Inhibition of Mettl3 ameliorates osteoblastic senescence by mitigating m6A modifications on Slc1a5 via Igf2bp2-dependent mechanisms.

Age-related osteoporosis is characterized by a marked decrease in the number of osteoblasts, which has been partly attributed to the senescence of cells of the osteoblastic lineage. Epigenetic studies have provided new insights into the mechanisms of current osteoporosis treatments and bone repair pathophysiology. N6-methyladenosine (m6A) is a novel transcript modification that plays a major role in cellular senescence and is essential for skeletal development and internal environmental stability. Bioinformatics analysis revealed that the expression of the m6A reading protein Igf2bp2 was significantly higher in osteoporosis patients. However, the role of Igf2bp2 in osteoblast senescence has not been elucidated. In this study, we found that Igf2bp2 levels are increased in ageing osteoblasts induced by multiple repetition and H2O2. Increasing Igf2bp2 expression promotes osteoblast senescence by increasing the stability of Slc1a5 mRNA and inhibiting cell cycle progression. Additionally, Mettl3 was identified as Slc1a5 m6A-methylated protein with increased m6A modification. The knockdown of Mettl3 in osteoblasts inhibits the reduction of senescence, whereas the overexpression of Mettl3 promotes the senescence of osteoblasts. We found that administering Cpd-564, a specific inhibitor of Mettl3, induced increased bone mass and decreased bone marrow fat accumulation in aged rats. Notably, in an OVX rat model, Igf2bp2 small interfering RNA delivery also induced an increase in bone mass and decreased fat accumulation in the bone marrow. In conclusion, our study demonstrated that the Mettl3/Igf2bp2-Slc1a5 axis plays a key role in the promotion of osteoblast senescence and age-related bone loss.

The efficacy of nutritional screening indexes in predicting the incidence of osteosarcopenia and major osteoporotic fracture in the elderly.

INTRODUCTION: The effect of nutritional status on osteosarcopenia (OS) and major osteoporotic fracture (MOF) among the elderly is still unclear. So we aimed to compare the efficacy of the Mini-Nutrition Assessment-Short Form (MNA-sf), the Geriatric Nutritional Risk Index (GNRI) and Controlling Nutritional Status (CONUT) for predicting OS and MOF among the elderly. MATERIALS AND METHODS: A total of 409 participants were enrolled in this prospective study. Blood biochemical indexes, nutritional status, and bone- and muscle-related examinations were assessed at initial visit to the outpatient. Participants were divided into 4 groups: (1) control; (2) osteopenia/osteoporosis; (3) sarcopenia; (4) osteosarcopenia, and then followed for 5 years, recording the occurrence time of MOF. RESULTS: The frequency values of osteopenia/osteoporosis, sarcopenia, and OS, at baseline, were respectively 13.4, 16.1, and 12% among the study samples. Correlation analysis showed that nutritional status scores were associated with body mass index, handgrip strength, albumin, bone mineral density, and physical functions. According to multivariate models, poor nutritional status was significantly associated with a higher risk of OS and MOF (P < 0.05). Survival analysis showed that the MOF rate in malnutrition group was significantly higher than normal nutrition group (P < 0.05). The receiver operator characteristic curve shows that the value of MNA-sf to diagnose OS and MOF is greater (P < 0.05). CONCLUSION: The poor nutritional status was associated with a higher risk of both OS and MOF. MNA-sf showed a superior diagnostic power for OS and MOF among the elderly. Early nutrition assessments and interventions may be key strategies to prevent OS and fractures.

Vitamin D delays intervertebral disc degeneration and improves bone quality in ovariectomized rats.

