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Abstract Platelets are a significant component of the cell population in the tumour microenvironment (TME). Platelets influence other immune cells and perform cross-talk with tumour cells, playing an important role in tumour development. Extracellular vesicles (EVs) are small membrane vesicles released from the cells into the TME. They can transfer biological information, including proteins, nucleic acids, and metabolites, from secretory cells to target receptor cells. This process affects the progression of various human diseases, particularly cancer. In recent years, several studies have demonstrated that platelet-derived extracellular vesicles (PEVs) can help regulate the malignant biological behaviours of tumours, including malignant proliferation, resistance to cell death, invasion and metastasis, metabolic reprogramming, immunity, and angiogenesis. Consequently, PEVs have been identified as key regulators of tumour progression. Therefore, targeting PEVs is a potential strategy for tumour treatment. Furthermore, the extensive use of nanomaterials in medical research has indicated that engineered PEVs are ideal delivery systems for therapeutic drugs. Recent studies have demonstrated that PEV engineering technologies play a pivotal role in the treatment of tumours by combining photothermal therapy, immunotherapy, and chemotherapy. In addition, aberrant changes in PEVs are closely associated with the clinicopathological features of patients with tumours, which may serve as liquid biopsy markers for early diagnosis, monitoring disease progression, and the prognostic assessment of patients with tumours. A comprehensive investigation into the role and potential mechanisms of PEVs in tumourigenesis may provide novel diagnostic biomarkers and potential therapeutic strategies for treating human tumours.

Background: Periodontitis is one of the most common chronic oral inflammatory diseases. Over the past decade, herpes viruses, particularly Epstein-Barr virus (EBV), have been considered promising pathogenic candidates for periodontitis. However, the specific mechanism by which EBV contributes to the development of periodontitis is still unknown. This study aimed to explore the mechanism of EBV underlying the inflammatory response in human gingival fibroblasts (HGFs). Materials and methods: HGFs were stimulated with different concentrations of EBV (104, 105, 106, 107, and 108 DNA copies/mL) for 0, 8, 24, or 48 hours. The mRNA levels of interleukin (IL)-1β, tumour necrosis factor-α (TNF-α), IL-8, monocyte chemoattractant protein-1 (MCP-1), and Toll-like receptor 9 (TLR9) were measured using quantitative real-time polymerase chain reaction (PCR). Enzyme-linked immunosorbent assays (ELISAs) were performed for determining the mRNA and protein levels of IL-1β, TNF-α, IL-8, and MCP-1. Real-time PCR and ELISA were performed to determine the protein levels of IL-1β, TNF-α, IL-8, and MCP-1. Activation of the TLR9/myeloid differentiation factor 88 (MyD88)/nuclear factor kappa B (NF-κB) pathway was evaluated using western blotting. Results: The expressions of IL-1β, TNF-α, IL-8, and MCP-1 were significantly upregulated in HGFs under EBV stimulation in a concentration- and time-dependent manner. EBV promoted TLR9 and MyD88 expression and induced NF-κB transcription. On the contrary, the upregulation of these factors and the activation of NF-κB pathway were drastically inhibited by TLR9 antagonists. Conclusions: Our findings demonstrate that EBV promotes the production of inflammatory cytokines IL-1β and TNF-α and chemokines IL-8 and MCP-1 in HGFs through the TLR9/MyD88/NF-κB pathway.

BackgroundMindfulness training has been shown to promote positive mental health outcomes and related changes in neural networks such as the default mode network, which has a central node in the posterior cingulate cortex (PCC). Previous work from our group reported on the impact of a novel, neurofeedback augmented mindfulness training (NAMT) task on regulation of PCC hemodynamic activity in typically developing adolescents. The present pilot study aimed to expand on this finding by examining the pre-post changes of the NAMT task on resting-state functional connectivity of the PCC.MethodsThirty-one typically developing adolescents (14.77 ± 1.23 years; 45% female) underwent a resting-state functional magnetic resonance imaging scan both before and after completing the NAMT task. A linear mixed effects model was used to assess for changes in functional connectivity of the PCC across the two resting-state runs.ResultsData did not support the hypothesized decrease in connectivity between the PCC seed and other DMN regions from pre- to post-NAMT task. However, we observed a significant increase in functional connectivity between the PCC and a cluster encompassing the left hippocampus and amygdala following completion of the NAMT task (run 1 Fisher’s Z = 0.16; run 2 Fisher’s Z = 0.26).ConclusionAlthough preliminary, this finding suggests NAMT has the potential to strengthen connectivity between default mode and salience regions. We speculate that such changed connectivity may facilitate enhanced self-referential and emotional processing in adolescents.Clinical trial registrationhttps://clinicaltrials.gov/, identifier NCT04053582.

Abstract High‐frequency oscillatory activity in cognition‐related neural circuits during wakefulness consistently induces the growth of dendritic spines and axonal terminals. Although these structural changes are essential for cognitive functions, it is hypothesized that if these newly expanded structures fail to establish functional connections, they may become superfluous. Sleep is believed to facilitate the reduction of such redundant structures to maintain neural homeostasis. However, the mechanisms underlying this pruning process during sleep remain poorly understood. In this study, that melatonin type 3 receptors (MT3Rs) are selectively expressed in the stellate neurons of the medial entorhinal cortex (MEC) is demonstrated, an area where high melatonin levels are detected during sleep. Activation of MT3Rs during sleep initiates the shrinkage of dendritic spines in stellate neurons by downregulating neural network activity and dephosphorylating synaptic proteins in the MEC. This process is disrupted when MT3R expression is knocked down or when MT3Rs are blocked during sleep. Notably, interference with MT3Rs in the MEC during sleep impairs the acquisition of spatial memory but does not affect object memory acquisition following sleep. These findings reveal novel molecular mechanisms involving melatonin and MT3Rs in the regulation of dendritic spine shrinkage during sleep, which is crucial for the acquisition and consolidation of spatial memory.

