Real-Time Monitoring on the Chinese Giant Salamander Using RPA-LFD.

The Chinese giant salamander (Andrias davidianus), listed as an endangered species under "secondary protection" in China, faces significant threats due to ecological deterioration and the expansion of human activity. Extensive field investigations are crucial to ascertain the current status in the wild and to implement effective habitat protection measures to safeguard this species and support its population development. Traditional survey methods often fall short due to the elusive nature of the A. davidianus, presenting challenges that are time-consuming and generally ineffective. To overcome these obstacles, this study developed a real-time monitoring method that uses environmental DNA (eDNA) coupled with recombinase polymerase amplification and lateral flow strip (RPA-LFD). We designed five sets of species-specific primers and probes based on mitochondrial genome sequence alignments of A. davidianus and its close relatives. Our results indicated that four of these primer/probe sets accurately identified A. davidianus, distinguishing it from other tested caudata species using both extracted DNA samples and water samples from a tank housing an individual. This method enables the specific detection of A. davidianus genomic DNA at concentrations as low as 0.1 ng/mL within 50 min, without requiring extensive laboratory equipment. Applied in a field survey across four sites in Huangshan City, Anhui Province, where A. davidianus is known to be distributed, the method successfully detected the species at three of the four sites. The development of these primer/probe sets offers a practical tool for field surveying and monitoring, facilitating efforts in population recovery and resource conservation for A. davidianus.

The challenge of managing ischemic stroke in brucellosis: a case report.

A 64-year-old woman was admitted to the hospital for sudden weakness in one of her left limbs. The patient was diagnosed with acute ischemic stroke (IS) of undetermined cause and received intravenous thrombolysis. Following thrombolysis, the patient's left limb weakness improved, but she subsequently developed recurrent high fever and delirium. Further diagnostic tests revealed that she had been infected with Brucella melitensis. The patient showed significant improvement during anti-infection treatment for Brucellosis and secondary prevention treatment for IS. However, her condition unexpectedly worsened on the 44th day after admission due to a hemorrhagic stroke (HS), which required an urgent craniotomy. Immunohistochemical analysis of the hematoma sample collected during the operation showed the presence of CD4+ and CD8+ T lymphocytes surrounding the blood vessels. This case highlights the unique challenge of managing IS in brucellosis and sheds light on the potential role of T lymphocytes in the immune response related to stroke.

Excess phosphate promotes SARS­CoV­2 N protein­induced NLRP3 inflammasome activation via the SCAP­SREBP2 signaling pathway.

Hyperphosphatemia or severe acute respiratory syndrome coronavirus 2 (SARS­CoV­2) infection can promote cardiovascular adverse events in patients with chronic kidney disease. Hyperphosphatemia is associated with elevated inflammation and sterol regulatory element binding protein 2 (SREBP2) activation, but the underlying mechanisms in SARS­CoV­2 that are related to cardiovascular disease remain unclear. The present study aimed to elucidate the role of excess inorganic phosphate (PI) in SARS­CoV­2 N protein­induced NLRP3 inflammasome activation and the underlying mechanisms in vascular smooth muscle cells (VSMCs). The expression levels of SARS­CoV­2 N protein, SREBP cleavage­activating protein (SCAP), mature N­terminal SREBP2, NLRP3, procaspase­1, cleaved caspase­1, IL­1ß and IL­18 were examined by western blotting. The expression levels of SREBP2, HMG­CoA reductase, HMGCS1, low density lipoprotein receptor, proprotein convertase subtilisin/kexin type 9 (PCSK9), SREBP1c, fatty acid synthase, stearyl coenzyme A desaturase 1, acetyl­CoA carboxylase α and ATP­citrate lyase were determined by reverse transcription­quantitative PCR. The translocation of SCAP or NLRP3 from the endoplasmic reticulum to the Golgi was detected by confocal microscopy. The results showed that excess PI promoted SCAP­SREBP and NLRP3 complex translocation to the Golgi, potentially leading to NLRP3 inflammasome activation and lipogenic gene expression. Furthermore, PI amplified SARS­CoV­2 N protein­induced inflammation via the SCAP­SREBP pathway, which facilitates NLRP3 inflammasome assembly and activation. Inhibition of phosphate uptake with phosphonoformate sodium alleviated NLRP3 inflammasome activation and reduced SREBP­mediated lipogenic gene expression in VSMCs stimulated with PI and with SARS­CoV­2 N protein overexpression. Inhibition of SREBP2 or small interfering RNA­induced silencing of SREBP2 effectively suppressed the effect of PI and SARS­CoV­2 N protein on NLRP3 inflammasome activation and lipogenic gene expression. In conclusion, the present study identified that PI amplified SARS­CoV­2 N protein­induced NLRP3 inflammasome activation and lipogenic gene expression via the SCAP­SREBP signaling pathway.

