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Duodenal stump fistula (DSF) is a serious complication of radical gastrectomy for gastric cancer. Herein, we illustrated an innovative choice for treating duodenal stump fistulas by placing a modified sump drainage through trocar puncture into the DSF-related abscess (DSF-abscess) cavity. We retrospectively analyzed 974 consecutive patients who underwent gastrectomy for gastric cancer between 2011 and 2021. Of these patients, 34 who developed postoperative duodenal stump fistulas postoperatively were enrolled into our study, and their clinical data were retrospectively assessed. From January 2011 to December 2017, 15 patients received conventional treatments (percutaneous catheter drainage, PCD group) known as the traditional percutaneous method, and 19 patients from January 2018 to December 2021 received new treatments (Troca's SD group) consisting of conventional therapies and placement of a modified sump drainage through trocar puncture into DSF-abscess cavity. The demographics, clinical characteristics and treatment outcomes were compared between two groups. Compared with the PCD group, the rates of postoperative complications, duodenostomy creation, subsequent surgery, fistula healing rates of the DSF, and length of postoperative hospital stay were significantly decreased in the Troca SD group. However, there was no significant difference in the abscess recurrence rate and mortality rates. Trocar puncture with a modified sump drainage is an safe, effective, and technically feasible treatment for duodenal stump fistula after radical gastrectomy for gastric cancer. This novel technique should be further investigated using large-scale RCT research.

SIVA-1 has been shown to affect apoptotic processes in various different cell lines, and SIVA-1 significantly contributes to the decreased responsiveness of cancer cells to some chemotherapy agents. However, whether SIVA-1 has potential application in gastric cancer remains unknown. Therefore, the objective of this investigation was to clarify the distinct function of SIVA-1 in chemotherapeutic drug resistance within a living murine model with gastric malignancy, and initially elucidate the underlying mechanisms. In an established multidrug-resistant gastric cancer xenograft mouse model, lentivirus, named Lv-SIVA-1, was injected into xenograft tumors, and increased the mRNA and protein expression of endogenous SIVA-1 in tumors. Immunohistochemical assays of xenograft tumor showed that SIVA-1 was significantly upregulated, and the protein expression levels of SIVA-1 were highly increased, as detected by Western blotting. In addition, we detected the role of SIVA-1 in cell proliferation and cell apoptosis in gastric cancer cells by TUNEL and found that SIVA-1 decreased tumor cell apoptosis and promoted tumor growth in vivo. Using a TMT assay between tumor tissues of experimental and control groups, differentially expressed proteins were examined and three potential biomarkers of multidrug resistance (ARF, MDM2, and p53) were screened. We further investigated the molecular mechanism by which SIVA-1 played an efficient role against chemotherapies and found that overexpressed SIVA-1 leads to increased ARF and MDM2 expression and suppressed expression of p53 in tumor tissue. In conclusion, SIVA-1 plays a significant role in the multidrug resistance of gastric tumors. In addition, overexpressed SIVA-1 positively regulates cell proliferation, adjusts cycle progression, and reduces the response to drug treatment for gastric cancer in an ARF/MDM2/p53-dependent manner. This novel research provides a basis for chemical management of gastric cancer through regulation of SIVA-1 expression.

