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Abstract This article proposes an integrated framework for adaptive QoS provision in IEEE 802.16e broadband wireless access networks based on cross-layer design. On one hand, an efficient admission control (AC) algorithm is proposed along with a semi-reservation scheme to guarantee the connection-level QoS. First, to guarantee the service continuity for handoff connections and resource efficiency, our semi-reservation scheme considers both users' handoff probability and average resource consumption together, which effectively avoids resource over-reservation and insufficient reservation. For AC, a new/handoff connection is accepted only when the target cell has enough resource to afford both instantaneous and average resource consumption to meet the average source rate request. On the other hand, a joint resource allocation and packet scheduling scheme is designed to provide packet-level QoS guarantee in term of "QoS rate", which can ensure fairness for the services with identical priority level in case of bandwidth shortage. Particularly, an enhanced bandwidth request scheme is designed to reduce unnecessary BR delay and redundant signaling overhead caused by the existing one in IEEE 802.16e, which further improves the packet-level QoS performance and resource efficiency for uplink transmission. Simulation results show that the proposed approach not only balances the tradeoff among connection blocking rate, connection dropping rate, and connection failure rate, but also achieves low mean packet dropping rate (PDR), small deviation of PDR, and low QoS outage rate. Moreover, high resource efficiency is ensured.

Background and Aims: Lipoprotein lipase (LPL) is responsible for the lipolytic processing of triglyceride-rich lipoproteins, the deficiency of which causes severe hypertriglyceridemia. Liver LPL expression is high in suckling rodents but relatively low at adulthood. However, the regulatory mechanism and functional significance of liver LPL expression are incompletely understood. We have established the zinc finger protein ZBTB20 as a critical factor for hepatic lipogenesis. Here, we evaluated the role of ZBTB20 in regulating liver Lpl gene transcription and plasma triglyceride metabolism., Approach and Results: Hepatocyte-specific inactivation of ZBTB20 in mice led to a remarkable increase in LPL expression at the mRNA and protein levels in adult liver, in which LPL protein was mainly localized onto sinusoidal epithelial cells and Kupffer cells. As a result, the LPL activity in postheparin plasma was substantially increased, and postprandial plasma triglyceride clearance was significantly enhanced, whereas plasma triglyceride levels were decreased. The dysregulated liver LPL expression and low plasma triglyceride levels in ZBTB20-deficient mice were normalized by inactivating hepatic LPL expression. ZBTB20 deficiency protected the mice against high-fat diet-induced hyperlipidemia without causing excessive triglyceride accumulation in the liver. Chromatin immunoprecipitation and gel-shift assay studies revealed that ZBTB20 binds to the LPL promoter in the liver. A luciferase reporter assay revealed that ZBTB20 inhibits the transcriptional activity of LPL promoter. The regulation of LPL expression by ZBTB20 is liver-specific under physiological conditions., Conclusions: Liver ZBTB20 serves as a key regulator of LPL expression and plasma triglyceride metabolism and could be a therapeutic target for hypertriglyceridemia., (© 2021 American Association for the Study of Liver Diseases.)

Background: Coronary microembolization (CME) is a complicated problem that commonly arises in the context of coronary angioplasty. MicroRNAs play crucial roles in cardiovascular diseases. However, the role and mechanism of miR-181a-5p in CME-induced myocardial injury remains unclear., Methods: We established CME rat models. Cardiac function was detected by echocardiography. Haematoxylin-basic fuchsin-picric acid staining was used to measure micro-infarction size. Serum samples and cell culture supernatants were evaluated via enzyme-linked immunosorbent assay. Cellular reactive oxygen species were determined by dichloro-dihydro-fluorescein diacetate assay, and the other oxidative stress related parameters were assayed by spectrophotometry. The dual-luciferase reporter (DLR) assay and RNA pulldown were conducted to validate the association between miR-181a-5p and X-linked inhibitor of apoptosis protein (XIAP). The expression of miR-181a-5p and XIAP mRNA were determined by quantitative reverse transcription polymerase chain reaction. Proteins were evaluated via immunoblotting. The viability of the cell was evaluated via cell counting kit-8 assay., Results: The miR-181a-5p level was significantly increased in CME myocardial tissues. Downregulation of miR-181a-5p improved CME-induced cardiac dysfunction and alleviated myocardial oxidative stress and inflammatory injury, whereas miR-181a-5p exhibited the opposite effects. Then, the DLR assay and RNA pulldown results revealed that miR-181a-5p directly targeting on XIAP. The XIAP level was found to be remarkably decreased after CME. XIAP overexpression attenuated CME-induced myocardial oxidative stress and inflammatory injury. Finally, in vitro rescue experiments revealed that knockdown of XIAP could abolish the protective effects of miR-181a-5p knockdown on hypoxia-induced cardiomyocyte oxidative stress and inflammatory injury., Conclusions: Downregulation of miR-181a-5p alleviates CME-induced myocardial damage by suppressing myocardial oxidative stress and inflammation through directly targeting XIAP., (Copyright and License information: Journal of Geriatric Cardiology 2021.)

