Do people who highly value happiness tend to ruminate?

Previous studies have suggested that an extremely strong desire for happiness might ironically reduce a person’s well-being, particularly among Western people. According to the goal progress theory and the theory of valuing happiness, rumination might explain the relationship between valuing happiness and well-being. Based on these theoretical rationales, this study examined the following hypotheses: (1) valuing happiness is significantly associated with rumination, (2) people who experience low life stress have a stronger association between valuing happiness and rumination, and (3) people with more interdependent self-construal have a weaker association between valuing happiness and rumination. University students in Japan participated in a cross-sectional study (N = 350; Study 1) and a 4-weeks longitudinal study (N = 329; Study 2). They responded to a packet of questionnaires assessing valuing happiness, trait rumination, depressive symptoms, negative events, and interdependent self-construal. Consistent with our hypothesis, valuing happiness was concurrently and longitudinally associated with increased rumination after controlling for depressive symptoms. However, negative events did not moderate the association between valuing happiness and rumination. Furthermore, Study 1, but not Study 2, indicated that the association between valuing happiness and rumination was stronger among students with highly interdependent self-construal than those with less interdependent self-construal. The preset findings indicated that valuing happiness might be a factor that perpetuates rumination. More sophisticated evidence on the influence of valuing happiness on rumination can lead to effective psychotherapies for decreasing rumination and depression

Sclerite formation in the hydrothermal-vent “scaly-foot” gastropod — possible control of iron sulfide biomineralization by the animal

A gastropod from a deep-sea hydrothermal field at the Rodriguez triple junction, Indian Ocean, has scale-shaped structures, called sclerites, mineralized with iron sulfides on its foot. No other organisms are known to produce a skeleton consisting of iron sulfides. To investigate whether iron sulfide mineralization is mediated by the gastropod for the function of the sclerites, we performed a detailed physical and chemical characterization. Nanostructural characterization of the iron sulfide sclerites reveals that the iron sulfide minerals pyrite (FeS2) and greigite (Fe3S4) form with unique crystal habits inside and outside of the organic matrix, respectively. The magnetic properties of the sclerites, which are mostly consistent with those predicted from their nanostructual features, are not optimized for magnetoreception and instead support use of the magnetic minerals as structural elements. The mechanical performance of the sclerites is superior to that of other biominerals used in the vent environment for predation as well as protection from predation. These characteristics, as well as the co-occurrence of brachyuran crabs, support the inference that the mineralization of iron sulfides might be controlled by the gastropod to harden the sclerites for protection from predators. Sulfur and iron isotopic analyses indicate that sulfur and iron in the sclerites originate from hydrothermal fluids rather than from bacterial metabolites, and that iron supply is unlikely to be regulated by the gastropod for iron sulfide mineralization. We propose that the gastropod may control iron sulfide mineralization by modulating the internal concentrations of reduced sulfur compounds

Development of split-force-controlled body weight support (SF-BWS) robot for gait rehabilitation

This study introduces a body-weight-support (BWS) robot actuated by two pneumatic artificial muscles (PAMs). Conventional BWS devices typically use springs or a single actuator, whereas our robot has a split force-controlled BWS (SF-BWS), in which two force-controlled actuators independently support the left and right sides of the user’s body. To reduce the experience of weight, vertical unweighting support forces are transferred directly to the user’s left and right hips through a newly designed harness with an open space around the shoulder and upper chest area to allow freedom of movement. A motion capture evaluation with three healthy participants confirmed that the proposed harness does not impede upper-body motion during laterally identical force-controlled partial BWS walking, which is quantitatively similar to natural walking. To evaluate our SF-BWS robot, we performed a force-tracking and split-force control task using different simulated load weight setups (40, 50, and 60 kg masses). The split-force control task, providing independent force references to each PAM and conducted with a 60 kg mass and a test bench, demonstrates that our SF-BWS robot is capable of shifting human body weight in the mediolateral direction. The SF-BWS robot successfully controlled the two PAMs to generate the desired vertical support forces

Cell adhesion molecules nectins and associating proteins: Implications for physiology and pathology

Nectins have recently been identified as new cell adhesion molecules (CAMs) consisting of four members. They show immunoglobulin-like structures and exclusively localize at adherens junctions (AJs) between two neighboring cells. During the formation of cell–cell junctions, nectins function in cooperation with or independently of cadherins, major CAMs at AJs. Similar to cadherins, which are linked to the actin cytoskeleton by binding to catenins, nectins also bind to afadin through their C-terminal region and are linked to the actin cytoskeleton. In addition to nectins, there are nectin-like molecules (Necls), which resemble nectins in their structures and consist of five members. Nectins and Necls are involved in the formation of various kinds of cell–cell adhesion, and also play key roles in diverse cellular functions including cell movement, proliferation, survival, and differentiation. Thus, nectins and Necls are crucial for physiology and pathology of multicellular organisms

(-)-Epigallocatechin Gallate Reduces Platelet-Derived Growth Factor-BB-Stimulated Interleukin-6 Synthesis in Osteoblasts: Suppression of SAPK/JNK

