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Abstract Background Obesity is well-established as a significant contributor to the development of insulin resistance (IR) and diabetes, partially due to elevated plasma saturated free fatty acids like palmitic acid (PA). Grb10-interacting GYF Protein 2 (GIGYF2), an RNA-binding protein, is widely expressed in various tissues including the liver, and has been implicated in diabetes-induced cognitive impairment. Whereas, its role in obesity-related IR remains uninvestigated. Methods In this study, we employed palmitic acid (PA) exposure to establish an in vitro IR model in the human liver cancer cell line HepG2 with high-dose chronic PA treatment. The cells were stained with fluorescent dye 2-NBDG to evaluate cell glucose uptake. The mRNA expression levels of genes were determined by real-time qRT-PCR (RT-qPCR). Western blotting was employed to examine the protein expression levels. The RNA immunoprecipitation (RIP) was used to investigate the binding between protein and mRNA. Lentivirus-mediated gene knockdown and overexpression were employed for gene manipulation. In mice, an IR model induced by a high-fat diet (HFD) was established to validate the role and action mechanisms of GIGYF2 in the modulation of HFD-induced IR in vivo. Results In hepatocytes, high levels of PA exposure strongly trigger the occurrence of hepatic IR evidenced by reduced glucose uptake and elevated extracellular glucose content, which is remarkably accompanied by up-regulation of GIGYF2. Silencing GIGYF2 ameliorated PA-induced IR and enhanced glucose uptake. Conversely, GIGYF2 overexpression promoted IR, PTEN upregulation, and AKT inactivation. Additionally, PA-induced hepatic IR caused a notable increase in STAU1, which was prevented by depleting GIGYF2. Notably, silencing STAU1 prevented GIGYF2-induced PTEN upregulation, PI3K/AKT pathway inactivation, and IR. STAU1 was found to stabilize PTEN mRNA by binding to its 3’UTR. In liver cells, tocopherol treatment inhibits GIGYF2 expression and mitigates PA-induced IR. In the in vivo mice model, GIGYF2 knockdown and tocopherol administration alleviate high-fat diet (HFD)-induced glucose intolerance and IR, along with the suppression of STAU1/PTEN and restoration of PI3K/AKT signaling. Conclusions Our study discloses that GIGYF2 mediates obesity-related IR by disrupting the PI3K/AKT signaling axis through the up-regulation of STAU1/PTEN. Targeting GIGYF2 may offer a potential strategy for treating obesity-related metabolic diseases, including type 2 diabetes. Graphical Abstract

Background: Diabetes Mellitus (DM), a chronic metabolic disease characterized by elevated blood glucose, is caused by various degrees of insulin resistance and dysfunctional insulin secretion, resulting in hyperglycemia. The loss and failure of functional β-cells are key mechanisms resulting in type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). Aim of review: Elucidating the underlying mechanisms of β-cell failure, and exploring approaches for β-cell neogenesis to reverse β-cell dysfunction may provide novel strategies for DM therapy. Key scientific concepts of review: Emerging studies reveal that genetic susceptibility, endoplasmic reticulum (ER) stress, oxidative stress, islet inflammation, and protein modification linked to multiple signaling pathways contribute to DM pathogenesis. Over the past few years, replenishing functional β-cell by β-cell neogenesis to restore the number and function of pancreatic β-cells has remarkably exhibited a promising therapeutic approach for DM therapy. In this review, we provide a comprehensive overview of the underlying mechanisms of β-cell failure in DM, highlight the effective approaches for β-cell neogenesis, as well as discuss the current clinical and preclinical agents research advances of β-cell neogenesis. Insights into the challenges of translating β-cell neogenesis into clinical application for DM treatment are also offered.