Objective: To analyze the genetic and clinical characteristics of MYO15A variants associated non-syndromic autosomal recessive deafness3 (DFNB3). Methods: The hearing test and high-throughput sequencing data of 108 families with non-syndromic hearing loss, who visited the Center of Genetics and Prenatal Diagnosis in the First Affiliated Hospital of Zhengzhou University from November 2016 to February 2019, were retrospectively analyzed to investigate the characteristics of MYO15A variation. Results: Compound heterozygous MYO15A variations were detected in nine patients from eight families, accounting for 7.4% of all 108 families. The variants were c.5910+1G>A/c.9417_9418insTA, c.4234T>G/c.8324G>T, c.3926A>T/c.5002delC, c.9690+1G>A/c.10257_10259delCTT, c.8324G>T/c.10419_10423delCAGCT, c.4519C>T/c.6454G>C, c.6177+1G>T/c.10257_10259delCTT and c.5692C>T/c.7396-1G>A. All patients had severe to profound hearing loss. Among the 14 variations, 12 variations were located in the main structural domains, including 5 in motor domain, 3 in FERM domain, 3 in MyTH4 domain and 1 in IQ motif. The c.3926A>T, c.4234T>G, c.4519C>T, c.5002delC, c.6454G>C, c.8324G>T, c.9417_9418insTA and c.10419_10423delCAGCT had not been reported in the Human Gene Mutation Database up to February 2020. According to the guidelines of the American College of Medical Genetics and Genomics (ACMG), 6 reported variants and the first reported c.4519C>T, c.5002delC, c.9417_9418insTA and c.10419_10423delCAGCT were identified as pathogenic variants, while c.8324G>T was likely pathogenic variant, and c.3926A>T, c.4234T>G and c.6454G>C were variants of uncertain significance. Conclusions: The variations of MYO15A in patients with DFNB3 are mainly complex heterozygous. The clinical phenotypes are mostly severe to profound hearing loss, and the mutation loci are mainly in the motor, FERM and MyTH4 domains.

MiRNAs can be used as promising diagnostic biomarkers of heart failure, while lncRNAs act as competing endogenous RNAs of miRNAs. In this study, we collected peripheral blood monocytes from subjects with or without HF to explore the association between certain lncRNAs, miRNAs and HF. Heart failure patients with preserved or reduced ejection fraction were recruited for investigation. ROC analysis was carried out to evaluate the diagnostic values of certain miRNAs and lncRNAs in HF. Luciferase assays were used to study the regulatory relationship between above miRNAs and lncRNAs. LncRNA overexpression was used to explore the effect of certain miRNAs in H9C2 cells. Expression of miR-30c was significantly decreased in the plasma and peripheral blood monocytes of patients suffering from heart failure, especially in these with reduced ejection fraction. On the contrary, the expression of lncRNA-CASC7 was remarkably increased in the plasma and peripheral blood monocytes of patients suffering from heart failure. Both miR-30c and lncRNA-CASC7 expression showed a promising efficiency as diagnostic biomarkers of heart failure. Luciferase assays indicated that miR-30c played an inhibitory role in lncRNA-CASC7 and IL-11 mRNA expression. Moreover, the overexpression of lncRNA-CASC7 suppressed the expression of miR-30c while evidently increasing the expression of IL-11 mRNA and protein in H9C2 cells. This study clarified the relationship among miR-30c, lncRNA-CASC7 and IL-11 expression and the risk of heart failure and showed that lncRNA-CASC7 is potentially involved in the pathogenesis of HF via modulating the expression of miR-30c., (© 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)

