Biomechanical analysis of adjacent segments after correction surgery for adult idiopathic scoliosis: a finite element analysis.

The biomechanical aspects of adjacent segment degeneration after Adult Idiopathic Scoliosis (AdIS) corrective surgery involving postoperative changes in motion and stress of adjacent segments have yet to be investigated. The objective of this study was to evaluate the biomechanical effects of corrective surgery on adjacent segments in adult idiopathic scoliosis by finite element analysis. Based on computed tomography data of the consecutive spine from T1-S1 of a 28-year-old male patient with adult idiopathic scoliosis, a three-dimensional finite element model was established to simulate the biomechanics. Two posterior long-segment fixation and fusion operations were designed: Strategy A, pedicle screws implanted in all segments of both sides, and Strategy B, alternate screws instrumentation on both sides. The range of motion (ROM), Maximum von Mises stress value of intervertebral disc (IVD), and Maximum von Mises stress of the facet joint (FJ) at the fixation adjacent segment were calculated and compared with data of the preoperative AdIS model. Corrective surgery decreased the IVD on the adjacent segments, increased the FJ on the adjacent segments, and decreased the ROM of the adjacent segments. A greater decrease of Maximum von Mises stress was observed on the distal adjacent segment compared with the proximal adjacent segment. The decrease of Maximum von Mises stress and increment of Maximum von Mises stress on adjacent FJ in strategy B was greater than that in strategy A. Under the six operation modes, the change of the Maximum von Mises stress on the adjacent IVD and FJ was significant. The decrease in ROM in the proximal adjacent segment was greater than that of the distal adjacent segment, and the decrease of ROM in strategy A was greater than that in strategy B. This study clarified the biomechanical characteristics of adjacent segments after AdIS corrective surgery, and further biomechanical analysis of two different posterior pedicle screw placement schemes by finite element method. Our study provides a theoretical basis for the pathogenesis, prevention, and treatment of adjacent segment degeneration after corrective surgery for AdIS.

Sesamin-mediated high expression of BECN2 ameliorates cartilage endplate degeneration by reducing autophagy and inflammation.

Lumbar disc degeneration (LDD) is a prevalent clinical spinal disease characterized by the calcification and degeneration of the cartilage endplate (CEP), which significantly reduces nutrient supply to the intervertebral disc. Traditional Chinese medicine offers a conservative and effective approach for treating LDD. We aimed to investigate the molecular mechanisms underlying the therapeutic effects of Sesamin in LDD treatment. Transcriptome sequencing was used to analyze the effect of Sesamin on LPS-induced ATDC5. We explored the role of BECN2, a target gene of Sesamin, in attenuating LPS-induced degeneration of ATDC5 cells. Our results revealed the identification of 117 differentially expressed genes (DEGs), with 54 up-regulated and 63 down-regulated genes. Notably, Sesamin significantly increased the expression of BECN2 in LPS-induced ATDC5 cell degeneration. Overexpressed BECN2 enhanced cell viability and inhibited cell apoptosis in LPS-induced ATDC5 cells, while BECN2 knockdown reduced cell viability and increased apoptosis. Furthermore, BECN2 played a crucial role in attenuating chondrocyte degeneration by modulating autophagy and inflammation. Specifically, BECN2 suppressed autophagy by reducing the expression of ATG14, VPS34, and GASP1, and alleviated the inflammatory response by decreasing the expression of inflammasome proteins NLRP3, NLRC4, NLRP1, and AIM2. In vivo experiments further supported the beneficial effects of Sesamin in mitigating LDD. This study provides novel insights into the potential molecular mechanism of Sesamin in treating LDD, highlighting its ability to mediate autophagy and inflammation inhibition via targeting the BECN2. This study provides a new therapeutic strategy for the treatment of LDD, as well as a potential molecular target for LDD.

Overexpression of S100A1 in Osteosarcoma Inhibits Tumor Proliferation and Progression.

