Reciprocal regulation of flower induction by ELF3α and ELF3ß generated via alternative promoter usage.

Flowering is critical for sexual reproduction and fruit production. Several pear (Pyrus sp.) varieties produce few flower buds, but the underlying mechanisms are unknown. The circadian clock regulator EARLY FLOWERING3 (ELF3) serves as a scaffold protein in the evening complex that controls flowering. Here, we report that the absence of a 58-bp sequence in the 2nd intron of PbELF3 is genetically associated with the production of fewer flower buds in pear. From rapid amplification of cDNA ends sequencing results, we identified a short, previously unknown transcript from the PbELF3 locus, which we termed PbELF3ß, whose transcript level was significantly lower in pear cultivars that lacked the 58-bp region. The heterologous expression of PbELF3ß in Arabidopsis (Arabidopsis thaliana) accelerated flowering, whereas the heterologous expression of the full-length transcript PbELF3α caused late flowering. Notably, ELF3ß was functionally conserved in other plants. Deletion of the 2nd intron reduced AtELF3ß expression and caused delayed flowering time in Arabidopsis. AtELF3ß physically interacted with AtELF3α, disrupting the formation of the evening complex and consequently releasing its repression of flower induction genes such as GIGANTEA (GI). AtELF3ß had no effect in the absence of AtELF3α, supporting the idea that AtELF3ß promotes flower induction by blocking AtELF3α function. Our findings show that alternative promoter usage at the ELF3 locus allows plants to fine-tune flower induction.

PIK3CA variants selectively initiate brain hyperactivity during gliomagenesis.

Glioblastoma is a universally lethal form of brain cancer that exhibits an array of pathophysiological phenotypes, many of which are mediated by interactions with the neuronal microenvironment1,2. Recent studies have shown that increases in neuronal activity have an important role in the proliferation and progression of glioblastoma3,4. Whether there is reciprocal crosstalk between glioblastoma and neurons remains poorly defined, as the mechanisms that underlie how these tumours remodel the neuronal milieu towards increased activity are unknown. Here, using a native mouse model of glioblastoma, we develop a high-throughput in vivo screening platform and discover several driver variants of PIK3CA. We show that tumours driven by these variants have divergent molecular properties that manifest in selective initiation of brain hyperexcitability and remodelling of the synaptic constituency. Furthermore, secreted members of the glypican (GPC) family are selectively expressed in these tumours, and GPC3 drives gliomagenesis and hyperexcitability. Together, our studies illustrate the importance of functionally interrogating diverse tumour phenotypes driven by individual, yet related, variants and reveal how glioblastoma alters the neuronal microenvironment.

Comparative efficacy and complications of single and dual growing rods for early-onset scoliosis: an updated meta-analysis.

PURPOSE: This updated meta-analysis aimed to compare single and dual growing rods, including both traditional growing rod and magnetically controlled growing rod (MCGR) used in the treatment of early-onset scoliosis (EOS) with regard to deformity correction, spinal growth, and complications. METHODS: This meta-analysis was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines using articles extracted from PubMed, EMBASE databases, and Cochrane Library databases. Only articles reporting the complications and the imaging parameters before and after growing rods in the patients diagnosed with EOS were included. We extracted and statistically analyzed the data deemed relevant for this study, and used the Newcastle-Ottawa Scale to assess the risk of bias in each study. Data synthesis and statistical analyses were performed using R software. RESULTS: Fifteen eligible articles containing 409 participants (n = 185, single growing rods; n = 224, dual growing rods) were identified. The meta-analysis found no significant differences in the preoperative and postoperative major Cobb angle, T1-S1 distance, thoracic kyphosis, and coronal balance between single and dual rods groups. The final follow-up major Cobb angle (P = 0.01; standardized mean difference, - 0.42 [95% confidence interval (CI), - 0.74 to - 0.10]; I2 = 23%) was significantly smaller in dual rods group than single-rod group. However, no significant differences in the correction rate of angle (major Cobb angle and kyphosis angle) and changes in the T1-S1 distance between the two groups were observed. Moreover, there were no significant differences in the metalwork failure, infection, or proximal junctional kyphosis between single and dual rods groups. However, total complications (P = 0.03; risk ratio (RR), 0.79 [95% CI, 0.63-0.98]; I2 = 29%) and distraction failure in MCGR (P = 0.04; RR, 0.38 [95% CI, 0.14-0.98]; I2 = 11%) were significantly lower in dual rods group than single-rod group. CONCLUSION: This updated meta-analysis found that patients with dual growing rods had fewer complications, especially distraction failure in MCGR, than those with single growing rod. However, none of deformity correction, spinal growth, or other complications differed between single and dual growing rods. Therefore, we believe that dual growing rods do not provide strong advantages over single growing rod in the treatment of EOS.

