Dynamic optimization of the sit-to-stand movement

The purpose of this study was to clarify criteria that can predict trajectories during the sit-to-stand movement. In particular, the minimum jerk and minimum torque-change models were examined. Three patterns of sit-to-stand movement from a chair, i.e., upright, natural, and leaning forward, were measured in five young participants using a 3-D motion analysis device (200 Hz). The trajectory of the center of mass and its smoothness were examined, and the optimal trajectories predicted by both models were evaluated. Trajectories of the center of mass predicted by the minimum torque-change model, rather than the minimum jerk model, resembled the measured movements in all rising movement patterns. The upright pattern required greater extension torque of the knee and ankle joints at the instant of seat-off. The leaning-forward pattern required greater extension hip torque and higher movement cost than the natural and upright patterns. These results indicate that the natural sit-to-stand movement might be a result of dynamic optimization.     

Prevalence of Sexual Victimization and Correlates of Forced Sex in Japanese Men Who Have Sex with Men

Studies of men who have sex with men (MSM) in diverse geographic and cultural contexts have identified health challenges affecting this population. MSM might be particularly vulnerable to sexual victimization and forced sex. The aim of this research study was to examine prevalence of sexual victimization and correlates of forced sex among Japanese MSM. We recruited a sample of 5,731 Japanese MSM who completed an internet-administered survey. Participants reported on history of different types of sexual victimization, unprotected anal sex, other health risk behaviors, exposure to gay-related teasing and bullying, depression, and suicidality. Over one-fifth of the sample (21.4%) reported experiencing at least one form of sexual victimization, and 8.7% reported a history of forced sex. MSM who had ever experienced forced sex were significantly more likely to report experiencing psychological risks (depression OR = 1.55, 95% CI = 1.28–1.89; attempted suicide OR = 2.25, 95% CI = 1.81–2.81; other forms of bullying OR = 1.38, 95% CI = 1.13–1.68) and other behavioral risks (unprotected anal sex OR = 1.56, 95% CI = 1.29–1.90; sex venue attendance OR = 1.27, 95% CI = 1.04–1.54; methamphetamine use OR = 1.57, 95% CI  = 1.05–1.36), compared to MSM who had not experienced forced sex. Efforts to develop holistic and integrated health services for Japanese MSM are warranted, particularly related to psychosocial determinants of HIV prevention. However, due to cultural factors that emphasize familial and social relations and that stigmatize same-sex behavior, Japanese MSM might experience challenges to seeking social support and health services. Interventions must be provided in safe and non-judgmental settings where Japanese MSM feel comfortable disclosing their health and social support needs.     

Polycomb Group Protein Ezh2 Regulates Hepatic Progenitor Cell Proliferation and Differentiation in Murine Embryonic Liver

In embryonic liver, hepatic progenitor cells are actively proliferating and generate a fundamental cellular pool for establishing parenchymal components. However, the molecular basis for the expansion of the progenitors maintaining their immature state remains elusive. Polycomb group proteins regulate gene expression throughout the genome by modulating of chromatin structure and play crucial roles in development. Enhancer of zeste homolog 2 (Ezh2), a key component of polycomb group proteins, catalyzes tri-methylation of lysine 27 of histone H3 (H3K27me3), which trigger the gene suppression. In the present study, we investigated a role of Ezh2 in the regulation of the expanding hepatic progenitor population in vivo. We found that Ezh2 is highly expressed in the actively proliferating cells at the early developmental stage. Using a conditional knockout mouse model, we show that the deletion of the SET domain of Ezh2, which is responsible for catalytic induction of H3K27me3, results in significant reduction of the total liver size, absolute number of liver parenchymal cells, and hepatic progenitor cell population in size. A clonal colony assay in the hepatic progenitor cells directly isolated from in vivo fetal livers revealed that the bi-potent clonogenicity was significantly attenuated by the Ezh2 loss of function. Moreover, a marker expression based analysis and a global gene expression analysis showed that the knockout of Ezh2 inhibited differentiation to hepatocyte with reduced expression of a number of liver-function related genes. Taken together, our results indicate that Ezh2 is required for the hepatic progenitor expansion in vivo, which is essential for the functional maturation of embryonic liver, through its activity for catalyzing H3K27me3.     

Subcellular localization of the epitheliopeptide, Hym-301, in hydra

Peptides, as signaling molecules, play a number of roles in cell activities. An epitheliopeptide, Hym-301, has been described as a peptide involved in morphogenesis in hydra. However, little is known about the intracellular location of the peptide or its specific functions. To investigate the mechanism of morphogenesis that involves peptidic molecules, we have examined the intracellular localization of Hym-301 in hydra by using immunohistochemical and immunogold electron-microscopic analyses. We have found that the pattern of distribution of mature peptide is slightly different from that of its mRNA, and that the peptide is stored in vesicles located adjacent to the cell membrane. We have also found that the peptide is released both extracellularly and internally to the cytoplasm of the cells. Based upon these observations, we have constructed a possible model mechanism of homeostatic regulation of the distribution of the Hym-301 peptide in a dynamic tissue context.     

