Macrozoobenthic community structure in a poikilohaline Mediterranean lagoon (Laki Lagoon, northern Aegean)

The community structure of the macrobenthic fauna was studied in the overall area of Laki Lagoon in September 1997 (salinity 32–35 psu) and monthly from February 1998 to February 1999 in the innermost part of the lagoon (salinity 0.1–6.8 psu). Community structure was analyzed by means of uni- and multivariate methods. In September 1997, the macrofauna in the outer part of the lagoon was characterized by a higher diversity and the occurrence of both lagoonal and marine species, and in the innermost part by a higher total abundance and the occurrence of a few lagoonal species. The combination of distance from the sea, depth, salinity and sediment organic matter correlated best with the spatial distribution pattern of the macrobenthic fauna. Community structure in the innermost part of the lagoon showed a seasonal periodicity. Species composition during spring 1998, at 0.1–2.0 psu, was similar to that in September 1997. During summer the macrobenthic fauna became impoverished, but recovered from late summer onwards. The salinity increase during summer (up to 5–7 psu) was followed by the appearance of marine species in the innermost part of the lagoon. Total abundance displayed a peak in late spring and a lower one in mid-autumn. The seasonal dynamics of the faunal assemblage was mainly governed by water temperature. Predation pressure by Atherina boyeri may have contributed to quantitative community changes during autumn.     

The Laboratory Rat as an Animal Model for Osteoporosis Research

Osteoporosis is an important systemic disorder, affecting mainly Caucasian women, with a diverse and multifactorial etiology. A large variety of animal species, including rodents, rabbits, dogs, and primates, have been used as animal models in osteoporosis research. Among these, the laboratory rat is the preferred animal for most researchers. Its skeleton has been studied extensively, and although there are several limitations to its similarity to the human condition, these can be overcome through detailed knowledge of its specific traits or with certain techniques. The rat has been used in many experimental protocols leading to bone loss, including hormonal interventions (ovariectomy, orchidectomy, hypophysectomy, parathyroidectomy), immobilization, and dietary manipulations. The aim of the current review is not only to present the ovariectomized rat and its advantages as an appropriate model for the research of osteoporosis, but also to provide information about the most relevant age and bone site selection according to the goals of each experimental protocol. In addition, several methods of bone mass evaluation are assessed, such as biochemical markers, densitometry, histomorphometry, and bone mechanical testing, that are used for monitoring and evaluation of this animal model in preventive or therapeutic strategies for osteoporosis.Abbreviations: BMD, bone mineral density; DEXA, dual-energy X-ray absorptiometry; μCT, microcomputerized tomography; pQCT, peripheral quantitative computerized tomographyOsteoporosis is a multifactorial skeletal disease, characterized by reduction in bone mass and disruption of the microarchitectural structure of bone tissue, resulting in loss of mechanical strength and increased risk of fracture.² The disorder can be localized or involve the entire skeleton. Generalized osteoporosis can be primary (postmenopausal and senile) or secondary. In the European Union, osteoporosis is a leading cause of mortality and morbidity in the elderly and a key factor in the high cost of medical care.³⁴Although osteoporosis usually makes its appearance late in life, and age is a major risk factor, its roots can be tracked back into adolescence. Particularly during periods of rapid bone growth, dietary calcium levels are of high importance.³⁴ Other factors that contribute to the pathogenesis of osteoporosis are lifestyle and genetic and hormonal attributes.^13,71 Reduced physical activity increases the rate of bone loss, and muscle contraction is the prevailing source of skeletal loading. Regarding hormonal factors, women, especially in the decade after menopause, can show a severe reduction of bone mass, thus explaining the high incidence of osteoporotic fractures in women compared with men.³⁴The multiple factors implicated in osteoporosis, its obscure pathogenesis, the dramatic decline in quality of life, high incidence of the disorder (especially in postmenopausal women), financial cost, and high mortality, make the need for further experimentation in animal models imperative. Experimental research can improve our understanding of pathogenesis and of the activity of pharmaceutical agents in the prevention or treatment of the disease. Although many aspects of the disorder have been revealed, others remain unclear, including the mechanisms involved in calcium homeostasis in the extracellular space and its effect on bone physiology and disease⁶⁵ and the cell and molecular pathways triggered after mechanical loading to orchestrate bone renewal.⁵³ Current research is focused on new therapeutic possibilities targeting the osteolytic enzymes of the osteoclast and the mechanisms activating bone progenitor cells and those controlling apoptosis as new potential treatments.^63,64Many therapeutic advances in the management of osteoporosis were studied first in diverse animal models and then entered clinical practice.^31,67,69 All of these models should fulfill similar basic criteria: they must comply with national and local ethical and legislative considerations, be accessible to experimental centers, be easy and safe to handle, have a low cost of acquisition, require little maintenance, reliably reproduce the disease and the biological material to be examined should be readily available. Laboratory rats meet most of these criteria. In addition, the availability of detailed knowledge of the rat skeleton and protocols for rapid induction of osteopenia, have increased this model''s popularity. Here we review the advantages and limitations of the use of the laboratory rat in osteoporosis research.     

