Strategies for patients with recurrent nasopharyngeal carcinoma involved internal carotid artery who are intolerant to embolization.

BACKGROUND: The surgical treatment of recurrent nasopharyngeal carcinoma (rNPC) involving the internal carotid artery (ICA) is challenging, as the massive bleeding caused by intraoperative rupture of the ICA is life-threatening. We reported that ICA embolization is an effective pretreatment to avoid fatal bleeding, but some patients cannot tolerate the procedure. We used endovascular vascular protection (ICA stents), vascular sacrifice (bypass grafting) and extravascular vascular protection (transcervical external stent placement) of the ICA to provide alternative options for these patients. METHODOLOGYy: This study enrolled patients with rNPC adjacent to or invading the ICA who were unsuitable for ICA embolization from January 2015 to June 2020. ICA pretreatment combined with endoscopic nasopharyngectomy (ENPG) was performed for the 30 patients. We report the survival outcome and incidence of complications after ICA pretreatment. RESULTS: ICA pretreatment was performed for the 30 enrolled patients, among whom 8 underwent endoscopic-assisted transcervical protection of the parapharyngeal ICA combined with ENPG, 6 underwent bypass grafting, and 16 underwent ICA stent implantation followed by ENPG. After pretreatment, at a median follow-up of 43 months (range, 2-80 months), the 3-year locoregional overall survival (OS), progression-free survival (PFS), locoregional recurrence-free survival (LRRFS), and distant metastasis-free survival (DMFS) were 62.9%, 61.3%, 70.2%, and 71.4%, respectively. CONCLUSIONS: ICA pretreatment combined with salvage ENPG enables the feasible and effective resection of rNPC lesions involving the ICA in patients who cannot tolerate ICA embolization. Therefore, this treatment may be an effective method for improving outcomes. Multidisciplinary therapy is needed to reduce operation-related complications.

Integrative analyses of radiation-related genes and biomarkers associated with breast cancer.

OBJECTIVE: In addition to significantly reducing breast cancer recurrence risk, radiotherapy also prolongs patients' lives. However, radiotherapy-related genes and biomarkers still remain poorly understood. The present study aimed to identify radiation-associated genes in breast cancer. MATERIALS AND METHODS: Breast cancer data were downloaded from Gene Expression Omnibus (GEO) and UCSC Xena database. The gene ontology (GO) enrichment and gene set enrichment analysis (GSEA) were performed for annotation and integrated discovery. Protein-protein interaction (PPI) network was constructed by STRING database and hub genes were identified. Then, immunohistochemistry and tissue expression of key genes was analyzed by using the Human Protein Atlas (HPA) and GEPIA database. Genes associated with prognosis were identified by performing univariate cox analysis. RESULTS: We identified 341 differentially expressed genes related to radiotherapy in breast cancer patients. PPI analysis revealed a total of 129 nodes and 516 interactions and identified five hub genes (EGFR, FOS, ESR1, JUN, and IL6). In addition, 11 SDEGs THBS1, SERPINA11, NFIL3, METTL7A, KCTD12, HSPA6, EGR1, DDIT4, CCDC3, C11orf96, and BCL2A1 candidate genes can be used as potential diagnostic markers. The calibration curve and ROC indicate good probability consistencies of 3-years and 5-year survival rates of patients between estimation and observation. CONCLUSIONS: Our findings provide novel insight into the functional characteristics of breast cancer through integrative analysis of GEO data and suggest potential biomarkers and therapeutic targets for breast cancer.

Association of Ubiquitin C-Terminal Hydrolase-L1 (Uch-L1) serum levels with cognition and brain energy metabolism.

