Second cistron in CACNA1A gene encodes a transcription factor mediating cerebellar development and SCA6.

The CACNA1A gene, encoding the voltage-gated calcium channel subunit α1A, is involved in pre- and postsynaptic Ca(2+) signaling, gene expression, and several genetic neurological disorders. We found that CACNA1A coordinates gene expression using a bicistronic mRNA bearing a cryptic internal ribosomal entry site (IRES). The first cistron encodes the well-characterized α1A subunit. The second expresses a transcription factor, α1ACT, which coordinates expression of a program of genes involved in neural and Purkinje cell development. α1ACT also contains the polyglutamine (polyQ) tract that, when expanded, causes spinocerebellar ataxia type 6 (SCA6). When expressed as an independent polypeptide, α1ACT-bearing an expanded polyQ tract-lacks transcription factor function and neurite outgrowth properties, causes cell death in culture, and leads to ataxia and cerebellar atrophy in transgenic mice. Suppression of CACNA1A IRES function in SCA6 may be a potential therapeutic strategy.

Local Confinement Effects of Block Copolymers Driving Self-Assembly of Nanoparticles into Discrete Pancake-Shaped Superlattices.

The utilization of polymer conformations to construct a variety of superlattices is a common method within the field. However, this technique often results in only long-range ordering rather than the formation of distinct superlattices. In this study, a well-organized array of discrete pancake-shaped superlattices (DPSs) is successfully obtained through the utilization of air-liquid interface self-assembly, facilitated by the confined environment created by a block copolymer. It is crucial to note that both the self-assembly behavior and resulting morphologies of the DPSs can be precisely tuned by adjusting several experimental parameters, most notably the concentration and molecular architecture of the block copolymers. Furthermore, this work provides valuable insights into the formation processes and mechanisms underpinning the DPSs. The approach described here is both straightforward and efficacious, establishing a strong foundation for subsequent research and the development of non-close-packed superlattice structures.

A High-Relative-Bandwidth Doherty Power Amplifier with Modified Load Modulation Network for Wireless Communications.

This paper presents a novel load modulation network to realize a broadband Doherty power amplifier (DPA). The proposed load modulation network consists of two generalized transmission lines and a modified coupler. A comprehensive theoretical analysis is carried out to explain the operation principles of the proposed DPA. The analysis of the normalized frequency bandwidth characteristic shows that a theoretical relative bandwidth of approximately 86% can be obtained across a normalized frequency range of 0.4-1.0. The complete design process that allows the design of the large-relative-bandwidth DPA based on derived parameter solutions is presented. A broadband DPA operating between 1.0 GHz and 2.5 GHz was fabricated for validation. Measurements demonstrate that the DPA can deliver an output power of 43.9-44.5 dBm with a drain efficiency of 63.7-71.6% in the 1.0-2.5 GHz frequency band at the saturation level. Moreover, a drain efficiency of 45.2-53.7% can be obtained at the 6 dB power back-off level.

Transcriptomic analysis reveals the regulatory mechanism underlying the indirubin-mediated amelioration of dextran sulfate sodium-induced colitis in mice.

CONTEXT: Aryl hydrocarbon receptor (AhR) agonists are potential therapeutic agents for ulcerative colitis (UC). Indirubin (IDR), which is a natural AhR ligand approved for leukemia treatment, ameliorates dextran sulfate sodium (DSS)-induced colitis in mice. However, the therapeutic mechanisms of IDR are unknown, limiting its application. OBJECTIVE: This study explores the therapeutic mechanisms of IDR in DSS-induced colitis using transcriptomic analysis. MATERIALS AND METHODS: Male BALB/c mice were categorized to six groups: normal, DSS model (2% DSS), IDR treatment (10, 20 and 40 mg/kg), and sulfasalazine (520 mg/kg) groups. The drugs were intragastrically administered for 7 consecutive days. The disease activity index (DAI) was recorded. After euthanasia, the colon length was measured, and histopathological examination, immunohistochemistry staining using F4/80, and colonic transcriptomic analysis were conducted. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blotting (WB) were conducted to verify our findings. RESULTS: Compared with DSS, IDR treatment decreased the DAI score by 64.9% and increased colon length by 26.2%. Moreover, it alleviated mucosal injury and reduced macrophage infiltration. Transcriptomic analysis identified several downregulated genes (Igkvs and Nlrp3), as well as Nlrp3/Il1ß and hemoglobin gene networks, after IDR treatment. The abundances of NF-κB p65, NLRP3, IL-1ß, and HBA decreased by 69.1, 59.4, 81.1, and 83.0% respectively, after IDR treatment. DISCUSSION AND CONCLUSION: Apart from the well-documented NF-κB signalling pathway, IL-17A, and NLRP3-IL-1ß, the suppression of haemoglobin-induced lipid peroxidation could be a previously unknown mechanism of IDR. Our study can help improve its application for UC treatment.

