[Infection status and Molecular types of Rhinovirus among Cases of Acute Respiratory Tract Infections in Luohe City, Henan Province, from 2017 to 2022].

Objective: To understand the infection status and molecular types of rhinovirus (RV) among cases of Acute Respiratory Infections (ARIs) in Luohe City, Henan Province, from 2017 to 2022. Methods: From October 2017 to June 2022, clinical and epidemiological data were collected from 2 270 cases of ARIs at Luohe Central Hospital in Henan Province. Throat swab specimens were obtained from these cases. Real-time quantitative polymerase chain reaction (qPCR) was used to screen for RV-positive specimens. Subsequently, the positive samples were subjected to nested reverse transcription polymerase chain reaction (nested RT-PCR) to amplify the full-length VP1 region. Using the MEGA software, along with 169 RV reference strains recommended by the International Committee on Taxonomy of Viruses, a phylogenetic tree was constructed to determine RV types. Results: Among the 2 270 cases of ARIs, there were 1 283 male cases (56.52%). The median age (Q1, Q3) was 3 (1, 6) years, with the population under 5 years old accounting for 68.59% (1 557/2 270). RV was detected in 137 cases (6.04%), of which 68 cases (49.64%) showed co-detection with other viruses, with the most common being co-detection with enterovirus, accounting for 14.60% (20/137). The RV detection rates in the age groups of 0~4 years, 5~14 years, 15~59 years, and≥60 years were 6.42% (100/1 557), 4.69% (21/448), 3.80% (6/158), and 9.35% (10/107), respectively, with no statistically significant differences (χ2=5.310, P=0.150). The overall detection rates of RV before (2017-2019) and during (2020-2022) the COVID-19 pandemic showed no statistically significant difference (χ2=1.823, P=0.177). A total of 109 VP1 sequences were obtained, including 62 types. Among them, RV-A, RV-B, and RV-C had 42, 3, and 17 types respectively. Conclusion: RV is one of the predominant pathogens in ARIs cases in Luohe City, Henan Province, from 2017 to 2022. Multiple types of RV co-circulate without any apparent dominant type.

[Outcomes and complications of open versus closed reduction and internal fixation for Delbet type â ¡ and â ¢ hip fractures in children and adolescents].

OBJECTIVE: To compare the outcomes and complications of open versus closed reduction and internal fixation for Delbet type Ⅱ and Ⅲ hip fractures in children and adolescents. METHODS: We retrospectively analyzed the data of 42 patients with Delbet type Ⅱ (22 cases) and Ⅲ (20 cases) hip fractures (including 24 male and 18 female patients with a mean age of 8.19± 3.23 years, range 2-15 years) admitted in the Fifth and Third Affiliated Hospital of Southern Medical University from January, 2013 to January, 2022. Nineteen of the patients received closed and 23 underwent open reduction and internal fixation. The operation time, postoperative healing time, and Ratliff standard hip function results were compared between the two groups, and the incidences of such complications as premature epiphyseal closure and femoral head necrosis were analyzed. RESULTS: All the patients were followed up for 13-84 months (mean 36.04±8.23 months). The operation time of closed reduction and internal fixation was significantly shorter than that of open surgery (68.23±24.68 vs 119.71±32.75 min, P < 0.05). All the patients showed good fracture healing after the operations with similar healing time between the two groups (3.32±0.31 vs 3.18±0.20 months, P > 0.05). The rate of excellent and good hip joint function was 90.48% in the overall patients and showed no significant difference between the two groups (17/19 vs 21/23, P > 0.05). The incidences of premature epiphyseal closure (3/19 in closed vs 4/23 in open reduction group, P > 0.05) and femoral head necrosis (2/19 vs 1/23, P > 0.05) were comparable between the two groups. CONCLUSIONS: In children and adolescents, open reduction can achieve definite surgical effect for Delbet type Ⅱ and Ⅲ hip fractures, but closed reduction and internal fixation are recommended when anatomic reduction can be achieved. Premature epiphyseal closure and femoral head necrosis are common and serious complications of these fractures.

[Analysis of safety and factors influencing the surgical efficacy of benign biliary stenosis treated with autologous gastric flap repair with the vascular tip].