OBJECTIVE: In recent years, many researchers have taken serum ubiquitin c-terminal hydrolase (Uch-L1) as an indicator of post-traumatic brain injury and associated it with cognitive impairment. Alzheimer's disease is characterized by cognitive impairment and energy metabolism disorders. The purpose of this study was to detect whether serum Uch-L1 is related to cognition and brain energy metabolism in healthy people, and to explore whether it can be used as an early blood marker of Alzheimer's disease. PATIENTS AND METHODS: In this prospective cohort study, adult outpatients from a Grade 3A hospital were recruited. They completed the 18F-FDG-PET/CT examination in the nuclear medicine department and were screened by the Mini Mental State scale (MMSE) and the Montreal Cognitive Assessment scale (MoCA). Blood samples were collected from all outpatients to detect the concentration of serum Uch-L1, and the mean standard uptake value (SUVmean) of energy metabolism in the hippocampus during PET/CT examination was collected. RESULTS: A total of 37 participants, 14 participants with cognitive impairment (MMSE score < 27) and 23 controls (MMSE score 27-30) were included. There was a significant difference in the SUVmean of the hippocampus between the cognitive impairment group and the normal control group (p < 0.05). There was a significant correlation between the SUVmean of the hippocampus and the total score of MMSE in all participants [r = 0.439, 95% CI: (0.139-0.668), p = 0.007]. There were also significant correlations between serum Uch-L1 and MMSE. Based on the significant differences of demographic variables between groups, we conducted a multivariate linear regression analysis of MMSE cognitive scores based on age (X1), length of education (X2) and SUVmean of hippocampus (X3). The regression equation is as follows: Y = 25.709-0.072 X1 + 0.422 X2 + 0.232 X3. CONCLUSIONS: Brain cognitive ability is closely related to energy metabolism and serum Uch-L1 concentration, so serum Uch-L1 may become a blood marker for extensive screening of dementia in the future. We look forward to the introduction of a more accurate and low-cost method for detecting serum Uch-L1 concentration.

Establishment and verification of a nomogram for predicting severe acute pancreatitis.

OBJECTIVE: The purpose of this study was to establish a nomogram for predicting the severity of acute pancreatitis (AP) and verify its predictive value. PATIENTS AND METHODS: A total of 571 AP patients received by Ordos Central Hospital from January 2015 to December 2018 were included in this study. According to the 2012 Revised Atlanta classification, the included subjects were classified into severe AP (SAP) group and non-severe AP (NSAP) group [including patient with mild AP (MAP) and moderately SAP (MSAP)]. The baseline characteristics, imageological data and pathological data within 24 h after the disease onset between the two groups were analyzed using One-way analysis of variance (one-way ANOVA). R language was used for establishing a predictive nomogram, whose performance was verified by clinical data of 150 AP cases collected from December 2018 to December 2019. RESULTS: One-way ANOVA shows that SAP and NSAP patients show significant differences in sex, calcium ions, creatinine, neutrophils ratio, lymphocytes ratio and eosinophils ratio (p<0.05). A predictive nomogram was accordingly established using the six indicators. Validation on this predictive nomogram showed high internal validation concordance index (C-index) of 0.69 (95% CI, 0.64-0.74), and high external validation C-index of 0.71 (95% CI, 0.67-0.76). CONCLUSIONS: This nomogram can be used as a clinical tool to predict the severity of SAP.

Five lncRNAs associated with the survival of hepatocellular carcinoma: a comprehensive study based on WGCNA and competing endogenous RNA network.

OBJECTIVE: The competing endogenous RNA (ceRNA) presents a comprehensive regulatory network among lncRNAs, miRNAs and mRNA. The ceRNA provides significant information in understanding the pathology of cancer. This study aimed to explore a lncRNA-associated ceRNA network for predicting the overall survival of patients with hepatocellular carcinoma (HCC). MATERIALS AND METHODS: In this study, RNA-sequencing data of HCC were downloaded from The Cancer Genomes Atlas (TCGA) database. The module-trait relationship was analyzed with Weighted gene co-expression network analysis (WGCNA). The key module associated with tumor was identified, as well as the involved lncRNAs, mRNAs and miRNAs. The preliminary ceRNA network was constructed with Cytoscape. The survival analysis was further performed to screen survival-relevant lncRNAs, mRNAs and miRNAs, and then the survival-associated ceRNA network was reconstructed. RESULTS: Eventually, 5 lncRNAs, 10 miRNAs, and 25 mRNAs were included in the reconstructed ceRNA network. CONCLUSIONS: The identified lncRNAs were promising candidate biomarkers in HCC diagnosis and therapeutics. This analysis process was effective to construct ceRNA network. The result will be conductive to explore the significant lncRNAs and regulatory mechanism.