Treponema pallidum (Tp) has a well-known ability to evade the immune system and can cause neurosyphilis by invading the central nervous system (CNS). Microglia are resident macrophages of the CNS that are essential for host defense against pathogens, this study aims to investigate the interaction between Tp and microglia and the potential mechanism. Here, we found that Tp can exert significant toxic effects on microglia in vivo in Tg (mpeg1: EGFP) transgenic zebrafish embryos. Single-cell RNA sequencing results showed that Tp downregulated autophagy-related genes in human HMC3 microglial cells, which is negatively associated with apoptotic gene expression. Biochemical and cell biology assays further established that Tp inhibits microglial autophagy by interfering with the autophagosome-lysosome fusion process. Transcription factor EB (TFEB) is a master regulator of lysosome biogenesis, Tp activates the mechanistic target of rapamycin complex 1 (mTORC1) signaling to inhibit the nuclear translocation of TFEB, leading to decreased lysosomal biogenesis and accumulated autophagosome. Importantly, the inhibition of autophagosome formation reversed Tp-induced apoptosis and promoted microglial clearance of Tp. Taken together, these findings show that Tp blocks autophagic flux by inhibiting TFEB-mediated lysosomal biosynthesis in human microglia. Autophagosome accumulation was demonstrated to be a key mechanism underlying the effects of Tp in promoting apoptosis and preventing itself from clearing by human microglia. This study offers novel perspectives on the potential mechanism of immune evasion employed by Tp within CNS. The results not only establish the pivotal role of autophagy dysregulation in the detrimental effects of Tp on microglial cells but also bear considerable implications for the development of therapeutic strategies against Tp, specifically involving mTORC1 inhibitors and autophagosome formation inhibitors, in the context of neurosyphilis patients. Author summary Treponema pallidum (Tp) is the causative agent of syphilis and poses a significant threat to the central nervous system (CNS), potentially leading to neurosyphilis. Given Tp’s remarkable ability to circumvent host immune defenses, comprehending its immune evasion mechanisms within the CNS is of paramount importance to devise effective treatment strategies for neurosyphilis. This study aimed to explore the interplay between Tp and microglia, vital immune cells residing in the CNS. Both in vivo and in vitro analyses revealed considerable toxicity of Tp on microglia. Furthermore, Tp infection was found to impede lysosomal biosynthesis, leading to a diminished pool of lysosomes available for autophagosome fusion. Consequently, the autophagic flux was disrupted, resulting in the accumulation of autophagosomes. Our findings underscore the pivotal role of autophagosome accumulation as a key mechanism exploited by Tp to promote microglial cell apoptosis and evade clearance within the human CNS. This investigation sheds new light on the potential immune evasion strategies employed by Tp in the CNS context.

Abstract Based on the favorable ionic conductivity and structural stability, sodium superionic conductor (NASICON) materials especially utilizing multivalent redox reaction of vanadium are one of the most promising cathodes in sodium‐ion batteries (SIBs). To further boost their application in large‐scale energy storage production, a rational strategy is to tailor vanadium with earth‐abundant and cheap elements (such as Fe, Mn), reducing the cost and toxicity of vanadium‐based NASICON materials. Here, the Na3.05V1.03Fe0.97(PO4)3 (NVFP) is synthesized with highly conductive Ketjen Black (KB) by ball‐milling assisted sol‐gel method. The pearl‐like KB branch chains encircle the NVFP (p‐NVFP), the segregated particles possess promoted overall conductivity, balanced charge, and modulated crystal structure during electrochemical progress. The p‐NVFP obtains significantly enhanced ion diffusion ability and low volume change (2.99%). Meanwhile, it delivers a durable cycling performance (87.7% capacity retention over 5000 cycles at 5 C) in half cells. Surprisingly, the full cells of p‐NVFP reveal a remarkable capability of 84.9 mAh g−1 at 20 C with good cycling performance (capacity decay rate is 0.016% per cycle at 2 C). The structure modulation of the p‐NVFP provides a rational design on the superiority of others to be put into practice.

Abstract The accelerating electrification has sparked an explosion in lithium‐ion batteries (LIBs) consumption. As the lifespan declines, the substantial LIBs will flow into the recycling market and promise to spawn a giant recycling system. Nonetheless, since the lack of unified guiding standard and nontraceability, the recycling of end‐of‐life LIBs has fallen into the dilemma of low recycling rate, poor recycling efficiency, and insignificant benefits. Herein, tapping into summarizing and analyzing the current status and challenges of recycling LIBs, this outlook provides insights for the future course of full lifecycle management of LIBs, proposing gradient utilization and recycling‐target predesign strategy. Further, we acknowledge some recommendations for recycling waste LIBs and anticipate a collaborative effort to advance sustainable and reliable recycling routes.

