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Abstract Objective We investigated the different life styles among the diet structures and exercise patterns of 100 patients with refractory gout and 79 healthy volunteers; of these, we selected 39 patients and 20 healthy volunteers for serum proton magnetic resonance (1H-NMR) metabolic network detection. We determined the potential biomarkers of refractory gout and attempted to explore the relation between potential biomarkers and diet structures and exercise patterns. Methods The study employed a questionnaire survey to analyze diet structures and exercise patterns from 100 patients of refractory gout and 79 healthy volunteers. At the same time, using 1H-NMR metabolic technology to analyze the metabolites present in the serum samples obtained from 39 patients of refractory gout (group B) and 20 healthy subjects (group A). Employing MestReNova (Version 8.0.1) to analyze the metabolites maps, collecting the NMR results, further importing into SIMCA-P+ 14.0 software (Umetrics, Sweden) for principal component analysis (PCA), partial least squares discriminant analysis (PLS-DA), and orthogonal partial least squares discriminant analysis (OPLS-DA) statistical analysis. Combining patterns recognition and multivariate statistics, potential biomarkers were searched. Other experimental data, including creatinine and adiponectin, were counted by the SPSS21.0. The measurement data were expressed by X ± S and t test. The counting data were expressed in percent and performed by X 2 test. Results Our results revealed that patients with gout tended to be obese, and there were differences in their lifestyle with exercise, sleep, and smoking, as well as in their preference for fructose drinks, alcohol, and total and structural distribution of meat, milk, eggs, and so on when compared with the healthy volunteers. Importantly, we found the adiponectin in the gout group was lower as compared to the healthy group. Further, metabolomics in combination with KEGG analysis revealed that the biosynthesis of aminoacyl tRNA, biosynthesis of valine, leucine, and isoleucine, metabolism of alanine, aspartic, and glutamate, metabolism of glycine, serine, and threonine, phenylalanine, glycolysis/gluconeogenesis, ketone body synthesis and degradation, metabolism of d‐glutamine, citric acid cycle (TCA cycle), triglyceride metabolism, and others could be used as specific biomarkers of this disease. Conclusion Recurrent refractory gout and formation of tophus may be related to the diet structures and lifestyles between the patients and the healthy people, and their abnormal metabolic network may be related to the disorder of mitochondrial energy metabolism, which further results in abnormal metabolism of glucose, lipids, amino acids, and deposition of uric acid in joints, peripheral connective tissue, and kidney, inducing an inflammatory response.

Study Design: Retrospective cohort study. Objective: Odontoid synchondrosis fracture is rare, and there is a paucity of literature on its surgical treatments. This case series study analyzed patients treated with C1 to C2 internal fixation with or without anterior atlantoaxial release and discussed the clinical effectiveness of the procedure. Methods: Data were retrospectively collected from a single-center cohort of patients who had undergone surgical treatments for displaced odontoid synchondrosis fracture. The operation time and blood loss volume were recorded. Neurological function was assessed and classified using the Frankel grades. The odontoid process tilting angle (OPTA) was used to evaluate fracture reduction. Fusion duration and complications were also analyzed. Results: Seven patients (1 boy and 6 girls) were included in the analysis. Three patients underwent anterior release and posterior fixation surgery, and the other 4 underwent posterior-only surgery. The fixation segment was C1 to C2. The average follow-up period was 34.7 ± 8.5 months. The average operation time was 145.7 ± 45.3 min, with an average blood loss volume of 95.7 ± 33.3 mL. The OPTA was corrected from 41.9° ± 11.1° preoperative to 2.4° ± 3.2° at the final follow-up (P <.05). The preoperative Frankel grade of 1 patient was grade C, of 2 patients was grade D, and of 4 patients was grade E. The neurological function of the patients in grade C and grade D recovered to grade E at the final follow-up. None of the patients developed a complication. All the patients achieved odontoid fracture healing. Conclusion: Posterior C1 to C2 internal fixation with or without anterior atlantoaxial release is a safe and effective method for treating young children with displaced odontoid synchondrosis fracture. