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Liver cirrhosis is the most common condition resulting in ascites, and ascites is the most common complication of cirrhosis. Ascites is associated with decreased quality of life, increased risk of infection, renal impairment, and overall decreased survival.1-3 Patients with massive ascites frequently present with abdominal discomfort, shortness of breath, decreased appetite, spontaneous bacterial peritonitis, and abdominal wall hernias. 4,5 In addition to dietary management (e.g., sodium and fluid restriction, and abstinence from alcohol) and diuretics, therapeutic paracentesis is a common therapy in the setting of ascites, particularly for patients with massive and refractory ascites. 1,5The goal of paracentesis should be to provide symptomatic relief that lasts as long as possible while at the same time preventing complications such as paracentesis-induced circulatory dysfunction (PICD). PICD was first described by Ginsèt al 6 in 1988, and usually occurs following large-volume paracentesis (> 5-6 L) and result in faster reaccumulation of ascites, hyponatremia, renal impairment, and shorter survival. The incidence of PICD approaches 80% when a large-volume paracentesis is performed without additional therapeutic management; the incidence is reduced to 15 to 35% when volume expanders (discussed below) are used. Knowledge of the pathophysiology, clinical presentation, diagnosis, and prevention of PICD will assist the interventional radiologist in the proper clinical management of patients with massive and refractory ascites. PathophysiologyThe exact pathophysiology of PICD is not entirely understood. PICD was initially thought to occur secondary to fluid shifting after paracentesis, resulting in decreased circulating volume. 7Although, simple fluid shifting may be contributory, additional studies demonstrated that decreased systemic vascular resistance also plays an essential role in PICD. [8][9][10] One of the causes of decreased systemic vascular resistance is believed to result from increased nitric oxide synthesis secondary to shear stress caused by increased cardiac output postparacentesis. 11 Increased cardiac output is also believed to lead to a reflex mechanism of decreased systemic vascular resistance, possibly through short-term downregulation of the sympathetic nervous system and renin release secondary to cardiac volume receptor activation. 12 Decreased intra-abdominal pressure is another possible contributing factor to the decreased systemic vascular resistance 13 after paracentesis.The resulting effective hypovolemia due to arteriolar vasodilation in turn leads to a prolonged activation of the sympathetic nervous system and the renin-angiotensin-aldosterone pathway. Increased plasma renin activity in particular is Keywords ► paracentesis ► ascites ► complication ► circulatory dysfunction AbstractParacentesis-induced circulatory dysfunction is a complication of large volume paracentesis that leads to faster reaccumulation of ascites, hyponatremia, renal impairment, and shorter survival. Knowledge of ...

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Proteins and protein networks associated with cochlear pathogenesis in the Ames waltzer (av) mouse, a model for deafness in Usher syndrome 1F (USH1F), were identified. Cochlear protein from wild-type and av mice at postnatal day 30, a time point in which cochlear pathology is well established, was analyzed by quantitative 2D gel electrophoresis followed by mass spectrometry (MS). The analytic gel resolved 2270 spots; 69 spots showed significant changes in intensity in the av cochlea compared with the control. The cochlin protein was identified in 20 peptide spots, most of which were up-regulated, while a few were down-regulated. Analysis of MS sequence data showed that, in the av cochlea, a set of full-length isoforms of cochlin was up-regulated, while isoforms missing the N-terminal FCH/LCCL domain were down-regulated. Protein interaction network analysis of all differentially expressed proteins was performed with Metacore software. That analysis revealed a number of statistically significant candidate protein networks predicted to be altered in the affected cochlea. Quantitative PCR (qPCR) analysis of select candidates from the proteomic and bioinformatic investigations showed up-regulation of Coch mRNA and those of p53, Brn3a and Nrf2, transcription factors linked to stress response and survival. Increased mRNA of Brn3a and Nrf2 has previously been associated with increased expression of cochlin in human glaucomatous trabecular meshwork. Our report strongly suggests that increased level of cochlin is an important etiologic factor leading to the degeneration of cochlear neuroepithelia in the USH1F model.