Association of D-dimer to albumin ratio with adverse cardiovascular outcomes in ischaemic heart failure patients with diabetes mellitus: a retrospective cohort study.

OBJECTIVE: To determine the association of D-dimer to albumin ratio (DAR) with major adverse cardiovascular events (MACE) after percutaneous coronary intervention (PCI) in ischaemic heart failure patients with diabetes mellitus. DESIGN: A retrospective observational cohort study. SETTING: Single centre in Beijing, China, conducted at one of the largest cardiology centres in China. PARTICIPANTS: From June 2017 to June 2019, 3707 patients with heart failure and concomitant multiple vessel disease undergoing elective PCI were screened. A total 1021 of patients were enrolled after exclusion and the follow-up period was up to 36 months. PRIMARY AND SECONDARY OUTCOME MEASURES: The MACE was the primary measured outcome. The secondary outcomes were all-cause mortality, non-fatal myocardial infarction and any revascularisation. METHODS: These participants were grouped according to DAR tertiles. The cumulative incidence functions, Cox regression, restricted cubic spline and receiver operating characteristic curves were used to determine the association between DAR and outcomes. The subgroup analysis was also performed. RESULTS: After follow-up, MACE occurred in 404 (39.6%) participants. The cumulative hazards curve manifested significant differences in MACE, all-cause mortality and any revascularisation (log-rank test: all p<0.001). In adjusted models, DAR was an independent risk factor of MACE (tertile 2: HR 1.82, 95% CI 1.37 to 2.42; tertile 3: HR 1.74, 95% CI 1.28 to 2.36) and all-cause mortality (tertile 2: HR 2.04, 95% CI 1.35 to 3.11; tertile 3: HR 1.89, 95% CI 1.20 to 2.98). The optimal cut-off of DAR was 1.2. In the stratified analysis, sex, age, hypertension, hypercholesterolaemia, total revascularisation and any interfered vessel did not affect the independent predictive ability. CONCLUSION: Higher DAR was independently associated with MACE and all-cause mortality after PCI in ischaemic heart failure patients with diabetes mellitus.

Identification of Reduced mTOR T1262 Phosphorylation as a Novel Mechanism and Therapeutic Target of Apoptosis in Senescent Cardiomyocytes: Aging and Cardiomyocyte Apoptosis.

The mechanisms through which aging increases heart injury remain partially understood. Protein phosphorylation plays a critical regulatory role in cell survival and death. Using an unbiased phosphoproteomics approach, we aimed to identify the proteins whose phosphorylation could be causatively related to aging-related cardiomyocyte apoptosis and elucidate the underlying mechanisms. Comparative phosphoproteomics was conducted on cardiac tissues obtained from young (8 weeks) and aged (24 months) mice. Our findings revealed that the Mammalian Target of Rapamycin phosphorylation at T1262 (mTORT1262) was reduced in the aging heart. Immunohistochemical and Western blot analyses confirmed these findings in aging myocardia and D-galactose-induced senescent AC16 cardiomyocytes. In hypoxia/reoxygenation cardiomyocytes, mTORT1262 phosphorylation deficiency (mTORT1262A, lentivirus-mediated transfection) inhibited AKT1, suppressed NF-κB, activated FOXO1/3a signaling, and ultimately exacerbated apoptosis. Conversely, mTORT1262 pseudophosphorylation (mTORT1262E) exhibited opposite effects. Through bioinformatics and CO-IP, purinergic receptor P2X4 (P2X4R) was found to be the possible receptor responsible for mTORT1262 phosphorylation. Knockdown of P2X4R increased apoptosis, whereas its overexpression decreased it. In senescent cardiomyocytes, P2X4R expression and mTORT1262 and AKT1S473 phosphorylation were reduced, NF-κB signaling was suppressed, and FOXO1/3a signaling was activated. We demonstrated that P2X4R downregulation and the subsequent reduction of mTORT1262 phosphorylation is a novel mechanism contributing to cardiomyocyte apoptosis in aging hearts. The P2X4R-mTOR-AKT1 signaling pathway represents a potential therapeutic target against accelerated cardiac injury in aging.

