Global trends and developments in mindfulness interventions for diabetes: a bibliometric study.

BACKGROUND: Diabetes is a metabolic disorder posing a global threat to health. Many scholars are dedicated to developing non-pharmacological therapies, and mindfulness intervention is among the potentially effective approaches. Due to the rapid increase in relevant research in recent years, along with the diverse focus and interventions used in studies, it has become challenging for practitioners to quickly comprehend the key features of this field and the directions worth paying attention to. Bibliometric analysis, in response, can help scholars understand this field and identify points of interest. METHODS: Publications related to mindfulness intervention in diabetes from the establishment of the Web of Science Core Collection (WOSCC) to September 2023 were searched. We employed four bibliometric techniques: General Analysis of Publications, Collaborative Network Analysis, Co-citation Analysis, and Keyword Analysis. The CiteSpace 6.1.R was used to analyze the literature with the strongest citation bursts, while VOSviewer 1.6.13 was used to provide visualizations of publicly available data by analyzing co-citations or co-authorship affiliations. RESULTS: We found a total of 387 articles. The results indicate that research on this topic has been steadily increasing over time. The United States is the top producer of relevant publications, with Tilburg University being the institution that publishes the most articles. The journal "Mindfulness" has the highest publication count. In the collaborative network analysis, the United States emerged as the main hub for global cooperation in this research field, contributing 182 articles with a total of 5872 citations. The journal "Diabetes Care" was frequently cited and played a central role. The keyword analysis revealed that researchers have shown a strong interest in how mindfulness interventions affect the mental health of diabetic individuals. Additionally, there is a focus on studying elderly diabetic groups and exploring how mindfulness interventions impact metabolic diseases. These areas are currently the main research priorities. CONCLUSION: Our findings demonstrate the current trend and hotspots in mindfulness intervention and offer some directions for future research.

Effects of mind-body therapies on schizophrenia: A systematic review and network meta-analysis.

OBJECTIVE: The objective of this meta-analysis is to evaluate and compare the effectiveness of different mind-body therapies in reducing the symptoms of schizophrenia. METHODS: A systematic search was performed using databases such as PubMed, Embase, Cochrane Library, Web of Science, and Scopus. Randomized controlled trials that assessed the effects of mind-body therapies on patients with schizophrenia were included. The search covered the period between the inception of each database and November 17th, 2022. The methodological quality of the trials was assessed using the Cochrane risk of bias tool. A network meta-analysis was conducted to compare the effects of various mind-body therapies, including Yoga, Mindfulness, Tai Chi, Baduanjin, and Yijinjing. RESULTS: The analysis included 22 randomized controlled trials involving a total of 2064 subjects. The network meta-analysis revealed that Yoga and Mindfulness interventions were more effective than other mind-body therapies in reducing the symptoms of schizophrenia. Specifically, Yoga improved PANSS-positive symptom scores (SUCRA: 74.8 %) and PANSS-negative symptom scores (SUCRA: 80.4 %), whereas Mindfulness improved PANSS-positive symptom scores (SUCRA: 85.6 %). CONCLUSION: The findings of this study indicate that Yoga may be a promising intervention for the treatment of schizophrenia. However, the small sample size and the low quality of the included studies have limited the generalizability of our findings Therefore, this study must be understood with caution, and further investigation is warranted when more relevant studies emerge.

Electroacupuncture regulates hepatic cholesterol synthesis by HMGCR deubiquitination in rats.

This experiment was designed to explore the effect and mechanism of electroacupuncture (EA) for hyperlipidemia and hepatic cholesterol synthesis in rats. Liver and adipose tissues were assessed histologically, and body and liver weight, serum and liver lipid levels, expression of mTOR/ubiquitin-specific peptidase 20 (USP20)/recombinant 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR), and phosphorylation of mTOR and USP20 were measured. In vitro deubiquitination assays with liver cytosol were conducted. EA at Fenglong point ameliorated hyperlipidemia and hepatocyte steatosis, and decreased p-USP20, p-mTOR and HMGCR expression in the liver by reducing deubiquitination. Furthermore, EA decreased feeding-induced lipid biosynthesis in the liver. Concomitantly, EA prevented the induction of phosphorylated USP20 and mTOR, and HMGCR expression; and reduced the deubiquitination of HMGCR after re-feeding. This experiment demonstrated that EA can effectively improve hyperlipidemia and reduce hepatic cholesterol synthesis by counteracting the deubiquitination activity of HMGCR in hyperlipidemic rats.

