Coral spawning in the Gulf of Oman and relationship to latitudinal variation in spawning season in the northwest Indian Ocean

Despite a wealth of information on sexual reproduction in scleractinian corals, there are regional gaps in reproductive records. In the Gulf of the Oman in the Arabian Sea, reproductive timing was assessed in four common species of broadcast spawning corals using field surveys of gamete maturity and aquarium observations of spawning activity. The appearance of mature gametes within the same month for Acropora downingi, A. hemprichii, Cyphastrea microphthalma and Platygyra daedalea (≥ 75% of colonies, n = 848) indicated a synchronous and multi-specific spawning season. Based on gamete disappearance and direct observations, spawning predominantly occurred during April in 2013 (75- 100% of colonies) and May in 2014 (77-94% of colonies). The difference in spawning months between survey years was most likely explained by sea temperature and the timing of lunar cycles during late-stage gametogenesis. These reproductive records are consistent with a latitudinal gradient in peak broadcast spawning activity at reefs in the northwestern Indian Ocean which occurs early in the year at low latitudes (January to March) and progressively later in the year at mid (March to May) and high (June to September) latitudes

Metabolic control and bone health in adolescents with type 1 diabetes

<p>Abstract</p> <p>Background</p> <p>Adults with type 1 diabetes (T1D) have decreased bone mineral density (BMD) and increased fracture risk, yet the etiologies remain elusive. Early detection of derangements in bone biomarkers during adolescence could lead to timely recognition. In adolescents with T1D, we evaluated the relationships between metabolic control, BMD, and bone anabolic and turnover markers.</p> <p>Methods</p> <p>Cross-sectional study of 57 adolescent subjects with T1D who had HbA1c consistently ≥ 9% (Poor Control, PC n = 27) or < 9% (Favorable Control, FC n = 30) for two years prior to enrollment. Subjects had T1DM for at least three years and were without diabetes complications, known celiac disease, or other chronic diseases.</p> <p>Results</p> <p>There were no differences between HbA1c groups in BMD, components of the IGF system, or 25-hydroxyvitamin D status. The prevalence of 25-hydroxyvitamin D abnormalities was similar to that seen in the general adolescent population. Few patients met the recommended dietary allowance (RDA) for vitamin D or calcium.</p> <p>Conclusions</p> <p>These data provide no evidence of association between degree of metabolic control and BMD in adolescents with T1D. Adolescents with T1D have a high prevalence of serum 25-hydroxyvitamin D abnormalities. Longitudinal studies are needed to evaluate the predictive value of vitamin D abnormalities on fracture risk.</p

Targeted Overexpression of Osteoactivin in Cells of Osteoclastic Lineage Promotes Osteoclastic Resorption and Bone Loss in Mice

This study sought to test whether targeted overexpression of osteoactivin (OA) in cells of osteoclastic lineage, using the tartrate-resistant acid phosphase (TRAP) exon 1B/C promoter to drive OA expression, would increase bone resorption and bone loss in vivo. OA transgenic osteoclasts showed ∼2-fold increases in OA mRNA and proteins compared wild-type (WT) osteoclasts. However, the OA expression in transgenic osteoblasts was not different. At 4, 8, and 15.3 week-old, transgenic mice showed significant bone loss determined by pQCT and confirmed by μ-CT. In vitro, transgenic osteoclasts were twice as large, had twice as much TRAP activity, resorbed twice as much bone matrix, and expressed twice as much osteoclastic genes (MMP9, calciton receptor, and ADAM12), as WT osteoclasts. The siRNA-mediated suppression of OA expression in RAW264.7-derived osteoclasts reduced cell size and osteoclastic gene expression. Bone histomorphometry revealed that transgenic mice had more osteoclasts and osteoclast surface. Plasma c-telopeptide (a resorption biomarker) measurements confirmed an increase in bone resorption in transgenic mice in vivo. In contrast, histomorphometric bone formation parameters and plasma levels of bone formation biomarkers (osteocalcin and pro-collagen type I N-terminal peptide) were not different between transgenic mice and WT littermates, indicating the lack of bone formation effects. In conclusion, this study provides compelling in vivo evidence that osteoclast-derived OA is a novel stimulator of osteoclast activity and bone resorption

Ras-association domain family 1C protein promotes breast cancer cell migration and attenuates apoptosis