Ferroptosis induced by the biocontrol agent Pythium oligandrum enhances soybean resistance to Phytophthora sojae.

Ferroptosis is a newly discovered form of cell death accompanied by iron accumulation and lipid peroxidation. Both biotic and abiotic stresses can induce ferroptosis in plant cells. In the case of plant interactions with pathogenic Phytophthora oomycetes, the roles of ferroptosis are still largely unknown. Here, we performed transcriptome analysis on soybean plants treated with the biocontrol agent Pythium oligandrum, a soilborne and non-pathogenic oomycete capable of inducing plant resistance against Phytophthora sojae infection. Expression of homologous soybean genes involved in ferroptosis and resistance was reprogrammed upon P. oligandrum treatment. Typical hallmarks for characterizing ferroptosis were detected in soybean hypocotyl cells, including decreased glutathione (GSH) level, accumulation of ferric ions, and lipid peroxidation by reactive oxygen species (ROS). Meanwhile, ferroptosis-like cell death was triggered by P. oligandrum to suppress P. sojae infection in soybean. Protection provided by P. oligandrum could be attenuated by the ferroptosis inhibitor ferrostatin-1 (Fer-1), suggesting the critical role of ferroptosis in soybean resistance against P. sojae. Taken together, these results demonstrate that ferroptosis is a P. oligandrum-inducible defence mechanism against oomycete infection in soybean.

The effects of smoking on clinical and structural outcomes after rotator cuff repair: a systematic review and meta-analysis.

BACKGROUND: Several factors have been reported to adversely affect clinical and structural outcomes after rotator cuff repair (RCR). However, the effects of smoking on rotator cuff healing and clinical outcomes remain controversial. The purpose of this study was to compare the clinical and structural outcomes after RCR between smokers and nonsmokers. We hypothesized that there would be no significant difference in the clinical scores after RCR and that smoking would be associated with a significantly increased risk of retear and reoperation. METHODS: This systematic review was performed in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines using the PubMed, Cochrane Library, and Embase databases. We included only articles in which patients underwent arthroscopic and open RCR, the clinical outcome scores were reported for smokers and nonsmokers, and the number of rotator cuff retears and reoperations were reported. Data relevant to this study were extracted and statistically analyzed. We used the Newcastle-Ottawa Scale to assess the risk of bias in each study and calculated the I2 value to quantify the effect of heterogeneity. RESULTS: Fourteen eligible articles were identified, with 73,817 participants (8553 smokers and 65,264 nonsmokers). The meta-analysis demonstrated that there were no significant differences in the American Shoulder and Elbow Surgeons score (P = .10), Simple Shoulder Test score (P = .19), University of California-Los Angeles score (P = .09), or visual analog scale score (P = .19) between smokers and nonsmokers after surgery, but the Constant score was significantly lower (P = .005) for smokers. Smoking was significantly associated with an increased risk of retear (P = .002; risk ratio, 2.06 [95% confidence interval, 1.30-3.28]; I2 = 31%) and reoperation (P < .001; risk ratio, 1.29 [95% confidence interval, 1.20-1.40]; I2 = 36%) in patients after RCR. CONCLUSION: Besides the Constant score, which was lower in smokers, there were no significant differences in the clinical scores after RCR between smokers and nonsmokers. However, smoking was associated with a significantly increased risk of retear and reoperation.

