The cytokinin receptor OHK4/OsHK4 regulates inflorescence architecture in rice via an IDEAL PLANT ARCHITECTURE1/WEALTHY FARMER'S PANICLE-mediated positive feedback circuit.

Inflorescence architecture is important for rice (Oryza sativa) grain yield. The phytohormone cytokinin (CK) has been shown to regulate rice inflorescence development; however, the underlying mechanism mediated by CK perception is still unclear. Employing a forward genetic approach, we isolated an inactive variant of the CK receptor OHK4/OsHK4 gene named panicle length1, which shows decreased panicle size due to reduced inflorescence meristem (IM) activity. A 2-amino acid deletion in the long α-helix stalk of the sensory module of OHK4 impairs the homodimerization and ligand-binding capacity of the receptor, even though the residues do not touch the ligand-binding domain or the dimerization interface. This deletion impairs CK signaling that occurs through the type-B response regulator OsRR21, which acts downstream of OHK4 in controlling inflorescence size. Meanwhile, we found that IDEAL PLANT ARCHITECTURE1(IPA1)/WEALTHY FARMER'S PANICLE (WFP), encoding a positive regulator of IM development, acts downstream of CK signaling and is directly activated by OsRR21. Additionally, we revealed that IPA1/WFP directly binds to the OHK4 promoter and upregulates its expression through interactions with 2 TCP transcription factors, forming a positive feedback circuit. Altogether, we identified the OHK4-OsRR21-IPA1 regulatory module, providing important insights into the role of CK signaling in regulating rice inflorescence architecture.

Chronic inhalation of H2S in low concentration induces immunotoxicity and inflammatory effects in lung tissue of rats.

Hydrogen sulfide (H2S) is a typical odour compound mainly causing respiratory and central nervous system symptoms. However, the immunotoxicity of inhaled H2S and the underlying mechanisms remain largely unknown. In this study, a low-dose inhalation exposure to H2S was arranged to observe inflammatory response and immunotoxicity in lung tissue of rats. Low concentrations of H2S exposure affected the immune level of pulmonary tissue and peripheral blood. Significant pathological changes in lung tissue in the exposure group were observed. At low concentration, H2S not only induced the upregulation of AQP-4 and MMP-9 expression but also stimulated immune responses, initiating various anti-inflammatory and inflammatory factors, altering tissue homeostatic environments. The TNF and chemokine signaling pathway played an important role which can promote the deterioration of pulmonary inflammatory processes and lead to lung injury and fibrosis. Excessive immune response causes an inflammatory effect and blood-gas barrier damage. These data will be of value in evaluating future occupational health risks and providing technical support for the further development of reliable, sensitive, and easy-to-use screening indicators of exposure injury.

Songorine inhibits oxidative stress-related inflammation through PI3K/AKT/NRF2 signaling pathway to alleviate lipopolysaccharide-induced septic acute lung injury.

OBJECTIVE: The present study aimed to investigate the protective action and mechanism of songorine on sepsis-induced acute lung injury (ALI). METHODS: The sepsis-induced ALI mouse and cell models were established by lipopolysaccharide (LPS) induction. Lung injury was assayed by hematoxylin and eosin staining, lung injury score, and lung wet-to-dry (W/D) weight ratio. Apoptosis in lung tissues was evaluated by TUNEL assay, and the expression of apoptosis-related markers (Bcl2, Bax, and caspase-3) was measured by western blotting. Levels of pro-inflammatory factors and oxidative stress markers in the bronchoalveolar lavage fluid (BALF) of mice were measured by ELISA and RT-qPCR. The expression of PI3K/AKT/NRF2 pathway-related proteins was analyzed by western blotting. RESULTS: Songorine treatment at 40 mg/kg mitigated sepsis-induced ALI, characterized by improved histopathology, lung injury score, and lung W/D weight ratio (p < 0.05). Moreover, songorine markedly attenuated sepsis-induced apoptosis in lung tissues; this was evidenced by an increase in Bcl2 levels and a decrease in Bax and caspase-3 levels (p < 0.01). Also, songorine reduced levels of proinflammatory cytokines (TNF-α, IL-6, IL-1ß and MPO) and oxidative stress regulators (SOD and GSH) in the BALF of LPS-induced sepsis mice and RAW264.7 cells (p < 0.05). In addition, songorine upregulated the PI3K/AKT/NRF2 pathway-related proteins in LPS-induced sepsis mice and RAW264.7 cells (p < 0.05). Furthermore, LY294002 (a PI3K inhibitor) treatment reversed the protective effect of songorine on sepsis-induced ALI. CONCLUSION: Songorine inhibits oxidative stress-related inflammation in sepsis-induced ALI via the activation of the PI3K/AKT/NRF2 signaling pathway.

