Reduced expression of semaphorin 3A in osteoclasts causes lymphatic expansion in a Gorham-Stout disease (GSD) mouse model. / ç ´éª¨ç»†èƒžä¸­ä¿¡å·ç´ 3Aè¡¨è¾¾çš„å‡å°‘å¯¼è‡´å°é¼ GSDæ¨¡åž‹ä¸­æ·‹å·´ç®¡æ‰©å¼ .

Gorham-Stout disease (GSD) is a sporadic chronic disease characterized by progressive bone dissolution, absorption, and disappearance along with lymphatic vessel infiltration in bone-marrow cavities. Although the osteolytic mechanism of GSD has been widely studied, the cause of lymphatic hyperplasia in GSD is rarely investigated. In this study, by comparing the RNA expression profile of osteoclasts (OCs) with that of OC precursors (OCPs) by RNA sequencing, we identified a new factor, semaphorin 3A (Sema3A), which is an osteoprotective factor involved in the lymphatic expansion of GSD. Compared to OCPs, OCs enhanced the growth, migration, and tube formation of lymphatic endothelial cells (LECs), in which the expression of Sema3A is low compared to that in OCPs. In the presence of recombinant Sema3A, the growth, migration, and tube formation of LECs were inhibited, further confirming the inhibitory effect of Sema3A on LECs in vitro. Using an LEC-induced GSD mouse model, the effect of Sema3A was examined by injecting lentivirus-expressing Sema3A into the tibiae in vivo. We found that the overexpression of Sema3A in tibiae suppressed the expansion of LECs and alleviated bone loss, whereas the injection of lentivirus expressing Sema3A short hairpin RNA (shRNA) into the tibiae caused GSD-like phenotypes. Histological staining further demonstrated that OCs decreased and osteocalcin increased after Sema3A lentiviral treatment, compared with the control. Based on the above results, we propose that reduced Sema3A in OCs is one of the mechanisms contributing to the pathogeneses of GSD and that expressing Sema3A represents a new approach for the treatment of GSD.

The limiting effect of genome size on xylem vessel diameter is shifted by environmental pressures in seed plants.

Current and previous studies have extensively studied the physiological and ecological consequences of genome size (GS) on plants because of the limiting effect of GS on cell size. However, it is still obscure whether such limiting effect could be shifted by environmental pressures, or not. Here, we compiled a global dataset comprised of GS, xylem vessel diameter (V dia), xylem hydraulic conductivity (K S), P 50 (xylem water potential at the loss of 50% maximum K S), and climate factors of 251 phylogeny and habitat divergent species from 59 families. The results showed that GS could limit the V dia of the species from the same family sampled in the similar climate conditions. But the expected positive relationship between GS and V dia became uncertain and even negative across different environmental conditions. V dia was strongly positively coordinated with mean annual temperature (MAT), mean annual precipitation (MAP), and potential evapotranspiration (PET). Furthermore, V dia as the anatomic foundation of plant hydraulic performance was strongly positively coordinated with K S and negatively coordinated with -P 50. The strong environmental selection on K S and P 50 explained the concerted regulation of V dia by environmental factors. The findings revealed the combined regulation of GS and environmental pressures on xylem cell size and thus affected plant eco-physiological performance. The shifted cell size limiting effect of GS by environmental factors manifests plants great plasticity under changed environmental conditions.

The Relationship between Mobile Phone Anxiety and Sleep Quality Occupational Therapy in Adolescents and Its Internal Mechanism.

With the development of the Internet era, the application of smartphones in life is quite useful, and the penetration rate of smartphones will be further increased in the future, making teenagers increasingly dependent on mobile phones. Teenagers are under great academic pressure, and excessive reliance on mobile phones will inevitably affect the formation of normal values. Teenagers, as a special group, deserve our attention. Mobile phone dependence has become a social problem. In this paper, the Pittsburgh Sleep Quality Index was used to evaluate the sleep quality of adolescents, and the factors affecting the sleep quality of adolescents were explored from three dimensions of behaviour, physiology, and emotion based on the sleep quality model. In this study, structural equation modelling was used to test the multiple mediating effects and analyze the relationship between mobile phone anxiety and sleep quality. Through the analysis of the internal mechanism of the two, the results show that the average score of adolescents' anxiety about mobile phone use is 32.87, and the standard deviation is 10.67. The difference between mobile phone anxiety and sleep quality was statistically significant (P < 0.001); good sleep quality can alleviate the prediction effect of mobile phone anxiety on anxiety and provide reference for promoting the physical and mental health development of adolescents.