Objective: To investigate the complication rate and risk factors associated with using autologous gastric flap tissue with a vascular tip to treat benign biliary strictures. Methods: A retrospective analysis was conducted on clinical data of 92 patients with benign biliary stenosis who applied autologous gastric flap tissue to repair the stenosis at the PLA General Hospital from January 2006 to May 2022. Among them, there were 40 males and 52 females, aged from 25 to 79 (50.5±12.9) years. The perioperative clinical data of the patients were recorded(Body Mass Index、preoperative platelets et.), and a multivariate logistic regression model was used to analyze the factors influencing postoperative complications. Long-term follow-up was conducted to evaluate the long-term efficacy of autologous gastric flap tissue with vascular tissues for benign biliary stenosis surgery. Results: The incidence of recent postoperative complications in patients was 26.1%, and univariate analysis showed that preoperative bile-intestinal anastomosis, positive intraoperative bile bacterial culture, low preoperative hemoglobin, and low preoperative platelet count were significantly associated with the occurrence of postoperative complications after biliary stenosis repair with a vascularized gastric flap (P<0.05). Multifactorial analysis showed that low preoperative platelets (OR=0.990, 95%CI: 0.982-0.998, P=0.015), low preoperative hemoglobin (OR=4.953, 95%CI: 1.405-15.010, P=0.012) and positive intraoperative bile bacterial culture (OR=19.338, 95%CI: 3.618-103.360, P<0.001) were independent risk factors for the development of postoperative complications. The excellent long-term follow-up rate of patients was 92.0%. Conclusions: The procedure of repairing benign biliary stenosis with a vascularized gastric flap preserves the function of the sphincter of Oddi and reconstructs the normal physiological passage of the bile duct. This procedure is safe and feasible and provides a reliable option for the surgical treatment of bile duct injury and bile duct stenosis.

QTc interval prolongation during recovery from brief high-intensity intermittent exercise in obese adults.

The risk of malignant arrhythmias is higher during extremely intense exercise and after its cessation. It is still unclear whether high-intensity interval exercise (HIE), an increasingly popular option in preventive and rehabilitative medicine, can lead to an impaired electrophysiological milieu, as revealed by QT interval prolongation on an electrocardiogram. This study investigated heart rate-corrected QT interval (QTc) dynamics during recovery from HIE in obese adults. In total, 13 obese males (age: 24.3 ± 4.6 years old; body mass index: 31.6 ± 4.1 kg/m2) underwent: (1) HIE: an HIE session of four 30-s all-out cycling efforts interspersed with 4­min recovery periods; (2) REC: a recovery session 24 h after HIE; and (3) CON: a control session of no treatment. The QT interval was measured before HIE, REC, and CON, and then at 30-min intervals thereafter, for up to 3 h. QTc values were obtained using Bazett, Fridericia, Framingham, Hodges, and Rautaharju correction formulas. Acute HIE led to a significant increase in QTc for each correction (by 5-47 ms, all p < 0.05), and QTc was significantly longer during early recovery from acute exercise (HIE) compared with CON corrected with the Bazett (by 49 ms), Fridericia (by 11 ms), Hodges (by 27 ms), and Rautaharju (by 15 ms) formulas (all p < 0.05). Further, the QTc for each correction at most of the observation points in the REC trial was significantly longer (by 5-10 ms, all p < 0.05) than the corresponding value of the CON. In conclusion, in obese adults, the risk of QTc prolongation increased after brief HIE, and the risk may be sustained for more than 24 h.

Radiomics signature based on FDG-PET predicts proliferative activity in primary glioma.

AIM: To investigate a radiomics method based on 2-[18F]-fluoro-2-deoxy-d-glucose (FDG) positron-emission tomography (PET) to non-invasively evaluate proliferative activity in gliomas. MATERIALS AND METHODS: A total of 123 patients with histopathologically confirmed primary glioma were reviewed retrospectively and assigned randomly into the primary cohort (n=82) and validation cohort (n=41). Tumour proliferative activity was defined by the Ki-67 index based on immunohistochemistry. Standard uptake value (SUV) maps were generated, and 1,561 radiomics features were extracted. Radiomics features were selected through the sequential application of three algorithms. Three predictive signatures were generated: a radiomics signature, a clinical signature, and a fusion signature. The predictive performances were evaluated by receiver operating characteristic (ROC) curve analysis, and patient prognoses were stratified based on the Ki-67 index and the signature with the most reliable performance. RESULTS: Nine radiomics features were selected to construct the radiomics signature that achieved an accuracy of 81.7% and 73.2% and an area under the curve (AUC) of 0.88 and 0.76 in the primary cohort and the validation cohort, respectively. The clinical signature and fusion signature demonstrated comparable performance in the primary cohort but were over-fitted judging from the result in the validation cohort. Both the Ki-67 index and the radiomics signature could stratify patients into two distinctive prognostic groups, and the difference within each prognostic group was not statistically significant. CONCLUSION: Radiomics signature based on 18F-FDG-PET is a promising method for the non-invasive measurement of glioma proliferative activity and facilitates the prediction of patient prognoses.

