Practical study on the application of full-cycle fast track surgical nursing model in patients with replantation of severed fingers: A retrospective analysis.

To explore the effect of full-cycle fast track surgical (FTS) nursing in patients with replantation of severed fingers, and observe its effect on functional recovery of replanted fingers and quality of life of patients. From January 2021 to December 2022, 86 patients with replantation of severed fingers were selected from Rizhao People's Hospital, 41 patients were given routine perioperative care, 45 patients were given full-cycle rapid rehabilitation surgical care. Compare the relevant indexes of the 2 groups of patients during hospitalization. Three months after discharge, the finger function recovery of the 2 groups were compared, and the quality of life of the patients was scored with the QL-Index scale, and the satisfaction was evaluated at the same time. The first time of getting out of bed and the time of hospitalization in the full-cycle FTS nursing group were significantly shorter than those in the conventional nursing group, and the incidence of postoperative nausea, vomiting, constipation and venous thromboembolism were significantly lower than those in the conventional nursing group. The anxiety score was significantly lower than that in the conventional nursing group, the difference was statistically significant (P < .05). There was no significant difference in the incidence of arteriovenous crisis between the 2 groups (P > .05). Three months after discharge, the scores of finger sensation and movement, quality of life and satisfaction of patients in the FTS nursing group were higher than those in the conventional nursing group, and the difference was statistically significant (P < .05). Full-cycle fast track surgical nursing model can improve the in-patient experience, reduce the incidence of complications, promote rapid rehabilitation, improve the quality of life of patients, and improve satisfaction.

Current trends of high-risk gene Cul3 in neurodevelopmental disorders.

Cul3 encodes Cullin-3, a core component of the ubiquitin E3 ligase that is involved in protein ubiquitination. Recent studies have identified Cul3 as a high-confidence risk gene in neurodevelopmental disorders (NDDs), especially autism spectrum disorder (ASD). Different strategies have been used to generate animal models with Cul3 deficiency in the central nervous system, including whole-brain knockout (KO), cell-type specific conditional KO (cKO), and brain region-specific knockdown. In this review, we revisited the basic properties of CUL3 and its function under physiological and pathological conditions. Recent clinical studies including case reports and large cohort sequencing studies related to CUl3 in NDDs have been summarized. Moreover, we characterized the behavioral, electrophysiological, and molecular changes in newly developed Cul3 deficiency models. This would guide further studies related to Cul3 in CNS and provide potential therapeutic targets for Cul3-deficiency-induced NDDs, including ASD.

Inhibition of transition-metal dissolution with an inert soluble product interface constructed by high-concentration electrolyte.

The formation of a compact and stable cathode electrolyte interphase (CEI) film is a promising way to improve the high voltage resistance of lithium-ion batteries (LIBs). However, challenges arise due to the corrosion of hydrogen fluoride (HF) and the dissolution of transition metal ions (TMs) in harsh conditions. To address this issue, researchers have constructed an anion-derived CEI film enriched with LiF and LiPO2F2 soluble product on the surface of LiNi0.5Mn1.5O4 (LNMO) cathode in highly concentrated electrolytes (HCEs). The strong binding of LiF and LiPO2F2 generated an inert LiPO2F2 soluble product interface, which inhibited HF corrosion and maintained the spinel structure of LNMO, contributing to a capacity retention of 92% after 200 cycles at 55°C in the resulting cell with a soluble LiPO2F2-containing CEI film. This new approach sheds light on improving the electrode/electrolyte interface for high-energy LIBs.

Improving performances of the electrode/electrolyte interface via the regulation of solvation complexes: a review and prospect.

The electrode/electrolyte interface (EEI) is a research hotspot in lithium-ion batteries, while the electrolyte solvation complex can be regarded as a factor that cannot be ignored in determining the performance of the EEI. From the perspective of the electrolyte solvation complex, this review summarizes the effects of solvation complexes on the composition of an EEI film and the Li+ desolvation process, and further clarifies the internal mechanism of the electrolyte composition controlling solvation chemistry. Finally, combined with doubtful points that are not comprehensively considered in the regulation of solvated complexes, this review puts forward some cutting-edge views, which are of great significance for future guidance in improving the performance of lithium-ion batteries.

