Bio-Inspired Superhydrophilic Self-Assembled Coronavirus-Like Pt-WC/CNT for Hydrogen Evolution Reaction.

This study presents a novel approach to enhance the catalytic activity of composite materials by promoting active surface exposure and improving hydrogen transfer performance. Through a self-assembly route involving tailored gas-solid and galvanic replacement reactions, Pt-WC/CNT catalysts with superhydrophilicity and coronavirus-like structure are synthesized. These unique structural features contribute to a remarkable enhancement in the electrocatalytic performance of the hydrogen evolution reaction (HER). Notably, the Pt-WC/CNT catalyst exhibits an outstanding intrinsic activity and efficient bubble transfer properties, leading to a high turnover frequency of 34.97 H2·s-1 at an overpotential of 100 mV. This value is 4.8 times higher than that achieved by commercial Pt/C catalysts (7.30 H2·s-1), establishing Pt-WC/CNT as one of the most active catalysts reported to date. Moreover, the combination of gas-solid and galvanic replacement reactions in the synthesis process offers a scalable route for the production of Pt-loading controllable composite catalysts, thus challenging the dominance of commercial Pt/C catalysts.

XCR1+ conventional dendritic cell-induced CD4+ T helper 1 cell activation exacerbates cardiac remodeling after ischemic myocardial injury.

Cardiac remodeling has no established therapies targeting inflammation. CD4+ T-cell subsets have been reported to play significant roles in healing process after ischemic myocardial injury, but their detailed mechanisms of activation remain unknown. To explore immune reactions during cardiac remodeling, we applied a non-surgical model of coronary heart disease (CHD) induced by a high-fat diet (HFD-CHD) in SR-BI-/-/ApoeR61h/h mice. Flow cytometry analyses throughout the period of progressive cardiac dysfunction revealed that CD4+ T Helper 1 (Th1) cells were predominantly activated in T-cell subsets. Probucol was reported to attenuate cardiac dysfunction after coronary artery ligation model (ligation-MI) in rats. To determine whether probucol suppress cardiac remodeling after HFD-CHD, we treated SR-BI-/-/ApoeR61h/h mice with probucol. We found treatment with probucol in HFD-CHD mice reduced cardiac dysfunction, with attenuated activation of Th1 cells. RNA-seq analyses revealed that probucol suppressed the expression of CXCR3, a Th1-related chemokine receptor, in the heart. XCR1+ cDC1 cells, which highly expresses the CXCR3 ligands CXCL9 and CXCL10, were predominantly activated after HFD-CHD. XCR1+ cDC1 lineage skewing of pre-DC progenitors was observed in bone marrow, with subsequent systemic expansion of XCR1+ cDC1 cells after HFD-CHD. Activation of CXCR3+ Th1 cell and XCR1+ cDC1 cells was also observed in ligation-MI. Notably, post-MI depletion of XCR1+ cDC1 cells suppressed CXCR3+ Th1 cell activation and prevented cardiac dysfunction. In patient autopsy samples, CXCR3+ Th1 and XCR1+ cDC1 cells infiltrated the infarcted area. In this study, we identified a critical role of XCR1+ cDC1-activated CXCR3+ Th1 cells in ischemic cardiac remodeling.

A Dietary Oxysterol, 7-Ketocholesterol, Exacerbates Imiquimod-Induced Psoriasis-like Dermatitis in Steatohepatitic Mice.