AI/ML to Relationship Between Circadian Rhythm of Blood Pressure and Left Ventricular Hypertrophy in Patients with Hypertension.

Objective: The objective of this experiment was to investigate the relationship between the circadian rhythm of blood pressure and left ventricular hypertrophy (LVH) in patients with hypertension. Methods: A total of 500 hypertension patients with documented circadian rhythm of blood pressure were selected for this study. The researchers collected general patient data and fasting blood samples. The following parameters were measured within subgroups of hypertensive patients: age, sex ratio, BMI, fasting blood glucose, total cholesterol, triacylglycerol, HDL-C, LDL-C, duration of hypertension, antihypertensive drug usage, and statin intake. Results: The results of the study showed that LVH hypertension had a significantly higher proportion of grade 3 hypertension compared to non-LVH hypertension (P < .001). Additionally, LVH hypertension displayed higher mean systolic blood pressure levels over a 24-hour period (P = .002), during daytime (P = .029), and during nighttime (P < .001). The 24-hour pulse pressure (P < .001) and pulse pressure index (P = 0.001) were also significantly higher in patients with LVH hypertension. Furthermore, the rate of blood pressure decline at night was significantly lower in the LVH hypertension group compared to the control group (P < .001). B-type natriuretic peptide (BNP) levels (P = .034) and left ventricular mass index (LVMI) (P < .001) were significantly higher in patients with LVH hypertension compared to non-LVH patients. Conclusions: The findings of this study suggest a close association between hypertensive LVH and the weakening or disappearance of the circadian rhythm of blood pressure. It was also observed that the level of blood pressure classification and plasma BNP levels were increased in patients with LVH hypertension.

New mitogenomes from the genus Cricotopus (Diptera: Chironomidae, Orthocladiinae): Characterization and phylogenetic implications.

Cricotopus is a large and diverse genus of non-biting midges composed of several subgenera. Complete mitogenome sequences are available for very few Cricotopus species. The subgenus Pseudocricotopus unites species with unusual morphological structures in adult male and pupal stages, however, molecular methods are needed to verify the placement of this subgenus within Cricotopus. We obtained mitogenomes of C. (Pseudocricotopus) cf. montanus and nine other Cricotopus species for phylogenetic analysis, coupled with two Rheocricotopus species and one Synorthocladius species as outgroups. The structure of the mitogenome was similar among these Cricotopus species, exhibiting A+T bias and retaining ancestral gene order. Mutation rate, estimated as Ka/Ks, varied among genes, and was highest for ATP8 and lowest for COI. The phylogenetic relationships among species of Cricotopus, Rheocricotopus and Synorthocladius was reconstructed using Bayesian inference and maximum likelihood estimation. The phylogenetic trees confirmed placement of subgenus Pseudocricotopus, represented by Cricotopus cf. montanus, within Cricotopus. Our study increases the library of chironomid mitogenomes and provides insight into the properties of their constituent genes.

SARS-CoV-2 nucleocapsid protein promotes TMAO-induced NLRP3 inflammasome activation by SCAP-SREBP signaling pathway.