Abstract Background To evaluate the myocardial microcirculation perfusion of patients with acute ST-segment elevation myocardial infarction (STEMI) with a different index of microcirculatory resistance (IMR) after percutaneous coronary intervention (PCI) by myocardial contrast echocardiography (MCE) and analyse the value of MCE in predicting myocardial perfusion after PCI. Methods Fifty-six patients with acute STEMI who underwent an emergency PCI were selected from October 2018 to October 2019 in our hospital. According to the IMR values measured during PCI treatment, the patients were divided into three groups. Traditional ultrasound and MCE were performed one week after PCI. The left ventricular ejection fraction (LVEF), ventricular wall motion score index (WMSI), A value, β value and A × β value (which refers to the patient’s myocardial blood flow) were measured. The receiver operating characteristic curve was drawn to evaluate the effectiveness of the MCE parameters in the diagnosis of myocardial microcirculation perfusion disorders. Results The results showed that there was no significant difference in the LVEF among the groups. The WMSI in Group 3 was statistically different from that in Groups 1 and 2 (P

Abstract Background Dermatofibrosarcoma protuberans (DFSP) is a superficial fibroblastic tumor characterized by high rate of local recurrence and low metastatic potential. Fibrosarcomatous transformation can rarely arise in DFSP either de novo or as recurrent, which represents a form of tumor progression and carries an increased risk of metastasis over classic DFSP. Cytogenetically, DFSP is characterized by a recurrent unbalanced chromosome translocation t (17;22)(q22;q13), leading to the formation of COL1A1-PDGFB fusion transcript that is present in more than 90% of cases. Alternative fusions involving the PDGFD with partners of COL6A3 or EMILIN2 have recently been documented in less than 2% of cases. Herein, we report a DFSP with fibrosarcomtous morphology harboring a novel TNC-PDGFD fusion. Case presentation A 54-year-old female presented with a slowly growing mass in the right thigh. Excision demonstrated a 2-cm ovoid, well-circumscribed, gray-white, mass. Microscopic examination revealed a partially encapsulated subcutaneous nodule without dermal connection. The neoplasm was composed of cellular and fairly uniform spindle cells with brisk mitoses, arranged in elongated fascicles and herringbone patterns, with focal collagenized stroma. The neoplastic cells were positive for CD34 and smooth muscle actin. Fluorescence in-situ hybridization analyses showed negative for COL1A1-PDGFB fusion as well as NTRK1/2/3 rearrangements. A subsequent RNA sequencing detected an in-frame fusion between exon 15 of TNC and exon 6 of PDGFD. This fusion was further confirmed by nested reverse transcription polymerase chain reaction amplification followed by Sanger sequencing. A diagnosis of fibrosarcomatous DFSP was rendered and the patient was in good status at a follow-up of 12 months after the operation. Conclusions We report a fibrosarcomatous DFSP with novel TNC-PDGFD fusion, which adds to the pathologic and genetic spectrum of PDGFD-rearranged DFSP.

Abstract As a cathode for sodium‐ion batteries (SIBs), Na3V2(PO4)2F3 (NVPF) with 3D open framework is a promising candidate due to its high working voltage and large theoretical capacity. However, the severe capacity degradation and poor rate capability hinder its practical applications. The present study demonstrated the optimization of Na‐storage performance of NVPF via delicate lattice modulation. Aliovalent substitution of V3+ at Na+ in NVPF induces the generation of electronic defects and expansion of Na+‐migration channels, resulting in the enhancement in electronic conductivity and acceleration of Na+‐migration kinetics. It is disclosed that the formed stronger NaO bonds with high ionicity than VO bonds lead to the significant increase in structural stability and ionicity in the Na+‐substituted NVPF (NVPF‐Nax). The aforementioned effects of Na+ substitution achieve the unprecedented electrochemical performance in the optimized Na3.14V1.93Na0.07(PO4)2F3 (NVPF‐Na0.07). As a result, NVPF‐Na0.07 delivers a high‐rate capability (77.5 mAh g−1 at 20 C) and ultralong cycle life (only 0.027% capacity decay per cycle over 1000 cycles at 10 C). Sodium‐ion full cells are designed using NVPF‐Na0.07 as cathode and Se@reduced graphene oxide as anode. The full cells exhibit excellent wide‐temperature electrochemical performance from −25 to 25°C with an outstanding rate capability (96.3 mAh g−1 at 20 C). Furthermore, it delivered an excellent cycling performance over 300 cycles with a capacity retention exceeding 90% at 0.5 C under different temperatures. This study demonstrates a feasible strategy for the development of advanced cathode materials with excellent electrochemical properties to achieve high‐efficiency energy storage.

