Classification of mindfulness experiences from gamma-band effective connectivity: Application of machine-learning algorithms on resting, breathing, and body scan.

BACKGROUND AND OBJECTIVE: Practicing mindfulness is a mental process toward interoceptive awareness, achieving stress reduction and emotion regulation through brain-function alteration. Literature has shown that electroencephalography (EEG)-derived connectivity possesses the potential to differentiate brain functions between mindfulness naïve and mindfulness experienced, where such quantitative differentiation could benefit telediagnosis for mental health. However, there is no prior guidance in model selection targeting on the mindfulness-experience prediction. Here we hypothesized that the EEG effective connectivity could reach a good prediction performance in mindfulness experiences with brain interpretability. METHODS: We aimed at probing direct Directed Transfer Function (dDTF) to classify the participants' history of mindfulness-based stress reduction (MBSR), and aimed at optimizing the prediction accuracy by comparing multiple machine learning (ML) algorithms. Targeting the gamma-band effective connectivity, we evaluated the EEG-based prediction of the mindfulness experiences across 7 machine learning (ML) algorithms and 3 sessions (i.e., resting, focus-breathing, and body-scan). RESULTS: The support vector machine and naïve Bayes classifiers exhibited significant accuracies above the chance level across all three sessions, and the decision tree algorithm reached the highest prediction accuracy of 91.7 % with the resting state, compared to the classification accuracies with the other two mindful states. We further conducted the analysis on essential EEG channels to preserve the classification accuracy, revealing that preserving just four channels (F7, F8, T7, and P7) out of 19 yielded the accuracy of 83.3 %. Delving into the contribution of connectivity features, specific connectivity features predominantly located in the frontal lobe contributed more to classifier construction, which aligned well with the existing mindfulness literature. CONCLUSION: In the present study, we initiated a milestone of developing an EEG-based classifier to detect a person's mindfulness experience objectively. The prediction accuracy of the decision tree was optimal to differentiate the mindfulness experiences using the local resting-state EEG data. The suggested algorithm and key channels on the mindfulness-experience prediction may provide guidance for predicting mindfulness experiences using the EEG-based classification embedded in future wearable neurofeedback systems or plausible digital therapeutics.

Mitochondria in tumor immune surveillance and tumor therapies targeting mitochondria.

Mitochondria play a central role in cellular energy production and metabolic regulation, and their function has been identified as a key factor influencing tumor immune responses. This review provides a comprehensive overview of the latest advancements in understanding the role of mitochondria in tumor immune surveillance, covering both innate and adaptive immune responses. Specifically, it outlines how mitochondria influence the function of the tumor immune system, underscoring their crucial role in modulating immune cell behavior to either promote or inhibit tumor development and progression. Additionally, this review highlights emerging drug interventions targeting mitochondria, including novel small molecules with significant potential in cancer therapy. Through an in-depth analysis, it explores how these innovative strategies could improve the efficacy and outlook of tumor treatment.

Neoadjuvant immunochemotherapy followed by ex situ lung auto-transplant (Oto procedure) for central lung cancer: A case report with literature review.

Sleeve and double-sleeve lobectomies are lung-sparing techniques for treating central lung cancers. However, if the tumour extends to involve the bronchi and vessels, lung auto-transplantation may be an alternative to pneumonectomy. Neoadjuvant therapy after surgery is the most common strategy for patients with extensive central lung cancer. Herein, we report a case of central lung cancer in a patient who underwent immunochemotherapy as neoadjuvant therapy following lung auto-transplantation. A 68-year-old man with stage IIIA non-small cell lung cancer and left upper lobe squamous cell carcinoma underwent neoadjuvant immunochemotherapy. Following partial regression, a multidisciplinary team decided on a back-table procedure with auto-lung transplantation after pneumonectomy to preserve pulmonary function. The patient had an uneventful recovery and was discharged after three weeks with no residual tumour or lymph node metastases. Lung auto-transplantation can be successfully performed in non-lung transplantation centres, potentially broadening treatment options for patients with central lung cancer.

Promoting mercury removal in high humidity environments by hydrophobic modified activated carbon with methyl functional group.