Development of the ARDS-derived gene panel for lung adenocarcinoma prognosis stratification and experiment validation of CCL20 expression.

Acute respiratory distress syndrome (ARDS) is a life-threatening condition characterized by lung inflammation and high mortality rates. Lung cancer, specifically lung adenocarcinoma (LUAD), is a major cause of cancer-related deaths worldwide. Patients with LUAD, particularly those undergoing chemotherapy, are more likely to develop ARDS. ARDS inflicts major malfunctioning in the immune system. We suspected a certain shared pathogenic mechanism between these diseases. This study analyzed 503 LUAD patients from the TCGA-LUAD cohort as the training set, 85 LUAD cases from the GSE30219 cohort as the validation set, and 24 RNA-seq samples from ARDS mice model and control groups in the GSE2411 cohort. The differentially expressed genes (DEGs) of ARDS were analyzed using the limma package and screened by Cox and Lasso analysis. ssGSEA and xCell algorithms were utilized for immune landscaping. RT-qPCR analysis was used to determine the mRNA levels of key genes in both the LPS-induced ARDS model and human LUAD cell lines. We identified DEGs between ARDS and control groups, which were highly associated with cytokine production and leukocyte migration. A prognosis model for LUAD patients was developed based on the expressions of the key genes in the ARDS-derived DEGs, including FMO3, IL1R2, CCL20, CFTR, and GADD45G. A satisfactory efficacy was observed in both the training and validation cohorts. The model demonstrated increased effectiveness in predicting the intratumor immune profile and mutation status of LUAD. Moreover, we utilized LPS to induce the ARDS model, which resulted in elevated expressions of IL1R2 and CCL20. Additionally, CCL20 was upregulated in cancerous LUAD cell lines. We developed an ARDS-based model for stratifying LUAD prognosis. CCL20 was found to be elevated in both the ARDS model and LUAD, suggesting a shared underlying mechanism of these two diseases.

Rice kinesin-related protein STD1 and microtubule-associated protein MAP65-5 cooperatively control microtubule bundling.

MAIN CONCLUSIONS: STD1 specifically interacts with MAP65-5 in rice and they cooperatively control microtubule bundles in phragmoplast expansion during cell division. Microtubules play critical roles during the cell cycle progression in the plant cell. We previously reported that STEMLESS DWARF 1 (STD1), a kinesin-related protein, was localized specifically to the phragmoplast midzone during telophase to regulate the lateral expansion of phragmoplast in rice (Oryza sativa). However, how STD1 regulates microtubule organization remains unknown. Here, we found that STD1 interacted directly with MAP65-5, a member of the microtubule-associated proteins (MAPs). Both STD1 and MAP65-5 could form homodimers and bundle microtubules individually. Compared with MAP65-5, the microtubules bundled by STD1 were disassembled completely into single microtubules after adding ATP. Conversely, the interaction of STD1 with MAP65-5 enhanced the microtubule bundling. These results suggest STD1 and MAP65-5 might cooperatively regulate microtubule organization in the phragmoplast at telophase.

Ectopic odorant receptors responding to flavor compounds in skin health and disease: Current insights and future perspectives.

