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BackgroundHand arm vibration disease (HAVD) is one of the legal occupational diseases in China, and its pathogenesis is not clear. Operators exposed to electric vibration tools for a long time have an increased risk of HAVD.ObjectiveTo conduct a systematic evaluation of the effects of vibration operations on workers' upper limb nerves, blood vessels, and muscles.MethodsRelevant studies on the effects of hand-transmitted vibration on HAVD were searched and collected from the China Knowledge Infrastructure, Wanfang, and PubMed databases, and the literature was published from January 1974 to April 2021. The quality of cohort and case-control studies was assessed by the Newcastle-Ottawa Scale (NOS), and the quality of cross-sectional studies was by the evaluation criteria recommended by the Agency for Healthcare Quality and Research (AHRQ). Statistical analyses of outcome indicators (OR) in the included literature were performed using RevMan 5.4.1 software, effect sizes in the literature on vibration-induced white finger and neurosensory impairment were combined using a random-effect model, those that included carpal tunnel syndrome were combined using a fixed-effect model, and subgroup and publication bias analyses were also performed. To explore sources of study heterogeneity, meta-regression was performed using Stata 16.0 software, and sensitivity analyses were performed on the included literature.ResultsA total of 716 papers were retrieved from the databases, and 18 articles were retrieved by manual searching. A total of 34 papers were included after excluding those not meeting the criteria. Of the papers, 11004, 7270, and 1722 subjects related to vibration-induced white finger, neurosensory impairment, and carpal tunnel syndrome, respectively. The results of meta-analysis showed that compared with the control group, the combined ORs of hand-transmitted vibration exposure were 4.25 (95%CI: 2.72−6.65) for vibration-induced white finger, 4.03 (95%CI: 2.46−6.61) for neurosensory impairment, and 2.44 (95%CI: 1.61−3.71) for carpal tunnel syndrome. Heterogeneity was identified in the original studies related to vibration-induced white finger (I2=81%, P < 0.001) and neurosensory impairment (I2=90%, P < 0.001), except carpal tunnel syndrome (I2=23%, P < 0.001). The results of sensitivity analysis showed that the combined effect sizes (ORs) were stable and reliable. The results of meta-regression showed that the factors contributing to high heterogeneity of combined vibration-induced white finger and neurosensory impairment were time of publication (t=−2.10, P=0.049) and working age (t=−2.40, P=0.032), respectively.ConclusionHand-transmitted vibration is a risk factor for vibration-induced white finger, neurosensory impairment, and carpal tunnel syndrome in operators.

Paris polyphylla var. yunnanensis is an endangered medicinal plant endemic to China with great economic importance for the pharmaceutical industry. Two significant barriers to its commercial development are the long duration of its seed germination and the frequency of interspecific hybridization. We developed a method for clonal propagation of Paris polyphylla var. yunnanensis and successfully applied it to selected elite wild plants, which could become cultivar candidates based on their biomass production and saponin content. In comparison to the traditional method, somatic embryogenesis produced an average of 63 somatic embryos per gram of callus in just six weeks, saving 12 to 15 months in plantlet production. The produced in vitro plantlets were strong and healthy and 94% survived transplanting to soil. Using this method, four candidate cultivars with diverse morphologies and geographic origins were clonally reproduced from selected elite wild accessions. In comparison to those obtained with the traditional P. polyphylla propagation technique, they accumulated higher biomass and polyphyllin levels in rhizomes plus adventitious roots during a five-year period. In conclusion, somatic embryogenesis-based methods offer an alternate approach for the rapid and scaled-up production of P. polyphylla, as well as opening up species conservation options.