Background: Osteosarcoma is the most common primary malignant tumor of bone. Abnormal expression of S100A1 protein is closely related to the occurrence and development of malignant tumors. However, S100A1 in osteosarcoma has not been studied. Methods: All osteosarcoma tissues were collected from patients who received surgical therapy at the Affiliated Hospital of Inner Mongolia Medical University, China in 2020. QRT-PCR and western blot assays were used to detect the expression of S100A1 in osteosarcoma tissues and cells. The negative effect of S100A1 on osteosarcoma cell growth was confirmed by vitro and vivo experiments. Results: S100A1 inhibited the growth of osteosarcoma cells in vitro. Overexpression of S100A1 may inhibit the proliferation of osteosarcoma cells by preventing the activation of AKT signaling pathway by western blot assay. Finally, animal experiments confirmed that overexpression of S100A1 could inhibit the proliferation of osteosarcoma cells. Overexpression of S100A1 obtained better survival benefit in mice. Conclusion: Our findings provided a new insight to the treatment of osteosarcoma. It also raised the possibility that S100A1 could be used in targeted therapies for osteosarcoma.

miR-142-3p and HMGB1 Are Negatively Regulated in Proliferation, Apoptosis, Migration, and Autophagy of Cartilage Endplate Cells.

BACKGROUND: Cartilage endplate (CEP) degeneration plays a vital role in the pathological process of intervertebral disc degeneration. It has been previously reported that microRNAs may participate in the occurrence and development of intervertebral disc degeneration through regulating its target genes directly. The regulatory roles of miR-142-3p/HMGB1 in some orthopedic diseases have been determined successively, but there was no report about the degeneration of CEP. Therefore, we aimed to determine the regulation of miR-142-3p/HMGB1 or potential molecular mechanisms on proliferation, apoptosis, migration, and autophagy of CEP cells. METHODS: The target gene of miR-142-3p was determined by double luciferase assay. We selected ATDC5 cell lines. CCK-8 method was used to detect cell proliferation. Real-time fluorescence quantitative polymerase chain reaction was used to determine gene expression levels, and western blot analysis was used to determine protein expression levels. We chose flow cytometry to measure cell apoptosis and cell cycle. RESULTS: The result of luciferase detection showed that the target gene of miR-142-3p in CEP cells was HMGB1. Knockdown of the miR-142-3p inhibited the expression level of HMGB1, the proliferation and migration of CEP cells, but it promoted apoptosis of CEP cells. In addition, the detection results of the proteins related to apoptosis or autophagy showed that knockdown of miR-142-3p promoted apoptosis and autophagy. CONCLUSION: The negative regulation of miR-142-3p/HMGB1 can affect the proliferation, apoptosis, migration, and autophagy of CEP cells. Our results provide a new idea for the targeted treatment of CEP degeneration by inhibiting the expression of HMGB1.

Low expression of miR-142-3p promotes intervertebral disk degeneration.

BACKGROUND: Intervertebral disk degeneration (IDD) is a degenerative disease characterized by cytoplasm loss and extracellular matrix degradation. Numerous evidence reported that miRNAs participated in IDD development. Nevertheless, the function of miR-142-3p in IDD development remains unknown. This study mainly explored the potential role and function of miR-142-3p in IDD development. METHODS: One percent fetal bovine serum was used to induce the degeneration of ATDC5 cells, and miR-142-3p level was examined by qRT-PCR. Then, miR-142-3p mimic/inhibitor and its corresponding negative control were transfected into ATDC5 normal and degenerative cells. Viability, migration, invasion, apoptosis, cycle, Bax, Bcl-2, P62, and Beclin1 expression levels were assessed using CCK8, wound healing assay, annexin V-FITC/PI staining, western blot, and qRT-PCR, respectively. RESULTS: The results revealed that the expression levels of MMP13, ADAMTS5, MMP3, and Col-X were increased as well as the expression levels of SOX-9 and Col-II were reduced in ATDC5 degenerative cells, indicating the degeneration model was constructed. We observed that miR-142-3p was decreased in ATDC5 degenerative cells and its suppression could promote ATDC5 cell degeneration. However, miR-142-3p overexpression could reverse the cell viability inhibition, as well as apoptosis and autophagy enhancement in ATDC5 degenerative cells. CONCLUSIONS: Our results proved that miR-142-3p may play an important role in disk degeneration. Further animal study is needed to illustrate the role of the miR-142-3p in IDD development.