Patients with psoriasis are at a higher risk of developing nonalcoholic fatty liver disease. We previously identified an oxidized derivative of cholesterol, 7-ketocholesterol (7KC), in diet-induced steatohepatitic mice. Here, we investigated whether 7KC exacerbates psoriasis-like dermatitis by accelerating steatohepatitis in mice. A high-fat/high-cholesterol/high-sucrose/bile salt diet (nonalcoholic steatohepatitis (NASH) diet) with or without 0.0125% 7KC was fed to C57BL/6 mice (7KC or control group) for three weeks to induce steatohepatitis. A 5% imiquimod cream was then applied to the ears and dorsal skin for four days to induce psoriasis-like dermatitis. Hepatic lipid accumulation and inflammatory cell infiltration were exacerbated in the 7KC group compared with the control group after three weeks. Serum tumor necrosis factor-α (TNF-α) levels were also elevated in the 7KC group (108.5 ± 9.8 vs. 83.1 ± 13.1 pg/mL, p < 0.005). Imiquimod cream increased the psoriasis area severity index (PASI) score in mice in the 7KC group (9.14 ± 0.75 vs. 5.17 ± 1.17, p < 0.0001). Additionally, Tnfa, Il23a, Il17a, and Il22 mRNA levels in the dorsal lesion were significantly upregulated. Finally, Th17 cell differentiation and the TNF signaling pathway were enhanced in the dorsal lesions and liver of mice in the 7KC group. These data suggest that steatohepatitis and psoriasis are linked by a potent, diet-related factor.

The Correlation of Family Resilience with Sleep Quality and Depression of Parents of Children with Epilepsy.

PURPOSE: The present study aims to investigate the correlation between family resilience, sleep quality, and depression in parents of children with epilepsy. DESIGN AND METHODS: The parents of 157 children with epilepsy were assessed using the shortened Chinese version of the Family Resilience Assessment Scale (FRAS-SC) to measure the resilience level of families of children with epilepsy. The Pittsburgh Sleep Quality Index (PSQI) was used to determine the sleep quality of the subjects. The Self-Rating Depression Scale (SDS), a self-rating scale for evaluating depression, was used. RESULTS: The FRAS-SC total score was 97.9 ± 9.0. The PSQI total score was 6.41 ± 3.79, and the detection rate of sleep disorders was 37.6%. The SDS total score was 51.63 ± 10.73, and the detection rate of moderate-severe depressive symptoms was 21.6%. The FRAS-SC total score and all items (except USR) were negatively correlated with the PSQI total score (P < .05). The FRAS-SC total score and all items were significantly and negatively correlated with the SDS total score (P < .01). The degree of explanation of family resilience for sleep quality and depression was 3.5% and 14.9%, respectively. CONCLUSIONS: The higher the level of family resilience, the better sleep quality and the less depression the parents of children with epilepsy will get. PRACTICAL IMPLICATIONS: Relevant intervention measures based on family resilience will help to improve the sleep quality of parents of children with epilepsy and alleviate depression. And then improve the family's ability to care for children with epilepsy.

Progranulin deficiency leads to enhanced age-related cardiac hypertrophy through complement C1q-induced ß-catenin activation.

AIMS: Age-related cardiac hypertrophy and subsequent heart failure are predicted to become increasingly serious problems in aging populations. Progranulin (PGRN) deficiency is known to be associated with accelerated aging in the brain. We aimed to evaluate the effects of PGRN deficiency on cardiac aging, including left ventricular hypertrophy. METHODS AND RESULTS: Echocardiography was performed on wild-type (WT) and PGRN-knockout (KO) mice every 3 months from 3 to 18 months of age. Compared to that of WT mice, PGRN KO mice exhibited age-dependent cardiac hypertrophy and cardiac dysfunction at 18 months. Morphological analyses showed that the heart weight to tibia length ratio and cross-sectional area of cardiomyocytes at 18 months were significantly increased in PGRN KO mice relative to those in WT mice. Furthermore, accumulation of lipofuscin and increases in senescence markers were observed in the hearts of PGRN KO mice, suggesting that PGRN deficiency led to enhanced aging of the heart. Enhanced complement C1q (C1q) and activated ß-catenin protein expression levels were also observed in the hearts of aged PGRN KO mice. Treatment of PGRN-deficient cardiomyocytes with C1q caused ß-catenin activation and cardiac hypertrophy. Blocking C1q-induced ß-catenin activation in PGRN-depleted cardiomyocytes attenuated hypertrophic changes. Finally, we showed that C1 inhibitor treatment reduced cardiac hypertrophy and dysfunction in old KO mice, possibly by reducing ß-catenin activation. These results suggest that C1q is a crucial regulator of cardiac hypertrophy induced by PGRN ablation. CONCLUSION: The present study demonstrates that PGRN deficiency enhances age-related cardiac hypertrophy via C1q-induced ß-catenin activation. PGRN is a potential therapeutic target to prevent cardiac hypertrophy and dysfunction.