Exendin-4 promotes bone formation in diabetic states via HDAC1-Wnt/ß-catenin axis.

Exendin-4 has been found to have hypoglycemic effect and prevent bone loss in diabetic patients, but its mechanism of preventing bone loss is still unclear. In this study, high-fat diet combined with streptozotocin was used to establish type 2 diabetes mellitus (T2DM) mice, and bone marrow mesenchyme stem cells (BMSCs) were isolated for osteogenic induction in vitro. Alizarin red staining and ALP activity detection were used to observe the effect of exendin-4 on osteogenic differentiation of BMSCs. Western blot was used to detect the proteins expression in BMSCs. In vivo, the effects of exendin-4 treatment on body weight, blood glucose, bone density and bone quality of T2DM mice were observed by treatment with exendin-4. The results showed that exendin-4 promoted osteogenic differentiation of T2DM derived BMSCs, down-regulated histone deacetylase 1 (HDAC1) and p-ß-Catenin proteins expression, and up-regulated Wnt3, ß-Catenin and runt-related transcription factor 2 (Runx 2) proteins expression. In vivo, exendin-4 effectively suppressed the blood glucose and increased body weight of T2DM mice, and significantly improved bone density and bone quality of the right tibia. Interestingly, by over-expression of HDAC1 in BMSCs, the effect of exendin-4 on promoting osteogenic differentiation of BMSCs was attenuated, and the regulation of Wnt3a, ß-Catenin, p-ß-Catenin or Runx2 proteins were reversed. By injecting adenovirus containing HDAC1 into the right tibia of mice, the effect of exendin-4 on bone density and bone quality of T2DM mice was significantly attenuated. All above results suggest that the HDAC1-Wnt/ß-Catenin signal axis is involved in the anti-diabetic bone loss effect of exendin-4, and HDAC1 may be the target of exendin-4.

LncRNA ANRIL promotes multiple myeloma progression and bortezomib resistance by EZH2-mediated epigenetically silencing of PTEN.

Multiple myeloma (MM) is a plasma cell malignancy of bone marrow. In the present study, we aimed to study the function and potential mechanism of the antisense non-coding RNA in the INK4 Locus (ANRIL) in MM. The expression levels of ANRIL in MM patients and healthy donors were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). The effects and mechanisms of ANRIL in MM were evaluated by cell viability assay, BrdU incorporation assay, tumor xenograft model, flow cytometry, western blot, RNA immunoprecipitation (RIP), transcriptome RNA sequencing, and chromatin immunoprecipitation (ChIP). We found that ANRIL was upregulated in MM patients and cell lines, and associated with advanced international staging system (ISS) stage and poor overall survival. Enforced ANRIL expression promoted proliferation and tumor xenograft growth of MM cells, while knockdown of ANRIL exhibited opposite effects. Moreover, ANRIL overexpression increased the half-maximal inhibitory concentration (IC50) of bortezomib and reduced bortezomib-induced apoptosis in MM cells. ANRIL was found to accumulate in the nuclei of MM cells, and interact with EZH2 by RIP assay. Transcriptome RNA sequencing identified PTEN as a target of ANRIL in MM cells. In the ChIP assay, knockdown of ANRIL reduced EZH2 occupancy and H3K27me3 binding to the promoter region of PTEN. Furthermore, EZH2 knockout or PTEN restoration abrogated the effects caused by ANRIL overexpression in MM cells. Our results indicated that ANRIL exerted oncogenic functions and conferred chemoresistance of MM cells by EZH2-mediated epigenetically silencing of PTEN.

