Paclobutrazol Enhanced Stem Lodging Resistance of Direct-Seeded Rice by Affecting Basal Internode Development.

The objectives of this study were to explore the mechanism of stem mechanical strength in direct-seeded rice (DSR) as affected by paclobutrazol, especially its related endogenous hormone and cell wall component changes in culm tissue and response to the application of paclobutrazol. Field experiments were conducted in Changchun County, Jilin Province, China, by using two japonica rice varieties, Jiyujing and Jijing305, with soaking seeds in paclobutrazol at concentrations of (0 mg L-1, S0; 50 mg L-1; S1; 100 mg L-1; S2; 150 mg L-1, S3; 200 mg L-1, S4) in 2021 and 2022. The results suggest that the application of paclobutrazol increased the grain yield and reduced the lodging rate of DSR. Compared with the S0 treatments, soaking the seeds in paclobutrazol treatments rapidly shortened the length of the basal internode by decreasing the endogenous indole acetic acid (IAA) and gibberellin A3 (GA3) contents in culm tissue. The larger breaking strength (M) was attributed to a higher section modulus (SM) and bending stress (BS). The higher mechanical tissue thickness in culm tissue under paclobutrazol treatments, which was raised by higher endogenous zeatin and zeatin riboside (Z+ZR) content in culm tissue, increased the culm diameter, culm wall thickness, and section modulus (SM) of the internode. Compared with the S0 treatments, soaking the seeds in paclobutrazol treatments increased the cellulose content, lignin content, activities of lignin-related enzymes, and expression of key genes in lignin biosynthesis, as well as resulted in a higher bending stress (BS) to enhance the culm breaking strength (M).

Characterization of distinct microbiota associated with androgenetic alopecia patients treated and untreated with platelet-rich plasma (PRP).

BACKGROUND: Androgenic alopecia (AGA) is the most common type of hair loss in men, and there are many studies on the treatment of hair loss by platelet-rich plasma (PRP). The human scalp contains a huge microbiome, but its role in the process of hair loss remains unclear, and the relationship between PRP and the microbiome needs further study. Therefore, the purpose of this study was to investigate the effect of PRP treatment on scalp microbiota composition. METHODS: We performed PRP treatment on 14 patients with AGA, observed their clinical efficacy, and collected scalp swab samples before and after treatment. The scalp microflora of AGA patients before and after treatment was characterized by amplifying the V3-V4 region of the 16 s RNA gene and sequencing for bacterial identification. RESULTS: The results showed that PRP was effective in the treatment of AGA patients, and the hair growth increased significantly. The results of relative abundance analysis of microbiota showed that after treatment, g_Cutibacterium increased and g_Staphylococcus decreased, which played a stable role in scalp microbiota. In addition, g_Lawsonella decreased, indicating that the scalp oil production decreased after treatment. CONCLUSIONS: The findings suggest that PRP may play a role in treating AGA through scalp microbiome rebalancing.

Chromosomal polymorphisms and susceptibility to menstrual disorders: a retrospective analysis of 24,578 women.

PURPOSE: To evaluate the association between the polymorphic variants of chromosomes and menstrual disorders. METHODS: The data from our previous retrospective, single-center cohort study were re-analyzed. Women with regular menstruation were included as controls. Women with menstrual cycle abnormalities were subgrouped according to reproductive causes. The frequency of chromosomal polymorphisms was compared between groups. Regression analysis was used to adjust for potential confounding variables. RESULT: A total of 24,578 women composed of 8062 women with regular cycles as the control group and 16,516 women as the menstrual cycle irregularity group were included. When compared with the control group, the incidence of chromosomal polymorphisms in the total menstrual cycle irregularity group, Polycystic ovary syndrome group, and Primary ovarian insufficiency group were significantly higher (4.49% versus 5.34%, P = 0.004, 4.49% versus 5.35%, P = 0.018 and 4.49% versus 5.94%, P = 0.002, respectively). The incidences of inv(9) in the Primary ovarian insufficiency group were significantly higher than that in the control individuals (1.0% versus 1.6%, P = 0.024). Logistic regression analysis showed an effect of chromosomal polymorphisms on menstrual cycle irregularity (OR: 1.62, 95% CI: 1.234-2.187, P = 0.007; adjusted OR: 1.46, 95% CI: 1.153-1.819, P < 0.001). The result demonstrated an effect of chromosomal polymorphisms on the Primary ovarian insufficiency group (OR: 2.52, 95% CI: 1.307-5.177, P < 0.001; adjusted OR: 2.61, 95% CI: 1.371-4.605, P < 0.001). CONCLUSION: The study suggests chromosomal polymorphisms adversely affect female menstrual cycle irregularity.

