Yin Shi

Background: Electroacupuncture has been shown to effectively reduce anti-Müllerian hormone levels and improve follicular development in polycystic ovary syndrome. However, the mechanism of action is yet to be deciphered. Long noncoding RNAs have been shown to play an important role in polycystic ovary syndrome and function as competing endogenous RNAs to regulate target genes. Therefore, the aim of this study was to observe whether the effect of electroacupuncture on anti-Müllerian hormone involves modulation of the long noncoding RNA LOC103691336. Methods: A polycystic ovary syndrome rat model was established and treated with low-frequency electroacupuncture at CV3 and CV4. Estrous cycle, ovarian morphology, and the levels of anti-Müllerian hormone and testosterone in the serum and ovaries were measured. Follicular granulosa cells of rats in each group were collected for in vitro experiments. High-throughput sequencing and bioinformatics methods were applied to analyze anti-Müllerian hormone–related long noncoding RNAs, and LOC103691336 was identified as the long noncoding RNA most closely related to anti-Müllerian hormone. Silencing of LOC103691336 was applied to observe its effect on the expression of anti-Müllerian hormone. Argonaute 2 RNA immunoprecipitation assays and RNA pulldown were used to observe whether LOC103691336 functions as a miR-138-5p sponge to regulate anti-Müllerian hormone. Results: Estrus cycle and ovarian morphology were improved by electroacupuncture. Expression levels of anti-Müllerian hormone and testosterone were significantly reduced in ovarian tissues and peripheral serum ( P < 0.01 and P < 0.05). High-throughput sequencing and bioinformatic analysis showed a close relationship between LOC103691336 and anti-Müllerian hormone. After silencing LOC103691336 expression, LOC103691336 and anti-Müllerian hormone levels were reduced in rat follicular granulosa cells ( P < 0.01). Furthermore, Argonaute 2 RNA immunoprecipitation assay and RNA pulldown results showed that LOC103691336 regulated anti-Müllerian hormone by binding to miR-138-5p. After electroacupuncture, LOC103691336 and anti-Müllerian hormone levels were significantly reduced in follicular granulosa cells ( P < 0.01), whereas miR-138-5p expression levels were significantly increased ( P < 0.01). Conclusion: Our results demonstrated that the effect of electroacupuncture on anti-Müllerian hormone levels may be mediated by reductions in abnormal LOC103691336 expression levels and increased miR-138-5p levels in this polycystic ovary syndrome rat model.

Crohn's disease can progress from non-stricturing, non-penetrating inflammation (B1) to stricturing (B2) or penetrating (B3) complications, yet risk is commonly recognized only after structural damage is established. This narrative review examines clinical, endoscopic, genomic, circulating, stool, tissue, imaging, radiomic, and computational biomarkers relevant to behavioral-progression risk and separates direct B1-to-B2 or source-defined B3 evidence from related prognostic and mechanistic evidence, while distinguishing internal penetrating from perianal fistulizing disease when source reporting permits. Structured searches of PubMed/MEDLINE, Embase, and Web of Science, supplemented by citation tracking, informed the selection of longitudinal human studies, prediction models, and mechanistic studies relevant to candidate feature selection. Ileal involvement, perianal fistulizing disease, persistent inflammatory burden, and endoscopic severity provide reproducible risk enrichment but insufficient individual-level precision. Genomic scores, plasma and stool proteins, tissue transcriptomics, shear-wave elastography, radiomics, and machine-learning models suggest potential value for multimodal risk stratification, but most lack independent external validation, calibration, transportability, and demonstrated incremental value over routinely available clinical variables. Direct prospective evidence is substantially more developed for B2 stricturing progression than for incident internal B3 penetrating progression; internal penetrating disease and perianal fistulizing disease are treated as distinct outcomes. Mechanistic studies suggest divergent fibrostenotic and tissue-destructive programs that provide biological guidance for biomarker selection. No biomarker or multimodal model identified in this review was ready to support routine biomarker-guided treatment escalation. Future studies should use well-characterized B1 baselines, prespecified structural outcomes, and prospective decision-impact testing that quantifies overtreatment.

