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“Venous thromboembolism (VTE) has important heritable components. In the past 20 years, knowledge in this field has greatly increased with the identification PARP inhibitor drugs of a number of gene variants causing hypercoagulability.

The two main mechanisms are loss-of-function of anticoagulant proteins and gain-of-function of procoagulants, the latter owing to increased synthesis or impaired downregulation of a normal protein or, more rarely, to synthesis of a functionally hyperactive molecule. Diagnosis of thrombophilia is useful to determine the causes of VTE, recognizing that this multifactorial disease can also be influenced by various acquired factors including cancer, surgery, trauma, prolonged immobilization, or reproduction-associated risk factors. Diagnosis of inherited thrombophilia rarely affects the acute or long-term management of VTE. However, the risk of recurrent VTE is increased in anticoagulant-deficient patients and in homozygotes for buy MK-2206 gain-of-function mutations. Screening for inherited thrombophilia in thrombosis-free

individuals is indicated only for relatives of a proband who is anticoagulant-deficient or has a family history of VTE. In families with thrombophilia and Flavopiridol manufacturer VTE, primary antithrombotic prophylaxis during risk situations lowers the rate of incident VTE. In this Review, we discuss the main causes of inherited thrombophilia, the associated clinical manifestations, and the implications for antithrombotic prophylaxis in the affected individuals.”
“Malakoplakia is a rare form of chronic granulomatous

inflammation in mammals, and usually affects the urinary tract in humans. In this report, we present a case of granulomatous nephritis consistent with malakoplakia in a 4-year-old male cynomolgus monkey. Gross examination showed that the kidney was markedly enlarged and adhered to the surrounding organs. Histology showed that there was diffuse interstitial infiltration of histiocytes with abundant foamy eosinophilic cytoplasm resembling von Hansemann cells, PAS-positive granular cytoplasm and occasional PAS- and iron-positive intracellular small inclusion bodies. Electron microscopy showed that these histiocytes contained abundant lysosomes and phagolysosomes but no obvious Michaelis-Gutmann bodies. Based on these findings, a diagnosis of granulomatous nephritis consistent with early malakoplakia was made. This is the first report in a monkey of a renal lesion consistent with malakoplakia.