[The association between Cathepsin S and pulmonary function and CT phenotypes in patients with chronic obstructive pulmonary disease].

Objective: To explore the value of cathepsin S in the bronchoalveolar lavage fluid (BALF) of patients with chronic obstructive pulmonary disease (COPD) in the evaluation of pulmonary function and CT phenotypes. Method: From April 2014 to April 2017, 46 patients with stable COPD were enrolled, and 29 healthy volunteers served as the control group. The patients were divided into 4 subgroups: GOLD Ⅰ(n=12), GOLD Ⅱ(n=6), GOLD Ⅲ(n=14), GOLD Ⅳ(n=14). The levels of cathepsin S and IFN-γ in BALF were determined by enzyme-linked immunosorbent assay (ELISA). The percentage ratio of low attenuation area to total lung area (LAA%), two times the ratio of airway wall thickness to outer diameter(2T/D), and the ratio of wall area to total cross-sectional area (WA) were measured by HRCT. Results: There were significant differences in the levels of cathepsin S in BALF between the groups (F=6.639, P=0.000). BALF cathepsin S levels were as follows: GOLD Ⅳ grou P>GOLD Ⅲ grou P>GOLD Ⅱ grou P>GOLD group Ⅰ >healthy control group (P value were all<0.05); LAA grade 3>LAA grade 2>LAA grade 1>LAA grade 0 (P value were all<0.05). Correlation analysis showed that BALF cathepsin S levels were correlated negatively with FEV(1)/FVC, FEV(1)% predicted, and DLCO% (r value was -0.065、-0.576、-0.392, respectively, P value were all<0.05), and but positively with RV/TLC%, LAA%, 2T/D, WA and IFN-γ(r value was 0.695, 0.497, 0.142, 0.309, 0.148, respectively, P value were all<0.05). Conclusion: The levels of cathepsin S were associated with the degree of airflow limitation and emphysema phenotype in COPD.

[The inhibition effects of apatinib on cell proliferation, migration and apoptosis in esophageal carcinoma via Ras/Raf/MEK/ERK and JAK2/STAT3 pathways].