Anti-inflammatory effects of amarogentin on 2,4-dinitrochlorobenzene-induced atopic dermatitis-like mice and in HaCat cells.

BACKGROUND: Amarogentin (AMA) is a secoiridoid glycoside extracted from Swertia and Gentiana roots and exhibits many biological effects such as antioxidative, anti-inflammatory, and antitumor activities. Atopic dermatitis (AD) is a chronic inflammatory skin disease caused by disorders in the regulation of multiple inflammatory cytokines. No effective cure has been found for AD now. METHODS: We constructed the HaCat and splenocyte model and tested the inhibitory effect of AMA on IL-4, IL-6, and IL-13 secretions using enzyme-linked immunosorbent assay (ELISA). The AD mouse model was constructed and treated with AMA, the severity of skin lesions was observed, epidermal tissue was collected, and epidermal thickness and mast cell infiltration were observed using hematoxylin and eosin and toluidine blue staining, respectively. The expression of kallikrein-related peptidase 7 (KLK7) and filaggrin (FLG) was detected using immunostaining and Western blot analysis. The mRNA expression of KLK7 and FLG was detected using quantitative polymerase chain reaction (qPCR). Blood immunoglobulin E (IgE) secretion was detected. RESULTS: AMA inhibited IL-6 secreted by tumor necrosis factor (TNF)-α-induced HaCaT cells and reduced IL-4 and IL-13 secreted by phytohemagglutinin (PHA)-induced primary cells in the mice spleen. It was found that the treatment of AMA with 2,4-dinitrochlorobenzene-induced AD-like mice could promote the recovery of dermatitis, reduce the score of dermatitis severity and the scratching frequency, treat the skin lesions, reduce the epidermal thickness, decrease the infiltration of mast cells, reduce the IgE level in serum, decrease the expression levels of AD-related cytokines, increase protein and mRNA expression of FLG, and reduce the protein and mRNA expression of KLK7 in the skin tissues of AD-like mice. CONCLUSION: In conclusion, AMA inhibits inflammatory response at the cellular level, and AMA reduces the validation response of specific dermatitis mice, relieves pruritus, and repairs the damaged skin barrier.

Effect of different concentrations of foliar iron fertilizer on chlorophyll fluorescence characteristics of iron-deficient rice seedlings under saline sodic conditions.

The effectiveness of iron is reduced in saline conditions, which can easily lead to iron deficiency and inhibit photosynthesis in rice. In this study, 4-week-old Fe-deficient rice seedlings were treated under saline sodic stress (50 mM) to different concentrations (0, 0.2%, 0.4%, 0.8%, 1.6%, and 3.2%) of foliar iron fertilizer (FeEDDHA). Differences in prompting fluorescence and the MR820 signal of rice leaves after 7 days of treatment were probed using the JIP-test. The results show that the performances of the two rice varieties were in general agreement. Under iron deficiency and soda salinity stress conditions, rice growth was inhibited, and the pigment content, specific energy flux, quantum yield, performance of the active PSII reaction center (PIABS) and the oxidation (Vox) and reduction rates (Vred) of PSI were reduced. These indicators first increase and then decrease with increasing iron fertiliser concentrations. The best results were obtained with the Fe3 treatment (0.8%). Fluorescence parameters such as the relative variable fluorescence (WK and VJ) and the quantum yield of energy dissipation (φDo) showed opposite trends. This suggests that iron deficiency/excess and soda saline stress disrupt the electron and energy transport in the photosystem. Appropriate iron fertilization concentration can repair the photosynthetic electron transport chain, improve electron transport efficiency and promote balanced energy distribution. Therefore, we suggest that moderate amounts of Fe are beneficial for improving the electron and energy transport properties of the photosystem, while spraying high concentrations of Fe fertilizer has a negative effect on improving salt tolerance in rice.

