In this study we evaluated the indications, complications, and the spectrum of histopathological results of percutaneous renal needle biopsy (PRNB) performed in our clinic. Between June 1990 and December 2006, 679 PRNBs were performed on native kidneys of 614 children (304 boys, 310 girls) with a mean age of 10.4 years. Most frequent indications for PRNB were nephrotic syndrome (47%), hematuria, and/or proteinuria (15.9%), acute renal failure (14.6%) and complex renal manifestations (18.9%). The overall complication rate was 15.2%. The most common complications were perirenal hematoma (12.4%) and macroscopic hematuria (2.6%). The most frequent histopathological group of diseases were glomerulopathies; these were diagnosed in 376 patients (61.2%) and included membranoproliferative glomerulonephritis (11.1%), mesangial proliferation (10.7%), diffuse proliferative glomerulonephritis (7.7%), and focal segmental glomerulosclerosis (7.3%) as the most frequent. The second most frequent group of histopathology was manifestations secondary to systemic diseases; these were shown in 195 patients (31.8%). Amyloidosis (11.4%) and Henoch-Schönlein nephritis (9.9%) made the majority of this group. In conclusion, our study demonstrated that PRNB is a safe procedure with usually transient complications showing the most frequent renal diseases that cause diagnostic and therapeutic difficulties for pediatric nephrologists.

Sepsis is one of the most important risk factors in acute respiratory distress syndrome (ARDS). beta-Glucan is a potent reticuloendothelial modulating agent, the immunobiological activity of which is mediated in part by an increase in the number and function of macrophages. In this study, we investigated the putative protective role of beta-glucan against sepsis-induced lung injury. Sepsis was induced by cecal ligation and puncture (CLP) in Wistar rats. The control group received saline, and the treatment groups received beta-glucan or beta-glucan + beta-1,3-D-glucanase. Five hours thereafter, plasma tumor necrosis factor (TNF) alpha, interleukin (IL) 1beta, and IL-6 levels were determined. Presence of lung injury was determined via lung tissue myeloperoxidase (MPO) activity, intercellular adhesion molecule (ICAM) 1 levels, and histopathological examination at 18 h after CLP. In a separate set of experiments, survival was monitored for 7 days after CLP. beta-Glucan treatment led to a significant increase in survival rate (63% in glucan-treated rats vs 38% in saline-treated rats). Administration of the beta-glucan inhibitor abrogated beta-glucan's survival benefit (50%). After CLP, plasma TNF-alpha, IL-1beta, and IL-6 concentrations were increased in control animals. When beta-glucan was administered, it completely blocked the elevation of TNF-alpha, IL-1beta, and IL-6. Administration of beta-1,3-D-glucanase suppressed glucan-induced decrease in cytokines. Animals treated with beta-glucan showed a significant reduction in lung injury score, a marked decrease in ICAM-1 expression, and a significant decrease in MPO levels. In contrast, beta-1,3-D-glucanase caused a significantly increased MPO and ICAM-1 levels in the lung. These data reveal that beta-glucan treatment improved the course of CLP-induced peritonitis and attenuated the lung injury. Administration of beta-glucanase inhibited the beta-glucan activity and resulted in enhanced lung injury.

Object The authors conducted a study to determine the effectiveness of mitomycin C in preventing postlaminectomy peridural fibrosis in rabbits. Methods Laminectomies were performed at L-4 in 12 rabbits. Color-coded cotton pads soaked either with 0.02% mitomycin C or saline were applied in a blinded fashion to the operative sites, with saline-treated laminectomy sites serving as controls. The rabbits were killed 30 days after surgery. The extent of peridural fibrosis was evaluated by histological analysis. The mitomycin C—treated sites showed significantly decreased peridural fibrosis. Conclusions Peridural fibrosis can be a devastating condition that develops after laminectomy. Topical application of mitomycin C may be a successful method of preventing postlaminectomy peridural fibrosis.

The role of transforming growth factor beta1 (TGF beta1) in airway remodeling in asthma and chronic obstructive pulmonary disease (COPD) has not been fully described. To evaluate the possible pathogenetic role of TGF beta1 in asthma and COPD, immunohistochemical expression of TGF beta1 was described in bronchial biopsies from patients with asthma and COPD compared with healthy individuals. Twelve subjects with asthma, 13 subjects with COPD, and 10 healthy individuals enrolled in the study. Bronchial biopsies were stained with hematoxylin and eosin and anti-TGF beta1 antibody. As a result, immunoreactive TGF beta1 was mainly localized in association with connective tissue in all groups. The staining intensity was not statistically different among the groups in bronchial epithelium, whereas it was significantly higher in the group of asthma in the submucosa. Because there is evidence showing a significant increase of staining intensity in the submucosa from asthmatics but not from subjects with COPD, we may conclude that TGF beta1 may play a significant role in pathogenesis of asthma but not in COPD.