Simvastatin induces apoptosis of nasopharyngeal carcinoma cells through NF-κB signaling pathway.

OBJECTIVE: The aim of this study was to investigate the mechanism of simvastatin-induced apoptosis in nasopharyngeal carcinoma (NPC) cells. MATERIALS AND METHODS: CNE1 and HK1 cell lines were treated with different concentrations of simvastatin for different time course. Subsequently, Cell Counting Kit-8 (CCK-8), colony formation assay, and flow cytometry were conducted to evaluate cell activity, colony formation ability, as well as cell cycle of NPC cells, respectively. The mRNA expressions of p21, Bim, and cyclin D1 were examined by qPCR. Meanwhile, the protein expression levels of apoptosis-related proteins (including caspase-3, Bax, Bcl-2) were detected by Western blot. Caspase-3 activity was determined to estimate cell apoptosis. An NPC xenotransplantation model was constructed to further determine the role of simvastatin in vivo. In addition, NF-κB activity was assessed through Luciferase reporter gene assay and Western blot. RESULTS: Simvastatin treatment lead to significantly reduced viability of NPC cells and the number of cell colonies dose-dependently and time-dependently. Meanwhile, simvastatin treatment caused cell cycle arrest in G0/G1 phase, remarkably downregulated expression of cyclin D1, and upregulated expressions of p21 and Bim. In addition, simvastatin induced apoptosis of NPC cells and enhanced the Luciferase activity of caspase-3. Western blot results indicated that simvastatin promoted the protein level of Bax and caspase-3, whereas suppressed the protein expression of Bcl-2. In vivo experiments showed that simvastatin was able to suppress the growth of NPC cells. Further studies demonstrated that simvastatin remarkably attenuated the Luciferase activity of pNF-κB-Luc, thereby specifically inhibiting the NF-κB signaling pathway. CONCLUSIONS: Simvastatin inhibits proliferation and promotes apoptosis of NPC cells by inhibiting the NF-κB pathway.

Sulphuric acid-mediated weathering on Taiwan buffers geological atmospheric carbon sinks.

The chemical composition of the Gaoping River in Taiwan reflects the weathering of both silicate and carbonate rocks found in its metasedimentary catchment. Major dissolved ion chemistry and radiocarbon signatures of dissolved inorganic carbon (DIC) reveal the importance of pyrite-derived sulphuric acid weathering on silicates and carbonates. Two-thirds of the dissolved load of the Gaoping River derives from sulphuric acid-mediated weathering of rocks within its catchment. This is reflected in the lowest reported signatures DI14C for a small mountainous river (43 to 71 percent modern carbon), with rock-derived carbonate constituting a 14C-free DIC source. Using an inverse modelling approach integrating riverine major dissolved ion chemistry and DI14C, we provide quantitative constraints of mineral weathering pathways and calculate atmospheric CO2 fluxes resulting from the erosion of the Taiwan orogeny over geological timescales. The results reveal that weathering on Taiwan releases 0.31 ± 0.12 MtC/yr, which is offset by burial of terrestrial biospheric organic carbon in offshore sediments. The latter tips the balance with respect to the total CO2 budget of Taiwan such that the overall system acts as a net sink, with 0.24 ± 0.13 MtC/yr of atmospheric CO2 consumed over geological timescales.

Molecular mechanism for the influence of gender dimorphism on alcoholic liver injury in mice.