Known to be involved in bone-cartilage metabolism, Vitamin D (VD) may play a role in human's disc pathophysiology. Given that postmenopausal women are prone to suffer VD deficiency and intervertebral disc degeneration (IDD), this study is intended to investigate whether VD can delay IDD in ovariectomized rats by improving bone microstructure and antioxidant stress. Female Sprague-Dawley rats were randomly allocated into four groups: sham, oophorectomy (OVX)+VD deficiency (VDD), OVX, and OVX+VD supplementation (VDS). In vivo, after a 6-month intervention, imaging and pathology slice examinations showed that IDD induced by OVX was significantly alleviated in VDS and deteriorated by VDD. The expressions of aggrecan and Collagen II in intervertebral disc were reduced by OVX and VDD, and elevated by VDS. Compared with the OVX+VDD and OVX group vertebrae, OVX+VDS group vertebrae showed significantly improved endplate porosity and lumbar bone mineral density with increased percent bone volume and trabecular thickness. Furthermore, 1α,25(OH)2D3 restored the redox balance (total antioxidant capacity, ratio of oxidized glutathione/glutathione) in the disc. The cocultivation of 1α,25(OH)2D3 and nucleus pulposus cells (NPCs) was conducted to observe its potential ability to resist excessive oxidative stress damage induced by H2O2. In vitro experiments revealed that 1α,25(OH)2D3 reduced the senescence, apoptosis, and extracellular matrix degradation induced by H2O2 in NPCs. In conclusion, VDS exhibits protective effects in OVX-induced IDD, partly by regulating the redox balance and preserving the microstructure of endplate. This finding provides a new idea for the prevention and treatment of IDD.

The influence of iris -ciliary angle (ICA) on the vault after implantation of V4c implantable collamer lens: a chain mediation model of ICL haptic related factors.

BACKGROUND: This study aims to identify the relationship between iris -ciliary angle (ICA) and the vault. Additionally, we also seek to investigate the chain mediating effects of the ICL haptic related factors on this relationship. METHODS: The participants were categorized into three groups according to the ICA value as follows: low ICA group (< 35°); moderate ICA group (35°-70°); high ICA group (> 70°). We compared the preoperative ocular characteristics and postoperative examinations among the three groups. Multiple variable stepwise regression was performed to establish the vault prediction formula. The Process V4.0 in SPSS and Hayes's PROCESS model 6 was conducted to further elucidate the mediating effects of the final tip point of ICL haptic and the ICL arc-lens arc on the relationship between the ICA and vault. RESULTS: There was a significant difference in the positions of the ICL haptic among three ICA groups. The regression vault equation was Vault = 679.42-7.26*TCA + 192.30*ACD-196.37*CLR + 73.21* STS(horizontal).A significant negative correlation was found between the ICA and vault (P < 0.01).The chain mediation model revealed that the final tip point of ICL haptic and the ICL arc-Lens arc were sequential mediators between ICA and vault (effect = -1.63, 95% CI = -2.72--0.73). CONCLUSION: The ICA was associated with vault via the mediation effect of the final tip point of the ICL haptic and the ICL arc -lens arc. Assessment of ICL haptic related parameters adds significant information to interpret the vault after surgery.

Role of ferroptosis and immune infiltration in intervertebral disc degeneration: novel insights from bioinformatics analyses.

Background: Intervertebral disc degeneration (IVDD), which contributes to stenosis of the spinal segment, commonly causes lower back pain. The process of IVDD degradation entails gradual structural adjustments accompanied by extreme transformations in metabolic homeostasis. However, the molecular and cellular mechanisms associated with IVDD are poorly understood. Methods: The RNA-sequencing datasets GSE34095 and GSE56081 were obtained from the Gene Expression Omnibus (GEO) database. Ferroptosis-related differentially expressed genes (DEGs) were identified from these gene sets. The protein-protein interaction (PPI) network was established and visualized using the STRING database and Cytoscape software, and the key functional modules of ferroptosis-related genes were identified. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed on the DEGs. Weighted gene co-expression network analysis (WGCNA), immune infiltration analysis in the GEO database, and other GSE series were used as validation datasets. The xCELL algorithm was performed to investigate the immune cell infiltration differences between the degenerated IVDD and control groups. Results: The major genes involved in nucleus pulposus tissue immune infiltration and ferroptosis-related genes were mined by bioinformatics analysis. A total of 3,056 DEGs were obtained between the IVDD tissue and control groups. The DEGs were enriched in the cell cycle; apoptosis; necroptosis; and the PI3K-Akt, Hippo, and HIF-1 signaling pathways. PCR and Western blot techniques were utilized to confirm the differential ferroptosis-related genes. The results indicated that the protein expression levels of NCOA4 and PCBP1 were elevated, while the protein expression level of GPX4 was reduced in NPCs following IL-1ß treatment. Our study has found that severe disc tissue degeneration leads to a noteworthy increase in the expression of CD8A in naive T cells, CCR7 in memory CD4+ cells, GZMB in natural killer (NK) cells, and CD163 and CD45 in macrophages. Conclusion: Our data demonstrate that ferroptosis occurs in IVDD, suggesting that ferroptosis may also increase IVDD improvement by triggering immune infiltration. This work was conducted to further understand IVDD pathogenesis and identify new treatment strategies.