Complications and risk factors of percutaneous endoscopic transforaminal discectomy in the treatment of lumbar spinal stenosis.

BACKGROUND: With the advancements in surgical methods, optical designs, and surgical instruments, percutaneous endoscopic transforaminal discectomy (PETD) has become an effective and minimally invasive procedure to treat lumbar spinal stenosis (LSS) in recent years. Few studies have focused on the complications associated with the treatment of LSS using percutaneous endoscopic lumbar discectomy (PELD). This study aimed to summarize the complications of PETD and identify the associated risk factors. METHODS: Complications in a total of 738 consecutive LSS patients who underwent single-level PETD were retrospectively recorded and analyzed between January 2016 and July 2020. In addition, a matched case-control study was designed, and according to the date of operation, the control group was matched with patients without complications, with a matching ratio of 1:3. Demographic parameters included age, sex, BMI, smoking and drinking status, comorbidity, and surgical level. The radiological parameters included grade of surgical-level disc degeneration, number of degenerative lumbar discs, grade of lumbar spinal stenosis, degenerative lumbar scoliosis, lumbar lordosis, disc angle, and disc height index. Univariate analysis was performed using independent samples t-test and chi-squared test. RESULTS: The incidence of different types of complications was 9.76% (72/738). The complications and occurrence rates were as follows: recurrence of LSS (rLSS), 2.30% (17/738); persistent lumbosacral or lower extremity pain, 3.79% (28/738); dural tear, 1.90% (14/738); incomplete decompression, 0.81% (6/738); surgical site infection, 0.41% (3/738); epidural hematoma, 0.27% (2/738); and intraoperative posterior neck pain, 0.27% (2/738). Univariate analysis demonstrated that age, the grade of surgical-level disc degeneration (P < 0.001) and the number of disc degeneration levels (P = 0.004) were significantly related to the complications. CONCLUSION: Complications in the treatment of LSS using PELD included rLSS, persistent pain of the lumbosacral or lower extremity, dural tear, incomplete decompression, surgical site infection, epidural hematoma, and intraoperative posterior neck pain. In addition, old age, severe grade of surgical-level disc degeneration and more disc degeneration levels significantly increased the incidence of complications.

Apcdd1 stimulates oligodendrocyte differentiation after white matter injury.

Wnt signaling plays an essential role in developmental and regenerative myelination of the CNS, therefore it is critical to understand how the factors associated with the various regulatory layers of this complex pathway contribute to these processes. Recently, Apcdd1 was identified as a negative regulator of proximal Wnt signaling, however its role in oligodendrocyte (OL) differentiation and reymelination in the CNS remain undefined. Analysis of Apcdd1 expression revealed dynamic expression during OL development, where its expression is upregulated during differentiation. Functional studies using ex vivo and in vitro OL systems revealed that Apcdd1 promotes OL differentiation, suppresses Wnt signaling, and associates with ß-catenin. Application of these findings to white matter injury (WMI) models revealed that Apcdd1 similarly promotes OL differentiation after gliotoxic injury in vivo and acute hypoxia ex vivo. Examination of Apcdd1 expression in white matter lesions from neonatal WMI and adult multiple sclerosis revealed its expression in subsets of oligodendrocyte (OL) precursors. These studies describe, for the first time, the role of Apcdd1 in OLs after WMI and reveal that negative regulators of the proximal Wnt pathway can influence regenerative myelination, suggesting a new therapeutic strategy for modulating Wnt signaling and stimulating repair after WMI.

Combining serum and urine biomarkers in the early diagnosis of mild cognitive impairment that evolves into Alzheimer's disease in patients with the apolipoprotein E ϵ4 genotype.