The production of synthetic polyploids for plant breeding is compromised by high levels of mixoploids and low numbers of solid polyploid regenerants during in vitro induction. Somatic embryogenesis could potentially contribute to the maximization of solid polyploid production due to the single cell origin of regenerants. In the present study, a novel procedure for establishing homogeneous tetraploid embryogenic cell lines in Magnolia officinalis has been established. Embryogenic cell aggregate (ECA) about 100–200 μm across, and consisting of dozens of cells, regenerated into a single colony of new ECAs and somatic embryos following colchicine treatment. Histological analysis indicated that the few cells that survived some colchicine regimes still regenerated to form a colony. In some colonies, 100% tetraploid somatic embryos were obtained without mixoploid formation. New granular ECA from single colonies with 100% tetraploid somatic embryos were isolated and cultured individually to proliferate into cell lines. These cell lines were confirmed to be homogeneous tetraploid by flow cytometry. Many tetraploid somatic embryos and plantlets were differentiated from these cell lines and the stability of ploidy level through the somatic embryogenesis process was confirmed by flow cytometry and chromosome counting. The establishment of homogeneous polyploid cell lines, which were presumed to represent individual polyploidization events, might expand the phenotypic variations of the same duplicated genome and create novel breeding opportunities using newly generated polyploid plantlets.

Abstract Background Autophagy is an evolutionarily conserved system for the degradation of intracellular components in eukaryotic organisms. Autophagy plays essential roles in preventing premature senescence and extending the longevity of vascular plants. However, the mechanisms and physiological roles of autophagy in preventing senescence in basal land plants are still obscure. Results Here, we investigated the functional roles of the autophagy-related gene PpATG3 from Physcomitrella patens and demonstrated that its deletion prevents autophagy. In addition, Ppatg3 mutant showed premature gametophore senescence and reduced protonema formation compared to wild-type (WT) plants under normal growth conditions. The abundance of nitrogen (N) but not carbon (C) differed significantly between Ppatg3 mutant and WT plants, as did relative fatty acid levels. In vivo protein localization indicated that PpATG3 localizes to the cytoplasm, and in vitro Y2H assays confirmed that PpATG3 interacts with PpATG7 and PpATG12. Plastoglobuli (PGs) accumulated in Ppatg3, indicating that the process that degrades damaged chloroplasts in senescent gametophore cells was impaired in this mutant. RNA-Seq uncovered a detailed, comprehensive set of regulatory pathways that were affected by the autophagy mutation. Conclusions The autophagy-related gene PpATG3 is essential for autophagosome formation in P. patens. Our findings provide evidence that autophagy functions in N utilization, fatty acid metabolism and damaged chloroplast degradation under non-stress conditions. We identified differentially expressed genes in Ppatg3 involved in numerous biosynthetic and metabolic pathways, such as chlorophyll biosynthesis, lipid metabolism, reactive oxygen species removal and the recycling of unnecessary proteins that might have led to the premature senescence of this mutant due to defective autophagy. Our study provides new insights into the role of autophagy in preventing senescence to increase longevity in basal land plants.

Fusarium equiseti (JMF-01), as an entomopathogenic fungus, can effectively control agricultural pests and has the potential to be a biocontrol agent. To promote mycelial growth and sporulation, we investigated the optimal submerged culture conditions for F. equiseti. In this study, we used the single-factor method and Box–Behnken design and determined the virulence of the submerged culture against Myzus persicae after optimization. As a result, the highly significant factors affecting the spore concentration of strain JMF-01 were the primary inoculum density and the initial pH, and the highly significant factor affecting the mycelial biomass was the medium-to-flask ratio. The highest mycelial biomass value was 0.35 g when the incubation time was 5.68 days, the initial pH was 5.11, the medium-to-flask ratio was 0.43, and 1 mL of the primary inoculum with spore density of 0.97 × 107 conidia/mL was added. When the incubation time was 6.32 days, the initial pH was 4.46, the medium-to-flask ratio was 0.35, the primary inoculum density was 1.32 × 107 conidia/mL of 1 mL, and the highest spore concentration of 6.49 × 108 blastospores/mL was obtained. Compared with the unoptimized medium conditions, the optimized submerged culture had the highest mycelial biomass and spore concentration, which were 3.46 and 2.06 times higher, respectively. The optimized submerged culture was highly pathogenic toward M. persicae, reaching a 95% mortality rate. Our results provide optimal submerged culture conditions for F. equiseti and lay the basis for later research to expand production for pest control.