Background: Guillain–Barré syndrome (GBS) is an immune‐mediated neuropathy that may be influenced by infectious, demographic, and healthcare‐related factors. Although increasing attention has been paid to neurological complications during the COVID‐19 pandemic, the global burden, inequalities, and future trends of GBS remain insufficiently characterized. Methods: This population‐based observational epidemiological study used data from the Global Burden of Disease Study 2021 to assess the burden of GBS across 204 countries and territories from 1990 to 2021. The main outcomes included prevalence, years lived with disability (YLDs), age‐standardized prevalence rate (ASPR), age‐standardized YLD rate (ASYR), and estimated annual percentage change (EAPC). Analyses were stratified by sex, age group, country, region, and socio‐demographic index (SDI). Inequality analysis, decomposition analysis, Joinpoint regression, and Bayesian age‐period‐cohort modeling were further used to assess socioeconomic disparities, driving factors, temporal changes, and future trends. Results: From 1990 to 2021, the global burden of GBS increased substantially. In 2021, the global number of prevalent cases reached 471,850, and the ASPR was 5.91 per 100,000 population. The corresponding number of YLDs was 139,639, with an ASYR of 1.75 per 100,000 population. The burden was lowest among children younger than 5 years and increased progressively with age. Males generally had a higher burden than females, particularly among older adults. Low‐SDI regions experienced disproportionately higher ASPR and ASYR, indicating substantial global inequalities. The increases observed after 2019 temporally coincided with the COVID‐19 pandemic; however, this association should be interpreted cautiously. Decomposition analysis suggested that epidemiological changes, population growth, and population aging collectively contributed to the increasing burden of GBS. Conclusion: The global burden of GBS increased markedly from 1990 to 2021, with substantial regional, sex‐, age‐, and SDI‐related heterogeneity. The post‐2019 increase temporally coincided with the COVID‐19 pandemic, but causal inference should be avoided due to the observational nature of this study. Strengthening neurological surveillance, improving early diagnosis and treatment capacity, and reducing healthcare disparities in low‐SDI regions may help mitigate the future burden of GBS.

Background: PCOS is far more than an ovarian disorder; it is a systemic metabolic crisis affecting 11–13% of women. This review maps its extra-ovarian reach into the liver, heart, muscle, and pancreas. Methods: We analyzed how the "pathophysiological quartet"—insulin resistance, hyperandrogenism, inflammation, and oxidative stress—coordinates systemic damage. Results: PCOS prevalence skyrockets to 28.3% in women with obesity. Key findings include a 51.61% prevalence of MASLD in obese patients and a 2–4 fold increase in cardiovascular and type 2 diabetes risk. These manifestations are rooted in a shared metabolic "soil," creating a vicious cycle of androgen excess and multi-organ dysfunction, including sarcopenia and β-cell exhaustion. Conclusion: Fragmented care is insufficient. The systemic nature of PCOS demands a paradigm shift toward integrated, multidisciplinary management, treating the patient as a metabolic whole.

Objective: The aim of this study was to analyze and compare the differential expression of peptides within the follicular fluid of polycystic ovary syndrome (PCOS) patients versus normal women by using peptidomics techniques. The underlying mechanisms involved in PCOS pathogenesis will be explored, together with screening and identification of potential functional peptides via bioinformatics analysis.Materials and methods: A total of 12 patients who underwent in vitro fertilization and embryo transfer (IVF-ET) at the Reproductive Medicine Center of Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine from 1 September 2022 to 1 November 2022 were included in this study. The follicular fluid of PCOS patients (n = 6) and normal women (n = 6) were collected. The presence and concentration differences of various peptides were detected by the LC-MS/MS method. GO and KEGG analysis were performed on the precursor proteins of the differentially-expressed peptides, and protein network interaction analysis was carried out to identify functionally-relevant peptides among the various peptides.Results: A variety of peptides within the follicular fluid of PCOS versus normal patients were detected by peptidomics techniques. Altogether, 843 upregulated peptides and 236 downregulated peptides were detected (absolute fold change ≥2 and p < 0.05). Of these, 718 (718 = 488 + 230) peptides were only detected in the PCOS group, while 205 (205 = 174 + 31) were only detected in the control group. Gene Ontology enrichment and pathway analysis were performed to characterize peptides through their precursor proteins. We identified 18 peptides from 7 precursor proteins associated with PCOS, and 4 peptide sequences were located in the functional domains of their corresponding precursor proteins.Conclusion: In this study, differences in the follicular development of PCOS versus normal patients were revealed from the polypeptidomics of follicular development, which thus provided new insights for future studies on the pathological mechanisms of PCOS development.

Background: Moxibustion is a potential therapy for inflammatory bowel disease-related depression, but its specific mechanism of action is unclear. This study aimed to investigate the molecular mechanism by which moxibustion alleviates depressive behavior in rats with Crohn’s disease (CD).Methods: The CD rat model was established with 2,4,6-trinitrobenzenesulfonic acid. Treatment with moxibustion was applied to Tianshu (ST25, bilateral), Qihai (CV6), and Baihui (GV20) acupoints, and the effect of moxibustion was compared with that of the combination of moxibustion plus indoleamine-2,3-dioxygenase 1 (IDO1) inhibitor, 1-methyltryptophan (1-MT). The effects of moxibustion and moxibustion plus 1-MT combination on colonic inflammation and depressive behavior (assessed by forced swimming test, sucrose preference test, and open field test) were investigated. The changes in IDO1, TNF-α, and IL-1β in rat colon and hippocampus were assessed by Western blot (WB). Gas chromatography-mass spectrometry, immunofluorescence staining, and WB were applied to detect kynurenine pathway (KP) metabolites, hippocampal neuronal activity, and microglia activation, respectively.Results: Both moxibustion and moxibustion plus 1-MT combination significantly alleviated intestinal inflammation and depressive behavior, downregulated the levels of IDO1 in the colon and hippocampus, and inhibited inflammation-inducing factors IL-1β and TNF-α, as well as the kynurenine/tryptophan (KYN/TRP) ratio of KP metabolites, and upregulated the kynurenic acid (KYNA)/KYN ratio and the KYNA/quinolinic acid (QUIN) ratio in the hippocampus in rats with CD; Hippocampal ionized calcium-binding adaptor molecule-1 (Iba-1), c-fos protein expression, activated microglia, and neuronal activation was also significantly reduced by moxibustion and moxibustion plus 1-MT. The addition of 1-MT did not significantly increase the therapeutic effect of moxibustion.Conclusion: Moxibustion can improve depressive behavior in rats with CD, which may be related to its regulation of KP metabolism in the gut-brain axis and inhibition of hippocampal microglia activation and neuronal activation.