Possession of the apolipoprotein E (APOE) ϵ4 genotype is a major predictor of progression to Alzheimer's disease (AD), particularly in patients with mild cognitive impairment (MCI). However, the use of APOE genotyping in the diagnosis of MCI is limited due to its low sensitivity and specificity, which often results in a high false-positive rate. In this study, we found that there was a significant decrease in serum BDNF and notable increase in urine AD7c-NTP in MCI patients who harbored the APOE ϵ4 allele. Both serum BDNF and urine AD7c-NTP had higher positive predictive values and were more sensitive biomarkers of MCI. Additionally, a testing strategy employing serum BDNF and urine AD7c-NTP revealed increases in sensitivity, positive and negative predictive values, and predictive ability compared with the use of either biomarker alone, suggested that combinatorial detection might have great potential for translation to the clinic.

Recompression after percutaneous transforaminal endoscopic decompression for degenerative lumbar spinal stenosis: risk factors and outcomes of two different reoperation procedures.

Purpose: To determine the risk factors for recompression after percutaneous transforaminal endoscopic decompression (PTED) for the treatment of degenerative lumbar spinal stenosis (DLSS) and compare the outcomes of PTED and posterior lumbar interbody fusion (PLIF) as revision surgery. Methods: We retrospectively evaluated 820 consecutive DLSS patients who underwent PTED at our institution. 26 patients developed postoperative recompression and underwent reoperation. In total, 208 patients with satisfactory clinical outcomes were enrolled in the control group. The demographic and imaging data of each patient were recorded. Univariate and multivariate analyses were performed to assess risk factors for recompression. Additionally, patients with recompression were divided into PTED and PLIF groups according to the reoperation procedure. The clinical outcomes of the two groups were compared using independent-sample t-tests. Results: The grade of surgical-level disc degeneration [odds ratio (OR): 2.551, p = 0.045] and the number of disc degeneration levels (OR: 11.985, p < 0.001) were independent risk factors for recompression after PTED. There was no significant difference in the visual analog score (VAS) and Oswestry disability index (ODI) two weeks postoperatively between the PTED and PLIF groups for surgical treatment. However, the mean VAS of back pain (14.1 vs. 20.5, p = 0.016) and ODI (16.0 vs. 21.8, p = 0.016) of patients in the PLIF group were smaller than those in the PTED group at the final follow-up. Conclusion: More severe degeneration and degenerated levels indicate a higher recompression rate after PTED. Although both PTED and PLIF could achieve immediate relief postoperatively in the treatment of recompression, the final follow-up results showed that the outcome of PLIF appeared better than that of PTED.

Gut mycobiome alterations in obesity in geographically different regions.

The gut fungi play important roles in human health and are involved in energy metabolism. This study aimed to examine gut mycobiome composition in obese subjects in two geographically different regions in China and to identify specific gut fungi associated with obesity. A total of 217 subjects from two regions with different urbanization levels [Hong Kong (HK): obese, n = 59; lean, n = 59; Kunming (KM): obese, n = 50; lean, n = 49. Mean body mass index (BMI) for obesity = 33.7] were recruited. We performed deep shotgun metagenomic sequencing on fecal samples to compare gut mycobiome composition and trophic functions in lean and obese subjects across these two regions. The gut mycobiome of obese subjects in both HK and KM were altered compared to those of lean subjects, characterized by a decrease in the relative abundance of Nakaseomyces, Schizosaccharomyces pombe, Candida dubliniensis and an increase in the abundance of Lanchanceathermotolerans, Saccharomyces paradox, Parastagonospora nodorum and Myceliophthorathermophila. Reduced fungal - bacterial and fungal - fungal correlations as well as increased negative fungal-bacterial correlations were observed in the gut of obese subjects. Furthermore, the anti-obesity effect of fungus S. pombe was further validated using a mouse model. Supplementing high-fat diet-induced obese mice with the fungus for 12 weeks led to a significant reduction in body weight gain (p < 0.001), and an improvement in lipid and glucose metabolism compared to mice without intervention. In conclusion, the gut mycobiome composition and functionalities of obese subjects were altered. These data shed light on the potential of utilizing fungus-based therapeutics for the treatment of obesity. S. pombe may serve as a potential fungal probiotic in the prevention of diet-induced obesity and future human trials are needed.