It is known that women develop alcoholic liver injury more rapidly and have a lower alcohol toxic threshold than men. However, the detailed molecular mechanisms remain unclear. The precise mechanism responsible for the sex difference needs to be determined. Female and male mice were given ethanol by intragastric infusion every day for 4 weeks. The pathological changes were detected by hematoxylin-eosin, Sirius red, oil red O, periodic acid-Schiff, and Hochest33258 staining in the liver of female and male mice. The related gene and protein expression of hepatocytes stress, proliferation and apoptosis, glycogen synthesis, lipid metabolism, and hepatic fibrosis were also systematically analyzed in the female and male mice. Livers from ethanol-treated female mice had more serious hepatocyte necrosis, liver fibrosis ( P < 0.01), substantial micro/macrovesicular steatosis ( p < 0.01), glycogen consumption ( p < 0.05), and hepatocytes apoptosis ( p < 0.05) than ethanol-treated male mice. The expression of heat shock protein 27 (HSP27), HSP70, proliferating cell nuclear antigen, B-cell lymphoma/leukemia-2 (Bcl-2), and phosphorylated signal transducer and activators of transcription 3 (p-STAT3) was higher in ethanol-treated male mice than ethanol-treated female mice ( P < 0.05 or P < 0.01). But, the expression of Bax (Bcl-2-associated X protein), Caspase 3, CYP2E1 (cytochrome P4502E1), and transforming growth factor ßl had the contrary results. Our study suggested that ethanol treatment induced more expression of HSP27 and HSP70, faster hepatocyte proliferation, higher level of glycogen, and interleukin-6 signaling pathway activation, but less hepatocyte apoptosis and CYP2E1 expression in male mice than female mice, which could be helpful to understand the molecular mechanism for the influence of sex difference on alcoholic liver injury.

MiR-378 promotes the cell proliferation of non-small cell lung cancer by inhibiting FOXG1.

OBJECTIVE: To identify the functioning mode of miR-378 on non-small cell lung cancer (NSCLC) and provide therapeutic targets for NSCLC. PATIENTS AND METHODS: Expression levels of miR-378 in human NSCLC tissue samples and NSCLC-derived cell lines were measured by using quantitative Real-time polymerase chain reaction (PCR). Cell proliferation capacity was assessed by methyl thiazolyl tetrazolium (MTT) assay and colony formation assay. Cell apoptosis and cell cycle distribution were identified by flow cytometry. Downstream target gene was confirmed by using luciferase and Western blotting assays. RESULTS: MiR-378 was significantly elevated in NSCLC tissues when compared with para-carcinoma tissues (n=42). Decreased-miR-378 could attenuate cell proliferation capacity, as well as promoted cell apoptosis and induced cell cycle arrest at G0/G1 phase. FOXG1 was chosen as the target gene of miR-378 by bioinformatics analysis and luciferase reporter assay. Moreover, restoration of miR-378 could impair the tumor suppression role of downregulated-miR-378 on NSCLC growth. CONCLUSIONS: Decreased-miR-378 exerted tumor-suppressive effects on NSCLC growth via targeting FOXG1 in vitro, which provided an innovative and candidate target for diagnosis and treatment of NSCLC.

Identification of glutathione S-transferases in Bemisia tabaci (Hemiptera: Aleyrodidae) and evidence that GSTd7 helps explain the difference in insecticide susceptibility between B. tabaci Middle East-Minor Asia 1 and Mediterranean.