Phosphoglycerate dehydrogenase promotes proliferation and bortezomib resistance through increasing reduced glutathione synthesis in multiple myeloma.

The serine synthesis pathway (SSP) is active in multiple cancers. Previous study has shown that bortezomib (BTZ) resistance is associated with an increase in the SSP in multiple myeloma (MM) cells; however, the underlying mechanisms of SSP-induced BTZ resistance remain unclear. In this study, we found that phosphoglycerate dehydrogenase (PHGDH), the first rate-limiting enzyme in the SSP, was significantly elevated in CD138+ cells derived from patients with relapsed MM. Moreover, high PHGDH conferred inferior survival in MM. We also found that overexpression of PHDGH in MM cells led to increased cell growth, tumour formation, and resistance to BTZ in vitro and in vivo, while inhibition of PHGDH by short hairpin RNA or NCT-503, a specific inhibitor of PHGDH, inhibited cell growth and BTZ resistance in MM cells. Subsequent mechanistic studies demonstrated PHGDH decreased reactive oxygen species (ROS) through increasing reduced glutathione (GSH) synthesis, thereby promoting cell growth and BTZ resistance in MM cells. Furthermore, adding GSH to PHGDH silenced MM cells reversed S phase arrest and BTZ-induced cell death. These findings support a mechanism in which PHGDH promotes proliferation and BTZ resistance through increasing GSH synthesis in MM cells. Therefore, targeting PHGDH is a promising strategy for MM therapy.

Protease-activated receptor 2 deficiency in hematopoietic lineage protects against myocardial infarction through attenuated inflammatory response and fibrosis.

Ischaemic heart disease is one of the leading causes of death. Protease-activated receptor 2 (PAR2) is widely expressed within the cardiovascular system and is known to mediate inflammatory processes in various immunocytes, such as macrophages, mastocytes and neutrophils. Here, we investigated whether activating macrophage PAR2 modulates cardiac remodelling in a murine model of myocardial infarction. Myocardial infarction was produced by the permanent ligation of the left anterior descending coronary artery (LAD) in C57BL/6J background wild-type (WT) mice transplanted with bone marrow from WT or PAR2 knockout (PAR2 KO) mice. Hematopoietic deficiency of PAR2 had improvement of left ventricular systolic dysfunction and dilatation and decreased fibrosis deposition in remote zone at 1 week after LAD ligation. Inactivation of PAR2 also led to less recruitment of macrophages in myocardium, which was accompanied by decreased expression of pro-inflammatory cytokines. Furthermore, cultured cardiac fibroblasts (CFs) were activated and showed a fibrotic phenotype after being co-cultured in medium containing PAR2-activating macrophage, which enhances interferon-beta (INF-ß) expression. The beneficial effects of macrophages with INF-ß neutralisation or PAR2-deletion ameliorates the JAK/STAT3 pathway in CFs, which might be attributed to CF activation. These data suggest that macrophage-derived IFN-ß plays a crucial role in adverse cardiac remodelling after myocardial infarction, at least in part, through a PAR2-dependent mechanism.

High COX-2 expression in cancer-associated fibiroblasts contributes to poor survival and promotes migration and invasiveness in nasopharyngeal carcinoma.