Objective: To detect gene mutation sassociated with deafness in four Waardenburg syndrome (WS) type Ⅱ patients, and to explore the possible mechanism of molecular genetics. Methods: All patients with WS were identified at the genetic and prenatal diagnosis center of the First Affiliated Hospital of Zhengzhou University from August 2015 to December 2018.Clinical materials and peripheral blood were collected from patients and family members. The genes associated with deafness of the patients were tested by next generation sequencing(NGS). And suspected mutations were verified by Sanger sequencing. Results: All patients carried heterozygous mutations in SOX10, they were c.355_356insTCAGGCAGCGC, c.1106_1107insTGGGGCCCCCCACACTA, c.511T>C (p.Y171H), c.91_100del. According to the guidelines for genetic variation of the Amercian College of Medical Genetics and Genomics (ACMG), three frameshift mutations were pathogenic mutations, one missense mutation was likely pathogenic mutation. Conclusion: Application of next generation sequencing technologies make gene diagnosis of Waardenburg syndrome efficiently and accurately.

Myocardial infarction (MI) is a life-threatening cardiac event that results in extreme damage to the heart muscle. The Wnt signaling pathway has been implicated in the development of heart diseases. Hence, the current study aimed to investigate the role of microRNA (miRNA) in association with the Wnt signaling pathway to identify potential candidates for MI therapy. Differentially expressed miRNAs associated with MI occurrence were screened, and miR-494 was selected for subsequent experiments. Sprague-Dawley rats were included to establish a MI model via intraperitoneal injection of 0.1 mg/kg atropine sulfate and 40 mg/kg pentobarbital sodium. Then, the interaction between miR-494 and LRG1 was identified. The effect of miR-494 on expression of the Wnt signaling pathway-related genes, proliferation, migration, and invasion ability of fibroblasts and vascular endothelial cells (VECs) was subsequently evaluated through a series of gain- and loss-of-function experiments. The results revealed that miR-494 was poorly expressed and LRG1 was highly expressed in MI rats. miR-494 targets and downregulates LRG1, which resulted in the inactivation of the Wnt signaling pathway and promoted proliferation, migration, and invasion ability of fibroblasts and VECs. In conclusion, this study provided evidence suggesting that overexpressed miR-494 could potentially promote the proliferation, migration, and invasion of fibroblasts and VECs in MI through the inactivation of the Wnt signaling pathway by binding to LRG1., (Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.)

Background: Long non-coding RNAs (lncRNAs) play a central role in regulating heart diseases. In the present study, we examined the effects of lncRNA taurine up-regulated gene 1 (TUG1) in ischemia/reperfusion (I/R)- or hydrogen peroxide-challenged cardiomyocytes, with specific focus on autophagy-induced cell apoptosis., Methods: The expressions of miR-142-3p and TUG1 in H 2 O 2 -challenged cardiomyocytes and I/R-injured heart tissue were measured by RT-qPCR. Cell death was measured by trypan blue staining assay. Cell apoptosis was determined by Annexin V/PI staining and TUNEL assay. Autophagy was examined by quantifying cells or tissues containing LC3 + autophagic vacuoles by immunofluorescence, or by measuring the expressions of autophagy-related biomarkers by Western blot. The direct interaction between miR-142-3p and TUG1, high mobility group box 1 protein (HMGB1), or Ras-related C3 botulinum toxin substrate 1 (Rac1) was examined using luciferase reporter assay. The significance of miR-142-3p and TUG1 on cell apoptosis or autophagy was examined using both gain-of-function and loss-of-function approaches. The importance of HMGB1 or Rac1 was assessed using siRNA-mediated gene silencing., Results: miR-142-3p was down-regulated, while TUG1 up-regulated in H 2 O 2 -challenged cardiomyocytes in vitro and I/R-injured heart tissues in vivo. Functionally, inhibition of TUG1 and overexpression of miR-142-3p inhibited cell apoptosis and autophagy in cardiomyocytes. The function of TUG1 were achieved by sponging miR-142-3p and releasing the suppression of the putative targets of miR-142-3p, HMGB1 and Rac1. Both HMGB1 and Rac1 essentially mediated cell apoptosis and autophagy induced by TUG1., Conclusions: TUG1, by targeting miR-142-3p and up-regulating HMGB1 and Rac1, plays a central role in stimulating autophagic cell apoptosis in ischemia/hypoxia-challenged cardiomyocytes. Down-regulating TUG1 or up-regulating miR-142-3p may ameliorate myocardial injury and protect against acute myocardial infarction., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Objective: To determine whether serum prealbumin levels are associated with long-term survival after hepatectomy in patients with primary hepatocellular carcinoma(HCC)., Methods: A consecutive sample of 526 patients with HCC who underwent potentially curative hepatectomy from August 2007 to August 2010 was retrospectively analyzed. Patients were classified as having normal or reduced serum prealbumin based on cut-off values of 200 or 182 mg/L., Results: Multivariate analysis identified the preoperative level of serum prealbumin as an independent prognostic factor of long-term survival (P < 0.05): Survival was significantly better for those with normal levels than for those with reduced levels, based on either cut-off value. Similar results were observed in subgroup analyses based on the degree of cirrhosis, level of ɑ-fetoprotein and Barcelona Clinic Liver Cancer stage., Conclusions: Preoperative level of serum prealbumin may be useful for predicting long-term survival in patients with HCC after hepatectomy., (© 2019 Wiley Periodicals, Inc.)