Nuclear lamins are differentially expressed in retinal neurons of the adult rat retina

Lamins are type V intermediate filament proteins that support nuclear membranes. They are divided into A-type lamins, which include lamin A and C, and B-type lamins, which include lamin B1 and B2. In the rat brain, lamin A and C are expressed in relatively equal amounts, while the expressions of lamin B1 and B2 vary depending on the cell type. Lamins play important roles in normal morphogenesis and function. In the nervous system, their abnormal expression causes several neurodegenerative diseases such as peripheral neuropathy, leukodystrophy and lissencephaly. The retina belongs to the central nervous system (CNS) and has widely been used as a source of CNS neurons. We investigated the expression patterns of lamin subtypes in the adult rat retina by immunohistochemistry and found that the staining patterns differed when compared with the brain. All retinal neurons expressed lamin B1 and B2 in relatively equal amounts. In addition, horizontal cells and a subpopulation of retinal ganglion cells expressed lamin A and C, while photoreceptor cells expressed neither lamin A nor C, and all other retinal neurons expressed lamin C only. This differential expression pattern of lamins in retinal neurons suggests that they may be involved in cellular differentiation and expression of cell-specific genes in individual retinal neurons.     

A Kinetic Analysis on the Enhancement of Superoxide Generation from Rice Leaf Disks Stimulated with Proteoglucomannan after Pretreatment with Concanavalin A

We have identified by differential plaque hybridization, human cDNA clones encooding a member of a heat-shock protein family (hsp 90α) in the cDNA library of Adenovirus Type 12 E1A transfected HeLa cells. The complete nucleotide sequence of one of the clones (pHB76–114A) was identified. The sequence of 2912 base pairs had a single reading frame with a coding potential for an 84,672-Da protein. The amino acid sequence was highly homologous, but not identical, to that of the human hsp 90α gene isolated from human peripheral blood lymphocytes [M. Yamazaki, K. Akaogi, T. Miwa, T. Imai, E. Soeda and K. Yokoyama, Nucleic Acids Res., 17, 7108 (1989)]. This cDNA hybridized with RNA species which increased 5- to 20-fold upon heat shock and more than 5-fold in the differentiation stage of human Tera 2 cells.     

MARCKS regulates lamellipodia formation induced by IGF‐I via association with PIP2 and β‐actin at membrane microdomains

Myristoylated alanine‐rich C kinase substrate (MARCKS) is considered to participate in formation of F‐actin‐based lamellipodia, which represents the first stage of neurite formation. However, the mechanism of how MARCKS is involved in lamellipodia formation is not precisely unknown. Using SH‐SY5Y cells, we demonstrated here that MARCKS was translocated from cytosol to detergent‐resistant membrane microdomains, known as lipid rafts, within 30 min after insulin‐like growth factor‐I (IGF‐I) stimulation, which was accompanied by MARCKS dephosphorylation, β‐actin accumulation in lipid rafts, and lamellipodia formation. The protein kinase C inhibitor, Ro‐31‐8220, and Rho‐kinase inhibitors, HA1077 and Y27632, themselves decreased basal phosphorylation levels of MARCKS and coincidently elicited translocation of MARCKS to lipid rafts. On the other hand, the phosphoinositide 3‐kinase inhibitor, LY294002, abolished IGF‐I‐induced dephosphorylation, translocation of MARCKS to lipid rafts, and lamellipodia formation. Treatment of cells with neomycin, a PIP₂‐masking reagent, attenuated the translocation of MARCKS to lipid rafts and the lamellipodia formation induced by IGF‐I, although dephosphorylation of MARCKS was not affected. Immunocytochemical and immunoprecipitation analysis indicated that IGF‐I stimulation induced the translocation of MARCKS to lipid rafts in the edge of lamellipodia and formation of the complex with PIP₂. Moreover, we demonstrated that knockdown of endogenous MARCKS resulted in significant attenuation of IGF‐I‐induced β‐actin accumulation in the lipid rafts and lamellipodia formation. These results suggest a novel role for MARCKS in lamellipodia formation induced by IGF‐I via the translocation of MARCKS, association with PIP₂, and accumulation of β‐actin in the membrane microdomains. J. Cell. Physiol. 220: 748–755, 2009. © 2009 Wiley‐Liss, Inc.