Perioperative acute kidney injury: The renoprotective effect and mechanism of dexmedetomidine.

Dexmedetomidine (DEX) is a highly selective and potent α2-adrenoceptor (α2-AR) agonist that is widely used as a clinical anesthetic to induce anxiolytic, sedative, and analgesic effects. In recent years, a growing body of evidence has demonstrated that DEX protects against acute kidney injury (AKI) caused by sepsis, drugs, surgery, and ischemia-reperfusion (I/R) in organs or tissues, indicating its potential role in the prevention and treatment of AKI. In this review, we summarized the evidence of the renoprotective effects of DEX on different models of AKI and explored the mechanism. We found that the renoprotective effects of DEX mainly involved antisympathetic effects, reducing inflammatory reactions and oxidative stress, reducing apoptosis, increasing autophagy, reducing ferroptosis, protecting renal tubular epithelial cells (RTECs), and inhibiting renal fibrosis. Thus, the use of DEX is a promising strategy for the management and treatment of perioperative AKI. The aim of this review is to further clarify the renoprotective mechanism of DEX to provide a theoretical basis for its use in basic research in various AKI models, clinical management, and the treatment of perioperative AKI.

Evaluation of nocturnal apnea and airflow limitation as indicators for cognitive dysfunction in patients with chronic obstructive pulmonary disease/obstructive sleep apnea hypopnea syndrome overlap syndrome.

OBJECTIVE: The aim of this study is to investigate how much intermittent hypoxemia and airflow limitation contribute to cognitive impairment in overlap syndrome (OS), which is the coexistence of two common diseases, obstructive sleep apnea hypopnea syndrome (OSAHS) and chronic obstructive pulmonary disease (COPD). METHODS: We conducted a cross-sectional study of patients with OSAHS, COPD or OS, compared with normal controls, to determine the association between sleep apnea/pulmonary function-related indicators and cognitive dysfunction in individuals with OSAHS, COPD or OS. RESULTS: A total of 157 participants were recruited. Both OSAHS and OS presented lower adjusted Montreal cognitive assessment (MoCA) scores compared with COPD group. In addition, the MoCA score was significantly lower in COPD group compared with control group. The incidence of cognitive impairment was 57.4% in OSAHS group, and 78% in OS group, which were significantly higher than COPD group (29%) and control group (8.8%). Furthermore, a broader range of cognitive domains were affected in OS group compared with OSAHS group. Elevated levels of oxygen desaturation index (ODI) and/or apnea hypopnea index (AHI) were positively correlated with increased Epworth sleeping scale (ESS) in OSAHS and OS. Forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1) and peak expiratory flow (PEF) were positively correlated with cognitive scores in OSAHS but not in OS. Serum level of hypoxia-inducible factor-1α (HIF-1α) was significantly higher in OS. Logistic regression identified ODI as an independent risk factor for cognitive impairment in OS, while severity of snoring and PEF were independent risk factors in OSAHS. DISCUSSION: This study revealed significant cognitive impairment in OS, OSAHS and COPD. Sleep-related indicators are warranted in OS patients for detection, differentiation and grading of cognitive impairment, whereas pulmonary functions are warranted in OSAHS patients for detection and early intervention of cognitive impairment.

Enhanced Oxidation of Organic Compounds by the Ferrihydrite-Ferrate System: The Role of Intramolecular Electron Transfer and Intermediate Iron Species.

Previous studies mostly held that the oxidation capacity of ferrate depends on the involvement of intermediate iron species (i.e., FeIV/FeV), however, the potential role of the metastable complex was disregarded in ferrate-based heterogeneous catalytic oxidation processes. Herein, we reported a complexation-mediated electron transfer mechanism in the ferrihydrite-ferrate system toward sulfamethoxazole (SMX) degradation. A synergy between intermediate FeIV/FeV oxidation and the intramolecular electron transfer step was proposed. Specifically, the conversion of phenyl methyl sulfoxide (PMSO) to methyl phenyl sulfone (PMSO2) suggested that FeIV/FeV was involved in the oxidation of SMX. Moreover, based on the in situ Raman test and chronopotentiometry analysis, the formation of the metastable complex of ferrihydrite/ferrate was found, which possesses higher oxidation potential than free ferrate and could achieve the preliminary oxidation of organics via the electron transfer step. In addition, the amino group of SMX could complex with ferrate, and the resulting metastable complex of ferrihydrite/ferrate would combine further with SMX molecules, leading to intramolecular electron transfer and SMX degradation. The ferrate loss experiments suggested that ferrihydrite could accelerate the decomposition of ferrate. Finally, the effects of pH value, anions, humic acid, and actual water on the degradation of SMX by ferrihydrite-ferrate were also revealed. Overall, ferrihydrite demonstrated high catalytic capacity, good reusability, and nontoxic performance for ferrate activation. The ferrihydrite-ferrate process may be a green and promising method for organic removal in wastewater treatment.

