Chronic Sinusitis: The Empiric Treatment Strikes Back: Is CRS Directly Caused by Infectious Agent(s)?

Chronic sinusitis leads to unresolved infection and inflammation resulting in tissue remodeling, then further propagates the vicious cycle of deterioration and dysfunction of the sinuses’ natural defense mechanisms, and yet another cycle of infection and mucosal injury. Antibiotic therapy targeting pathogens classically implicated in sinusitis could augment the risk of therapeutic failure through the natural selection of resistant and/or virulent pathogens, especially in the presence of Gram-negative E. coli. Our recent demonstration of highly pathogenic E. coli, detected through intraoperative biopsy of sinus tissue, allowed the resolution of chronic sinusitis symptoms upon E. coli targeted therapy. The isolated E. coli carried three genes, each coding biofilm formation, which may, in part, account for the chronicity of E. coli sinusitis. We recommend that, patients with chronic sinusitis be considered for intraoperative biopsy for unusual pathogens, therefore allowing targeted therapy. In the future, use of vaccines and biofilm inhibitors might be an effective therapeutic consideration

Evaluation of cardiac muscle microvessel density in children diagnosed with cyanotic heart defects

Abstract: Angiogenesis is largely an adaptive response to tissue hypoxia, which occurs in a wide variety of situations. Interestingly, the extent of hypoxia-induces angiogenesis in the cardiac muscle of children diagnosed with congenital cyanotic heart defects is not well established. Thus, the aim of this study was to 1) estimate the cardiac muscle microvessel density (MVD) in children diagnosed with cyanotic (study group) and non-cyanotic (control group) heart defects and to 2) evaluate the prognostic significance of MVD value in the development of ventricular dysfunction in the postoperative period. The study group included 42 children diagnosed with cyanotic heart defects. The control group comprised 33 patients with a diagnosis of non-cyanotic heart failure. The collected tissue included cardiac muscle sections from the right atrium and interventricular or interatrial wall during surgical correction of the defect. Immunocytochemistry with monoclonal mouse anti-human antibodies against CD31, CD34 and CD105 was employed to estimate the MVD value. The mean cardiac muscle MVD, defined by CD34 expression, was 596.7 ± 32.6 microvessels per 1 mm2 in the study group, which was notsignificantly different from the mean MVD in the control group (461.2 ± 30.5). Interestingly, in non-cyanotic heart defects, an inner area of subendocardial meshwork was estimated to have 75.3 ± 7.0 microvessels per 1 mm2, compared to 92.8 ± 10.9 microvessels per 1 mm2 (p = 0.0082) in patients with cyanotic heart defects. No significant correlations between MVD value and ventricular dysfunction were found. Cyanotic heart defects resulting in chronic hypoxia might provoke angiogenesis in the subendocardial meshwork of the heart wall. The process seems to be independent of the type of cyanotic heart disease and most likely takes place during antenatal development. A ventricular dysfunction observed in some cases of cyanotic heart defects could not be predicted by the estimation of MVD

Nephrotic syndrome unfavorable course correlates with downregulation of podocyte vascular endothelial growth factor receptor (VEGFR)-2

Idiopathic nephrotic syndrome (INS) in children is most commonly caused by primary glomerulopathies. Morphological lesions observed in INS might be secondary to inflammatory factors of mainly extra-renal origin. The vascular endothelial growth factor (VEGF) family is regarded as playing a crucial role in this pathomechanism. The aim of the present work was to analyze the possible relation between VEGF-C and VEGF receptor (VEGFR)-2 expressions at electron microscopy level in different INS cases. The study group comprised 18 children with minimal change disease (MCD), 30 patients diagnosed with diffuse mesangial proliferation (DMP) and 11 subjects with focal segmental glomerulosclerosis (FSGS). An indirect immunohistochemical assay employing monoclonal anti-VEGF-C and anti-VEGFR-2 antibodies was applied in the study. The immunohistochemical expression of VEGF-C within podocyte cytoplasm was significantly increased in DMP subjects who were resistant to steroids and in all FSGS patients compared to MCD children and controls (p < 0.05). VEGF-C over-expression in these cases was followed by downregulation of VEGFR-2. Nephrotic syndrome progression correlates with the downregulation of podocyte VEGFR-2. For this reason, decreased VEGFR-2 expression in the podocyte processes of children with idiopathic nephrotic syndrome might be regarded as a potent factor of unfavorable prognosis. (Folia Histochemica et Cytobiologica 2011; Vol. 49, No. 3, pp. 472&#8211;478