Sirtuin 3 (SIRT3), the nicotinamide adenine dinucleotide (NAD⁺)-dependent deacetylase, acts as a metabolic modulator mainly located in mitochondria via regulating the process of the relevant biochemical processes by targeting crucial mediators. Recently, owing to its dual role in cancer, SIRT3 has attracted extensive attention. Cancer cells have different metabolic patterns from normal cells, and SIRT3-mediated metabolism reprogramming could be critical in the cancer context, which is closely related to the mechanism of metabolism reprogramming, metastasis, and chemoresistance in tumor cells. Therefore, it is crucial to elucidate the relevant pathological mechanisms and take appropriate countermeasures for the progression of clinical strategies to inhibit the development of cancer. In this review, existing available data on the regulation of cancer metabolism reprogramming, metastasis, and chemoresistance progression of SIRT3 are detailed, as well as the status quo of SIRT3 small molecule modulators is updated in the application of cancer therapy, aiming to highlight strategies directly targeting SIRT3-mediated tumor-suppressing and tumor-promoting, and provide new approaches for therapy application. Furthermore, we offer an effective evidence-based basis for the evolvement of potential personalized therapy management strategies for SIRT3 in cancer settings.

Objective To explore whether acupuncture combined with moxibustion could inhibit epithelialmesenchymal transition in Crohn’s disease by affecting the transforming growth factor β 1 (TGF- β 1)/Smad3/Snail pathway. Methods Sixty-three patients with Crohn’s disease were randomly divided into an observation group (31 cases) receiving moxibustion at 43 °C combined with acupuncture, and a control group (32 cases) receiving moxibustion at 37 °C combined with sham acupuncture using a random number table. Patients were treated for 12 weeks. Crohn’s Disease Activity Index (CDAI) was used to evaluate disease activity. Hematoxylin-eosin staining and transmission electron microscopy were utilized to observe the morphological and ultrastructural changes. Immunohistochemistry was used to detect the expression of transforming growth factor β 1 (TGF-β 1), T β R1, T β R2, Smad3, Snail, E-cadherin and fibronectin in intestinal mucosal tissues. Results The decrease of the CDAI score, morphological and ultrastructural changes were more significant in observation group. The expression levels of TGF- β 1, Tβ R2, Smad3, and Snail in the observation group were significantly lower than those before the treatment (PPPP<0.05). Conclusions Moxibustion at 43 °C combined with acupuncture may suppress TGF-β 1/Smad3/Snail pathway-mediated epithelial-mesenchymal transition of intestinal epithelial cells in Crohn’s disease patients by inhibiting the expression levels of TGF-β 1, Tβ R2, Smad3, and Snail. (Registration No. ChiCTR-IIR-16007751)

Objective. To investigate the mechanism of action of herb-partitioned moxibustion on CD from the perspective of autophagy and immunity. Methods. The expression of microtubule-associated protein LC3II and SQSTM1/p62 in the colon tissues was detected by immunohistochemistry. Western blot was used to detect the expression of autophagic and immune-related proteins in the colon, such as LC3II, SQSTM1/p62, Beclin1, ATG16L1, NOD2, IRGM, IL-1β, IL-17, and TNF-β. mRNA levels of immune factors, such as IL-1β, IL-17, and TNF-β, and autophagy signaling molecules, such as PI3KC, AKT1, LKB1, and mTOR, were detected by RT-qPCR. Results. Herb-partitioned moxibustion reduced the protein levels of ATG16L1, NOD2, IRGM, LC3II, and Beclin1 ( ) and both the protein and mRNA levels of IL-1β, IL-17, and TNF-β in CD rats ( or ), and it also increased the expression of SQSTM1/p62 protein ( ). The modulatory effects of herb-partitioned moxibustion on ATG16L1, NOD2, IRGM, LC3II, TNF-β, and IL-17 protein and IL-1β protein and mRNA were better than those of mesalazine ( or ). Herb-partitioned moxibustion also reduced colon PI3KC, AKT1, and LKB1 mRNA expressions in CD rats ( or ) and increased mTOR protein expression ( ). And the modulatory effect of herb-partitioned moxibustion on AKT1 mRNA was better than that of mesalazine ( ). Conclusion. Herb-partitioned moxibustion may inhibit excessively activated autophagy and modulate the expression of immune-related factors by regulating the LKB1-mTOR-PI3KC signal transduction networks, thereby alleviating intestinal inflammation in CD rats.