Multiple variants in collagen genes are associated with the susceptibility to lumbar disc herniation in the Chinese population.

PURPOSE: Lumbar disc herniation (LDH) is an important cause of back pain and sciatica, but its aetiology is not fully understood. Single-nucleotide polymorphisms (SNPs) in specific collagen genes are known to increase the risk of lumbar disc degeneration. We performed a case-control study among the Chinese Han population to investigate whether genetic variations in collagen genes were associated with the risk of LDH or not. METHODS: We genotyped SNPs selected from 1000 Genome Projects using Agena MassARRAY technology. Three hundred and eighty-four LDH cases were compared with 384 controls of similar age, using the odds ratio and 95% confidence interval to calculate the susceptibility in several genetic models. RESULTS: Our results revealed that subjects with the rs6122316-C variant of the COL9A3 gene had a higher likelihood of LDH than subjects with the allele T variant in both the codominant and recessive models. In addition, after gender stratification analysis, we found significant associations between rs16970089 and rs740024 and LDH risk in females. Age stratification analysis illustrated that rs16970089 and rs6122316 were also correlated with LDH risk in people over 50 years. The smoking stratification illustrated that rs2071358 and rs740024 had an increased association with LDH risk in smokers. And after drinking stratification, we also observed the significance between rs740024 and LDH risk. CONCLUSIONS: Variants in genes for COL1A1, COL9A3 and COL2A1 significantly influence the risk of LDH. Large and well-designed studies are needed to confirm and explain these conclusions. These slides can be retrieved under Electronic Supplementary Material.

Investigation of the STOX1 polymorphism on lumbar disc herniation.

BACKGROUND: Lumbar disc herniation (LDH) is a common musculoskeletal disorder affliction and associated with several genes polymorphism. Storkhead box 1 (STOX1) gene is a transcriptional factor related with several signaling pathways including inflammatory pathway. However, little is known about single-nucleotide polymorphisms (SNPs) of STOX1 associated with LDH risk. METHODS: We conducted a case-control study among 508 LDH cases and well-matched 508 controls, and six candidate SNPs in STOX1 were genotyped by Agena MassARRAY. Chi-squared test, genetic model, and haploview analysis were used to evaluate associations. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by unconditional logistic regression. RESULTS: In the allelic model analysis, we found the minor allele "T" of rs7903209 and "A" of rs4472827 were associated with an increased risk of LDH (p = .029, p = .016). Furthermore, in the genotype model analysis, rs7903209 polymorphism was associated with the increased susceptibility of LDH based on dominant (p = .033) and additive model (p = .024); and rs4472827 variant was found to play a harmful role in the LDH risk based on genotype (p = .014), dominant (p = .012), and additive model (p = .015). In the haplotype analysis, the haplotype "GT" in block (rs10998461 and rs10998468) decreased LDH risk (OR = 0.7, 95% CI = 0.52-0.93, p = .016). Functional assessment indicated that rs7903209 and rs4472827 polymorphisms may influence the expression of STOX1. CONCLUSION: Our results provide evidence for polymorphisms of rs7903209 and rs4472827 in STOX1 associated with LDH risk in Chinese Han population.

CHRNA5/CHRNA3 gene cluster is a risk factor for lumbar disc herniation: a case-control study.