Morphology of caterpillars and pupae of European Maculinea species (Lepidoptera: Lycaenidae) with an identification table

Ofthe four recognized Maculinea species that occur in Europe, three (M. teleius, M. nausitlzous, and M. alcon) are found on damp meadows, and may co-occur; sometimes their larval instars even occupy the same host ant nest. It is, therefore, important to be able to distinguish between the caterpillars of these species for effective conservation. We present the morphology of the larvae and pupae of these three species, and a simple key to their identification. Inter-specific differences among larvae and pupae, and within-species differences among larval instars, are underlined in order to enable their proper identification. The length, colour and distribution of bristles are considered the best features for species and instar identification. The morphology ofthe described species is compared with that of the other European species, M. arion

Expression of galectin-3 in nephrotic syndrome glomerulopaties in children.

BACKGROUNDGalectins are a family of ancient animal carbohydrate binding proteins; the name is from their description as beta-galactoside-specific lectins. They have been strongly implicated in inflammation and cancer. Studies of the association of galectins with various aspects of kidney disease in humans are still at an early stage. In line with the above, the aim of the present report was to analyse the immunohistochemical expression of galectin-3 (the only chimera galectin currently identified) in renal biopsy specimens of children with idiopathic nephrotic syndrome (INS).PATIENTS AND METHODSEighteen children with minimal change disease (MCD), 30 with diffuse mesangial proliferation (DMP) and 11 with focal segmental glomerulosclerosis (FSGS) treated between 2003 and 2006 in the Department of Paediatric Cardiology and Nephrology, Poznan University of Medical Sciences. An indirect immunohistochemical protocol using a polyclonal rabbit antibody against human galectin-3 was employed.RESULTSIn the control, MCD and DMP children who responded to steroid therapy anti-galectin-3 reactivity was present both in renal cortex and medulla. It was the strongest within cortical collecting ducts and subjectively less expressed in distal tubules. The total number of galectin-3 positive cortical and medullary segments of collecting ducts was significantly higher in the subjects who did not respond to steroid therapy These patients revealed also immunohistochemical reactivity of galectin-3 within nuclei of individual glomerular mesangial cells (

The expression of Platelet-derived Growth factor receptors (PDGFRs) and their correlation with overall survival of patients with ovarian cancer

Objectives: The main aim of the study was to investigate the expression of Platelet-Derived Growth Factor Receptors alpha (PDGFR-alpha) and beta (PDGFR-beta) in malignant and benign ovarian tumors. We performed an analysis of the correlation of PDGFRs expression and stage of the disease, tumor grade and histopathological type of epithelial ovarian cancer (EOC). Additionally, we evaluated patient prognosis according to PDGFR expression.  Material and methods: Our study group was composed of 52 samples of EOCs, 35 samples of benign ovarian tumors (BOTs), and 21 samples of unchanged ovaries (UOs). The samples were collected from patients who had been operated on in the Division of Gynecological Surgery of the Poznan University of Medical Sciences.  Results: PDGFR-alpha was found to be expressed more frequently in cancer cells of EOCs, when compared with tumor cells of BOTs and epithelium of UOs. On the other hand, PDGFR-alpha receptors were present less frequently in the stroma of EOCs, when compared with the stroma of BOTs and UOs. Comparing the studied groups, there were no statistically significant differences in the expression of PDGFR-beta. The expression of both PDGFRs was not related to the FIGO stage, grade or histopathological type of EOCs. The expression of the PDGFR-beta receptor in cancer cells was associated with an improved overall survival among patients with EOCs. Patient prognosis was not affected by either PDGFR-alpha expres- sion or by PDGFR-beta tumor stroma expression.  Conclusions: The expression of PDGFR-alpha is significantly different when comparing EOCs, BOTs and UOs. However, the prognosis of EOC only seems to be affected by PDGFR-beta expression in cancer cells.

