mátrai, and Csaba Bödör

TJ, Davis Z, Gardiner A, et al. Unmutated Ig V(H) genes are associated with a more aggressive form of chronic lymphocytic leukemia. Blood. 1999; 94: 1848–1854. 12 Zenz T

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. J. Vasc. Interv. Radiol., 2012, 23 (1), 76–79. 68 Orringer, M. B., Bluett, M., Deeb, G. M.: Aggressive treatment of chylothorax complicating transhiatal

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Magyar Sebészet
Authors: Zoltán Mátrai, János Papp, Csaba Polgár, Erika Hitre, István Köves, Edit Oláh, Judit Andi, Andrea Kiss, István Vámosi Nagy, László Tóth, and Zsolt Orosz

Aggressive Fibromatosis (desmoid tumor) J Clin Oncol 24 7 1195 203 . 28. J Church

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safety profile of the CD19-directed defined composition CAR T cell product JCAR017 in relapsed/refractory aggressive B-NHL patients: Potential for outpatient administration. 2017; 130: 1552

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-Kovacic A, et al. Aggressive B-cell lymphomas in patients with myelofibrosis receiving JAK1/2 inhibitor therapy. Blood 2018; 132: 694–706. 46 Islam MS. Concurrent chronic lymphocytic

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Righi, L., Volante, M., Tavaglione, V. és mtsai: Somatostatin receptor tissue distribution in lung neuroendocrine tumours: a clinicopathologic and immunohistochemical study of 218 ’clinically aggressive’ cases. Ann. Oncol., 2010, 21 , 548

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Acta Veterinaria Hungarica
Authors: Anna Linda Nógrádi, Iain Cope, Márton Balogh, and János Gál

The authors present eight cases of gastric dilatation and volvulus (GDV) in guinea pigs from the Department and Clinic of Exotic Animal and Wildlife Medicine, University of Veterinary Medicine, Budapest, Hungary between 2012 and 2016. Seven animals were operated on and two survived. Gastric torsion has been noted in many mammalian species. Gastric volvulus has a high morbidity and high mortality rate with a guarded to poor prognosis in all of these species. How GDV develops is still not widely understood. Postmortem examinations, in both our cases and previously reported cases, have failed to reveal the exact causes of the gastric torsions. The aetiology of gastric torsion in guinea pigs is probably multifactorial. Feeding fewer meals per day, eating rapidly, decreased food particle size, exercise, stress after a meal, competition, age, and an aggressive or fearful temperament, are all likely and potential risk factors for GDV development in a similar fashion to dogs. Sex, breeding, dental diseases, anatomical abnormalities, pain and pregnancy may also be contributing factors.

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The glomerular filtration barrier is a highly specialized tri-layer structure with unique functional properties. Podocyte dysfunction and cytoskeletal disorganization leads to disruption of the slit diaphragma, and proteinuria. Inflammatory diseases involving the kidney as well as inherited podocytopathies or diabetic nephropathy cause injury of the podocyte network. Focal segmental glomerulosclerosis (FSGS) is a pathologic entity that is a common cause of nephrotic syndrome with severe proteinuria in both adults and children. Several causative genes have been identified in the pathogenesis of FSGS. Mutations of the transient receptor potential canonical-6 (TRPC6), a non-selective cation channel that is directly activated by diacylglycerol (DAG), cause a particularly aggressive form of FSGS. Angiotensin II, acting through its AT1 receptor, plays a critical role in generation of proteinuria and progression of kidney injury in a number of kidney diseases, including FSGS. Mounting evidence suggest the central role of TRPC6 and perhaps other TRPC channels in the pathogenesis of FSGS as well as of acquired forms of proteinuria such as diabetic nephropathy or hypertension. Identification of signaling pathways downstream of TRPC6 may provide novel targets for the treatment of proteinuria and prevent progression of podocyte injury.

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