The H2O content in the flue gas seriously inhibits the application of activated carbon injection adsorption mercury technology. Hydrophobic activated carbon was prepared by hexamethyldisiloxane (HMDSO) vapour deposition, the contact angle of water for hydrophobically modified AC increased from 42° to 143°, and H2O adsorption capacity decreased from 17.28 mg/g to 3.05 mg/g when relative humidity was 95%. The simulation results of water channels show that the number of water molecules escaping from the modified AC loaded with hydrophobic functional groups increased by 325%. When the water vapour content was 30%, the mercury removal efficiency of modified AC increased from 58.82% to 89.60% compared with AC, and the adsorption capacity increased by 10.6 µg/g. In high-humidity environments, NO and SO2 can produce corresponding acids for oxidising Hg0, thereby enhancing the adsorption efficiency of Hg0, while NH3 completes with Hg0 for the active sites on the surface of AC, which has an inhibitory effect.

Light signaling-dependent regulation of plastid RNA processing in Arabidopsis.

Light is a vital environmental signal that regulates the expression of plastid genes. Plastids are crucial organelles that respond to light, but the effects of light on plastid RNA processing following transcription remain unclear. In this study, we systematically examined the influence of light exposure on plastid RNA processing, focusing on RNA splicing and RNA editing. We demonstrated that light promotes the splicing of transcripts from the plastid genes rps12, ndhA, atpF, petB, and rpl2. Additionally, light increased the editing rate of the accD transcript at nucleotide 794 (accD-794) and the ndhF transcript at nucleotide 290 (ndhF-290), while decreasing the editing rate of the clpP transcript at nucleotide 559 (clpP-559). We have identified key regulators of signaling pathways, such as CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1), ELONGATED HYPOCOTYL 5 (HY5), and PHYTOCHROME-INTERACTING FACTORs (PIFs), as important players in the regulation of plastid RNA splicing and editing. Notably, COP1 was required for GENOMES UNCOUPLED1 (GUN1)-dependent repression of clpP-559 editing in the light. We showed that HY5 and PIF1 bind to the promoters of nuclear genes encoding plastid-localized RNA processing factors in a light-dependent manner. This study provides insight into the mechanisms underlying light-mediated post-transcriptional regulation of plastid gene expression.

Deapi-platycodin D3 attenuates osteoarthritis development via suppression of PTP1B.

Dysregulated chondrocyte metabolism is an essential risk factor for osteoarthritis (OA) progression. Maintaining cartilage homeostasis represents a promising therapeutic strategy for the treatment of OA. However, no effective disease-modifying therapy is currently available to OA patients. To discover potential novel drugs for OA, we screened a small-molecule natural product drug library and identified deapi-platycodin D3 (D-PDD3), which was subsequently tested for its effect on extracellular matrix (ECM) properties and on OA progression. We found that D-PDD3 promoted the generation of ECM components in cultured chondrocytes and cartilage explants and that intra-articular injection of D-PDD3 delayed disease progression in a trauma-induced mouse model of OA. To uncover the underlying molecular mechanisms supporting these observed functions of D-PDD3, we explored the targets of D-PDD3 via screening approach integrating surface plasmon resonance with liquid chromatography-tandem mass spectrometry. The results suggested that D-PDD3 targeted tyrosine-protein phosphatase non-receptor type 1 (PTP1B), deletion of which restored chondrocyte homeostasis and markedly attenuated destabilization of the medial meniscus induced OA. Further cellular and molecular analyses showed that D-PDD3 maintained cartilage homeostasis by directly binding to PTP1B and consequently suppressing the PKM2/AMPK pathway. These findings demonstrated that D-PDD3 was a potential therapeutic drug for the treatment of OA and that PTP1B served as a protein target for the development of drugs to treat OA. This study provided significant insights into the development of therapeutics for OA treatment, which, in turn, helped to improve the quality of life of OA patients and to reduce the health and economic burden.

Osteoarthritis is a degenerative disease with a high prevalence and consequently causes a burden to society. However, there is no convincing DMOAD exhibiting effective therapeutic effects on OA. In this study, we screened a small-molecule natural product drug library and identified D-PDD3, which was subsequently tested for its effect on extracellular matrix properties and on OA progression. Further cellular and in vivo experiments showed that D-PDD3 maintains cartilage homeostasis by directly binding to PTP1B and consequently suppressing the PKM2/AMPK pathway. Our results provided fundamental evidence for applying D-PDD3-based therapies against OA, which, in turn, helps to improve the quality of life in OA patients and to reduce the health and economic burden.

Comparative efficacy of balanced crystalloids versus 0.9% saline on delayed graft function and perioperative outcomes in kidney transplantation: a meta-analysis of randomised controlled trials.

