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The role of competition in community structure and species interactions is universal. However, how one quantifies the outcome of competitive interactions is frequently debated. Here, we review the strengths and weaknesses of the target-neighbor design, a type of additive design where one of the competing species is reduced to a single individual and where controls and analyses are used for the target, but not for the neighbors. We conducted a literature review to determine how the target-neighbor design has been typically used and analyzed. We found that historically, targets were often smaller than neighbors and introduced after neighbor establishment; thus, targets would have little effect on neighbors. However, as co-establishment of targets and neighbors of similar size is now common, the target is more likely to affect the neighbors than in its earlier usage. This can be problematic, because if targets have a significant effect on neighbor performance, bias is introduced into the assessment of the target results. As target treatment controls are necessary to determine the absolute effect of neighbors on target growth, we advocate that analysis of the neighbor competitive response serves as a necessary control for unexpected target x neighbor interactions. [ABSTRACT FROM AUTHOR]

Parathyroid hormone (PTH) is a major physiologic regulator of calcium, phosphorous, and skeletal homeostasis. Cells of the osteoblastic lineage are key targets of PTH action in bone, and recent evidence suggests that osteocytes might be important in the anabolic effects of PTH. To understand the role of PTH signaling through the PTH/PTHrP receptors (PPR) in osteocytes and to determine the role(s) of these cells in mediating the effects of the hormone, we have generated mice in which PPR expression is specifically ablated in osteocytes. Transgenic mice in which the 10 kb-Dmp1 promoter drives a tamoxifen-inducible Cre-recombinase were mated with animals in which exon 1 of PPR is flanked by lox-P sites. In these animals, osteocyte-selective PPR knockout (Ocy-PPRcKO mice) could be induced by administration of tamoxifen. Histological analysis revealed a reduction in trabecular bone and mild osteopenia in Ocy-PPRcKO mice. Reduction of trabeculae number and thickness was also detected by micro-computed tomography analysis whereas bone volume fraction (BV/TV%) was unchanged. These findings were associated with an increase in Sost and sclerostin expression. When Ocy-PPRcKO mice were subjected to a low-calcium diet to induce secondary hyperparathyroidism, their blood calcium levels were significantly lower than littermate controls. Moreover, PTH was unable to suppress Sost and sclerostin expression in the Ocy-PPRcKO animals, suggesting an important role of PTH signaling in osteocytes for proper bone remodeling and calcium homeostasis. [ABSTRACT FROM AUTHOR]

Describes an induction process to manipulate nutrient conditions in order to induce secondary metabolite production in marine strains which normally produce little. Benefit of this for the isolation of natural products for use in pharmaceutical compounds; Presentation of a method for testing crude extracts of antimicrobial activity combined with thin layer chromatography characterization of the extracts.

Determines the capability of the Crangon septemspinosa egg to symbiotically relate with a bacterium to protect itself against Lagenidium myophilum, a known shrimp pathogen. Antifungal testing of the egg surface bacteria with standard inhibition diffusion; Demonstration of an epibiotic bacterium's inhibitory action against a related organism.

Parathyroid hormone (PTH) is the only Food and Drug Administration-approved anabolic agent to treat osteoporosis; however, the cellular targets of PTH action in bone remain controversial. PTH modulates bone turnover by binding to the PTH/PTH-related peptide (PTHrP) type 1 receptor (PPR), a G-protein-coupled receptor highly expressed in bone and kidneys. Osteocytes, the most abundant cells in adult bone, also express PPR. However, the physiological relevance of PPR signaling in osteocytes remains to be elucidated. Toward this goal, we generated mice with PPR deletion in osteocytes (Ocy- PPRKO). Skeletal analysis of these mice revealed a significant increase in bone mineral density and trabecular and cortical bone parameters. Osteoblast activities were reduced in these animals, as demonstrated by decreased collagen type I α1 mRNAand receptor activator of NF-κBligand (RANKL) expression. Importantly, when subjected to an anabolic or catabolic PTHregimen, Ocy-PPRKO animals demonstrated blunted skeletal responses. PTH failed to suppress SOST/Sclerostin or induce RANKL expression in Ocy-PPRKO animals compared with controls. In vitro, osteoclastogenesis was significantly impaired in Ocy-PPRKO upon PTH administration, indicating that osteocytes control osteoclast formation through a PPR-mediated mechanism. Taken together, these data indicate that PPR signaling in osteocytes is required for bone remodeling, and receptor signaling in osteocytes is needed for anabolic and catabolic skeletal responses. [ABSTRACT FROM AUTHOR]

Although bone responds to its mechanical environment, the cellular and molecular mechanisms underlying the skeleton's response to mechanical unloading are not completely understood. Osteocytes are the most abundant yet least understood cells in bones and are thought to be responsible for sensing stresses and strains inbone. Sclerostin, a product of the SOST gene, is produced postnatally primarily by osteocytes and is a negative regulator of bone formation. Recent studies show SOST is mechanically regulated at both mRNA and protein levels. During prolonged bed rest and immobilization, circulating sclerostin increases, both in humans and in animal models and its increase is associated with a decrease in parathyroid hormone (PTH). To investigate whether SOST/sclerostin up-regulation in mechanical unloading is a cell-autonomous response or a hormonal response to decreased PTH levels, we subjected osteocytes to an in vitro unloading environment, achieved by the NASA Rotating Wall Vessel (RWV) system. To perform these studies, we generated a novel osteocytic cell line (Ocy454) which produces high levels of SOST/sclerostin at early and in the absence of differentiation factors. Importantly, these osteocytes recapitulated the in vivo response to mechanical unloading with increased expression of SOST (3.4 ± 1.9 fold, p<0.001), sclerostin (4.7 ± 0.1 fold, p< 0.001), and the RANKL/OPG (2.5 ± 0.7 fold, p <0.001) ratio. This data demonstrates, for the first time a cell-autonomous increase in SOST/Sclerostin and RANKL/OPG ratio in the setting of unloading. Thus, targeted osteocyte therapies could hold promise as novel osteoporosis and disuse-induced bone loss treatments by directly modulating the mechnosensing cells in bone. [ABSTRACT FROM AUTHOR]

Hematopoietic progenitors are regulated in their respective niches by cells of the bone marrow microenvironment. The bone marrow microenvironmerit is composed of a variety of cell types, and the relative contribution of each of these cells for hematopoietic lineage maintenance has remained largely unclear. Osteocytes, the most abundant yet least understood cells in bone, are thought to initiate adaptive bone remodeling responses via osteoblasts and osteoclasts. Here we report that these cells regulate hematopoiesis, constraining myelopoiesis through a Gso-mediated mechanism that affects G-CSF production. Mice lacking Gsa in osteocytes showed a dramatic increase in myeloid cells in bone marrow, spleen, and peripheral blood. This hematopoietic phenomenon was neither intrinsic to the hematopoietic cells nor dependent on osteoblasts but was a consequence of an altered bone marrow microenvironment imposed by Gsa deficiency in osteocytes. Conditioned media from osteocyte-enriched bone explants significantly increased myeloid colony formation in vitro, which was blocked by G-CSF-neutralizing antibody, indicating a critical role of osteocyte-derived G-CSF in the myeloid expansion. [ABSTRACT FROM AUTHOR]