Detection of Interaction Effects in a Nonparametric Concurrent Regression Model.

Many methods have been developed to study nonparametric function-on-function regression models. Nevertheless, there is a lack of model selection approach to the regression function as a functional function with functional covariate inputs. To study interaction effects among these functional covariates, in this article, we first construct a tensor product space of reproducing kernel Hilbert spaces and build an analysis of variance (ANOVA) decomposition of the tensor product space. We then use a model selection method with the L1 criterion to estimate the functional function with functional covariate inputs and detect interaction effects among the functional covariates. The proposed method is evaluated using simulations and stroke rehabilitation data.

The movement and settlement behaviour of cyprids of Balanus reticulatus on the surfaces of the titanium alloys.

The motion paths of Balanus reticulatus cyprids were similar on all the titanium alloys surfaces. On the parallel grinding surfaces, the temporary attachment duration and the settlement ratio of the cyprids were influenced by the roughness and the composition of the surfaces and correlated positively. The surface roughness could also change the contact area and the numbers of the attachment points of the cyprids in the similar pattern. Consequently, the roughness and the composition of the surfaces regulated the cyprid settlement by the temporary attachment duration. The cross grinding increased the temporary attachment duration but drastically decreased the settlement ratio to 0 compared to the parallel grinding, possibly due to the voids and the drastic decrease of the contact area and the numbers of the attachment points of the cyprids on the cross grinding surface, respectively. The cross grinding therefore significantly reduced the cyprid settlement compared to the parallel grinding.

miR-378a-5p inhibits the proliferation of colorectal cancer cells by downregulating CDK1.

BACKGROUND: MicroRNAs (miRNAs) play an important role in tumor occurrence. The role of miR-378a-5p and CDK1 in colorectal cancer (CRC) was investigated in this study. METHODS: Investigation of TCGA database and the detection of miR-378a-5p expression in colorectal cancer pathological tissues and colorectal cancer cell lines were undertaken by using qRT-PCR. We performed cell function experiments (CCK-8 assay, EdU assay, colony formation assay, wound healing assay, transwell assay, cell apoptosis assessment, and cell cycle assessment) and nude mouse tumor formation experiments to evaluate the effects of miR-378a-5p on proliferation, metastasis, and invasion to explore the role of miR-378a-5p in vivo and in vitro. Next, through TCGA database, immunohistochemical staining of pathological tissues, and cell function experiments, the role of the target gene CDK1 of miR-378a-5p was verified by database prediction, and dual luciferase reporter gene experiments in colorectal cancer cells were performed. Finally, whether upregulation of CDK1 restores the inhibitory effect of overexpression of miR-378a-5p on the proliferation of CRC cells was studied by overexpression of CDK1. RESULTS: Bioinformatic analysis showed significant downregulation of miR-378a-5p levels in colorectal cancer (CRC). Cell function experiments and tumor xenograft mouse models confirmed the low expression of miR-378a-5p within CRC tissues, which indicated the tumor suppressive role of miR-378a-5p in CRC. To better explore the regulation of miR-378a-5p in CRC, we predicted and validated cell cycle-dependent protein kinase 1 (CDK1) as the miR-378a-5p target gene and observed that miR-378a-5p suppressed CRC cell proliferation by targeting CDK1. CONCLUSION: The results of this study help to elucidate the mechanism by which miR-378a-5p can be used as a tumor marker to inhibit the growth of colorectal cancer and CDK1, which is related to the prognosis of colorectal cancer patients. MiR-378a-5p inhibits CRC cell proliferation by suppressing CDK1 expression, which may become a possible therapeutic target for treatment of CRC.