Vascular endothelial cells (ECs) senescence plays a crucial role in vascular aging that promotes the initiation and progression of cardiovascular disease. The mutation of Grb10-interacting GYF protein 2 (GIGYF2) is strongly associated with the pathogenesis of aging-related diseases, whereas its role in regulating ECs senescence and dysfunction still remains elusive. In this study, we found aberrant hyperexpression of GIGYF2 in senescent human ECs and aortas of old mice. Silencing GIGYF2 in senescent ECs suppressed eNOS-uncoupling, senescence, and endothelial dysfunction. Conversely, in nonsenescent cells, overexpressing GIGYF2 promoted eNOS-uncoupling, cellular senescence, endothelial dysfunction, and activation of the mTORC1-SK61 pathway, which were ablated by rapamycin or antioxidant N-Acetyl-l-cysteine (NAC). Transcriptome analysis revealed that staufen double-stranded RNA binding protein 1 (STAU1) is remarkably downregulated in the GIGYF2-depleted ECs. STAU1 depletion significantly attenuated GIGYF2-induced cellular senescence, dysfunction, and inflammation in young ECs. Furthermore, we disclosed that GIGYF2 acting as an RNA binding protein (RBP) enhances STAU1 mRNA stability, and that the intron region of the late endosomal/lysosomal adaptor MAPK and mTOR activator 4 (LAMTOR4) could bind to STAU1 protein to upregulate LAMTOR4 expression. Immunofluorescence staining showed that GIGYF2 overexpression promoted the translocation of mTORC1 to lysosome. In the mice model, GIGYF2flox/flox Cdh-Cre+ mice protected aged mice from aging-associated vascular endothelium-dependent relaxation and arterial stiffness. Our work discloses that GIGYF2 serving as an RBP enhances the mRNA stability of STAU1 that upregulates LAMTOR4 expression through binding with its intron region, which activates the mTORC1-S6K1 signaling via recruitment of mTORC1 to the lysosomal membrane, ultimately leading to ECs senescence, dysfunction, and vascular aging. Disrupting the GIGYF2-STAU1-mTORC1 signaling cascade may represent a promising therapeutic approach against vascular aging and aging-related cardiovascular diseases.

In wireless communication wiretap channel, for the eavesdropper to obtain the legitimate receiver decoding rules situation, this paper proposes a LT-SLT fountain code anti-eavesdropping channel coding design. This method targets the Luby Transform (LT) code transmission for some of the original symbols of the Shifted LT (SLT) code and utilizes the fountain code to receive the correct symbols in different noise channels with differential characteristics so that the decoding process of the eavesdropper changes and cannot be decoded in synchronization with the legitimate receivers, and then the partial symbols of the recovered source are different from those of the legitimate receivers. When these symbols continue to participate in SLT decoding, increasing the untranslated rate of the eavesdropper. Experimental results show that although the method proposed in this paper increases the number of decoded symbols by a small amount, the eavesdropper untranslated rate of this scheme gets improved by about 15% when the main channel or the wiretap channel is varied individually, compared with LT code and SLT code. When both the main channel and the wiretap channel are varied simultaneously, the untranslated rate of the eavesdropper in this scheme gets approximately 30% higher compared to LT code and SLT code, and the untranslated rate of the eavesdropper in this scheme gets approximately 14% higher compared to SLT-LT fountain code. When the main channel is worse or slightly better than the wiretap channel, the untranslated rate of eavesdroppers of this scheme is better than that of SLT-LT fountain code, which effectively ensures secure transmission of information.

Fountain code can significantly increase eavesdroppers’ untranslated efficiency in the wireless communication eavesdropping channel. The secondary LT coding anti-eavesdropping scheme with fountain code degree-1 is the subject of a theoretical investigation in this paper. The fact that its channel security capacity is greater than that of traditional LT code is first deduced from an information-theoretic standpoint, and the impact of source symbol length on decoding complexity and decoding overhead is then examined. The experimental results show that, compared with the traditional anti-eavesdropping twice fountain code, selecting long source symbols for double LT coding, when the main channel is better than the eavesdropping channel, can ensure that the eavesdropper has a higher untranslated efficiency, and can effectively reduce the fountain code decoding complexity and the number of encoded symbols sent by the source to improve the efficiency of information transmission.

The prediction of pause fillers plays a crucial role in enhancing the naturalness of synthesized speech. In recent years, neural networks, including LSTM, BERT, and XLNet, have been employed for pause fillers prediction modules. However, these methods have exhibited relatively lower accuracy in predicting pause fillers. This paper introduces the utilization of the RoBERTa model for predicting Chinese pause fillers and presents a novel approach to training the RoBERTa model, effectively enhancing the accuracy of Chinese pause fillers prediction. Our proposed approach involves categorizing text from different speakers into four distinct style groups based on the frequency and position of Chinese pause fillers. The RoBERTa model is trained on these four groups of data, which incorporate different styles of fillers, thereby ensuring a more natural synthesis of speech. The Chinese pause fillers prediction module is evaluated on systems such as Parallel Tacotron2, FastPitch, and Deep Voice3, achieving a notable 26.7% improvement in word-level prediction accuracy compared to the BERT model, along with a 14% enhancement in position-level prediction accuracy. This substantial improvement results in a significant enhancement of the naturalness of the generated speech.