BACKGROUND: Lumbar disc herniation, a type of chronic low back pain syndrome, is caused by the lumbar intervertebral disk degeneration. Genetic variation in the CHRNA5/CHRNA3 has shown strong associations with smoking-related diseases. This study's aim is to test whether single-nucleotide polymorphisms in the CHRNA5/CHRNA3 gene are associated with lumbar disc herniation risk. METHODS: The genotype frequency distributions of the polymorphisms were detected by polymerase chain reaction-restriction fragment length polymorphism in 380 lumbar disc herniation patients (case group) and 400 healthy individuals (control group). Allelic, genotypic, and haplotype analyses were performed. RESULTS: We found that the individuals with rs8040868 CT genotype had a 0.46-fold higher risk of lumbar disc herniation than those with rs8040868 TT genotype, in men group (OR = 0.46, 95% CI 0.25-0.84, p = 0.012). Also among women, rs8040868 CT + CC genotype still reduced the risk of lumbar disc herniation under the dominant model (OR = 0.50, 95% CI 0.28-0.89, p = 0.019). Haplotype analysis showed that compared with the CHRNA5 "TACAACCG" wild-type, the "TACACCCG" haplotype was found to be associated with a decreased risk of lumbar disc herniation (LDH) (OR = 0.79, 95% CI 0.63-1.00, p = 0.047), while, in the less than 50-year-old group, CHRNA5 "TACACCCG" increased the risk of LDH (OR = 1.46, 95% CI 1.01-2.13, p = 0.047). CONCLUSIONS: Our data suggest that gene variance in the CHRNA5/CHRNA3 is associated with risk of lumbar disc herniation in the case-control study.

Correlation of EYS polymorphisms with lumbar disc herniation risk among Han Chinese population.

BACKGROUND: Lumbar disc herniation (LDH) is a common spinal disease in clinical practice. Once lumbar disc herniation occurs, it seriously reduces patient's quality of life. The EYS (eyes shut homolog) was discovered in recent years and it may be related to lumbar disc herniation. So we conducted a case-control study to explore the relationship between EYS polymorphism and lumbar disc herniation risk. METHODS: We selected 5 single-nucleotide polymorphisms (SNPs) of EYS gene in a case-control study with 508 cases and 508 healthy controls to evaluate the relatedness by using genetic model, haplotype, and stratification analysis. RESULTS: We found that the minor alleles of rs62413038 (OR = 1.21, 95%CI: 1.01-1.43, p = .036) and rs9450607 (OR = 1.26, 95% CI: 1.05-1.53, p = .016) were associated with an increased risk of lumbar disc herniation in the allelic model analysis. In the genotypic model analysis, rs62413038 displayed a significantly increased risk of lumbar disc herniation in log-additive models (OR = 1.20, 95% CI: 1.01-1.43, p = .039). While the rs9450607 was also obviously associated with an increased lumbar disc herniation risk in recessive (OR = 1.98, 95% CI: 1.24-3.13, p = .004) and log-additive models (OR = 1.27, 95% CI: 1.05-1.55, p = .014). In addition, in the haplotype analyses of the SNPs, we found that the "CGGA" haplotype of rs1482456, rs9342097, rs9450607, and rs7757884 was associated with lumbar disc herniation. (OR = 0.52, 95% CI: 0.30-0.89, p = .017). CONCLUSION: These results suggest that EYS polymorphism may be associated with lumbar disc herniation among Han Chinese population. It also opens up a new exploration direction for the etiology of lumbar disc herniation.

Association of glypican-6 polymorphisms with lumbar disk herniation risk in the Han Chinese population.

BACKGROUND: Lumbar disk herniation (LDH) is a degenerative disorder, which partly results from complex genetic factors. The aim of the study was to investigate the potential associations between glypican-6 (GPC6) variants and LDH risk in Han Chinese population. METHODS: A total of 508 Han Chinese LDH patients and 508 healthy controls were recruited in this study. Six single-nucleotide polymorphisms (SNPs) in GPC6 were selected and genotyped using an Agena MassARRAY platform. We used logistic regression method to evaluate the linkage between GPC6 variants and LDH risk by calculating the odds ratio (OR) and 95% confidence intervals (CIs) in multiple genetic models. HaploReg database was used for SNP functional annotation. RESULTS: Our result revealed GPC6 rs4773724 was associated with a decreased risk of LDH in allele model (OR = 0.82, 95% CI: 0.68-0.98, p = 0.026), whereas rs1008993 increased the LDH risk (OR = 1.34, 95% CI: 1.05-1.71, p = 0.020). Besides, we also found rs4773724 and rs9523981 were associated with susceptibility of LDH among individuals whose age are less than 45. And rs1008993 was associated with increased LDH risk in males. Furthermore, Haplotype analysis showed that the TT (rs4773724, rs1008993) haplotype and GC (rs4773724, rs1008993) haplotype had the opposite effects on the susceptibility of LDH. CONCLUSIONS: For the first time, we suggest that rs4773724 and rs1008993 in GPC6 were considered as a protective factor and a risk factor for LDH in Han Chinese population, respectively. These results provide new ideas for the treatment and prevention of LDH in Han Chinese population.