BACKGROUND: Delayed graft function after kidney transplantation is linked to poor graft survival and increased chronic allograft injury. Recent guidelines suggest using balanced crystalloids over 0.9% saline owing to better metabolic profiles, but their impact on DGF remains unclear. METHODS: We searched PubMed, Embase, and Cochrane Central Registry of Clinical Trials from inception until February 29, 2024, and included RCTs that randomised adult participants to receive either intravenous balanced fluids or 0.9% saline intraoperatively. We pooled data using a random-effects model and present risk ratios (RRs) or mean differences, with 95% confidence intervals (CIs). We assessed individual study risk of bias using the modified Cochrane tool and certainty of evidence using GRADE. Outcomes analysed were delayed graft function incidence, vasopressor requirements, length of hospital stay, and postoperative metabolic profiles. RESULTS: Of 106 publications identified, we included 11 RCTs (n=1717). Pooled analysis showed that the use of balanced fluids was associated with a lower incidence of delayed graft function compared with 0.9% saline (RR 0.82, 95% CI: 0.69 to 0.98, P=0.01, moderate certainty). Balanced crystalloids were associated with higher postoperative serum pH, higher serum bicarbonate, and lower serum chloride concentration, but effects on vasopressor requirements, length of hospital stay, and serum creatinine were uncertain. CONCLUSIONS: Balanced crystalloid intravenous fluid therapy reduced delayed graft function incidence and maintained more favourable serum chemistry profiles compared with 0.9% saline in patients undergoing kidney transplantation. However, crystalloid type did not significantly influence vasopressor requirements and length of hospital stay.

Macrophage autophagy protects against acute kidney injury by inhibiting renal inflammation through the degradation of TARM1.

Macroautophagy/autophagy activation in renal tubular epithelial cells protects against acute kidney injury (AKI). However, the role of immune cell autophagy, such as that involving macrophages, in AKI remains unclear. In this study, we discovered that macrophage autophagy was an adaptive response during AKI as mice with macrophage-specific autophagy deficiency (atg5-/-) exhibited higher serum creatinine, more severe renal tubule injury, increased infiltration of ADGRE1/F4/80+ macrophages, and elevated expression of inflammatory factors compared to WT mice during AKI induced by either LPS or unilateral ischemia-reperfusion. This was further supported by adoptive transfer of atg5-/- macrophages, but not WT macrophages, to cause more severe AKI in clodronate liposomes-induced macrophage depletion mice. Similar results were also obtained in vitro that bone marrow-derived macrophages (BMDMs) lacking Atg5 largely increased pro-inflammatory cytokine expression in response to LPS and IFNG. Mechanistically, we uncovered that atg5 deletion significantly upregulated the protein expression of TARM1 (T cell-interacting, activating receptor on myeloid cells 1), whereas inhibition of TARM1 suppressed LPS- and IFNG-induced inflammatory responses in atg5-/- RAW 264.7 macrophages. The E3 ubiquitin ligases MARCHF1 and MARCHF8 ubiquitinated TARM1 and promoted its degradation in an autophagy-dependent manner, whereas silencing or mutation of the functional domains of MARCHF1 and MARCHF8 abolished TARM1 degradation. Furthermore, we found that ubiquitinated TARM1 was internalized from plasma membrane into endosomes, and then recruited by the ubiquitin-binding autophagy receptors TAX1BP1 and SQSTM1 into the autophagy-lysosome pathway for degradation. In conclusion, macrophage autophagy protects against AKI by inhibiting renal inflammation through the MARCHF1- and MARCHF8-mediated degradation of TARM1.Abbreviations: AKI, acute kidney injury; ATG, autophagy related; Baf, bafilomycin A1; BMDMs, bone marrow-derived macrophages; CCL2/MCP-1, C-C motif chemokine ligand 2; CHX, cycloheximide; CQ, chloroquine; IFNG, interferon gamma; IL, interleukin; IR, ischemia-reperfusion; MAP1LC3/LC3, microtubule-associated protein 1 light chain 3; LPS, lipopolysaccharide; MARCHF, membrane associated ring-CH-type finger; NC, negative control; NFKB, nuclear factor of kappa light polypeptide gene enhancer in B cells; NLRP3, NLR family, pyrin domain containing 3; NOS2, nitric oxide synthase 2, inducible; Rap, rapamycin; Wort, wortmannin; RT-qPCR, real-time quantitative polymerase chain reaction; Scr, serum creatinine; SEM, standard error of mean; siRNA, small interfering RNA; SYK, spleen tyrosine kinase; TARM1, T cell-interacting, activating receptor on myeloid cells 1; TAX1BP1, Tax1 (human T cell leukemia virus type I) binding protein 1; TECs, tubule epithelial cells; TNF, tumor necrosis factor; WT, wild type.