The Bemisia tabaci (Gennadius) (Hemiptera:Aleyrodidae) species complex includes invasive and destructive pests of field crops, and the sibling species MEAM1 and MED are its two most damaging members. Previous research indicated that the replacement of Middle East-Minor Asia 1 (MEAM1) by Mediterranean (MED) as the dominant B. tabaci species in China can be mainly attributed to MED's greater tolerance to insecticides. Glutathione S-transferases (GSTs) play important roles in the detoxification of hydrophobic toxic compounds. To increase our understanding of differences in insecticide resistance between B. tabaci MEAM1 and MED, we searched the genomic and transcriptomic databases and identified 23 putative GSTs in both B. tabaci MEAM1 and MED. Through measuring mRNA levels of 18 of the GSTs after B. tabaci MEAM1 and MED adults were exposed to the insecticide imidacloprid, we found that the expression levels were increased more in B. tabaci MED than in MEAM1 (in particular, the expression level of GST-d7 was increased by 4.39-fold relative to the control). Knockdown of GST-d7 in B. tabaci MED but not in B. tabaci MEAM1 resulted in a substantial increase in the mortality of imidacloprid-treated adults. These results indicate that differences in GST-d7 may help explain why insecticide tolerance is greater in B. tabaci MED than in B. tabaci MEAM1.

MiR-93 inhibition ameliorates OGD/R induced cardiomyocyte apoptosis by targeting Nrf2.

OBJECTIVE: To identify the expression changes of microRNA 93 (miR-93) in oxygen-glucose deprivation/reoxygenation (OGD/R) injury in cardiomyocytes and its mechanism of mediating OGD/R and inducing apoptosis. MATERIALS AND METHODS: Primary cardiomyocytes were extracted and OGD/R model in cardiomyocytes was established in vitro. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect the expressions of miR-93, and Western blot assay was applied to measure the protein levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and caspase-3. Flow cytometry was utilized to examine the cardiomyocyte apoptosis rate. RESULTS: The apoptosis rate was increased after OGD/R in cardiomyocytes, accompanied by remarkable rise of miR-93 expression. After transfection of miR-93 antagomir, the apoptosis rate of cardiomyocyte induced by OGD/R was down-regulated, and the expression of cleaved caspase-3 was decreased. Meanwhile, the results of qRT-PCR and Western blot showed that the levels of Nrf2 mRNA and protein expression were up-regulated after the miR-93 level was inhibited, and luciferase reporter assay affirmed that Nrf2 was a target molecule for OGD/R-induced apoptosis mediated by miR-93. CONCLUSIONS: miR-93 mediates OGD/R-induced hypoxia/reoxygenation injury apoptosis in cells by targeting Nrf2.

Analysis on the relationship and mechanism of high blood pressure and vascular aging on the condition that the gender and age matches.

OBJECTIVE: The relationship between hypertension and the mechanism of the expression of T-lymphocyte Kv1.3 channels in vascular aging has been analyzed in this study based on the gender and age matches' principle. PATIENTS AND METHODS: Thirty patients have been consecutively chosen with vascular aging caused by hypertension (group A), while 30 cases of high blood pressure not merged with vascular aging (group B) were chosen, and 30 cases of healthy volunteers (group C), conforming to gender and age 1:1 and the closest matching principle, were studied. The aim of this study was to separate the peripheral blood mononuclear cells and give intervention of 0.2 nmol/L ANGII to CD4 + T-lymphocytes, and store them in the incubator 48 h. The difference of Kv1.3 channel current of CD4 + T-lymphocyte, mRNA, angiotensin receptor (AT1R) protein mRNA, and IFN-γ density has also been compared. RESULTS: The membrane capacitance, peak current, and current density of group A, are higher than those of the other two groups, and the differences have statistical significance (p<0.05). After adding ANGII intervention to group A, the expression levels of T-lymphocyte Kv1.3 potassium channels mRNA, AT1R mRNA, and IFN-γ are significantly increased, so that the difference has statistical significance p<0.05, while the other two groups have no significant change (p>0.05). The levels of Kv1.3 potassium channels, AT1R mRNA, and IFN-γ of group A before and after the intervention are significantly higher than those of the other two groups, and the differences are statistically significant (p<0.05). CONCLUSIONS: Vascular aging caused by hypertension may be linked to the increase of Kv1.3 potassium channel activity of T-lymphocyte, while ANGII can improve the high expression of Kv1.3 potassium channel and AT1R, to stimulate lymph cells to secrete IFN-γ.