Association study between matrix metalloproteinase-3 gene (MMP3) polymorphisms and ankylosing spondylitis susceptibility.

BACKGROUND: Ankylosing spondylitis (AS) is the second most common cause of inflammatory arthritis worldwide affecting the axial skeleton. Single nucleotide polymorphisms (SNPs) of matrix metalloproteinase-3 (MMP3) in the development of AS has few been investigated in Chinese population. METHODS: A total of 362 patients with AS and 362 healthy controls were enrolled in the study. Five SNPs in MMP3 genotypes were identified by Agena MassARRAY. Chi-squared tests and genetic model were used to evaluate associations. RESULTS: rs522616 had a significant risk of AS development compared to those with the TT genotype (p = 0.008). By multiple logistic regression models analysis, in codominant model, rs522616 CT genotypes also had a 1.44-fold risk (95% CI = 1.06-1.96, p = 0.008) for AS development compared to those with TT genotypes. In recessive model, the CC genotypes was a significantly reduced AS risk for individuals with TT/CT genotype (OR = 0.64; 95% CI = 0.41-0.99, p = 0.040). CONCLUSION: The present study suggests that MMP3 rs522616 polymorphism is associated with AS susceptibility and MMP3 might be a potential diagnostic biomarker for AS. Further independent studies with larger cohorts are warranted to validate our findings in different populations.

Does Body Mass Index and Height Influence the Incident Risk of Ischemic Stroke in Newly Diagnosed Type 2 Diabetes Subjects?

OBJECTIVE: To estimate the incident risk of ischemic stroke (IS) in newly diagnosed type 2 diabetes (T2D) subjects according to different body mass index (BMI) and height categories. METHODS: A total of 25,130 newly diagnosed T2D subjects were included in this study. All T2D subjects were enrolled consecutively from the Chronic Disease Surveillance System (CDSS) of Ningbo. Standardized incidence ratio (SIR) and its 95% confidence interval (95% CI) stratified by BMI categories and height quartiles were used to estimate the incident risk of IS in T2D subjects. RESULTS: In total, 22,795 subjects completed the follow-up. Among them, 1268 newly diagnosed IS cases were identified, with 149,675 person-years. The SIRs of normal BMI (18.5-24.0 kg/m2), overweight (24.0-28.0 kg/m2), and obese (≥28.0 kg/m2) in overall subjects were 2.56 (95% CI 1.90-3.13), 2.13 (95% CI 1.90-3.13), and 1.87 (95% CI 1.29-2.43), respectively (P trend < 0.01), comparing to the general population of Ningbo. For each 1 kg/m2 increment in BMI, the SIR was 0.948 (95% CI 0.903-0.999). For height quartiles, the SIRs of male subjects in quartile 1 (<160 cm), quartile 2 (161-165 cm), quartile 3 (165-170 cm), and quartile 4 (≥171 cm) were 2.27 (95% CI 1.99-2.56), 2.01 (95% CI 1.67-2.45), 1.37 (95% CI 1.05-1.68), and 0.91 (95% CI 0.40-1.32), respectively (P trend < 0.01). While for female subjects, the SIRs in quartile 1 (<155 cm), quartile 2 (156-160 cm), quartile 3 (161-165 cm), and quartile 4 (≥166 cm) were 3.57 (95% CI 3.11-3.49), 2.96 (95% CI 2.61-3.31), 1.94 (95% CI 1.51-2.36), and 1.71 (95% CI 0.95-2.47), respectively (P trend < 0.01). CONCLUSION: Compared to the general population of Ningbo, T2D subjects had a higher incident risk of IS. Furthermore, the IS incident risk was not only higher in newly diagnosed T2D subjects with normal BMI but also lower in taller newly diagnosed T2D subjects.