Severe lupus induced by the tumor necrosis factor-alpha inhibitor Anbainuo: a case report.

In rare cases, clinical inhibitors of the pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) can induce symptoms of lupus erythematosus (drug-induced lupus, DIL), but this adverse response usually resolves rapidly upon drug withdrawal. We report the case of a 25-year-old Asian woman with rheumatoid arthritis exhibiting severe prolonged DIL even after the termination of TNF-α inhibitor treatment. The patient had been treated intermittently using Traditional Chinese Medicine for 11 years, but this therapy failed to effectively control her clinical symptoms. Subsequently, methotrexate and hydroxychloroquine were prescribed, but a reduced white blood cell count was detected. Finally, the TNF-α inhibitor Anbainuo was prescribed. However, after 2 months of treatment, the patient exhibited elevated serum creatinine, anti-double-stranded DNA (+++), anti-nuclear antibody (1:1000), and urine protein (+++) accompanied by buccal erythema, hair loss, and hand shaking, consistent with Anbainuo-induced lupus, lupus nephritis, and lupus encephalopathy. Moreover, her serum creatinine level remained high after Anbainuo withdrawal and prolonged steroid and immunosuppressive therapy. Careful and sustained monitoring for adverse reactions to Anbainuo (and other TNF-α inhibitors) is recommended.

Immunostimulatory Potential of MoS2 Nanosheets: Enhancing Dendritic Cell Maturation, Migration and T Cell Elicitation.

BACKGROUND: Due to their extraordinary physical and chemical properties, MoS2 nanosheets (MSNs) are becoming more widely used in nanomedicine. However, their influence on immune systems remains unclear. MATERIALS AND METHODS: Two few-layered MSNs at sizes of 100-250 nm (S-MSNs) and 400-500 nm (L-MSNs) were used in this study. Bone marrow-derived dendritic cells (DCs) were exposed to both MSNs at different doses (0, 8, 16, 32, 64, 128 µg/mL) for 48 h and subjected to analyses of surface marker expression, cytokine secretion, lymphoid homing and in vivo T cell priming. RESULTS: Different-sized MSNs of all doses did not affect the viability of DCs. The expression of CD40, CD80, CD86 and CCR7 was significantly higher on both S-MSN- and L-MSN-treated DCs at a dose of 128 µg/mL. As the dose of MSN increased, the secretion of IL-12p70 remained unchanged, the secretion of IL-1ß decreased, and the production of TNF-α increased. A significant increase in IL-6 was observed in the 128 µg/mL L-MSN-treated DCs. In particular, MSN treatment dramatically improved the ex vivo movement and in vivo homing ability of both the local resident and blood circulating DCs. Furthermore, the cytoskeleton rearrangement regulated by ROS elevation was responsible for the enhanced homing ability of the MSNs. More robust CD4+ and CD8+ T cell proliferation and activation (characterized by high expression of CD107a, CD69 and ICOS) was observed in mice vaccinated with MSN-treated DCs. Importantly, exposure to MSNs did not interrupt LPS-induced DC activation, homing and T cell priming. CONCLUSION: Few-layered MSNs ranging from 100 to 500 nm in size could play an immunostimulatory role in enhancing DC maturation, migration and T cell elicitation, making them a good candidate for vaccine adjuvants. Investigation of this study will not only expand the applications of MSNs and other new transition metal dichalcogenides (TMDCs) but also shed light on the in vivo immune-risk evaluation of MSN-based nanomaterials.

[Electroacupuncture at "Zusanli"(ST36) promotes gastrointestinal motility possibly by suppres-sing excessive autophagy via AMPK/ULK1 signaling in rats with functional dyspepsia].