Microstructural and physiological responses to cadmium stress under different nitrogen levels in Populus cathayana females and males.

Although increasing attention has been paid to the relationships between heavy metal and nitrogen (N) availability, the mechanism underlying adaptation to cadmium (Cd) stress in dioecious plants has been largely overlooked. This study examined Cd accumulation, translocation and allocation among tissues and cellular compartments in Populus cathayana Rehder females and males. Both leaf Cd accumulation and root-to-shoot Cd translocation were significantly greater in females than in males under a normal N supply, but they were reduced in females and enhanced in males under N deficiency. The genes related to Cd uptake and translocation, HMA2, YSL2 and ZIP2, were strongly induced by Cd stress in female roots and in males under a normal N supply. Cadmium largely accumulated in the leaf blades of females and in the leaf veins of males under a normal N supply, while the contrary was true under N deficiency. Furthermore, Cd was mainly distributed in the leaf epidermis and spongy tissues of males, and in the leaf palisade tissues of females. Nitrogen deficiency increased Cd allocation to the spongy tissues of female leaves and to the palisade tissues of males. In roots, Cd was preferentially distributed to the epidermis and cortices in both sexes, and also to the vascular tissues of females under a normal N supply but not under N deficiency. These results suggested that males possess better Cd tolerance compared with females, even under N deficiency, which is associated with their reduced root-to-shoot Cd translocation, specific Cd distribution in organic and/or cellular compartments, and enhanced antioxidation and ion homeostasis. Our study also provides new insights into engineering woody plants for phytoremediation.

Developmental Responses of Root Hairs to Mg Deficiency.

Magnesium (Mg), an essential element for plants is easily leached in acidic and sandy soils. Magnesium deficiency induces the initiation and elongation of root hairs, which allows the plant roots to acquire more Mg under Mg-limited conditions. However, the signals involved in the regulatory cascade leading to the induction of root hair development under Mg deficiency are largely unknown to date. Recent studies have revealed that many chemical signal molecules such as ethylene, nitric oxide, auxin, reactive oxygen, and calcium regulate the root hair development induced owing to Mg deficiency. This mini-review intends to briefly discuss the role of these chemical signals in the induction of root hair development under Mg-deficient conditions.

Humanin analogue, S14G-humanin, has neuroprotective effects against oxygen glucose deprivation/reoxygenation by reactivating Jak2/Stat3 signaling through the PI3K/AKT pathway.

Stroke, characterized by a disruption of blood supply to the brain, is a major cause of morbidity and mortality worldwide. Although humanin, a 24-amino acid polypeptide, has been identified to have multiple neuroprotective functions, the level of humanin in plasma has been demonstrated to decrease with age, which likely limits the effects against stroke injury. A potent humanin analogue, S14G-humanin (HNG), generated by replacement of Ser14 with glycine, has been demonstrated to have 1,000-fold stronger biological activity than humanin. The present study established an in vitro oxygen glucose deprivation/reoxygenation (OGD/R) model using SH-SY5Y neuroblastoma cells to mimic the in vivo ischemia/reperfusion injury in stroke. Adding HNG (0-10 µg/l) to SH-SY5Y cells to different extents blocked OGD/R-induced reduction of cell viability and antioxidative capacity, as well as decreased the elevated apoptosis rate induced by OGD/R, with the most evident effects at 1 µg/l HNG. Janus kinase 2 (Jak2)/signal transducer and activator of transcription 3 (Stat3) signaling was attenuated in OGD/R processes, yet reactivated with HNG treatment. FLLL32 (5 µM), a specific inhibitor of the signal, abolished effects of HNG on anti-apoptosis and antioxidation in OGD/R processes. Co-treatment with HNG and FLLL32 failed to interrupt upregulation of cytochrome c, B-cell lymphoma 2-associated X protein and cleaved caspase-3 provoked by OGD/R. Similar to FLLL32, Jak2/Stat3 signaling activated by HNG was also repressed by inhibitor of phosphoinositide 3-kinase (PI3K; 10 µM LY294002) or protein kinase B (AKT; 5 µM MK-2206 2HCl). These data collectively indicated that HNG has neuroprotective effects against OGD/R by reactivating Jak2/Stat3 signaling through the PI3K/AKT pathway, suggesting that HNG may be a promising agent in the management of stroke.