PDMS with Tunable Side Group Mobility and Its Highly Permeable Membrane for Removal of Aromatic Compounds.

Polydimethylsiloxane (PDMS), as the benchmark of organophilic membrane materials, still faces challenges for removal of aromatic compounds due to the undesirable transport channels. In this work, we propose to reconstruct the PDMS conformation with tunable side group mobility by introducing phenyl as rigid molecular spacer to relieve steric hindrance of large-sized aromatic molecules; meanwhile, polymer segments are loosely stacked to provide additional degrees of freedom as increasing the permeant size. Moreover, the reconstructed PDMS is engineered into the composite membrane with prevention of condensation of aromatic compounds in the substrate pores. The resulting thin-film composite membrane achieved one order of magnitude higher flux (11.8 kg m-2 h-1 ) with an equivalent separation factor (12.3) compared with the state-of-the-art membranes for aromatic removal. The permeant-customized membrane molecular and microstructure designing strategy opens a new avenue to develop membranes for specific separation targets.

Arabidopsis SMAX1 overaccumulation suppresses rosette shoot branching and promotes leaf and petiole elongation.

ARABIDOPSIS: SMAX1/SMXL (SUPPRESSOR OF MAX2 1/SMAX1-LIKE) proteins function as transcriptional repressors in karrikin and strigolactone (SL) signaling pathways and regulate plant architecture. MAX2 is a common factor in the two signaling pathways and a component of the SCF complex that modulates the proteasome-mediated degradation of SMAX1/SMXLs. SMXL6, 7, and 8 proteins promote shoot branching and inhibit petiole elongation. Our study found that the accumulation of SMAX1 suppresses rosette shoot branching and increases cauline branches on the primary inflorescence stem, plant height, petiole length, and leaf length/width ratio. The SMAX1 accumulation enhances the expression of BRC1, HB53, HB40, and HB21 that modulate shoot branching. SMAX1 also regulates the expression of the genes involved in auxin transport, cytokinin signaling pathway, and SL biosynthesis. The expression analyses of these genes suggest that excessive SMAX1 should accelerate the transport of auxin and the biosynthesis of SL in plants. High SL concentration suppresses the bud development in smax1D mutant that accumulates SMAX1 protein in plant. However, the effects of cytokinin and auxin on shoot branching remain elusive in the mutant with excessive SMAX1. SMAX1 regulates leaf shape and petiole length via modulating TCP1 expression. Our findings reveal a novel function of SMAX1 and new mechanism of shoot branching.

A nanobody-horseradish peroxidase fusion protein-based competitive ELISA for rapid detection of antibodies against porcine circovirus type 2.