Pentacyclic triterpene carboxylic acids derivatives integrated piperazine-amino acid complexes for α-glucosidase inhibition in vitro.

Eighteen derivatives of pentacyclic triterpene carboxylic acids (Maslinic acid, Corosolic acid and Asiatic acid) have been prepared by coupling the piperazine complex of l-amino acids at the C-28 site of the parent compounds. The α-glucosidase inhibitory activities of the pristine derivatives were evaluated in vitro. The results indicated that the inhibitory activity of some compounds (15e IC50 = 591 µM, 16e IC50 = 423 µM) was closed to that of the reference acarbose (IC50 = 347 µM) in ethanol-water system. In addition, compound 16e (IC50 = 380 µM) showed superior inhibitory activity than acarbose (IC50 = 493 µM) in the measurement system with DMSO as solvent. The comparison of two different solvent systems showed that the derivatives had better α-glucosidase inhibitory activity in the DMSO system than that of in ethanol-water system. Regrettably, all of the as-synthesized derivatives exhibited inferior α-glucosidase inhibitory activities than those of the parent compounds in both test solvent systems. Furthermore, the result of enzyme kinetics demonstrated that the inhibition mechanism of compound 16e was noncompetitive inhibition with the inhibition constant Ki = 552 µM.

[Effects of PES and 2,4-DCP on the Extracellular Polymeric Substances and Microbial Community of Anaerobic Granular Sludge].

The effects of polyether sulfone (PES) microplastics and 2,4-dichlorophenol (2,4-DCP) on the loosely-bound extracellular polymeric substances (LB-EPS) and tightly-bound EPS (TB-EPS) of anaerobic granular sludge were investigated. In addition, high-throughput sequencing technology was used to analyze the changes in the microbial community and gene functions in the anaerobic granular sludge. The results revealed that the chemical oxygen demand (COD) removal rates of the 2,4-DCP and PES+2,4-DCP experimental groups were 35% and 37%, which were 57% and 55% lower than that of the blank control group, while the COD removal rates of the PES experimental group remained around 90%. After the addition of the PES microplastics and 2,4-DCP, the protein and polysaccharide contents in the LB-EPS decreased compared with the control group, and the polysaccharide content in TB-EPS increased the least. In presence of the PES microplastics and 2,4-DCP, the activity of coenzyme F420 was inhibited. Through high-throughput sequencing, the microbial richness and diversity of the anaerobic granular sludge in the experimental group were reduced with the addition of the PES microplastics or 2,4-DCP. In the control group and the experimental group, the dominant bacteria at the phylum level were Proteobacteria (13.45%-44.47%), Firmicutes (6.86%-21.67%), and Actinobacteria (3.16%-18.11%). The abundance of ß-Proteobacteria in the PES+2,4-DCP experimental group was reduced by 15.28%, while the abundance of γ-Proteobacteria increased by 28.44% compared with the control group. Based on the phylogenetic investigation of the communities using the reconstruction of unobserved states (PICRUSt) analysis, it was found that in the experimental group with the PES microplastics or 2,4-DCP, the genes related to the sludge energy metabolism function were 0.25%-0.72% more than the control group; therefore, the abundance of genes related to the transport function group decreased significantly.

Influence of polyether sulfone microplastics and bisphenol A on anaerobic granular sludge: Performance evaluation and microbial community characterization.

