Abstract Concentrated growth factor (CGF) is an autogenuous product that contains highly concentrated number of platelets and can be derived from venous blood by selective centrifugation. It has been speculated that local growth factors in human platelets (insulinlike growth factor, IGF; transforming growth factor, TGF-b; platelet derived growth factor, PDGF) would enhance healing of grafts and also counteract resorption. The osteogensis effect of CGF and acellular dermal matrix (ADM) for alveolar cleft defects was evaluated in this study. Twenty alveolar cleft patients were divided randomly into two groups. One group underwent guided bone regeneration (GBR) using acellular dermal matrix film combined with alveolar bone grafting using iliac crest bone grafts (GBR group), while the other group underwent alveolar bone grafting combined with CGF (CGF group). Cone beam computed tomography (CBCT) images were obtained at 1 week and 6 months following the procedure. Using Mimics 17.0 software, the bone resorption rate and bone density improvement rate were calculated and compared between the two groups. Although not significant between ADM and CGF in bone resorption rate, the bone density improvement in cases with CGF(61.62 ± 4.728%) was much better than in cases with ADM (27.05 ± 5.607%) (p = 0.0002). Thus, CGF could be recommended to patients with alveolar cleft as a better choice.

ABSTRACT This study aimed to investigate the expression and mechanism of N- methyl -D- aspartate receptor 1 (NMDAR1) in the pathogenesis of Alzheimer disease (AD). Eighty adult Wistar rats were randomly divided into 4 groups (n=20 each) to receive an injection of 0, 5, 7 and 10 μl of 1 μg/μl amyloid-β 42 (Aβ1-42) in the hippocampus. Twenty rats in normal control group were injected with equal volume of saline. After 10 days, the hippocampus was isolated from 5 randomly selected rats in each group. The NMDAR1 protein and mRNA expression was determined by immunohistochemical staining and qRT-PCR. The aquaporin-1 (AQP-1) mRNA expression was also measured by qRT-PCR. We found that both NMDAR1 and AQP-1 expression in Aβ1-42 groups was increased in a dose-dependent manner. NMDAR1 and AQP-1 expression in 7 and 10 μl Aβ1-42 groups was significantly higher compared with 0 μl Aβ1-42 group (P <0.01). Further, the 10 μl Aβ1-42 group was randomly divided into 3 subgroups: AD-NMDA, AD-MK-801, and AD-Ctrl subgroup, which was given an intraperitoneal injection of NMDAR agonist NMDA, NMDAR antagonist MK-801 and saline, respectively. The relative APQ-1 expression in each subgroup was determined by qRT-PCR and Western blot analysis after 24 h. The AQP-1 expression was significantly decreased in AD-MK-801 group (P < 0.05), but was markedly increased in AD-NMDA group when compared with AD-Ctrl group (P <0.01). Our study suggested that expression abnormity of NMDAR1 is involved in the pathogenesis of AD. NMDAR1 might regulate the pathogenic process through stimulating the expression of AQP-1.

Abstract: Aflatoxin B1 (AFB1), produced by Aspergillus flavus and Aspergillus parasiticus, is one of the major mycotoxins to affect animal health. AFB1 contamination of aquafeed is widespread, especially in countries with humid, tropical climates. The most applied method for protecting animals against aflatoxicosis is the use of clay minerals. Growth performance, immunosuppressive effects (bactericidal activity, lysozyme activity, albumin/globulin ratio, alternative complement pathway activity, and protein content), and pathology parameters were used to evaluate the response of yellow catfish (Pelteobagrus fulvidraco) to increasing concentrations of AFB1 and test the protective effect of dietary supplementation with a bentonite (dioctahedral montmorillonite) based AFB1 binder. Triplicate groups of yellow catfish with an average weight of 2.0 ± 0.1 g were fed diets containing 0, 200, 500, and 1,000 μg/kg of AFB1 alone, or diets containing 0, 200, 500, and 1,000 μg/kg of AFB1 along with 2 g/kg AFB1 binder, for 12 weeks. Results showed that diets containing increasing amounts of AFB1 had a significantly lower (P = 0.002) survival rate. There was a statistical significant reduction in weight gain, final body weight, and specific growth rate, and an increase in feed conversion ratio (FCR) influenced by the levels of AFB1 in the diet (P < 0.001 for all parameters), as well as increasing protection due to the presence of the binder (P = 0.046, P = 0.014, P = 0.038, and P = 0.485, respectively). The immunosuppressive nature of AFB1 in yellow catfish diets was confirmed through observation of lower bactericidal activity (P = 0.001), lower lysozyme activity (P = 0.006), reduced total protein (P = 0.002), and enhanced albumin/globulin ratio (P = 0.004). Fish fed diets contaminated with AFB1 and supplemented with the AFB1 binder showed better improvement in FCR (P = 0.019). These results indicate that AFB1 has a negative impact on yellow catfish growth and survival rate. The AFB1 binder protected fish from the toxic effects of AFB1.