Gender differences in cardiovascular mortality by C-reactive protein level in the United States: evidence from the National Health and Nutrition Examination Survey III.

BACKGROUND: The association between C-reactive protein (CRP) and cardiovascular (CV) mortality by gender has not been previously described using a data set that is representative of the US population. METHODS: We used Cox proportional hazards models to explore gender differences in CRP-associated mortality via the National Health and Nutrition Examination Survey III 1988-1994 linked to the National Death Index with mortality follow-up through 2006. We examined CV mortality as well as all-cause mortality hazards. RESULTS: The final sample size included a total of 13,878 individuals (7,364 women and 6,514 men) with a median follow up of 18.2 years. All models controlled for race, age, smoking, high-density lipoprotein, hypertension, diabetes mellitus, waist circumference, and total cholesterol. Men with a CRP >3.0 mg/L relative to those with a CRP ≤3.0 mg/L had elevated CV mortality hazards (hazard ratio [HR] 1.79, 95% CI 1.23-2.60) and all-cause mortality hazards (HR 1.57, 95% CI 1.29-1.90). In women, elevated CRP was not significantly associated with either increased CV (HR 1.20, 95% CI 0.90-1.59) or all-cause mortality hazards (HR 1.09, CI 0.93-1.29). CONCLUSION: National guidelines from various agencies that make recommendations on the diagnostic and prognostic use of CRP have treated men and women equally. We find that there may be reason to tailor recommendations based upon one's gender.

Dual recognition elements for selective determination of progesterone based on molecularly imprinted electrochemical aptasensor.

A novel molecularly imprinted electrochemical aptasensor (MIEAS) was constructed for selective progesterone (P4) detection based on SnO2-graphene (SnO2-Gr) nanomaterial and gold nanoparticles (AuNPs). SnO2-Gr with a large specific area and excellent conductivity improved the adsorption capacity of P4. Aptamer, as biocompatible monomer, was captured by AuNPs on modified electrode through Au-S bond. An electropolymerized molecularly imprinted polymer (MIP) film consisted of p-aminothiophenol as chemical functional monomer and P4 as template molecule. Due to the synergetic effect of MIP and aptamer towards P4, this MIEAS exhibited better selectivity than the sensor with MIP or aptamer as single recognition element. The prepared sensor had a low detection limit of 1.73 × 10-15 M in a wide linear range from 10-14 M to 10-5 M. Satisfactory recovery obtained in tap water and milk samples proved that this sensor had great potential in environmental and food analysis.

Engineering crop Phytophthora resistance by targeting pathogen-derived PI3P for enhanced catabolism.

Phytophthora pathogens lead to numerous economically damaging plant diseases worldwide, including potato late blight caused by P. infestans and soybean root rot caused by P. sojae. Our previous work showed that Phytophthora pathogens may generate abundant phosphatidylinositol 3-phosphate (PI3P) to promote infection via direct association with RxLR effectors. Here, we designed a disease control strategy for metabolizing pathogen-derived PI3P by expressing secreted Arabidopsis thaliana phosphatidylinositol-4-phosphate 5-kinase 1 (AtPIP5K1), which can phosphorylate PI3P to PI(3,4)P2. We fused AtPIP5K1 with the soybean PR1a signal peptide (SP-PIP5K1) to enable its secretion into the plant apoplast. Transgenic soybean and potato plants expressing SP-PIP5K1 showed substantially enhanced resistance to various P. sojae and P. infestans isolates, respectively. SP-PIP5K1 significantly reduced PI3P accumulation during P. sojae and soybean interaction. Knockout or inhibition of PI3 kinases (PI3Ks) in P. sojae compromised the resistance mediated by SP-PIP5K1, indicating that SP-PIP5K1 action requires a supply of pathogen-derived PI3P. Furthermore, we revealed that SP-PIP5K1 can interfere with the action of P. sojae mediated by the RxLR effector Avr1k. This novel disease control strategy has the potential to confer durable broad-spectrum Phytophthora resistance in plants through a clear mechanism in which catabolism of PI3P interferes with RxLR effector actions.