Storage oil breakdown plays an important role in the life cycle of many plants by providing the carbon skeletons that support seedling growth immediately following germination. 1-Butanol, a specific inhibitor of phospholipase D (PLD)-dependent production of the signalling molecule phosphatidic acid (PA), inhibited Arabidopsis seed germination. N-Acylethanolamines (NAEs), which have been shown to inhibits PLDα1 activity, have no effect on seed germination. However, mobilization profile of triacylglycerols (TAG) that induced by each compound has not been reported. To gain deeper insights into the mode of mobilization of TAG during NAE 12:0 or 1-butanol treatment, we conducted a detailed comparative analysis of the effect of NAE 12:0, DMSO, 1-butanol and tert-butanol on Arabidopsis seed germination and fatty acid composition, tert-butanol and DMSO served as the corresponding controls treatment respectively. Our data show that 1-butanol, but not the inactive tert-butanol isomer, inhibited Arabidopsis seed germination, which is accompanied by a with retardation of the mobilization of triacylglycerols (TAG). In contrast, NAE 12:0 did not affect mobilization of TAG, nor did it significantly delay seed germination as monitored by radicle and cotyledon emergence. 1-Butanol induced RNA degradation in seeds and seedlings. We speculate that the large-scale degradation of RNA under the induction of 1-butanol may lead to abnormal gene expression in genes necessary for seed germination, including the genes needed for the mobilization of oil bodies, and thus cause a delay of seed germination. To the best of our knowledge, we report for the first time that 1-butanol delays the mobilization of TAG. Keywords: Germination, 1-butanol, N-Acylethanolamines, Triacylglycerols, Fatty acid

NUTCRACKER (NUC) is a transcription factor expressed in multiple tissues, but little is known about its physiological roles. In this study, we explored the physiological function of NUC with the Arabidopsis knockout, rescue, and overexpression lines. We found that NUC overexpression promoted development at the germination, seedling, and juvenile stages. NUC overexpression increased resistance to nitrogen (N) deficiency stress by increasing the chlorophyll content, suppressing anthocyanin accumulation, and increasing the biomass under N deficiency. In contrast, the absence of NUC did not affect such characteristics. N deficiency significantly increased the expression of NUC in leaves but did not affect the expression of NUC in roots. The overexpression of NUC promoted primary root length under both normal and N deficiency conditions. Furthermore, we found that the N-responsive and lateral-root-related genes TGA1 and NRT2.4 had NUC-binding sites in their promoter regions and that their expression was upregulated by NUC under N deficiency. The overexpression of the NUC increased the number and length of the lateral roots under N deficiency through inducible promotion. Multiple lines of investigation suggest that the regulatory function of the NUC could be bypassed through its redundant MAGPIE (MGP) when the NUC is absent. Our findings provide novel insight into NUC’s functions and will assist efforts to improve plants’ development and resistance to nutrient stresses.

Background Lecanicillium lecanii is an entomopathogenic fungi, which was isolated from insects suffering from disease. Now, it is an effective bio-control resource that can control agricultural pests such as whitefly and aphids. There are many studies on the control of various agricultural pests by L. lecanii, but no report on its control of Bemisia tabaci biotype-Q exists. In this work, we studied the susceptibility of B. tabaci Q-biotype (from Ningxia, China) to L. lecanii JMC-01 in terms of nymph mortality and the changes in detoxifying protective enzymes activities. Methods B. tabaci nymphs were exposed to L. lecanii JMC-01 conidia by immersion with the host culture. Mortality was assessed daily for all nymph stages. The detoxifying and protective enzyme activity changes, weight changes, and fat, and water contents of the nymphs were determined spectrophotometrically. Results All instars of B. tabaci died after being infested with 1 × 108 conidia/mL. The 2nd-instar nymphs were the most susceptible, followed by the 3rd-instar nymphs. The corrected cumulative mortality of the 2nd- and 3rd-instar nymphs was 82.22% and 75.55%, respectively. The levels of detoxifying and protective enzymes initially increased and then decreased. The highest activities of carboxylesterase, acetylcholinesterase, peroxidase, and catalase occurred on the 3rd day, reaching 10.5, 0.32, 20, and 6.3 U/mg prot, respectively. These levels were 2.2-, 4.3-, 2.4-, and 1.4-fold the control levels, respectively. The highest activities of glutathione-S transferase and superoxide dismutase on the 2nd day were, respectively, 64 and 43.5 U/mg prot. These levels were, respectively, 2.7 and 1.1-fold that of the control level. The water and fat content in the infected B. tabaci nymphs decreased and differed significantly from the control levels. The weight increased continuously in the first 24 h, decreasing thereafter. At 72 h, the infestation level was about 0.78-fold that of the control level. Conclusions The studied L. lecanii JMC-01 strain is pathogenic to the B. tabaci Q-biotype. This strain interferes with the normal functioning of detoxifying and protective enzymes, and is also involved in the disruption of normal physiological metabolism in B. tabaci.