The retention of polyether sulfone (PES) and bisphenol A (BPA) in wastewater has received extensive attention. The effects of PES and BPA on the removal of organic matter by anaerobic granular sludge were investigated. We also analyzed the changes in the electron transport system and the effects on the composition of extracellular polymeric substances (EPS), as well as alternations of the microbial community in the anaerobic granular sludge. In the experimental groups which received BPA, the removal of the chemical oxygen demand (COD) were significantly suppressed, which an average removal efficiency of less than 65%, 30% lower than that of the control group. In the loosely-bound EPS (LB-EPS) excitation-emission matrix (EEM) spectra, the absorption peak of tryptophan disappeared when the BPA pollutants was added, which it was present in the control group without added pollutants. The addition of PES and BPA also affected protease, acetate kinase, and coenzyme F420 activities in the anaerobic granular sludge. Especially, the coenzyme F420 reduced from 0.0045 to 0.0017 µmol/L in the presence of PES and BPA. The relative abundance of Spirochaetes decreased in the presence of PES and BPA, while the relative abundance of Bacteroidetes increased from 12.98% to 22.87%. At the genus level, in the presence of PES and BPA, the relative abundance of Acinetobacter increased from 2.20% to 9.64% and Hydrogenophaga decreased sharply from 15.58% to 0.12%.

Characterization of quantum and classical correlations in the Earth's curved space-time.

The preparation of quantum systems and the execution of quantum information tasks between distant users are always affected by gravitational and relativistic effects. In this work, we quantitatively analyze how the curved space-time background of the Earth affects the classical and quantum correlations between photon pairs that are initially prepared in a two-mode squeezed state. More specifically, considering the rotation of the Earth, the space-time around the Earth is described by the Kerr metric. Our results show that these state correlations, which initially increase for a specific range of satellite's orbital altitude, will gradually approach a finite value with increasing height of satellite's orbit (when the special relativistic effects become relevant). More importantly, our analysis demonstrates that the changes of correlations generated by the total gravitational frequency shift could reach the level of [Formula: see text] within the satellite's height at geostationary Earth orbits.

TRIM21 and PHLDA3 negatively regulate the crosstalk between the PI3K/AKT pathway and PPP metabolism.

PI3K/AKT signaling is known to regulate cancer metabolism, but whether metabolic feedback regulates the PI3K/AKT pathway is unclear. Here, we demonstrate the important reciprocal crosstalk between the PI3K/AKT signal and pentose phosphate pathway (PPP) branching metabolic pathways. PI3K/AKT activation stabilizes G6PD, the rate-limiting enzyme of the PPP, by inhibiting the newly identified E3 ligase TIRM21 and promotes the PPP. PPP metabolites, in turn, reinforce AKT activation and further promote cancer metabolic reprogramming by blocking the expression of the AKT inhibitor PHLDA3. Knockout of TRIM21 or PHLDA3 promotes crosstalk and cell proliferation. Importantly, PTEN null human cancer cells and in vivo murine models are sensitive to anti-PPP treatments, suggesting the importance of the PPP in maintaining AKT activation even in the presence of a constitutively activated PI3K pathway. Our study suggests that blockade of this reciprocal crosstalk mechanism may have a therapeutic benefit for cancers with PTEN loss or PI3K/AKT activation.

Exposure to polyamide 66 microplastic leads to effects performance and microbial community structure of aerobic granular sludge.

Microplastic polyamide 66 (PA66) was used to explore its mechanism of influence on the contaminants removal from aerobic granular sludge (AGS) and the corresponding change to the microbial community. Results showed that the removal pollution efficiency of the experimental groups with PA66 were inhibited during the early treatment stage. However, as the experiment progressed, the removal efficiencies of chemical oxygen demand (COD) (92.66%, 93.10%, 93.11%, 93.79%) and ammonia nitrogen (94.25%, 94.58%, 95.61%, 94.73%) were similar in the addition 0 g/L (A), 0.1 g/L (B), 0.2 g/L (C) and 0.5 g/L (D) PA66 beakers at the last 10 days. On the first day, the intensity of fluorescence peaks representing tryptophan protein-like and aromatic protein-like substances of loosely-bound extracellular polymeric substances (LB-EPS) indicated that the PA66 microplastic caused damage to the sludge structure, and the intensity of fluorescence peaks representing fulvic acid-like and humic acid-like substances were stronger than those in the control beaker (A). Microbial community analysis showed that the main phyla were Firmicutes (49.11%, 59.77%, 44.33%, 41.21%), Proteobacteria (26.44%, 11.96%, 31.44%, 19.4%) and Bacteroidetes (9.24%, 13.05%, 11.89%, 14.71%) in the four beakers. According to Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, genes representing [T] Signal transduction mechanisms illustrated that adding PA66 microplastic resulted in more signaling molecules in the AGS.