Objective: To investigate the in vitro and in vivo effects of apatinib in esophageal squamous cell carcinoma and the underlying mechanisms. Methods: The esophageal cancer cells, KYSE-150 and ECA-109, were divided into control group and apatinib treatment group at the concentrations of 2.5, 5, 10, 20 and 40 µmol/L respectively. All of experiments were performed in triplicate. MTT and colony formation assays were used to measure cell proliferation. Transwell assay was used to determine the migration capacity. The effect of apatinib on cell cycle and apoptosis was analyzed by flow cytometry. The expression of VEGF and VEGFR-2 was measured by real-time quantitative PCR (qRT-PCR). The concentration of VEGF in the cell supernatant was assessed by enzyme-linked immunosorbent assay (ELISA). The expression levels of MEK, ERK, p-MEK, p-ERK, JAK2, STAT3 and p-STAT3 after VEGF stimulation were detected by Western blot. Furthermore, the nude mice xenograft model was established. The tumor-bearing mice were randomly divided into control group, apatinib low dose treatment group (250 mg) and apatinib high dose treatment group (500 mg), respectively. Tumor inhibition rates of different groups were calculated. And then the expressions of VEGF and VEGFR2 were detected in xenograft tissues by immunohistochemical staining. Results: In the presence of 20 µmol/L and 40 µmol/L of apatinib for 24 hours, the migration cell numbers of KYSE-150 and ECA-109 were 428.67±4.16 and 286.67±1.53 as well as 1 123.67±70.00 and 477.33±26.84, respectively, that were significantly lower than control group (P<0.05 for all). In addition, after treatment with 10 µmol/L, 20 µmol/L and 40 µmol/L of apatinib for 7 days on KYSE-150 and ECA-109, the colony formation rates were (65.12±25.48)%, (58.19±24.73)% and (29.10±22.40)% as well as (70.61±15.14)%, (61.12±17.21)% and (43.09±11.13)%, respectively. The colony formation rates of 20 µmol/L and 40 µmol/L of apatinib treatment groups were significantly lower than control group (100.00±0.00, P<0.05). The cell cycle ratio of G(2)/M phase and apoptosis rate of control group and 20 µmol/L apatinib group in KYSE-150 cells were (12.14±2.13)% and (3.49±0.74)% as well as (26.27±3.30)% and (15.65±1.54)%, respectively. The corresponding ratios in ECA-109 cells were (3.44±0.57)% and (6.31±1.43)% as well as (22.64±2.36)% and (49.26±1.62)%, respectively. The results show that apatinib suppressed cell cycle progression at G(2)/M phase and induced cell apoptosis in both KYSE-150 and ECA-109 cells (P<0.05 for all). In the presence of 20 µmol/L and 40 µmol/L of apatinib in KYSE-150 cells, the relative levels of VEGF mRNA were (42.57±10.43)% and (25.69±1.24)%, and those of VEGF-2 mRNA were (36.09±10.82)% and (13.99±6.54)%, which were all significantly decreased compared to control group (100.00±0.00, P<0.05 for all). For ECA-109 cells, the relative expression of VEGF and VEGFR2 showed similar tendency (P<0.05 for all). Moreover, after treatment with 20 µmol/L and 40 µmol/L of apatinib in KYSE-150 cells, the VEGF concentrations were (766.48±114.27) pg/ml and (497.40±102.18)pg/ml, which were significantly decreased compared to control group [(967.41±57.75) pg/ml, P<0.05)]. The results in ECA-109 were consistent (P<0.05). Furthermore, after treatment with 40 µmol/L of apatinib in KYSE-150 and ECA-109, the relative expression of p-MEK and p-ERK were 0.49±0.05 and 0.28±0.03 as well as 0.63±0.03 and 1.22±0.15, which were significantly lower than control group (1.23±0.19 and 0.66±0.07 as well as 1.03±0.20 and 1.76±0.20; P<0.05). The relative expression of STAT3, p-STAT3 in control group and experimental group were 0.96±0.15 and 0.85±0.16 as well as 0.62±0.09 and 0.36±0.13, respectively. The results showed that the protein levels of STAT3 and p-STAT3 were significantly lower than the control group (P<0.05 for all). The inhibition rates of apatinib in xenograft nude mice were 29.25% and 19.96% for 250 mg and 500 mg treatment groups. The concentration of VEGF were (25.11±4.12) pg/ml, (16.40±2.81) pg/ml and (15.04±4.88)pg/ml for control, 250 mg and 500 mg treatment groups, respectively. Conclusions: Apatinib can inhibit cell proliferation, induce apoptosis and suppress migration of esophageal cancer cells in vitro and in vivo. This effect was mainly mediated via the alterations of Ras/Raf/MEK/ERK pathway and JAK2/STAT3 pathway.

Screening and functional analysis of micro-RNAs that regulate the expression of the tumor suppression TP53 gene.

OBJECTIVE: With gradual increase of cancer incidence and mortality rates, the regulatory mechanism of cancer has become a hotspot. It has been known that the expression of TP53 is closely associated with the occurrence of cancer. The microRNA (miRNA)-mediated regulation of the expression of numerous proto-oncogenes has been reported. This study aimed to identify miRNAs that regulate the expression of TP53 gene. MATERIALS AND METHODS: The sequence of TP53 gene was downloaded from NCBI and analyzed with TargetScan software to predict potential miRNAs that regulate TP53 expression. miR-122 was selected as the most potential miRNA for regulating TP53. miR-122 mimics and inhibitor were synthesized and transfected into Hela cells. The expression of TP53 mRNA was measured by qRT-PCR. The cell proliferation, migration, and invasion ability were assessed by CCK-8, scratch wounding, and transwell invasion assay, respectively. RESULTS: Cells transfected with miR-122 mimics exhibited significantly lower TP53 expression (p < 0.05), but significantly increased cell proliferation and migration compared with blank control group (p < 0.05). Notably, cells in miR-122 mimics and control groups had similar invasion ability (p > 0.05). However, cells in miR-122 inhibitor group exhibited significantly higher TP53 expression (p < 0.05), but significantly reduced cell proliferation and invasion ability. The migration ability of cells in miR-122 inhibitor group was similar to cells in control group (p > 0.05). CONCLUSIONS: The selected miR-122 effectively inhibited the expression of TP53 gene in Hela cells, and enhanced their proliferation, migration, and invasion.

[Correlation analysis of serum secreted frizzled-related protein 5 levels with airway inflammation and insulin resistance in chronic obstructive pulmonary disease patients].