The role of Serpina3n in the reversal effect of ATRA on dexamethasone-inhibited osteogenic differentiation in mesenchymal stem cells.

BACKGROUND: Glucocorticoid-induced osteoporosis (GIOP) is the most common secondary osteoporosis. Patients with GIOP are susceptible to fractures and the subsequent delayed bone union or nonunion. Thus, effective drugs and targets need to be explored. In this regard, the present study aims to reveal the possible mechanism of the anti-GIOP effect of all-trans retinoic acid (ATRA). METHODS: Bone morphogenetic protein 9 (BMP9)-transfected mesenchymal stem cells (MSCs) were used as an in vitro osteogenic model to deduce the relationship between ATRA and dexamethasone (DEX). The osteogenic markers runt-related transcription factor 2 (RUNX2), alkaline phosphatase (ALP), and osteopontin were detected using real-time quantitative polymerase chain reaction, Western blot, and immunofluorescent staining assay. ALP activities and matrix mineralization were evaluated using ALP staining and Alizarin Red S staining assay, respectively. The novel genes associated with ATRA and DEX were detected using RNA sequencing (RNA-seq). The binding of the protein-DNA complex was validated using chromatin immunoprecipitation (ChIP) assay. Rat GIOP models were constructed using intraperitoneal injection of dexamethasone at a dose of 1 mg/kg, while ATRA intragastric administration was applied to prevent and treat GIOP. These effects were evaluated based on the serum detection of the osteogenic markers osteocalcin and tartrate-resistant acid phosphatase 5b, histological staining, and micro-computed tomography analysis. RESULTS: ATRA enhanced BMP9-induced ALP, RUNX2 expressions, ALP activities, and matrix mineralization in mouse embryonic fibroblasts as well as C3H10T1/2 and C2C12 cells, while a high concentration of DEX attenuated these markers. When DEX was combined with ATRA, the latter reversed DEX-inhibited ALP activities and osteogenic markers. In vivo analysis showed that ATRA reversed DEX-inhibited bone volume, bone trabecular number, and thickness. During the reversal process of ATRA, the expression of retinoic acid receptor beta (RARß) was elevated. RARß inhibitor Le135 partly blocked the reversal effect of ATRA. Meanwhile, RNA-seq demonstrated that serine protease inhibitor, clade A, member 3N (Serpina3n) was remarkably upregulated by DEX but downregulated when combined with ATRA. Overexpression of Serpina3n attenuated ATRA-promoted osteogenic differentiation, whereas knockdown of Serpina3n blocked DEX-inhibited osteogenic differentiation. Furthermore, ChIP assay revealed that RARß can regulate the expression of Serpina3n. CONCLUSION: ATRA can reverse DEX-inhibited osteogenic differentiation both in vitro and in vivo, which may be closely related to the downregulation of DEX-promoted Serpina3n. Hence, ATRA may be viewed as a novel therapeutic agent, and Serpina3n may act as a new target for GIOP.

Efficacy and Safety of Long-Term Intravenous Tranexamic Acid Administration for Blood Management in Revision Surgery for Femoral Shaft Nonunion: A Retrospective Case-Control Study.

