Efficacy of PE-PLIF with a novel ULBD approach for lumbar degeneration diseases: a large-channel endoscopic retrospective study.

PURPOSE: This study aims to assess the effectiveness of Percutaneous Endoscopic Posterior Lumbar Interbody Fusion (PE-PLIF) combined with a novel Unilateral Laminotomy for Bilateral Decompression (ULBD) approach using a large-channel endoscope in treating Lumbar Degenerative Diseases (LDD). METHODS: This retrospective analysis evaluates 41 LDD patients treated with PE-PLIF and ULBD from January 2021 to June 2023. A novel ULBD approach, called 'Non-touch Over-Top' technique, was utilized in this study. We compared preoperative and postoperative metrics such as demographic data, Visual Analogue Scale (VAS) for pain, Oswestry Disability Index (ODI), Japanese Orthopedic Association (JOA) score, surgical details, and radiographic changes. RESULTS: The average follow-up duration was 14.41 ± 2.86 months. Notable improvements were observed postoperatively in VAS scores for back and leg pain (from 5.56 ± 0.20 and 6.95 ± 0.24 to 0.20 ± 0.06 and 0.12 ± 0.05), ODI (from 58.68 ± 0.80% to 8.10 ± 0.49%), and JOA scores (from 9.37 ± 0.37 to 25.07 ± 0.38). Radiographic measurements showed significant improvements in lumbar and segmental lordosis angles, disc height, and spinal canal area. A high fusion rate (97.56% at 6 months, 100% at 12 months) and a low cage subsidence rate (2.44%) were noted. CONCLUSIONS: PE-PLIF combined with the novel ULBD technique via a large-channel endoscope offers significant short-term benefits for LDD management. The procedure effectively expands spinal canal volume, decompresses nerve structures, improves lumbar alignment, and stabilizes the spine. Notably, it improves patients' quality of life and minimizes complications, highlighting its potential as a promising LDD treatment option.

Dynamic Recrystallization Constitutive Model and Texture Evolution of Metastable ß Titanium Alloy TB8 during Thermal Deformation.

The mechanical properties of metastable ß-titanium alloys are highly susceptible during the thermal mechanical processing (TMP). In this process, the recrystallization process plays an important role in determining the microstructure and texture evolution. The implementation of dynamic recrystallization (DRX), a process for achieving ß-grain refinement, is considered of great significance for the improvement of the properties of metastable ß-titanium alloys and their industrial production. Along these lines, in this work, an isothermal compression test of TB8 titanium alloy was carried out by using a Gleeble-3500 thermal simulator. As a result, the rheological stress behavior was analyzed, the thermal processing map was accurately established based on the stress-strain curve, and the optimal processing interval was determined. The DRX kinetic and the DRX grain size models were developed, on the basis of which a new DRX intrinsic model was established to improve the material parameters. Therefore, the actual situation in the working process could be better predicted. The microstructural evolution of TB8 titanium alloy during thermal deformation was comprehensively investigated using the electron backscatter diffraction (EBSD) technique. The obtained results demonstrate a close correlation between the diversity of DRX mechanisms in TB8 alloy and the distribution of dislocation density. Four microstructural textures during thermal deformation were identified, in which the cube texture of (001) <010> and the R-Gorss Nd texture of (110) <110> dominate. Due to the random orientation of the dynamically recrystallized grains, the strength of the R-Gorss Nd texture of (110) <110> increases with the increase in the volume fraction of DRX. On the contrary, it was verified that the dynamic recrystallization behavior has a significant weakening impact on the cube texture of (001) <010>.

The efficacy and safety of ultrasonic bone scalpel for removing retrovertebral osteophytes in anterior cervical discectomy and fusion: A retrospective study.