Objective: To investigate the relationship between serum secreted frizzled-related protein 5(sfrp5) levels, insulin resistance, and airway inflammation in patients with chronic obstructive pulmonary disease(COPD). Method: A total of 178 COPD patients visiting our respiratory outpatient clinic from February 2015 to January 2017 were enrolled, and 99 healthy control subjects from the same time period were selected. Serum sfrp5 levels were compared between the 2 groups. Serum sfrp5 and inflammatory cytokines in induced sputum were observed in the 4 subgroups: insulin resistant COPD group [homeostasis model assessment of insulin resistance (HOMA-IR)≥2.29], non-insulin resistant COPD group, non-COPD insulin resistant group, and healthy control group. Results: Serum sfrp5 levels were found to be significantly higher in the COPD group as compared to the healthy control group (t=-14.29, P<0.001). Serum sfrp5 levels in the insulin resistant COPD group [(8±3)ng/ml] were significantly lower than that of the non-insulin resistant COPD group [(10±5)ng/ml], non-COPD insulin resistant group [(13±3)ng/ml], and normal control group [(14±4)ng/ml, F=35.85, P<0.01]. The insulin resistant COPD group had higher levels of In(Homa-IR), as well as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in induced sputum as compared to the non-insulin resistant COPD group, non-COPD insulin resistant group, and healthy control group (F values were 64.968, 41.40, 64.15, respectively, P value <0.01 for all items). The non-insulin resistant COPD group had higher levels of In(HOMA-IR) as well as TNF-α and IL-6 in induced sputum as compared to the non-COPD insulin resistant group and healthy control group. FEV(1)/FVC and FEV(1)% predicted were significantly lower in the insulin resistant COPD group as compared to those of non-insulin resistant COPD group and non-COPD insulin resistant group, and healthy control group (F values were 2.481 and 8.37, respectively, P value<0.05 for all items). FEV(1)/FVC and FEV(1)% predicted were significantly lower in the non-insulin resistant COPD group as compared to those of the healthy control group and non-COPD insulin-resistant group. Serum sfrp5 levels were positively correlated to FEV(1)/FVC and FEV(1) predicted (r values were 0.466 and 0.412, respectively; P values were <0.001 and 0.007, respectively) and inversely correlated to In(HOMA-IR) and TNF-α and IL-6 in induced sputum (r values were -0.304, -0.459, -0.517, respectively; P values were <0.001, 0.002, <0.001, respectively). BMI, ln(HOMA-IR), and IL-6 in induced sputum were independent related factors (r(2) values were 0.286, 0.176, 14.69, respectively; P values were <0.01 for all items) Conclusion: Sfrp5 may be concurrently associated with COPD and insulin resistance; insulin resistance may be associated with airway inflammation and airflow limitation. Sfrp5 may be involved in the development of COPD and may be the key link by which insulin resistance exerts its effects on airway inflammation.

Shortage of dNTPs underlies altered replication dynamics and DNA breakage in the absence of the APC/C cofactor Cdh1.

The APC/C-Cdh1 ubiquitin-ligase complex targets cell cycle regulators for proteosomal degradation and helps prevent tumor development and accumulation of chromosomal aberrations. Replication stress has been proposed to be the main driver of genomic instability in the absence of Cdh1, but the real contribution of APC/C-Cdh1 to efficient replication, especially in normal cells, remains unclear. Here we show that, in primary MEFs, acute depletion or permanent ablation of Cdh1 slowed down replication fork movement and increased origin activity. Partial inhibition of origin firing does not accelerate replication forks, suggesting that fork progression is intrinsically limited in the absence of Cdh1. Moreover, exogenous supply of nucleotide precursors, or ectopic overexpression of RRM2, the regulatory subunit of Ribonucleotide Reductase, restore replication efficiency, indicating that dNTP availability could be impaired upon Cdh1 loss. Indeed, we found reduced dNTP levels in Cdh1-deficient MEFs. Importantly, DNA breakage is also significantly alleviated by increasing intracellular dNTP pools, strongly suggesting that genomic instability is the result of aberrant replication. These observations highlight the relevance of APC/C-Cdh1 activity during G1 to ensure an adequate supply of dNTPs to the replisome, prevent replication stress and the resulting chromosomal breaks and, ultimately, suppress tumorigenesis.

Induction of cell cycle arrest and apoptosis by grape seed procyanidin extract in human bladder cancer BIU87 cells.