α-Ketoglutaric acid ameliorates intervertebral disk degeneration by blocking the IL-6/JAK2/STAT3 pathway.

Intervertebral disk degeneration (IVDD) is the major cause of low back pain. Alpha-ketoglutaric acid (α-KG), an important intermediate in energy metabolism, has various functions, including epigenetic regulation, maintenance of redox homeostasis, and antiaging, but whether it can ameliorate IVDD has not been reported. Here, we examined the impacts of long-term administration of α-KG on aging-associated IVDD in adult rats. In vivo and in vitro experiments showed that α-KG supplementation effectively ameliorated IVDD in rats and the senescence of nucleus pulposus cells (NPCs). α-KG supplementation significantly attenuated senescence, apoptosis, and matrix metalloproteinase-13 (MMP-13) protein expression, and it increased the synthesis of aggrecan and collagen II in IL-1ß-treated NPCs. In addition, α-KG supplementation reduced the levels of IL-6, phosphorylated JAK2 and STAT3, and the nuclear translocation of p-STAT3 in IL-1ß-induced degenerating NPCs. The effects of α-KG were enhanced by AG490 in NPCs. The underlying mechanism may involve the inhibition of JAK2/STAT3 phosphorylation and the reduction of IL-6 expression. Our findings may help in the development of new therapeutic strategies for IVDD.NEW & NOTEWORTHY Alpha-ketoglutaric acid (α-KG) exerted its protective effect on nucleus pulposus cells' (NPCs) degeneration by inhibiting the senescence-associated secretory phenotype and extracellular matrix degradation. The possible mechanism may be associated with negatively regulating the JAK2/STAT3 phosphorylation and the decreased IL-6 expression, which could be explained by a blockage of the positive feedback control loop between IL-6 and JAK2/STAT3 pathway.

The complete chloroplast genome of Primula amethystina subsp. argutidens (Primulaceae).

Primula amethystina subsp. argutidens (Franchet) W. W. Smith & H. R. Fletcher (1942) is a blooming plant of the family Primulaceae. Here, we sequenced, assembled, and annotated the complete chloroplast (cp) genome of P. amethystina subsp. argutidens. The cp genome of P. amethystina subsp. argutidens is 151,560 bp in length with a GC content of 37%. The assembled genome has a typical quadripartite structure, containing a large single-copy (LSC) region of 83,516 bp, a small single-copy (SSC) region of 17,692 bp, and a pair of inverted repeat (IR) regions of 25,176 bp. The cp genome contains 115 unique genes, including 81 protein-coding genes, four rRNA genes, and 30 tRNA genes. Phylogenetic analysis showed that P. amethystina subsp. argutidens was closely related to P. amethystina.

Predictors and nomogram of in-hospital mortality in sepsis-induced myocardial injury: a retrospective cohort study.

