Evaluation of Turkish seaweeds for antiprotozoal, antimycobacterial and cytotoxic activities

As part of our continuing research on seaweeds, crude MeOH extracts of two green, three brown and six red algae collected from Marmara, Black, Aegean and Mediterranean Seas were screened. Four parasitic protozoa, i.e. Plasmodium falciparum, Trypanosoma brucei rhodesiense, T. cruzi, Leishmania donovani and the tubercle bacillus Mycobacterium tuberculosis were used as test organisms for the in vitro assays. The selective toxicity of the extracts was also determined against mammalian L6 cells. All seaweed extracts were active against T. brucei rhodesiense; the Dasya pedicellata extract was the most potent (IC₅₀ value 0.37 µg/mL). The same extract also weakly inhibited the growth of T. cruzi (IC₅₀ 62.02 µg/mL). All seaweed extracts also showed leishmanicidal activity (IC₅₀ values 16.76–69.98 µg/mL). The majority of the extracts also exhibited antiplasmodial potential and the most potent extracts were those from D. pedicellata (IC₅₀ 0.38 µg/mL), Codium bursa (IC₅₀ 1.38 µg/mL) and Caulerpa rasemosa (IC₅₀ 3.12 µg/mL). One brown and two red algal extracts showed some weak activity against Mycobacterium tuberculosis (MIC values 125–256 µg/mL). Except for the extract of Dasya pedicellata, none of the extracts displayed any cytotoxicity. This is the second study investigating the antiprotozoal activities of Turkish marine algae and identifies Dasya pedicellata, an understudied algal species, as a candidate for further studies. Copyright © 2010 John Wiley & Sons, Ltd.     

STAT3 and STAT1 mediate IL-11-dependent and inflammation-associated gastric tumorigenesis in gp130 receptor mutant mice

Deregulated activation of STAT3 is frequently associated with many human hematological and epithelial malignancies, including gastric cancer. While exaggerated STAT3 signaling facilitates an antiapoptotic, proangiogenic, and proproliferative environment for neoplastic cells, the molecular mechanisms leading to STAT3 hyperactivation remain poorly understood. Using the gp130(Y757F/Y757F) mouse model of gastric cancer, which carries a mutated gp130 cytokine receptor signaling subunit that cannot bind the negative regulator of cytokine signaling SOCS3 and is characterized by hyperactivation of the signaling molecules STAT1 and STAT3, we have provided genetic evidence that IL-11 promotes chronic gastric inflammation and associated tumorigenesis. Expression of IL-11 was increased in gastric tumors in gp130(Y757F/Y757F) mice, when compared with unaffected gastric tissue in wild-type mice, while gp130(Y757F/Y757F) mice lacking the IL-11 ligand-binding receptor subunit (IL-11Ralpha) showed normal gastric STAT3 activation and IL-11 expression and failed to develop gastric tumors. Furthermore, reducing STAT3 activity in gp130(Y757F/Y757F) mice, either genetically or by therapeutic administration of STAT3 antisense oligonucleotides, normalized gastric IL-11 expression and alleviated gastric tumor burden. Surprisingly, the genetic reduction of STAT1 expression also reduced gastric tumorigenesis in gp130(Y757F/Y757F) mice and coincided with reduced gastric inflammation and IL-11 expression. Collectively, our data have identified IL-11 as a crucial cytokine promoting chronic gastric inflammation and associated tumorigenesis mediated by excessive activation of STAT3 and STAT1.     

Health-related quality of life issues after cosmetic breast implant surgery in Finland

The purpose of this study is to compare women with cosmetic breast implants with population controls to examine health-related quality of life. A questionnaire including quality-of-life questions was mailed to 399 Finnish women who had had cosmetic breast implants during the years 1973-2002. The response rate of the study was 85. Results were compared with average Finnish women from a representative population sample. There were no differences in total score of health-related quality of life between women with breast implants and controls. Women with breast implants had lower health-related quality of life in dimensions of distress and sexual activity and partly also in dimensions of sleeping and mental function when compared with controls. On the other hand, operated women reported significantly less discomfort and symptoms than controls. Differences in health-related quality of life between women with breast implants and controls were largest in dimensions of distress, sexual activity, sleeping, and symptoms.     

Lumbosacral extrarenal Wilms' tumour: a case report and literature review

Occurrence of extrarenal Wilms' tumour (WT) is very exceptional and the diagnosis is almost always made after surgical intervention. The tumour can be located in the retroperitoneum, uterus, cervix, testes, skin and even in the thorax. The exact mechanism whereby a WT occurs in extrarenal tissues is not known. The presence of ectopic metanephric blastema cells or the WT gene that cause transformation of extrarenal primitive mesonephric or pronephric remnants into WT are both considered in the embryogenesis. Although ultrasonography and CT scan are both helpful in the definition of retroperitoneal tumours, there is no characteristic finding to diagnose an extrarenal WT before surgery. However the histological characteristics are the same as in intrarenal WT, a retroperitoneal teratoma should be clearly investigated for a possible admixture of WT cells. Patients with extrarenal WT are given the same treatment protocol as patients with stage III WT. In this paper, a 5-year-old female patient with an extrarenal WT located in the lumbosacral region is presented. Conclusion: as a rule, diagnosis of extrarenal Wilms' tumour is made after surgery. Surgical excision is the treatment of choice and the same general therapeutic rules should be followed as when the kidney were affected. Stage III guidelines for chemotherapy and radiotherapy are appropriate in these patients.     