Tumor-derived exosomal ICAM1 promotes bone metastasis of triple-negative breast cancer by inducing CD8+ T cell exhaustion.

Exosomes, which are nanosized extracellular vesicles, have emerged as crucial mediators of the crosstalk between tumor cells and the immune system. Intercellular adhesion molecule 1 (ICAM1) plays a crucial role in multiple immune functions as well as in the occurrence, development and metastasis of cancer. As a glycoprotein expressed on the cell membrane, ICAM1 is secreted extracellularly on exosomes and regulates the immunosuppressive microenvironment. However, the role of exosomal ICAM1 in the immune microenvironment of breast cancer bone metastases remains unclear. This study aimed to elucidated the role of exosomal ICAM1 in facilitating CD8+ T cell exhaustion and subsequent bone metastasis in triple-negative breast cancer (TNBC). We demonstrated that TNBC cells release ICAM1-enriched exosomes, and the binding of ICAM1 to its receptor is necessary for the suppressive effect of CD8 T cell proliferation and function. This pivotal engagement not only inhibits CD8+ T cell proliferation and activation but also initiates the development of an immunosuppressive microenvironment that is conducive to TNBC tumor growth and bone metastasis. Moreover, ICAM1 blockade significantly impairs the ability of tumor exosomes to bind to CD8+ T cells, thereby inhibiting their immunosuppressive effects. The present study elucidates the complex interaction between primary tumors and the immune system that is mediated by exosomes and provides a foundation for the development of novel cancer immunotherapies that target ICAM1 with the aim of mitigating TNBC bone metastasis.

Intracellular calcium dysregulation in heart and brain diseases: Insights from induced pluripotent stem cell studies.

The central nervous system (CNS) plays a role in regulating heart rate and myocardial contractility through sympathetic and parasympathetic nerves, and the heart can impact the functional equilibrium of the CNS through feedback signals. Although heart and brain diseases often coexist and mutually influence each other, the potential links between heart and brain diseases remain unclear due to a lack of reliable models of these relationships. Induced pluripotent stem cells (iPSCs), which can differentiate into multiple functional cell types, stem cell biology and regenerative medicine may offer tools to clarify the mechanisms of these relationships and facilitate screening of effective therapeutic agents. Because calcium ions play essential roles in regulating both the cardiovascular and nervous systems, this review addresses how recent iPSC disease models reveal how dysregulation of intracellular calcium might be a common pathological factor underlying the relationships between heart and brain diseases.

PDZK1 protects against mechanical overload-induced chondrocyte senescence and osteoarthritis by targeting mitochondrial function.

Mechanical overloading and aging are two essential factors for osteoarthritis (OA) development. Mitochondria have been identified as a mechano-transducer situated between extracellular mechanical signals and chondrocyte biology, but their roles and the associated mechanisms in mechanical stress-associated chondrocyte senescence and OA have not been elucidated. Herein, we found that PDZ domain containing 1 (PDZK1), one of the PDZ proteins, which belongs to the Na+/H+ Exchanger (NHE) regulatory factor family, is a key factor in biomechanically induced mitochondrial dysfunction and chondrocyte senescence during OA progression. PDZK1 is reduced by mechanical overload, and is diminished in the articular cartilage of OA patients, aged mice and OA mice. Pdzk1 knockout in chondrocytes exacerbates mechanical overload-induced cartilage degeneration, whereas intraarticular injection of adeno-associated virus-expressing PDZK1 had a therapeutic effect. Moreover, PDZK1 loss impaired chondrocyte mitochondrial function with accumulated damaged mitochondria, decreased mitochondrion DNA (mtDNA) content and increased reactive oxygen species (ROS) production. PDZK1 supplementation or mitoubiquinone (MitoQ) application alleviated chondrocyte senescence and cartilage degeneration and significantly protected chondrocyte mitochondrial functions. MRNA sequencing in articular cartilage from Pdzk1 knockout mice and controls showed that PDZK1 deficiency in chondrocytes interfered with mitochondrial function through inhibiting Hmgcs2 by increasing its ubiquitination. Our results suggested that PDZK1 deficiency plays a crucial role in mediating excessive mechanical load-induced chondrocyte senescence and is associated with mitochondrial dysfunction. PDZK1 overexpression or preservation of mitochondrial functions by MitoQ might present a new therapeutic approach for mechanical overload-induced OA.