Development and validation of a preoperative prediction model for follicular thyroid carcinoma.

OBJECTIVE: The low pre- and intraoperative diagnostic rates in follicular thyroid carcinoma (FTC) often lead to inadequate surgical resection and necessitate further completion surgery. Therefore, the preoperative prediction of FTC in thyroid nodules is essential. DESIGN AND PATIENT: Patients were categorized into two data sets: the modelling data set, which included 3649 patients admitted to our centre between January 2014 and December 2016, and the validation data set, which included 1253 patients admitted between January and December 2017. Patient data from the FTC and non-FTC groups were initially included in a modelling data set to establish a preoperative prediction model. This model was subsequently employed in a validation data set for external validation of the predictive value. The positivity rate for FTC predicted by the model was compared with that of the intraoperative frozen sections. RESULTS: The preoperative serum thyroglobulin level, nodule diameter, calcification status, solidity and blood supply were selected as predictors for the model. The regression equation was as follows: Y = 0.010 × (thyroglobulin level) + 0.556 × (nodule diameter) + 0.675 × (calcification status) + 2.355 × (nodule component) + 1.072*(blood flow) - 9.787. The model positively predicted FTC at values of Y ≥ -4.11. The accuracy, sensitivity, specificity, positive likelihood ratio and negative likelihood ratio of the prediction model were 89.2%, 90.2%, 87.7%, 39.2 and 0.11, respectively. External validation of the model demonstrated acceptable results. The positive prediction rate of the model was 90.7% (78/86), which was significantly higher than that of the intraoperative frozen sections (10.5% [9/86]; P < 0.0001). CONCLUSIONS: We successfully established and validated a simple and reliable preoperative prediction model for FTC using the preoperative thyroglobulin level and ultrasonographic features of the thyroid nodules. This model may improve the preoperative evaluation of FTC in clinical settings and facilitate the development of a reasonable surgical programme for FTC.

Application of Continuous and Intermittent Intraoperative Nerve Monitoring in Thyroid Surgery.

BACKGROUND: Whether continuous intraoperative nerve monitoring (C-IONM) can further reduce the incidence of recurrent laryngeal nerve injury compared with intermittent intraoperative nerve monitoring (I-IONM) in high-risk thyroid surgery is still controversial. This observational study aimed to evaluate the incidence of vocal cord paralysis (VCP) in high-risk thyroid surgeries performed with I-IONM and C-IONM. MATERIALS AND METHODS: High-risk thyroid surgical patients operated with I-IONM or C-IONM by the same group of surgeons in the thyroid surgery department of our institution between January 2014 and February 2018 were analyzed. Differences in the incidence rates of temporary and permanent VCP between the two groups were compared. A P-value < 0.05 was considered statistically significant. RESULTS: A total of 344 patients who underwent high-risk thyroid surgery (550 nerves at risk [NARs]) were observed, with 238 patients (374 NARs) operated with I-IONM and 106 patients (173 NARs) operated with C-IONM. The incidence of temporary and permanent VCP was 1.9% (7/374) and 0.8% (3/374) in the I-IONM group and 1.2% (2/173) and 0% (0/173) in the C-IONM group, respectively, showing no statistical difference (P = 0.726 and P = 0.555). The incidence rate of impending recurrent laryngeal nerve injuries successfully prevented in the C-IONM group was 5.2% (9/173). CONCLUSIONS: Both I-IONM and C-IONM are equally safe and effective in high-risk thyroid surgery. C-IONM can help predict impending recurrent laryngeal nerve injury in real time and has a good warning feature, thereby minimizing critical maneuvers in high-risk thyroid surgery.

Mer activation ameliorates nerve injury-induced neuropathic pain by regulating microglial polarization and neuroinflammation via SOCS3 in male rats.