Impact of postoperative pituitary tumor adrenal insufficiency and hormone replacement therapy (HRT) on tumor recurrence.

OBJECTIVE: The present study was aimed to investigate the impact of postoperative pituitary tumor adrenal insufficiency and hormone replacement therapy (HRT) on tumor recurrence. PATIENTS AND METHODS: The prospective study included 143 pituitary tumor patients as study subjects. Within 6 months after the operation, the study was planned to explore differences (if any) between the tumor recurrence rate of patients treated with hormone replacement therapy and the patients without hormone replacement therapy. Also, the relation of tumor reoccurrence was studied with pituitary tumor adrenal insufficiency. RESULTS: The age, gender of patients as well as the size of the tumor had no significant correlation with postoperative pituitary tumor adrenal insufficiency. Further, the short-term follow-up lasting for 0.5 to 2.5 years after the operation, the hormone replacement therapy of hydrogenation had no significant impact on tumor recurrence rate. CONCLUSIONS: The age, patient gender and the size of the tumor were not independent risk factors leading to postoperative pituitary tumor adrenal insufficiency. However, the occurrence rate of adrenal insufficiency of patients in high age group was higher than that of patients in low age group. Also, the occurrence rate of adrenal insufficiency of patients (whose one or several hormones dramatically decreased before the operation) was significantly higher than that of patients (whose hormone level did not decrease before the operation). So, the patients in high age group and whose one or several hormones dramatically decreased before the operation should be paid more attention to the condition of adrenal insufficiency and should be ready for hormone replacement.

Osteogenic potential of three different autogenous bone particles harvested during implant surgery.

OBJECTIVES: The aim was to compare the osteoblast activity and osteogenic potential of autogenous bone particles harvested using three different techniques and determine the most advantageous method of collecting autogenous bone particles. SUBJECTS AND METHODS: Bone particles were harvested from 20 patients during dental implant surgery using bone scraping, low-speed drilling and bone trap filtering. After the osteoblasts were cultured, cell proliferation, migration, mineralization, transcription of osteogenesis-related genes, secretion of osteogenesis-related proteins and osteoinductive protein content in the bone particle matrix were evaluated. RESULTS: Osteoblast activity and osteogenic potential were higher in bone samples harvested by scraper or low-speed drilling than in samples harvested by bone trap filter. Although these parameters were slightly lower in the low-speed drilling group than in the scraper group, significant differences were found only in bone Gla protein levels. However, the levels of osteoinductive proteins in the bone particle matrix were significantly higher in the low-speed drilling group than in the scraper group. CONCLUSIONS: Low-speed drilling is a recommendable and effective technique for collecting autogenous bone particles. In implant operations, low-speed drilling can be considered the first-line option, and if the quantity of harvested bone is insufficient, bone shavings obtained by the scraper may be considered.

Mechanism of action of KIAA1456 gene on the proliferation and apoptosis of alveolar epithelial cells.

OBJECTIVE: To explore the mechanism by which KIAA1456 acts on alveolar epithelial cells through lentiviral transfection. MATERIALS AND METHODS: After constructing a KIAA1456 gene vector, 293T cells were co-transfected with lentiviral vectors and after incubation cells were examined by fluorescence microscopy. CCL-149 cells were transfected with LV-KIAA1456 and were examined by fluorescence microscopy. The proliferation capacity of transfected CCL-149 cells was evaluated using flow cytometry. The effect of KIAA1456 overexpression on CCL-149 cells proliferation was studied using the CCK-8 method. RESULTS: The expression level of KIAA1456 in the LV- KIAA1456 group was significantly higher compared with the LV-Con group and the blank group. Compared with the LV-Con and the blank groups, the proportion of responding cells in G2/M phase showed statistically significant differences. Viable cells had adarker color and higher OD value measured by ELISA. Compared with the control and the blank groups, the growth and proliferation in the CCL-149 transfection group were significantly slower. CONCLUSIONS: KIAA1456 gene inhibited the proliferation of CCL-149 cells by negative regulation of the G2/M cell cycle. We suggest that it can be used as a specific target for the treatment of alveolar epithelium.