Two new Ag(I) coordination polymers (CPs), namely, Ag(L)(Htp) (1) and [Ag(L)]·(Htp)·2H 2 O (2) were synthesized from the long flexible ligand of 1,6-bis(2-methylbenzimidazolyl)hexane (L), terephthalic acid (H 2 tp) and different silver(I) salts using hydrothermal and sonochemical methods, These CPs were characterized by elemental analysis, IR spectra, scanning electron microscopy, single-crystal and powder X-ray diffraction analysis. 1 features a uninodal 3-connected 2D hcb layered structure, while 2 exhibits an infinite 1D linear chain and ultimately extended into 3D supramolecular framework via O-H⋯O and Ag⋯O interactions. In addition, the effect of various sonication concentrations of the initial reagents, ultrasonic time and power of ultrasound irradiation on the size and morphology of nanostructured 1 and 2 were evaluated. Nano-sized 1 and 2 exhibit relatively high performance as UV light driven photocatalysts for the degradation of methylene blue., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Objective: To analyze the mutations of PAX3 gene in two Waardenburg syndrome type Ⅰ (WS1) pedigrees and make prenatal diagnosis for the high-risk 18-week-old fetus. Methods: PAX3 gene was first analyzed by Sanger sequencing and multiplex ligation-dependent probe amplification(MLPA) for detecting pathogenic mutation of the probands of the two pedigrees. The mutations were confirmed by MLPA and Sanger in parents and unrelated healthy individuals.Prenatal genetic diagnosis for the high-risk fetus was performed by amniotic fluid cell after genotyping. Results: A heterozygous PAX3 gene gross deletion (E7 deletion) was identified in all patients from WS1-01 family, and not found in 20 healthy individuals.Prenatal diagnosis in WS1-01 family indicated that the fetus was normal. Molecular studies identified a novel deletion mutation c. 1385&#95;1386delCT within the PAX3 gene in all affected WS1-02 family members, but in none of the unaffected relatives and 200 healthy individuals. Conclusions: PAX3 gene mutation is etiological for two WS1 families. Sanger sequencing plus MLPA is effective and accurate for making gene diagnosis and prenatal diagnosis.

Objective: To explore the impact and mechanism of electro-acupuncture (EA) on olfactory ensheathing cells (OECs) transplantation of spinal cord injury (SCI) axonal regeneration., Methods: In the experiment, 72 adult Sprague Dawley male rats weighted (220±20) g underwent contusion and transection method to cause the T9 model of spinal cord injury, were randomly divided into four groups involving model group, EA group,OECs group,and EA+OECs group. 5% fluorescein gold (FG) solution of 0.5 µl was injected into rats' spinal cord at 4 weeks and 8 weeks after SCI, a series of tests were performed including fluorescein gold(FG) retrograde tagging, BBB scores., Results: (1)The BBB scores level among four groups had no differences from the 1st day to the 1st week after the SCI (P>0.05). From the 3rd week after the SCI, the BBB scores level in EA+ OECs group were obviously higher than that of other groups (P<0.05). (2)The result of the fluorescein gold (FG) retrograde tagging showed at 4 weeks and 8 weeks after treatment FG positive nerve fibers were observed in SCI region. In EA+OECs group the number of FG positive nerve fibers was more than other three groups, and the fibers were more regularly arranged than other three groups., Conclusion: The combination of electro-acupuncture and OECs transplantation can recover the pathway of nerve conduction and promote nerve fibers regeneration and hind limb function recovery for SCI rat, and can guide the trend of the axonal regeneration.