BACKGROUND: Sepsis-induced myocardial injury (SIMI) is a common organ dysfunction and is associated with higher mortality in patients with sepsis. We aim to construct a nomogram prediction model to assess the 28-day mortality in patients with SIMI. . METHOD: We retrospectively extracted data from Medical Information Mart for Intensive Care (MIMIC-IV) open-source clinical database. SIMI was defined by Troponin T (higher than the 99th percentile of upper reference limit value) and patients with cardiovascular disease were excluded. A prediction model was constructed in the training cohort by backward stepwise Cox proportional hazards regression model. The concordance index (C-index), area under the receiver operating characteristics curve (AUC), net reclassification improvement (NRI), integrated discrimination improvement (IDI), calibration plotting and decision-curve analysis (DCA) were used to evaluate the nomogram. RESULTS: 1312 patients with sepsis were included in this study and 1037 (79%) of them presented with SIMI. The multivariate Cox regression analysis in all septic patients revealed that SIMI was independently associated with 28-day mortality of septic patients. The risk factors of diabetes, Apache II score, mechanical ventilation, vasoactive support, Troponin T and creatinine were included in the model and a nomogram was constructed based on the model. The C-index, AUC, NRI, IDI, calibration plotting and DCA showed that the performance of the nomogram was better than the single SOFA score and Troponin T. CONCLUSION: SIMI is related to the 28-day mortality of septic patients. The nomogram is a well-performed tool to predict accurately the 28-day mortality in patients with SIMI.

Loss of Histone Methyltransferase KMT2D Attenuates Angiogenesis in the Ischemic Heart by Inhibiting the Transcriptional Activation of VEGF-A.

Angiogenesis occurred after myocardial infarction (MI) protects heart failure (HF). The aim of our study was to explore function of histone methyltransferase KMT2D (MLL4, mixed-lineage leukemia 4) in angiogenesis post-MI. Western blotting showed that KMT2D protein expression was elevated in MI mouse myocardial. Cardiomyocyte-specific Kmt2d-knockout (Kmt2d-cKO) mice were generated, and echocardiography and immunofluorescence staining detected significantly attenuated cardiac function and insufficient angiogenesis following MI in Kmt2d-cKO mice. Cross-talk assay suggested that Kmt2d-KO H9c2-derived conditioned medium attenuates EA.hy926 EC function. ELISA further identified that VEGF-A released from Kmt2d-KO H9c2 was significantly reduced. CUT&Tag and RT-qPCR revealed that KMT2D deficiency reduced Vegf-a mRNA expression and enrichment of H3K4me1 on the Vegf-a promoter. Moreover, KMT2D silencing in ECs also suppressed endothelial function. Our study indicates that KMT2D depletion in both cardiomyocytes and ECs attenuates angiogenesis and that loss of KMT2D exacerbates heart failure after MI in mice.

Association Between Poor Nutritional Status and Increased Risk for Subsequent Vertebral Fracture in Elderly People with Percutaneous Vertebroplasty.

Background: The relationship between a poor nutritional state and the risk of fractures has not been investigated. This study aimed to investigate the ability of the Controlling Nutritional Status (CONUT) and Geriatric Nutritional Risk Index (GNRI) to predict the incidence of subsequent vertebral fracture (SVF) after percutaneous vertebroplasty (PVP). Methods: A total of 307 women and 138 men over 50 years old who underwent PVP for osteoporotic vertebral compression fracture (OVCF) were included. Blood biochemical indexes, body mass index (BMI), bone mineral density (BMD), physical function, and muscle strength were measured at baseline. Cox regression analysis was used to determine whether nutritional state was an independent predictor for SVF. Results: During follow-up, 35 (25.4%) men and 85 (27.7%) women suffered SVF. Patients with SVF had lower BMI, serum albumin levels, GNRI scores, grip strength, lumbar BMD, and Short-Physical Performance Battery (SPPB) scores and higher fall rates and CONUT scores (P < 0.05). Compared with normal nutrition, mild malnutrition was associated with higher risk for SVF (women: HR 2.37, p=0.001, men: HR 2.97, p=0.021 by GNRI; women: HR 2.36, p=0.005, men: HR 3.62, p=0.002 by CONUT) after adjusting for confounding factors. Those with moderate-severe malnutrition also had a higher risk of SVF. Kaplan-Meier analysis showed that poor nutrition state was significantly associated with lower SVF-free survival (P<0.05). The area under curve (AUC) for predicting SVF was 0.65 and 0.73 for the GNRI and 0.67 and 0.66 for the CONUT in men and women, respectively. Conclusion: GNRI and CONUT are simple and effective tools for predicting SVF in patients undergoing PVP. Health management and nutrition supplement after PVP is a potentially effective prevention strategy against SVF.