OBJECTIVE: The aim of this study was to evaluate the effects of grape seed procyanidin extract (GSPE) on cell proliferation and apoptosis in human bladder cancer BIU87 cells and to investigate its molecular mechanism in vitro. MATERIALS AND METHODS: BIU87 cells were treated with different concentrations of GSPE for 24h in vitro while an untreated group was taken as control. MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay, Hoechst 33258 staining, flow cytometry, RT-PCR and Western blot were used to detect the anti-proliferation and apoptotic induction effects of GSPE on BIU87 cells. RESULTS: It was found that GSPE inhibited the cell growth through cell cycle arrest at G1 phase and induced cell apoptosis in BIU87 cells in a dose-dependent manner. Semi-quantitated RT-PCR and Western blot analyses indicated that GSPE increased caspase-3 (p<0.01), but decreased the expression of cyclinD1, CDK4 and survivin (p<0.01). CONCLUSIONS: GSPE inhibits cell proliferation by inducing cell cycle arrest and apoptosis in BIU87 cells, and the effect may be related with its down-regulation of cyclinD1, CDK4 and survivin.

Melioidosis acquired by a traveler from Papua New Guinea.

Melioidosis is an infectious disease caused by Burkholderia pseudomallei. Melioidosis is of public health importance in endemic areas, particularly in tropical and sub-tropical areas. We describe a case of melioidosis contracted by a man with diabetes from Papua New Guinea that was evaluated using multi-locus sequence typing and whole genome sequencing.

Development of expressed sequence tag-simple sequence repeat markers for Chrysanthemum morifolium and closely related species.

With the development of chrysanthemum breeding in recent years, an increasing number of wild species in genera related to Chrysanthemum were introduced to extend the genetic resources and facilitate the genetic improvement of chrysanthemums via hybridization. However, few simple sequence repeat (SSR) markers are available for marker-assisted breeding and population genetic studies of chrysanthemum and closely related species. Expressed sequence tags (ESTs) in public databases and cross-species transferable markers are considered to be a cost-effective means for developing sequence-based markers. In this study, 25 EST-SSRs were successfully developed from Chrysanthemum EST sequences for Chrysanthemum morifolium and closely related species. In total, 4164 unigene sequences were assembled from 7180 ESTs of chrysanthemum in GenBank, which were subsequently used to screen for the presence of microsatellites with the SSRIT software. The screening criteria were 8, 5, 4, and 3 repeating units for di-, tri-, tetra-, and penta- and higher-order nucleotides, respectively. Moreover, 310 SSR loci from 296 sequences were identified, and 198 primer pairs for SSR amplification were designed with the Primer Premier 5.0 software, of which 25 SSR loci showed polymorphic amplification in 52 species and varieties belonging to Chrysanthemum, Ajania, and Opisthopappus. The application of EST-SSR markers to the identification of intergeneric hybrids between Chrysanthemum and Ajania was demonstrated. Therefore, EST-SSRs can be developed for species that lack gene sequences or ESTs by utilizing ESTs of closely related species.

Effects of different exercise durations on Keap1-Nrf2-ARE pathway activation in mouse skeletal muscle.

The purpose of this study was to investigate the effects of acute exercise stress on the nuclear factor-erythroid2 p45-related factor 2 (Nrf2)/antioxidant response element (ARE) transactivation, Kelch-like ECH-associated protein 1 (Keap1) cytosolic protein and Nrf2 nucleoprotein expressions, Nrf2 target genes mRNA expressions, and glutathione redox (GSH/GSSG) ratio level; with a particular focus on the changes in Keap1-Nrf2-ARE pathway activation following different durations of exercise. Wild-type mice (C57BL/6J, two months old) were separated into one-hour and six-hour treadmill running groups, as well as a non-exercise control group (n = 10 in each group). Measurements of Nrf2/ARE transactivation, Nrf2 nucleoprotein expressions, Keap1 cytosolic protein expression, Nrf2 target genes' mRNA expressions (superoxide dismutase-1 [SOD1], superoxide dismutase-2 [SOD2], γ-glutamyl cysteine ligase-modulatory [GCLm], γ-glutamyl cysteine ligase-catalytic [GCLc], glutathione reductase [GR], glutathione peroxidase-1 [Gpx1], catalase [CAT], and hemoxygenase-1 [Ho-1]), and GSH/GSSG ratio were carried out immediately after exercise. The results showed significant increases in Keap1-Nrf2-ARE pathway activation and the mRNA expressions of six measured enzymes in skeletal muscle after six hours of exercise; while in the one-hour exercise group, there was no change in Keap1-Nrf2-ARE pathway activation and only two enzymes' mRNA expressions were increased. It is suggested that the changes in Keap1-Nrf2-ARE pathway activation and its target genes' mRNA expressions were dependent on the exercise duration, with longer duration associated with higher responses.