Equol exerts a protective effect on postmenopausal osteoporosis by upregulating OPG/RANKL pathway.

BACKGROUD: Estrogen deficiency is the leading cause of postmenopausal osteoporosis(PMOP) and phytoestrogens soy isoflavones (SI) have been shown to improve PMOP. Equol (Eq), an in vivo metabolite of phytoestrogens soy isoflavones (SI), has a more stable structure and stronger biological activity than its parent compound and has the greatest estrogenic activity. However, there are few studies on the therapeutic effect of Eq on PMOP. PURPOSE: To explore the therapeutic effect and mechanisms of Eq on POMP. METHODS: Osteoblast-like cells ROS1728 were cultured with different doses of Eq, estradiol (E2), separately. The effect of Eq on the proliferation, apoptosis, cell cycle of osteoblasts were detected by CCK-8 and flow cytometry, and the expression of OPG/RANK/RANKL signaling pathway of osteoblasts was detected by Quantitative real-time PCR (qRT-PCR) and Western blot (WB), and RNA silencing technology were carried out to explore the receptors through which Eq plays a role. Then PMOP rat model was established and treated by Eq or E2 to further verification of the effect and mechanism of Eq on PMOP. RESULT: Eq promoted the proliferation and inhibited the apoptosis of osteoblasts and increased the proportion of osteoblasts in the S phase and G2/M phase in a dose-dependent manner. Mechanistically, Eq treatment upregulated the expression of OPG and OPG/RANKL ratio in osteoblasts and this regulatory effect was mainly mediated through the ERß receptor. Furthermore, in vivo study, Eq improved microstructure and BMD of the femur of PMOP rat model, which imitated the osteoprotective effect of E2. Moreover, the Eq or E2 treatment increased serum levels of Ca, 1,25(OH)2D3, bone Gla-protein(BGP), and Type I procollagen (PC1), and reduced serum levels of phosphorus (P), parathyroid hormone(PTH), pyridinol (PYD), tartrate-resistant acid phosphatase (TRAP) and urinary level of deoxypyridinoline (DPD) in the treatment OVX group compared with the untreated OVX group. Meanwhile, Eq or E2 markedly induced the mRNA and protein expression of OPG and OPG/RANKL ratio. CONCLUSION: Eq can combine with ERß and exert a protective effect on PMOP by upregulating OPG/RANKL pathway.

Effects of Mobile Phone-Based Telemedicine Management in Patients With Type 2 Diabetes Mellitus: A Randomized Clinical Trial.

BACKGROUND: This study aims to explore the effect of mobile phone-based telemedicine management of glycemic control of type 2 diabetes mellitus (T2DM). METHODS: Patients with T2DM were followed up in Chongqing Jiulongpo District Yuzhoulu Community Health Center, and randomly divided into the telemedicine group (n=47) and the control group (n=50). The control group received regularly routine intervention. The telemedicine management group used the mobile phone to manage their health condition remotely. RESULTS: Both groups had similar baseline characteristics. After a follow-up period of 12 months intervention, the weight, body mass index, waist circumference, systolic blood pressure, body fat percentage, body fat mass, body water and muscle mass, fasting blood glucose, glycosylated hemoglobin, total costs of diabetes treatment for 1 month and the quality-of-life score were significantly improved in the telemedicine group (P<0.05). And compared with the control group, body fat composition, fasting blood glucose, glycosylated hemoglobin and the cost of change shows a significant improvement (P<0.05). Positive correlation was detected between fasting blood glucose and body composition parameters, such as body fat percentage, lean body mass and body fat mass in the telemedicine group (r=0.56, P<0.05; r=0.37, P<0.05; r=0.56, P<0.05). CONCLUSIONS: Compared with conventional intervention, the mobile phone-based telemedicine management can help patients with T2DM to improve glycemic level and quality of life.