OBJECTIVE: To explore the effect of electroacupuncture (EA) at "Zusanli" (ST36) on gastrointestinal motility and expression of autophagy marker LC3 and autophagy signaling pathway molecule AMP-activated protein kinase (AMPK) in rats with functional dyspepsia (FD), so as to explore its mechanisms underlying improvement of FD. METHODS: A total of 40 male SD rats were randomly divided into blank control, model, EA, AMPK inhibitor and EA＋AMPK inhibitor groups, with 8 rats in each group. The FD model was established by tail-clip (30 min/time, twice daily) ＋ single day feeding, and gavage of normal saline (2 mL/time, twice a day) for 2 successive weeks. For rats of EA and EA＋AMPK inhibitor groups, EA (4 Hz, 1.0 mA) was applied to bilateral ST36 for 20 min, once daily for 7 successive days. For rats of the AMPK-inhibitor and EA＋AMPK inhibitor groups, Compound C (20 mg/kg) solution was administered by intraperitoneal injection before every EA administration. The gastric residual rate and small intestinal transit rate were calculated based on the weight of stomach and length of ink propelling and total small intestine, respectively. The expression levels of c-kit, microtubule-associated protein 1 light chain 3, Beclin 1, phosphorylated (p)-AMPK and p-unc-51 like autophagy activating kinase 1(ULK1) in the gastric antrum tissue were detected by using Western blot. RESULTS: Compared with the blank control group, the gastric residual rate and the expression levels of LC3-Ⅱ/LC3Ⅰ， Beclin 1, p-AMPK and p-ULK1 proteins were significantly increased, and the small intestinal transit rate and the expression of c-kit protein obviously decreased in the model group (P<0.01). After EA intervention, modeling-induced increase of gastric residual rate and the expression of LC3-Ⅱ/LC3Ⅰ， Beclin 1, p-AMPK and p-ULK1 proteins, and decrease of small intestinal transit rate and expression of c-kit protein were reversed in the EA, AMPK inhibitor and EA＋AMPK inhibitor groups (P<0.05, P<0.01). The therapeutic effect of EA and EA＋AMPK was significantly superior to that of AMPK inhibitor in down-regulating the expression of LC3Ⅱ/LC3Ⅰ， Beclin 1, p-AMPK and p-ULK1 proteins and in up-regulating the expression of c-kit protein (P<0.05, P<0.01). No significant differences were found among the EA, AMPK inhibitor and EA＋AMPK inhibitor groups in lowering gastric residual rate and elevating the small intestinal transit rate (P>0.05). CONCLUSION: EA at ST36 can promote gastrointestinal motility in FD rats, which is possibly mediated by inhibiting excessive autophagy of interstitial cells of Cajal via down-regulating AMPK/ULK1 signaling.

Isodunnianol alleviates doxorubicin-induced myocardial injury by activating protective autophagy.

Recurrent cardiotoxicity limits the clinical application of doxorubicin (DOX); however the detailed molecular mechanism of DOX cardiotoxicity remains unclear. In the current study, we found that a natural product extracted from Illicium verum, isodunnianol (IDN), mitigates DOX-induced cardiotoxicity by regulating autophagy and apoptosis both in vitro and in vivo. DOX suppressed protective autophagy and induced apoptosis in H9C2 cardiac myoblasts. Additionally, IDN demonstrated up-regulated autophagy and reduced apoptosis through the activation of the AMPK-ULK1 pathway. In addition, the beneficial effects of IDN on DOX which induced myocardial injury were dependent on AMPK and ULK1 phosphorylation. Similar results were also observed in a DOX-induced cardiotoxicity rat model. The combination of IDN and DOX resulted in decreased apoptosis and inflammatory myocardial fibrosis compared to the DOX mono-treatment group. In summary, our findings provide novel insights into the prevention of DOX-related toxicity by isodunnianol, a food source natural product, warranting further investigation.

Electroacupuncture inhibits NLRP3 inflammasome activation through CB2 receptors in inflammatory pain.

The therapeutic effect of electroacupuncture (EA) on inflammatory pain has been well recognized clinically. The inflammasome promotes the maturation of the inflammatory cytokines, and EA can stimulate cannabinoid CB2 receptors in inflamed tissues. In this study we investigated whether EA inhibits NLRP3 inflammasome activation through CB2 receptors and thus relieving inflammatory pain. Assay of Caspase-1 activity and western blotting revealed that complete Freund's adjuvant (CFA) injection activated the NLRP3 inflammasome in the skin tissue in rats, which was attenuated by EA treatment. Immunofluorescence labeling showed that NLRP3 inflammasome elicited by CFA in the skin macrophages were decreased by EA. Nociceptive behavioral tests demonstrated that in CB2 receptor knockout mice, the EA effects on NLRP3 inflammasomes were largely attenuated. In addition, in vitro studies in a macrophage cell line showed that CB2 receptor stimulation inhibited the NLRP3 inflammasome activation. Thus, our results suggest a novel signaling pathway through which CB2 receptors are involved in the analgesic effect of EA on inflammatory pain. Stimulation of CB2 receptors inhibits NLRP3 inflammasome activation in inflamed skin tissues. These results suggest that EA reduces the inflammatory pain by inhibiting the activation of NLRP3 inflammasome through CB2 receptors. Our findings provide novel information about the mechanisms through which EA and CB2 receptor activation reduce inflammatory pain.