Background: This study delves into the intricacies of resistant hypertension (RH), a prevalent yet enigmatic chronic cardiovascular ailment that is linked to a myriad of complications. Although its full pathogenesis is still shrouded in mystery, the field of proteomics offers a beacon of hope, with its potential to shed light on the proteins that orchestrate the tapestry of life. Harnessing the power of proteomics is essential for demystifying the pathogenesis of RH, enabling more precise diagnostics and treatments, and ultimately improving prognostic outcomes. Methods: Our approach was to employ rigorous statistical analyses to home in on proteins with significant expression variances between our two cohorts. We complemented this with bioinformatics tools to unravel the intricate functions and pathways of these proteins. By synthesizing these insights with the clinical profiles of our patients, we were able to distill a set of definitive biomarkers with diagnostic potential. In our quest for clarity, we also embarked on a retrospective journey, amassing and scrutinizing clinical data from both RH and hypertension (HTN) patients. We crafted and rigorously assessed risk factor models to evaluate their diagnostic prowess. Results: Our exploration spanned across 30 blood samples from RH patients and 20 from those grappling with HTN. Our inquiry yielded some compelling revelations: (1) RH patients showcased 29 unique proteins, in contrast to the 59 unique proteins found in HTN patients. A deeper dive into the proteomic data unveiled molecular functions predominantly tied to lipid metabolism, protein networking, and oxidative stress, with a spotlight on pathways such as cholesterol metabolism, coagulation, and the complement cascade. (2) By charting receiver operating characteristic curves and rigorously analyzing the proteomic data, we surfaced 11 proteins with notable diagnostic potential, tightly interwoven with clinical metrics. Conclusion: Our research has pinpointed 11 proteins that stand as promising serum biomarkers, endowed with significant diagnostic value. This discovery marks a stride towards a more nuanced understanding and management of resistant hypertension.

Abstract This study investigates the expression and significance of urinary protein and coagulation‐fibrinolysis indicators in preeclampsia, categorized into mild preeclampsia (109 cases) and severe preeclampsia (97 cases) based on disease severity. Additionally, 110 patients with gestational hypertension (gestational hypertension group) were included for comparative analysis. General information, laboratory indicators, urinary protein, and coagulation‐fibrinolysis indicator levels were collected for each group. Significant differences were observed in blood pressure among groups (P .05). Total cholesterol, triglycerides, and low‐density Lipoprotein levels in severe preeclampsia were higher than those in mild preeclampsia and gestational hypertension groups, whereas high‐density lipoprotein, albumin, and platelet levels were lower in severe preeclampsia. No significant differences were observed in prothrombin time or D‐dimer levels among groups (P > .05). Urinary protein, urinary protein quantification, activated partial thromboplastin time, thrombin time, and fibrinogen were identified as influencing factors for adverse maternal and infant outcomes in severe preeclampsia patients. The study concludes that urinary protein and coagulation‐fibrinolysis indicators are elevated in preeclampsia, particularly in severe preeclampsia cases, suggesting their potential use as diagnostic influencing factors for severe preeclampsia.

Abstract. Pancreatic β-cell failure due to a reduction in function and mass has been defined as a primary contributor to the progression of type 2 diabetes (T2D). Reserving insulin-producing β-cells and hence restoring insulin production are gaining attention in translational diabetes research, and β-cell replenishment has been the main focus for diabetes treatment. Significant findings in β-cell proliferation, transdifferentiation, pluripotent stem cell differentiation, and associated small molecules have served as promising strategies to regenerate β-cells. In this review, we summarize current knowledge on the mechanisms implicated in β-cell dynamic processes under physiological and diabetic conditions, in which genetic factors, age-related alterations, metabolic stresses, and compromised identity are critical factors contributing to β-cell failure in T2D. The article also focuses on recent advances in therapeutic strategies for diabetes treatment by promoting β-cell proliferation, inducing non-β-cell transdifferentiation, and reprograming stem cell differentiation. Although a significant challenge remains for each of these strategies, the recognition of the mechanisms responsible for β-cell development and mature endocrine cell plasticity and remarkable advances in the generation of exogenous β-cells from stem cells and single-cell studies pave the way for developing potential approaches to cure diabetes.

Ectopic thyroid arises from abnormal development of thyroid primordial tissues as it migrates to the lower interstitium during the embryonic period, which can occur at various locations during the descent process. However, ectopic thyroid in the subdiaphragmatic area is extremely rare. In this case, we report a case of ectopic thyroid located in the hepatoduodenal ligament. The 60-year-old female patient was admitted to hospital with gallbladder stones and cholecystitis. Preoperative imaging showed a mass in the hepatoduodenal ligament. As the patient declined a needle biopsy of the mass, the nature of the mass remained unclear prior to surgery. The patient subsequently underwent laparoscopic cholecystectomy and exploratory resection of the mass. The histopathology of the resected mass showed the characteristics of ectopic thyroid, and immunohistochemical staining revealed positive expression of thyroid transcription factor-1 and thyroglobulin. The diagnosis of ectopic thyroid was established. Upon confirming the diagnosis, comprehensive neck examination revealed the presence of a normally functioning thyroid gland. Throughout the four-year follow-up period, the patient’s thyroid ultrasonography and thyroid function tests indicated no abnormalities. Ectopic thyroid in the hepatoduodenal ligament and surrounding areas is an extremely rare clinical abnormality, achieving a clear diagnosis before initiating treatment offers diagnostic and treatment insights and clues for clinicians when differentiating masses within this region.

Background/purpose: The ligature-induced periodontitis model is an effective approach to induce inflammation and bone loss similar to that of human periodontitis. Previous clinical and in vitro studies have shown the involvement of lymphocytes in periodontitis, while, the local and systemic profile of immune cells associated with periodontitis in the ligature-induced periodontitis model in mice remains unclear. Materials and methods: Experimental periodontitis was constructed in mice by ligating around the maxillary second molars for 14 and 28 days, respectively. Alveolar bone loss was assessed by micro-computed tomography (micro-CT). Hematoxylin and eosin (H&E) and tartrate-resistant acid phosphatase (TRAP) staining were used to evaluate the histological changes in the periodontal tissues. B and T cells in the cervical lymph nodes, spleen, and peripheral blood were analyzed by flow cytometry. Results: The 14-day ligation effectively induced significant periodontal inflammation and alveolar bone loss in C57BL/6J mice, which were progressive and maintained for a relatively long-term period until day 28. In addition, CD3+ T cells and CD19+ B cells were the dominant population in both health and disease, and the B cell population within the cervical lymph nodes (LN) increased significantly under periodontitis condition, while, no significant differences of the T and B cell population among the spleen and peripheral blood were observed. Conclusion: The ligature-induced periodontitis mice model was established to perform a longitudinal assessment of changes in periodontal tissues morphologically and histologically, meanwhile, explore the local and systemic changes of the predominant immune-associated cells.