Imatinib mesylate inhibits proliferation and exerts an antifibrotic effect in human breast stroma fibroblasts

Tumor stroma plays an important role in cancer development. In a variety of tumors, such as breast carcinomas, a desmoplastic response, characterized by stromal fibroblast and collagen accumulation, is observed having synergistic effects on tumor progression. However, the effect of known anticancer drugs on stromal cells has not been thoroughly investigated. Imatinib mesylate is a selective inhibitor of several protein tyrosine kinases, including the receptor of platelet-derived growth factor, an important mediator of desmoplasia. Recently, we have shown that imatinib inhibits the growth and invasiveness of human epithelial breast cancer cells. Here, we studied the effect of imatinib on the proliferation and collagen accumulation in breast stromal fibroblasts. We have shown that it blocks the activation of the extracellular signal-regulated kinase and Akt signaling pathways and up-regulates cyclin-dependent kinase inhibitor p21(WAF1), leading to the inhibition of fibroblast proliferation, by arresting them at the G(0)/G(1) phase of the cell cycle. Imatinib inhibits more potently the platelet-derived growth factor-mediated stimulation of breast fibroblast proliferation. By using specific inhibitors, we have found that this is due to the inhibition of the Akt pathway. In addition, imatinib inhibits fibroblast-mediated collagen accumulation. Conventional and quantitative PCR analysis, as well as gelatin zymography, indicates that this is due to the down-regulation of mRNA synthesis of collagen I and collagen III-the main collagen types in breast stroma-and not to the up-regulation or activation of collagenases matrix metalloproteinase 2 and matrix metalloproteinase 9. These data indicate that imatinib has an antifibrotic effect on human breast stromal fibroblasts that may inhibit desmoplastic reaction and thus tumor progression.     

The Aminoacyl-tRNA Synthetase and tRNA Expression Levels Are Deregulated in Cancer and Correlate Independently with Patient Survival

Aminoacyl-tRNA synthetases (ARSs) are essential enzymes that load amino acids to their cognate tRNA molecules. The expression of certain ARSs and tRNAs has been shown to be deregulated in cancer, presumably to accommodate elevated protein synthesis requirements. In this work, the expression of cytoplasmic ARSs and tRNAs in ten TCGA cancers has been systematically examined. ARSs were found to be mostly upregulated in tumours and their upregulation often correlated with worse patient survival. tRNAs were found to be either upregulated or downregulated in tumours and their expression sometimes correlated to worse survival outcomes. However, although the expression of most ARSs and tRNAs was deregulated in tumours when compared to healthy adjacent tissues, only in a few cases, and independently, did it correlate to patient survival. These data point to the general uncoupling of concomitant ARS and tRNA expression deregulation and patient survival, highlighting the different ARS and tRNA requirements in cancers.     

Impaired desensitization of a human polymorphic α2B-adrenergic receptor variant enhances its sympatho-inhibitory activity in chromaffin cells

Recent advances in tumor biology have revealed that a detailed analysis of the complex interactions of tumor cells with their adjacent microenvironment (tumor stroma) is mandatory in order to understand the various mechanisms involved in tumor growth and the development of metastasis. The mutual interactions between tumor cells and cellular and non-cellular components (extracellular matrix = ECM) of the tumor microenvironment will eventually lead to a loss of tissue homeostasis and promote tumor development and progression. Thus, interactions of genetically altered tumor cells and the ECM on the one hand and reactive non-neoplastic cells on the other hand essentially control most aspects of tumorigenesis such as epithelial-mesenchymal-transition (EMT), migration, invasion (i.e. migration through connective tissue), metastasis formation, neovascularisation, apoptosis and chemotherapeutic drug resistance. In this mini-review we will focus on these issues that were recently raised by two review articles in CCS.     

Polyamines induce aggregation of LHC II and quenching of fluorescence in vitro

Dissipation of excess excitation energy within the light-harvesting complex of Photosystem II (LHC II) is a main process in plants, which is measured as the non-photochemical quenching of chlorophyll fluorescence or qE. We showed in previous works that polyamines stimulate qE in higher plants in vivo and in eukaryotic algae in vitro. In the present contribution we have tested whether polyamines can stimulate quenching in trimeric LHC II and monomeric light-harvesting complex b proteins from higher plants. The tetramine spermine was the most potent quencher and induced aggregation of LHC II trimers, due to its highly cationic character. Two transients are evident at 100μM and 350μM for the fluorescence and absorbance signals of LHC II respectively. On the basis of observations within this work, some links between polyamines and the activation of qE in vivo is discussed.