Prediction of Talc Content in Wheat Flour Based on a Near-Infrared Spectroscopy Technique.

A procedure for the prediction of talc content in wheat flour based on radial basis function (RBF) neural network and near-infrared spectroscopy (NIRS) data is described. In this study, 41 wheat flour samples adulterated with different concentrations of talc were used. The diffuse reflectance spectra of all samples were collected by NIRS analyzer in the spectral range of 400 to 2,500 nm. A sample of outliers was eliminated by Mahalanobis distance based on near-infrared spectral scanning, and the remaining 40 wheat flour samples were used for spectral characteristic analysis. A calibration set of 26 samples and a prediction set of 14 samples of wheat flour were built as a result of sample set partitioning based on joint x-y distances division. A comparison of Savitzky-Golay smoothing, multiplicative scatter correction (MSC), first derivation, second derivation, and standard normal variation in the modeling showed that MSC has the best preprocessing effect. To develop a simpler, more efficient prediction model, the correlation coefficient method (CCM) was used to reduce spectral redundancy and determine the maximum correlation informative wavelength (MIW). From the full 1,050 wavelengths, 59 individual MIWs were finally selected. The optimal combined detection model was CCM-MSC-RBF based on the selected MIWs, with a determination of prediction coefficients of prediction (Rp) of 0.9999, root-mean-square error of prediction of 0.0765, and residual predictive deviation of 65.0909. The study serves as a proof of concept that NIRS technology combined with multivariate analysis has the potential to provide a fast, nondestructive and reliable assay for the prediction of talc content in wheat flour.

PPARγ activation reduces ischemia/reperfusion-induced metastasis in a murine model of hepatocellular carcinoma.

Ischemia/reperfusion (I/R) injury during liver resection or transplantation for the treatment of hepatocellular carcinoma (HCC) may increase the risk of metastasis. Peroxisome proliferator-activated receptor-γ (PPARγ) activation has been observed to exert a protective effect against hepatic I/R injury. However, whether PPARγ activation exerts a protective effect against I/R-associated liver metastasis remains unknown. Therefore, the present study aimed to investigate the effects of the PPAR agonist rosiglitazone and the specific PPARγ antagonist GW9662 on tumor metastasis following hepatic I/R. An experimental mouse model of hepatic I/R-induced HCC metastasis was designed in order to determine the effects of I/R on tumor metastasis in the liver. Four groups were established: Sham, control (I/R), rosiglitazone (Ro) and rosiglitazone with GW9662 (Ro + GW) groups. In the latter two groups, the treatments were administered intravenously 1 h prior to the induction of ischemia. Tumor load was measured 12 days after the procedure. Furthermore, tissue analyses were conducted to determine the expression levels of alanine aminotransferase, myeloperoxidase (MPO), matrix metalloproteinase (MMP)-9, vascular cell adhesion molecule (VCAM)-1, nuclear factor (NF)-κB and PPARγ. Rosiglitazone pretreatment appeared to significantly mitigate hepatic I/R injury, as indicated by serological and histological analysis. The levels of VCAM-1, MPO and MMP-9 expression in the Ro group were significantly reduced at 8 h following ischemia compared with those in the control and Ro + GW groups. In addition, rosiglitazone inhibited the I/R-induced activation of NF-κB, and GW9662 attenuated the inhibitory effect. To the best of our knowledge, the present study is the first to report on the expression and the functional roles of PPARγ in I/R-associated metastasis. Short-term treatment of mice with rosiglitazone, a potent PPARγ agonist, confers protective effects against hepatic I/R-associated metastasis. Thus, PPARγ may be a potential therapeutic target for the protection of the liver against I/R-associated metastasis.

Expression and function of hematopoiesis-stimulating factor receptors on the GPI- and GPI+ hematopoietic stem cells of patients with paroxysmal nocturnal hemoglobinuria/aplastic anemia syndrome.