Abstract Most patients with hypertension are complicated with insulin resistance (IR), which is one of the risk factors of hypertension and can increase the level of serum homocysteine (Hcy) by affecting Hcy's metabolic enzyme and insulin level. Investigations in recent years have shown that Hcy is an independent risk factor for cardiovascular diseases. At present, folic acid is the prominent medicine used to reduce Hcy, but its effection for Hcy has an obvious individual difference, which is closely related to individual genes. Moreover, folic acid is chiefly used in patients with Hcy ≥15 μmol/L, but Hcy ≥10 μmol/L has had an adverse effect on the cardiovascular system. Randomized clinical trials have shown that dapagliflozin can improve IR. Therefore, whether it can reduce Hcy has become a new direction. This study was a retrospective case–control study. Patients with high serum Hcy and hypertension complicated with IR were divided into two groups: the dapagliflozin group (n = 166) and the control group (n = 198). Before and after 12 weeks of treatment, the changes in serum Hcy and IR index were measured and compared. We found that dapagliflozin could reduce the serum Hcy level of patients with hypertension and IR to a certain extent. Dapagliflozin could be a viable option for hypertension complicated with IR and hyperhomocysteinemia. However, these findings need to be further confirmed in future randomized clinical trials with a large number of samples.

Abstract. Background:. Pancreatic β-cells elevate insulin production and secretion through a compensatory mechanism to override insulin resistance under metabolic stress conditions. Deficits in β-cell compensatory capacity result in hyperglycemia and type 2 diabetes (T2D). However, the mechanism in the regulation of β-cell compensative capacity remains elusive. Nuclear factor-Y (NF-Y) is critical for pancreatic islets' homeostasis under physiological conditions, but its role in β-cell compensatory response to insulin resistance in obesity is unclear. Methods:. In this study, using obese (ob/ob) mice with an absence of NF-Y subunit A (NF-YA) in β-cells (ob, Nf-ya βKO) as well as rat insulinoma cell line (INS1)-based models, we determined whether NF-Y-mediated apoptosis makes an essential contribution to β-cell compensation upon metabolic stress. Results:. Obese animals had markedly augmented NF-Y expression in pancreatic islets. Deletion of β-cell Nf-ya in obese mice worsened glucose intolerance and resulted in β-cell dysfunction, which was attributable to augmented β-cell apoptosis and reactive oxygen species (ROS). Furthermore, primary pancreatic islets from Nf-ya βKO mice were sensitive to palmitate-induced β-cell apoptosis due to mitochondrial impairment and the attenuated antioxidant response, which resulted in the aggravation of phosphorylated c-Jun N-terminal kinase (JNK) and cleaved caspase-3. These detrimental effects were completely relieved by ROS scavenger. Ultimately, forced overexpression of NF-Y in INS1 β-cell line could rescue palmitate-induced β-cell apoptosis, dysfunction, and mitochondrial impairment. Conclusion:. Pancreatic NF-Y might be an essential regulator of β-cell compensation under metabolic stress.

Colon adenocarcinoma (COAD) is among the most prevalent cancers worldwide, ranking as the third most prevalent malignancy in incidence and mortality. The somatostatin receptor (SSTR) family comprises G-protein-coupled receptors (GPCRs), which couple to inhibitory G proteins (Gi and Go) upon binding to somatostatin (SST) analogs. GPCRs are involved in hormone release, neurotransmission, cell growth inhibition, and cancer suppression. However, their roles in COAD remain unclear. This study used bioinformatics to investigate the expression, prognosis, gene alterations, functional enrichment, and immunoregulatory effects of the SSTR family members in COAD. SSTR1-4 are differentially downregulated in COAD, and low SSTR2 expression indicates poor survival. Biological processes and gene expression enrichment of the SSTR family in COAD were further analyzed using the Kyoto Encyclopedia of Genes and Genomes and Gene Ontology. A strong correlation was observed between SSTR expression and immune cell infiltration. We also quantified SSTR2 expression in 25 COAD samples and adjacent normal tissues using quantitative real-time polymerase chain reaction. We analyzed its correlation with the dendritic cell–integrin subunit alpha X marker gene. The biomarker exploration of the solid tumors portal was used to confirm the correlation between SSTR2 with immunomodulators and immunotherapy responses. Our results identify SSTR2 as a promising target for COAD immunotherapy. Our findings provide new insights into the biological functions of the SSTR family and their implications for the prognosis of COAD.

Abstract Background Partial restoration combined with periodontal root coverage surgery can be applied to the treatment of non-carious cervical lesions (NCCLs) accompanied with gingival recessions in clinical practice. However, the feasibility of NCCL partial restorative treatment from a biomechanical perspective remains unclear. This study aimed to investigate the effect of partial restorations on stress distributions in the NCCLs of mandibular first premolars via three-dimensional finite element analysis. Methods Three-dimensional finite element models of buccal wedge-shaped NCCLs in various locations of a defected zenith (0 mm, 1 mm, and 2 mm) were constructed and divided into three groups (A, B, and C). Three partially restored NCCL models with different locations of the lower restoration border (1 mm, 1.5 mm, and 2 mm), and one completely restored NCCL model were further constructed for each group. The following restorative materials were used in all restoration models: composite resin (CR), glass-ionomer cement (GIC), and mineral trioxide aggregate (MTA). The first principal stress distributions under buccal oblique loads of 100 N were analyzed. Restoration bond failures were also evaluated based on stress distributions at dentin-restoration interfaces. Results When the partial restoration fully covered the defected zenith, the first principal stress around the zenith decreased and the maximum tensile stress was concentrated at the lower restoration border. When the partial restoration did not cover the defected zenith, the first principal stress distribution patterns were similar to those in unrestored models, with the maximum tensile stress remaining concentrated at the zenith. As the elastic modulus of the restorative material was altered, the stress distributions at the interface were not obviously changed. Restoration bond failures were not observed in CR, but occurred in GIC and MTA in most models. Conclusions Partial restorations that fully covered defected zeniths improved the stress distributions in NCCLs, while the stress distributions were unchanged or worsened under other circumstances. CR was the optimal material for partial restorations compared to GIC and MTA.

Abstract Oxidative stress had been linked to hypertensive renal impairment in previous investigations. Superoxide dismutase (SOD) was a clinically available oxidative stress biomarker. The association between SOD and the microalbuminuria in hypertensive patients has not been established. From January 2017 to December 2018, data on 690 patients with essential hypertension were collected retrospectively at Shandong Provincial Qianfoshan Hospital. Patients were divided into hypertension with microalbuminuria group (HM) and hypertension without microalbuminuria group (NHM). Clinical data from patients were collected and compared between the two groups. Spearman correlation analysis was used to analyze the correlation between UACR and SOD. Univariate and multivariate logistic regression analyses were used to screen for the risk factors for HM. Our research included 556 patients in the NHM group and 134 patients in the HM group. Spearman correlation analysis showed a negative correlation between SOD and UACR (P