Histone methyltransferase KMT2D contributes to the protection of myocardial ischemic injury.

Histone H3 lysine 4 (H3K4) methyltransferase 2D (KMT2D) plays an important role in cell development in early life. However, the function of KMT2D in adult cells such as cardiomyocytes or neurons has not been reported. In this study, cardiomyocyte-specific KMT2D knockout (KMT2D-cKO) and control (KMT2D-Ctl) mice were exposed to sham or myocardial ischemia (MI) surgery. Depletion of KMT2D aggravated the ischemic area, led to the increased mortality (26.5% in KMT2D-cKO vs 12.5% in KMT2D-Ctl) of the mice, and weakened the left ventricular systolic function. RNA-seq analysis in cardiac tissues identified genes whose expression was changed by MI and KMT2D deletion. Combined with the genome-wide association study (GWAS) analysis, cardiac disease-associated genes Rasd1, Thsd7a, Ednra, and Tns1 were identified. The expression of the Rasd1 was significantly decreased by MI or the loss of KMT2D in vivo. Meanwhile, ChIP assays demonstrated that either MI or loss of KMT2D attenuated monomethylated H3K4 (H3K4me1) enrichment on the enhancer of Rasd1. By generating a KMT2D knockout (H9C2-KO) H9C2 monoclone, we verified that the expression of Rasd1 was controlled by KMT2D, and the expression of Rasd1 was decreased by serum starvation but not low-(O2) treatment in H9C2 cells. KMT2D has a protective effect on ischemic myocardium by regulating cardiac disease-associated genes including Rasd1. KMT2D is required for the H3K4me1 deposition on the enhancer of Rasd1. Our data for the first time suggest that KMT2D-mediated Rasd1 expression may play an important protective effect on adult cells during nutritional deficiency caused by ischemic injury.

Computed tomography-based paravertebral muscle density predicts subsequent vertebral fracture risks independently of bone mineral density in postmenopausal women following percutaneous vertebral augmentation.

BACKGROUND: The risk of subsequent vertebral fractures (SVF) after the primary vertebral fracture cannot be explained by lower bone mineral density (BMD) alone. Computed tomography (CT) measurements of paravertebral muscle density (PMD) are recognized radiographic markers used to predict physical function, fragile fractures. AIMS: This study aims to investigate the relationship between PMD and the risk of SVF in cohorts of postmenopausal women, and to determine if combining both PMD and BMD measures derived from CT can improve the accuracy of predicting SVF. METHODS: This study enrolled 305 postmenopausal women between the ages of 50 and 88 for 3 years of follow-up studies. Trabecular attenuation (Hounsfield units, HU) was measured at L1 level and muscle attenuation of paravertebral muscle at L3 level on preoperative lumbar CT scans to determine the L1 BMD and L3 PMD. Kaplan-Meier analysis was applied to evaluate SVF-free survival. The hazard ratios (HRs) of PMD for SVF events were estimated with the Cox proportional hazards model. The predictive values of L1 BMD and L3 PMD for SVF were quantified using the Receiver-Operating Characteristic (ROC) curve. RESULT: During the 3 years of follow-up studies, 88 patients (28.9%) suffered an SVF. ROC curve analysis demonstrated that an L3 PMD threshold of 32 HU had a sensitivity of 89.8% and a specificity of 62% for the prediction of SVF. Kaplan-Meier analysis showed that L3 PMD ≤ 32 HU was significantly associated with lower SVF-free survival (p < 0.001; log-rank test). After adjusting for age, BMI, diabetes, postoperative osteoporosis treatment, handgrip strength, L1 BMD, multivariate analyses also indicated a persistent modest effect of L3 PMD on SVF-free survival. The area under the ROC curve of L3 PMD and L1 BMD, combined to predict the risk of SVF, was 0.790, which was significantly higher than the value for L1 BMD alone (0.735). L3 PMD and L1 BMD significantly improved the accuracy of SVF risk prediction compared with L1 BMD alone, which was confirmed by reclassification improvement measures. The inclusion of handgrip strength and postoperative osteoporosis treatment in the model further improved SVF prediction accuracy, and PMD remained significant in the model. CONCLUSION: Decreased L3 PMD is an independent risk predictor of SVF. Combined CT-based L1 BMD and L3 PMD can significantly improve the accuracy of predicting the risk of SVF in postmenopausal women who have suffered prior osteoporotic vertebral fractures.

