Iatrogenic coronary artery fistula in a patient with a single coronary artery.

Here, we report on a case of coronary artery fistula that developed following the repair of a double-outlet right ventricle (DORV) with infundibular pulmonary stenosis in a patient who has a single coronary artery. The major concern in this case was that of reduction of coronary blood flow from the patient's only coronary artery to the myocardium distal to the fistula.

HIN-1, a putative cytokine highly expressed in normal but not cancerous mammary epithelial cells.

To identify molecular alterations implicated in the initiating steps of breast tumorogenesis, we compared the gene expression profiles of normal and ductal carcinoma in situ (DCIS) mammary epithelial cells by using serial analysis of gene expression (SAGE). Through the pair-wise comparison of normal and DCIS SAGE libraries, we identified several differentially expressed genes. Here, we report the characterization of one of these genes, HIN-1 (high in normal-1). HIN-1 expression is significantly down regulated in 94% of human breast carcinomas and in 95% of preinvasive lesions, such as ductal and lobular carcinoma in situ. This decrease in HIN-1 expression is accompanied by hypermethylation of its promoter in the majority of breast cancer cell lines (>90%) and primary tumors (74%). HIN-1 is a putative cytokine with no significant homology to known proteins. Reintroduction of HIN-1 into breast cancer cells inhibits cell growth. These results indicate that HIN-1 is a candidate tumor suppressor gene that is inactivated at high frequency in the earliest stages of breast tumorogenesis.

[Pathophysiology of hemodynamic shock (circulatory failure). Part 2]. / Patofiziologija hemodinamskog soka (krvotocnog urusaja) (drugi dio).

In the second part of the review authors stress the importance of extent and duration of tissue shock hypoenergosis and body reactive capacity for the clinical outcome of the syndrome. Functional restitution, decrease of functional organ capacity, permanent absence of certain organs' function and death, represent a possible clinical status caused by and developed during the shock syndrome. Progressive pathologic alteration of tissue function and structure correlates well with the degree of tissue hypoenergosis. A short detailed description of the tissue alterations is outlined in the paper. The shock syndrome very often consists of parallel pathogenic processes which therefore can be classified as a complex pathogenic forms of the shock. A list of clinical disorders which develop due to a complex shock pathogenesis, are outlined in the paper. Tentative relative contribution of individual pathogenic processes are estimated for various diseases. Clinical symptoms and signs, as well as laboratory parameters give a valuable information which points to the level of shock development and reversibility. Correlation of clinical parameters and pathophysiologic processes are outlined. Simple predictive rules are re-discussed in the scope of underlying pathophysiology. In addition, a related hemodynamic disorders are shortly discussed in the paper.

[The pathophysiology of hemodynamic shock syndrome (part one)]. / Patofiziologija hemodinamskog soka (krvotocnog urusaja) (prvi dio).

Hemodynamic shock syndrome represents an acute circulatory failure leading to a multiple organ failure. Such circulatory failure develops due to a decrease of arteriovenous blood pressure gradient as a consequence of three independent groups of pathogenic mechanisms (cardiogenic, vasohypotonic and hypovolemic), all of which lead to the common pathogenic pathways. A decrease of arteriovenous pressure gradient induces vasomotoric responses, reactive body fluids redistribution, endocrine, metabolic as well as tissue energy adjustments. In this review a comprehensive synopsis of pathogenic processes is outlined. The cardiogenic mechanisms include the acute systolic and/or diastolic heart failure. Vasohypotonic mechanisms (neurogenic, septic and anaphylactic) are due to vascular tonus missadjustment. Hypovolemia caused by blood, plasma, water and electrolytes losses and/or sequestration, leads to decrease of pressure gradient as soon as the extent of hypovolemia overcomes the compensatory vascular capacity. The decrease of tissue perfusion is direct consequence of the arteriovenous pressure gradient loss. Tissue hypoperfusion causes a progressive depletion of cellular ATP concentration (cellular hypoenergosis), which very often falls lower than 0,1 mmol/L. Cellular hypoenergosis plays the critical role in conversion of negative homeostatic regulation into a positive feedback mode. Positive homeostatic regulation (circuli vitiosi) amplifies deterioration of arteriovenous blood pressure gradient, which reversely intensifies the degree of energy depletion in the tissues. Such homeostatic conversion plays a critical role in the development of progressive phase (systemic failure, decompensation) of the shock.

Our 10-year experience with embolized Wilms' tumor.

In the Department of Pediatric Surgery, Clinical Hospital Center Rebro in Zagreb, during the last 10 years a new method of invasive diagnostic and at the same time therapeutic procedure for the treatment of Wilms' tumor has been introduced. The treatment is preoperative Percutaneous Transcatheter Intraarterial Embolization (PTIE) of the renal artery. The aim of this procedure is to reduce vascularization, to decrease the mass of kidney affected by the tumor, to separate it from the surrounding tissue, to decrease intraoperative spillage of malignant cells into the blood stream and their metastasizing. As a result nephrectomy is easier to perform. It has been confirmed that it is best to perform nephrectomy 48 hours after embolization. The authors present their own experience with 33 patients, ranging from 1 to 16 years of age.