Wpływ chirurgicznego leczenia rozejścia linii szwu mechanicznego u chorych po zabiegu ominięcia żołądka sposobem Roux na gospodarkę węglowodanową oraz stężenia hormonów jelitowych &#8212; badanie wstępne

Introduction: Staple-line disruption (SLD) following Roux-en-Y gastric bypass (RYGB) results in weight regain. This study evaluated glucose homeostasis and gut hormonal changes following surgical repair of gastrogastric fistula. Material and methods: Three patients with SLD underwent an oral 75 g glucose tolerance test (OGTT) before (baseline) and one week after gastric pouch restoration. Plasma glucose, insulin and glucagon glucose-dependent insulinotropic polypeptide (GIP) and glucagonlike peptide&#8211;1 (GLP-1) were measured in the OGTT samples. Fasting plasma levels of ghrelin and leptin were assessed. Results: Restoration of gastric pouch provided moderate amelioration of glucose metabolism and gut hormones, yet without complete normalisation of glucose homeostasis at one week after surgery. Duodenal passage exclusion resulted in early improvement of control fasting plasma glucose with decrease of glucagon from 18.5 to 15 (ng/mL, by 19%), relatively stable insulin and decline of incretin hormones (GIP and GLP-1). Post-challenge measurements confirmed amelioration of glycaemic control with decrease of plasma glucose from 182 to 158 mg/dL at 60 minutes. Surgical re-intervention resulted in exacerbation of GIP response with brisk rise in plasma level, accompanied by considerable increase of peak insulin concentration. The overall post-challenge glucagon and GLP-1 responses were decreased. Marked decrease in fasting plasma ghrelin and leptin were observed. Conclusions: Our report gives further insight into the hormonal mechanisms underlying the effects of surgically altered anatomy of different parts of the small intestine on glucose homeostasis that is highly important, since it may facilitate novel conservative therapies of diabetes without the need for surgery.Wstęp: Rozejście linii szwu mechanicznego (SLD) po operacji ominięcia żołądka sposobem Roux (RYGB) skutkuje nawrotem otyłości. W badaniu poddano ocenie zmiany gospodarki węglowodanowej oraz stężeń hormonów jelitowych po chirurgicznym leczeniu przetoki żołądkowo-żołądkowej. Materiały i metody: Trzech chorych z SLD poddano doustnemu testowi obciążenia 75 g glukozy (DTOG) przed oraz jeden tydzień po zabiegu odtworzenia proksymalnego zbiornika żołądkowego. W próbkach krwi pobranych podczas DTOG oceniano osoczowe stężenie glukozy, insuliny, glukagonu, insulinotropowego peptydu zależnego od glukozy (GIP) oraz glukagonopodobnego peptydu 1 (GLP-1). We krwi pobranej na czczo oceniano dodatkowo stężenie greliny oraz leptyny. Wyniki: Odtworzenie proksymalnego zbiornika żołądkowego prowadzi do umiarkowanej poprawy metabolizmu glukozy oraz stężeń hormonów jelitowych, jednakże bez całkowitej normalizacji homeostazy węglowodanowej w jeden tydzień od zabiegu operacyjnego. Wyłączenie pasażu dwunastniczego skutkowało wczesną poprawą kontroli stężenia glukozy na czczo, ze spadkiem stężenia glukagonu z 18,5 do 15 (ng/ml, o 19%), względnie stałym stężeniem insuliny oraz spadkiem stężeń hormonów inkretynowych (GIP i GLP-1). Pomiary dokonane po obciążeniu glukozą potwierdziły poprawę kontroli glikemii ze spadkiem osoczowego stężenia glukozy z 182 do 158 mg/dl w 60 minucie testu. Zabieg chirurgiczny skutkował nasileniem sekrecji GIP z wyraźnym wzrostem osoczowego stężenia tego hormonu po obciążeniu glukozą, z towarzyszącym znacznym wzrostem najwyższego stężenia insuliny. Całkowite stężenie glukagonu oraz GLP-1 po obciążeniu glukozą malało. Zaobserwowano znaczny spadek stężenia greliny oraz leptyny na czczo. Wnioski: Praca pozwala na dalsze poznanie mechanizmów hormonalnych leżących u podstaw wpływu chirurgicznie zmienionej anatomii różnych części jelita cienkiego na homeostazę węglowodanową. Poznanie tych mechanizmów jest bardzo istotne z punktu widzenia klinicznego, gdyż w przyszłości może przyczynić się do wprowadzenia nowych metod leczenia zachowawczego cukrzycy, bez konieczności wykonywania operacji bariatrycznych