Clinical disease caused by weakly pathogenic mycobacterial species, Mycobacterium bovis Bacille Calmette-Guérin (BCG) and non-tuberculous environmental mycobacteria (EM), which is known as Mendelian susceptibility to mycobacterial disease (MSMD), is a rare entity defined recently. Infections with the more virulent Mycobacterium species, M. tuberculosis, may have largely gone unnoticed in these patients due to early death. Mutations in five proteins (IFNgammaR1, IFNgammaR2, IL-12/IL-23Rbeta1, IL-12/IL-23p40 and STAT1) have been found in MSMD. These patients are prone to surprisingly few other infectious diseases mainly to salmonellosis. Here we present three IL-12/IL-23Rbeta1 deficient patients from three different families and with different genetic mutations, who presented exclusively with Salmonella infections. Bacteremia and lymph node involvement were common clinical expressions. Leukocytoclastic vasculitis developed in one of these patients. Two patients were not inoculated with BCG, the third patient did not develop BCG infection although BCG vaccine had been given twice at ages of 1 and 7 years. All three patients responded well to antibiotic treatment. In conclusion, patients with chronic, recurrent or complicated Salmonella infections should be screened for MSMD, particularly for IL-12/IL-23p40/IL-12R/-23Rbeta1 deficiency. Conversely, in patients with genetic IL-12/-23Rbeta1 deficiency a full evaluation for Salmonella infection is required. IL-12/IL-23p40/IL-12R/IL-23Rbeta1 deficiency seem to be underdiagnosed in patients with salmonellosis, and since such patients need prolonged therapy, diagnosis is important.

Survivin is an inhibitor of apoptosis protein, which is overexpressed in many carcinomas, including lung carcinoma. The aim of this immunohistochemical study was to investigate the role of survivin in the early steps of lung carcinogenesis and non-small cell lung carcinomas (NSCLC), and its relationship with expression of p53 protein, a tumor suppressor gene involved in cell cycle control. In the normal bronchial epithelium, low-grade atypical adenomatous hyperplasia (AAH) and non-neoplastic lung parenchyma adjacent to tumor, survivin was found completely negative. Expression of survivin was detected in the areas of squamous metaplasia and dysplasia as well as high-grade AAH lesions adjacent to tumor. Survivin was expressed in 50 (64%) and p53 in 41 (53%) NSCLC. Survivin expression was significantly correlated with lymph node metastasis (p=0.02). There was no correlation between survivin and p53 expression. The patients with expression of survivin had significantly worse prognosis (Log-rank test, p=0.003). Multivariate Cox regression analysis showed TNM stage (p<0.001) and survivin expression (p=0.003) as independent prognostic indicators. In conclusion, survivin expression might be an early step in lung carcinogenesis. Survivin expression might also be used as a prognostic indicator predicting the worse outcome in NSCLC, and might be a novel target for the treatment of patients with preinvasive lesions of lung and NSCLC.

The treatment strategy of differentiating lung carcinomas into small-cell lung carcinoma and non-small-cell lung carcinoma has been satisfactory until recently. The introduction of novel cytotoxic agents that affect a patient's response to therapy has made further differentiation important. Non-small-cell carcinoma represents a heterogeneous group of cancers with varying histologic subtypes, hence the necessity to subgroup them. In the case of adenocarcinoma and squamous cell cancer, their different responses to novel therapeutic agents and their higher occurrence make differentiation between them even more important. New markers such as desmoglein-3 (positive for squamous carcinoma) and Napsin A (positive for adenocarcinoma), which show improved specificity and sensitivity, may be particularly useful for this type of differentiation. In our study, 124 surgically resected specimens were used: 57 adenocarcinoma, 42 squamous cell carcinoma, 16 large-cell carcinoma, 1 small-cell carcinoma, and 8 typical carcinoid tumor samples. The sensitivity to desmoglein-3 and Napsin A was 92.8% and 85.9%, whereas specificity was 100% and 97%, respectively. The use of a desmoglein-3 and Napsin A double-staining strategy in our study confirmed that these markers are useful in differentiating pulmonary squamous cell carcinoma and pulmonary adenocarcinoma from other subtypes.

Malignant pleural mesothelioma (MPM) is a rare and asbestosis-associated tumor. MPM commonly invades locally, mostly in the lung, heart, pericardium, chest wall, and vertebrae. Distant metastasis of MPM is very rare. Here we report a patient with MPM who presented with multiple unusual distant metastases. The patient's thorax tomography demonstrated right-sided, irregularly-thickened pleura with nodular masses and invasion of the chest wall into the subcutaneous area. The patient underwent biopsy for a subcutaneous mass in the right anterior chest wall. Pathologic examination revealed a malignant mesenchymal tumor. During follow-up, he suffered from a painful nodule on the scalp and nodules on the fingers, as well as weakness in his right arm. Cranial magnetic resonance imaging illustrated a 1 cm nodule in the left cerebellar hemisphere. Histopathologic examination of the biopsy from the nodule on the scalp revealed a typical mixed type of MPM, with calretinin, vimentin and creatine 5/6 positivity. Distant metastases can be seen in MPM and a biopsy of metastatic regions can yield the diagnosis.