Validity of the I­FEED classification in assessing postoperative gastrointestinal impairment in patients undergoing elective lumbar spinal surgery with general anesthesia: a prospective observational study.

BACKGROUND: The I-FEED classification, scored 0-8, was reported to accurately describe the clinical manifestations of gastrointestinal impairment after colorectal surgery. Therefore, it is interesting to determine whether the I-FEED scoring system is also applicable to patients undergoing lumbar spine surgery. METHODS: Adult patients undergoing elective lumbar spine surgery were enrolled, and the I-FEED score was measured for 4 days after surgery. The I-FEED scoring system incorporates five elements: intake (score: 0, 1, 3), feeling nauseated (score: 0, 1, 3), emesis (score: 0, 1, 3), results of physical exam (score: 0, 1, 3), and duration of symptoms (score: 0, 1, 2). Daily I-FEED scores were summed, and the highest overall score is used to categorize patients into one of three categories: normal (0-2 points), postoperative gastrointestinal intolerance (POGI; 3-5 points), and postoperative gastrointestinal dysfunction (POGD; 6 + points). The construct validity hypothesis testing determines whether the I-FEED category is consistent with objective clinical findings relevant to gastrointestinal impairment, namely, the longer length of hospital stay (LOS), higher inhospital medical cost, more postoperative gastrointestinal medical treatment, and more postoperative non-gastrointestinal complications. RESULTS: A total of 156 patients were enrolled, and 25.0% of patients were categorized as normal, 49.4% POGI, and 25.6% POGD. Patients with higher I-FEED scores agreed with the four validity hypotheses. Patients with POGD had a significantly longer length of hospital stay (1 day longer median stay; p = 0.049) and more inhospital medical costs (approximately 500 Taiwanese dollars; p = 0.037), and more patients with POGD required rectal laxatives (10.3% vs. 32.5% vs. 32.5%; p = 0.026). In addition, more patients with POGD had non-gastrointestinal complications (5.1% vs. 11.7% vs. 30.0%; p = 0.034). CONCLUSION: This study contributes preliminary validity evidence for the I-FEED score as a measure for postoperative gastrointestinal impairment after elective lumbar spine surgery.

Research Progress of Drug Delivery Systems Targeting the Kidneys.

Chronic kidney disease (CKD) affects more than 10% of the global population, and its incidence is increasing, partially due to an increase in the prevalence of disease risk factors. Acute kidney injury (AKI) is an independent risk factor for CKD and end-stage renal disease (ESRD). The pathogenic mechanisms of CKD provide several potential targets for its treatment. However, due to off-target effects, conventional drugs for CKD typically require high doses to achieve adequate therapeutic effects, leading to long-term organ toxicity. Therefore, ideal treatments that completely cure the different types of kidney disease are rarely available. Several approaches for the drug targeting of the kidneys have been explored in drug delivery system research. Nanotechnology-based drug delivery systems have multiple merits, including good biocompatibility, suitable degradability, the ability to target lesion sites, and fewer non-specific systemic effects. In this review, the development, potential, and limitations of low-molecular-weight protein-lysozymes, polymer nanomaterials, and lipid-based nanocarriers as drug delivery platforms for treating AKI and CKD are summarized.

Role of m6A modifications in immune evasion and immunotherapy.

RNA modification has garnered increasing attention in recent years due to its pivotal role in tumorigenesis and immune surveillance. N6-methyladenosine (m6A) modification is the most prevalent RNA modification, which can affect the expression of RNA by methylating adenylate at the sixth N position to regulate the occurrence and development of tumors. Dysregulation of m6A affects the activation of cancer-promoting pathways, destroys immune cell function, maintains immunosuppressive microenvironment, and promotes tumor cell growth. In this review, we delve into the latest insights into how abnormalities in m6A modification in both tumor and immune cells orchestrate immune evasion through the activation of signaling pathways. Furthermore, we explore how dysregulated m6A modification in tumor cells influences immune cells, thereby regulating tumor immune evasion via interactions within the tumor microenvironment (TME). Lastly, we highlight recent discoveries regarding specific inhibitors of m6A modulators and the encapsulation of m6A-targeting nanomaterials for cancer therapy, discussing their potential applications in immunotherapy.