Accumulating evidence has demonstrated that M1 microglial polarization and neuroinflammation worsen the development of neuropathic pain. However, the mechanisms underlying microglial activation during neuropathic pain remain incompletely understood. Myeloid-epithelial-reproductive tyrosine kinase (Mer), which is a member of the Tyro-Axl-Mer (TAM) family of receptor tyrosine kinases, plays a crucial role in the regulation of microglial polarization. However, the effect of Mer on microglial polarization during neuropathic pain has not been determined. In this study, western blotting, immunofluorescence analysis, quantitative polymerase chain reaction (qPCR), and enzyme-linked immunosorbent assay (ELISA) were used to examine the role of Mer in pain hypersensitivity and microglial polarization in rats with chronic constriction injury (CCI) of the sciatic nerve. The results indicated that Mer expression in microglia was prominently increased in the spinal cords of rats subjected to CCI. Furthermore, treatment with recombinant protein S (PS, an activator of Mer) alleviated mechanical allodynia and thermal hyperalgesia, promoted the switch in microglia from the M1 phenotype to the M2 phenotype, and ameliorated neuroinflammation in rats subjected to CCI. However, the use of suppressor of cytokine signalling 3 (SOCS3) siRNA abolished these changes. These results indicated that Mer regulated M1/M2 microglial polarization and neuroinflammation and may be a potential target for treating neuropathic pain.

Omaveloxolone ameliorates isoproterenol-induced pathological cardiac hypertrophy in mice.

Nuclear factor erythroid 2-related factor 2 (Nrf2) is an important transcriptional regulator that plays a protective role against various cardiovascular diseases. Omaveloxolone is a newly discovered potent activator of Nrf2 that has a variety of cytoprotective functions. However, the potential role of omaveloxolone in the process of pathological cardiac hypertrophy and heart failure are still unknown. In this study, an isoproterenol (ISO)-induced pathological cardiac hypertrophy model was established to investigate the protective effect of omaveloxolone in vivo and in vitro. Our study first confirmed that omaveloxolone administration improved ISO-induced pathological cardiac hypertrophy in mice and neonatal cardiomyocytes. Omaveloxolone administration also diminished ISO-induced cardiac oxidative stress, inflammation and cardiomyocyte apoptosis. In addition, omaveloxolone administration activated the Nrf2 signaling pathway, and Nrf2 knockdown almost completely abolished the cardioprotective effect of omaveloxolone, indicated that the cardioprotective effect of omaveloxolone was directly related to the activation of the Nrf2 signaling. In summary, our study identified that omaveloxolone may be a promising therapeutic agent to mitigate pathological cardiac hypertrophy.

How hetero-single-atom dispersion reconstructed electronic structure of carbon materials and regulated Fenton-like oxidation pathways.

Single-atom catalysts (SACs) have emerged as competitive candidates for Fenton-like oxidation of micro-pollutants in water. However, the impact of metal insertion on the intrinsic catalytic activity of carrier materials has been commonly overlooked, and the environmental risk due to metal leaching still requires attention. In contrast to previous reports, where metal sites were conventionally considered as catalytic centers, our study investigates, for the first time, the crucial catalytic role of the carbon carrier modulated through hetero-single-atom dispersion and the regulation of Fenton-like oxidation pathways. The inherent differences in electronic properties between Fe and Co can effectively trigger long-range electron rearrangement in the sp2-carbon-conjugated structure, creating more electron-rich regions for peroxymonosulfate (PMS) complexation and initiating the electron transfer process (ETP) for pollutant degradation, which imparts the synthesized catalyst (FeCo-NCB) with exceptional catalytic efficiency despite its relatively low metal content. Moreover, the FeCo-NCB/PMS system exhibits enduring decontamination efficiency in complex water matrices, satisfactory catalytic stability, and low metal leaching, signifying promising practical applications. More impressively, the spatial relationship between metal sites and electron density clouds is revealed to determine whether high-valent metal-oxo species (HVMO) are involved during the decomposition of surface complexes. Unlike single-type single-atom dispersion, where metal sites are situated within electron-rich regions, hetero-single-atom dispersion can cause the deviation of electron density clouds from the metal sites, thus hindering the in-situ oxidation of metal within the complexes and minimizing the contribution of HVMO. These findings provide new insights into the development of carbon-based SACs and advance the understanding of nonradical mechanisms underpinning Fenton-like treatments.

Sequential bio-treatment of ammonia-rich wastewater from Chinese medicine residue utilization: Regulation of dissolved oxygen.