Effect of home processing on the distribution and reduction of pesticide residues in apples.

The effect of home processing (washing, peeling, coring and juicing) on residue levels of chlorpyrifos, ß-cypermethrin, tebuconazole, acetamiprid and carbendazim in apple segments was investigated. The pesticide residues were determined by UPLC-MS/MS and GC with a flame photometric (FPD) and electron capture detection (ECD). The results indicated that the pesticide residue levels in the apple peel and core were higher compared with in the apple flesh. After peeled and cored apple was processed into apple juice and pomace, chlorpyrifos, ß-cypermethrin and tebuconazole were concentrated in the apple pomace. However, residues of acetamiprid and carbendazim were exceptions. The apple pomace was free of acetamiprid, which was mainly present in the apple juice. After washing the mean loss of chlorpyrifos, ß-cypermethrin, tebuconazole, acetamiprid and carbendazim from apples under recommended dosage and twofold higher dosage were 17-21%, 6.7-7.1%, 13-32%, 42-67% and 47-50%, respectively. The pesticide residues were significantly reduced in the edible part of the apple except for ß-cypermethrin during peeling and coring process. The removal effect of apple juicing was found to be the most pronounced on ß-cypermethrin residue, which was reduced in the range of 81-84%, and the reductions of chlorpyrifos, tebuconazole, acetamiprid and carbendazim upon apple juicing were in the range of 15-36%.

Antioxidant enzyme activities and lipid peroxidation induced by eicosapentaenoic acid (EPA) in PC12 cells.

Eicosapentaenoic acid (EPA) is one of the major dietary polyunsaturated fatty acids and induces apoptosis in several cancer cells. In this study, the EPA induced lipid peroxidation and response of antioxidative enzymes have been investigated in rat pheochromocytoma PC12 cells to elucidate the mechanisms of apoptosis induced by the polyunsaturated fatty acid EPA. We have analyzed superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities and glutathione (GSH) contents in PC12 cells after exposure to different concentrations of EPA. Lipid peroxidation was shown to increase in the presence of EPA as an indication of the oxidative damage. Lipid peroxidation was enhanced by EPA in a dose-dependent manner, and the loss of cell viability was partially reversed by vitamin E. In the case of antioxidant enzyme activities, SOD and GPX activities and GSH contents increased significantly at 50 micromol/L EPA and were respectively 2.41-fold (p < 0.01), 3.49-fold (p < 0.05), and 1.43-fold (p < 0.05) higher than controls. The CAT activity at 10 micromol/L had the highest value and was increased by 25.83% (p < 0.05) compared to control. The results suggest that in PC12 cells the mechanism of apoptosis induced by EPA may be partly due to lipid peroxidation.

Mapping QTL associated with resistance to Fusarium head blight in the Nanda2419 x Wangshuibai population. II: type I resistance.

Fusarium head blight (FHB) is a serious disease in wheat and barley affecting both yield and quality. To identify genes for resistance to infection, the RIL population derived from 'Nanda2419' x 'Wangshuibai' and the parents were evaluated for percentage of infected spikes (PIS) in four different environments. Using a 2,960 cM marker framework map constructed for this population, ten chromosome regions were detected for their association with type I resistance through interval mapping with Mapmaker/QTL, among which QTLs mapped in the intervals of Xwmc349--Xgwm149 on chromosome 4B, of Xwmc96--Xgwm304 on chromosome 5A and of Xgwm408--Xbarc140 on chromosome 5B were revealed in at least three environments and have Wangshuibai as the source of resistance alleles. Qfhi.nau-4B and Qfhi.nau-5A had larger effects and explained up to 17.5 and 27.0% of the phenotypic variance, respectively. To detect epistasis QTLs, two-locus interactions were examined by whole genome scan. Interactions of five locus pairs were found to have significant effects on type I resistance with the LOD score ranging 3.8-6.5 and four of them conferred resistance in parental phase. The one with the most significant effect was Xcfd42--Xgwm469 (6D)/Xwmc390-2--Xbd04 (2A) pair. No QTL x E interaction was detected for PIS. It was found that flowering time did not have significant effects on PIS in this population. Our studies indicated that Wangshuibai is useful for breeding for both type I and type II scab resistance and the markers associated with the QTLs could be used in marker-assisted selection and isolation of scab-resistance QTLs.