Skin, the largest organ of human body, acts as a barrier to protect body from the external environment and is exposed to a myriad of flavor compounds, especially food- and plant essential oil-derived odorant compounds. Skin cells are known to express various chemosensory receptors, such as transient potential receptors, adenosine triphosphate receptors, taste receptors, and odorant receptors (ORs). We aim to provide a review of this rapidly developing field and discuss latest discoveries related to the skin ORs activated by flavor compounds, their impacts on skin health and disease, odorant ligands interacting with ORs exerting specific biological effects, and the mechanisms involved. ORs are recently found to be expressed in skin tissue and cells, such as keratinocytes, melanocytes, and fibroblasts. To date, several ectopic skin ORs responding to flavor compounds, are involved in different skin biological processes, such as wound healing, hair growth, melanin regulation, pressure stress, skin barrier function, atopic dermatitis, and psoriasis. The recognition of physiological role of skin ORs, combined with the fact that ORs belong to a highly druggable protein family (G protein-coupled receptors), underscores the potential of skin ORs responding to flavor compounds as a novel regulating strategy for skin health and disease.

The gut odorant receptor and taste receptor make sense of dietary components: A focus on gut hormone secretion.

Odorant receptors (ORs) and taste receptors (TRs) are expressed primarily in the nose and tongue in which they transduce electrical signals to the brain. Advances in deciphering the dietary component-sensing mechanisms in the nose and tongue prompted research on the role of gut chemosensory cells. Acting as the pivotal interface between the body and dietary cues, gut cells "smell" and "taste" dietary components and metabolites by taking advantage of chemoreceptors-ORs and TRs, to maintain physiological homeostasis. Here, we reviewed this novel field, highlighting the latest discoveries pertinent to gut ORs and TRs responding to dietary components, their impacts on gut hormone secretion, and the mechanisms involved. Recent studies indicate that gut cells sense dietary components including fatty acid, carbohydrate, and phytochemical by activating relevant ORs, thereby modulating GLP-1, PYY, CCK, and 5-HT secretion. Similarly, gut sweet, umami, and bitter receptors can regulate the gut hormone secretion and maintain homeostasis in response to dietary components. A deeper understanding of the favorable influence of dietary components on gut hormone secretion via gut ORs and TRs, coupled with the facts that gut hormones are involved in diverse physiological or pathophysiological phenomena, may ultimately lead to a promising treatment for various human diseases.

Understanding the mechanism underlying the anti-diabetic effect of dietary component: a focus on gut microbiota.

Diabetes has become one of the biggest non-communicable diseases and threatens human health worldwide. The management of diabetes is a complex and multifaceted process including drug therapy and lifestyle interventions. Dietary components are essential for both diabetes management and health and survival of trillions of the gut microbiota (GM). Herein, we will discuss the relationship between diets and GM, the mechanism linking diabetes and gut dysbiosis, and the effects of dietary components (nutrients, phytochemicals, probiotics, food additives, etc.) on diabetes from the perspective of modulating GM. The GM of diabetic patients differs from that of health individuals and GM disorder contributes to the onset and maintenance of diabetes. Studies in humans and animal models consolidate that dietary component is a key regulator of diabetes and increasing evidence suggests that the alteration of GM plays a salient role in dietary interventions for diabetes. Given that diabetes is a major public health issue, especially that diabetes is linked with a high risk of mortality from COVID-19, this review provides compelling evidence for that targeting GM by dietary components is a promising strategy, and offers new insights into potential preventive or therapeutic approaches (dietary and pharmacological intervention) for the clinical management of diabetes.

Sucrose promotes D53 accumulation and tillering in rice.