At the cellular level, the remodelling of membrane lipids and production of heat shock proteins are the two main strategies whereby plants survive heat stress. Although many studies related to glycerolipids and HSPs under heat stress have been reported separately, detailed alterations of glycerolipids and the role of HSPs in the alterations of glycerolipids still need to be revealed. In this study, we profiled the glycerolipids of wild-type Arabidopsis and its HSP101-deficient mutant hot-1 under two types of heat stress. Our results demonstrated that the alterations of glycerolipids were very similar in wild-type Arabidopsis and hot-1 during heat stress. Although heat acclimation led to a slight decrease of glycerolipids, the decrease of glycerolipids in plants without heat acclimation is more severe under heat shock. The contents of 36:x monogalactosyl diacylglycerol (MGDG) were slightly increased, whereas that of 34:6 MGDG and 34:4 phosphatidylglycerol (PG) were severely decreased during moderate heat stress. Our findings suggested that heat acclimation could reduce the degradation of glycerolipids under heat shock. Synthesis of glycerolipids through the prokaryotic pathway was severely suppressed, whereas that through the eukaryotic pathway was slightly enhanced during moderate heat stress. In addition, HSP101 has a minor effect on the alterations of glycerolipids under heat stress.

MYB transcription factors (TFs) are one of the largest TF families in plants to regulate numerous biological processes. However, our knowledge of the MYB family in Physcomitrella patens is limited. We identified 116 MYB genes in the P. patens genome, which were classified into the R2R3-MYB, R1R2R3-MYB, 4R-MYB, and MYB-related subfamilies. Most R2R3 genes contain 3 exons and 2 introns, whereas R1R2R3 MYB genes contain 10 exons and 9 introns. N3R-MYB (novel 3RMYB) and NR-MYBs (novel RMYBs) with complicated gene structures appear to be novel MYB proteins. In addition, we found that the diversity of the MYB domain was mainly contributed by domain shuffling and gene duplication. RNA-seq analysis suggested that MYBs exhibited differential expression to heat and might play important roles in heat stress responses, whereas CCA1-like MYB genes might confer greater flexibility to the circadian clock. Some R2R3-MYB and CCA1-like MYB genes are preferentially expressed in the archegonium and during the transition from the chloronema to caulonema stage, suggesting their roles in development. Compared with that of algae, the numbers of MYBs have significantly increased, thus our study lays the foundation for further exploring the potential roles of MYBs in the transition from aquatic to terrestrial environments.

A20 is a ubiquitin-editing enzyme that is known to regulate inflammatory signaling and cell death. However, A20 mutations are also frequently found in multiple malignancies suggesting a potential role as a tumor suppressor as well. We recently described a novel role for A20 in regulating the wnt-beta-catenin signaling pathway and suppressing colonic tumor development in mice. The underlying mechanisms for this phenomenon are unclear. To study this, we first generated A20 knockout cell lines by genome-editing techniques. Using these cells, we show that loss of A20 causes dysregulation of wnt-dependent gene expression by RNAseq. Mechanistically, A20 interacts with a proximal signaling component of the wnt-signaling pathway, receptor interacting protein kinase 4 (RIPK4), and regulation of wnt-signaling by A20 occurs through RIPK4. Finally, similar to the mechanism by which A20 regulates other members of the receptor interacting protein kinase family, A20 modifies ubiquitin chains on RIPK4 suggesting a possible molecular mechanism for A20's control over the wnt-signaling pathway.