In this study, we present a novel surgical method that utilizes the ultrasonic bone scalpel (UBS) for the removal of large retrovertebral osteophytes in anterior cervical discectomy and fusion (ACDF) and evaluate its safety and efficacy in comparison to the traditional approach of using high-speed drill (HSD). A total of 56 patients who underwent ACDF for retrovertebral osteophytes were selected. We recorded patients' baseline information, operation time, intraoperative blood loss, complications, JOA and VAS scores, and other relevant data. The mean operation time and the mean intraoperative blood loss in the UBS group were less than those in the HSD group (P < 0.05). Although both groups exhibited considerable improvements in JOA and VAS scores following surgery, there was no statistically significant difference between the two groups (P > 0.05). Additionally, no significant disparities were found in bone graft fusion between the two groups at 6- and 12-months postsurgery. Notably, neither group exhibited complications such as dura tear or spinal cord injury. Our study found that the use of UBS reduced operative time, minimized surgical bleeding, and led to clinical outcomes comparable to HSD in ACDF. This technique offers an effective and safe method of removing large retrovertebral osteophytes.

Ganoderic acid A slows osteoarthritis progression by attenuating endoplasmic reticulum stress and blocking NF-Κb pathway.

Osteoarthritis (OA) is a prevalent degenerative pathology, however, there exists a lack of cost-effective pharmacological interventions that efficaciously inhibit its progression. ganoderic acid A (GAA), a triterpenoid derived from Ganoderma lucidum, possesses antiapoptotic and -inflammatory effects. Our objective was to better understand the therapeutic effects of GAA on OA as well as to elucidate the underlying mechanisms of its action. To establish an OA cell model in vitro, chondrocytes (CHONs) were treated with interleukin (IL)-1ß. Subsequently, the investigation was conducted afterward according to the following indicators: cell viability, apoptosis, inflammation, and extracellular matrix (ECM) degradation. Western blotting analysis (WB) was employed to assess both endoplasmic reticulum (ER) stress and proteins associated with the nuclear factor-kappa B (NF-κB) signaling pathway. Furthermore, based on molecular docking studies, GAA exhibits a significant binding competence to p65. OA mouse models were constructed by performing a destabilization medial meniscus (DMM) operation. Moreover, histopathology and immunohistochemistry were used to determine the GAA therapeutic effect in reducing OA in vivo. Our findings revealed that GAA has antiapoptotic, anti-inflammatory, and anti-ECM degradation effects by inhibiting the ER stress and NF-κB axis in CHONs in vitro. Furthermore, our findings suggest that GAA may attenuate the progression of osteoarthritis in vivo. GAA can protect CHONs by regulating apoptosis, ECM changes, and inflammation thereby preventing OA progression. These promising results indicate that GAA may be a therapeutic agent for OA treatment.

Thermosensitive hydrogel for cartilage regeneration via synergistic delivery of SDF-1α like polypeptides and kartogenin.

Regeneration of injured articular cartilage is limited by low early-stage recruitment of stem cells and insufficient chondrogenic differentiation. Hydrogels are widely used to repair cartilage because they have excellent mechanical and biological properties. In this study, a dual drug-loaded thermosensitive hydroxypropyl chitin hydrogel (HPCH) system was prepared to release stromal-derived factor-1α-like polypeptides (SDFP) and kartogenin (KGN) for stem-cell recruitment and chondrogenic differentiation. The hydrogel had a network structure that promoted cell growth and nutrient exchange. Moreover, it was temperature sensitive and suitable for filling irregular defects. The system showed good biocompatibility in vitro and promoted stem-cell recruitment and chondrogenic differentiation. Furthermore, it reduced chondrocyte catabolism under inflammatory conditions. Animal experiments demonstrated that the dual-drug hydrogel systems can promote the regeneration of articular cartilage in rats. This study confirmed that an HPCH system loaded with KGN and SDFP could effectively repair articular cartilage defects and represents a viable treatment strategy.

Association between CTLA-4 gene polymorphism and risk of rheumatoid arthritis: a meta-analysis.