One task of nonparallel speech conversion is to convert the source speaker’s speech samples to the target speaker’s speech samples, keeping the content unchanged. In view of the advantages of MaskCycleGAN-VC in nonparallel speech conversion, such as small model size and superior performance, our paper uses the basic structure of MaskCycleGAN-VC to improve it and proposes a cyclic boundary method filling in the frame MaskCycleGAN-VC (CBFMCycleGAN-VC) model, which predicts the voice of a person as he ages by using voice samples of his younger self. First, this paper adds speech preprocessing modules, including the Chebyshev low-pass filter and adaptive filter, which increases the robustness of the system. Second, our paper considers the time-domain difference in the weight parameters, which makes it easier to grasp the mapping law of the time-domain structure, with a faster convergence speed. Last, the circular boundary method is introduced to avoid the ringing effect, to enhance the connection between the filled frame and the adjacent frame, and to obtain a better generator. The simulation results show that the CBFMCycleGAN-VC model is more suitable for the speech conversion task of predicting the voices of elderly people, and the convergence speed is faster. The converted voice is also closer to the voice of the target speaker in the time domain and frequency domain. Under the condition that the accuracy rate is similar to that of MaskCycleGAN-VC, the MOS score is 17.5% higher than that of MaskCycleGAN-VC.

In recent years, physical layer security technology has provided a new way to solve the problem of secure transmissions in wireless communications from an information theory perspective by using physical layer security coding and the inherent characteristics of the channel. As a nonsystematic code, Luby transform (LT) code has the characteristics of random coding and rateless, therefore, eavesdroppers cannot directly obtain useful information from leaked code symbols. As a shifted LT (SLT) code, the SLT codes can efficiently recover information, with a smaller decoding overhead. Therefore, we propose an SLT-LT joint code anti-eavesdropping scheme based on random symbol sets. Based on the environment of the main channel, the sender selects a set of random symbols to send to legitimate receivers as known symbols and uses these random symbols and message symbols to form source symbols for the SLT-LT concatenated coding to increase the bit error rate (BER) of the eavesdroppers. The experimental results show that, compared with other anti-eavesdropping LT schemes, our proposed scheme only adds a small amount of decoding overhead but has a better security performance.

Abstract Ferroptosis, a recently identified and iron-dependent cell death, differs from other cell death such as apoptosis, necroptosis, pyroptosis, and autophagy-dependent cell death. This form of cell death does not exhibit typical morphological and biochemical characteristics, including cell shrinkage, mitochondrial fragmentation, nuclear condensation. The dysfunction of lipid peroxide clearance, the presence of redox-active iron as well as oxidation of polyunsaturated fatty acid (PUFA)-containing phospholipids are three essential features of ferroptosis. Iron metabolism and lipid peroxidation signaling are increasingly recognized as central mediators of ferroptosis. Ferroptosis plays an important role in the regulation of oxidative stress and inflammatory responses. Accumulating evidence suggests that ferroptosis is implicated in a variety of cardiovascular diseases such as atherosclerosis, stroke, ischemia-reperfusion injury, and heart failure, indicating that targeting ferroptosis will present a novel therapeutic approach against cardiovascular diseases. Here, we provide an overview of the features, process, function, and mechanisms of ferroptosis, and its increasingly connected relevance to oxidative stress, inflammation, and cardiovascular diseases.

Arginase is a key hydrolase in the urea cycle that hydrolyses L-arginine to urea and L-ornithine. Increasing number of studies in recent years demonstrate that two mammalian arginase isoforms, arginase 1 (ARG1) and arginase 2 (ARG2), were aberrantly upregulated in various types of cancers, and played crucial roles in the regulation of tumor growth and metastasis through various mechanisms such as regulating L-arginine metabolism, influencing tumor immune microenvironment, etc. Thus, arginase receives increasing focus as an attractive target for cancer therapy. In this review, we provide a comprehensive overview of the physiological and biological roles of arginase in a variety of cancers, and shed light on the underlying mechanisms of arginase mediating cancer cells growth and development, as well as summarize the recent clinical research advances of targeting arginase for cancer therapy.