Cholesteatoma is a destructive and abnormal skin growth consisting of keratinizing squamous epithelium in the middle ear. Its molecular mechanisms remain poorly understood. Here, we found that the NF-κB inflammatory signaling pathway was highly activated in cholesteatoma. NF-κB activation increased the expression of microRNA-802 (miR-802) and chromatin immunoprecipitation assays showed that P65 could uniquely bind to miR-802 promoter. miR-802 overexpression promoted keratinocyte cell proliferation and cell cycle progression, while inhibition of miR-802 decreased these effects. From computational analysis and luciferase report assays, miR-802 directly repressed PTEN expression by targeting its 3'-UTR. Our results demonstrate that the NF-κb/miR-802/PTEN signaling pathway plays an important role in the development of cholesteatoma.

Tussilagone (TSL) and its allied sesquiterpenoids were considered as the main active principles of the flower buds of Tussilago farfara, which has been widely used in China as an antitussive herbal medicine. Six new bisabolane-type sesquiterpenoids, tussfararins A-F (1-6), along with 12 known sesquiterpenoids, were isolated from the flower buds of T. farfara. Structures of the new compounds were elucidated by extensive spectroscopic analysis. The biological analysis showed that compounds 1, 3, 6, and 7 inhibited nitric oxide (NO) production in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells with IC50 values of 13.6-24.4 µM., (Georg Thieme Verlag KG Stuttgart · New York.)

The pyridyl-lead complexes [Pb(m)-C5H4N](-) (m = 1-4), which are produced from the reactions between lead clusters formed by laser ablation and the pyridine molecules seeded in argon carrier gas, are studied by photoelectron (PE) spectra and density functional theory. The adiabatic electron affinity (EA) of [Pb(m)C5H4N](-) is obtained from PE spectra at photon energies of 308 and 193 nm. Theoretical calculation is carried out to elucidate their structures and bonding modes. A variety of geometries for the isomers are optimized to search for the lowest-energy geometry. By comparing the theoretical results, including the EA and simulated density of state spectra, with the experimental determination, the lowest-energy structures for each species are obtained. The following analysis of the molecular orbital composition provides the evidence that the pyridyl binds on lead clusters through the Pb-C sigma bond. Moreover, there is an apparent spin-state transition from triplet state toward singlet state for the ground-state structure of [Pb(m)C5H4N](-) with an increase of lead cluster.

Objective: To investigate the plasticity and the role of plasticity in the auditory cortex of rats which experienced tinnitus by screening the plasticity markers immediately early gene c-fos and the NMDA receptor's subtype NR2A., Methods: Thirty white Wistar rats were randomly distributed into 3 groups: sodium salicylate group (n = 12), physiological saline group (n = 12) and normal control group (n = 6). Tinnitus were induced by salicylate administration and tested by behavioral conditioning studies, and then immunohistochemical staining was used to observe the expression of c-fos and NR2A in the auditory cortex of each group., Results: Behavioral evidence indicated that all of the twelve rats in the sodium salicylate group perceived tinnitus. Fos-positive neurons were observed in all rats, while they appeared as typical dark dots, corresponding to a labeling restricted to their nucleus. NR2A protein was mainly expressed in the cytoplast and membrane of the cortical pyramidal cells. The expression of c-fos and NR2A immunoreactive neurons in auditory cortexes of the sodium salicylate group was significantly higher than that of other two control groups., Conclusions: The higher expression of c-fos and NR2A indicate that the neurotransmitters and receptors should be involved in the tinnitus, as well as suggest that neuronal plasticity occurs in the auditory cortex of rats experienced tinnitus, which may be played an important role in the mechanism of tinnitus.