Exogenous Klotho ameliorates extracellular matrix degradation and angiogenesis in intervertebral disc degeneration via inhibition of the Rac1/PAK1/MMP-2 signaling axis.

Intervertebral disc degeneration (IDD) is highly ubiquitous in the aged population and is an essential factor for low back pain and spinal disability. Because of the association between IDD and senescence, we investigated the ability of the anti-aging drug Klotho to inhibit age-dependent advancement of nucleus pulposus cell (NPC) degeneration. The results indicated that 400 pM exogenous Klotho significantly ameliorated extracellular matrix degradation and angiogenesis. Moreover, we demonstrated that the suppression of angiogenesis and extracellular matrix catabolism was related to inhibition of the Ras-related C3 botulinum toxin substrate 1 (Rac1)/PAK1 axis and matrix metalloproteinase 2 protein expression by exogenous Klotho cotreatment with a Rac1 inhibitor, gene overexpression in NPCs, and stimulation of human umbilical vein endothelial cells with conditioned medium from NPCs. The treatment also preserved the NPC phenotype, viability, and matrix content. In conclusion, these results suggest that the new anti-aging drug Klotho is a potential treatment strategy to mitigate IDD, and thus, provides an innovative understanding of the molecular mechanism of IDD. DATA AVAILABILITY: All data supporting the findings of this study are available from the corresponding authors upon reasonable request.

Presence of ginsenoside re during in vitro maturation protects porcine oocytes from heat stress.

Heat stress (HS) affects the development of porcine gametes and embryos negatively, induces the decrease of reproductive ability significantly, threatens global pig production. Ginsenoside Re (GRe), is a main bioactive component of ginseng, shows very specific anti-apoptotic, antioxidant and anti-inflammatory activities. To investigate the alleviating effect of GRe on the in vitro maturation of porcine oocyte under the HS, the polar body extrusion rate, intracellular levels of reactive oxygen species (ROS) and glutathione (GSH), ATP content, mitochondrial membrane potential (MMP) were assessed. For the current study, porcine cumulus-oocyte complexes (COCs) randomly divided into four groups: the control, GRe, HS and HS + GRe group. The results showed that HS inhibited the cumulus cell expansion and polar body extrusion rate, the levels of GSH and MMP, the ATP content, the gene expression of Nrf2 of porcine oocytes and the parthenogenetic activation (PA) embryo development competence, but GRe treatment could partly neutralize these adverse effects. Furthermore, HS increased the ROS formation and percentage of apoptosis, the gene expression of HSP90, CASP3 and CytoC of porcine oocytes, but GRe could weaken the effect on Cyto C and BAX expression induced by HS. Taken together, these results showed that the presence of GRe during in vitro maturation protects porcine oocytes from HS. These findings lay a foundation for GRe may be used as a potential protective drug to protect porcine oocytes against HS damage.

Ascorbic acid promotes nucleus pulposus cell regeneration by regulating proliferation during intervertebral disc degeneration.