To effectively treat actual ammonia-rich Chinese medicine residue (CMR) resource utilization wastewater, we optimized an anaerobic-microaerobic two-stage expanded granular sludge bed (EGSB) and moving bed sequencing batch reactor (MBSBR) combined process. By controlling dissolved oxygen (DO) levels, impressive removal efficiencies were achieved. Microaeration, contrasting with anaerobic conditions, bolstered dehydrogenase activity, enhanced electron transfer, and enriched the functional microorganism community. The increased relative abundance of Synergistetes and Proteobacteria facilitated hydrolytic acidification and fostered nitrogen and phosphorus removal. Furthermore, we examined the impact of DO concentration in MBSBR on pollutant removal and microbial metabolic activity, pinpointing 2.5 mg/L as the optimal DO concentration for superior removal performance and energy conservation.

Implementation and Evaluation of Discharge Planning for Patients Undergoing Umbilical Cord Blood Transplantation.

BACKGROUND Umbilical cord blood transplantation (UCBT) patients have high rates of unplanned readmissions and poor quality of life (QoL). The aim of this study was to evaluate the effects of discharge planning on unplanned readmissions, self-efficacy, QoL, and clinical outcomes. MATERIAL AND METHODS Patients who received their first UCBT from April 2022 to March 2023 were included. Participants (n=72) were assigned to a control group (CG: received usual care) or an intervention group (IG: received discharge planning from admission to 100 days after UCBT). The cumulative readmission rates 30 days after discharge and 100 days after UCBT were analyzed using the log-rank test. Self-efficacy and QoL were assessed at admission and 100 days after UCBT using the General Self-Efficacy Scale and FACT-BMT version 4, clinical outcomes derived from medical records. RESULTS Sixty-six patients completed the study. Discharge planning did not reduce readmission rates 30 days after discharge (20.59% vs 31.25%, P=0.376) or 100 days after UCBT (29.41% vs 34.38%, P=0.629). However, the IG showed significantly better self-efficacy (P<0.001), and except for social and emotional well-being, all the other dimensions and 3 total scores of FACT-BMT in the IG were higher than for the controls at 100 days after UCBT (P<0.05). CONCLUSIONS The discharge planning program can improve self-efficacy and QoL of UCBT recipients. The implementation of discharge planning for patients undergoing UCBT was necessary for successful hospital-to-home transitions.

RGS19 activates the MYH9/ß-catenin/c-Myc positive feedback loop in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is one of the most common fatal cancers worldwide, and the identification of novel treatment targets and prognostic biomarkers is urgently needed because of its unsatisfactory prognosis. Regulator of G-protein signaling 19 (RGS19) is a multifunctional protein that regulates the progression of various cancers. However, the specific function of RGS19 in HCC remains unclear. The expression of RGS19 was determined in clinical HCC samples. Functional and molecular biology experiments involving RGS19 were performed to explore the potential mechanisms of RGS19 in HCC. The results showed that the expression of RGS19 is upregulated in HCC tissues and is significantly associated with poor prognosis in HCC patients. RGS19 promotes the proliferation and metastasis of HCC cells in vitro and in vivo. Mechanistically, RGS19, via its RGS domain, stabilizes the MYH9 protein by directly inhibiting the interaction of MYH9 with STUB1, which has been identified as an E3 ligase of MYH9. Moreover, RGS19 activates ß-catenin/c-Myc signaling via MYH9, and RGS19 is also a transcriptional target gene of c-Myc. A positive feedback loop formed by RGS19, MYH9, and the ß-catenin/c-Myc axis was found in HCC. In conclusion, our research revealed that competition between RGS19 and STUB1 is a critical mechanism of MYH9 regulation and that the RGS19/MYH9/ß-catenin/c-Myc feedback loop may represent a promising strategy for HCC therapy.

MG53 ameliorates nerve injury induced neuropathic pain through the regulation of Nrf2/HO-1 signaling in rats.