Femoral shaft nonunion is a complication that seriously affects physiological functions. We aimed to assess the effectiveness and safety of short- and long-term intravenous tranexamic acid (TXA) administration in the perioperative period of revision surgery for femoral shaft nonunion. In this retrospective study, 53 patients undergoing double-locking plates with channel bone grafting technology for the treatment of femoral shaft nonunion were divided into 3 groups: the patients in group A without use TXA during hospitalization, the patients in group B received intravenous (IV) 1-g TXA at 30 min before the surgery and deep soaked 1-g TXA for 5 min before closing the incision, and then 1-g TXA IV again 6 h after surgery, and the patients in group C received 1-g TXA IV before the operation, 1-g TXA topically during the operation, and subsequent long-term 1-g TXA IV until discharged. The primary outcomes were total blood loss (TBL) and hidden blood loss (HBL). The secondary outcomes included actual hemoglobin (Hb) loss values, transfusion requirement, number of units transfused, postoperative laboratory values (Hb, hematocrit, fibrinogen, and D-dimer), visual analogue scale (VAS) scores, and hospitalization time. The mean TBL was lower in group C than in group A (1168 mL vs. 2714 mL, P < 0.001) and group B (1168 mL vs. 1557 mL, P = 0.008). The differences in HBL volumes were also significant between groups A and C (P < 0.001) and between groups A and B (P < 0.01). The actual Hb loss in the 3 groups showed a consistent trend with TBL, but no significant differences between groups B and C (P = 0.23). On postoperative day (POD) 3, the Hb level was higher in group C than in group A (111.1 g/L vs. 94.6 g/L, P = 0.02). No significant differences were found in VAS, hospital stay, thromboembolic complications, incision-related complications, and TXA adverse reactions among groups. Long-term intravenous TXA during hospitalization can effectively reduce perioperative blood loss, Hb drop, and postoperative hyperfibrinolysis, but is associated with an increased incidence of adverse reactions.

Proposal for detecting ring current via electron vortices.

In an intense circularly polarized laser field, the excitation of the atoms shows a strong dependence on the orbital helicity. The resonant excitation starting from the ground state with $ m = - 1 $m=-1 occurs much more easily in the left-handed circularly polarized (LCP with $ m = + 1 $m=+1) pulse than in the right-handed circularly polarized (RCP with $ m = - 1 $m=-1) pulse. In this Letter, we numerically demonstrate that the orbital-helicity-dependent two-photon-resonant excitation leads to the photoelectron vortex pattern in the polarization plane being sensitive to the sequence of the two counter-rotating circularly polarized pulses in xenon, which enables the detection of the ring currents associated with different quantum states. These results also provide an effective way for controlling the rotational symmetry of the electron vortex.

IGF-1 reverses the osteogenic inhibitory effect of dexamethasone on BMP9-induced osteogenic differentiation in mouse embryonic fibroblasts via PI3K/AKT/COX-2 pathway.

Glucocorticoid-Induced Osteoporosis (GIOP) is a prevalent clinical complication caused by large dose administration of glucocorticoids, such as Dexamethasone (Dex) and Prednisone. GIOP may lead to fractures and even Osteonecrosis of the Femoral Head (ONFH). It has been reported that glucocorticoids inhibit osteogenesis via the suppression of osteogenic differentiation in Mesenchymal Stem Cells (MSCs), but the precise mechanism underlying this suppression awaits further investigation. Meanwhile, novel and efficacious therapies are recommended to cope with GIOP. In this study, we demonstrated that Dex had the inhibitory effect on Bone Morphogenetic Protein 9 (BMP9)-induced ALP activities and matrix mineralization in Mouse Embryonic Fibroblasts (MEFs). In addition, the study confirmed that Dex decreased the expression of osteogenic markers such as Runx2 and OPN. However, the inhibitory effect of Dex on these osteogenic markers can be reversed when combined with insulin-like growth factor 1 (IGF-1). Regarding the inhibitory mechanism, we found that the level of AKT and p-AKT can be decreased by Dex and that Ly294002, the PI3K inhibitor, can block the reversal effect of IGF-1. Moreover, the knockdown or inhibition of COX-2 produced similar results to those of Ly294002. Our findings indicated that IGF-1 may reverse the osteogenic inhibitory effect of Dex via PI3K/AKT pathway, which may be associated with the up-regulation of COX-2. This study may provide new clinical management strategy for GIOP cases.