Clinical values of serum C5a in Alzheimer's disease patients with different dementia stages.

Alzheimer's disease (AD) is characterized by abnormal inflammatory responses, and complement C5a (C5a) is known to initiate inflammation. This study aimed to investigate the associations between serum C5a, inflammatory responses, and cognitive function in AD patients. A total of 242 AD patients and 132 age-matched controls were included. Enzyme-linked immunosorbent assay revealed increased levels of C5a, interleukin (IL)-4, IL-6, IL-10, IL-1ß, and tumor necrosis factor (TNF)-α with advancing stages of AD. Pearson correlation coefficient and receiver operating characteristic curve revealed positive correlations between serum C5a levels, inflammatory cytokine levels, Neuropsychiatric Inventory (NPI) and Activities of Daily Living (ADL) scores, and negative correlations with Mini-mental State Examination (MMSE) and Montreal cognitive assessment (MoCA) scores. Serum C5a above 68.68 pg/mL could aid in the diagnosis of AD. Multivariable logistic analysis revealed that serum C5a was an independent risk factor for IL-1ß/IL-6/IL-10/TNF-α and an independent protective factor for IL-4. Higher serum C5a levels were associated with lower MMSE and MoCA scores. In conclusion, elevated serum C5a levels were beneficial for AD diagnosis and predictive of inflammation and cognitive dysfunction.

Investigating the Immunogenic Cell Death-Dependent Subtypes and Prognostic Signature of Triple-Negative Breast Cancer.

Recently, immunotherapy has emerged as a promising and effective method for treating triple-negative breast cancer (TNBC). However, challenges still persist. Immunogenic cell death (ICD) is considered a prospective treatment and potential combinational treatment strategy as it induces an anti-tumor immune response by presenting the antigenic epitopes of dead cells. Nevertheless, the ICD process in TNBC and its impact on disease progression and the response to immunotherapy are not well understood. In this study, we observed dysregulation of the ICD process and verified the altered expression of prognostic ICD genes in TNBC through quantitative real-time polymerase chain reaction (qRT-PCR) analysis. To investigate the potential role of the ICD process in TNBC progression, we determined the ICD-dependent subtypes, and two were identified. Analysis of their distinct tumor immune microenvironment (TIME) and cancer hallmark features revealed that Cluster 1 and 2 corresponded to the immune "cold" and "hot" phenotypes, respectively. In addition, we constructed the prognostic signature ICD score of TNBC patients and demonstrated its clinical independence and generalizability. The ICD score could also serve as a potential biomarker for immune checkpoint blockade and may aid in the identification of targeted effective agents for individualized clinical strategies. Supplementary Information: The online version contains supplementary material available at 10.1007/s43657-023-00133-x.

Immunocyte profiling changes in patients received epidural versus intravenous analgesia after pancreatectomy: A randomized controlled trial.

BACKGROUND: Perioperative immunosuppressants, such as surgical stress and opioid use may downregulate anti-cancer immunocytes for patients undergoing pancreatectomy. Thoracic epidural analgesia (TEA) may attenuate these negative effects and provide better anti-cancer immunocyte profile change than intravenous analgesia using opioid. METHODS: We randomly assigned 108 adult patients undergoing pancreatectomy to receive one of two 72-h postoperative analgesia protocols: one was TEA, and the other was intravenous patient-controlled analgesia (IV-PCA). The perioperative proportional changes of immunocytes relevant to anticancer immunity-namely natural killer (NK) cells, cytotoxic T cells, helper T cells, mature dendritic cells, and regulatory T (Treg) cells were determined at 1 day before surgery, at the end of surgery and on postoperative day 1,4 and 7 using flow cytometry. In addition, the progression-free survival and overall survival between the two groups were compared. RESULTS: After surgery, the proportions of NK cells and cytotoxic T cells were significantly decreased; the proportion of B cells and mature dendritic cells and Treg cells were significantly increased. However, the proportions of helper T cells exhibited no significant change. These results were comparable between the two groups. Furthermore, there were no significant differences in progression-free survival (52.75 [39.96] and 57.48 [43.66] months for patients in the TEA and IV-PCA groups, respectively; p = 0.5600) and overall survival (62.71 [35.48] and 75.11 [33.10] months for patients in the TEA and IV-PCA groups, respectively; p = 0.0644). CONCLUSIONS: TEA was neither associated with favorable anticancer immunity nor favorable oncological outcomes for patients undergoing pancreatectomy.