[Manual acupuncture versus electroacupuncture for menopausal syndrome:a randomized controlled trial].

OBJECTIVE: To compare the clinical therapeutic effects and safety on menopausal symptoms between manual acupuncture (MA) and electroacupuncture (EA). METHODS: Fifty patients were randomized into an MA group (25 cases) and an EA group (25 cases). In the MA group, the regular needling technique and pseudo-EA were used at Guanyuan (CV 4), Zigong (EX-CA 1), Tianshu (ST 25) and Sanyinjiao (SP 6). In the EA group, the acupoints were the same as the MA group and stimulated with EA and pseudo-MA (no manipulation applied in treatment), with disperse-dense wave, 10 Hz/50 Hz, 0.5 to 1.0 mA. In the two groups, the needles were retained for 30 min. The treatment was given once every two days, three times a week, totally for 8 consecutive weeks. The results of the menopause rating scale (MRS), the menopause-specific quality of life (MENQOL), the self-rating anxiety scale (SAS) and the self-rating depression scale (SDS), follicle stimulating hormone (FSH), luteinizing hormone (LH) and estradiol (E2) as well as adverse reactions were evaluated before treatment, in 4 and 8 weeks of treatment separately. RESULTS: Compared with those before treatment, the scores of MRS, MENQOL, SAS and SDS were all reduced in the 4 and 8 weeks of treatment in the two groups (all P<0.05). The results in 8 weeks of treatment were lower than those in 4 weeks of treatment in the two groups (all P<0.05). The differen-ces were not significant statistically between the two groups (all P>0.05). Compared with those before treatment, the levels of FSH and LH reduced and E2 increased after treatment in the two groups, without significant differences (all P>0.05). The differences were not significant statistically between the two groups (all P>0.05). The severe adverse reactions were not found in the treatment of the two groups. CONCLUSIONS: Both manual acupuncture and electroacupuncture relieve the symptoms of depression and anxiety in menopausal syndrome,improve the living quality and do not induce apparent changes in serological sex hormones in the patients.

Selective Production of Toluene from Biomass-Derived Isoprene and Acrolein.

Toluene is a basic chemical that is currently produced from petroleum resources. In this paper, we report a new route for the effective synthesis of toluene from isoprene and acrolein, two reactants readily available from biomass, through a simple two-step reaction. The process includes Diels-Alder cycloaddition of isoprene and acrolein in a Zn-containing ionic liquid at room temperature to produce methylcyclohex-3-enecarbaldehydes (MCHCAs) as intermediates, followed by M (M=Pt, Pd, Rh)/Al2 O3 -catalyzed consecutive dehydrogenation-decarbonylation of the MCHCAs at 573 K to generate toluene with an overall yield up to 90.7 %. Model reactions indicated that a synergistic inductive effect of the C=C double bond and the aldehyde group in MCHCA plays a key role in initiating the consecutive dehydrogenation-decarbonylation, and that methyl benzaldehydes are the key intermediates in the gas-phase transformation of MCHCAs. Microcalorimetric adsorption of CO on different catalysts showed that decarbonylation of the substrate occurs more likely on the strong adsorption sites. To the best of our knowledge, it is the first report of Pt/Al2 O3 -catalyzed consecutive dehydrogenation-decarbonylation of a given compound in one reactor. This work provides a highly efficient and environmental friendly route to toluene by utilizing two compounds that can be prepared from biomass.

Long-Term Cognitive Improvement After Benfotiamine Administration in Patients with Alzheimer's Disease.

