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Humpback whales Megaptera novaeangliae that breed in the western North Pacific (WNP) are listed as endangered under the US Endangered Species Act. Previous research in the WNP concluded that the full extent of humpback whale breeding areas is unknown. Recovering this endangered population requires identifying all associated breeding grounds and potential threats in those locations. Prior to 2015, humpback whales were known to occur in the Mariana Archipelago (within the WNP), but their population identity and habitat use there were unknown. To determine the population identity of humpback whales in the Mariana Archipelago and whether the area serves as a breeding ground for these whales, small-boat photo-identification and biopsy sampling surveys were conducted in the southern portion of the archipelago during February and March 2015-2018. A total of 14 mother-calf pairs and 27 other non-calf whales were encountered. Seven non-calves were re-sighted in multiple years, including 4 females associated with calves in one or more years. Competitive behavior was observed in multiple years. Comparisons with other North Pacific humpback whale catalogs resulted in matches to breeding (Japan and Philippines) and feeding (Russia) grounds in the WNP. DNA profiling of 28 biopsy samples identified 24 individuals (14 females, 10 males) representing 7 mitochondrial DNA haplotypes. The haplotype frequencies from the Mariana Archipelago showed the greatest identity with the Ogasawara breeding ground and Commander Islands feeding ground in the WNP. This study establishes the Mariana Archipelago as a breeding area for endangered WNP humpback whales, which should be considered in ongoing research and conservation efforts.

We have discovered two molecular features at radial velocities of -35 km s-1 and 0 km s-1 toward the infrared Double Helix Nebula (DHN) in the Galactic center with NANTEN2. The two features show good spatial correspondence with the DHN. We have also found two elongated molecular ridges at these two velocities distributed vertically to the Galactic plane over 0.°8. The two ridges are linked by broad features in velocity and are likely connected physically with each other. The ratio between the 12CO J = 2-1 and J = 1-0 transitions is 0.8 in the ridges which is larger than the average value 0.5 in the foreground gas, suggesting the two ridges are in the Galactic center. An examination of the K band extinction reveals a good coincidence with the CO 0 km s-1 ridge and is consistent with a distance of 8 ± 2 kpc. We discuss the possibility that the DHN was created by a magnetic phenomenon incorporating torsional Alfvén waves launched from the circum-nuclear disk and present a first estimate of the mass and energy involved in the DHN. © 2014. The American Astronomical Society. All rights reserved.

It has been recently demonstrated that NKG2D is an activating costimulatory receptor on natural killer (NK) cells, natural killer T (NKT) cells, activated [CD8.sup.+] T cells, and [gamma][delta] T cells, which respond to cellular stress, such as inflammation, transformation, and infection. Here we show that intestinal inflammation in colitic SCID mice induced by adoptive transfer of [CD4.sup.+][CD45RB.sup.high] T cells is characterized by significant increase of [CD4.sup.+][NKG2D.sup.+] T cells and constitutive expression of NKG2D ligands, such as H60, Mult-1, and Rae-1, by lamina propria [CD11c.sup.+] dendritic cells. Furthermore, treatment with nondepleting and neutralizing anti-NKG2D MAb after transfer of [CD4.sup.+][CD45RB.sup.high] T cells into SCID mice significantly suppressed wasting disease with colitis, abrogated leukocyte infiltration, and reduced production of IFN-[gamma] by lamina propria [CD4.sup.+] T cells. These findings demonstrate that NKG2D signaling pathway is critically involved in [CD4.sup.+] T cell-mediated disease progression and suggest a new therapeutic target for inflammatory bowel diseases. NKG2D; [CD4.sup.+] T cells; chronic colitis; inflammatory bowel disease

FTY720, a sphingosine-derived immunomodulator, causes immunosuppression via enhancement of lymphocyte sequestration into secondary lymphoid organs, thereby preventing their antigen-activated T cell egress to sites of inflammation. FTY720 is highly effective in inhibiting autoimmunity in various animal models. However, there is little known about how FTY720 controls the migration property of memory T cells. Here, we demonstrated that FTY720 pre%nts the development of colitis induced by the adoptive transfer of lamina propria (LP) colitogenic effector memory CD[4.sup.+] T cells ([T.sub.EM] cells; CD45R[B.sup.low]WCD[44.sup.high]CD62[L.sup.-]) into severe combined immunodeficiency (SCID) mice and suppresses interferon-% interleukin-2, and tumor necrosis factor-a production by LP CD[4.sup.+] T cells. The numbers of spleen, peripheral blood, mesentefic lymph node, and LP CD[4.sup.+] T cells in FTY720-treated mice were significantly reduced compared with those in control mice. Notably, LP CD[4.sup.+] [T.sub.EM] cells as well as splenic CD[4.sup.+]CD45R[B.sup.high] T cells expressed several spingosine-l-phosphate receptors that are targets for FRY720. Furthermore, FTY720 also prevented the development of colitis induced by the adoptive transfer of splenic CD[4.sup.+]CD45R[B.sup.high] T cells into SCID mice. Collectively, the present data indicate that FTY720 treatment may offer the potential not only to prevent the onset of disease but also to treat memory T cell-mediated autoimmune diseases including inflammatory bowel diseases. therapy; migration; I cell doi:10.1152/ajpgi.00496.2005

The biochemical functions of the Cbfa1 core-binding factor were characterized in fetal mice with mutated Cbfa1 genes. The mutated mice died after birth due to a complete lack of bone formation that was induced by the disruption of the Cbfa1 gene. Histological analysis of the skeleton of the mice indicated the presence of low levels of osteopontin and osteolacin. Furthermore, maturational arrest occured during the early stage of osteoblast differentiation in the mutated mice embryos.