Plant lifespan is affected by factors with genetic and environmental bases. The laws governing these two factors and how they affect plant lifespan are unclear. Here we show that the acyl chain length (ACL) of phosphatidylserine (PS) is correlated with plant lifespan. Among the detected eight head-group classes of membrane lipids with lipidomics based on triple quadrupole tandem mass spectrometry, the ACL of PS showed high diversity, in contrast to the ACLs of the other seven classes, which were highly conserved over all stages of development in all plant species and organs and under all conditions that we studied. Further investigation found that acyl chains of PS lengthened during development, senescence, and under environmental stresses and that increasing length was accelerated by promoted- senescence. The acyl chains of PS were limited to a certain carbon number and ceased to increase in length when plants were close to death. These findings suggest that the ACL of PS can count plant lifespan and could be a molecular scale ruler for measuring plant development and senescence.

Senescence is the last phase of the plant life cycle and has an important role in plant development. Degradation of membrane lipids is an essential process during leaf senescence. Several studies have reported fundamental changes in membrane lipids and phospholipase D (PLD) activity as leaves senesce. Suppression of phospholipase Dα1 (PLDα1) retards abscisic acid (ABA)-promoted senescence. However, given the absence of studies that have profiled changes in the compositions of membrane lipid molecules during leaf senescence, there is no direct evidence that PLD affects lipid composition during the process. Here, we show that application of n-butanol, an inhibitor of PLD, and N-Acylethanolamine (NAE) 12∶0, a specific inhibitor of PLDα1, retarded ABA-promoted senescence to different extents. Furthermore, phospholipase Dδ (PLDδ) was induced in leaves treated with ABA, and suppression of PLDδ retarded ABA-promoted senescence in Arabidopsis. Lipid profiling revealed that detachment-induced senescence had different effects on plastidic and extraplastidic lipids. The accelerated degradation of plastidic lipids during ABA-induced senescence in wild-type plants was attenuated in PLDδ-knockout (PLDδ-KO) plants. Dramatic increases in phosphatidic acid (PA) and decreases in phosphatidylcholine (PC) during ABA-induced senescence were also suppressed in PLDδ-KO plants. Our results suggest that PLDδ-mediated hydrolysis of PC to PA plays a positive role in ABA-promoted senescence. The attenuation of PA formation resulting from suppression of PLDδ blocks the degradation of membrane lipids, which retards ABA-promoted senescence.

Abstract Replacement of expensive and rare platinum with metal–nitrogen–carbon catalysts for oxygen reduction reactions in proton exchange membrane fuel cells is hindered by their inferior activity. Herein, we report a highly active iron-nitrogen-carbon catalyst by optimizing the carbon structure and coordination environments of Fe-N4 sites. A critical high-temperature treatment with ammonium chloride and ammonium bromide not only enhances the intrinsic activity and density of Fe-N4 sites, but also introduces numerous defects, trace Br ions and creates mesopores in the carbon framework. Notably, surface Br ions significantly improve the interaction between the ionomer and catalyst particles, promoting ionomer infiltration and optimizing the O2 transport and charge transfer at triple-phase boundary. This catalyst delivers a high peak power density of 1.86 W cm−2 and 54 mA cm−2 at 0.9 ViR-free in a H2-O2 fuel cells at 80 °C. Our findings highlight the critical role of interface microenvironment regulation.

Abstract In pursuing cheap and effective oxygen reduction catalysts, the Fe/N/C system emerges as a promising candidate. Nevertheless, the structural transformations of starting materials into Fe- and N-doped carbon catalysts remains poorly characterized under pyrolytic conditions. Here, we explore the evolution of Fe species and track the formation of Fe–N4 site development by employing diverse in-situ diagnostic techniques. In-situ heating microscopy reveals the initial formation of FeOx nanoparticles and subsequent internal migration within the carbon matrix, which stops once FeOx is fully reduced. The migration and decomposition of nanoparticles then leads to carbon layer reconstruction. Experimental and theoretical analysis reveals size-dependent behavior of FeOx where nanoparticles below 7 nm readily release Fe atoms to form Fe–N4 while nanoparticles with sizes >10 nm tend to coalesce and impede Fe–N4 site formation. The work visualizes the pyrolysis process of Fe/N/C materials, providing theoretical guidance for the rational design of catalysts.