BACKGROUND: The widespread popularity of porcine circovirus type 2(PCV2) has seriously affected the healthy development of the pig industry and caused huge economic losses worldwide. A rapid and reliable method is required for epidemiological investigation and evaluating the effect of immunization. However, the current methods for PCV2 antibody detection are time-consuming or very expensive and rarely meet the requirements for clinical application. we have constructed the platform for expressing the nanobody(Nb)­horseradish peroxidase(HRP) fusion protein as an ultrasensitive probe to detect antibodies against the Newcastle disease virus(NDV), previously. In the present work, an Nb-HRP fusion protein-based competitive ELISA(cELISA) for rapid and simple detection antibodies against PCV2 was developed using this platform to detect anti-PCV2 antibodies in clinical porcine serum. RESULTS: Using phage display technology, 19 anti-PCV2-Cap protein nanobodies were screened from a PCV2-Cap protein immunized Bactrian camel. With the platform, the PCV2-Nb15­HRP fusion protein was then produced and used as a sensitive reagent for developing a cELISA to detect anti­PCV2 antibodies. The cut­off value of the cELISA is 20.72 %. Three hundreds and sixty porcine serum samples were tested by both newly developed cELISA and commercial kits. The sensitivity and specificity were 99.68 % and 95.92 %, respectively. The coincidence rate of the two methods was 99.17 %. When detecting 620 clinical porcine serum samples, a good consistent (kappa value = 0.954) was found between the results of the cELISA and those of commercial kits. CONCLUSIONS: In brief, the newly developed cELISA based PCV2-Nb15­HRP fusion protein is a rapid, low-cost, reliable and useful nanobody-based tool for the serological evaluation of current PCV2 vaccine efficacy and the indirect diagnosis of PCV2 infection.

Selective inhibition of caspases in skeletal muscle reverses the apoptotic synaptic degeneration in slow-channel myasthenic syndrome.

Slow-channel syndrome (SCS) is a congenital myasthenic disorder caused by point mutations in subunits of skeletal muscle acetylcholine receptor leading to Ca(2+) overload and degeneration of the postsynaptic membrane, nuclei and mitochondria of the neuromuscular junction (NMJ). In both SCS muscle biopsies and transgenic mouse models for SCS (mSCS), the endplate regions are shrunken, and there is evidence of DNA damage in the subsynaptic region. Activated caspase-9, -3 and -7 are intensely co-localized at the NMJ, and the Ca(2+)-activated protease, calpain, and the atypical cyclin-dependent kinase (Cdk5) are overactivated in mSCS. Thus, the true mediator(s) of the disease process is not clear. Here, we demonstrate that selective inhibition of effector caspases, caspase-3 and -7, or initiator caspase, caspase-9, in limb muscle in vivo by localized expression of recombinant inhibitor proteins dramatically decreases subsynaptic DNA damage, increases endplate area and improves ultrastructural abnormalities in SCS transgenic mice. Calpain and Cdk5 are not affected by this treatment. On the other hand, inhibition of Cdk5 by expression of a dominant-negative form of Cdk5 has no effect on the degeneration. Together with previous studies, these results indicate that focal activation of caspase activity at the NMJ is the principal pathological process responsible for the synaptic apoptosis in SCS. Thus, treatments that reduce muscle caspase activity are likely to be of benefit for SCS patients.

SIRT1 expression is refractory to hypoxia and inflammatory cytokines in nucleus pulposus cells: Novel regulation by HIF-1α and NF-κB signaling.

Hypoxia and a marked increase in inflammatory cytokines are common hallmarks of intervertebral disc degeneration; these events disrupt the normal balance between extracellular matrix (ECM) degradation and synthesis in degenerative intervertebral discs. SIRT1, one of the NAD+-dependent class III histone deacetylases, controls cellular processes and is regulated by hypoxia and inflammatory cytokines in a cell-type-dependent manner. SIRT1 protects degenerative human nucleus pulposus cells against apoptosis. However, the role of SIRT1 in inflammation in intervertebral discs is still unclear. The current study showed that in rat NP cells, as in other cells, SIRT1 suppressed the induction of the mRNA expression of proteases that degrade ECM induced by TNF-α. Moreover, real-time PCR, transfection, and loss- and gain-of-function experiments revealed that SIRT1 mRNA and protein expression were refractory to hypoxia and HIF-1α. Additionally, SIRT1 mRNA and protein expression and the activity of the SIRT1 promoter were not affected by inflammatory cytokines but were sustained by NF-κB signaling in the presence or absence of TNF-α. In summary, the present study suggested that SIRT1 is not affected by hypoxia and inflammatory cytokines in rat intervertebral discs. Moreover, not HIF-1α but NF-κB signaling is critical for the maintenance of SIRT1 expression in NP cells under physiologic and pathophysiologic conditions.