IntroductionPreeclampsia (PE), at early onset, is likely to be diagnosed as gestational hypertension (GH). Some cases of GH rapidly progress to PE within a short period of time, increasing the mortality rate of pregnant women and adverse events in neonates during the peripartum period. Oxidative stress participates in the occurrence and progression of PE. However, it is unknown whether the progression of GH to PE can be predicted.MethodsA total of 1548 patients diagnosed with PE (649 cases) or GH (899 cases) from January 2016 to June 2022 were selected as the study subjects. The 1548 patients were randomly divided into the training set (1083 cases) and the validation set (465 cases) in a 7:3 ratio. General and clinical data were collected to construct a risk factor prediction model for PE.ResultsWe found that (1) Systolic blood pressure (SBP), and uric acid (UA)/ superoxide dismutase (SOD) were the risk factors for the progression of GH to PE; (2) A nomogram was constructed from the prediction model, and the area under the curve (AUC) was 0.95, with a sensitivity of 87.4%, a specificity of 92.8%; (3) Build a model simplified scoring system. PE was most strongly predicted by UA/SOD (100 points), SBP (29 points), and serum potassium (19 points). The AUC was 0.92, with a sensitivity of 91.0%, a specificity of 81.7%. The clinical decision analysis curve shows that the model exhibits positive benefits when the threshold probability is at 0.01–0.91.ConclusionThese findings show that UA/SOD can predict progression of GH to PE.

Methylation has a close relationship with immune reactions, metastasis, and cancer cell growth. Additionally, RNA methylation-related proteins have emerged as potential cancer therapeutic targets. The connection between the tumor microenvironment (TME) and methylation-related genes (MRGs) remains unclear. We explored the expression patterns of the MRGs in the genome and transcriptional fields of 796 prostate cancer (PCa) samples using two separate data sets. We identified a relationship between patient clinicopathological characteristics, prognosis, TME cell infiltrating qualities, and different MRG changes, as well as the identification of two distinct molecular groupings. Then, we formed an MRGs model to predict overall survival (OS), and we tested the accuracy of the model in patients with PCa. In addition, we developed a very accurate nomogram to improve the MRG model’s clinical applicability. The low-risk group had fewer tumor mutational burden (TMB), greater tumor immune dysfunction and exclusion (TIDE) ratings, fewer mutant genes, and better OS prospects. We discuss how MGRs may affect the prognosis, clinically important traits, TME, and immunotherapy responsiveness in PCa. In order to get a better understanding of MRGs in PCa, we could further explore the prognosis and create more effective immunotherapy regimens to open new avenues.

Optically pumped magnetometers (OPMs) can capture brain activity but are susceptible to magnetic noise. The objective of this study was to evaluate a novel methodology used to reduce magnetic noise in OPM measurements. A portable magnetoencephalography (MEG) prototype was developed with OPMs. The OPMs were divided into primary sensors and reference sensors. For each primary sensor, a synthetic gradiometer (SG) was constructed by computing a secondary sensor that simulated noise with signals from the reference sensors. MEG data from a phantom with known source signals and six human participants were used to assess the efficacy of the SGs. Magnetic noise in the OPM data appeared predominantly in a low frequency range (p < 0.01), enhanced the signal-to-noise ratio (SNR) (p < 0.001) and improved the accuracy of source localization (p < 0.02). The SGs precisely revealed movement-evoked magnetic fields in MEG data recorded from human participants. SGs provided an effective method to enhance SNR and improve the accuracy of source localization by suppressing noise. Software-simulated SGs may provide new opportunities regarding the use of OPM measurements in various clinical and research applications, especially those in which movement is relevant.

Rational: Cholesterol sulfate (CS) is the most abundant known sterol sulfate in human plasma, and it plays a significant role in the control of metabolism and inflammatory response, which contribute to the pathogenesis of insulin resistance, β-cell dysfunction and the resultant development of diabetes. However, the role of CS in β-cells and its effect on the development of diabetes remain unknown. Here, we determined the physiological function of CS in pancreatic β-cell homeostasis.Materials and Methods: Blood CS levels in streptozotocin (STZ)- or high-fat diet-induced diabetic mice and patients with type 1 or 2 diabetes were determined by LC-MS/MS. The impact of CS on β-cell mass and insulin secretion was investigated in vitro in isolated mouse islets and the β-cell line INS-1 and in vivo in STZ-induced diabetic mice. The molecular mechanism of CS was explored by viability assay, EdU incorporation analysis, flow cytometry, intracellular Ca2+ influx analysis, mitochondrial membrane potential and cellular ROS assays, and metabolism assay kits.Results: Plasma CS levels in mice and humans were significantly elevated under diabetic conditions. CS attenuated diabetes in a low-dose STZ-induced mouse model. Mechanistically, CS promoted β-cell proliferation and protected β-cells against apoptosis under stressful conditions, which in turn preserved β-cell mass. In addition, CS supported glucose transporter-2 (GLUT2) expression and mitochondrial integrity, which then resulted in a less reactive oxygen species (ROS) generation and an increase in ATP production, thereby enabling insulin secretion machinery in the islets to function adequately.Conclusion: This study revealed a novel dual role of CS in integrating β-cell survival and cell function, suggesting that CS might offer a physiologic approach to preserve β-cells and protect against the development of diabetes mellitus.

Salt stress is an adverse environmental factor for plant growth and development. Under salt stress, plants can activate the selective autophagy pathway to alleviate stress. However, the regulatory mechanism of selective autophagy in response to salt stress remains largely unclear. Here, we report that the selective autophagy receptor PagNBR1 (neighbor of BRCA1) is induced by salt stress in Populus. Overexpression of PagNBR1 in poplar enhanced salt stress tolerance. Compared with wild type (WT) plants, the transgenic lines exhibited higher antioxidant enzyme activity, less reactive oxygen species (ROS), and higher net photosynthesis rates under salt stress. Furthermore, co-localization and yeast two-hybrid analysis revealed that PagNBR1 was localized in the autophagosome and could interact with ATG8 (autophagy-related gene). PagNBR1 transgenic poplars formed more autophagosomes and exhibited higher expression of ATG8, resulting in less accumulation of insoluble protein and insoluble ubiquitinated protein compared to WT under salt stress. The accumulation of insoluble protein and insoluble ubiquitinated protein was similar under the treatment of ConA in WT and transgenic lines. In summary, our results imply that PagNBR1 is an important selective autophagy receptor in poplar and confers salt tolerance by accelerating antioxidant system activity and autophagy activity. Moreover, the NBR1 gene is an important potential molecular target for improving stress resistance in trees.