Nasopharyngeal carcinoma (NPC) has the highest rate of metastasis among head and neck cancers, and distant metastasis is the major reason for treatment failure. We have previously shown that high cyclooxygenase-2 (COX-2) expression is associated with a poor prognosis of patients with NPC and inhibits chemotherapy-induced senescence in NPC cells. In this study, we found that COX-2 was upregulated in cancer-associated fibroblasts (CAFs) derived from NPC by RNA-Seq. Furthermore, elevated COX-2 expression in CAF was detected in NPC patients with poor survival and distant metastasis by using immunohistochemistry. Then, we identified that COX-2 is highly expressed in CAF at the distant metastasis site in seven paired NPC patients. High expression of COX-2 and secretion of prostaglandin E2, a major product catalyzed by COX-2 in fibroblasts, promotes migration and invasiveness of NPC cells in vitro. On the contrary, inhibition of COX-2 has the opposite effect in vitro as well as in the COX-2-/- mouse with the lung metastasis model in vivo. Mechanistically, we discovered that COX-2 elevates tumor necrosis factor-α expression in CAF to promote NPC cell migration and invasiveness. Overall, our results identified a novel target in CAF promoting NPC metastasis. Our findings suggested that high expression of COX-2 in CAF may serve as a new prognostic indicator for NPC metastasis and provide the possibility of targeting CAF for treating advanced NPC.

High NEK2 confers to poor prognosis and contributes to cisplatin-based chemotherapy resistance in nasopharyngeal carcinoma.

Nasopharyngeal carcinoma (NPC) is a common malignant tumor in southern China and Southeast Asia, but the molecular mechanism of its pathogenesis is poorly understood. Our previous work demonstrated that NEK2 is overexpressed in multiple cancers. However, how NEK2 involves in NPC development remains to be elucidated. In this study, we firstly identified NEK2, located at +1q32-q33, a late event in NPC pathogenesis, overexpressed in the stage III-IV and paired sequential recurrent patients with NPC by immunohistochemistry. Furthermore, Kaplan-Meier analysis indicated high NEK2 conferred an inferior overall survival in NPC. In addition, cisplatin experiments with cell counting kit-8, colony formation, and a xenograft mice model of NPC demonstrated that NEK2 contributed to proliferation and cisplatin resistance in vitro and in vivo. On the contrary, downregulation of NEK2 by short hairpin RNA inhibited NPC cell growth and increased the sensitivity of cisplatin treatment in vitro. Thus, increased expression of NEK2 protein could not be predicted for poor survival but used as a novel biomarker for recurrence of NPC. Targeting NEK2 has the potential to eradicate the cisplatin-based chemotherapy resistant NPC cells.

Pressure Overload Impairs Cardiac Function in Long-Chain Fatty Acid Transporter CD36-Knockout Mice.

CD36 is one of the important transporters of long-chain fatty acids (LCFAs) in the myocardium. We previously reported that CD36-deficient patients demonstrate a marked reduction of myocardial uptake of LCFA, while myocardial glucose uptake shows a compensatory increase, and are often accompanied by cardiomyopathy. However, the molecular mechanisms and functional role of CD36 in the myocardium remain unknown.The current study aimed to explore the pathophysiological role of CD36 in the heart. Methods: Using wild type (WT) and knockout (KO) mice, we generated pressure overload by transverse aortic constriction (TAC) and analyzed cardiac functions by echocardiography. To assess cardiac hypertrophy and fibrosis, histological and molecular analyses and measurement of ATP concentration in mouse hearts were performed.By applying TAC, the survival rate was significantly lower in KO than that in WT mice. After TAC, KO mice showed significantly higher heart weight-to-tibial length ratio and larger cross-sectional area of cardiomyocytes than those of WT. Although left ventricular (LV) wall thickness in the KO mice was similar to that in the WT mice, the KO mice showed a significant enlargement of LV cavity and reduced LV fractional shortening compared to the WT mice with TAC. A tendency for decreased myocardial ATP concentration was observed in the KO mice compared to the WT mice after TAC operation.These data suggest that the LCFA transporter CD36 is required for the maintenance of energy provision, systolic function, and myocardial structure.

Short-term effects of nanoscale Zero-Valent Iron (nZVI) and hydraulic shock during high-rate anammox wastewater treatment.