Shoot branching is regulated by multiple signals. Previous studies have indicated that sucrose may promote shoot branching through suppressing the inhibitory effect of the hormone strigolactone (SL). However, the molecular mechanisms underlying this effect are unknown. Here, we used molecular and genetic tools to identify the molecular targets underlying the antagonistic interaction between sucrose and SL. We showed that sucrose antagonizes the suppressive action of SL on tillering in rice and on the degradation of D53, a major target of SL signalling. Sucrose inhibits the gene expression of D3, the orthologue of the Arabidopsis F-box MAX2 required for SL signalling. Overexpression of D3 antagonizes sucrose inhibition of D53 degradation and enables the SL inhibition of tillering under high sucrose. Sucrose prevents SL-induced degradation of D14, the SL receptor involved in D53 degradation. In contrast to D3, D14 overexpression enhances D53 protein levels and sucrose-induced tillering, even in the presence of SL. Our results show that sucrose inhibits SL response by affecting key components of SL signalling and, together with previous studies reporting the inhibition of SL synthesis by nitrate and phosphate, demonstrate the central role played by SLs in the regulation of plant architecture by nutrients.

The URL1-ROC5-TPL2 transcriptional repressor complex represses the ACL1 gene to modulate leaf rolling in rice.

Moderate leaf rolling is beneficial for leaf erectness and compact plant architecture. However, our understanding regarding the molecular mechanisms of leaf rolling is still limited. Here, we characterized a semi-dominant rice (Oryza sativa L.) mutant upward rolled leaf 1 (Url1) showing adaxially rolled leaves due to a decrease in the number and size of bulliform cells. Map-based cloning revealed that URL1 encodes the homeodomain-leucine zipper (HD-Zip) IV family member RICE OUTERMOST CELL-SPECIFIC 8 (ROC8). A single-base substitution in one of the two conserved complementary motifs unique to the 3'-untranslated region of this family enhanced URL1 mRNA stability and abundance in the Url1 mutant. URL1 (UPWARD ROLLED LEAF1) contains an ethylene-responsive element binding factor-associated amphiphilic repression motif and functions as a transcriptional repressor via interaction with the TOPLESS co-repressor OsTPL2. Rather than homodimerizing, URL1 heterodimerizes with another HD-ZIP IV member ROC5. URL1 could bind directly to the promoter and suppress the expression of abaxially curled leaf 1 (ACL1), a positive regulator of bulliform cell development. Knockout of OsTPL2 or ROC5 or overexpression of ACL1 in the Url1 mutant partially suppressed the leaf-rolling phenotype. Our results reveal a regulatory network whereby a transcriptional repression complex composed of URL1, ROC5, and the transcriptional corepressor TPL2 suppresses the expression of the ACL1 gene, thus modulating bulliform cell development and leaf rolling in rice.

Narrow Leaf21, encoding ribosomal protein RPS3A, controls leaf development in rice.

Leaf morphology influences photosynthesis, transpiration, and ultimately crop yield. However, the molecular mechanism of leaf development is still not fully understood. Here, we identified and characterized the narrow leaf21 (nal21) mutant in rice (Oryza sativa), showing a significant reduction in leaf width, leaf length and plant height, and increased tiller number. Microscopic observation revealed defects in the vascular system and reduced epidermal cell size and number in the nal21 leaf blade. Map-based cloning revealed that NAL21 encodes a ribosomal small subunit protein RPS3A. Ribosome-targeting antibiotics resistance assay and ribosome profiling showed a significant reduction in the free 40S ribosome subunit in the nal21 mutant. The nal21 mutant showed aberrant auxin responses in which multiple auxin response factors (ARFs) harboring upstream open-reading frames (uORFs) in their 5'-untranslated region were repressed at the translational level. The WUSCHEL-related homeobox 3A (OsWOX3A) gene, a key transcription factor involved in leaf blade lateral outgrowth, is also under the translational regulation by RPS3A. Transformation with modified OsARF11, OsARF16, and OsWOX3A genomic DNA (gDNA) lacking uORFs rescued the narrow leaf phenotype of nal21 to a better extent than transformation with their native gDNA, implying that RPS3A could regulate translation of ARFs and WOX3A through uORFs. Our results demonstrate that proper translational regulation of key factors involved in leaf development is essential to maintain normal leaf morphology.

Improved dual luciferase reporter (DLR) assay to determine the protein stability.