Abstract Objective Sleep disorders as a preclinical symptom of synucleinopathies become more prevalent in older adults. Synucleinopathies might be caused by the abnormal aggregation of alpha‐synuclein in the brain, which was indicated by alpha‐synuclein levels in cerebrospinal fluid (CSF). We aimed to investigate associations of sleep characteristics with CSF alpha‐synuclein in older adults. Methods Our study recruited 536 cognitively intact individuals (aged between 40 and 90 years old) from the Chinese Alzheimer’s Biomarker and Lifestyle study. Sleep behaviors were assessed by Pittsburgh Sleep Quality Index and total alpha‐synuclein in CSF was measured by enzyme‐linked immune‐sorbent assay. We used multiple linear and non‐linear regression models for research. Results Significant non‐linear associations of CSF alpha‐synuclein with sleep time and duration were revealed. Individuals who went to bed and fell asleep too early or late tended to have lower CSF alpha‐synuclein (reflection point for time to bed and fall asleep were 10:26 p.m. and 10:40 p.m.). Lower CSF alpha‐synuclein was also observed in individuals with either excessive or insufficient sleep duration (reflection point: 7.24 hours). Besides, overall poor sleep quality (β = −0.0621; P = 0.0242), longer sleep latency (β = −0.0415; P = 0.0174) and lower sleep efficiency (β = 0.0036; P = 0.0017) showed linear associations with lower CSF alpha‐synuclein. Sleep disturbances and daytime dysfunction were not significantly associated with CSF alpha‐synuclein. Interpretation Poor sleep was associated with lower levels of CSF alpha‐synuclein in older adults, which may provide new insight into the prevention of synucleinopathies.

Employing the new nitronyl nitroxide biradical ligand biNIT-3Py-5-Ph (2-(5-phenyl-3-pyridyl)-bis(4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide)), a 16-spin Cu-radical complex, [Cu8(biNIT-3Py-5-Ph)4(hfac)16] 1, and three 2p-3d-4f chain complexes, {[Ln(hfac)3][Cu(hfac)2]2(biNIT-3Py-5-Ph)2}n (LnⅢ= Gd 2, Tb 3, Dy 4; hfac = hexafluoroacetylacetonate), have been prepared and characterized. X-ray crystallographic analysis revealed in all derivatives a common cyclic [Cu-biNIT]2 secondary building unit in which two bi-NIT-3Py-5-Ph biradical ligands and two CuII ions are associated via the pyridine N atoms and NO units. For complex 1, two such units assemble with four additional CuII ions to form a discrete complex involving 16 S = 1/2 spin centers. For complexes 2–4, the [Cu-biNIT]2 units are linked by LnIII ions via NO groups in a 1D coordination polymer. Magnetic studies show that the coordination of the aminoxyl groups with Cu or Ln ions results in behaviors combining ferromagnetic and antiferromagnetic interactions. No slow magnetic relaxation behavior was observed for Tb and Dy derivatives.

Summary: The development of high-performance cathodes for sodium-ion batteries (SIBs) is one key issue required for the success of large-scale energy storage systems. In addition to performance degradation during cycling, electrode materials are usually hampered by instability when stored in various environments severely restricting their practical application. Here, we report a stable cathode material that shows no obvious capacity attenuation in various storage conditions. The cathode is composed of regular and homogeneous Na3V2(PO4)2O2F0.99Cl0.01 (NVPFCl) microcubes, with electrochemical properties, including high specific capacity (128.2 mA h g-1 at 0.1 C), excellent rate capability (79.8 mA h g-1 at 20 C), long-term cycle life, and all-climate performance. Studies using in/ex situ characterization and electrode kinetics are implemented to reveal the possible reasons for the stability and electrochemical activity of NVPFCl. This work may provide a pathway for the development of all-climate and storage-stable SIB cathode materials.