The stability and resilience of an anaerobic ammonium oxidation (anammox) system under transient nanoscale Zero-Valent Iron (nZVI) (50, 75 and 100 mg L-1), hydraulic shock (2-fold increase in flow rate) and their combination were studied in an up-flow anaerobic sludge blanket reactor. The response to the shock loads can be divided into three phases i.e. shock, inertial and recovery periods. The effects of the shock loads were directly proportional to the shock intensity. The effluent quality was gradually deteriorated after exposure to high nZVI level (100 mg L-1) for 2 h. The higher effluent sensitivity index and response caused by unit intensity of shock was observed under hydraulic and combined shocks. Notably, the specific anammox activity and the content of heme c were considerably reduced during the shock phase and the maximum loss rates were about 30.5% and 24.8%, respectively. Nevertheless, the extracellular polymeric substance amount in the shock phase was enhanced in varying degrees and variation tendency was disparate at all the tested shock loads. These results suggested that robustness of the anammox system was dependent on the magnitude shocks applied and the reactor resistance can be improved by reducing hydraulic retention time with the increase of nZVI concentration under these circumstances.

[Influencing factors for needlestick injuries in student nurses].

OBJECTIVE: To investigate the needlestick injuries in student nurses during nine months of in-ternship in our hospital, and reveal the high-risk periods, risk procedures, and influencing factors for needlestick injuries, and explore the prevention approaches. METHODS: Three hundred and fifty student nurses who interned at our hospital from April to December 2014 and from July 2014 to March 2015 were surveyed using self-de-signed questionnaires. Three hundred and forty questionnaires were recovered and 334 out of them were valid. Data were collected and questionnaires were analyzed. RESULTS: The incidence of needlestick injuries was 60.8%; the incidence of needlestick injuries was substantially higher at the early stage than at the late stage of the internship, and higher in the day shift than in the night shift. Moreover, the incidence of needlestick injuries was the highest during the removal of a syringe or infusion needle, accounting for 24.3% of the total incidence. Some other significant factors for needlestick injuries in student nurses included education level, reports on oc-cupational exposure, constant update of nursing knowledge, regular hematological examination, and relevant training experiences. According to 61.7% of student nurses, clinical operations were affected due to underlying concern about needlestick injuries. CONCLUSION: More attention should be paid to high incidence of needlestick injuries in student nurses, especially at the early stage of their internship. To reduce the incidence of needlestick injuries, education on occupational protection should be given to student nurses in advance, and the pre-job training should be enhanced.

Active anaerobic methane oxidation in the groundwater table fluctuation zone of rice paddies.

Rice paddies are globally important sources of methane emissions and also active regions for methane consumption. However, the impact of fluctuating groundwater levels on methane cycling has received limited attention. In this study, we delved into the activity and microbial mechanisms underlying anaerobic oxidation of methane (AOM) in paddy fields. A comprehensive approach was employed, including 13C stable isotope assays, inhibition experiments, real-time quantitative reverse transcription PCR, metagenomic sequencing, and binning technology. Geochemical profiles revealed the abundant coexistence of both methane and electron acceptors in the groundwater table fluctuation (GTF) zone, at a depth of 40-60 cm. Notably, the GTF zone exhibited the highest rate of AOM, potentially linked to the reduction of iron oxides and nitrate. Within this zone, Candidatus Methanoperedens (belonging to the ANME-2d group) dominated the Archaea population, accounting for a remarkable 85.4 %. Furthermore, our results from inhibition experiments, RT-qPCR, and metagenome-assembled genome (MAG) analysis highlighted the active role of Ca. Methanoperedens GTF50 in the GTF zone. This microorganism could independently mediate AOM process through the intriguing "reverse methanogenesis" pathway. Considering the similarity in geochemical conditions across different paddy fields, it is likely that Ca. Methanoperedens-mediated AOM is prevalent in the GTF zones.

Targeting gut microbial nitrogen recycling and cellular uptake of ammonium to improve bortezomib resistance in multiple myeloma.