Impact of polymorphisms of the DNA repair gene XRCC1 and their role in the risk of prostate cancer.

OBJECTIVE: We conducted a case-control study to examine the role of XRCC1 codons 194 (Arg>Trp), 280 (Arg>His) and 399 (Arg>Gln) polymorphisms in the risk of prostate cancer. METHODS: This study included 572 consecutive primary prostate cancer patients and 572 controls between January 2011 and January 2014. The polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was performed to detect XRCC1 codons 194 (Arg>Trp), 280 (Arg>His) and 399 (Arg>Gln) polymorphisms. RESULTS: Compared with the control subjects, the prostate cancer cases had a habit of cigarette smoking (χ(2)=18.13, P<0.001) and a family history of cancer (χ(2)=25.23, P<0.001). Conditional logistic regression analysis showed that the subjects carrying Trp/Trp genotype were more likely to greatly increase the prostate cancer when compared with Arg/Arg genotype, and the adjusted OR was 2.04(1.24-3.41). We did not find significant association between XRCC1 194 (Arg>Trp) polymorphism and clinical stage and Gleason score of prostate cancer (P>0.05). CONCLUSION: Our results show an increased risk for prostate cancer in individuals with XRCC1 194 (Arg>Trp) polymorphism, and a significant interaction between XRCC1 194 (Arg>Trp) polymorphism and tobacco smoking, alcohol drinking and family history of cancer.

Skeletal muscle calpain acts through nitric oxide and neural miRNAs to regulate acetylcholine release in motor nerve terminals.

Cholinergic overactivity in diseases of neuromuscular transmission elicits a retrograde signal resembling homeostatic synaptic plasticity that downregulates transmitter release. Understanding this compensatory pathway could provide insights into novel therapeutic avenues and molecular mechanisms underlying learning and memory. Here we identify nitric oxide as a possible source of this signal in pathological human and mouse muscle samples and link this signaling pathway to changes in synaptic function in the neuromuscular junction. We further show that neuronal nitric oxide synthase is regulated by cholinergic excess through activation of skeletal muscle calpain and its effect on Cdk5 and CaMKII, leading to direct modulation of presynaptic function. Finally, we show that this signaling pathway acts through specific miRNA control of presynaptic vesicle protein expression. The control of presynaptic miRNA levels by postsynaptic activity represents a novel mechanism for the modulation of synaptic activity in normal or pathological conditions.

A conserved eEF2 coding variant in SCA26 leads to loss of translational fidelity and increased susceptibility to proteostatic insult.

The autosomal dominant spinocerebellar ataxias (SCAs) are a genetically heterogeneous group of disorders exhibiting cerebellar atrophy and Purkinje cell degeneration whose subtypes arise from 31 distinct genetic loci. Our group previously published the locus for SCA26 on chromosome 19p13.3. In this study, we performed targeted deep sequencing of the critical interval in order to identify candidate causative variants in individuals from the SCA26 family. We identified a single variant that co-segregates with the disease phenotype that produces a single amino acid substitution in eukaryotic elongation factor 2. This substitution, P596H, sits in a domain critical for maintaining reading frame during translation. The yeast equivalent, P580H EF2, demonstrated impaired translocation, detected as an increased rate of -1 programmed ribosomal frameshift read-through in a dual-luciferase assay for observing translational recoding. This substitution also results in a greater susceptibility to proteostatic disruption, as evidenced by a more robust activation of a reporter gene driven by unfolded protein response activation upon challenge with dithiothreitol or heat shock in our yeast model system. Our results present a compelling candidate mutation and mechanism for the pathogenesis of SCA26 and further support the role of proteostatic disruption in neurodegenerative diseases.

[Inhibitory effect of inositol hexaphosphate on proliferation of LNCaP cells and its relation to IGFBP 3 expression].