Intervertebral disc degeneration (IVDD) affects human health. Ascorbic acid (AA) deficiency is a major factor that contributes to the development of degenerative disc disease in the elderly. Here, as a novel treatment with promising applications, we demonstrate that AA treatment inhibited senescence and maintained the proliferation of nucleus pulposus (NP) cells during long-term culture. AA-treated NP cells and acupuncture-treated rat models exhibited degenerative resistance during cell passaging and AA increased cell proliferation and decreased time-related senescence. Interestingly, Kyoto Encyclopedia of Genes and Genomes pathway mapping revealed five top enriched pathways and four pathways were associated with the aldehyde dehydrogenase (ALDH) enzyme family, especially proliferation-related ALDH1A3. Collectively, our findings demonstrate that ALDH1A3 expression was increased by AA treatment, which counteracted degeneration in NP cells over time and rejuvenated maintenance of proliferation in NP cells, which has a promising therapeutic implications in IVDD.

Association Between Abdominal Obesity and Subsequent Vertebral Fracture Risk.

BACKGROUND: Obesity had been previously considered to be a protective factor against osteoporosis or fractures; however, recent research indicates that obesity, especially abdominal obesity, may increase the risk of some types of fractures. OBJECTIVE: We explored the effects of abdominal obesity on subsequent vertebral fracture (SVF) after percutaneous vertebral augmentation (PVA). STUDY DESIGN: A prospective observational cohort study. SETTING: Department of Spinal Surgery of a hospital affiliated with a medical university. METHODS: A total of 390 women and 237 men aged > 50 years suffering from osteoporotic vertebral fracture (OVF) were included. Weight, height, bone mineral density (BMD), abdominal circumference, and other basic information were measured at baseline and 1-year follow-up visit. RESULTS: During follow-up, 80 (33.7%) men and 143 (36.7%) women incurred SVF. Greater waist circumference (WC) and waist-to-hip ratio (WHR) increased the risk of SVF in men (WC: HR 1.83, P = 0.016; WHR: HR 1.63, P = 0.045) and women (WC: HR 2.75, P = 0.001; WHR: HR 2.63, P = 0.001) after adjustment for BMD and other potential confounders. Compared with normal BMI, being overweight was associated with lower SVF risk (women: HR 0.55, P = 0.044; men: HR 0.46, P = 0.046), and obesity was associated with greater SVF risk (women: HR 4.53, P < 0.001; men: HR 3.77, P < 0.001) in both genders. We observed a nonlinear relationship between BMI and SVF with a U-shaped curve; after adjusting BMD, this became a reverse J-curve. LIMITATIONS: There was no further statistical analysis of the relationship between abdominal obesity and other fracture sites. Asymptomatic SVF may underestimate the impact of abdominal obesity on the occurrence of SVF. CONCLUSIONS: Abdominal obesity was significantly associated with a higher risk of SVF after PVA. Management of body type after PVA may be an effective prevention strategy against SVF.

Changes in intervertebral distraction: A possible factor for predicting dysphagia after anterior cervical spinal surgery.

OBJECTIVE: Dysphagia following anterior cervical spine surgery (ACSS) is common. This study aimed to determine if change in intervertebral distraction following ACSS is associated with early dysphagia. METHODS: We retrospectively examined patients who underwent ACSS for myelopathy and/or radiculopathy in our institution. The Bazaz score and the Chinese version of the Swallowing-Quality of Life survey were used to assess postoperative swallowing function. Change in intervertebral distraction was defined as the difference between the preoperative and postoperative mean values of the anterior and posterior intervertebral distances at the surgical site. Potential risk factors examined included age, gender, body mass index, operative time, blood loss volume, level of surgery, as well as radiographic data including Cobb angle, T1 slope, sagittal vertical axis, and intervertebral distraction. RESULTS: Among the 289 patients, the incidence of dysphagia was 58.1% 1 week after ACSS. Patients who underwent surgery involving C3/4 or involving three or more levels had worse Swallowing-Quality of Life and Bazaz scores. The optimal cutoff value for change in intervertebral distraction for predicting dysphagia 1 week after surgery was 6.10 mm. Change in intervertebral distraction ≥ 6.10 mm, surgery involving C3/4, and surgery involving three or more levels were significantly and independently associated with early dysphagia. CONCLUSION: A correlation between early dysphagia and change in intervertebral distraction ≥ 6.10 mm could be confirmed. In addition, patients undergoing ACSS involving C3-4 or multilevel surgery (≥3) must be monitored carefully postoperatively for dysfunctional swallowing.