Influence of configuration and anchor in ligamentous augmentation to prevent proximal junctional kyphosis: A finite element study.

Ligament augmentation has been applied during spinal surgery to prevent proximal junctional kyphosis (PJK), but the configuration and distal anchor strategies are diverse and inconsistent. The biomechanics of different ligament augmentation strategies are, therefore, unclear. We aimed to create a finite element model of the spine for segments T6-S1. Model Intact was the native form, and Model IF was instrumented with a pedicle screw from segments T10 to S1. The remaining models were based on Model IF, with ligament augmentation configurations as common (CM), chained (CH), common and chained (CHM); and distal anchors to the spinous process (SP), crosslink (CL), and pedicle screw (PS), creating SP-CH, PS-CHM, PS-CH, PS-CM, CL-CHM, CL-CH, and CL-CM models. The range of motion (ROM) and maximum stress on the intervertebral disc (IVD), PS, and interspinous and supraspinous ligaments (ISL/SSL) was measured. In the PS-CH model, the ROM for segments T9-T10 was 73% (of Model Intact). In the CL-CHM, CL-CH, CL-CM, PS-CM, and PS-CHM models, the ROM was 8%, 17%, 7%, 13%, and 30%, respectively. The PS-CH method had the highest maximum stress on IVD and ISL/SSL, at 80% and 72%, respectively. The crosslink was more preferable as the distal anchor. In the uppermost instrumented vertebrae (UIV) + 1/UIV segment, the CM was the most effective configuration. The PS-CH model had the highest flexion load on the UIV + 1/UIV segment and the CL-CM model provided the greatest reduction. The CL-CM model should be verified in a clinical trial. The influence of configuration and anchor in ligament augmentation is important for the choice of surgical strategy and improvement of technique.

Identifying the potential role of IL-1ß in the molecular mechanisms of disc degeneration using gene expression profiling and bioinformatics analysis.

PURPOSE: We performed a bioinformatics analysis to identify the key genes that were differentially expressed between degenerative intervertebral disc (IVD) cells with and without exposure to interleukin-1ß and explore the related signaling pathways and interaction networks. METHODS: The microarray data were downloaded from the Gene Expression Omnibus (27,494). Then, analyses of the gene ontology, signaling pathways, and interaction networks for the differentially expressed genes (DEGs) were conducted using tools including the Database for Annotation, Visualization, and Integrated Discovery, Metascape, Gene Set Enrichment Analysis, Search Tool for the Retrieval of Interacting Genes, Cytoscape, Venn method, and packages of the R computing language. RESULTS: A total of 260 DEGs were identified, including 161 upregulated and 99 downregulated genes. Gene Ontology annotation analysis showed that these DEGs were mainly associated with the extracellular region, chemotaxis, taxis, cytokine activity, and cytokine receptor binding. A Kyoto Encyclopedia of Genes and Genomes signaling pathway analysis showed that these DEGs were mainly involved in the of cytokine-cytokine receptor interaction, rheumatoid arthritis, tumor necrosis factor signaling pathway, Salmonella infection, and chemokine signaling pathway. The interaction network analysis indicated that 10 hub genes, including CXCL8, CXCL1, CCL20, CXCL2, CXCL5, CXCL3, CXCL6, C3, PF4, and GPER1 may play key roles in IVD degeneration. CONCLUSIONS: Bioinformatic analysis showed that CXCL8 and other nine key genes may play a role in the development of disc degeneration induced by inflammatory reactions and can be used to identify potential target genes for therapeutic applications in IVD degeneration.