Sarcopenia in overweight and obese patients is a predictive factor for postoperative complication in gastric cancer: A prospective study.

BACKGROUND: Sarcopenia is a syndrome characterized by progressive and generalized loss of skeletal muscle mass and strength. This study aims to explore the prevalence of sarcopenia in overweight and obese gastric cancer (GC) patients and figured out the impacts of sarcopenia on the postoperative complication of overweight and obese GC patients. METHODS: According to the recommended body-mass index (BMI) for Asian populations by WHO, we conducted a prospective study of overweight and obese gastric cancer patients (BMI ≥ 23 kg/m2) under curative gastrectomy from August 2014 to December 2015. Including lumbar skeletal muscle index, handgrip strength and gait speed as the sarcopenic components were measured before surgery. Patients were followed up after gastrectomy to gain the actual clinical outcomes. Factors contributing to postoperative complications were analyzed by univariate and multivariate analysis. RESULTS: Total of 206 overweight or obese patients were enrolled in this study, 14 patients were diagnosed sarcopenia and were demonstrated having significantly association with higher risk of postoperative complications, higher hospital costs, and higher rate of 30-days readmission compared with the non-sarcopenic ones. On the basis of univariate and multivariate analysis, sarcopenia was an independent risk factor for postoperative complication of overweight and obese patients with gastric cancer (P = 0.002). CONCLUSION: Sarcopenia is an independent predictor of postoperative complications in overweight or obese patients with gastric cancer after radical gastrectomy.

Ion transport peptide (ITP) regulates wing expansion and cuticle melanism in the brown planthopper, Nilaparvata lugens.

Ion transport peptide (ITP) and its alternatively spliced homologous ITP-like (ITPL) products play important roles in various insect developmental processes. We found for the first time that alternative 5' untranslated regions (5' UTRs) of ITPL (NilluITPLs-1, -2, -3 and -4) control spatiotemporal expression in the brown planthopper, Nilaparvata lugens, as demonstrated by reverse-transcription quantitative PCR. By using an alternative 5' UTR, NilluITPL-1 was expressed exclusively in the male reproductive system, resulting in the production of the NilluITPL seminal fluid protein. Interestingly, NilluITPLs-3 and -4 were expressed exclusively in the integument, indicating a specialized function for NilluITPL during ecdysis and eclosion. We investigated the functions of NilluITP and NilluITPL using RNA interference (RNAi). We did not observe apparent phenotypes when expression of NilluITPLs was suppressed. However, when NilluITP expression was suppressed, the insect exhibited melanism and failed wing expansion, indicating that NilluITP is a neuropeptide associated with wing expansion in addition to bursicon. Additionally, in contrast to bursicon, the insects showed increased melanism when NilluITP was eliminated by RNAi. Unlike previous studies of ITP/ITPL in other species, NilluITP was very important in the control of N. lugens postecdysial behaviours but was not critical during ecdysis. Thus, the functions of ITP and ITPL are more complex in insects than previously thought.

Clinical evaluation of salivary carbohydrate antigen 125 and leptin in controls and parotid tumours.