The human gut microbiota is known for its highly heterogeneous composition across different individuals. However, relatively little is known about functional differences in its ability to ferment complex polysaccharides. Through ex vivo measurements from healthy human donors, we show that individuals vary markedly in their microbial metabolic phenotypes (MMPs), mirroring differences in their microbiota composition, and resulting in the production of different quantities and proportions of Short Chain Fatty Acids (SCFAs) from the same inputs. We also show that aspects of these MMPs can be predicted from composition using 16S rRNA sequencing. From experiments performed using the same dietary fibers in vivo, we demonstrate that an ingested bolus of fiber is almost entirely consumed by the microbiota upon passage. We leverage our ex vivo data to construct a model of SCFA production and absorption in vivo, and argue that inter-individual differences in quantities of absorbed SCFA are directly related to differences in production. Though in vivo studies are required to confirm these data in the context of the gut, in addition to in vivo read outs of SCFAs produced in response to specific fiber spike-ins, these data suggest that optimizing SCFA production in a given individual through targeted fiber supplementation requires quantitative understanding of their MMP.

Mindfulness training (MT) reduces self-referential processing and promotes interoception, the perception of sensations from inside the body, by increasing one’s awareness of and regulating responses to them. The posterior cingulate cortex (PCC) and the insular cortex (INS) are considered hubs for self-referential processing and interoception, respectively. Although MT has been consistently found to decrease PCC, little is known about how MT relates to INS activity. Understanding links between mindfulness and interoception may be particularly important for informing mental health in adolescence, when neuroplasticity and emergence of psychopathology are heightened. We examined INS activity during real-time functional magnetic resonance imaging neurofeedback-augmented mindfulness training (NAMT) targeting the PCC. Healthy adolescents (N = 37; 16 female) completed the NAMT task, including Focus-on-Breath (MT), Describe (self-referential processing), and Rest conditions, across three neurofeedback runs and two non-neurofeedback runs (Observe, Transfer). Regression coefficients estimated from the generalized linear model were extracted from three INS subregions: anterior (aINS), mid (mINS), and posterior (pINS). Mixed model analyses revealed the main effect of run for Focus-on-Breath vs. Describe contrast in aINS [R2 = 0.39] and pINS [R2 = 0.33], but not mINS [R2 = 0.34]. Post hoc analyses revealed greater aINS activity and reduced pINS activity during neurofeedback runs, and such activities were related to lower self-reported life satisfaction and less pain behavior, respectively. These findings revealed the specific involvement of insula subregions in rtfMRI-nf MT.

ABSTRACT Prebiotics confer benefits to human health, often by promoting the growth of gut bacteria that produce metabolites valuable to the human body, such as short-chain fatty acids (SCFAs). While prebiotic selection has strongly focused on maximizing the production of SCFAs, less attention has been paid to gases, a by-product of SCFA production that also has physiological effects on the human body. Here, we investigate how the content and volume of gas production by human gut microbiota are affected by the chemical composition of the prebiotic and the community composition of the microbiota. We first constructed a linear system model based on mass and electron balance and compared the theoretical product ranges of two prebiotics, inulin and pectin. Modeling shows that pectin is more restricted in product space, with less potential for H2 but more potential for CO2 production. An ex vivo experimental system showed pectin degradation produced significantly less H2 than inulin, but CO2 production fell outside the theoretical product range, suggesting fermentation of fecal debris. Microbial community composition also impacted results: methane production was dependent on the presence of Methanobacteria, while interindividual differences in H2 production during inulin degradation were driven by a Lachnospiraceae taxon. Overall, these results suggest that both the chemistry of the prebiotic and the composition of the microbiota are relevant to gas production. Metabolic processes that are relatively prevalent in the microbiome, such as H2 production, will depend more on substrate, while rare metabolisms such as methanogenesis depend more strongly on microbiome composition. IMPORTANCE Prebiotic fermentation in the gut often leads to the coproduction of short-chain fatty acids (SCFAs) and gases. While excess gas production can be a potential problem for those with functional gut disorders, gas production is rarely considered during prebiotic design. In this study, we combined the use of theoretical models and an ex vivo experimental platform to illustrate that both the chemical composition of the prebiotic and the community composition of the human gut microbiota can affect the volume and content of gas production during prebiotic fermentation. Specifically, more prevalent metabolic processes such as hydrogen production were strongly affected by the oxidation state of the probiotic, while rare metabolisms such as methane production were less affected by the chemical nature of the substrate and entirely dependent on the presence of Methanobacteria in the microbiota.

Abstract Background The term “loss-of-only-child family” means that the only child in a family passed away or is disabled due to an accident or other events. The parents who cannot conceive or do not adopt another child, are known as Shidu parents in China. This study compares the physical and mental health of Shidu parents with those parents who have not experienced such loss. Methods The target group is comprised of parents being Shidu for more than 1 year (N = 95) and the control group is comprised of parents with a living child (N = 97) from the same area as the Shidu parents. Socio-demographic information and physical health outcomes were collected by the adapted questionnaires. PCL-C (PTSD Checklist-Civilian Version), CES-D (Center for Epidemiological Studies Depression Scale) and GHQ-12 (General Health Questionnaire) were applied to evaluate the parents’ physical and mental status. Results Shidu parents have a higher risk of developing PTSD and depression, and suffer more severe psychiatric disorders compared to parents with a living child. The rate of PTSD in the Shidu group was up to 32.6% and the scores of PCL-C are much higher than the control group. The physical status of Shidu parents were much worse than that of the control group, characterized by higher morbidity of chronic diseases and more hospital visits. Conclusions Shidu parents have more severe mental health problems and a higher rate of chronic diseases than parents who have a living child. Loss of the only child is the most traumatic event for the parents, which is a serious and unique problem in Chinese society that deserves attention. More studies and support are desired to improve the physical and mental health of Shidu parents.

Background: The heartache from the devastating 8.0 magnitude Wenchuan earthquake, which killed nearly 90,000 people in western China, is still felt despite the large-scale recovery and reconstruction of the affected areas. This study investigated the relationships of earthquake-trauma exposures and personality with posttraumatic stress disorder (PTSD), to identify the long-term consequences of the Wenchuan earthquake on the survivors and the risk factors related to chronic PTSD. We hope the findings can contribute to developing new health care prevention and interventions for the survivors.Methods: We collected a sample of 490 people over 3 years after the Wenchuan earthquake, using questionnaires about demographic information and the traumatic experience in earthquake, the Impact of Event Scale-Revised (IES-R), and the Eysenck Personality Questionnaires (EPQ), to find the consequences of the Wenchuan earthquake on the survivors and the potential factors related to the long-term morbidity of PTSD.Result: Traumatic experiences, such as witnessing someone being seriously injured, having your house seriously damaged, and having close relatives severely injured, were associated with developing PTSD. Personality measured by EPQ was also closely related to PTSD. Regression analyses indicated that a potential linear model characterized the relationship between PTSD, neuroticism and psychoticism, yet extraversion/introversion were not significant factors. In the multivariate logistic regression, neuroticism (a continuous variable measured by EPQ) was of more significance in predicting the morbidity of long-term PTSD, compared with other variables [odds ratio (OR) = 1.113, 95% confidence interval (CI) = 1.081-1.146, Wald Value = 50.467, P < 0.001]. The final path diagram built a model indicated the moderating role of personality in the relationship between traumatic experiences and PTSD (CMIN/DF = 2.324, P < 0.001; CFI = 0.879 < 0.8; RMSEA = 0.05 < 0.08).Conclusion: This study demonstrated the role of personality traits and subjective exposure experiences regarding the vulnerability associated with PTSD after earthquake. Among all personality traits, neuroticism is considered a vulnerability factor of PTSD, and other personality traits also moderate the effects of traumatic experiences associated with PTSD. These findings might be useful for psychologists to develop intervention strategies for people suffered natural disasters, and to help individuals with PTSD to heal fully.