Comparisons in analgesic effects between ultrasound-guided erector spinae plane block and surgical intercostal nerve block after video-assisted thoracoscopic surgery: A randomized controlled trial.

STUDY OBJECTIVE: This study aimed to compare the analgesic effects of anesthesiologist-administrated erector spinae plane block (ESPB) and surgeon-administrated intercostal nerve block (ICNB) following video-assisted thoracoscopic surgery (VATS). DESIGN: Randomized, controlled, double-blinded study. SETTING: Operating room, postoperative recovery room and ward in two centers. PATIENTS: One hundred patients, ASA I-III and scheduled for elective VATS. INTERVENTIONS: The anesthesiologist-administrated ESPB under ultrasound guidance or surgeon-administrated ICNB under video-assisted thoracoscopy was randomly provided during VATS. Regular oral non-opioid analgesic combined with intravenous rescue morphine were prescribed for multimodal analgesia after surgery. MEASUREMENTS: The primary outcomes were the pain score and morphine consumption during 48 h after surgery. Postoperative pain intensity were assessed using the 10-cm visual analogue scale at 1 h, 24 h, and 48 h after surgery. Morphine consumption at these time points was compared between the two study groups. Furthermore, oral weak opioid rescue analgesic was also provided at 24 h after surgery. Postoperative quality of recovery at 24 h was also assessed using the QoR-15 questionnaire, along with duration of chest tube drainage and hospital stay were compared as secondary outcomes. MAIN RESULTS: Patients in the two study groups had comparable baseline characteristics, and surgical types were also similar. Postoperative VAS changes at 1 h, 24 h, and 48 h after surgery were also comparable between the two study groups. Both groups had low median scores (<4.0) at all time points (all p > 0.05). Patients in the ESPB group required statistically non-significant higher 48-h morphine consumption [3 (0-6) vs. 0 (0-6) mg in the ESPB group and ICNB group respectively; p = 0.135] and lower numbers of oral rescue analgesic (0.4 ± 1.2 vs. 1.0 ± 1.8 in the ESPB group and ICNB group respectively; p = 0.059). Additionally, patients in the two study groups had similar QoR15 scores and lengths of hospital stay. CONCLUSIONS: Both anesthesiologist-administered ultrasound-guided ESPB and surgeon-administered VATS ICNB were effective analgesic techniques for patients undergoing VATS for tumor resection.

Integrated transcriptome and proteome analysis provides insights into CpFPA1 for floral induction in Chimonanthus praecox (Magnoliidae) without FLC in genome.

KEY MESSAGE: We used transcriptomic and proteomic association analysis to reveal the critical genes/proteins at three key flower bud differentiation stages and overexpression of CpFPA1 in Arabidopsis resulted in earlier flowering. Wintersweet (Chimonanthus praecox), a rare winter-flowering woody plant, is well known for its unique blooming time, fragrance and long flowering period. However, the molecular mechanism of flowering in C. praecox remains poorly unclear. In this study, we used transcriptomic and proteomic association analysis to reveal the critical genes/proteins at three key flower bud (FB) differentiation stages (FB.Apr, FB.May and FB.Nov) in C. praecox. The results showed that a total of 952 differential expressed genes (DEGs) and 40 differential expressed proteins (DEPs) were identified. Gene ontology (GO) enrichment revealed that DEGs in FB.Apr/FB.May comparison group were mainly involved in metabolic of biological process, cell and cell part of cellular component and catalytic activity of molecular function. In the EuKaryotic Orthologous Groups (KOG) functional classification, DEPs were predicted mainly in the function of general function prediction only (KOG0118), post-translational modification, protein turnover and chaperones. The autonomous pathway genes play an essential role in the floral induction. Based on transcriptome and proteome correlation analysis, six candidate genes associated with the autonomous pathway were identified, including FPA1, FPA2a, FPA2b, FCA, FLK, FY. Furthermore, CpFPA1 was isolated and functionally characterized, and ectopic expression of CpFPA1 in Arabidopsis Columbia (Col-0) resulted in earlier flowering. These data could contribute to understand the function of CpFPA1 for floral induction and provide information for further research on the molecular mechanisms of flowering in wintersweet.