Cytotoxic T lymphocyte-associated protein 4 (CTLA-4) gene polymorphisms may be involved in the risk of Rheumatoid arthritis (RA). However, evidence for the association remains controversial. Therefore, we performed a meta-analysis to confirm the relationship between CTLA-4 gene polymorphisms and RA. The pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to assess the strength of association. Stratified analysis was conducted by ethnicity. In total, 66 case-control studies including 21681 cases and 23457 controls were obtained. For rs3087243 polymorphism, significant association was detected in Asians (A vs. G: OR=0.77, 95%CI=0.65-0.90, P=0.001; AA vs. GG: OR=0.67, 95%CI=0.48-0.94, P=0.02) and Caucasians (A vs. G: OR=0.89, 95%CI=0.86-0.93, P<0.00001; AA vs. GG: OR=0.81, 95%CI=0.75-0.88, P<0.00001). For rs231775 polymorphism, significant association was observed in the overall (G vs. A: OR =1.16, 95%CI=1.08-1.25, P<0.0001; GG vs. AA: OR=1.29, 95%CI=1.12-1.50, P=0.0006), and in Asians (G vs. A: OR=1.27, 95%CI=1.10-1.47, P=0.001; GG vs. AA: OR=1.58, 95%CI=1.24-2.01, P=0.0002), but not in Caucasians. However, there was no association between rs5742909 polymorphism and RA. This meta-analysis confirmed that rs3087243 and rs231775 polymorphism were associated with the risk of RA in both overall population and ethnic-specific analysis, but there was no association between rs5742909 polymorphism and RA risk.

Src Homology 2 Domain-Containing Protein Tyrosine Phosphatase Promotes Inflammation and Accelerates Osteoarthritis by Activating ß-Catenin.

Osteoarthritis (OA) is a chronic articular disease characterized by cartilage degradation, subchondral bone remodeling and osteophyte formation. Src homology 2 domain-containing protein tyrosine phosphatase (SHP2) has not been fully investigated in the pathogenesis of OA. In this study, we found that SHP2 expression was significantly increased after interleukin-1ß (IL-1ß) treatment in primary mouse chondrocytes. Inhibition of SHP2 using siRNA reduced MMP3, MMP13 levels, but increased AGGRECAN, COL2A1, SOX9 expression in vitro. On the contrary, overexpression of SHP2 exerted the opposite results and promoted cartilage degradation. Mechanistically, SHP2 activated Wnt/ß-catenin signaling possibly through directly binding to ß-catenin. SHP2 also induced inflammation through activating Mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB) pathways. Our in vivo studies showed that SHP2 knockdown effectively delayed cartilage destruction and reduced osteophyte formation in the mouse model of OA induced by destabilization of the medial meniscus (DMM). Altogether, our study identifies that SHP2 is a novel and potential therapeutic target of OA.

Inhibiting Monoacylglycerol Lipase Suppresses RANKL-Induced Osteoclastogenesis and Alleviates Ovariectomy-Induced Bone Loss.

Osteoporosis is a common chronic metabolic bone disease characterized by reduced trabecular bone and increased bone fragility. Monoacylglycerol lipase (MAGL) is a lipolytic enzyme to catalyze the hydrolysis of monoglycerides and specifically degrades the 2-arachidonoyl glycerol (2-AG). Previous studies have identified that 2-AG is the mainly source for arachidonic acid and the most abundant endogenous agonist of cannabinoid receptors. Considering the close relationship between inflammatory mediators/cannabinoid receptors and bone metabolism, we speculated that MAGL may play a role in the osteoclast differentiation. In the present study, we found that MAGL protein expression increased during osteoclast differentiation. MAGL knockdown by adenovirus-mediated shRNA in bone marrow-derived macrophages demonstrated the suppressive effects of MAGL on osteoclast formation and bone resorption. In addition, pharmacological inhibition of MAGL by JZL184 suppressed osteoclast differentiation, bone resorption, and osteoclast-specific gene expression. Activation of the Mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB) pathways was inhibited by JZL184 and deletion of MAGL. Our in vivo study indicated that JZL184 ameliorated bone loss in an ovariectomized mouse model. Furthermore, overexpressing H1 calponin partially alleviated the inhibition caused by JZL184 or MAGL deletion on osteoclastogenesis. Therefore, we conclude that targeting MAGL may be a novel therapeutic strategy for osteoporosis.

NR1D1 modulates synovial inflammation and bone destruction in rheumatoid arthritis.