Adaptive radiations are well-known for animals and plants, but not for microbes. Here, Hehemann et al. show that there has been a recent adaptive radiation of bacteria in the Vibrionaceae to use different forms of alginate and that this radiation has been mediated by horizontal gene transfer.

The principle of image super-resolution reconstruction (SR) is to pass one or more low-resolution (LR) images through information processing technology to obtain the final high-resolution (HR) image. Convolutional neural networks (CNN) have achieved better results than traditional methods in the process of an image super-resolution reconstruction. However, if the number of neural network layers is increased blindly, it will cause a significant increase in the amount of calculation, increase the difficulty of training the network, and cause the loss of image details. Therefore, in this paper, we use a novel and effective image super-resolution reconstruction technique via fast global and local residual learning model (FGRLR). The principle is to directly train a low-resolution small image on a neural network without enlarging it. This will effectively reduce the amount of calculation. In addition, the stacked local residual block (LRB) structure is used for non-linear mapping, which can effectively overcome the problem of image degradation. After extracting features, use 1 × 1 convolution to perform dimensional compression, and expand the dimensions after non-linear mapping, which can reduce the calculation amount of the model. In the reconstruction layer, deconvolution is used to enlarge the image to the required size. This also reduces the number of parameters. We use skip connections to use low-resolution information for reconstructing high-resolution images. Experimental results show that the algorithm can effectively shorten the running time without affecting the quality of image restoration.

Innate-like B lymphocytes play an important role in innate immunity in periodontal disease through Toll-like receptor (TLR) signaling. However, it is unknown how innate-like B cell apoptosis is affected by the periodontal infection-associated innate signals. This study is to determine the effects of two major TLR ligands, lipopolysaccharide (LPS) and CpG-oligodeoxynucleotides (CpG-ODN), on innate-like B cell apoptosis. Spleen B cells were isolated from wild type (WT), TLR2 knockout (KO) and TLR4 KO mice and cultured with E. coli LPS alone, P. gingivalis LPS alone, or combined with CpG-ODN for 2 days. B cell apoptosis and expressions of specific apoptosis-related genes were analyzed by flow cytometry and real-time PCR respectively. P. gingivalis LPS, but not E. coli LPS, reduced the percentage of AnnexinV+/7-AAD- cells within IgMhighCD23lowCD43-CD93- marginal zone (MZ) B cell sub-population and IgMhighCD23lowCD43+CD93+ innate response activator (IRA) B cell sub-population in WT but not TLR2KO or TLR4KO mice. CpG-ODN combined with P. gingivalis LPS further reduced the percentage of AnnexinV+/7-AAD- cells within MZ B cells and IRA B cells in WT but not TLR2 KO or TLR4 KO mice. Pro-apoptotic CASP4, CASP9 and Dapk1 were significantly down-regulated in P. gingivalis LPS- and CpG-ODN-treated B cells from WT but not TLR2 KO or TLR4 KO mice. Anti-apoptotic IL-10 was significantly up-regulated in P. gingivalis LPS- and CpG-ODN-treated B cells from WT and TLR2 KO but not TLR4 KO mice. These results suggested that both TLR2 and TLR4 signaling are required for P. gingivalis LPS-induced, CpG-ODN-enhanced suppression of innate-like B cell apoptosis.

Molybdenum cofactor (Moco) is required for the activities of Moco-dependant enzymes. Cofactor for nitrate reductase and xanthine dehydrogenase (Cnx1) is known to be involved in the biosynthesis of Moco in plants. In this work, a soybean (Glycine max L.) Cnx1 gene (GmCnx1) was transferred into soybean using Agrobacterium tumefaciens-mediated transformation method. Twenty seven positive transgenic soybean plants were identified by coating leaves with phosphinothricin, bar protein quick dip stick and PCR analysis. Moreover, Southern blot analysis was carried out to confirm the insertion of GmCnx1 gene. Furthermore, expression of GmCnx1 gene in leaf and root of all transgenic lines increased 1.04-2.12 and 1.55-3.89 folds, respectively, as compared to wild type with GmCnx1 gene and in line 10 , 22 showing the highest expression. The activities of Moco-related enzymes viz nitrate reductase (NR) and aldehydeoxidase (AO) of T1 generation plants revealed that the best line among the GmCnx1 transgenic plants accumulated 4.25 μg g(-1) h(-1) and 30 pmol L(-1), respectively (approximately 2.6-fold and 3.9-fold higher than non-transgenic control plants).In addition, overexpression ofGmCnx1boosted the resistance to various strains of soybean mosaic virus (SMV). DAS-ELISA analysis further revealed that infection rate of GmCnx1 transgenic plants were generally lower than those of non-transgenic plants among two different virus strains tested. Taken together, this study showed that overexpression of a GmCnx1 gene enhanced NR and AO activities and SMV resistance, suggesting its important role in soybean genetic improvement.

Methylation has a close relationship with immune reactions, metastasis, and cancer cell growth. Additionally, RNA methylation-related proteins have emerged as potential cancer therapeutic targets. The connection between the tumor microenvironment (TME) and methylation-related genes (MRGs) remains unclear. We explored the expression patterns of the MRGs in the genome and transcriptional fields of 796 prostate cancer (PCa) samples using two separate data sets. We identified a relationship between patient clinicopathological characteristics, prognosis, TME cell infiltrating qualities, and different MRG changes, as well as the identification of two distinct molecular groupings. Then, we formed an MRGs model to predict overall survival (OS), and we tested the accuracy of the model in patients with PCa. In addition, we developed a very accurate nomogram to improve the MRG model’s clinical applicability. The low-risk group had fewer tumor mutational burden (TMB), greater tumor immune dysfunction and exclusion (TIDE) ratings, fewer mutant genes, and better OS prospects. We discuss how MGRs may affect the prognosis, clinically important traits, TME, and immunotherapy responsiveness in PCa. In order to get a better understanding of MRGs in PCa, we could further explore the prognosis and create more effective immunotherapy regimens to open new avenues. [ABSTRACT FROM AUTHOR]