OBJECTIVES: We determined the correlation between saliva and serum for CA125 and leptin, and evaluated their clinical screening potential for parotid tumours. SUBJECTS AND METHODS: Serum, acid-stimulated bilateral parotid saliva and chewing-stimulated whole saliva were collected and measured the levels of CA125 and leptin with electrochemiluminescence immunoassay and enzyme-linked immunosorbent assay for healthy controls and patients with unilateral parotid tumour. Intra- and intergroup comparisons were made among them. Correlations and receiver operating curve analyses were also conducted. RESULTS: There was no correlation between salivary and serum CA125 (r = -0.157-0.265, P > 0.05), while significant correlation was found for leptin (r = 0.219-0.761, P < 0.05). Leptin levels in tumour parotid saliva and CA125 levels in whole saliva were elevated significantly (P < 0.001) and showed screening potential for parotid tumours. Salivary and serum leptin levels were significantly higher in women than in men (P < 0.001). CONCLUSIONS: Salivary CA125 might originate primarily from salivary gland and tumour rather than from blood, while salivary leptin might originate from both blood and salivary gland. Multiple sources might contribute to the significantly elevated CA125 in whole saliva. Whole saliva CA125 and parotid saliva leptin reflected the occurrence of parotid tumours, while serum CA125 and leptin did not. Salivary CA125 and leptin could not distinguish malignant parotid tumours. When detecting leptin level, the influence of subjects' sex must be considered.

Selenium protects reproductive system and foetus development in a rat model of gestational lead exposure.

OBJECTIVE: Lead is a common environmental contaminant. Lead accumulation in the body is especially dangerous for pregnant women and newborns. Selenium is a trace element which may rectify the damaging effects of lead. Here we tested potential protective effects of selenium against gestational lead exposure. MATERIALS AND METHODS: Pregnant SD rats were exposed to 200 mg/L of lead acetate (given with water), with or without sodium selenite supplementation (2-8 mg/kg/day via intragastric administration). Pregnant rats not exposed to lead or selenium served as control animals. The outcomes in pregnant rats were serum lead and selenium levels, reproductive hormone (follicle-stimulating hormone, luteinizing hormone, prolactin, oestradiol, progesterone) levels, and uterine and ovarian morphological changes. The outcomes in the offspring were sex differentiation, survival rates (day 21 after birth), weight (days 0-35 after birth), weight of reproductive organs, and puberty onset (foreskin separation or vaginal opening). RESULTS: Selenium supplementation dose-dependently decreased serum lead levels, rectified reproductive hormone levels, and attenuated reproductive morphological changes caused by lead exposure. Lead exposure did not affect sex differentiation, but significantly (p < 0.05 vs. control animals) decreased the offspring weight on days 0-28 and the weight of their reproductive organs. Furthermore, lead exposure delayed the onset of puberty. These pathological changes were dose-dependently rectified or attenuated by selenium supplementation. CONCLUSIONS: Gestational lead exposure causes damages to the reproductive system of pregnant rats, and negatively modulates growth and reproductive system development of the offspring. These adverse effects are rectified or attenuated by selenium supplementation.

Feasibility of radical gastrectomy for elderly patients with gastric cancer.

BACKGROUND: The aim of this study was to evaluate the short-term safety and long-term benefits of radical gastrectomy for gastric cancer in elderly patients. METHODS: A total of 729 patients undergoing gastrectomy for adenocarcinoma between December 2008 and December 2011 were enrolled in this retrospective study. Patients were divided into three groups: young group (<65 years), young-old group (65-79 years) and old-old group (≥80 years). RESULTS: Lower albumin levels, higher ASA grades, comorbidities, tumors located in the upper third of the stomach and advanced TNM stages were more common in the young-old and old-old age groups. Overall complications increased significantly with advancing age (15.4%, 24.9%, 48.7%, respectively); respiratory complications largely contributed to the dramatic increase. Severe complications were similar between the young and young-old groups (3.9%, 3.7%), but were significantly increased in the old-old group (12.8%). In multivariate analysis, old-old age, multiple comorbidities and no epidural use were strong predictors for overall complications. Both overall survival and disease-specific survival (DSS) rates declined with advancing age. Multivariate analysis showed that old-old age and TNM stage ≥ II were major independent risk factors for the DSS rate. When adjusted for confounding factors, young-old age was not a risk factor. The median survival time for the old-old patients with stage III tumors was 12.9 months. CONCLUSIONS: It is relatively safe and beneficial for young-old patients to undergo radical gastrectomy as the young patients. However, the decision to perform radical gastrectomy for old-old patients with TNM stage III tumors should be made carefully.