Paroxysmal nocturnal hemoglobinuria/aplastic anemia (PNH/AA) syndrome presents a markedly increased population of cells deficient in glycophosphatidylinositol (GPI- cells) and signs of bone marrow failure, which requires treatment with hematopoiesis-stimulating factors, such as granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF). However, little is known about the effects of these stimulating factors on GPI- cells. In order to explore the effects of stimulating factors in PNH/AA, G-CSF receptor (CD114) and SCF receptor (CD117) expression levels on GPI+ and GPI- hematopoietic stem cells (HSCs) were measured by flow cytometry (FCM). The mean fluorescence intensity (MFI) values of signal transducer and activator of transcription 5 (STAT5) and phosphorylated (P)-STAT5 were measured in GPI+ and GPI- HSCs by FCM following stimulation with G-CSF or SCF in vitro. The expression levels of CD114 and CD117 on GPI- HSCs were significantly lower (P<0.01) than those on GPI+ HSCs in PNH/AA patients and normal controls. The MFI values of STAT5 in the GPI- and GPI+ HSCs of PNH/AA patients and normal controls were not significantly different. However, the MFI values of P-STAT5 in the GPI- HSCs of PNH/AA patients were significantly lower than those in the GPI+ HSCs of PNH/AA patients and normal controls prior to and following stimulation with G-CSF or SCF (P<0.01). The GPI- HSCs of PNH/AA patients responded poorly to stimulation by hematopoiesis-stimulating factors, which indicates that these factors can be used safely in patients with PNH/AA.

Speckle-type POZ (pox virus and zinc finger protein) protein gene deletion in ovarian cancer: Fluorescence in situ hybridization analysis of a tissue microarray.

The aim of the present study was to investigate the status of speckle-type POZ (pox virus and zinc finger protein) protein (SPOP) gene located on chromosome 17q21 in ovarian cancer (OC). The present study evaluated a tissue microarray, which contained 90 samples of ovarian cancer and 10 samples of normal ovarian tissue, using fluorescence in situ hybridization (FISH). FISH is a method where a SPOP-specific DNA red fluorescence probe was used for the experimental group and a centromere-specific DNA green fluorescence probe for chromosome 17 was used for the control group. The present study demonstrated that a deletion of the SPOP gene was observed in 52.27% (46/88) of the ovarian cancer tissues, but was not identified in normal ovarian tissues. Simultaneously, monosomy 17 was frequently identified in the ovarian cancer tissues, but not in the normal ovarian tissues. Furthermore, the present data revealed that the ovarian cancer histological subtype and grade were significantly associated with a deletion of the SPOP gene, which was assessed by the appearance of monosomy 17 in the ovarian cancer samples; the deletion of the SPOP gene was observed in a large proportion of serous epithelial ovarian cancer (41/61; 67.21%), particularly in grade 3 (31/37; 83.78%). In conclusion, deletion of the SPOP gene on chromosome 17 in ovarian cancer samples, which results from monosomy 17, indicates that the SPOP gene may serve as a tumor suppressor gene in ovarian cancer.

Preparation of a novel composite nanofiber gel-encapsulated human placental extract through layer-by-layer self-assembly.

Aqueous human placenta extract (HPE) has been previously used to treat chronic soft tissue ulcer; however, the optimal dosage of HPE has yet to be elucidated. The present study investigated a novel nanofiber gel composed through layer-by-layer (LbL) self-assembly, in which HPE was encapsulated. IKVAV, RGD, RAD16 and FGL-PA were screened and combined to produce an optimal vehicle nanofiber gel through LbL assembly. Subsequently, the aqueous HPE was encapsulated into this nanofiber at the appropriate concentration, and the morphology, particle size, drug loading efficacy, encapsulation rate, release efficiency and structure validation were detected. The encapsulation efficiency of all three HPE samples was >90%, the nanofiber gel exhibited a slow releasing profile, and the structure of HPE encapsulated in the nanofiber gel was unvaried. In conclusion, this type of novel composite nanocapsules may offer a promising delivery system for HPE.

Establishment of a rat autogenous arteriovenous fistula model following 5/6 nephrectomy.