Sarcopenic obesity defined by visceral adiposity was associated with osteoporotic vertebral fracture.

BACKGROUND: Previous studies have reported that the fracture risk related to sarcopenic obesity (SO) may be influenced by the distribution of fat mass. Therefore, it is useful to explore a body component suitable for defining obesity when predicting fracture risk. This study was an attempt to explore the contribution of SO defined by visceral adiposity on the incidence of osteoporotic fracture. METHODS: We enrolled 736 Chinese patients aged > 60 years in this prospective study. Sarcopenia was defined as low skeletal muscle index (SMI) with muscle strength or low SMI with low physical performance. Obesity was categorized as follows: (1) android to gynoid ratio (A/G ratio, men > 0.82, women > 0.65) as an indicator of visceral adiposity; (2) body fat percentage (men > 27.8%; women > 34.5%); and (3) body mass index (≥ 25 kg/m2). A Cox proportional hazard model was used to determine the association between SO and the risk of osteoporotic fracture. RESULTS: The incidence of SO was 8.7%; 9.0% in females and 8.1% in males. Of 223 (30.2%) patients with self-reported fractures. SO classified by A/G was associated with an increased risk of osteoporotic vertebral fracture (HR: 1.71, 95% CI: 1.07-2.72). High SMI was associated with a reduced risk of osteoporotic vertebral fracture (HR: 0.82, 95% CI: 0.72-0.93), higher BMI was associated with a higher risk vertebral fracture (HR: 1.12, 95% CI: 0.94-1.63), and higher A/G ratio was associated with a higher risk of any fracture (HR: 1.28, 95% CI: 1.14-1.43) and osteoporotic vertebral fracture (HR: 1.19, 95% CI: 1.05-1.36). CONCLUSIONS: Our findings suggest that SO, defined by visceral adiposity, was associated with the risk of osteoporotic vertebral fracture. Moreover, low SMI, low muscle strength and visceral adiposity were independently associated with osteoporotic fracture.

Establishing an appropriate Z score regression equation for Chinese pediatric coronary artery echocardiography: a multicenter prospective cohort study.

BACKGROUND: Z score utility is emphasized in classifying coronary artery lesions in Kawasaki disease patients. The present study is the largest such multicenter Chinese pediatric study about coronary artery diameter reference values and Z score regression equation to date. It is useful in Chinese pediatric echocardiography. METHODS: A multicenter cohort was assembled, which consisted of 852 healthy children between 1 month and 17 years of age, ten children were excluded because their ultrasound images were not clear, or lost in following up. Diameters of the right coronary artery, left coronary artery, and left anterior descending coronary artery were assessed using echocardiography. Data were body surface area (BSA)-corrected using BSA calculated via either the Stevenson BSA formula or the Haycock BSA formula. Coronary artery diameter reference values and Z score regression equations were established for use in the Chinese pediatric population. RESULTS: No difference was observed between coronary artery diameter data corrected using BSAste or BSAhay. Of the five assessed regression models, the exponential model exhibited the best fit and was therefore selected as the basis for derivation of the SZ method. When comparing Z scores, those produced by the SZ method conformed to the standard normal distribution, while those produced by the D method did not. In addition, there was a statistically significant difference between Z scores produced by the SZ and D methods (P < 0.05). CONCLUSIONS: Coronary artery diameter reference values for echocardiography were successfully established for use in the Chinese pediatric population, and a Z score regression equation more suitable for clinical use in this population was successfully developed.