Abstract Objectives Posthepatectomy liver failure (PHLF) is a severe complication of liver resection. We aimed to develop and validate a model based on extracellular volume (ECV) and liver volumetry derived from computed tomography (CT) for preoperative predicting PHLF in resectable hepatocellular carcinoma (HCC) patients. Methods A total of 393 resectable HCC patients from two hospitals were enrolled and underwent multiphasic contrast-enhanced CT before surgery. A total of 281 patients from our hospital were randomly divided into a training cohort (n = 181) and an internal validation cohort (n = 100), and 112 patients from another hospital formed the external validation cohort. CT-derived ECV was measured on nonenhanced and equilibrium phase images, and liver volumetry was measured on portal phase images. The model is composed of independent predictors of PHLF. The under the receiver operator characteristic curve (AUC) and calibration curve were used to reflect the predictive performance and calibration of the model. Comparison of AUCs used the DeLong test. Results CT-derived ECV, measured future liver remnant (mFLR) ratio, and serum albumin were independent predictors for PHLF in resectable HCC patients. The AUC of the model was significantly higher than that of the ALBI score in the training cohort, internal validation cohort, and external validation cohort (all p

Leuciscus merzbacheri (Zugmayer, 1912) is a cyprinid fish endemic to China, with a distribution range limited to Xinjiang Province. As a landmark species in the Junggar Basin, L. merzbacheri is of considerable significance regarding our understanding of the adaptive evolution of salt and alkali tolerance. In this study, the complete mitochondrial sequence of L. merzbacheri was obtained for the first time by high-throughput sequencing. The circular mitogenome is 16,609 bp in length and contains the standard 37 genes, including 13 protein-coding, 22 transfer RNA, and 2 ribosomal RNA genes, which is similar to that of other fish. The mitogenome contents of A, T, C, and G were 27.9, 26.3, 27.1, and 18.7%, respectively. Phylogenetically, L. merzbacheri was located on a new branch near the base of the phylogenetic tree, thereby suggesting an early origin.

Abstract Objectives To assess the value of myocardial extracellular volume (ECV) derived from contrast-enhanced chest computed tomography (CT) for longitudinal evaluation of cardiotoxicity in patients with breast cancer (BC) treated with anthracycline (AC). Materials and methods A total of 1151 patients with BC treated with anthracyclines, who underwent at least baseline, and first follow-up contrast-enhanced chest CT were evaluated. ECV and left ventricular ejection fraction (LVEF) were measured before (ECV0, LVEF0), during ((ECV1, LVEF1) and (ECV2, LVEF2)), and after (ECV3, LVEF3) AC treatment. ECV values were evaluated at the middle of left ventricular septum on venous phase images. Cancer therapy-related cardiac dysfunction (CTRCD) was recorded. Results Mean baseline LVEF values were 65.85% ± 2.72% and 102 patients developed CTRCD. The mean ECV0 was 26.76% ± 3.03% (N0 = 1151). ECV1, ECV2, and ECV3 (median interval: 61 (IQR, 46–75), 180 (IQR, 170–190), 350 (IQR, 341–360) days from baseline) were 31.32% ± 3.10%, 29.60% ± 3.24%, and 32.05% ± 3.58% (N1 = 1151, N2 = 841, N3 = 511). ECV1, ECV2, and ECV3 were significantly higher than ECV0 (p

Astrocyte inflammation activation is an important cause that hinders the recovery of motor function after cerebral ischemia. However, its molecular mechanism has not yet been clearly clarified. The peroxisome proliferator-activated receptor α (PPARα) is a ligand-activated nuclear transcriptional factor. This study aims to further clarify the role of PPARα in astrocyte inflammation activation after cerebral ischemia and to explore the underlying mechanism. Astrocyte activation was induced in an in vivo model by transient middle cerebral artery occlusion (tMCAO) in mice. The in vitro model was induced by an oxygen-glucose deprivation/reoxygenation (OGD/R) in a primary culture of mouse astrocyte. PPARα-deficient mice were used to observe the effects of PPARα on astrocyte activation and autophagic flux. Our results showed that PPARα was mainly expressed in activated astrocytes during the chronic phase of brain ischemia and PPARα dysfunction promoted astrocyte inflammatory activation. After cerebral ischemia, the expressions of LC3-II/I and p62 both increased. Autophagic vesicle accumulation was observed by electron microscopy in astrocytes, and the block of autophagic flux was indicated by an mRFP-GFP-LC3 adenovirus infection assay. A PPARα deficit aggravated the autophagic flux block, while PPARα activation preserved the lysosome function and restored autophagic flux in astrocytes after OGD/R. The autophagic flux blocker bafilomycin A1 and chloroquine antagonized the effect of the PPARα agonist on astrocyte activation inhibition. This study identifies a potentially novel function of PPARα in astrocyte autophagic flux and suggests a therapeutic target for the prevention and treatment of chronic brain ischemic injury.

Recent work has demonstrated that behavioral manipulations targeting specific cortical areas during prolonged wakefulness lead to a region-specific homeostatic increase in theta activity (5-9 Hz), suggesting that theta waves could represent transient neuronal OFF periods (local sleep). In awake rats, the occurrence of an OFF period in a brain area relevant for behavior results in performance errors. Here we investigated the potential relationship between local sleep events and negative behavioral outcomes in humans. Volunteers participated in two prolonged wakefulness experiments (24 h), each including 12 h of practice with either a driving simulation (DS) game or a battery of tasks based on executive functions (EFs). Multiple high-density EEG recordings were obtained during each experiment, both in quiet rest conditions and during execution of two behavioral tests, a response inhibition test and a motor test, aimed at assessing changes in impulse control and visuomotor performance, respectively. In addition, fMRI examinations obtained at 12 h intervals were used to investigate changes in inter-regional connectivity. The EF experiment was associated with a reduced efficiency in impulse control, whereas DS led to a relative impairment in visuomotor control. A specific spatial and temporal correlation was observed between EEG theta waves occurring in task-related areas and deterioration of behavioral performance. The fMRI connectivity analysis indicated that performance impairment might partially depend on a breakdown in connectivity determined by a "network overload." Present results demonstrate the existence of an association between theta waves during wakefulness and performance errors and may contribute explaining behavioral impairments under conditions of sleep deprivation/restriction. [ABSTRACT FROM AUTHOR]

An efficient method for the synthesis of indolylglycine derivatives is described. The oxidative coupling reactions of ethyl 2-(disubstituted amino) acetates with indoles proceeded smoothly in the presence of mrfa-chloroperoxybenzoic acid (mCPBA) under ambient conditions to produce indolylglycine derivatives in satisfactory to excellent yields. [ABSTRACT FROM AUTHOR]

