Metabolic syndrome: its features in overweight women with polycystic ovary syndrome as compared with obese women without ovarian dysfunction?

UNLABELLED: OVARIAN DYSFUNCTIOBJECTIVE: The study assesses the frequency of metabolic changes in overweight patients with or without polycystic ovary syndrome. MATERIAL AND METHODS: The study group was made up by 148 patients of whom 99 patients without polycystic ovary syndrome (group A, control group) and 49 with polycystic ovary syndrome (group B), that came in our endocrine unit for a weight loss program, in the September 2008 March 2009 period. Morphometric parameters (height, weight, body mass index), biological parameters (cholesterol, triglycerides, blood glucose, glycated hemoglobin) and body composition analysis by measuring the electrical bioimpedance, were evaluated. RESULTS: Patients with polycystic ovary syndrome have a higher percentage of total fat (38.22+/-7.2) than patients without polycystic ovary syndrome (36.316+/-5.65) (p<0.05), for the same characteristics. Glycated hemoglobin, blood glucose and triglycerides were found higher in group B patients. Furthermore, the amount of free testosterone is higher in group B patients compared to those in group A. The prevalence of metabolic syndrome was higher in polycystic ovary syndrome cases (26.13%) comparative with overweight cases (16.16%, p<0.01). CONCLUSIONS: In the group of overweight patients, the group of patients with polycystic ovary syndrome is a particular group showing more severe metabolic changes.

Giant uterine leiomyoma.

Uterine leiomyomas represent the most common benign tumors of the female reproductive tract. Giant uterine leiomyomas are very rare neoplasms and represents a great diagnosis and therapeutic challenge. This article illustrates a case of a 45-year old woman presented to our surgery department with a 10-month history of progressive increasing abdominal size, back pain, vague abdominal pressure sensations, weight loss, constipation and urinary frequency. Physical examination, laboratory evaluation, transabdominal ultrasound and computed tomography scanning suggested a giant abdominopelvic mass. Abdominal supracervical hysterectomy with bilateral salpingo-oophorectomy was performed. Histologically, the specimen was a 18.1 Kg uterine leiomyoma measuring 33/28/22 cm. The patient's postoperative course was uneventful and she was discharged from the hospital on the sixth postoperative day.

Peripheral blood neutrophil granulocytes from patients with head and neck squamous cell carcinoma functionally differ from their counterparts in healthy donors.

Solid tumors such as head and neck squamous cell carcinoma (HNSCC) display an intense interaction between tumoral factors and the immune system. Functional modulation of tumor-infiltrating and peripheral blood immune cells plays an important role during tumor progression. In this pilot study we compared biological functions of polymorphonuclear granulocytes (PMN) from the peripheral blood of HNSCC patients and healthy subjects. PMN were simultaneously isolated from the peripheral blood of HNSCC patients and healthy donors for functional analysis (apoptosis, production of reactive oxygen species (ROS), cytokine release and immunophenotyping). PMN from HNSCC patients showed a significantly lower inducible production of ROS (P = 0.02) and reduced spontaneous apoptosis (P= 0.008) compared with PMN from healthy donors. Under standard culture conditions, there was no significant difference regarding the release of inflammatory cytokines between PMN from HNSCC patients and PMN from healthy donors. Confirming previous observations, serum concentrations of PMN-related cytokines were significantly higher in the peripheral blood of HNSCC patients than in that of controls. Importantly, immunophenotyping revealed an increased number of immature PMN in PMN fractions isolated from HNSCC patients. Peripheral blood PMN from HNSCC patients and healthy donors show distinct functional differences. The presence of increased numbers of immature stages of PMN in HNSCC patients may partly contribute to the changes observed. After recruitment to and infiltration of the tumor, PMN may be further modulated in the local tumor microenvironment. This pilot study justifies functional analyses of myeloid cells in larger cohorts of patients with HNSCC.

[Innovations in biomarker development: a pathway towards individualized cancer therapy?]. / Moderne Methoden der Biomarkerentwicklung: eine Chance für die individualisierte Tumortherapie?