Long non-coding RNAs are involved in many infectious diseases. Our previous studies showed that lncRNA-ENST00000421645 expression is increased in T lymphocytes of neurosyphilis patients compared to healthy controls. However, whether lncRNA-ENST00000421645 has biological functions remains unclear. The current study was undertaken to understand the mechanism of lncRNA-ENST00000421645 in T lymphocyte function in neurosyphilis patients. The lncRNA-ENST00000421645 pull-down assay showed that lncRNA-ENST00000421645 acted on the acetylase NAT10. The chromatin immunoprecipitation (ChIP)-PCR results showed that lncRNA-ENST00000421645 promoted the acetylation of histone H3K27 adjacent to the Kank1 promoter, thereby promoting Kank1 protein expression. Kank1 promotes 14-3-3 protein expression, inhibits NF-kB activation, inhibits IFN-γ secretion by T lymphocytes, and promotes T lymphocyte apoptosis. Taken together, our findings suggest a novel mechanism that LncRNA-ENST00000421645 upregulates Kank1 to inhibit IFN-γ expression and promote T cell apoptosis in neurosyphilis.

Abstract Dietary shifts can alter the relative availability of different nutrients and are therefore associated with metabolic adaptation in animals. The Coccinellidae (ladybirds) exhibits three major types of feeding habits and provides a useful model to study the effects of dietary changes on the evolution of mitogenomes, which encode proteins directly involved in energy metabolism. Here, mitogenomes of three coccinellid species were newly sequenced. These data were combined with other ten previously sequenced coccinellid mitogenomes to explore the relationship between mitogenome evolution and diets. Our results indicate that mitogenomic data can be effectively used to resolve phylogenetic relationships of Coccinellidae. Strong codon usage bias in coccinellid mitogenomes was predominantly determined by nucleotide composition. The 13 mitochondrial protein‐coding genes (PCGs) globally evolved under negative constraints, with some PCGs showing a stronger purifying selection. Six PCGs (nad3, nad4L, and nad5 from Complex I; cox1 and cox3 from Complex IV; and atp6 from Complex V) displayed signs of positive selection. Of these, adaptive changes in cox3 were potentially associated with metabolic differences resulting from dietary shifts in Coccinellidae. Our results provide insights into the adaptive evolution of coccinellid mitogenomes in response to both dietary shifts and other life history traits.

This study stimulated functional microbial adaptation to the extreme environment of the Luliang oilfield reservoir and assessed the impact of indigenous microbial enhanced oil recovery treatment on the microbial community and oil recovery. By high-resolution pyro-sequencing, Acinetobacter, Pseudomonas, Sphingomonas, Thauera, Arcobacter and Hyphomonas were regarded as suitable candidates and a customised nutrient mixture was selected to activate the target microbes. The interfacial tension of crude oil and water decreased from 29.76 mN m−1 to 0.65 mN m−1 and the emulsion stability index increased from 5% to 92% after customised nutrient culture. The oil biodegradation experiments after the cultivation exhibited positive effects in degrading aromatics, resins and asphaltenes fractions and improving the mobility. Six target genera were activated markedly after 96 h of incubation. The oil recovery was enhanced from 51.2% to 60.7% using fermentation broth injection. Thus, injecting a customised nutrient mixture with injection brine into the stratum to stimulate functional microbes has the potential to enhance oil recovery in the Luliang oilfield.

The objective of this study was to investigate whether MTNR1B gene variants influence repaglinide response in Chinese patients with newly diagnosed type 2 diabetes mellitus (T2DM). A total of 300 patients with T2DM and 200 control subjects were enrolled to identify MTNR1B rs10830963 and rs1387153 genotypes by real-time polymerase chain reaction (PCR), with subsequent high-resolution melting (HRM) analysis. Ninety-five patients with newly diagnosed T2DM were randomly selected to undergo 8 weeks of repaglinide treatment (3 mg/day). After 8-week repaglinide monotherapy, patients with at least one G allele of MTNR1B rs10830963 showed a smaller decrease in fasting plasma glucose (FPG) (P = 0.031) and a smaller increase in homeostasis model assessment for beta cell function (HOMA-B) (P = 0.002) levels than those with the CC genotype did. The T allele carriers at rs1387153 exhibited a smaller decrease in FPG (P = 0.007) and smaller increases in postprandial serum insulin (PINS) (P = 0.016) and HOMA-B (P < 0.001) levels compared to individuals with the CC genotype. These data suggest that the MTNR1B rs10830963 and rs1387153 polymorphisms are associated with repaglinide monotherapy efficacy in Chinese patients with T2DM.