We developed a binary vector co-expressing firefly luciferase (FF) and Renilla luciferase (REN) to detect protein stability in response to different stimuli, and verified the functionality of the vector. The StrigoQuant-like reporter expressing FF and REN in one transcript is a sensitive tool for detecting protein abundance in different genotypes. However, we found that significant differences in the relative FF/REN ratio of empty StrigoQuant vector in different genotypes. Therefore, to determine the actual protein abundance, the relative FF/REN ratio of the protein of interest should be normalized to that of the empty vector.

[Effect of calorie-enriched formula on postoperative catch-up growth in infants with cyanotic congenital heart disease: a propective randomized controlled study].

OBJECTIVE: To study the effect of calorie-enriched formula on postoperative catch-up growth in infants with cyanotic congenital heart disease (CHD). METHODS: A total of 100 infants with cyanotic CHD who underwent surgical operation from January to December, 2017, were randomly divided into a high-calorie group (receiving calorie-enriched formula after surgery) and a conventional group (receiving standard formula after surgery), with 50 infants in each group. All infants were followed up for 6 months. The observation indices included body height, body weight, prealbumin, and N-terminal pro-brain natriuretic peptide before surgery, at the time of ventilator weaning and extubation after surgery, and at 1, 3, and 6 months after surgery. Height-for-age Z-score (HAZ), weight-for-age Z-score (WAZ), and weight-for-height Z-score (WHZ) were also assessed. Adverse reactions were recorded for both groups. RESULTS: There were 25 cases (50%) and 21 cases (42%) of malnutrition in the high-calorie group and the conventional group respectively before surgery (P > 0.05). The nutritional status of the two groups improved 6 months after surgery (P < 0.05). At 6 months after surgery, compared with the conventional group, the high-calorie group had a lower proportion of infants with malnutrition (18% vs 36%, P < 0.05) and also a lower proportation of infants with a WAZ score of < -2 (P < 0.05). The infants with malnutrion in the high-calorie group had higher HAZ, WAZ, and WHZ than those in the conventional group (P < 0.05). No gastrointestinal intolerance was observed in both groups during hospitalization. CONCLUSIONS: Compared with the standard formula, calorie-enriched formula can better help with postoperative catch-up growth in infants with cyanotic CHD.

DEGENERATED PANICLE AND PARTIAL STERILITY 1 (DPS1) encodes a cystathionine ß-synthase domain containing protein required for anther cuticle and panicle development in rice.

Degeneration of apical spikelets and reduced panicle fertility are common reasons for low seed-setting rate in rice (Oryza sativa). However, little is known about the underlying molecular mechanisms. Here, we report a novel degenerated panicle and partial sterility 1 (dps1) mutant that showed panicle apical degeneration and reduced fertility in middle spikelets. dps1 plants were characterized by small whitish anthers with altered cuticle morphology and absence of pollen grains. Amounts of cuticular wax and cutin were significantly reduced in dps1 anthers. Panicles of dps1 plants showed an accumulation of reactive oxygen species (ROS), lower antioxidant activity, and increased programmed cell death. Map-based cloning revealed that DPS1 encodes a mitochondrial-localized protein containing a cystathionine ß-synthase domain that showed the highest expression in panicles and anthers. DPS1 physically interacted with mitochondrial thioredoxin proteins Trx1 and Trx20, and it participated in ROS scavenging. Global gene expression analysis in dps1 revealed that biological processes related to fatty acid metabolism and ROS homeostasis were significantly affected, and the expression of key genes involved in wax and cutin biosynthesis were downregulated. These results suggest that DPS1 plays a vital role in regulating ROS homeostasis, anther cuticle formation, and panicle development in rice.

Reduction of ATPase activity in the rice kinesin protein Stemless Dwarf 1 inhibits cell division and organ development.