Despite multiple medical and scientific achievements, cancer remains a leading cause of death worldwide. Next to imaging technologies, molecular methods for early detection and for monitoring of the course of disease are of increasing interest. Thus, over the past years numerous studies have focused on the identification of biomarkers for cancer diagnosis, prognosis and response to therapy. The study of biomarkers seems to pose a high degree of complexity because many different types of molecules may, in principle, serve as potential biomarkers. In addition, these molecules can be produced either by the tumor or by the tumor-host in response to the presence of cancer. In this review the authors will address several major topics encompassed by the field of biomarker research. They will discuss the primary sources from which biomarker candidates can be 'mined' as well as the technological or methodological challenges associated with identification of biomarkers. Furthermore, the review will focus on current biomarker candidates for head and neck squamous cell carcinoma (HNSCC), with particular interest on several molecules yielding potential relevance for detection and prognosis of this type of cancer. Finally, several biomarker candidates with predictive potential for the response to therapy of HNSCC patients will be discussed, since identifying such molecules is crucial for developing individually-tailored and improved therapeutic strategies.

Primary hydatid cyst with an unusual location--a case report.

Human cystic echinococcosis, a zoonotic infection caused by Echinococcus granulosus, is still a largely extended public health problem in endemic regions (China, Middle East, Mediterranean region, South America, Russian Federation, etc.). Primary echinococcosis may develop in almost any organ (liver, lung, kidney, spleen, mediastinum, heart, brain, bones, pancreas, breast, ovaries, etc.). The liver and the lungs are the most frequently involved organs. Primary hydatid disease of the soft tissue is extremely rare, even in endemic areas. The paper will be focused on analyzing this rare disease. A 46-years old woman who came to our Department of Surgery with a 7/8 cm painless, round, palpable mass in the subcutaneous tissue of the proximal anteromedial side of the right thigh. Based on clinical and laboratory findings and imaging techniques we suspected a hydatid cyst. Conservative surgery associated with antihelminthic substances intraoperative and Albendazole postoperative was performed. After an uneventful recovery the patient was discharged 7 days after operation. No local or systemic recurrences were detected during 1 year follow up.

The cold case: are rhinoviruses perfectly adapted pathogens?

Rhinoviruses, which cause common cold, belong to the Picornaviridae family, small non-enveloped viruses (diameter 15-30 nm) containing a single-stranded RNA genome (about 7 kb). Over 100 different rhinoviral serotypes have been identified thus far, establishing rhinoviruses as the most diverse group of Picornaviridae. Based on receptor binding properties, rhinoviruses are divided into two classes: the major group binding to intracellular adhesion molecule-1 and the minor group binding to the very low density lipoprotein receptors. Interactions between virus and the receptor molecules cause a conformational change in the capsid, which is a prerequisite for viral uptake. Rhinoviruses trigger a chemokine response upon infection that may lead to exacerbation of the symptoms of common cold, i.e. asthma and inflammation. The following review aims to summarize the knowledge about rhinoviral infections and discusses therapeutical approaches against this almost perfectly adapted pathogen.

TRAIL activates acid sphingomyelinase via a redox mechanism and releases ceramide to trigger apoptosis.

We have previously shown that activation of the acid sphingomyelinase (ASM), the release of ceramide and the formation of ceramide-enriched membrane domains are central for the induction of apoptosis by CD95. Here, we demonstrate that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and CD95 activate the ASM via a redox mechanism resulting in release of ceramide and formation of ceramide-enriched membrane platforms. Ceramide-enriched membrane platforms serve to cluster DR5 upon stimulation. Antioxidants prevent TRAIL-mediated stimulation of ASM, the release of ceramide, the formation of ceramide-enriched membrane platforms and the induction of apoptosis by TRAIL. Further, ASM-deficient splenocytes fail to cluster DR5 in ceramide-enriched membrane domains upon TRAIL stimulation and resist TRAIL-induced apoptosis, events that were restored by addition of natural C(16)-ceramide. A dose-response analysis indicates that ceramide-enriched membrane platforms greatly sensitized tumor cells to TRAIL-induced apoptosis. Our data indicate that ceramide-enriched membrane platforms are required for the signaling of TRAIL-DR5 complexes under physiological conditions.

TNF-alpha induction by LPS is regulated posttranscriptionally via a Tpl2/ERK-dependent pathway.

Tpl2 knockout mice produce low levels of TNF-alpha when exposed to lipopolysaccharide (LPS) and they are resistant to LPS/D-Galactosamine-induced pathology. LPS stimulation of peritoneal macrophages from these mice did not activate MEK1, ERK1, and ERK2 but did activate JNK, p38 MAPK, and NF-kappaB. The block in ERK1 and ERK2 activation was causally linked to the defect in TNF-alpha induction by experiments showing that normal murine macrophages treated with the MEK inhibitor PD98059 exhibit a similar defect. Deletion of the AU-rich motif in the TNF-alpha mRNA minimized the effect of Tpl2 inactivation on the induction of TNF-alpha. Subcellular fractionation of LPS-stimulated macrophages revealed that LPS signals transduced by Tpl2 specifically promote the transport of TNF-alpha mRNA from the nucleus to the cytoplasm.