Abstract Background Novel therapeutic targets are urgently needed for treating drug-resistant non-small cell lung cancer (NSCLC) and overcoming drug resistance to molecular-targeted therapies. Regulator of G protein signaling 20 (RGS20) is identified as an upregulated factor in many cancers, yet its specific role and the mechanism through which RGS20 functions in NSCLC remain unclear. Our study aimed to identify the role of RGS20 in NSCLC prognosis and delineate associated cellular and molecular pathways. Methods Immunohistochemistry and lung cancer tissue microarray were used to verify the expression of RGS20 between NSCLC patients. CCK8 and cell cloning were conducted to determine the proliferation ability of H1299 and Anip973 cells in vitro. Furthermore, Transcriptome sequencing was performed to show enrichment genes and pathways. Immunofluorescence was used to detect the translocation changes of YAP to nucleus. Western blotting demonstrated different expressions of autophagy and the Hippo-PKA signal pathway. In vitro and in vivo experiments verified whether overexpression of RGS20 affect the proliferation and autophagy of NSCLC through regulating the Hippo pathway. Results The higher RGS20 expression was found to be significantly correlated with a poorer five-year survival rate. Further, RGS20 accelerated cell proliferation by increasing autophagy. Transcriptomic sequencing suggested the involvement of the Hippo signaling pathway in the action of RGS20 in NSCLC. RGS20 activation reduced YAP phosphorylation and facilitated its nuclear translocation. Remarkably, inhibiting Hippo signaling with GA-017 promoted cell proliferation and activated autophagy in RGS20 knock-down cells. However, forskolin, a GPCR activator, increased YAP phosphorylation and reversed the promoting effect of RGS20 in RGS20-overexpressing cells. Lastly, in vivo experiments further confirmed role of RGS20 in aggravating tumorigenicity, as its overexpression increased NSCLC cell proliferation. Conclusion Our findings indicate that RGS20 drives NSCLC cell proliferation by triggering autophagy via the inhibition of PKA-Hippo signaling. These insights support the role of RGS20 as a promising novel molecular marker and a target for future targeted therapies in lung cancer treatment.

BackgroundDigital health interventions (DHIs) have shown promising results for the management of chronic wounds. However, its effectiveness compared to usual care and whether variability in the type of intervention affects wound outcomes are unclear. ObjectiveThe main objective was to determine the effectiveness of DHIs on wound healing outcomes in adult patients with chronic wounds. The secondary objectives were to assess if there was any variation in wound healing outcomes across the various types of DHIs. MethodsIn total, 9 databases were searched for the literature up to August 1, 2023. Randomized controlled trials (RCTs), cohort studies, and quasi-experimental studies comparing the efficacy of DHIs with controls in improving wound outcomes in adult patients with chronic wounds were included. Study selection, data extraction, and risk of bias assessment were conducted independently by 2 reviewers. We assessed the quality of each RCT, cohort study, and quasi-experimental study separately using the Cochrane risk of bias tool, ROBINS-I, and the Joanna Briggs Institute Critical Appraisal tools checklists. Relative risks (RRs) and 95% CIs were pooled using the random effects model, and heterogeneity was assessed by the I2 statistic. Subgroup analysis and sensitivity analysis were also performed. ResultsA total of 25 studies with 8125 patients were included in this systematic review, while only 20 studies with 6535 patients were included in the meta-analysis. Efficacy outcomes in RCTs showed no significant differences between the DHIs and control groups in terms of wound healing (RR 1.02, 95% CI 0.93-1.12; P=.67) and all-cause mortality around 1 year (RR 1.08, 95% CI 0.55-2.12; P=.83). Compared with the control group, the use of DHIs was associated with significant changes in adverse events (RR 0.44, 95% CI 0.22-0.89; P=.02). Subgroup analysis suggested a positive effect of the digital platforms in improving wound healing (RR 2.19, 95% CI 1.35-3.56; P=.002). Although meta-analysis was not possible in terms of wound size, cost analysis, patient satisfaction, and wound reporting rates, most studies still demonstrated that DHIs were not inferior to usual care in managing chronic wounds. ConclusionsThe findings of our study demonstrate the viability of adopting DHIs to manage chronic wounds. However, more prominent, high-quality RCTs are needed to strengthen the evidence, and more detailed clinical efficacy research is required. Trial RegistrationPROSPERO CRD42023392415; https://tinyurl.com/4ybz6bs9