Several kinesins, the ATP-driven microtubule (MT)-based motor proteins, have been reported to be involved in many basic processes of plant development; however, little is known about the biological relevance of their ATPase activity. Here, we characterized the Oryza sativa (rice) stemless dwarf 1 (std1) mutant, showing a severely dwarfed phenotype, with no differentiation of the node and internode structure, abnormal cell shapes, a shortened leaf division zone and a reduced cell division rate. Further analysis revealed that a substantial subset of cells was arrested in the S and G2/M phases, and multinucleate cells were present in the std1 mutant. Map-based cloning revealed that STD1 encodes a phragmoplast-associated kinesin-related protein, a homolog of the Arabidopsis thaliana PAKRP2, and is mainly expressed in the actively dividing tissues. The STD1 protein is localized specifically to the phragmoplast midzone during telophase and cytokinesis. In the std1 mutant, the substitution of Val-40-Glu in the motor domain of STD1 significantly reduced its MT-dependent ATPase activity. Accordingly, the lateral expansion of phragmoplast, a key step in cell plate formation, was arrested during cytokinesis. Therefore, these results indicate that the MT-dependent ATPase activity is indispensible for STD1 in regulating normal cell division and organ development.

Knockdown of Rice MicroRNA166 Confers Drought Resistance by Causing Leaf Rolling and Altering Stem Xylem Development.

MicroRNAs are 19- to 22-nucleotide small noncoding RNAs that have been implicated in abiotic stress responses. In this study, we found that knockdown of microRNA166, using the Short Tandem Target Mimic (STTM) system, resulted in morphological changes that confer drought resistance in rice (Oryza sativa). From a large-scale screen for miRNA knockdown lines in rice, we identified miR166 knockdown lines (STTM166); these plants exhibit a rolled-leaf phenotype, which is normally displayed by rice plants under drought stress. The leaves of STTM166 rice plants had smaller bulliform cells and abnormal sclerenchymatous cells, likely causing the rolled-leaf phenotype. The STTM166 plants had reduced stomatal conductance and showed decreased transpiration rates. The STTM166 lines also exhibited altered stem xylem and decreased hydraulic conductivity, likely due to the reduced diameter of the xylem vessels. Molecular analyses identified rice HOMEODOMAIN CONTAINING PROTEIN4 (OsHB4), a member of HD-Zip III gene family, as a major target of miR166; moreover, rice plants overexpressing a miR166-resistant form of OsHB4 resembled the STTM166 plants, including leaf rolling and higher drought resistance. The genes downstream of miR166-OsHB4 consisted of polysaccharide synthesis-related genes that may contribute to cell wall formation and vascular development. Our results suggest that drought resistance in rice can be increased by manipulating miRNAs, which leads to developmental changes, such as leaf rolling and reduced diameter of the xylem, that mimic plants' natural responses to water-deficit stress.

Analysis of a customized cervical collar to improve neck posture during smartphone usage: a comparative study in healthy subjects.

PURPOSE: A slouching posture during smartphone usage increases gravitational loadings on the cervical spine, which may lead to neck pain and degeneration. The objective of the present study was to investigate the head, neck and trunk angles in different smartphone-usage postures, as well as the posture-correction effects and comfort scores of three neck collars. METHODS: This was a prospective cohort study in which 41 healthy young subjects aged 18-25 were recruited. The head, neck and trunk angles were measured in all participants during a neutral position and three smartphone-using postures, including sitting with and without back support and standing. The postural correction and comfort scores of three collars (Aspen Vista, Sport-aid and our customized 3D printed collars) were compared. RESULTS: Smartphone use increased the head and neck flexion angles in all postures, and sitting without back support showed the greatest head and neck flexion angles. The posture-correcting effect of the customized collar was better than the Aspen Vista and Sport-aid collars. In addition, the customized collar was more comfortable to wear than the other two collars in most contact areas. CONCLUSION: Smartphone use increased both the head and neck flexion in different postures, and the proposed customized 3D-printed cervical collar significantly reduced the head and neck angles. These slides can be retrieved under Electronic Supplementary Material.

Mutations in the Rice OsCHR4 Gene, Encoding a CHD3 Family Chromatin Remodeler, Induce Narrow and Rolled Leaves with Increased Cuticular Wax.

