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OBJECTIVE: High-risk (HR) human papillomavirus (HPV) is one of the major causes for most anal and penile cancers and oropharyngeal cancers in men, and vaccination against HPV is recommended for the prevention of these cancers. Data on HPV infection in Chinese men is still limited, which requires further investigation to guide vaccine development and assess the effectiveness of HPV vaccines. We thus studied the HR-HPV genotype distribution in HPV-infected men in Northern China. PATIENTS AND METHODS: Genital specimens were obtained from male patients (≥18 years old) at the clinic for sexually transmitted infections of the Shandong Provincial Hospital between January 2016 and December 2018. Samples were analyzed for 15 HR-HPV genotypes, and 2 low-risk HPV (LR-HPV) genotypes using a multiplex real-time quantitive polymerase chain reaction (qPCR) assay. RESULTS: Of 1,163 participants enrolled, 426 patients were diagnosed as verruca acuminata (CA) and 737 were asymptomatic men. The overall prevalence of HPV infection was 42% (489/1,163), and 27.4% (319/1,163) were positive for HR-HPV. HPV 16 (5.2%, 61/1,163) was the most common HR genotype overall, followed by HPV 52 (4.6%, 54/1,163), 51 (4.3%, 50/1,163), 18 (4.1%, 48/1,163), and 39 (4.0%, 47/1,163). Genotypes 16, 52, 39, 51, and 18 were most prevalent in CA patients, and 16, 51, 18, 59, and 39 in asymptomatic men. Prevalence of genotypes 31, 33, and 45 covered by the 9-valent HPV prophylactic vaccine was low in the assessed region. CONCLUSIONS: HPV 16, 52, 51, 18, 39, and 59 were the most common HR genotypes detected in men in Northern China. Importantly, HPV 39, 51, and 59 are not currently covered by either the 4-valent or 9-valent HPV vaccines. [ABSTRACT FROM AUTHOR]

In diverse application fields, the increasing requisitions of Wireless Sensor Networks (WSNs) have more and more research dedicated to the question of sensor nodes' deployment in recent years. For deployment of sensor nodes, some key points that should be taken into consideration are the coverage area to be monitored, energy consumed of nodes, connectivity, amount of deployed sensors and lifetime of the WSNs. This paper analyzes the wireless sensor network nodes deployment optimization problem. Wireless sensor nodes deployment determines the nodes' capability and lifetime. For node deployment in heterogeneous sensor networks based on different probability sensing models of heterogeneous nodes, the author refers to the organic small molecule model and proposes a molecule sensing model of heterogeneous nodes in this paper. DSmT is an extension of the classical theory of evidence, which can combine with any type of trust function of an independent source, mainly concentrating on combined uncertainty, high conflict, and inaccurate source of evidence. Referring to the data fusion model, the changes in the network coverage ratio after using the new sensing model and data fusion algorithm are studied. According to the research results, the nodes deployment scheme of heterogeneous sensor networks based on the organic small molecule model is proposed in this paper. The simulation model is established by MATLAB software. The simulation results show that the effectiveness of the algorithm, the network coverage, and detection efficiency of nodes are improved, the lifetime of the network is prolonged, energy consumption and the number of deployment nodes are reduced, and the scope of perceiving is expanded. As a result, the coverage hole recovery algorithm can improve the detection performance of the network in the initial deployment phase and coverage hole recovery phase. [ABSTRACT FROM AUTHOR]

A survey of mtDNA variation among populations of chum salmon Oncorhynchus keta around the Pacific Rim revealed four large population groups: Rim of the Sea of Japan, the Rim of the Okhotsk Sea and West Bering Sea, North-west Alaska and Gulf of Alaska. The observed population structure appears to reflect isolation by distance with limited gene flow between regions and larger amounts of gene flow between populations within these four regions. [ABSTRACT FROM AUTHOR]

Esophageal cancer is a malignant tumor with a high incidence in China. At pesent, advanced esophageal cancer patients are still frequently encountered. The primary treatment for resectable advanced esophageal cancer is surgery-based multimodality therapy, including preoperative neoadjuvant therapy, such as chemotherapy, chemoradiotherapy or chemotherapy plus immunotherapy, followed by radical esophagectomy with thoraco-abdominal two-field or cervico-thoraco-abdominal three-field lymphadenectomy via minimally invasive approach or thoracotomy. In addition, adjuvant chemotherapy, radiotherapy, or chemoradiotherapy, or immunotherapy may also be administered if suggested by postoperative pathological results. Although the treatment outcome of esophageal cancer has improved significantly in China, many clinical issues remain controversial. In this article, we summarize the current hotspots and important issues of esophageal cancer in China, including prevention and early diagnosis, treatment selection for early esophageal cancer, surgical approach selection, lymphadenectomy method, preoperative neoadjuvant therapy, postoperative adjuvant therapy, and nutritional support treatment.