Pulmonary arterial hypertension (PAH) is a severe complication of hereditary hemorrhagic telangiectasia (HHT); however, little is known about its clinical characteristics and prognosis. Nine newly diagnosed HHT-PAH patients were prospectively recruited between October 2007 and January 2016 and were followed up every half-year. Eighteen idiopathic pulmonary arterial hypertension (IPAH) patients, matched with HHT-PAH patients on mean pulmonary arterial pressure, pulmonary capillary wedge pressure, pulmonary vascular resistance, cardiac index, and World Health Organization (WHO) functional class (FC), were recruited. The clinical characteristics of HHT-PAH patients were described and the prognosis of these two cohorts were compared. Of HHT-PAH patients, 55.56% were WHO FC III. Kaplan–Meier survival analysis showed one- and three-year survival rates of HHT-PAH patients were 77.8% and 53.3% respectively, which were worse than matched IPAH patients (log rank: P = 0.047). HHT-PAH patients had higher red cell distribution width (14.88 ± 2.93% versus 13.19 ± 0.83%, P = 0.031), larger right ventricular anteroposterior diameter (34.67 ± 6.67 mm versus 28.56 ± 6.35 mm, P = 0.029), and lower mean corpuscular hemoglobin concentration (317.38 ± 17.71 g/L versus 335.72 ± 14.68 g/L, P = 0.011) than matched IPAH patients. Multivariate Cox proportional hazards regression analyses showed baseline total bilirubin independently predicted the mortality of HHT-PAH after adjusting by age, cardiac index, mixed venous oxygen saturation, or serum uric acid. HHT-PAH patients may have a worse prognosis than matched IPAH patients. Baseline total bilirubin may be a promising predictor for the long-term prognosis in HHT-PAH patients.

The family Miridae is one of the most species-rich families of insects. To better understand the diversity and evolution of mirids, we determined the mitogenome of Lygus pratenszs and re-sequenced the mitogenomes of four mirids (i.e., Apolygus lucorum, Adelphocoris suturalis, Ade. fasciaticollis and Ade. lineolatus). We performed a comparative analysis for 15 mitogenomic sequences representing 11 species of five genera within Miridae and evaluated the potential of these mitochondrial genes as molecular markers. Our results showed that the general mitogenomic features (gene content, gene arrangement, base composition and codon usage) were well conserved among these mirids. Four protein-coding genes (PCGs) (cox1, cox3, nad1 and nad3) had no length variability, where nad5 showed the largest size variation; no intraspecific length variation was found in PCGs. Two PCGs (nad4 and nad5) showed relatively high substitution rates at the nucleotide and amino acid levels, where cox1 had the lowest substitution rate. The Ka/Ks values for all PCGs were far lower than 1 (

Background: The aim of this study was to investigate the significance of positive expression of Mycobacterium tuberculosis, (MTB) antigen in the cerebrospinal fluid (CSF) monocytes in diagnosing tuberculous meningitis (TBM). Materials and Methods: A total of 50 inpatients of TBM, 30 viral meningitis and 20 healthy controls were studied at the 1 st , 2 nd , and 4 th week during their treatment course. Immunohistochemical assay were used to detect early secreted antigenic target 6 (ESAT-6) positive cells, and positive cases were also observed. Results: The percentage of positive cases and positive cells of ESAT-6 in CSF monocytes were all higher in the 1 st and 2 nd week than in the 4 th week in TBM patients (P < 0.01); and percentage of positive cases and positive cells of MTB antigen in CSF monocytes were higher in TBM patients than in viral meningitis and health control in the 1 st and 2 nd week (P < 0.01). The sensitivity was 90% and the specificity was 92% in the early stage (within 2 weeks) of TBM. Conclusion: The positive expression of ESAT-6 in CSF monocytes is helpful for the early diagnosis of TBM.