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to use proton nuclear magnetic resonance technology to analyze the metabolic pathways of invigorating the spleen and promoting Yang dehumidification and dredging collaterals (Cassia twig Peony Anemarrhenae and Rise Yang Dehumidification Decoction) in treating the acute attack of refractory gout and to find the target of traditional Chinese medicine (TCM). Method: Forty patients with acute refractory gout of spleen deficiency and dampness-heat type were recruited and randomly divided into TCM group and the Western medicine group, with 20 patients in each group. Serum samples were collected before and after 10 days of treatment for comparative analysis, and the metabolic pathways were identified. Combined with the results of TCM syndrome score, inflammatory indexes (C reactive protein, erythrocyte sedimentation rate), and creatinine, adiponectin, and cytokine (interleukin-6, tumor necrosis factor-α) levels before and after treatment, the mechanism of TCM action was analyzed. Results: Cassia twig Peony Anemarrhenae and Rise Yang Dehumidification Decoction were found to be better than Western medicine in alleviating joint swelling and pain, localized as well as systemic fever, and bitter and dry mouth. Furthermore, inflammatory indicators, cytokines, creatinine, and adiponectin levels were better in the TCM group than in the Western medicine group. In terms of metabolic pathways, the treatment of an acute attack of refractory gout with our TCM compounds resulted in better improvements in branched-chain amino acid (BCAA) metabolism, glycine, serine, and threonine metabolism, tyrosine metabolism, taurine, and low taurine metabolism, glycolysis/sugar dysplasia, synthesis and degradation of ketone body, D-glutamine metabolism, citric acid cycle (TCA cycle), glyceride metabolic pathways, etc., than the use of Western medicine. Conclusion: TCM compounds may improve the metabolic network of refractory acute gout by stimulating the above metabolic pathways to inhibit the inflammatory response, relieve joint pain, and augment glucose metabolism, energy metabolism, and lipid metabolism. These compounds are hence worthy of promotion.

Background: Alzheimer's disease (AD) is a neurodegenerative disorder distinguished by a swift cognitive deterioration accompanied by distinctive pathological hallmarks such as extracellular Aβ (β‐amyloid) peptides, neuronal neurofibrillary tangles (NFTs), sustained neuroinflammation, and synaptic degeneration. The elevated frequency of AD cases and its proclivity to manifest at a younger age present a pressing challenge in the quest for novel therapeutic interventions. Numerous investigations have substantiated the involvement of C/EBPβ in the progression of AD pathology, thus indicating its potential as a therapeutic target for AD treatment. Aims: Several studies have demonstrated an elevation in the expression level of C/EBPβ among individuals afflicted with AD. Consequently, this review predominantly delves into the association between C/EBPβ expression and the pathological progression of Alzheimer's disease, elucidating its underlying molecular mechanism, and pointing out the possibility that C/EBPβ can be a new therapeutic target for AD. Methods: A systematic literature search was performed across multiple databases, including PubMed, Google Scholar, and so on, utilizing predetermined keywords and MeSH terms, without temporal constraints. The inclusion criteria encompassed diverse study designs, such as experimental, case–control, and cohort studies, restricted to publications in the English language, while conference abstracts and unpublished sources were excluded. Results: Overexpression of C/EBPβ exacerbates the pathological features of AD, primarily by promoting neuroinflammation and mediating the transcriptional regulation of key molecular pathways, including δ‐secretase, apolipoprotein E4 (APOE4), acidic leucine‐rich nuclear phosphoprotein‐32A (ANP32A), transient receptor potential channel 1 (TRPC1), and Forkhead BoxO (FOXO). Discussion: The correlation between overexpression of C/EBPβ and the pathological development of AD, along with its molecular mechanisms, is evident. Investigating the pathways through which C/EBPβ regulates the development of AD reveals numerous multiple vicious cycle pathways exacerbating the pathological progression of the disease. Furthermore, the exacerbation of pathological progression due to C/EBPβ overexpression and its molecular mechanism is not limited to AD but also extends to other neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and multiple sclerosis (MS). Conclusion: The overexpression of C/EBPβ accelerates the irreversible progression of AD pathophysiology. Additionally, C/EBPβ plays a crucial role in mediating multiple pathways linked to AD pathology, some of which engender vicious cycles, leading to the establishment of feedback mechanisms. To sum up, targeting C/EBPβ could hold promise as a therapeutic strategy not only for AD but also for other degenerative diseases. [ABSTRACT FROM AUTHOR]