<p>Abstract</p> <p>Background</p> <p>The Ras association domain family 1 (RASSF1) gene is a Ras effector encoding two major mRNA forms, RASSF1A and RASSF1C, derived by alternative promoter selection and alternative mRNA splicing. RASSF1A is a tumor suppressor gene. However, very little is known about the function of RASSF1C both in normal and transformed cells.</p> <p>Methods</p> <p>Gene silencing and over-expression techniques were used to modulate RASSF1C expression in human breast cancer cells. Affymetrix-microarray analysis was performed using T47D cells over-expressing RASSF1C to identify RASSF1C target genes. RT-PCR and western blot techniques were used to validate target gene expression. Cell invasion and apoptosis assays were also performed.</p> <p>Results</p> <p>In this article, we report the effects of altering RASSF1C expression in human breast cancer cells. We found that silencing RASSF1C mRNA in breast cancer cell lines (MDA-MB231 and T47D) caused a small but significant decrease in cell proliferation. Conversely, inducible over-expression of RASSF1C in breast cancer cells (MDA-MB231 and T47D) resulted in a small increase in cell proliferation. We also report on the identification of novel RASSF1C target genes. RASSF1C down-regulates several pro-apoptotic and tumor suppressor genes and up-regulates several growth promoting genes in breast cancer cells. We further show that down-regulation of caspase 3 via overexpression of RASSF1C reduces breast cancer cells' sensitivity to the apoptosis inducing agent, etoposide. Furthermore, we found that RASSF1C over-expression enhances T47D cell invasion/migration <it>in vitro</it>.</p> <p>Conclusion</p> <p>Together, our findings suggest that RASSF1C, unlike RASSF1A, is not a tumor suppressor, but instead may play a role in stimulating metastasis and survival in breast cancer cells.</p

First distributional record of the giraffe seahorse, <i style="mso-bidi-font-style:normal">Hippocampus camelopardalis</i> Bianconi 1854 (Family: Syngnathidae) from Gulf of Kachchh waters, North west coast of India.

408-411Hippocampus camelopardalis was described based on the occurrence of a single specimen obtained from Mithapur reef region from the Gulf of Kachchh Marine National Park region, Gujarat. The discovery of this seahorse is considered as new record based on the review of earlier literature from Indian waters. The observed species is currently reported to occur from South African waters and present study infers its distributional range to Arabian Sea (Indian west coast). The observed specimen shows similarity to other seahorse species like H.trimaculatus and H.whitei based on the occurrence of three spots on its body and snout length respectively

The first record of shark attack on the Indo-Pacific hump-back Dolphin, <i>Sousa chinensis</i> (Osbeck, 1765) in Mithapur coast, India

1317-1319Present report is the documentation of shark attack on Indo-Pacific humpback dolphin, which was washed ashore at Mithapur coast in Gujarat, India. The crescent shaped tooth impregnation on the deceased dolphin revealed it was attacked by shark. As the animal was injured only in seven places, perhaps, the attack was due to competitive interaction between shark and dolphin. Morphometric measurements and description of the wounds on the dolphin were recorded and documented. This is the first report of shark attack on Indo-Pacific humpback dolphin from Gujarat coast

Reduced Bone Mineral Density in SOCS-2-Deficient Mice

Suppressor of cytokine signaling-2 (SOCS-2) is a member of the suppressor of cytokine signaling family, implicated in the negative regulation of cytokine action through inhibition of the Janus kinase (JAK) signal transducers and activators of transcription (STAT) signal transduction pathway. We have previously reported that SOCS-2-/- mice display an increased longitudinal skeletal growth associated with a deregulated GH/IGF-I signaling. The aim of the present study was to determine the role of SOCS-2 in the regulation of bone mineral density (BMD). Dual x-ray absorptiometry (DXA) analyses demonstrated that the areal BMD of the tibia was reduced in both 4-wk-old (-8.6%) and 15-wk-old (-6.0%) SOCS 2-/- mice compared with wild-type (WT) mice. The trabecular volumetric BMD, as measured by peripheral quantitative computerized tomography (pQCT) in the metaphyseal region of the distal femur, was reduced in both 4-wk-old (-10%) and 15-wk-old (-32%) SOCS 2-/- mice compared with WT mice. pQCT analyses in the diaphyseal region of tibia also revealed that the cortical volumetric BMD was reduced in both 4-wk-old (-7%) and 15-wk-old (-3%) SOCS 2-/- mice. The cortical cross-sectional area was reduced in 4-wk-old but not in 15-wk-old SOCS 2-/- mice. In conclusion, SOCS-2 inactivation results in reduced trabecular and cortical volumetric BMD. These effects are not consistent with an augmented GH/IGF-I signaling and, therefore, the mechanism behind the reduced BMD remains to be elucidated