Resumen: La aflatoxina B1 (AFB1), producida por Aspergillus flavus y Aspergillus parasiticus, es una de las principales micotoxinas que afectan la salud animal. La contaminación de alimentos acuícolas con AFB1 es común, especialmente en países con climas húmedos y tropicales. El método más usado para proteger a los animales contra la aflatoxicosis es el uso de arcillas. Para evaluar la respuesta del bagre amarillo (Pelteobagrus fulvidraco) a concentraciones crecientes de AFB1 y evaluar el efecto protector de una bentonita (montmorillonita dioctaédrica), se analizaron el crecimiento, efectos inmunosupresores (actividad bactericida, relación albúmina/globulina, actividad de la lisozima, actividad de la vía alternativa del complemento y contenido de proteínas) y parámetros patológicos. Grupos triplicados de P. fulvidraco, con un peso promedio de 2.0 ± 0.1 g, fueron alimentados durante 12 semanas con dietas que contenían 0, 200, 500 y 1,000 μg/kg de AFB1 pura, o dietas que contiendan 0, 200, 500 y 1,000 μg/kg de AFB1 junto con 2 g/kg de bentonita. Los resultados mostraron que las dietas con mayores cantidades de AFB1 tenían una tasa de supervivencia significativamente menor (P = 0.002). Hubo una reducción estadísticamente significativa del aumento de peso, el peso corporal final y la tasa de crecimiento específico y un aumento de la tasa de conversión alimenticia debido a los niveles de AFB1 en la dieta (P < 0.001 para todos los parámetros), así como mayor protección por la presencia de la bentonita (P = 0.046, P = 0.014, P = 0.038 y P = 0.485, respectivamente). La naturaleza inmunosupresora de AFB1 en las dietas del bagre amarillo se confirmó mediante la observación de una menor actividad bactericida (P = 0.001), una menor actividad de la lisozima (P = 0.006), una disminución de la proteína total (P = 0.002) y una mayor relación albúmina/globulina (P = 0.004). Los peces alimentados con dietas contaminadas con AFB1 y complementadas con la bentonita mostraron una mejora de la tasa de conversión alimenticia (P = 0.019). Estos resultados indican que la AFB1 tiene un impacto negativo en el crecimiento del bagre amarillo y la tasa de supervivencia. La bentonita protegió a los individuos de los efectos tóxicos de la AFB1.

The effects of Dangguibuxue Tang (DBT) on growth performance and immunity response in immunosuppressed broiler chicks were investigated in this study. 240 one-d-old broiler chicks (DaHeng S01) were randomly divided into 4 groups, 2.0% DBT-treatment (A), 0.5% DBT-treatment (B), cyclophosphamide-control (C), and control group (D). From 4 d to 7 d of age, chicks in group A, B and C were given cyclophosphamide (CY) at a dosage of 100mg/kg body weight (BW) daily by intraperitoneal injection to induce immunosuppression. Chicks in group D were given an equal volume of physiological saline daily by intraperitoneal injection and considered normal chicks. Groups A and B were supplemented with 2.0% or 0.5% of DBT in the drinking water from 8 d to 42 d of age. Groups C and D did not receive any additional medication. The results revealed that chicks from group B had lower feed:gain rate (FGR), lower total mortality, higher immunity organ indexes, higher levels of Newcastle disease (ND) antibody and infectious bursal disease (IBD) antibody, higher interleukin-2 and interleukin-6 levels, and greater lymphocyte proliferative responses to concanavalin A (ConA) during the experiment than those from group C. However, no significant difference in the immunity status in the two levels of DBT-treatment was observed. These results indicate that supplementation of 0.5% of DBT can improve both cellular immunity and humoral immunity in immunosuppressed broiler chicks.

OBJECTIVES: Plasmid pR ST98 is a hybrid resistance-virulence plasmid isolated from Salmonella enterica serovar Typhi (S. typhi). Previous studies demonstrated that pR ST98 could enhance the virulence of its host bacteria. However, the mechanism of pR ST98-increased bacterial virulence is still not fully elucidated. This study was designed to gain further insight into the roles of pR ST98 in host responses. METHODS: Human-derived macrophage-like cell line THP-1 was infected with wild-type (ST8), pR ST98-deletion (ST8-ΔpR ST98), and complemented (ST8-c-pR ST98) S. typhi strains. Macrophage autophagy was performed by extracting the membrane-unbound LC3-I protein from cells, followed by flow cytometric detection of the membrane-associated fraction of LC3-II. Intracellular bacterial growth was determined by colony-forming units (cfu) assay. Macrophage cell death was measured by flow cytometry after propidium iodide (PI) staining. Autophagy activator rapamycin (RAPA) was added to the medium 2 h before infection to investigate the effect of autophagy on intracellular bacterial growth and macrophage cell death after S. typhi infection. RESULTS: Plasmid pR ST98 suppressed autophagy in infected macrophages and enhanced intracellular bacterial growth and S. typhi-induced macrophage cell death. Pretreatment with RAPA effectively restricted intracellular bacterial growth of ST8 and ST8-c-pR ST98, and alleviated ST8 and ST8-c-pR ST98-induced macrophage cell death, but had no significant effect on ST8-ΔpR ST98. CONCLUSIONS: Plasmid pR ST98 enhances intracellular bacterial growth and S. typhi-induced macrophage cell death by suppressing autophagy.