Risk of all-cause and CHD mortality in women versus men with type 2 diabetes: a systematic review and meta-analysis.

OBJECTIVE: Previous studies have shown sex-specific differences in all-cause and CHD mortality in type 2 diabetes. We performed a systematic review and meta-analysis to provide a global picture of the estimated influence of type 2 diabetes on the risk of all-cause and CHD mortality in women vs men. METHODS: We systematically searched PubMed, EMBASE and Web of Science for studies published from their starting dates to Aug 7, 2018. The sex-specific hazard ratios (HRs) and their pooled ratio (women vs men) of all-cause and CHD mortality associated with type 2 diabetes were obtained through an inverse variance-weighted random-effects meta-analysis. Subgroup analyses were used to explore the potential sources of heterogeneity. RESULTS: The 35 analyzed prospective cohort studies included 2 314 292 individuals, among whom 254 038 all-cause deaths occurred. The pooled women vs men ratio of the HRs for all-cause and CHD mortality were 1.17 (95% CI: 1.12-1.23, I2 = 81.6%) and 1.97 (95% CI: 1.49-2.61, I2 = 86.4%), respectively. The pooled estimate of the HR for all-cause mortality was approximately 1.30 in articles in which the duration of follow-up was longer than 10 years and 1.10 in articles in which the duration of follow-up was less than 10 years. The pooled HRs for all-cause mortality in patients with type 2 diabetes was 2.33 (95% CI: 2.02-2.69) in women and 1.91 (95% CI: 1.72-2.12) in men, compared with their healthy counterparts. CONCLUSIONS: The effect of diabetes on all-cause and CHD mortality is approximately 17 and 97% greater, respectively, for women than for men.

Genetic variants in COL11A2 of lumbar disk degeneration among Chinese Han population.

BACKGROUND: Lumbar disk disease (LDD) is a common musculoskeletal disorder. Several predisposing genetic and environmental risk factors have been established for symptomatic LDD. METHODS: We conducted a case-control association study to investigate the role of the COL11A2 gene in LDD. Genotyping of 384 Chinese Han LDD patients and 384 Chinese Han controls was made for six single-nucleotide polymorphisms (SNPs) from COL11A2 by Agena Massarray. We evaluated these SNPs association with LDD using the chi-square test and genetic model analysis. RESULTS: The strongest associations with LDD were observed for polymorphisms in rs2071025. Carriers of "A" allele had an increased risk of LDD (OR = 1.47, 95% CI = 1.20-1.80, p = 0.0002) as compared with the "G" allele in allele model. We found that rs2071025 were associated with LDD in female and male from the stratification analyses (p < 0.05). Genetic models showed that rs986522(C) significantly increased the risk of LDD in female; however, in males, we did not find significant associations between the rs986522 and LDD risk. CONCLUSION: This study showed a genetic association with COL11A2 polymorphism in individuals with LDD. These data may provide novel insights into the pathogenesis of LDD, although further studies with larger numbers of participants worldwide are needed for validation of our conclusions.

Associations between Variants in BDNF/BDNFOS Gene and Lumbar Disc Herniation Risk among Han Chinese People.

Lumbar disc herniation (LDH) is a low back pain disorder and associated with several single nucleotide polymorphisms (SNPs). However, the role of brain-derived neurotrophic factor (BDNF) and BDNFOS gene in LDH susceptibility remains unknown. To examine whether the variants contribute to LDH, 7 SNPs were genotyped in 380 patients and 692 healthy controls among Han Chinese population. Multiple genetic models, stratification by age/gender and haploview analysis was used by calculating odds ratio (OR) and 95% confidence intervals (CIs). Rs11030064 in BDNFOS gene was associated with modified susceptibility for LDH at age ≤50 years but three loci (rs6265, rs11030104 and rs10767664) of BDNF gene increased LDH risk at age >50 years. Further, rs11030096 polymorphism in BDNFOS gene was associated with LDH the increased susceptibility of LDH in females. Haplotype analysis shown that haplotype "GCC" in the block (rs988712, rs7481311, and rs11030064) increased LDH risk (OR = 1.49, 95% CI = 1.06-2.10, p = 0.022) at age ≤50 years. However, there was no significant association between BDNF/BDNFOS gene and LDH risk in the overall before stratified analysis. For the first time, our results provide evidence on polymorphism of BDNF / BDNFOS gene associated with LDH risk in Chinese Han population.