The existing physical layer security technology based on fountain codes needs to ensure that the legal channel is superior to the eavesdropping channel; when the quality of the legal channel and the eavesdropping channel are close, the information security cannot be guaranteed. Aiming at this problem, this paper proposes a shifted Luby transform (SLT) code security scheme for partial information encryption, which is mainly divided into two stages, partial information encryption transfer and degree distribution adjustment. The main idea is that the source randomly extracts part of the information symbols, and performs XOR encryption with the random sequence containing the main channel noise sent by the legitimate receiver. Afterward, the degree distribution is adjusted using the number of transfer information symbols received by the legitimate receiver to improve the average degree of the encoded codewords. Since the eavesdropper can only obtain fewer information symbols in the initial stage, it is difficult to decode the generated coded symbols after the degree distribution adjustment, thereby ensuring the safe transmission of information. The experimental results show that, compared with other LT anti-eavesdropping schemes, even if the legitimate channel is not dominant, the proposed scheme still has better security performance and less decoding overhead.

Abstract Background Stroke is a serious cardiovascular disease and is also the leading cause of long-term disability in developing and developed countries. Because matrix metalloproteinase-9 (MMP-9) is associated with the risk of many cardiovascular diseases, we investigated the relationship between single nucleotide polymorphisms (SNPs) in MMP-9 and the risk of Ischemic stroke (IS) in a southern Chinese Han population. Methods This study included 250 stroke patients and 250 healthy controls. Genotyping was performed using the Agena MassARRAY system, and chi-squared tests and genetic models were used to evaluate the associations between MMP-9 SNPs and the risk of IS. Odds ratio (OR) and 95% confidence intervals (CIs) were calculated by unconditional logistic regression adjusted for age. Results Polymorphism rs3787268 was associated with increased the risk of IS. Specifically, the genotype “G/A” significantly correlated with IS risk in the co-dominant model [odds ratio (OR) = 1.62; 95% confidence interval (CI) = 1.10–2.41; p = 0.035)], while genotypes “G/A” and “A/A” may increase the risk of IS based on the dominant model (OR = 1.62; 95% CI = 1.12–2.35; p = 0.0097). This SNP was also significantly associated with IS risk in the log-additive model (OR = 1.33; 95% CI = 1.03–1.70; p = 0.026). Conversely, haplotype “C/G” appears to reduce the risk of IS (OR = 0.71; 95% CI = 0.54–0.95; p = 0.019). Conclusions Our study showed that the rs3787268 locus in the MMP-9 gene may increase risk of IS in a southern Chinese Han population and thus provide insight into the IS pathogenesis.

Abstract Background Single nucleotide polymorphisms (SNPs) in 3′-untranslated region (UTR) of genes related with cell-matrix adhesions and migration might affect miRNA binding and potentially affect the risk of cancer. The present study aimed to screen SNPs in 3′ UTR of cancer-related genes and investigate their contribution to the susceptibility of lung cancer. Methods Seven SNPs were selected and genotyped in a case-control study (322 lung cancer patients and 384 controls) among Chinese Han population. Odds ratio (OR) and 95% confidence intervals (CIs) were calculated by logistic regression adjusted for age and gender in multiple genetic models. Results In stratified analyses by gender, three (rs1064607, rs3796283 and rs2378456) of LPP gene were associated with a significantly increased susceptibility for lung cancer among male population. Besides, LPP rs2378456 weakened lung cancer risk in female. LPP rs1064607 polymorphism was significantly correlated with increased risk of lung adenocarcinoma. Furthermore, AA genotype of TNS3 rs9876 polymorphism was associated with lymphatic metastasis. Conclusion Our results provides evidence for the impact of LPP polymorphisms on the susceptibility to lung cancer in Chinese population.

Abstract Background Kidney cancer is the predominant form of malignancy of the kidney and accounts for approximately 3%–4% of all cancers. Renal cell cancer (RCC) represents more than 85% of kidney cancer. It has been reported that genetic factors may predispose individuals to RCC. This study evaluated the association between Acylphosphatase 2 (ACYP2) gene polymorphisms and RCC risk in the Han Chinese population. Methods Twelve single‐nucleotide polymorphisms (SNPs) in ACYP2 were genotyped using the Agena MassARRAY platform from 293 RCC patients and 495 controls. The Chi‐squared test, genetic models, haplotype, and stratification analyses were used to evaluate the association between SNPs and the risk of RCC. The relative risk was estimated using the odds ratio (OR) and 95% confidence interval (CI). Results We observed that the rs6713088 allele G (OR = 1.26, 95% CI: 1.03–1.53, p = .023) and rs843711 allele T (OR = 1.29, 95% CI: 1.06–1.57, p = .010) were associated with increased RCC risk. Genetic model analyses found that rs843711 was significantly associated with an increased RCC risk under the recessive model and log‐additive model after adjusting for age and gender. Haplotype analysis showed that the haplotype “TTCTCGCC” (OR = 0.67, 95% CI: 0.48–0.94, p = .021) was associated with a decreased risk of RCC in the Han Chinese population. Stratification analysis also found that rs6713088 and rs843711 were significantly associated with increased RCC risk. Conclusion In summary, the results suggested that ACYP2 polymorphisms could be used as a genetic marker for RCC. Additional functional and association studies are required to validate our results.