Distribution of protectin (CD59), a complement membrane attack inhibitor, in normal human tissues.

Protectin (CD59) is a recently discovered 18-20 kDa glycoprotein that effectively inhibits lysis by the membrane attack complex of the homologous complement system. This glycoprotein is widely distributed on the membranes of human blood cells (erythrocytes and leukocytes). By using immunofluorescence microscopy, protectin was observed in vascular endothelia throughout the body and in extravascular tissues. Cells expressing protectin were also found in ductal epithelia of pancreatic, biliary, and salivary systems, bronchi, and kidney collecting ducts. Furthermore, protectin was expressed in the epidermis and in the syncytiotrophoblast of placenta. The expression of protectin in endothelia, in various epithelial cells, and in placenta presumably protects autologous tissues and the fetoplacental unit from complement-mediated damage.     

Dyshematopoiesis in combined immune deficiency with congenital neutropenia

This report describes a patient with combined immune deficiency associated with congenital neutropenla (CID/CN) and reports a partial characterization of his hematopoletic abnormalities. The CID/CN syndrome described is characterized by neutropenla and by deficiencies in B-lymphoid and T-lymphoid cell number and function. Red cell and platelet counts were normal. In vitro assays indicate that the myeioid lineage was developmentally arrested at the level of the committed monocyte/granulocyte progenitor (CFU-GM), while precursors to the CFU-GM progenitor were normal. In vitro studies showed that the defect in myeiold development was not corrected with G-CSF or GM-CSF. However, combinations of cytokines present in conditioned media from the T-cell lines MO or C5MJ, or defined multiple cytokine combinations containing IL-1, IL-3, GM-CSF, kit ligand, IL-6, and IL-9, restored myelopoiesis in-vitro. In contrast, CBMJ-conditioned media did not correct deficiencies in immune function in the patient's lymphocytes and accessory cells. No abnormalities in the production of G-CSF, GM-CSF, M-CSF, or IL-1 from the patient could be identified to account for the defects in myelopoiesis orimmune function. © 1994 Wiley-Liss, Inc.     

Study of quality of life in patients with multiple sclerosis

INTRODUCTION: Multiple sclerosis (MS) is a neurological impairment mostly affecting younger adults substantially decreasing their working and living abilities. Different rating scales to determine disabilities are being used: EDSS, NRS, and CAMBS. The objective of this study was to assess the quality of life in MS patients, with reference to the disease itself and its treatment, comparing patients with MS and a matching healthy control group. METHODS AND SUBJECTS: Subjects were divided into two groups, a group of patients with MS and a control group of healthy subjects. There were 37 MS patients, 25 women and 12 men. Control group consisted of 51 subjects, 39 women and 12 men. There was no statistically significant sex difference. The mean age of the MS patients was 45.9 +/- 12.4 years, and of control group 42.4 +/- 10.3 years; yielding no statistically significant difference. The severity of impairment in MS patients according to EDSS scale was 3 to 3.5. The quality of life determined by the prediction and criterion variables was studied in both MS patients groups and control group. All variables were graded on a 1 to 5 scale. On statistical data processing chi2 test and t-test were used. RESULTS AND DISCUSSION: Predictors referring to family history, sexual life, social life, satisfaction with education, job, social environment, religious life, housing status, financial status and present family life did not differ between the MS and control group. MS patients were less satisfied with their place in society, their state of health and ways of spending their free time. The decrease of satisfaction correlated with the areas generally known to be directly or indirectly affected by MS. As to the criterion variable of 'satisfaction with former way of life' no significant differences were found, since the disease did not affect previous life achievements. MS patients were less satisfied with their status in society, their state of health and ways of spending their free time. Changes occurred as a consequence of substantial life changes caused by the disease, results of treatments and circumstances in which the patients lives. Results obtained indicated that patients were aware of their disease, lower quality of life that limited their daily activities and future plans. Answers referring to the state of health, social status, and sexual activities did not show any statistically significant difference between the groups of MS patients and healthy controls, although it could have been expected according to the experience and customary expectations in such cases. CONCLUSION: MS patients are mainly satisfied with what they have achieved previously as young people; they become dissatisfied in relation to the possible economic and social prospects, and they are aware of their disabilities and weaknesses, inability for professional development, working and workplace relationships, more difficult money acquisition, etc.     

Effect of chronic ethanol consumption on the expression of complement components and acute-phase proteins in liver

The complement system can provoke but also participate in the repair of liver injury. Here we investigated by microarray analysis the effect of chronic ethanol consumption on hepatic mRNA expression of complement components and acute-phase proteins in complement C3-deficient (C3(-/-)) and wild-type (C3(+/+)) mice. Up-regulation by ethanol of factor B, C1qA-chain and clusterin but down-regulation of factor H, Masp-2, factor D and the terminal components C6, C8alpha and C9 was seen in both strains. Ethanol up-regulated C2 and down-regulated C4bp only in C3(+/+) mice, while in C3(-/-) mice up-regulation of C1qB-chain and vitronectin was observed. The expression of factor B, C6, C1qB and factor I was lower but that of factor D higher in C3(-/-) than in C3(+/+) mice. Ethanol induced mRNA synthesis of many acute-phase proteins including SPARC and lipocalin-2, but reduced the expression of SAP. The induction of early classical and alternative pathway components and suppression of terminal pathway components and soluble regulators may thus contribute to alcohol-induced liver injury. Lipocalin-2 and SPARC emerge as new candidate markers for early detection of liver damage.