Influence of amoxicillin after pre-treatment on the extracellular polymeric substances and microbial community of anaerobic granular sludge.

A combined process coupling a Fe3O4 nanoparticles (Fe3O4 NPs) heterogeneous Fenton-like reaction and an anaerobic biological technology was investigated in order to effectively treat amoxicillin-containing wastewater. With the increase in the pretreatment degree, the average COD removal rate correspondingly increased from 84.8% to 92.4% using the anaerobic biological treatment, and the biodegradability and COD removal efficiency was improved by the pretreatment processes. During the process of amoxicillin degradation, hydroxyl free radicals tended to attack the lactamide, amide and pentacyclic rings of amoxicillin. In the excitation-emission matrix (EEM) spectra of soluble microbial products (SMPs), the absorption peak of humic acid gradually decreased with application of the pretreatment. The pretreatment products were more beneficial to the characteristics of anaerobic granular sludge. For the microbial community structure, the proportion of Methanothrix and Clostridia increased with addition the heterogeneous Fenton-like pretreatment, which favored conversion of organic contaminants to volatile fatty acids and biogas.

Controlled Synthesis of Porous Hierarchical ZnFe2O4 Micro-/Nanostructures with Multifunctional Photocatalytic Performance.

Engineering semiconductors with porous hierarchical micro-/nanostructures is a feasible strategy to obtain high solar-light utilization efficiency and strong photocatalytic performance. In this work, an integrated strategy of solvent evaporation and morphology-inherited annealing for the Fe-based metal-organic framework was developed to prepare the hierarchical spinel zinc ferrite (ZnFe2O4) micro-/nanostructure. The morphology and porosity of the hierarchical ZnFe2O4 structures can be adjusted by optimizing the annealing temperatures. Benefitting from magnetic separation performance, these highly visible light-responsive hierarchical ZnFe2O4 micro-/nanostructures are demonstrated to be multifunctional photocatalytic materials, and their photocatalytic activity and reproducibility were analyzed, and the photocatalytic mechanism was also investigated. This work provides a controlled and generic route for constructing novel hierarchical semiconductors with specific compositions and intriguing structures.

CCR5 is a suppressor for cortical plasticity and hippocampal learning and memory.

Although the role of CCR5 in immunity and in HIV infection has been studied widely, its role in neuronal plasticity, learning and memory is not understood. Here, we report that decreasing the function of CCR5 increases MAPK/CREB signaling, long-term potentiation (LTP), and hippocampus-dependent memory in mice, while neuronal CCR5 overexpression caused memory deficits. Decreasing CCR5 function in mouse barrel cortex also resulted in enhanced spike timing dependent plasticity and consequently, dramatically accelerated experience-dependent plasticity. These results suggest that CCR5 is a powerful suppressor for plasticity and memory, and CCR5 over-activation by viral proteins may contribute to HIV-associated cognitive deficits. Consistent with this hypothesis, the HIV V3 peptide caused LTP, signaling and memory deficits that were prevented by Ccr5 knockout or knockdown. Overall, our results demonstrate that CCR5 plays an important role in neuroplasticity, learning and memory, and indicate that CCR5 has a role in the cognitive deficits caused by HIV.

Methods for PTEN in Stem Cells and Cancer Stem Cells.

PTEN (phosphatase and tensin homologue) is the first tumor suppressor identified to have phosphatase activity and its gene is the second most frequently deleted or mutated tumor-suppressor gene associated with human cancers. Germline PTEN mutations are the cause of three inherited autosomal dominant disorders. Phosphatidylinositol 3,4,5,-triphosphate (PIP3), the product of the PI3 kinase, is one of the key intracellular targets of PTEN's phosphatase activity, although PTEN's phosphatase-independent activities have also been identified. PTEN is critical for stem cell maintenance, which contributes to its controlled tumorigenesis. PTEN loss leads the development of cancer stem cells (CSCs) that share properties with somatic stem cells, including the capacity for self-renewal and multi-lineage differentiation. Methods to isolate and functionally test stem cells and CSCs are important for understanding PTEN functions and the development of therapeutic approaches to target CSCs without having adverse effects on normal stem cells. Here, we describe protocols for the isolation and functional analysis of PTEN deficient embryonic stem cells, hematopoietic stem cells and leukemia-initiating cells (LICs), neural stem cells, and prostate stem cells and CSCs.