Leaf blade width, curvature, and cuticular wax are important agronomic traits of rice. Here, we report the rice Oschr4-5 mutant characterized by pleiotropic phenotypes, including narrow and rolled leaves, enhanced cuticular wax deposition and reduced plant height and tiller number. The reduced leaf width is caused by a reduced number of longitudinal veins and increased auxin content. The cuticular wax content was significantly higher in the Oschr4-5 mutant, resulting in reduced water loss rate and enhanced drought tolerance. Molecular characterization reveals that a single-base deletion results in a frame-shift mutation from the second chromodomain of OsCHR4, a CHD3 (chromodomain helicase DNA-binding) family chromatin remodeler, in the Oschr4-5 mutant. Expressions of seven wax biosynthesis genes (GL1-4, WSL4, OsCER7, LACS2, LACS7, ROC4 and BDG) and four auxin biosynthesis genes (YUC2, YUC3, YUC5 and YUC6) was up-regulated in the Oschr4-5 mutant. Chromatin immunoprecipitation assays revealed that the transcriptionally active histone modification H3K4me3 was increased, whereas the repressive H3K27me3 was reduced in the upregulated genes in the Oschr4-5 mutant. Therefore, OsCHR4 regulates leaf morphogenesis and cuticle wax formation by epigenetic modulation of auxin and wax biosynthetic genes expression.

Plane-to-plane analysis of mandibular misalignment in patients with facial asymmetry.

INTRODUCTION: Little is known regarding how the mandible rotates in facial asymmetry. The purpose of this study was to study mandibular misalignment with a new plane-to-plane analysis method in patients with facial asymmetry. METHODS: Optimal symmetry planes (OSPs) were generated by computing the greatest count of paired voxels on opposing sides of the computerized tomography image of the structure. The mandibular OSP was measured against the midfacial OSP for its alignment. The deviation angle formed by the 2 OSPs was broken down into a y-axis component (frontal deviation angle) and a z-axis component (horizontal deviation angle). Fifty-nine patients who sought correction for facial asymmetry were included for study. RESULTS: The new analysis method was feasible. Fifty patients (83%) had significant mandibular misalignment (deviation, ≥4° or 4 mm). The locations of the rotational axes exhibited significant variations that could explain the varied features of the asymmetry. The frontal deviation angle (mean, 3.80° ± 3.89°) was significantly larger than the horizontal deviation angle (mean, 2.77° ± 1.71°). There was no significant correlation between the horizontal deviation angle and the anterior deviation distance or the posterior deviation distance. CONCLUSIONS: Proper mandibular realignment was suggested to be the primary aim in surgical correction of most jawbone asymmetries. Because of the greatly varied rotational axes and the obscure z-axis rotation, realignment could be difficult with the traditional approach. The OSP-based analysis is advocated to guide planning.

The Arabidopsis U-box E3 ubiquitin ligase PUB30 negatively regulates salt tolerance by facilitating BRI1 kinase inhibitor 1 (BKI1) degradation.

The Arabidopsis U-box E3 ubiquitin ligases play an important role in the ubiquitin/26S proteasome-mediated protein degradation pathway. Recently, PUB30 has been reported to participate in the salt stress response during seed germination stage in abscisic acid (ABA)-independent manner, but the molecular mechanism remains to be elucidated. Here, we displayed that the pub30 mutant was more tolerant to salt stress during seed germination, whereas the mutant of its closest homologue PUB31 showed mild sensitivity to salt stress. PUB30 exhibited E3 ubiquitin ligase activity in vitro. PUB30 specifically interacted with BRI1 kinase inhibitor 1 (BKI1), a regulator playing dual roles in brassinosteroids signaling, in vitro and in vivo. We found that BKI1 protein was ubiquitinated and degraded by the 26S proteasome. The degradation of BKI1 was slowed down in the pub30-1 mutant compared with that in the wild type. The bki1 mutant was sensitive to salt, whereas the transgenic plants overexpressing BKI1 showed salt tolerant phenotype. All these results indicate that PUB30 negatively regulates salt tolerance probably through regulating the degradation of BKI1 and brassinosteroids signaling in Arabidopsis.