Mapping QTL associated with resistance to Fusarium head blight in the Nanda2419 x Wangshuibai population. I. Type II resistance.

Scab disease caused by Fusarium spp. has been a major concern for both wheat producers and consumers. Deployment of scab-resistant varieties is the major strategy to curb this disease. To identify the scab resistance genes in wheat cv. Wangshuibai, we produced a F(6:7) recombinant inbred line (RIL) population by crossing Wangshuibai with the scab-susceptible cultivar Nanda2419. The RILs were evaluated for scab resistance in the field by single floret inoculation in two replicates in 2002 and one replicate in 2003. The number of diseased spikelets (NDS) and the length of diseased rachides (LDR) were investigated to reflect the Type II resistance. Among 654 simple sequence repeat (SSR) markers surveyed, 326 were found to be polymorphic between the parents. A partial molecular map was constructed with these markers that covered over 2,210 cM of the wheat genome. Six chromosome regions showed association with both NDS and LDR in a one-way anova analysis, even though the variation explained by them varied between the two traits. Eight intervals were detected for their association with Type II resistance through interval mapping, five of which were not identified in single-point analysis. The quantitative trait loci (QTL) with large effects were the ones in the interval of Xgwm533-3-Xgwm533-1 on chromosome 3B and in the interval of Xwmc539-Xbarc024 on chromosome 6B, whose alleles favoring resistance originate from Wangshuibai. In addition, a QTL whose resistance allele originated from Nanda2419 was consistently detected in the interval of Xs1021m-Xgwm47-1 on chromosome 2B. These results suggest that Wangshuibai is the major source for Type II resistance in this population. The markers associated with these QTL would facilitate the use of scab-resistant genes of Wangshuibai in scab resistance breeding programs of wheat.

Coordination polymers based on cobridging of rigid and flexible spacer ligands: syntheses, crystal structures, and magnetic properties of [Mn(bpy)(H2O)(C4H4O4)].0.5bpy, Mn(bpy)(C5H6O4), and Mn(bpy)(C6H8O4).

Reactions of 4,4'-bipyridine (bpy) with Mn(C(4)H(4)O(4)).4H(2)O and Mn(C(5)H(6)O(4)).4H(2)O in methanolic aqueous solutions yielded [Mn(bpy)(H(2)O)(C(4)H(4)O(4))].0.5bpy (1) and Mn(bpy)(C(5)H(6)O(4)) (2), respectively, and reactions of freshly prepared Mn(OH)(2)(-)(2)(x)(CO(3))(x).yH(2)O, adipic acid and 4,4'-bipyridine in a methanolic aqueous solution afforded Mn(bpy)(C(6)H(8)O(4)) (3). The six-coordinate Mn atoms in 1 are interlinked by flexible succinato ligands to form layers, which are sustained by rigid bpy ligands into an 3D open framework with the free bpy molecules in tunnels. The ribbonlike chains in 2 result from Mn atoms bridged by glutarato ligands and are connected by bpy ligands into open layers. In 3, the Mn atoms are bridged by both bpy and adipato ligands to form 3D nanoporous frameworks and 2-fold interpenetration of the resulting 3D frameworks completes the crystal structure. In comparison with 1 and 2, compound 3 displays significant antiferromagnetic behavior at low temperature. The antiferromagnetic exchange becomes stronger from 1 through 2 to 3, and the antiferromagnetic ordering of Mn(2+) centers is related to the syn-syn bridging mode of the terminal carboxylate groups of alpha,omega-dicarboxylate anions. Crystal data: C(19)H(18)MnN(3)O(5) (1), monoclinic P2(1)/c, a= 11.686(2) A, b = 17.847(2) A, c = 8.852(1) A, beta = 99.67(1) degrees, V = 1819.9(4) A(3), Z = 4, D(c) = 1.545 g.cm(-3); C(15)H(14)MnN(2)O(4) (2), triclinic P, a = 8.145(2) A, b = 9.574(2) A, c = 10.180(1) A, alpha = 108.01(3) degrees, beta = 93.55(3) degrees, gamma = 105.30(1) degrees, V = 719.2(2) A(3), Z = 2, D(c) = 1.576 g.cm(-3); C(15)H(14)MnN(2)O(4) (3), triclinic P, a = 8.544(1) A, b= 8.881(1) A, c = 10.949(2) A, alpha = 108.81(1) degrees, beta = 95.40(1) degrees, gamma = 101.94(1) degrees, V = 757.7(2) A(3), Z = 2, D(c) = 1.557 g.cm(-3).