Association of IL-1A and IL-1B polymorphisms with ankylosing spondylitis among the Chinese Han population: a case-control study.

Ankylosing spondylitis (AS) is a complex and chronic inflammatory disease with a high heritage. Previous study has shown that IL-1A and IL-1B involved in inflammatory reaction. But little is known about single nucleotide polymorphisms (SNPs) of IL-1A and IL-1B associated with AS. We conducted a case-control study among 267 AS cases and 297 healthy controls from China. In the genetic model analysis, we found the "T" genotype of rs3783550 was associated with decreased AS risk in the dominant model (p = 0.044) and log-additive model (p = 0.023); the "C" genotype of rs3783546 was significantly associated with decreased AS risk based in the dominant model (p = 0.044) and log-additive model (p = 0.023). Additionally, the minor allele "A" of rs2853550 may also reduce the risk of AS in dominant (p = 0.025) and log-additive model (p = 0.024). Our results suggested that the polymorphisms of IL-1A and IL-1B are associated with the AS susceptibility in the Chinese Han population. Further studies are needed to characterize the functional sequences that cause AS.

The Association between GSTM1, GSTT1 Genetic Variants and Gastric Carcinoma Susceptibility in Chinese: A Systematic Review Article.

BACKGROUND: Glutathione S-transferases (GSTs) have been investigated as potential carcinoma susceptible genes. However, the relationship between GSTs (GSTM1, GSTT1) variants and gastric carcinoma (GC) risk has been controversial in Chinese population. METHODS: A comprehensive literature search strategy (PubMed, Chinese Biomedical Database, Chinese National Knowledge Infrastructure, Wan fang Database, etc.) was launched. Crude odds ratios (ORs) and confidence intervals (95% CI) were applied to estimate the strength of the association. RESULTS: Significant associations between GSTs genetic polymorphisms and GC were evidenced under random-effects model (OR GSTM1 =1.56, 95% CI: 1.39 to 1.76, I2=50.7%, P<0.0001; OR GSTT1 =1.24, 95% CI: 1.10 to 1.39, I2=43.6%, P=0.014; OR GSTM1-GSTT1 =1.51, 95% CI: 1.26 to 1.81, I2=59.7%, P=0.004). The pooled ORs were not qualitatively changed when any single study was omitted by sensitivity analysis. CONCLUSION: Our results indicated an increased GC risk in Chinese population with GSTM1 and GSTT1 null genotype and GSTM1-GSTT1 dual null genotype. Further multi-center studies are needed to investigate the gene-gene and gene-environment interactions on the susceptibility of GC.

Nutritional risk, malnutrition and nutritional support among hospitalized patients in orthopedics/spinal surgery of a Hohhot teaching hospital.

The evolution of nutritional status (the prevalence of nutritional risk, malnutrition, overweight and obesity) and the nutritional support of the hospitalized patients from admission to discharge or over a two-week period in orthopedics/ spinal surgery of a teaching hospital in Hohhot were investigated. 432 patients from two wards of the orthopedics/spinal surgery from Jan to Dec 2013, the traditional spinal surgery and the minimally invasive spinal surgery, were selected and detected in this study. The Nutritional Risk Score 2002 (NRS 2002) was used to determine the patients' nutritional status within 48 h after admission and during their hospitalization. The overall prevalence of nutritional risk, malnutrition, overweight and obesity at admission was 11.6%, 12.7%, 35.9% and 7.41%, respectively. Overall, there were 88.0% of the patients who were at nutritional risk received nutritional support, while 14.1% of non-risk patients received a redundant nutritional support. The overall prevalence of nutritional risk changed from 11.6% at admission to 19.4% upon discharge (p<0.05), and the prevalence of malnutrition changed from 12.7% to 20.6% (p<0.05). The prevalence of overweight and obesity, which changed from 35.9% to 31.0% and from 7.41% to 5.79% respectively, didn't experience statistically significant evolution. NRS 2002 was a feasible nutritional risk screening tool for patients in spinal surgery of orthopedics department. Patients' prevalence of nutritional risk and malnutrition increased significantly in spinal surgery of this hospital. Some inappropriate uses of nutritional support were observed in orthopedics/spinal surgery, and nutritional support guidelines or protocols should be promoted by a professional committee.