The sterol regulatory element-binding protein (SREBP) activation and cytokine level were significantly increased in coronavirus disease-19. The NLRP3 inflammasome is an amplifier for cellular inflammation. This study aimed to elucidate the modulatory effect of SARS-CoV-2 nucleocapsid protein (SARS-CoV-2 NP) on trimethylamine N-oxide (TMAO)-induced lipogenesis and NLRP3 inflammasome activation and the underlying mechanisms in vascular smooth muscle cells (VSMCs). Our data indicated that SARS-CoV-2 NP activates the dissociation of the SREBP cleavage activating protein (SCAP) from the endoplasmic reticulum, resulting in SREBP activation, increased lipogenic gene expression, and NLRP3 inflammasome activation. TMAO was applied to VSMC-induced NLRP3 inflammasome by promoting the SCAP-SREBP complex endoplasmic reticulum-to-Golgi translocation, which facilitates directly binding of SARS-CoV-2 NP to the NLRP3 protein for NLRP3 inflammasome assembly. SARS-CoV-2 NP amplified the TMAO-induced lipogenic gene expression and NLRP3 inflammasome. Knockdown of SCAP-SREBP2 can effectively reduce lipogenic gene expression and alleviate NLRP3 inflammasome-mediated systemic inflammation in VSMCs stimulated with TMAO and SARS-CoV-2 NP. These results reveal that SARS-CoV-2 NP amplified TMAO-induced lipogenesis and NLRP3 inflammasome activation via priming the SCAP-SREBP signaling pathway.

Membrane vesicles derived from Enterococcus faecalis promote the co-transfer of important antibiotic resistance genes located on both plasmids and chromosomes.

BACKGROUND: Bacterial membrane vesicles (BMVs) are novel vehicles of antibiotic resistance gene (ARG) transfer in Gram-negative bacteria, but their role in the spread of ARGs in Gram-positive bacteria has not been defined. The purpose of this study was to evaluate the role of MVs in the transmission of antimicrobial resistance in Gram-positive bacteria. METHODS: A linezolid-resistant Enterococcus faecalis CQ20 of swine origin was selected as the donor strain. Linezolid-susceptible E. faecalis SC032 of human origin, Enterococcus faecium BM4105 and Escherichia coli were selected as recipient strains. The presence of plasmids (pCQ20-1 and pCQ20-2) and an optrA-carrying transposon Tn6674 in CQ20, MVs and vesiculants was verified by WGS or PCR. MVs were isolated with density gradient centrifugation, and MV-mediated transformation was performed to assess the horizontal transferability of MVs. The MICs for CQ20 and its vesiculants were determined by the broth microdilution method. RESULTS: CQ20-derived MVs (CQ20-MV) were isolated, and PCR identified the presence of two plasmids and the optrA gene in the CQ20-MVs. MV-mediated transformation to E. faecalis SC032 and E. faecium BM4105 was successfully performed, and the WGS data also showed that both plasmids pCQ20-1 and pCQ20-2 and optrA-carrying transposon Tn6674 were transferred to E. faecalis SC032 and E. faecium BM4105, but failed for E. coli. Additionally, vesiculants that had acquired ARGs still had the ability to spread these genes via MVs. CONCLUSIONS: To our knowledge, this is the first report of MV-mediated co-transfer of ARG-carrying plasmids and transposons in the Gram-positive bacterium E. faecium.

Toxic effects and mechanisms of engineered nanoparticles and nanoplastics on lettuce (Lactuca sativa L.).

Engineered nanoparticles (ENPs) and nanoplastics (NPs) are typical nanoparticles in terrestrial environments. Till now, few studies have compared their toxicity and mechanism to plants. Here we investigated the effects of CuO, nZVI ENPs and polystyrene (PS) NPs on lettuce growth, metabolic functions, and microbial community structure. Results showed that low concentrations of nanoparticles decreased root biomass and promoted photosynthetic indicators, whereas increased reactive oxygen species (ROS) were detected in roots exposed to high concentrations of nanoparticles. High-dose CuO ENP exposure significantly raised the MDA content by 124.6 % compared to CK, causing the most severe membrane damage in the roots among the three types of nanoparticles. Although linoleic acid metabolism was down-regulated, the roots alleviated CuO stress by up-regulating galactose metabolism. Uptake of PS by roots similarly caused ROS production and activated the oxidative stress system by altering amino acid and vitamin metabolism. Faster microbial responses to nanoparticles were observed in the nZVI and PS networks. The root toxicity was indirectly mediated by ion release, NP uptake, or ROS generation, ultimately impacting root cell metabolism, rhizospheric microorganism and plant growth. These findings provide theoretical basis for assessing environmental impact of nanoparticles and their possible ecological risks.