OBJECTIVE: To investigate the effect of inositol hexaphosphate (IP6) on proliferation of human prostate carcinoma LNCaP cells and its relation to insulin-like growth factors binding protein-3 (IGFBP-3) expression. METHODS: The siRNA technology was used to silence the IGFBP-3 gene in LNCaP cells. LNCaP cells and IGFBP-3 gene silenced LNCaP cells were exposed to IP6 for 24 h. Cell viability was measured by MTT assay; cell cycle arrest and cell apoptosis were detected by flow cytometry. The expression levels of IGFBP-3 and Bcl-2 mRNA and protein were analyzed by real-time quantitative RT-PCR and Western blotting, respectively. RESULTS: The proliferation of LNCaP cells was be inhibited by IP6 in a dose dependent manner. After exposure to IP6 for 24 h, the cell viability in LNCaP cells and siRNA-treated LNCaP cells was 53.2%±11.6% and 82.3%±10.9%, respectively (P<0.05). After treatment of 1.5 mmol IP6，the apoptosis rate of LNCAP cells and siRNA-treated LNCAP cells was 40.48%±13.21% and 30.43%±10.65%, respectively (P<0.05). The proportion of G1 and G2 phase in LNCAP cells was 70.58%±8.25% and 5.64%±1.23%，after IP6 treatment the percentage of G1 phase cells decreased to 48.66%±11.23% and G2 phase cells increased to 31.11%±9.68%. However, for siRNA treated LNCAP cells, the proportion of G1 phase cells was 58.25%±12.36% and G2 phase cells was 23.85%±12.45%. Higher expression of IGFBP-3 and lower expression of Bcl-2 in LNCaP cells treated with IP6 were found at both mRNA and protein levels. IP6 treatment enhanced IGFBP-3 mRNA expression by 2.21±0.15 folds. In the contrast, expression of Bcl-2 mRNA decreased by 0.69±0.03 folds. Meanwhile, after IGFBP- gene silence Bcl-2 expression was not decreased. CONCLUSION: IP6 can inhibit the proliferation of LNCaP cells, which may be associated with the changes of IGFBP-3 level through Bcl-2 expression.

IMoVR-Net: A robust interpretable network for multi-ocular lesion recognition from TAO facial images.

Thyroid-associated ophthalmopathy (TAO) is an organ-specific autoimmune disease that seriously affects patient's life and health. However, the early diagnosis of TAO is highly dependent on the physician's subjective experience. Moreover, the currently proposed deep learning networks for eye diseases do not provide robust interpretability concerning feature learning paradigm, model structure, and the number of neurons. But the mentioned components are very important for model interpretability and are key factors that severely affect the transparency of the model. Therefore, a robust interpretable multi-orientation visual recognition network (IMoVR-Net) for TAO multi-ocular lesion recognition is proposed in this paper. Firstly, a multi-orientation visual cascaded encoder composed of the DenseGabor module and the dilated Gabor convolution group is proposed to achieve the fine extraction of multi-directional TAO lesion features by using a novel feature learning paradigm called alternating filtering. Besides, combining information theory and topology tool, an optimization rule based on topological energy entropy is proposed to provide a solid interpretable theory for determining the model structure. Finally, a clustering correlation analysis method is developed to accomplish the determination of the number of convolutional hidden neurons, providing robust interpretability for the selection of the number of neurons. Compared to other advanced models, the IMoVR-Net achieved state-of-the-art performance on different TAO ocular datasets with an average accuracy, sensitivity, precision, and F1 score of 0.878, 87.27 %, 0.875, and 87.39 %, respectively. The IMoVR-Net has good clinical application prospects due to its strong recognition ability and robust interpretability in feature extraction paradigm, model structure, and number of convolutional neurons.

Medical errors, affected sites, and adverse consequences among patients in the orthopaedic department: Does age matter?