We previously showed that the mitogen-activated protein (MAP) kinase superfamily, p44/p42 MAP kinase, p38 MAP kinase, and stress-activated protein kinase (SAPK)/c-Jun N-terminal (JNK), positively plays a part in the platelet-derived growth factor-BB- (PDGF-BB-) stimulated synthesis of interleukin-6 (IL-6), a potent bone resorptive agent, in osteoblast-like MC3T3-E1 cells while Akt and p70 S6 kinase negatively regulates the synthesis. In the present study, we investigated whether (-)-epigallocatechin gallate (EGCG), one of the major green tea flavonoids, affects the synthesis of IL-6 in these cells and the mechanism. EGCG significantly reduced the IL-6 synthesis and IL-6 mRNA expression stimulated by PDGF-BB, EGCG reduced the PDGF-BB-stimulated IL-6 synthesis also in primary-cultured osteoblasts. EGCG had no effect on the levels of osteocalcin and osteoprotegerin in MC3T3-E1 cells. The PDGF-BB-induced autophosphorylation of PDGF receptor β was not suppressed by EGCG. The PDGF-BB-induced phosphorylation of p44/p42 MAP kinase and p38 MAP kinase was not affected by EGCG. On the other hand, EGCG markedly suppressed the PDGF-BB-induced phosphorylation of SAPK/JNK. Finally, the PDGF-BB-induced phosphorylation of Akt and p70 S6 kinase was not affected by EGCG. These results strongly suggest that EGCG inhibits the PDGF-BB-stimulated synthesis of IL-6 via suppression of SAPK/JNK pathway in osteoblasts

Spiral ganglion cell degeneration‐induced deafness as a consequence of reduced GATA factor activity

Zinc‐finger transcription factors GATA2 and GATA3 are both expressed in the developing inner ear, although their overlapping versus distinct activities in adult definitive inner ear are not well understood. We show here that GATA2 and GATA3 are co‐expressed in cochlear spiral ganglion cells and redundantly function in the maintenance of spiral ganglion cells and auditory neural circuitry. Notably, Gata2 and Gata3 compound heterozygous mutant mice had a diminished number of spiral ganglion cells due to enhanced apoptosis, which resulted in progressive hearing loss. The decrease in spiral ganglion cellularity was associated with lowered expression of neurotrophin receptor TrkC that is an essential factor for spiral ganglion cell survival. We further show that Gata2 null mutants that additionally bear a Gata2 YAC (yeast artificial chromosome) that counteracts the lethal hematopoietic deficiency due to complete Gata2 loss nonetheless failed to complement the deficiency in neonatal spiral ganglion neurons. Furthermore, cochlea‐specific Gata2 deletion mice also had fewer spiral ganglion cells and resultant hearing impairment. These results show that GATA2 and GATA3 redundantly function to maintain spiral ganglion cells and hearing. We propose possible mechanisms underlying hearing loss in human GATA2‐ or GATA3‐related genetic disorders.Our results demonstrate that GATA2 and GATA3 redundantly function to maintain inner ear spiral ganglion cells and hearing. We propose possible mechanisms underlying hearing loss in human GATA2‐ or GATA3‐related genetic disorders.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/151287/1/gtc12705.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/151287/2/gtc12705_am.pd

Innate immune responses in Behçet disease and relapsing polychondritis

Behçet disease (BD) and relapsing polychondritis (RP) are chronic multisystem disorders characterized by recurrent flare-ups of tissue inflammation. Major clinical manifestations of BD are oral aphthae, genital aphthous ulcers, skin lesions, arthritis, and uveitis. Patients with BD may develop rare but serious neural, intestinal, and vascular complications, with high relapse rates. Meanwhile, RP is characterized by the inflammation of the cartilaginous tissues of the ears, nose, peripheral joints, and tracheobronchial tree. Additionally, it affects the proteoglycan-rich structures in the eyes, inner ear, heart, blood vessels, and kidneys. The mouth and genital ulcers with inflamed cartilage (MAGIC) syndrome is a common characteristic of BD and RP. The immunopathology of these two diseases may be closely related. It is established that the genetic predisposition to BD is related to the human leukocyte antigen (HLA)-B51 gene. Skin histopathology demonstrates the overactivation of innate immunity, such as neutrophilic dermatitis/panniculitis, in patients with BD. Monocytes and neutrophils frequently infiltrate cartilaginous tissues of patients with RP. Somatic mutations in UBA1, which encodes a ubiquitylation-related enzyme, cause vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic syndrome (VEXAS) with severe systemic inflammation and activation of myeloid cells. VEXAS prompts auricular and/or nasal chondritis, with neutrophilic infiltration around the cartilage in 52–60% of patients. Thus, innate immune cells may play an important role in the initiation of inflammatory processes underlying both diseases. This review summarizes the recent advances in our understanding of the innate cell-mediated immunopathology of BD and RP, with a focus on the common and distinct features of these mechanisms