Effects and mechanisms of polystyrene micro- and nano-plastics on the spread of antibiotic resistance genes from soil to lettuce.

Effects of microplastics (MPs) and nanoplastics (NPs) on the spread of antibiotic resistance genes (ARGs) in soil-plant systems are still unclear. To investigate the spread and mechanisms of ARGs from soil to lettuce, lettuce was exposed to soil spiked with two environmentally relevant concentrations of polystyrene MPs (100 µm) and NPs (100 nm). Results showed that microorganisms that carried ARGs in soil were increased after exposure to MPs/NPs, which led to an increase in ARGs in roots. NPs were absorbed by roots and can be transported to leaves. Analysis of transcriptomics, proteomics and metabolomics indicated that high concentration of NPs regulated the expression of related genes and proteins and improved the accumulation of flavonoids in the lettuce, therefore decreased the abundance of microorganisms that contained ARGs. Our work emphasizes the size and dose influences of MPs and NPs on the spread of ARGs from soil to plant.

Monocyte to high-density lipoprotein cholesterol ratio predicts poor outcomes in ischaemic heart failure patients combined with diabetes: a retrospective study.

BACKGROUND: The prevalence of ischaemic heart failure (HF) continues to increase. Diabetes mellitus (DM) concomitant with ischaemic HF increases the risk of major adverse cardiovascular events (MACEs). As a promising predictor for cardiovascular diseases, the predictive value of the monocyte to high-density lipoprotein cholesterol ratio (MHR) for MACE in the ischaemic HF with DM cohort has never been investigated before. OBJECTIVE: We aimed to investigate the MHR as a predictor for MACE in ischaemic HF patients with DM who underwent percutaneous coronary intervention (PCI). METHODS: This observational study enrolled 1049 patients with ischaemic HF and DM undergoing PCI from June 2017 to June 2019. The baseline data were collected. MACEs, including all-cause mortality, nonfatal myocardial infarction, and any revascularization, were recorded within the 36-month follow-up. The characteristics and incidence of MACE were analysed in four groups stratified by the quartiles of MHR. The hazard ratio for MACE was analysed with Cox regression models. The incidence of MACE in the four groups was evaluated by Kaplan‒Meier survival analysis. Restricted cubic spline analysis was performed to determine the nonlinear correlation between the MHR and MACE. RESULTS: After the 36-month follow-up, 407 patients (38.8%) experienced MACEs. The incidence of MACE was significantly higher among patients in the upper MHR quartile than among those in the lower MHR quartiles (23.4% vs. 36.0% vs. 41.4% and 54.6%; P < 0.001, respectively), which was consistent with the Kaplan‒Meier survival analyses (P < 0.0001). A multivariate Cox regression model showed that the MHR was an independent risk factor for MACE after variables were adjusted (adjusted HR: 2.11; 95% CI 1.47-3.03; P < 0.001). Its predictive effects on MACE showed no interaction with hypercholesterolemia (P > 0.05). CONCLUSION: The MHR was a significant and independent predictor of MACEs in ischaemic HF patients with DM undergoing PCI.

DNA barcodes and morphology reveal new species within the Rheotanytarsus guineensis species group from China (Diptera: Chironomidae).