To better understand the diversity and evolution of Odonata, we sequenced and annotated the complete mitochondrial genome (mitogenome) of Enallagma cyathigerum. This mitogenome was 16,661 bp in size and encoded the typical 37 genes, i.e. 13 protein-coding genes (PCGs), 22 transfer RNA genes (tRNAs) and two ribosomal RNA genes. The nucleotide composition of the E. cyathigerum mitogenome was significantly biased toward A and T, with an A + T content of 74.2%. Eleven PCGs started with a typical ATN codon, whereas the remaining two PCGs (nad1 and nad3) used TTG as the initial codon. All the 22 tRNAs had a typical secondary cloverleaf structure. The Bayesian phylogenetic analysis based on the concatenated nucleotide sequences of 13 PCGs strongly supported the sister relationship of E. cyathigerum and two Ischnura species from the same family Coenagrionidae. The phylogenetic tree strongly supported the monophyly of each of the two suborders (Zygoptera and Anisoptera) and recovered a phylogeny of Zygoptera + (Anisoptera + Anisozygoptera).

Skeletal muscle dysfunction in chronic obstructive pulmonary disease (COPD) patients is common. Neuromuscular Electrical Stimulation (NMES) is a powerful exercise training that may relieve muscle dysfunction in COPD. This study investigated whether electrical stimulation may have atypical adaptations via activation of miRNA related pathways in counteracting COPD muscle dysfunction. Forty-eight male Sprague-Dawley rats were randomly assigned to 3 groups. With the exception of the rats in the control group, the experimental rats were exposed to chronic intermittent hypoxia-hypercapnia (CIHH) (9∼11%O2,5.5∼6.5%CO2) for 2 or 4 weeks. Electrical stimulation was performed immediately after each CIHH session. Following assessment of the running capacity, biopsy samples were obtained from the gastrocnemius of the rats. The miR-1, miR-133a and miR-133b levels were measured, as well as their related proteins: phosphorylation of Akt (p-AKT), PGC-1alpha (PGC-1α), histone deacetylase 4 (HDAC4) and serum response factor (SRF). Myosin heavy chainIIa (MHCIIa) and myosin heavy chainIIb (MHCIIb) were also measured to assess fiber type changes. After 2 weeks, compared with the controls, only miR-1 and miR-133a were significantly increased (p

BackgroundChronic intermittent hypoxia-hypercapnia (CIHH) exposure leads to learnning and memory deficits in rats. Overactivation of N-methyl-D-aspartate receptors(NMDARs) can lead to the death of neurons through a process termed excitotoxicity, which is involved in CIHH-induced cognitive deficits. Excessively activated NR2B (GluN2B)-containing NMDARs was reported as the main cause of excitotoxicity. The ERK1/2 (extracellular signal-regulated kinase 1/2) signaling cascade acts as a key component in NMDARs-dependent neuronal plasticity and survival. Ca2+/calmodulin-dependent protein kinase II (CaMKII), synapse-associated protein 102 (SAP102) and Ras GTPase-activating protein (SynGAP) have been shown to be involved in the regulation of NMDAR-ERK signalling cascade. Recent studies revealed statins (the HMG-CoA reductase inhibitor) have effect on the expression of NMDARs. The present study intends to explore the potential effect of lovastatin on CIHH-induced cognitive deficits and the NR2B-ERK signaling pathway.Methods and findingsEighty male Sprague Dawley rats were randomly divided into five groups. Except for those in the control group, the rats were exposed to chronic intermittent hypoxia-hypercapnia (CIHH) (9 ∼ 11%O2, 5.5 ∼ 6.5%CO2) for 4 weeks. After lovastatin administration, the rats performed better in the Morris water maze test. Electron microscopy showed alleviated hippocampal neuronal synaptic damage. Further observation suggested that either lovastatin or ifenprodil (a selective NR2B antagonist) administration similarly downregulated NR2B subunit expression leading to a suppression of CaMKII/SAP102/SynGAP signaling cascade, which in turn enhanced the phosphorylation of ERK1/2. The phosphorylated ERK1/2 induced signaling cascade involving cAMP-response element-binding protein (CREB) phosphorylation and brain-derived neurotrophic factor (BDNF) activation, which is responsible for neuroprotection.ConclusionsThese findings suggest that the ameliorative cognitive deficits caused by lovastatin are due to the downregulation of excessive NR2B expression accompanied by increased expression of ERK signaling cascade. The effect of NR2B in upregulating pERK1/2 maybe due, at least in part, to inactivation of CaMKII/SAP102/SynGAP signaling cascade.