Background: Orthopaedics have become the focus of research on patient safety due to the high incidence of medical errors. Previous studies were based on all orthopaedic patients and rarely conducted empirical analyses from the perspective of age. This study aimed to fill the academic gap in the age variable by comparing medical errors, affected sites, and adverse consequences in orthopaedic patients. Methods: This retrospective study included 329 litigation claims against orthopaedists using data from China Judgments Online. First, we performed computer crawling and screened 5,237 litigation documents using keywords, including medical errors. Second, 2,536 samples were retained through systematic random sampling, and 549 irrelevant cases were deleted after manual reading. Finally, three clinicians from different medical departments selected 329 incidents related to orthopaedics for further analysis, according to the description of the lawsuits. Three other professional orthopaedists evaluated the patients' ages, affected sites of medical errors, and adverse consequences. Results: The greatest number of medical errors was observed in the joints (30.43%) for all orthopaedic patients. However, adult patients (aged 18-60 years) were most susceptible to errors in the extremities (30.42%). A higher rate of complications was associated with a higher rate of morbidity/mortality for the corresponding patients. Medical errors correlated with complications occurred in the following sites: joints (15.38%), extremities (12.50%), spine (16.95%), multiple sites (15.38%), and hands and feet (14.81%). In addition to surgical errors, over 10% of all orthopaedic patients experienced missed diagnoses. The incidence of insufficient adherence to informed consent obligations was 13.5% among adult patients and was much higher in paediatric and older adults patients. When orthopaedic patients suffered from medical technical errors, iatrogenic mortality/morbidity would decrease by 0.3% for one unit increase in age. Conclusion: Dividing patients into different ages demonstrated diverse results in terms of medical errors and affected sites. Negligence in diagnosis and examination can be fatal factors that endanger safety, and complications may cause morbidity/mortality. When patients suffered from technical errors, age is inversely proportional to mortality/morbidity. Special attention needs to be paid to technical errors in the younger older adults population (60-64 years old), which has inspired implications in promoting aging and public health.

Effect of dexmedetomidine on postoperative nausea and vomiting in female patients undergoing radical thoracoscopic lung cancer resection.

Introduction: Postoperative nausea and vomiting (PONV) is a prevalent postsurgical complication. The objective of our study was to compare the effect of different doses of dexmedetomidine on PONV in female patients undergoing radical thoracoscopic lung cancer resection. Methods: A total of 164 female patients undergoing elective thoracoscopic radical lung cancer surgery were enrolled and assigned to one of four groups. Patients received 0.2 µg/kg/h, 0.4 µg/kg/h, 0.8 µg/kg/h dexmedetomidine and normal saline in the Dex1, Dex2, Dex3 and Control groups, respectively. The primary outcome was the incidence of PONV during 48 h postoperatively. The second outcomes included the incidence of PONV and postoperative vomiting (POV) at four time points postoperatively (T1: PACU retention period; T2: PACU discharge to postoperative 12 h; T3: postoperative 12 h-postoperative 24 h; T4: postoperative 24 h-postoperative 48 h), the area under the curve of PONV grade (PONVAUC), PONV grade, POV grade and other postoperative recovery indicators. Results: The incidence of PONV differed among the four groups. The Dex2 group (29.27%) was lower than that in the Dex1 group (61.90%) and Control group (72.50%). The incidence of PONV at T2 in the Dex1 group (11.90%) and Dex2 group (9.76%) was lower than that in the Control group (42.50%). The incidence of PONV at T3 in the Dex2 group (29.27%) was lower than that in the Dex1 group (61.90%) and Control group (62.50%). The PONVAUC was lower in the Dex2 group than in the Control group. The incidence of POV at T3 in the Dex2 and Dex3 groups was lower than that in the Control group. The consumption of remifentanil, norepinephrine, PACU dwell time, VAS scores, postoperative PCA press frequency, and the time for the first postoperative oral intake were different among the four groups. The regression model shows that the Dex2 group is a protective factor for PONV. Conclusion: Dexmedetomidine can reduce the incidence of PONV and accelerate postoperative recovery in female patients undergoing radical thoracoscopic lung cancer resection. Compared with the other two dosages, 0.4 µg/kg/h dexmedetomidine is preferable. Clinical Trial Registration: chictr.org.cn, identifier ChiCTR2300071831.

Effect of preoperative natural killer cell on postoperative pulmonary complications in patients of lung cancer - A single-center retrospective cohort study.