The gut microbiome has been found to play a crucial role in the treatment of multiple myeloma (MM), which is still considered incurable due to drug resistance. In previous studies, we demonstrated that intestinal nitrogen-recycling bacteria are enriched in patients with MM. However, their role in MM relapse remains unclear. This study highlights the specific enrichment of Citrobacter freundii (C. freundii) in patients with relapsed MM. Through fecal microbial transplantation experiments, we demonstrate that C. freundii plays a critical role in inducing drug resistance in MM by increasing levels of circulating ammonium. The ammonium enters MM cells through the transmembrane channel protein SLC12A2, promoting chromosomal instability and drug resistance by stabilizing the NEK2 protein. We show that furosemide sodium, a loop diuretic, downregulates SLC12A2, thereby inhibiting ammonium uptake by MM cells and improving progression-free survival and curative effect scores. These findings provide new therapeutic targets and strategies for the intervention of MM progression and drug resistance.

Intestinal Microbes and Hematological Malignancies.

Hematological malignancies are diverse, with high malignancy characteristics, poor prognoses, and high mortality rates. The development of hematological malignancies is driven by genetic factors, tumor microenvironment factors, or metabolic factors; however, even when considering all of these factors, one still cannot fully estimate the risk of hematological malignancies. Several recent studies have demonstrated an intimate connection between intestinal microbes and the progression of hematological malignancies, and gut microbes play a primary role in the initiation and progression of hematological tumors through direct and indirect mechanisms. Thus, we summarize the correlation between intestinal microbes and hematological malignancies' onset, progression, and therapeutic effect in order to better understand how intestinal microbes affect their initiation and progression, especially in leukemia, lymphoma, and multiple myeloma, which may provide potential therapeutic targets for improving the survival of patients with hematological malignancies.

Long-term effects of soluble and insoluble ferric irons on anaerobic oxidation of methane in paddy soil.

Iron-dependent anaerobic oxidation of methane (Fe-AOM) is an important process to reduce methane emissions into the atmosphere. It is well known that iron bioavailability largely influences microbial iron reduction, but the long-term effects of different ferric irons on soil Fe-AOM remain unknown. In this work, paddy soil in the ferruginous zone was collected and inoculated with insoluble ferrihydrite and soluble EDTA-Fe(III) for 420 days. Stable isotope experiments, activity inhibition tests, and molecular biological techniques were performed to reveal the activity, microbial community, and possible mechanism of paddy soil Fe-AOM. The results showed that ferrihydrite was a better electron acceptor for long-term Fe-AOM cultivation. Although EDTA-Fe(III) is highly bioavailable and could stimulate Fe-AOM activity for a short time, it restricted the activity increase in the long term. The abundances of archaea, iron-reducing bacteria (IRB), and gene mcrA largely increased after cultivation, indicating the important roles of mcrA-carrying archaea and IRB. Remarkably, archaeal communities were similar, but bacteria were totally different with different ferric irons. The results of the microbial community and activity inhibition suggested that Fe-AOM was performed likely by the cooperation between archaea (Methanomassiliicoccaceae or pGrfC26) and IRB in the cultures.

Enhanced anaerobic oxidation of methane with the coexistence of iron oxides and sulfate fertilizer in paddy soil.

Iron oxides and sulfate are usually abundant in paddy soil, but their role in reducing methane emissions is little known. In this work, paddy soil was anaerobically cultivated with ferrihydrite and sulfate for 380 days. An activity assay, inhibition experiment, and microbial analysis were conducted to evaluate the microbial activity, possible pathways, and community structure, respectively. The results showed that anaerobic oxidation of methane (AOM) was active in the paddy soil. The AOM activity was much higher with ferrihydrite than sulfate, and an extra 10% of AOM activity was stimulated when ferrihydrite and sulfate coexisted. The microbial community was highly similar to the duplicates but totally different with different electron acceptors. The microbial abundance and diversity decreased due to the oligotrophic condition, but mcrA-carrying archaea increased 2-3 times after 380 days. Both the microbial community and the inhibition experiment implied that there was an intersection between iron and sulfur cycles. A "cryptic sulfur cycle" might link the two cycles, in which sulfate was quickly regenerated by iron oxides, and it might contribute 33% of AOM in the tested paddy soil. Complex links between methane, iron, and sulfur geochemical cycles occur in paddy soil, which may be significant in reducing methane emissions from rice fields.