Abstract Background Lumbar disc herniation (LDH) is a common spinal disease in clinical practice. Once lumbar disc herniation occurs, it seriously reduces patient's quality of life. The EYS (eyes shut homolog) was discovered in recent years and it may be related to lumbar disc herniation. So we conducted a case–control study to explore the relationship between EYS polymorphism and lumbar disc herniation risk. Methods We selected 5 single‐nucleotide polymorphisms (SNPs) of EYS gene in a case–control study with 508 cases and 508 healthy controls to evaluate the relatedness by using genetic model, haplotype, and stratification analysis. Results We found that the minor alleles of rs62413038 (OR = 1.21, 95%CI: 1.01–1.43, p = .036) and rs9450607 (OR = 1.26, 95% CI: 1.05–1.53, p = .016) were associated with an increased risk of lumbar disc herniation in the allelic model analysis. In the genotypic model analysis, rs62413038 displayed a significantly increased risk of lumbar disc herniation in log‐additive models (OR = 1.20, 95% CI: 1.01–1.43, p = .039). While the rs9450607 was also obviously associated with an increased lumbar disc herniation risk in recessive (OR = 1.98, 95% CI: 1.24–3.13, p = .004) and log‐additive models (OR = 1.27, 95% CI: 1.05–1.55, p = .014). In addition, in the haplotype analyses of the SNPs, we found that the “CGGA” haplotype of rs1482456, rs9342097, rs9450607, and rs7757884 was associated with lumbar disc herniation. (OR = 0.52, 95% CI: 0.30–0.89, p = .017). Conclusion These results suggest that EYS polymorphism may be associated with lumbar disc herniation among Han Chinese population. It also opens up a new exploration direction for the etiology of lumbar disc herniation.

Abstract Background Interleukin‐1β (IL‐1B) has been recognized as a pro‐inflammatory cytokine and associated with tumorigenesis. We aimed to evaluate the contribution of IL‐1B polymorphisms to the susceptibility of cervical cancer in Chinese Uygur population. Methods Seven variants were genotyped by Agena MassARRAY platform in 267 cervical cancer patients and 302 healthy controls. Allelic, genotypic, and haplotypic association analyses adjusted for age were investigated using odds ratios (OR) and 95% confidence intervals (CI). GEPIA and UALCAN databases were used to evaluate expression and prognostic of IL‐1B gene in cervical cancer. Results Our result revealed IL‐1B rs1143627‐AA (OR = 1.98, p = 0.029) and rs16944‐GG (OR = 2.01, p = 0.025) was associated with an increased risk of cervical cancer. Besides, we also found two protective single nucleotide polymorphisms (SNPs) rs3136558 (OR = 0.63, p = 0.011) and rs1143630 (OR = 0.63, p = 0.019). Haplotype ″TGA″ in the block (rs1143630, rs1143627, and rs16944) significantly decreased the susceptibility of cervical cancer (OR = 0.53, p = 0.0007). IL‐1B mRNA level was up‐regulated in the cervical cancer patients, which was related with poor prognosis in silico. Conclusions For the first time, our results provide evidence on polymorphism of IL‐1B gene associated with cervical cancer risk in Chinese Uygur population.