Objective: The regulatory mechanism of lncRNA MIR4435-2HG has been extensively investigated in human cancers other than melanoma. This study aims to elucidate the role of lncRNA MIR4435-2HG in melanoma., Material and Methods: The mRNA expression was detected by RT-qPCR. MTT assay, Transwell assay and Dual-Luciferase reporter assay were used to investigate the regulatory mechanism of lncRNA MIR4435-2HG., Results: Upregulation of lncRNA MIR4435-2HG was identified in melanoma and promoted melanoma cell proliferation, migration and invasion. In addition, lncRNA MIR4435-2HG serves as the ceRNA of miR-802. MiR-802 inhibited melanoma progression by downregulating lncRNA MIR4435-2HG. Besides, miR-802 directly targets FLOT2. And knockdown of FLOT2 restrained the progression of melanoma by downregulating lncRNA MIR4435-2HG and upregulating miR-802., Conclusions: LncRNA MIR4435-2HG promotes cell proliferation, migration and invasion in melanoma by sponging miR-802 and upregulating FLOT2.

Objective: To understand the changes on patterns of sleep duration of the China Health and Nutrition Survey (CHNS) cohort in 9 provinces from 2004 to 2011. Methods: Four rounds of CHNS data were used. Urban/rural, age and gender specific insufficient sleeping rates and excessive sleeping rates were analyzed. Results: In 2004, 2006, 2009 and 2011, a total of 274, 281, 329 and 304 children aged 3-5 years; 874, 806, 768 and 742 children aged 6-12 years; 789, 529, 426 and 367 children aged 13-17 years; 9 568, 9 530, 9 942 and 9 609 adults aged ≥18 years were surveyed respectively. The lowest insufficient sleeping rate was 53.9 % (200/371) in 3-17 years old children in rural area in 2006, the highest insufficient sleeping rate was 77.2 % (44/57) in 3-5 years old children in urban area in 2004. The insufficient sleeping rate increased in rural 3-5 years old children from 2004 to 2011. For the adults aged ≥18 years, the insufficient sleeping rate ranged from 4.2 % (82/1 954) in females aged 18-44 years in 2004 and 2009 to 20.8 % (211/1 015) in urban residents aged > 60 years in 2011. The insufficient sleeping rate in age-groups 44-59 years and ≥60 years increased in both males and females and in both urban area and rural area from 2004 to 2011. The gender specific excessive sleeping rate in 3-17 years old children was very low in both urban area and rural area and no difference was found in different rounds of survey. The excessive sleeping rate in adults ranged from 18.4 % (569/3 093) in urban population in 2011 to 32.5 % (1 617/4 969) in females in 2004. The excessive sleeping rate of adult decreased from 2004 to 2011. Conclusion: We should pay attention to the fact that the insufficient sleeping rate in adolescents is high and in increase in rural 3-5 years old children and adults aged ≥45 years.

Several previous studies have demonstrated that elevated levels of fibroblast growth factor-23 (FGF-23) may be involved in atherosclerosis and contribute to the high mortality rate of peritoneal dialysis (PD) patients. The aim of this study was to determine the precise role of FGF-23 in the pathogenesis of atherosclerosis in PD patients. Between April 2009 and January 2012, 62 PD patients and 25 control subjects were included in the study. An enzyme-linked immunosorbent assay was conducted to test for plasma FGF-23 levels. Carotid artery intima-media thickness (CIMT), left ventricular mass index (LVMI), and myocardial performance index (MPI) were determined by ultrasonography. Plasma Ca(2+), P(3+), calcium-phosphorus product, parathyroid hormone, N-terminal pro-brain natriuretic peptide, and cardiac troponin I were also detected. Plasma FGF-23 levels in PD patients were significantly higher than those in control subjects. PD patients with CIMT > 1.0 mm showed the highest levels of FGF-23. Plasma P(3+), calcium-phosphorous product, plasma parathyroid hormone, CIMT, LVMI, and MPI levels were positively associated with plasma FGF-23 levels. Multiple-stepwise regression analyses revealed that plasma P(3+), plasma parathyroid hormone, CIMT, LVMI, and MPI levels were strongly associated with plasma FGF-23 levels. However, no correlations were observed in plasma N-terminal pro-brain natriuretic hormone and cardiac troponin I levels. Plasma FGF- 23 levels may play an important role in the initiation and progression of atherosclerosis. Thus, detecting and defining plasma FGF-23 levels may be a promising biomarker for the early detection of atherosclerosis in PD patients.

PTEN is one of the most frequently mutated or deleted tumor suppressors in human cancers. NEDD4-1 was recently identified as the E3 ubiquitin ligase for PTEN; however, a number of important questions remain regarding the role of ubiquitination in regulating PTEN function and the mechanisms by which PTEN ubiquitination is regulated. In the present study, we demonstrated that p34, which was identified as a binding partner of NEDD4-1, controls PTEN ubiquitination by regulating NEDD4-1 protein stability. p34 interacts with the WW1 domain of NEDD4-1, an interaction that enhances NEDD4-1 stability. Expression of p34 promotes PTEN poly-ubiquitination, leading to PTEN protein degradation, whereas p34 knockdown results in PTEN mono-ubiquitination. Notably, an inverse correlation between PTEN and p34/NEDD4-1 levels was confirmed in tumor samples from colon cancer patients. Thus, p34 acts as a key regulator of the oncogenic behavior of NEDD4-1 and PTEN.