Modulating Dominant Facets of Pt through Multistep Selective Anchored on WC for Enhanced Hydrogen Evolution Catalysis.

Facilitating the exposure of the active crystal facets on the surfaces of composite catalysts is a representative route to promote catalytic activity. Based on a tailored galvanic replacement reaction, herein, a self-assembly route is reported to prepare Pt-WC/CNT with Pt (200) preferential orientation and well-dispersed structure, which are capable of substantially boosting electrocatalysis in hydrogen evolution reaction (HER). Formation mechanism reveals that the (200)-dominated Pt-based catalysts form in galvanic replacement reaction through selective anchored on WC, and the multistep galvanic replacement process plays a critical role to realize the Pt (200)-dominated growth in higher Pt loading catalyst. These unique structural features endow the Pt-WC/CNT with a high turnover frequency of 94.18 H2·s-1 at 100 mV overpotential, 7-fold higher than that of commercial Pt/C (13.55 H2·s-1), ranking it among the most active catalysts. In addition, this method, which combines with gas-solid reaction and galvanic replacement reaction, paves the way to scalable synthesis as Pt facets-controllable composite catalysts to challenge commercial Pt/C.

Nano-Silicon@Exfoliated Graphite/Pyrolytic Polyaniline Composite of a High-Performance Cathode for Lithium Storage.

In this paper, a Si@EG composite was prepared by liquid phase mixing and the elevated temperature solid phase method, while polyaniline was synthesized by the in situ chemical polymerization of aniline monomer to coat the surface of nano-silicon and exfoliated graphite composites (Si@EG). Pyrolytic polyaniline (p-PANI) coating prevents the agglomeration of silicon nanoparticles, forming a good conductive network that effectively alleviates the volume expansion effect of silicon electrodes. SEM, TEM, XRD, Raman, TGA and BET were used to observe the morphology and analyze the structure of the samples. The electrochemical properties of the materials were tested by the constant current charge discharge and cyclic voltammetry (CV) methods. The results show that Si@EG@p-PANI not only inhibits the agglomeration between silicon nanoparticles and forms a good conductive network but also uses the outermost layer of p-PANI carbon coating to effectively alleviate the volume expansion of silicon nanoparticles during cycling. Si@EG@p-PANI had a high initial specific capacity of 1491 mAh g-1 and still maintains 752 mAh g-1 after 100 cycles at 100 mA g-1, which shows that it possesses excellent electrochemical stability and reversibility.

The Interaction between Gut Microbiota and Host Amino Acids Metabolism in Multiple Myeloma.

Although novel therapies have dramatically improved outcomes for multiple myeloma (MM) patients, relapse is inevitable and overall outcomes are heterogeneous. The gut microbiota is becoming increasingly recognized for its influence on host metabolism. To date, evidence has suggested that the gut microbiota contributes to MM, not only via the progressive activities of specific bacteria but also through the influence of the microbiota on host metabolism. Importantly, the abnormal amino acid metabolism, as well as the altered microbiome in MM, is becoming increasingly apparent, as is the influence on MM progression and the therapeutic response. Moreover, the gut-microbiota-host-amino-acid metabolism interaction in the progression of MM has been highlighted. Modulation of the gut microbiota (such as fecal microbiota transplantation, FMT) can be modified, representing a new angle in MM treatment that can improve outcomes. In this review, the relationship between gut microbiota, metabolism, and MM, together with strategies to modulate the microbiota, will be discussed, and some unanswered questions for ongoing and future research will be presented.