The Rheotanytarsus guineensis species group (Diptera: Chironomidae) is a species diverse and taxonomically difficult group. Using DNA barcodes, we found five new species within the R. guineensis species group and reviewed the species group based on adult males from China. Rheotanytarsus guoae Lin & Yao sp. n., Rheotanytarsus miaoae Lin & Yao sp. n., Rheotanytarsus qiangi Lin & Yao sp. n., Rheotanytarsus yueqingensis Lin & Yao sp. n., and Rheotanytarsus yui Lin & Yao sp. n. are all described and figured. A key to known adult males of the R. guineensis species group worldwide is provided for the first time.

An injectable and light curable hyaluronic acid composite gel with anti-biofilm, anti-inflammatory and pro-healing characteristics for accelerating infected wound healing.

Bacterial biofilm formation and drug resistance are common issues associated with wound healing. Antimicrobial peptides (AMPs) are a new class of antimicrobial agents with the potential to solve these global health issues. New injectable adhesive antibacterial hydrogels have excellent prospects of becoming the next innovative wound-healing dressings. In this study, the hyaluronic acid was connected to the antibacterial peptide Plantaricin 149 (Pln149), obtaining HAD@AMP. HAD@AMP performed well in efficient antimicrobial activity, good histocompatibility, low drug resistance, low bacterial biofilm formation, and fast wound healing process which are essential for rapid healing of infected wound. During the hydrogel degradation process, Pln149 was released to inhibit bacterial communication and reduce bacterial biofilm formation. Meanwhile, HAD@AMP could up-regulate anti-inflammatory and pro-angiogenic factors, and down-regulate inflammatory factors to promote the healing of infected wounds, which provide a new idea for skin healing strategies.

New data on mitogenomes of Thienemanniella Kieffer, 1911 (Diptera: Chironomidae, Orthocladiinae).

The mitochondrial genome (mitogenome) has been widely used as a powerful marker in phylogenetic and evolutionary studies of various Dipteran groups. However, only a few mitogenomes from the Thienemanniella genus have been reported till now. Furthermore, there is still indeterminacy in the phylogenetic relationships of the genus Thienemanniella. In this study, mitogenomes of five Thienemanniella species were sequenced and analyzed newly. Combined with the published mitogenome of Thienemanniella nipponica, the obtained results showed that mitogenomes of Thienemanniella were conserved in structure, and all genes were observed to be arranged in the same gene order as the ancestral mitogenome. Nucleotide composition varied significantly among different genes, and the control region displayed the highest A + T content. All protein coding genes are subjected to purification selection, and the fastest evolving gene is ATP8. Maximum likelihood and Bayesian inference analyses showed the phylogeny of Thienemanniella which was supported in five topologies. Our present study provides valuable insight into the phylogenetic relationships of Thienemanniella species.

FGF21 prevents neuronal cell ferroptosis after spinal cord injury by activating the FGFR1/ß-Klotho pathway.

Spinal cord injury (SCI) is a kind of traumatic nervous system disease caused by neuronal death, causing symptoms like sensory, motor, and autonomic nerve dysfunction. The recovery of neurological function has always been a intractable problem that has greatly distressed individuals and society. Although the involvement of iron-dependent lipid peroxidation leading to nerve cell ferroptosis in SCI progression has been reported, the underlying mechanisms remain unaddressed. Thus, this study aimed to investigate the potential of recombinant human FGF21 (rhFGF21) in inhibiting ferroptosis of nerve cells and improving limb function after SCI, along with its underlying mechanisms. In vivo animal model showed that FGFR1, p-FGFR1, and ß-Klotho protein gradually increased over time after injury, reaching a peak on the third day. Moreover, rhFGF21 treatment significantly reduced ACSL4, increased GPX4 expression, reduced iron deposition, and inhibited ferroptosis. Meanwhile, rhFGF21 decreased cell apoptosis following acute spinal cord damage. In contrast, FGFR1 inhibitor PD173074 partially reversed the rhFGF21-induced therapeutic effects. Overall, this work revealed that rhFGF21 activates the FGFR1/ß-Klotho pathway to decrease ferroptosis of nerve cells, suggesting that FGF21 could be a new therapeutic target for SCI neurological rehabilitation.

The Maize ZmBES1/BZR1-9 Transcription Factor Accelerates Flowering in Transgenic Arabidopsis and Rice.