Abstract Background Radiation therapy is the cornerstone of treatment for adult-type diffuse gliomas, but recurrences are inevitable. Our study assessed the prognosis and recurrence pattern of different radiotherapy volumes after temozolomide-based chemoradiation in our institution. Methods The treatment plans were classified into two groups, the plan 1 intentionally involved the entire edema area while plan 2 did not. Retrospectively investigate the differences in outcomes of 118 adult-type diffuse gliomas patients between these two treatment plans. Then, patients who underwent relapse were selected to analyze their recurrence patterns. Continuous dynamic magnetic resonance images (MRI) were collected to categorized the recurrence patterns into central, in-field, marginal, distant, and cerebrospinal fluid dissemination (CSF-d) recurrence. Finally, the clinical and molecular characteristics which influenced progression were analyzed. Results Plan 1 (n = 63) showed a median progression-free survival (PFS) and overall survival (OS) of 9.5 and 26.4 months while plan 2 (n = 55) showed a median PFS and OS of 9.4 and 36.5 months (p = 0.418; p = 0.388). Treatment target volume had no effect on the outcome in patients with adult-type diffuse gliomas. And there was no difference in radiation toxicity (p = 0.388). Among the 90 relapsed patients, a total of 58 (64.4%) patients had central recurrence, 10 (11.1%) patients had in-field recurrence, 3 (3.3%) patients had marginal recurrence, 11 (12.2.%) patients had distant recurrence, and 8 (8.9%) patients had CSF-d recurrence. By treatment plans, the recurrence patterns were similar and there was no significant difference in survival. Reclassifying the progression pattern into local and non-local groups, we observed that oligodendroglioma (n = 10) all relapsed in local and no difference in PFS and OS between the two groups (p > 0.05). Multivariable analysis showed that subventricular zone (SVZ) involvement was the independent risk factor for non-local recurrence in patients with GBM (p

Abstract Background Clear cell renal cell cancer (ccRCC) is accompanied by T-cell infiltration. In this study, we sought to determine the difference in T-cell infiltration and the T-cell receptor (TCR) immune repertoire between ccRCC and peritumour tissue. Methods T-cell infiltration was examined using immunohistochemistry (IHC) and haematoxylin and eosin (HE) staining. The chi-squared test and Pearson correlation analysis were applied to evaluate the relationship between clinical traits and CD3, CD4, and CD8 expression. Immune repertoire sequencing (IR-Seq) was used to describe the profile of the TCR repertoire. Results The adjacent tissue showed increased expression of CD3, CD4 and CD8 compared with ccRCC tissue (P CD3 = 0.033; P CD4 = 0.014; P CD8 = 0.004). Indicated CD3+ T-cell density in ccRCC tissue was positively correlated with that in peritumour tissue (P = 0.010, r = 0.514), which implied the T cells in peritumour tissue directly infect the number of cells infiltrating in ccRCC tissue. Moreover, there was a positive correlation between Vimentin expression and indicated positive T-cell marker in ccRCC tissue (P CD3 = 0.035; P CD4 = 0.020; P CD8 = 0.027). Advanced stage revealed less CD4+ T-cell infiltration in ccRCC tissue (P CD4 = 0.023). The results from IR-Seq revealed an obvious increase in VJ and VDJ segment usage, as well as higher complementarity-determining region 3 (CDR3) amino acid (aa) clonotypes in ccRCC. The matched antigen recognized by the TCR of ccRCC may be potential targets. Conclusions The current study collectively demonstrates diminished T-cell infiltration and increased CDR3 aa diversity in ccRCC, which may be associated with immunotherapeutic targets for ccRCC patients.