Abstract Background ACYP2 gene may be involved in the process of telomere shortening which may be involved in the liver cancer. So, this research was to examine whether the ACYP2 gene polymorphism has impact on the risk of liver cancer in Chinese population. Methods Two hundred and fifty cirrhosis patients and 248 liver cancer patients were selected. Unconditional logistic regression was to calculate the odds ratio (OR) and 95% confidence intervals (CIs). Analyze the relationship between ACYP2 gene polymorphism and tumor using meta‐analysis. Analyze the expression of ACYP2 gene in liver cancer and its influence on the prognosis of liver cancer by databases (Ualcan, GTEX and Kaplan–Meier plotter). Results In the allele model, ACYP2 rs843720 was protection against the occurrence of cirrhosis developed into liver cancer (OR = 0.76, 95% CI: 0.58–0.99, p = 0.04). Rs1682111 and rs843720 play a protective role in the additive model (rs1682111: OR = 0.69, 95% CI: 0.52–0.93, p = 0.01; rs843720: OR = 0.73, 95% CI: 0.54–0.98, p = 0.04).While rs843645 G allele increased the risk of cirrhosis developed into liver cancer under the additive model (OR = 1.42, 95% CI: 1.02–2.00, p = 0.04).The haplotype analysis detected that “ATATCGCC” decreased the risk of cirrhosis developed into liver cancer (OR = 0.69, 95% CI: 0.51–0.92, 95% CI: p = 0.013); however, “TGAGCGTC” increased the risk of cirrhosis developed into liver cancer (OR = 1.48, 95% CI: 1.04–2.10, p = 0.027). Meta‐analysis shown that ACYP2 rs1682111 was associated with the risk of cancer (OR = 0.90, 95% CI: 0.78–1.05, p = 0.02). ACYP2 gene high expression was found to be associated with better OS for all liver patients. Conclusion Based on this research, we surmised that ACYP2 gene may be involved in the occurrence of liver cancer in Chinese populations.

Abstract Background Lumbar disk herniation (LDH) is a degenerative disorder, which partly results from complex genetic factors. The aim of the study was to investigate the potential associations between glypican‐6 (GPC6) variants and LDH risk in Han Chinese population. Methods A total of 508 Han Chinese LDH patients and 508 healthy controls were recruited in this study. Six single‐nucleotide polymorphisms (SNPs) in GPC6 were selected and genotyped using an Agena MassARRAY platform. We used logistic regression method to evaluate the linkage between GPC6 variants and LDH risk by calculating the odds ratio (OR) and 95% confidence intervals (CIs) in multiple genetic models. HaploReg database was used for SNP functional annotation. Results Our result revealed GPC6 rs4773724 was associated with a decreased risk of LDH in allele model (OR = 0.82, 95% CI: 0.68–0.98, p = 0.026), whereas rs1008993 increased the LDH risk (OR = 1.34, 95% CI: 1.05–1.71, p = 0.020). Besides, we also found rs4773724 and rs9523981 were associated with susceptibility of LDH among individuals whose age are less than 45. And rs1008993 was associated with increased LDH risk in males. Furthermore, Haplotype analysis showed that the TT (rs4773724, rs1008993) haplotype and GC (rs4773724, rs1008993) haplotype had the opposite effects on the susceptibility of LDH. Conclusions For the first time, we suggest that rs4773724 and rs1008993 in GPC6 were considered as a protective factor and a risk factor for LDH in Han Chinese population, respectively. These results provide new ideas for the treatment and prevention of LDH in Han Chinese population.

Abstract Background Laryngeal squamous cell carcinoma (LSCC) is one of the most prevalent malignant neoplasms of the upper respiratory tract. Studies have confirmed that an unstable chromosome constitution promotes the progress of laryngeal tumorigenesis, and ACYP2 has been confirmed as a telomere length‐related gene. However, to date, the association between ACYP2 polymorphisms and LSCC susceptibility has not been investigated. Methods We performed this study to explore the effect of 11 single‐nucleotide polymorphisms (SNPs) in ACYP2 on LSCC susceptibility in Chinese Han males. Unconditional logistic regression analysis adjusted for age was used to calculate the odds ratios and 95% confidence intervals. Results Based on allele and genotype models, our results showed that rs1682111 variant was significantly associated with a decreased LSCC susceptibility (p

Decoding overhead is a standard for measuring whether rateless coding is good or not. The product-code coding of Shifted RSD, a communication transmission scheme, is based on the joint decoding of rateless coding and channel coding at the network layer of feedback information, was proposed in this study in order to reduce the overhead of decoding in rateless coding in the wireless communication. This method combines rateless coding and channel coding at the network layer to decode, which results in multiple packets instead of one recovered by iterative decoding every time during decoding. The decoding is accomplished until all packets are decoded, and the original information of source is recovered. The decoding overhead used for recovering the original information can be reduced due to the increase in the number of packets recovered at a time. Experimental results show that the use of this method combining channel coding with rateless coding to decode requires less decoding overhead than using LT code or RSD code with feedback for decoding, thus improving the decoding capability of the receiving end. [ABSTRACT FROM AUTHOR]