Neuropathic pain is one of the most common types of chronic pain, and it arises as a direct consequence of a lesion or disease that affects the somatosensory system. Mitsugumin53 (MG53), which is a member of the TRIM family of proteins and is known as TRIM72, exerts protective effects on muscle, lung, kidney, brain, and other cells or tissues. Recently, increasing evidence has indicated that MG53 plays a vital role in regulating neuroinflammation and oxidative stress. However, the relationship between MG53 and neuropathic pain is unclear. In this study, we aimed to explore the role of MG3 in neuropathic pain after chronic constriction injury (CCI) to the sciatic nerve in rats. To explore the mechanism of MG53 regulating the development of neuropathic pain, the rats was injected (intrathecal injection) of recombinant human MG53 (rhMG53) protein and/or nuclear factor erythroid 2-related factor 2 (Nrf2) siRNA after CCI. Mechanical allodynia or thermal hyperalgesia was assessed by the 50% paw withdrawal threshold (PWT) or the paw withdrawal latency (PWL). The target molecules was detected using western blotting (WB), immunofluorescence (IF), quantitative real-time polymerase chain reaction (qPCR), enzyme-linked immunosorbent assay (ELISA), biochemical evaluations, and Dihydroethidium (DHE) staining. The results indicated that the expression level of MG53 in the spinal cord was increased after CCI in rats. Moreover, intrathecal injection with rhMG53 protein notably alleviated CCI-induced mechanical allodynia, thermal hyperalgesia, neuroinflammation，oxidative stress and the increased level of reactive oxygen species (ROS) via activation of the Nrf2/heme oxygenase-1 (HO-1) signaling pathway. However, administration of Nrf2 siRNA abrogated the analgesic, anti-inflammatory and antioxidant effects of rhMG53 in CCI model rats. Our study demonstrated that MG53 improved neuropathic pain, neuroinflammation, and oxidative stress via activation of the Nrf2/HO-1 signaling pathway in the spinal cord of CCI model rats, which suggested that MG53 may serve as a new target for the treatment of neuropathic pain.

Insight into Chinese medicine residue biochar combined with ultrasound for persulfate activation in atrazine degradation: Acanthopanax senticosus precursors, synergistic effects and toxicity assessment.

The synergistic activation of persulfate by multiple factors could degrade pollutants more efficiently. However, the co-activation method based on metal ions has the risk of leakage. The non-metallic coupling method could achieve the same efficiency as the metal activation and meanwhile release environmental stress. In this study, the original biochar (BC) was prepared through using Chinese medicinal residue of Acanthopanax senticosus as the precursor. Compared with other biochar, the pore size structure was higher and toxicity risk was lower. The ultrasonic (US)/Acanthopanax senticosus biochar (ASBC)/persulfate oxidation system was established for Atrazine (ATZ). Results showed that 45KHz in middle and low frequency band cooperated with ASBC600 to degrade nearly 70 % of ATZ within 50 min, and US promoted the formation of SO4- and OH. Meanwhile, the synergy index of US and ASBC was calculated to be 1.18, which showed positive synergistic effect. Finally, the potential toxicity was examined by using Toxicity Characteristic Leaching Procedure (TCLP) and luminescent bacteria. This study provides a promising way for the activation of persulfate, which is expected to bring a new idea for the win-win situation of pollutant degradation and solid waste resource utilization.

Light and nitrogen vacancy-intensified nonradical oxidation of organic contaminant with Mn (III) doped carbon nitride in peroxymonosulfate activation.

Recently, Mn-based materials have a great potential for selective removal of organic contaminants with the assistance of oxidants (PMS, H2O2) and the direct oxidation. However, the rapid oxidation of organic pollutants by Mn-based materials in PMS activation still presents a challenge due to the lower conversion of surface Mn (III)/Mn (IV) and higher reactive energy barrier for reactive intermediates. Here, we constructed Mn (III) and nitrogen vacancies (Nv) modified graphite carbon nitride (MNCN) to break these aforementioned limitations. Through analysis of in-situ spectra and various experiments, a novel mechanism of light-assistance non-radical reaction is clearly elucidated in MNCN/PMS-Light system. Adequate results indicate that Mn (III) only provide a few electrons to decompose Mn (III)-PMS* complex under light irradiation. Thus, the lacking electrons necessarily are supplied from BPA, resulting in its greater removal, then the decomposition of the Mn (III)-PMS* complex and light synergism form the surface Mn (IV) species. Above Mn-PMS complex and surface Mn (IV) species lead to the BPA oxidation in MNCN/PMS-Light system without the involvement of sulfate (SO4• ̶) and hydroxyl radicals (•OH). The study provides a new understanding for accelerating non-radical reaction in light/PMS system for the selective removal of contaminant.

Psychological Effects of a Structured Exercise Intervention During Umbilical Cord Blood Transplantation in Children and Adolescents.