BACKGROUND: The effect of preoperative natural killer (NK) cell abnormalities on postoperative pulmonary complications (PPCs) after thoracoscopic radical resection of lung cancer is still unclear. The main purpose of this study was to investigate the relationship between the preoperative NK cell ratio and PPCs. METHODS: The patients who underwent thoracoscopic radical resection for lung cancer were divided into a normal group and an abnormal group according to whether the proportion of preoperative NK cells was within the reference range. The main outcome was the incidence of PPCs during postoperative hospitalization. The demographic and perioperative data were collected. Propensity score matching was used to exclude systematic bias. Univariate logistic regression was used to test the relationship between the preoperative NK cell ratio and the incidence of PPCs. The restrictive cubic spline curve was used to analyze the dose-effect relationship between the preoperative NK cell ratio and the incidence of PPCs. RESULTS: A total of 4161 patients were included. After establishing a matching cohort, 910 patients were included in the statistical analysis. The incidence of PPCs in the abnormal group was greater than that in the normal group (55.2% vs. 31.6%). The incidence of PPCs first decreased and then increased with increasing NK cell ratio. The proportion of patients with Grade 3 or higher PPCs in the normal group was lower than that in the abnormal group [108 (23.7%) vs. 223 (49%)]. The indwelling time of the thoracic drainage tube in the abnormal group was longer than that in the normal group [3 (3, 4) vs. 3 (3, 5)]. A preoperative abnormal NK cell ratio constituted a risk factor for PPCs in each subgroup. CONCLUSION: Lung cancer patients with an abnormal proportion of peripheral blood NK cells before surgery were more likely to develop PPCs, their disease degree was more severe, and they had a prolonged duration of chest tube indwelling. Compared with those with abnormally high NK cell ratios, those with abnormally low NK cell ratios had more pronounced PPCs.

Efficient conversion of cane molasses into Tremella fuciformis polysaccharides with enhanced bioactivity through repeated batch culture.

Tremella fuciformis polysaccharide (TFPS) is a natural mushroom mucopolysaccharide widely used in health foods, medical care, cosmetic and surgical materials. In this study, we developed an efficient strategy for the repeated batch production of highly bioactive TFPS from the agro-industrial residue cane molasses. Cane molasses contained 39.92 % sucrose (w/w), 6.36 % fructose and 3.53 % glucose, all of which could be utilized by T. fuciformis spores, whereas, the TFPS production efficiency only reached 0.74 g/L/d. Corn cobs proved to be the best immobilized carrier that could tightly absorb spores and significantly shorten the fermentation lag period. The average yield of TFPS in eight repeated batch culture was 5.52 g/L with a production efficiency of 2.04 g/L/d. The average fermentation cycle after optimization was reduced by 61.61 % compared with the initial conditions. Compared to glucose as a carbon source, cane molasses significantly increased the proportion of low-molecular-weight TFPS (TFPS-2) in total polysaccharides from 3.54 % to 17.25 % (w/w). Moreover, TFPS-2 exhibited potent antioxidant capacity against four free radicals (O2-, ABTS+, OH, and DPPH). In conclusion, this study lays the foundation for the efficient conversion of cane molasses and production of TFPS with high bioactivity.

Nanocomposites of Conducting Polymers and 2D Materials for Flexible Supercapacitors.

Flexible supercapacitors (FSCs) with high electrochemical and mechanical performance are inevitably necessary for the fabrication of integrated wearable systems. Conducting polymers with intrinsic conductivity and flexibility are ideal active materials for FSCs. However, they suffer from poor cycling stability due to huge volume variations during operation cycles. Two-dimensional (2D) materials play a critical role in FSCs, but restacking and aggregation limit their practical application. Nanocomposites of conducting polymers and 2D materials can mitigate the above-mentioned drawbacks. This review presents the recent progress of those nanocomposites for FSCs. It aims to provide insights into the assembling strategies of the macroscopic structures of those nanocomposites, such as 1D fibers, 2D films, and 3D aerogels/hydrogels, as well as the fabrication methods to convert these macroscopic structures to FSCs with different device configurations. The practical applications of FSCs based on those nanocomposites in integrated self-powered sensing systems and future perspectives are also discussed.