Fish is one of the most extensive distributed organisms in the world. Fish taxonomy is an important component of biodiversity and the basis of fishery resources management. The DNA barcode based on a short sequence fragment is a valuable molecular tool for fish classification. However, the high dimensionality of DNA barcode sequences and the limitation of the number of fish species make it difficult to reasonably analyze the DNA sequences and correctly classify fish from different families. In this paper, we propose a novel deep learning method that fuses Elastic Net-Stacked Autoencoder (EN-SAE) with Kernel Density Estimation (KDE), named ESK model. In stage one, the ESK preprocesses original data from DNA barcode sequences. In stage two, EN-SAE is used to learn the deep features and obtain the outgroup score of each fish. In stage three, KDE is used to select a threshold based on the outgroup scores and classify fish from different families. The effectiveness and superiority of ESK have been validated by experiments on three datasets, with the accuracy, recall, F1-Score reaching 97.57%, 97.43%, and 98.96% on average. Those findings confirm that ESK can accurately classify fish from different families based on DNA barcode sequences.

Objective To explore the relationship and predictive function of blood urea nitrogen (BUN) level in association with major adverse cardiovascular event(MACE) subsequent to percutaneous coronary intervention(PCI) among patients diagnosed with acute coronary syndrome (ACS). Methods Between April 2017 and November 2017, ACS patients undergoing their initial PCI at the Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University were recruited. Following a 36-month follow-up period, 487 patients were included as 114 subjects experiencing MACE and 373 subjects without MACE. The Cox proportional hazards regression model was utilized to assess the risk ratio of MACE and its 95% confidence interval (CI) concerning BUN levels and ACS post-PCI. Additionally, the area under the receiver operating characteristic (ROC) curve (AUC) was applied to assess the predictive effect of BUN. Results After adjusting for confounding variables, Cox proportional hazards regression analysis revealed that the risk of MACE was approximately four times higher in the high BUN level group compared to the low BUN level group (OR=4.722,95% CI 1.716-12.993). Upon inclusion of BUN in both the basic prediction model and SCORE model for cardiovascular event risk, there was a significant increase in the AUC area (P＜ 0.001). Conclusions BUN levels can independently predict the risk of MACE following PCI in ACS patients, irrespective of traditional risk factors.

A subcortical pathway is thought to have evolved to facilitate fear information transmission, but direct evidence for its existence in humans is lacking. In recent years, rapid, preattentive, and preconscious fear processing has been demonstrated, providing indirect support for the existence of the subcortical pathway by challenging the necessity of canonical cortical pathways in fear processing. However, direct support also requires evidence for the involvement of subcortical regions in fear processing. To address this issue, here we investigate whether fear processing reflects the characteristics of the subcortical structures in the hypothesized subcortical pathway. Using a monocular/dichoptic paradigm, Experiment 1 demonstrated a same-eye advantage for fearful but not neutral face processing, suggesting that fear processing relied on monocular neurons existing mainly in the subcortex. Experiments 2 and 3 further showed insensitivity to short-wavelength stimuli and a nasal-temporal hemifield asymmetry in fear processing, both of which were functional characteristics of the superior colliculus, a key hub of the subcortical pathway. Furthermore, all three experiments revealed a low spatial frequency selectivity of fear processing, consistent with magnocellular input via subcortical neurons. These results suggest a selective involvement of subcortical structures in fear processing, which, together with the indirect evidence for automatic fear processing, provides a more complete picture of the existence of a subcortical pathway for fear processing in humans. [ABSTRACT FROM AUTHOR]

While most Vibrionaceae are considered generalists that thrive on diverse substrates, including animal-derived material, we show that Vibrio breoganii has specialized for the consumption of marine macroalga-derived substrates. Genomic and physiological comparisons of V. breoganii with other Vibrionaceae isolates revealed the ability to degrade alginate, laminarin, and additional glycans present in algal cell walls. Moreover, the widely conserved ability to hydrolyze animal-derived polymers, including chitin and glycogen, was lost, along with the ability to efficiently grow on a variety of amino acids. Ecological data showing associations with particulate algal material but not zooplankton further support this shift in niche preference, and the loss of motility appears to reflect a sessile macroalga-associated lifestyle. Together, these findings indicate that algal polysaccharides have become a major source of carbon and energy in V. breoganii, and these ecophysiological adaptations may facilitate transient commensal associations with marine invertebrates that feed on algae. [ABSTRACT FROM AUTHOR]

Objective: Chemotherapy-induced peripheral neuropathy (CIPN) is a common and severe adverse reaction in taxane-based chemotherapy. This study aimed to analyze the risk factors of peripheral neuropathy in patients with breast cancer receiving paclitaxel chemotherapy to provide a reference for the early prevention of CIPN., Methods: We included 350 patients with breast cancer who received chemotherapy for the first time at the Tangshan People's Hospital between August 2022 and June 2023 and were followed for at least 3 months after the end of chemotherapy. The incidence of CIPN in patients with breast cancer was calculated, and risk factors for CIPN were analyzed using logistic regression analysis., Results: The incidence rate of CIPN was 79.1%. Multifactor logistic regression analysis indicated that age ≥45 years [odds ratio (OR)=5.119, 95% confidence interval (CI)=1.395-18.780] and ≥60 years (OR=9.366, 95% CI=1.228-71.421), history of hypertension (OR=3.475, 95% CI=1.073-11.250), cumulative dose of chemotherapy drugs >900 mg (OR=4.842, 95% CI=1.961-5.946), vitamin D deficiency (OR=6.214, 95% CI=2.308-16.729), abnormal alanine aminotransferase (OR=3.154, 95% CI=1.010-9.844), anemia before chemotherapy (OR=2.770, 95% CI=1.093-7.019), infusion duration of chemotherapy drugs >30 min (OR=3.673, 95% CI=1.414-9.539), body mass index ≥24 kg/m 2 (OR=8.139, 95% CI=1.157-57.240), mild depression (OR=4.546, 95% CI=1.358-15.223), and major depression (OR=4.455, 95% CI=1.237-16.037) increased the risk of CIPN. Having a regular caregiver (OR=0.223, 95% CI=0.087-0.573), high levels of physical activity (OR=0.071, 95% CI=0.008-0.647), and strong social support (OR=0.048, 95% CI=0.003-0.682) were protective factors against CIPN., Conclusion: Clinical attention should be paid to patients with these risk factors, and active and effective preventive measures should be taken to reduce the occurrence of CIPN and improve the quality of life., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Lixian, Xiaoqian, Luyan, Lizhi, Rui, Hongyue, Caijie and Fenghui.)