Mitochondrial DNAs (mtDNAs) has been frequently used as genetic markers for the population genetic studies. In this study we used chum salmon (Oncorhynchus keta) from Korea, Japan andAmerica, and compared their mitochondrial NADH dehydrogenase subunit 3 (ND3) genes by DNA sequence analysis. Sequence variation was studied in the ND3 among total 11 individuals from three populations. The ND3 gene was amplified by PCR targeting parts of cytochrome oxidase III gene (COIII) and NADH dehydrogenase subunit 4L gene (ND4L). ND3 gene sequence, encoded 752 bps, presented some genetic variation in the chum salmon populations. The observed nucleotide variations inferred the distinct genetic differentiation of American salmons from Korean and Japanese chum salmons. Six sites of single nucleotide polymorphism (SNP) were explored in the ND3 locus. Denaturing gradient gel electrophoresis analysis also showed a clear heterogenous band in American salmons compared to Asian salmons.

Protein hydrolysates, prepared by enzymatic digestion of soybean protein and egg white albumin using several proteases, inhibited the crystal growth of calcium carbonate. Each hydrolysate showed different inhibitory activities, suggesting the key role of peptide structures in the inhibition. The deamidation of protein hydrolysates by glutaminase increased not only the inhibitory activity toward the crystal growth of calcium carbonate but also the resistance of the hydrolysates against peptic digestion. Furthermore, the addition of sodium chloride, citric acid, or lactose into the reaction mixture enhanced the inhibitory activity. The protein hydrolysates inhibited both nucleation and crystal growth of calcium carbonate and also affected the crystal morphology.

Quantitative immunoblot analyses were carried out to study the distribution of N-methyl-D-aspartate (NMDA) receptor subunit 2A and 2B (NR2A and NR2B, respectively) at the protein level in the adult rat brain. Highest levels of NR2A were detected in cerebral cortex and hippocampus, followed at more or less similar levels (about 36-72% of cerebral cortex) by striatum, thalamus, olfactory bulb, superior and inferior colliculi, and cerebellum. The lowest levels were detected in midbrain and lower brain stem (30-31% of cerebral cortex). The NR2B was more dramatic in differential distribution than the NR2A. Highest levels of NR2B were found in telencephalic (olfactory bulb, cerebral cortex, hippocampus, and striatum) and thalamic regions, and expression in superior and inferior colliculi, midbrain, lower brain stem, and cerebellum were significantly lower (4-25% of cerebral cortex). Interestingly, NR2B proteins were barely detectable in the cerebellum. When the postsynaptic density (PSD) fractions were compared, the amount of NR2B in the cerebellar PSD fraction was only 1.8% of that present in the cerebral PSD fraction where the subunit is highly enriched. Immunoblot analyses with a phosphotyrosine-specific antibody showed that the molecular sizes of major phosphotyrosine-containing proteins in forebrain and hindbrain are 180 and 45 kDa, respectively. The regional distribution of the 180 kDa major phosphotyrosine protein was very similar to that of NR2B, and the protein could be immunoprecipitated by NR2B antibody. Our data shows that NR2A and NR2B subunits are differentially distributed in the brain in an overlapping manner, and that the major phosphotyrosine-containing protein of 180 kDa in forebrain is the NR2B.

We carried out quantitative analyses of the developmental expression, subcellular localization of the N-methyl-D-aspartate receptor subunit 2A (NR2A) and 2B (NR2B), and tyrosine phosphorylation of NR2B. Immunoblot analyses showed that NR2A was not detected during the embryonic period and the first postnatal week but its expression reached 63.90% of adult at P14 and continued to increase until the fourth week, reaching a maximum at P30 (110% of adult). The NR2B was detected from as early as E14 (2.65% of adult) and its expression was transiently elevated at birth (43.73% of adult), decreasing for the first postnatal week, and then increased again rapidly in the second week (105.45% of adult at P14) with a maximum at P30 (123.34% of adult). There were 2.26 +/- 0.40-fold more NR2B than NR2A proteins in the forebrain PSD fractions, and NR2A and NR2B were enriched 2.75 +/- 0.35 and 4.65 +/- 0.25 fold, respectively, in the synaptosome, and 13.75 +/- 0.80 and 16.04 +/- 0.25-fold, respectively, in the PSD fraction from brain homogenate. The tyrosine phosphorylation of NR2B reached an adult level at around birth declining in the first postnatal week but recovered to the adult level by the end of the second week, while the amount of the protein itself increased 2.28-fold after birth, indicating that only a fraction of the proteins are phosphorylated in vivo. Our results indicate that expression and tyrosine phosphorylation of NR2B might be important for NMDA receptor functions in embryonic and early postnatal development.