HLA-DR2 gene and Spanish patients with ulcerative colitis.

BACKGROUND: An association with class II MHC genes has been described in ulcerative colitis, as in other diseases with immunological pathogenesis. Heterogeneous results have been reported, depending on the studied population. OBJECTIVE: To study the importance of these genes in our population, mainly the alleles of group HLA DR2 (gene HLA-DRB1). PATIENTS AND METHODS: We studied a total of 107 patients diagnosed of ulcerative colitis and 200 unaffected controls. Complete information about sex, age, family antecedent, age of onset, localization, complications, surgery and treatment was obtained from these patients. DNA was extracted from peripheral blood leukocytes and all the individuals were HLA-DRB1 genotyping. RESULTS AND CONCLUSIONS: We conclude that a positive association exists between DR15 and ulcerative colitis (p < 0.05). This positive association was characterized and various clinical parameters were analyzed, being concluded that DR1501 is more frequent in this disease (p < 0.05) and in benign manifestations; the frequency of the allele DR1502 was also found to be elevated in severe manifestations.

Uncoupling of immune complex formation and kidney damage in autoimmune glomerulonephritis.

The generation of autoantibody and subsequent tissue deposition of immune complexes (IC) is thought to trigger the pathogenic consequences of systemic autoimmune disease. Modulation of the autoantibody response disrupts pathogenesis by preventing the formation of ICs; however, uncoupling IC formation from subsequent inflammatory responses seems unlikely because of the apparent complexity of the IC-triggered inflammatory cascade. However, the disruption of a single gene, which encodes the gamma chain of the Fc receptor, was found to achieve this uncoupling in a spontaneous model of lupus nephritis, the New Zealand Black/New Zealand White (NZB/NZW) mouse. Gamma chain-deficient NZB/NZW mice generated and deposited IC and activated complement, but were protected from severe nephritis, thus defining another potential pathway for therapeutic intervention in autoimmune disease.

[Myocardial infarction following a bee sting. Apropos of a case and review of the literature]. / Infarctus du myocarde consécutif à une piqûre d'abeille. A propos d'un cas et revue de la littérature.

The authors report a case of limited inferior myocardial infarction in a young man following a bee sting. Coronary angiography, performed following the acute phase, showed angiographically healthy coronary arteries and minimal sequelae of myocardial necrosis in the inferior territory. The pathogenic role of the bee sting in myocardial necrosis was suggested by the timing of the events. The probable mechanism responsible for this myocardial infarction was severe coronary arterial spasm (partly mediated by psychological stress related to the intensity of the anaphylactic reaction) with secondary in situ thrombosis probably facilitated by cardiovascular collapse. The role of anaphylaxis, generating acute coronary insufficiency, is discussed in the light of this clinical case.

A heterologous radioimmunoassay system for human osteocalcin. Applications in performance sports girls.

Taking into account the involvement of the measurement of osteocalcin, a protein-containing gamma-carboxyglutamic acid (Gla), in investigating the physiopathology of bone and calcium metabolism, a radioimmunoassay (RIA) method useful in human clinics was developed. The reagents for the RIA of human osteocalcin namely, the radioiodination preparation, the reference preparation and the antiserum were obtained starting from bovine bone on account of the structure similarities between bovine and human osteocalcin. The reagents were incubated at 4 degrees C for 48 h followed by the polyethylene-glycol (PEG) separation technique. The sensitivity of the osteocalcin RIA method is 2.0 ng/ml, the intraassay precision is 3-5% and the interassay precision, 8-12% (coeficient of variation). Osteocalcin was measured in the sera of 3 groups of performance sports girls under basal conditions and being of more or less similar ages: rowing girls (n = 10, mean age 16 yr 6 mos), gymnast girls (n = 13, mean age 14 yr 8 mos) and table tennis girls (n = 9, mean age 16 yr). The same samples were used for the measurement of myoglobin. Osteocalcin quantification showed similar levels in the rowing and the table tennis girls, i.e. 11.91 +/- 3.39 ng/ml (X +/- SD) and 9.50 +/- 4.15 ng/ml, respectively. By contrast, in the gymnast girls, the osteocalcin levels were about 4 times higher (44.31 +/- 7.27 ng/ml) than in the other two groups. Myoglobin measurements showed lower levels in the gymnast group, than in the rowing and the table tennis groups, the latter two having similar levels. The multiplicative increase of osteocalcin in the gymnast girls is interpreted and commented in relation to their age and sexual development.