[Synthesis and anti-proliferative activity of fluoroquinolone (rhodanine unsaturated ketone) amide derivatives].

To discover novel antitumor rhodanine unsaturated ketones, a series of fluoroquinolone (rhodanine α, ß-unsaturated ketone) amine derivatives (5a-5r) were designed and synthesized with fluoroquinolone amide scaffold as a carrier. The structures of eighteen title compounds were characterized by elemental analysis, 1H NMR and MS. The in vitro anti-proliferative activity against Hep-3B, Capan-1 and HL60 cells was evaluated by MTT assay. The results showed that the title compounds not only had more significant anti-proliferative activity against three tested cancer cell lines than that of the parent ciprofloxacin 1, but also exhibited the highest activity against Capan-1 cells. The SAR revealed that some compounds carrying aromatic heterocyclic rings or phenyl attached to an electron-withdrawing carboxyl or sulfonamide substituent were comparable to or better than comparison doxorubicin against Capan-1 cells. As such, it suggests that fluoroquinolone (rhodanine α, ß-unsaturated ketone) amines are promising leads for the development of novel antitumor fluoroquinolones or rhodanine analogues.

[Synthesis and anti-proliferative activity of fluoroquinolone C-3 fused heterocyclic α,ß-unsaturated ketones derived from ciprofloxacin].

To discover novel antitumor fluoroquinolone lead compounds from a rational modification for antibacterial fluoroquinolones, a fused heterocyclic ketone corresponding to thiazolo[2,3- b][1,2,4]triazolone used as a bioisosteric replacement of the C-3 carboxylic acid group of ciprofloxacin 1, and further modification by a Claisen condensation reaction with substituted benzaldehydes formed novel fluoroquinolone C-3 fuse heterocyclic α, ß-unsaturated ketones as the title compounds (6a-6r), separately. The structures of eighteen title compounds were characterized by elemental analysis, 1H NMR and MS, and the in vitro anti-proliferative activity against human hepatoma Hep-3B cells, pancreatic Capan-1 cells and leukemia HL60 cells was evaluated by a MTT assay. The preliminary results showed that the title compounds not only had more significant anti-proliferative activity against three tested cancer cell lines than that of the parent ciprofloxacin 1, but also exhibited the highest activity against Capan-1 cells. In particular, compounds carrying an electron-withdrawing carboxyl (6k, 6m) or sulfonamide substituent (6q, 6r) attached to benzene ring were comparable to or better than constractive drug doxorubicin against Capan-1 cells. As such, it suggests that it is favorable for a fused heterocyclic α, ß-unsaturated ketone scaffold instead of the C-3 carboxylic acid group to improve the antitumor activity of fluoroquinolones.

[Synthesis and antitumor activity of fluoroquinolon-3-yl-s-triazole sulfide ketones and their derivatives from ciprofloxacin].

To discover an efficient strategy for the conversion of the antibacterial activity of fluoroquinolones into the antitumor activity, the three series of C-3 s-triazole-based derivatives including sulfide ketones (6a-6g), thiosemicarbazones (7a-7g) and fused heterocyclic thiazolotriazoles (8a-8g) were synthesized from ciprofloxacin (1), respectively. The structures were characterized by elemental analysis and spectral data. The antitumor activity was tested against three tumor cell lines (Hep-3B, Capan-1 and HL60) using the MTT assay. The three types of compounds all exhibited stronger anti-proliferative activities than ciprofloxacin in the test. The order of their activities was in compounds 7>8>6, and the order of selectivity against cancer cell lines was Capan-1, Hep-3B and HL60. Meanwhile, the SAR revealed that some compounds with electron-drawing group substituted such as fluoro- and nitro-phenyl compounds (6f, 7f, 8f) and (6g, 7g, 8g) displayed more significant activity than the control compounds, especially the IC50 values of thiosemicarbazone compounds 7f and 7g against Capan-1 was comparable to doxorubicin. Thus, a five-membered triazole as the C-3 bioisostere modified with the functionalized side-chain of sulfide-ketone thiosemicarbazone warrants special attention and further investigation.