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial hyperplasia, pannus formation, and cartilage and bone destruction. Nuclear receptor subfamily 1 group D member 1 (NR1D1) functions as a transcriptional repressor and plays a vital role in inflammatory reactions. However, whether NR1D1 is involved in synovial inflammation and joint destruction during the pathogenesis of RA is unknown. In this study, we found that NR1D1 expression was increased in synovial tissues from patients with RA and decreased in RA Fibroblast-like synoviocytes (FLSs) stimulated with IL-1ß in vitro. We showed that NR1D1 activation decreased the expression of proinflammatory cytokines and matrix metalloproteinases (MMPs), while NR1D1 silencing exerted the opposite effect. Furthermore, NR1D1 activation reduced reactive oxygen species (ROS) generation and increased the production of nuclear transcription factor E2-related factor 2 (Nrf2)-associated enzymes. Mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB) pathways were blocked by the NR1D1 agonist SR9009 but activated by NR1D1 silencing. NR1D1 activation also inhibited M1 macrophage polarization and suppressed osteoclastogenesis and osteoclast-related genes expression. Treatment with NR1D1 agonist SR9009 in collagen-induced arthritis (CIA) mouse significantly suppressed the hyperplasia of synovial, infiltration of inflammatory cell and destruction of cartilage and bone. Our findings demonstrate an important role for NR1D1 in RA and suggest its therapeutic potential.

Pristimerin Suppresses RANKL-Induced Osteoclastogenesis and Ameliorates Ovariectomy-Induced Bone Loss.

Osteoporosis is characterized by bone loss and destruction of trabecular architecture, which greatly increases the burden on the healthcare system. Excessive activation of osteoclasts is an important cause of osteoporosis, and suppression of osteoclastogenesis is helpful for the treatment of osteoporosis. Pristimerin, a natural compound, possesses numerous pharmacological effects via inactivating the NF-κB and MAPK pathways, which are closely related to osteoclastogenesis process. However, the relationship between Pristimerin and osteoclastogenesis requires further investigation. In this research, we examined the effect of Pristimerin on osteoclastogenesis and investigated the related mechanisms. Our results showed Pristimerin inhibited RANKL-induced osteoclast differentiation and osteoclastic bone resorption in vitro, with decreased expression of osteoclastogenesis-related markers including c-Fos, NFATc1, TRAP, Cathepsin K, and MMP-9 at both mRNA and protein levels. Furthermore, Pristimerin suppressed NF-κB and MAPK signaling pathways, reduced reactive oxygen species (ROS) production and activated the nuclear factor erythroid 2-related factor 2/heme oxygenase 1 (Nrf2/HO-1) signaling during osteoclastogenesis. Our in vivo experiments showed that Pristimerin remarkably ameliorated ovariectomy-induced bone loss, reduced serum levels of TNF-α, IL-1ß, IL-6, and RANKL, and increased serum level of osteoprotegerin (OPG). Therefore, our research indicated that Pristimerin is a potential chemical for the treatment of osteoporosis.

Vinpocetine inhibits RANKL-induced osteoclastogenesis and attenuates ovariectomy-induced bone loss.

Osteoporosis is a result of impaired bone formation and/or excessive bone resorption. Osteoclasts are the only cells in the body that have a bone resorption function. Inhibiting osteoclast activity and differentiation is a way to treat osteoporosis. The current pharmacological treatment for osteoporosis has many shortcomings, and more effective treatments are needed. Vinpocetine (Vinp), a derivative of the alkaloid vincamine, has been used to treat cerebrovascular disorders and cognitive impairment for a long time. Vinp inhibits mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB)-dependent inflammatory responses and oxidative damage in which osteoclasts are often involved. However, the effects of Vinp on the regulation of osteoclast activity remain unknown. In this study, we found that Vinp significantly inhibited receptor activator of NF-κB ligand (RANKL)-induced osteoclast and F-actin formation and decreased osteoclastic bone resorption in vitro. Vinp also suppressed the expression of osteoclast-specific genes, including NFATc1, c-Fos, tartrate-resistant acid phosphatase (TRAP), matrix metalloproteinase-9 (MMP-9), and cathepsin K (CTSK) at both the mRNA and protein levels. Vinp reduced activation of NF-κB, MAPK, and AKT signaling during osteoclastogenesis and prevented the production of reactive oxygen species with increased nuclear factor erythroid 2-related factor 2, heme oxygenase 1, and NAD(P)H:quinone acceptor oxidoreductase 1 expression. Animal experiments consistently demonstrated that Vinp treatment significantly attenuated ovariectomy-induced bone loss with a decrease in the osteoclast number and decreases in serum levels of RANKL, TRAP, interleukin-1ß, and tumor necrosis factor-alpha, as well as increased serum levels of osteoprotegerin. Taken together, our findings reveal that Vinp may be a potential pharmacological choice for preventing and treating osteoporosis.