Context. Dense molecular filaments are ubiquituous in the interstellar medium, yet their internal physical conditions and the role of gravity, turbulence, the magnetic field, radiation, and the ambient cloud during their evolution remain debated. Aims. We study the kinematics and physical conditions in the Musca filament, the ambient cloud, and the Chamaeleon-Musca complex to constrain the physics of filament formation. Methods. We produced CO(2–1) isotopologue maps with the APEX telescope that cut through the Musca filament. We further study a NANTEN2 12CO(1–0) map of the full Musca cloud, H I emission of the Chamaeleon-Musca complex, a Planck polarisation map, line radiative transfer models, Gaia data, and synthetic observations from filament formation simulations. Results. The Musca cloud, with a size of ~3–6 pc, contains multiple velocity components. Radiative transfer modelling of the CO emission indicates that the Musca filament consists of a cold (~10 K), dense (nH2 ∼ 104 cm−3) crest, which is best described with a cylindrical geometry. Connected to the crest, a separate gas component at T ~ 15 K and nH2 ∼ 103 cm−3 is found, the so-called strands. The velocity-coherent filament crest has an organised transverse velocity gradient that is linked to the kinematics of the nearby ambient cloud. This velocity gradient has an angle ≥30° with respect to the local magnetic field orientation derived from Planck, and the magnitude of the velocity gradient is similar to the transonic linewidth of the filament crest. Studying the large scale kinematics, we find coherence of the asymmetric kinematics from the 50 pc H I cloud down to the Musca filament. We also report a strong [C18O]/[13CO] abundance drop by an order of magnitude from the filament crest to the strands over a distance <0.2 pc in a weak ambient far-ultraviolet (FUV) field. Conclusions. The dense Musca filament crest is a long-lived (several crossing times), dynamic structure that can form stars in the near future because of continuous mass accretion replenishing the filament. This mass accretion on the filament appears to be triggered by a H I cloud–cloud collision, which bends the magnetic field around dense filaments. This bending of the magnetic field is then responsible for the observed asymmetric accretion scenario of the Musca filament, which is, for instance, seen as a V-shape in the position–velocity (PV) diagram. [ABSTRACT FROM AUTHOR]

Summary: This study evaluated the peri-implant bone repair in orchiectomized rats receiving intermittently PTH 1-34. The treatment returned the bone quality and quantity of the animals to normal in the computerized microtomography, laser confocal microscopy, and histological analysis. The PTH 1-34 promoted marked bone formation with increased volume, improved quality, and greater bone turnover. Introduction: Osteoporosis can be a problem in implant osseointegration. So this study aimed to evaluate the quantity and quality of peri-implant bone repair in orchiectomized Wistar rats receiving intermittently administered PTH 1-34. Methods: Animals (n = 24) were divided into 3 groups: healthy control (SHAM), orchiectomized (ORQ), and orchiectomized and treated with 0.5 μg/kg/day PTH 1-34 (TERI), and each received an implant in the right and left tibial metaphysis, which was allowed to repair for 60 days. The resultant bone formation was evaluated through computerized microtomography (micro-CT) to compare the percent bone volume (BV/TV), trabecular thickness (Tb.Th), trabecular number and separation (Tb.N, Tb.Sp), and bone implant contact (BIC) through the intersection surface (i.S) between groups. Laser confocal microscopy was used to evaluate fluorochrome areas for mineral apposition rate (MAR) and neoformed bone area (NBA). In addition, histological evaluation of calcified tissues with Stevenel blue and alizarin red staining was performed. Results: Treatment with PTH 1-34 returned the bone quality and quantity of the osteoporotic animal to normal, as the TERI group presented statistically significant higher values for BV/TV, Tb.Th, and BIC parameters compared with ORQ (p < 0.05), but when compared with SHAM (p > 0.05), no statistical difference was noted. In addition, in the bone turnover analysis (MAR, NBA) for TERI, the highest results are presented, followed by SHAM, and then ORQ (TERI × ORQ: p < 0.05). Conclusions: Intermittent treatment with PTH 1-34 on orchiectomized animals promoted marked bone formation with increased volume, improved quality, and greater bone turnover in the peri-implant space, returning the bone quality and quantity to the present standard in healthy animals. [ABSTRACT FROM AUTHOR]