Ubiquitin E3 ligase Nedd4-1 acts as a downstream target of PI3K/PTEN-mTORC1 signaling to promote neurite growth.

Protein ubiquitination is a core regulatory determinant of neural development. Previous studies have indicated that the Nedd4-family E3 ubiquitin ligases Nedd4-1 and Nedd4-2 may ubiquitinate phosphatase and tensin homolog (PTEN) and thereby regulate axonal growth in neurons. Using conditional knockout mice, we show here that Nedd4-1 and Nedd4-2 are indeed required for axonal growth in murine central nervous system neurons. However, in contrast to previously published data, we demonstrate that PTEN is not a substrate of Nedd4-1 and Nedd4-2, and that aberrant PTEN ubiquitination is not involved in the impaired axon growth upon deletion of Nedd4-1 and Nedd4-2. Rather, PTEN limits Nedd4-1 protein levels by modulating the activity of mTORC1, a protein complex that controls protein synthesis and cell growth. Our data demonstrate that Nedd4-family E3 ligases promote axonal growth and branching in the developing mammalian brain, where PTEN is not a relevant substrate. Instead, PTEN controls neurite growth by regulating Nedd4-1 expression.

Concerted activities of distinct H4K20 methyltransferases at DNA double-strand breaks regulate 53BP1 nucleation and NHEJ-directed repair.

Although selective binding of 53BP1 to dimethylated histone H4 lysine 20 (H4K20me2) at DNA double-strand breaks (DSBs) is a necessary and pivotal determinant of nonhomologous end joining (NHEJ)-directed repair, the enzymes that generate H4K20me2 at DSBs were unclear. Here, we determined that the PR-Set7 monomethyltransferase (H4K20me1) regulates de novo H4K20 methylation at DSBs. Rapid recruitment of PR-Set7 to DSBs was dependent on the NHEJ Ku70 protein and necessary for NHEJ-directed repair. PR-Set7 monomethyltransferase activity was required, but insufficient, for H4K20me2 and 53BP1 nucleation at DSBs. We determined that PR-Set7-mediated H4K20me1 facilitates Suv4-20 methyltransferase recruitment and catalysis to generate H4K20me2 necessary for 53BP1 binding. The orchestrated and concerted activities of PR-Set7 and Suv4-20 were required for proficient 53BP1 nucleation and DSB repair. This report identifies PR-Set7 as an essential component of NHEJ and implicates PR-Set7 as a central determinant of NHEJ-directed repair early in mammalian DSB repair pathway choice.

mTOR Inhibition ameliorates cognitive and affective deficits caused by Disc1 knockdown in adult-born dentate granule neurons.

Abnormalities during brain development are thought to cause psychiatric illness and other neurodevelopmental disorders. However, developmental processes such as neurogenesis continue in restricted brain regions of adults, and disruptions of these processes could contribute to the phenotypes of neurodevelopmental disorders. As previously reported, we show that Disc1 knockdown specifically in adult-born dentate gyrus (DG) neurons results in increased mTOR signaling, hyperexcitability, and neuronal structure deficits. Disc1 knockdown also resulted in pronounced cognitive and affective deficits, which could be reversed when the affected DG neurons were inactivated. Importantly, reversing increases in mTOR signaling with an FDA-approved inhibitor both prevented and treated these behavioral deficits, even when associated structural deficits were not reversed. Our findings suggest that a component of the affective and cognitive phenotypes in neurodevelopmental disorders may be caused by disruptions in adult-born neurons. Consequently, treatments directed at this cell population may have a significant impact on these phenotypes.