BACKGROUND: Children and adolescents undergoing umbilical cord blood transplantation (UCBT) are faced with severe fatigue and a decline in quality of life (QoL) during the inpatient period. OBJECTIVE: To investigate the effect of a structured exercise intervention on fatigue, QoL and clinical outcomes among children and adolescents during UCBT. METHODS: In this randomized controlled trial, participants (n = 48) were randomized to a control group (CG: usual care) or an intervention group (IG: a structured exercise intervention). Fatigue and QoL were assessed at hospital admission, 14 days after UCBT, and at discharge using linear mixed model analysis. In addition, engraftment kinetics, supportive treatment, transplant-related complications, and hospital length of stay were derived from medical records. RESULTS: 4 patients completed the study, the IG participated in an average of 2.12 (1.36-2.8) sessions with a duration of 24 (16-34) min weekly, and the total rate of adherence to the training program was 70.59%. For fatigue and QoL, there was a significant effect of time in the control group, with the total score of fatigue decreased from T1 to T2 (73.9vs 60.9, P = .001) and T1 to T3 (73.9vs 65.6, P = .049), and the QoL scores decreased from T1 to T2 (73.9vs 66.1, P = .043). The hospital length of stay was less in the intervention group (P = .034). CONCLUSION: Our randomized study indicated that structured exercise interventions might exert a protective effect by attenuating the decline in fatigue and QoL, and shortening duration of hospitalization.

Identification of MIR600HG/hsa-miR-342-3p/ANLN network as a potential prognosis biomarker associated with lmmune infiltrates in pancreatic cancer.

Pancreatic cancer is one of the tumors with the worst prognosis, causing serious harm to human health. The RNA network and immune response play an important role in tumor progression. While a systematic RNA network linked to the tumor immune response remains to be further explored in pancreatic cancer. Based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases, the MIR600HG/hsa-miR-342-3p/ANLN network was determined. WB and IHC were used to confirm the high expression of ANLN in pancreatic cancer. The prognostic model based on the RNA network could effectively predict the survival prognosis of patients. The analysis of immune infiltration showed that the MIR600HG/hsa-miR-342-3p/ANLN network altered the level of infiltration of T helper 2 (Th2) and effector memory T (Tem) cells. Furthermore, we found that the chemokines chemokine ligand (CCL) 5 and CCL14 may play a key role in immune cell infiltration mediated by the RNA network. In conclusion, this study constructed a prognostic model based on the MIR600HG/hsa-miR-342-3p/ANLN network and found that it may function in tumor immunity.

RNF125 attenuates hepatocellular carcinoma progression by downregulating SRSF1-ERK pathway.

Hepatocellular carcinoma (HCC) is one of the most deadly malignant cancers worldwide. Research into the crucial genes responsible for maintaining the aggressive behaviour of cancer cells is important for the clinical treatment of HCC. The purpose of this study was to determine whether the E3 ubiquitin ligase Ring Finger Protein 125 (RNF125) plays a role in the proliferation and metastasis of HCC. RNF125 expression in human HCC samples and cell lines was investigated using TCGA dataset mining, qRT‒PCR, western blot, and immunohistochemistry assays. In addition, 80 patients with HCC were studied for the clinical value of RNF125. Furthermore, the molecular mechanism by which RNF125 contributes to hepatocellular carcinoma progression was determined with mass spectrometry (MS), coimmunoprecipitation (Co-IP), dual-luciferase reporter assays, and ubiquitin ladder assays. We found that RNF125 was markedly downregulated in HCC tumour tissues, which was associated with a poor prognosis for patients with HCC. Moreover, the overexpression of RNF125 inhibited HCC proliferation and metastasis both in vitro and in vivo, whereas the knockdown of RNF125 exerted antithetical effects. Mechanistically, mass spectrometry analysis revealed a protein interaction between RNF125 and SRSF1, and RNF125 accelerated the proteasome-mediated degradation of SRSF1, which impeded HCC progression by inhibiting the ERK signalling pathway. Furthermore, RNF125 was detected to be the downstream target of miR-103a-3p. In this study, we identified that RNF125 is a tumour suppressor in HCC and inhibits HCC progression by inhibiting the SRSF1/ERK pathway. These findings provide a promising treatment target for HCC.