Association of rs4552569 and rs17095830 single-nucleotide polymorphisms with susceptibility to ankylosing spondylitis in east Asian population: a meta-analysis.

Several studies have been conducted in east Asian population to evaluate the association between rs4552569 and rs17095830 single-nucleotide polymorphisms (SNPs) with susceptibility to ankylosing spondylitis (AS), but the outcomes are inconsistent. A summary evaluation of the evidence supporting the associations has not been performed. Therefore,we performed this meta-analysis to access whether the two SNPs are related to ankylosing spondylitis. We systematically searched PubMed, EMBASE, Web of Science and Cochrane Library for papers published up until 3 February 2017, to obtain relevant studies using our research strategy. The allele/genotype frequencies were extracted from each study. We calculated the summary odds ratios (ORs) and 95% confidence intervals (CIs) to evaluate the associations between the two SNPs and AS risk. Four papers including five studies were obtained for this meta-analysis. The included studies suggested that there was no significant association between rs4552569 SNP and AS (C vs T, OR = 1.08, 95% CI: 0.96-1.22, P = 0.20).With regard to rs17095830 SNP, significant association was observed (G vs A, OR = 1.19, 95% CI: 1.06-1.33, P = 0.002). Based on a comprehensive analysis of the currently available evidence, rs4552569 SNP is not significantly associated with the predisposition of AS, while rs17095830 SNP is likely a susceptibility variant for AS in east Asian population. Further studies with different population groups are needed to confirm these potential associations.

Association between IGF-1 polymorphisms and risk of osteoporosis in Chinese population: a meta-analysis.

BACKGROUND: Several studies looking into the association between insulin-like growth factor-1 (IGF-1) gene polymorphisms and osteoporosis predisposition have been conducted among Chinese population with conflicting outcomes. The present systematic review and meta-analysis was performed to appraise and synthesize the existing evidence, so as to provide a more precise and reliable association between polymorphisms in IGF-1 gene and osteoporosis. METHODS: Five electronic databases including PubMed, EMBASE, ISI Web of Science, CNKI and Wanfang were systematically searched for potential studies. Summary odds ratio (OR) and corresponding 95% confidence interval (95% CI) were calculated to evaluate the association. The best-matching genetic model of inheritance was determined using a genetic-model free approach. RESULTS: Six case-control studies comprising 2068 osteoporosis patients and 2071 healthy controls were obtained for the meta-analysis. Dominant model was confirmed to be the best-matching genetic model (TT + TC versus CC). The overall data suggested that rs35767 polymorphism was significantly associated with osteoporosis vulnerability (OR 1.21, 95% CI 1.07, 1.37; P = 0.002). When stratifying the participants and performing subgroup-analysis according to source of patients, the result suggested that rs35767 was significantly correlated to osteoporosis in post-menopausal women subgroup (OR 1.29, 95% CI 1.08, 1.54; P = 0.005), but the correlation was not established in the subgroup of both gender (OR 1.14, 95% CI 0.96, 1.35; P = 0.12). CONCLUSION: Taken together, the findings of our current study suggested a significant association between rs35767 polymorphism and risk of osteoporosis in Chinese post-menopausal women.

Evolving Healthcare Quality in Top Tertiary General Hospitals in China during the China Healthcare Reform (2010-2012) from the Perspective of Inpatient Mortality.