The aim of this study was to establish a stable rat model of autogenous arteriovenous fistula (AVF) with chronic renal function insufficiency. Forty Sprague-Dawley rats were randomly divided into an experimental group (n=20) and sham surgery group (n=20) and a 5/6 nephrectomy model was established in the rats. One week later, in the experimental group, the ipsilateral caroid artery was inserted into the external jugular vein by a cuff technique to establish a carotid arteriovenous fistula; in the sham group, the external jugular vein and carotid artery were dissociated. At 7 and 28 days following the establishment of the AVF, the renal functions of the two groups were measured. Hematoxylin and eosin staining and double collagen and elastin staining were conducted to evaluate the area of intimal hyperplasia in the external jugular vein, and the expression of α-smooth muscle actin in the vein was investigated by immunohistochemistry. The creatinine and urea nitrogen levels in the experimental group at each time-point were significantly higher than those in the sham surgery group (P<0.05). The intimal hyperplasia of the external jugular vein of the experimental group was increased significantly compared with that in the sham group at each time-point (P<0.05). The model, which is easy to establish and simple to master, provides a new and feasible experimental method for the study of intimal hyperplasia associated with autogenous AVF in chronic renal insufficiency, and is worthy of wider use.

Ultrastructural identification of telocytes in the muscularis of chicken ileum.

Telocytes (TCs) are a specialized type of interstitial cells, characterized by a small cell body and long, thin processes, that have recently been identified in various cavitary and non-cavitary organs of humans and laboratory mammals. Chickens present significant economical and scientific notability; however, ultrastructural identification of TCs remains unclear in birds. The aim of the present study was to describe electron microscopic evidence for the presence of TCs in the chicken gut. The ileum of healthy adult broiler chickens (n=10) was studied by transmission electron microscopy. TCs are characterized by several, long (tens to hundreds of µm) prolongations called telopodes (Tps). Tps, which are below the resolving power of light microscopy, display podomeres (thin segments of ≤0.2 µm) and podoms (dilations accommodating caveolae, mitochondria and endoplasmic reticulum). TCs were observed in every field, but were predominantly located in the myenteric plexus and the lamina propria. Tps frequently establish close spatial relationships with immune cells, blood vessels and nerve endings. On the basis of their distribution and morphology, it was hypothesized that the different locations of TCs may be associated with different roles.

[Lipopolysaccharide induced expression of peroxiredoxin 1 in airway epithelial cell].

OBJECTIVE: To investigate the effect of lipopolysaccharide (LPS) on expression of peroxiredoxin 1 (prdx1) in airway epithelial cells. METHODS: The airway epithelium cell line BEAS-2B was cultivated, and the cells were stimulated with 0, 1, and 10 mg/L of LPS for 12 hours and 24 hours, and then were harvested for prdx1 expression detection. The mRNA expression of prdx1 was detected by reverse transcription-polymerase chain reaction (RT-PCR).The airway epithelium cells were stimulated with 0, 0.1 , 0.5, 1 , 5, and 10 mg/L of LPS for 12 hours, and were collected for determination of prdx 1 protein expression by Western blotting. RESULTS: RT-PCR results showed that the prdx1 mRNA expression was significantly increased within 12 hours of stimulation with elevation of the dosage of LPS. The prdx1 mRNA expression at 12 hours of stimulation by 10 mg/L LPS was significantly higher than that in control group (2.014 ± 0.197 vs. 0.644 ± 0.178, P<0.05). However, with prolongation of LPS stimulation time, the prdx1 mRNA expression at 24 hours was slightly declined. Western blotting results showed that the prdx1 protein expression was gradually increased with elevation of dosage of LPS. The prdx1 protein expression at 12 hours of stimulation with 5 mg/L LPS was significantly higher than that in control group (1.069 ± 0.175 vs. 0.328 ± 0.010, P<0.05), and the expression remained at high level at 12 hours of stimulation with 10 mg/L LPS (0.984 ± 0.220 ). CONCLUSION: 10 mg/Lof LPS can induce the mRNA and protein expression of prdx1 in BEAS-2B cell after 12 hours of stimulation.