In model plants, the BRI1-EMS suppressor 1 (BES1)/brassinazole-resistant 1 (BZR1) transcription factors play vital roles in regulating growth, development, and stimuli response. However, the roles of maize ZmBES1/BZR1 members are largely unknown. In this research, the ZmBES1/BZR1-9 gene was ectopically expressed in Arabidopsis and rice for the phenotyping of flowering. We found that the complementation and overexpression of ZmBES1/BZR1-9 in bes1-D mutant and wild type Arabidopsis both resulted in early flowering that was about 10 days shorter than in the untransformed control under long-day conditions. In addition, there was no difference in the rosette leaf number between all transgenic lines and the control. Subsequently, the ZmBES1/BZR1-9 gene was overexpressed in rice. It was found that overexpression lines of rice exhibited early flowering with heading dates that were 8 days shorter compared with untransformed plants. Moreover, the results of RNA-seq and qRT-PCR showed that five flowering-regulated genes, namely At2-MMP, AtPCC1, AtMYB56, AtPELPK1, and AtPRP10, were significantly up-regulated in all complementary and overexpressing lines of Arabidopsis. Meanwhile, the results of RNA-seq showed that 69 and 33 differentially expressed genes (DEGs) were up- and down-regulated in transgenic rice, respectively. Four flowering-related genes, namely OsGA20OX1, OsCCR19, OsBTBN19, and OsRNS4 were significantly up-regulated in transgenic lines. To sum up, our findings demonstrate that ZmBES1/BZR1-9 is involved in controlling flowering and provide insights into further underlying roles of BES1/BZR1s in regulating growth and development in crops.

DNA Barcode of symbiotic chironomids: Findings in the genus Symbiocladius (Diptera: Chironomidae).

Chironomidae of symbiotic habits have been recorded in different parts of the world, among commensals and parasites. There are different genera reported at the moment, however questions such as the origin of commensal or parasitic life, which occurred first or what are their benefits remain debatable. In order to contribute with information to elucidate the above mentioned issues, the present study reports the finding of immature stages of Symbiocladius (Acletus) wygodzinskyi Roback, 1965 in the Churup stream located in the Andes Cordillera (Peru), living on nymphs of Leptophlebiidae (Ephemeroptera). We present a morphological description of immature stages of this species and for the first time the sequence of COX1 gene S. (A.) wygodzinskyi. The genetic result also supports differences between the morphospecies of Symbiocladius (Symbiocladius) rhithrogenae Zavrel, 1924 and S. (A.) wygodzinskyi in 23%.

Guanine-rich RNA sequence binding factor 1 regulates neuronal ferroptosis after spinal cord injury in rats via the GPX4 signaling pathway.

Spinal cord injury (SCI) can trigger multiple forms of neuronal cell death. Among these, ferroptosis stands out as a particularly important style of cell death due to its iron overload-dependent lipid peroxidative regulatory mechanism. The guanine-rich RNA sequence binding factor 1 (GRSF1) is an RNA-binding protein that has been implicated in cellular senescence, mitochondrial function, oxidative stress, erythropoiesis, and embryonic brain development. However, the function of GRSF1 in neuronal ferroptosis after SCI remains unclear. Here, we established a SCI rat model in vivo and evaluated the function of GRSF1 on neuronal ferroptosis by inhibiting and overexpressing GRSF1. We firstly verified the protein expression of GRSF1 and GPX4 at different time points after SCI. According of changes in expression, we chose 3 d post SCI to assess the effect of GRSF1 on ferroptosis. We found that GRSF1 expression decreased after SCI. In addition, GRSF1 was mainly localized in the cytoplasm of neurons. The results also showed that overexpression of GRSF1 promoted recovery of neurological functional after SCI. Further investigation revealed that GRSF1 might attenuate neuronal ferroptosis by regulating the GPX4 protein expression levels. In summary, our findings indicate that GRSF1 attenuates injury in SCI and reduces neuron ferroptosis and promotes functional recovery via GPX4.