Influence of polymorphisms in insulin-like growth factor-1 on the risk of osteoporosis in a Chinese postmenopausal female population.

We conducted a case-control study in a Chinese postmenopausal population, and explore the potential role of the promoter region variation of the IGF-1 gene in bone mineral density and osteoporosis risk. 485 postmenopausal women with a primary diagnosis of osteoporosis and 485 age-matched controls were selected between 2012 and 2014. The Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) was used for rs35767, rs2288377 and rs5742612 of IGF-1 genotyping. By conditional regression analysis, individuals carrying TT genotype and CT+TT genotype of rs35767 were found to be correlated with an elevated risk of osteoporosis, with adjusted ORs (95% CI) of 1.90 (1.23-2.93) and 1.35 (1.04-1.76), respectively. Our study found that CT+TT genotype of rs35767 was significantly associated with moderate increased risk of osteoporosis in smokers and drinkers, and the ORs (95% CI) were 2.11 (1.06-4.20) and 2.36 (1.29-4.32), respectively. We found that those carrying CT+TT genotype of rs35767 had a significant lower BMD levels at L1-L4 vertebrae, femoral neck, total hip and trochanter compared to those with CC genotype. Our study suggests that TT genotype and CT+TT genotype of IGF-I rs35767 were associated with risk of osteoporosis and BMD levels.

[POSTERIOR LUMBAR INTERBODY FUSION FOR DOUBLE-SEGMENTAL BILATERAL ISTHMIC LUMBAR SPONDYLOLISTHESIS].

OBJECTIVE: To explore the effectiveness of posterior lumbar interbody fusion in the treatment of double-segmental bilateral isthmic lumbar spondylolisthesis. METHODS: Between February 2008 and December 2013, 17 patients with double-segmental bilateral isthmic lumbar spondylolisthesis were treated with posterior lumbar interbody fusion. There were 12 males and 5 females, with an age ranged 48-69 years (mean, 55.4 years). The disease duration ranged from 11 months to 17 years (median, 22 months). According to the Meyerding classification, 30 vertebrea were rated as degree I, 3 as degree II, and 1 as degree III. L4,5 was involved in 14 cases and L3,4 in 3 cases. The preoperative visual analogue scale (VAS) score was 8.6 ± 3.2. RESULTS: Cerebrospinal fluid leakage occurred in 2 cases because of intraoperative dural tear; primary healing of incision was obtained, with no operation related complication in the other patients. The patients were followed up 1-6 years (mean, 3.4 years). At last follow-up, VAS score was decreased significantly to 1.1 ± 0.4, showing significant difference when compared with preoperative score (t=7.652, P=0.008). X-ray films showed that slippage vertebral body obtained different degree of reduction, with a complete reduction rate of 85% (29/34) at 1 week after operation. All patients achieved bony union at 6-12 months (mean, 7.4 months). According to the Lenke classification, 13 cases were rated as grade A and 4 cases as grade B. No internal fixation loosening and fracture were observed during the follow-up. Intervertebral disc height was maintained, no loss of spondylolisthesis reduction was found. CONCLUSION: It can obtain satisfactory clinical result to use spinal canal decompression by posterior approach, and screw fixation for posterior fusion in treatment of double-segmental bilateral isthmic lumbar spondylolisthesis. The key points to successful operation include accurate insertion of screw, effective decompression, distraction before reduction, rational use of pulling screws, and interbody fusion.