To date, we still lack disease-modifying therapies for Alzheimer's disease (AD). Here, we report that long-term administration of benfotiamine improved the cognitive ability of patients with AD. Five patients with mild to moderate AD received oral benfotiamine (300 mg daily) over 18 months. All patients were examined by positron emission tomography with Pittsburgh compound B (PiB-PET) and exhibited positive imaging with ß-amyloid deposition, and three received PiB-PET imaging at follow-up. The five patients exhibited cognitive improvement as assayed by the Mini-Mental Status Examination (MMSE) with an average increase of 3.2 points at month 18 of benfotiamine administration. The three patients who received follow-up PiB-PET had a 36.7% increase in the average standardized uptake value ratio in the brain compared with that in the first scan. Importantly, the MMSE scores of these three had an average increase of 3 points during the same period. Benfotiamine significantly improved the cognitive abilities of mild to moderate AD patients independently of brain amyloid accumulation. Our study provides new insight to the development of disease-modifying therapy.

[Anti-inflammatory and analgesia effects of electroacupuncture device of point injection on rats of inflammatory pain].

OBJECTIVE: To explore the anti-inflammatory and analgesia mechanism of electroacupuncture (EA) device of point injection (PI) on rats of inflammatory pain. METHODS: 48 Sprague Dawley (SD) rats were randomly assigned into a control group, a model group, an EA+PI group, an EA device of PI (EAPI) group, an EA group and a PI group, eight rats in each one. The rats in the control group were subcutaneously injected with 50 µL of liquid paraffin oil solvent into the dorsum of left hindpaw, while rats in the remaining groups were treated with 50 µL of complete freund's adjuvant (CFA) at identical location to induce the model of inflammatory pain. After model establishment, the rats in the EA+PI group, EAPI group, EA group and PI group were treated with EA+PI,EA device of PI, EA and PI, respectively, once every other day (the 2nd day, 4th day and 6th day). Each treatment was given for 30 min. The mechanical withdrawal threshold, thermal withdrawal threshold and foot swelling before and 1 d to 6 d after model establishment were observed; the western blotting method was applied to measure IL-1ß expression in inflammatory tissue of skin. RESULTS: After model establishment, compared with the control group, the mechanical withdrawal threshold and thermal withdrawal threshold were reduced (all P<0.05) and the foot swelling was increased in the rest groups (all P<0.05). After treatment, the mechanical withdrawal threshold and thermal withdrawal threshold in the EAPI group were significantly increased compared with those in the EA+PI group, EA group and PI group (all P<0.05), but the foot swelling was reduced (all P<0.05). The IL-1ß expression in the model group was higher than that in the control group (P<0.05); after treatment, the IL-1ß expression in the EAPI group was lower than that in the model group, EA group and PI group (all P<0.05), but no significantly different from that in the EA+PI group (P>0.05). CONCLUSIONS: The efficacy of EA device of PI on inflammatory pain is superior to EA combined with PI, EA alone and PI alone, which is suitable for further popularization and application.

Exposure to pyrithiamine increases ß-amyloid accumulation, Tau hyperphosphorylation, and glycogen synthase kinase-3 activity in the brain.

Decreased thiamine-dependent enzyme activity and/or thiamine deficiency (TD) have been linked to Alzheimer's disease (AD). In this study, we administered pyrithiamine, an anti-thiamine compound, to both APP/PS1 transgenic mice and wild-type littermate control mice; alternatively, we induced TD by thiamine-depleted diet. Pyrithiamine treatment and diet-induced TD impaired the memory of wild-type mice, but had little effect on APP/PS1 mice. Pathophysiologically, pyrithiamine treatment and diet-induced TD aggravated ß-amyloid accumulation in the brain. This was demonstrated by increased ß-amyloid in the brains of wild-type mice using ELISA and by the number of amyloid plaques in the brains of APP/PS1 transgenic mice using immunochemical staining. Also, enhanced numbers of phosphorylated Tau-positive cells were observed in both APP/PS1 transgenic and wild-type mice. Furthermore, pyrithiamine decreased the phosphorylation rates of glycogen synthase kinase (GSK)-3ß and raised its enzymatic activity, but had little influence on GSK-3α. Diet-induced TD reduced the phosphorylated rates and increased the activities of GSK-3, GSK-3α, and GSK-3ß. These results suggest that when sufficient thiamine supplement is administered, pyrithiamine can cause AD-like pathological alterations similar to that of diet-induced TD.