Healthcare reforms (HR) initiated by many countries impacts on healthcare systems worldwide. Being one of fast developing countries, China launched HR in 2009. Better understanding of its impact is helpful for China and others in further pursuit of HR. Here we evaluate inpatient mortality, a proxy to healthcare quality, in 43 top tertiary hospitals in China during this critical period. This is a hospital-based observational study with 8 million discharge summary reports (DSR) from 43 Chinese hospitals from 2010-2012. Using DSRs, we extract the vita status as the outcome, in addition to age, gender, diagnostic codes, and surgical codes. Nearly all hospitals have expanded their hospitalization capacities during this period. As of year 2010, inpatient mortality (IM) across hospitals varies widely from 2‰ to 20‰. Comparing IM of year 2011 and 2012 with 2010, the overall IM has been substantially reduced (OR = 0.883 and 0.766, p-values<0.001), showing steady improvements in healthcare quality. Surgical IM correlates with the overall IM (correlation = 0.60, p-value <0.001), but is less uniform. Over these years, surgical IM has also been steadily reduced (OR = 0.890 and 0.793, p-values<0.001). Further analyses of treatments on five major diseases and six major surgeries revealed that treatments of myocardial infarction, cerebral hemorrhage and cerebral infarction have significant improvement. Observed temporal and spatial variations demonstrate that there is a substantial disparity in healthcare quality across tertiary hospitals, and that these hospitals are rapidly improving healthcare quality. Evidence-based assessment shed light on the reform impact. Lessons learnt here are relevant to further refining HR.

Comparative Study of Three Commonly Used Methods for Hospital Efficiency Analysis in Beijing Tertiary Public Hospitals, China.

BACKGROUND: Tertiary hospitals serve as the medical service center within the region and play an important role in the medical and health service system. They are also the key targets of public hospital reform in the new era in China. Through the reform of health system, the public hospital efficiency has changed remarkably. Therefore, this study aimed to provide some advice for efficiency assessment of public hospitals in China by comparing and analyzing the consistency of results obtained by three commonly used methods for examining hospital efficiency, that is, ratio analysis (RA), stochastic frontier analysis (SFA), and data envelopment analysis (DEA). METHODS: The theoretical basis, operational processes, and the application status of RA, SFA, and DEA were learned through literature analysis. Then, the empirical analysis was conducted based on measured data from 51 tertiary public hospitals in Beijing from 2009 to 2011. RESULTS: The average values of hospital efficiency calculated by SFA with index screening and principal component analysis (PCA) results and those calculated by DEA with index screening results were relatively stable. The efficiency of specialized hospitals was higher than that of general hospitals and that of traditional Chinese medicine hospitals. The results obtained by SFA with index screening results and the results obtained by SFA with PCA results showed a relatively high correlation (r-value in 2009, 2010, and 2011 were 0.869, 0.753, and 0.842, respectively, P < 0.01). The correlation between results obtained by DEA with index screening results and PCA results and results obtained by other methods showed statistical significance, but the correlation between results obtained by DEA with index screening results and PCA results was lower than that between results obtained by SFA with index screening results and PCA results. CONCLUSIONS: RA is not suitable for multi-index evaluation of hospital efficiency. In the given conditions, SFA is a stable efficiency analysis method. In the evaluation of hospital efficiency, DEA combined with PCA should be adopted with caution due to its poor stability.

[RESEARCH PROGRESS OF ROLE OF ESTROGEN AND ESTROGEN RECEPTOR ON ONSET AND PROGRESSION OF ADOLESCENT IDIOPATHIC SCOLIOSIS].

OBJECTIVE: To review the recent progress in research on the role of estrogen and estrogen receptor on the onset and progression of adolescent idiopathic scoliosis (AIS). METHODS: The recently published clinical and experimental literature at home and abroad on abnormality of estrogen and its receptor in AIS was reviewed and summarized. RESULTS: There are many abnormal changes of estrogen and estrogen receptor in most AIS patients, including higher serum estrogen concentration, unusual cellular response to estrogen, late age at menarche, and gene polymorphisms of estrogen receptor, which are closely associated with AIS predisposition, curve severity, and scoliosis progression. CONCLUSION: Estrogen and its receptor participate in the onset and progression of AIS by certain mechanisms, but exact mechanism remains indefinite, which needs further research to better define the role of estrogen and its receptor in AIS.