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Specimens of Dolichoperoides macalpini (Nicoll, 1914) (Digenea: Dolichoperoididae) were collected from Australian venomous snakes (Elapidae): Notechis scutatus Peters, 1861 and Austrelaps superbus (Günther, 1858) from Tasmania and surrounding islands and N. s. occidentalis Glauert, 1948 from wetlands near Perth, Western Australia. Despite variation in morphological measurements, genetic analysis showed that the one species of digeneans infected the snakes from all locations. This study presents the first DNA sequences for D. macalpini (internal transcribed spacer, 18S, 28S), confirming its placement in a family separate from the Reniferidae and Telorchiidae. Analysis of the infection dynamics of infection in Western Australian snakes showed significant differences in levels of infection between wetland locations, season and year of collection. Infection of D. macalpini was reported in the gastrointestinal tract, including the mouth, in freshly euthanised snakes in Western Australia, and in the lung in Tasmanian snakes, consistent with earlier reports. Differences in morphology and site of infection are suggested to be due to a combination of season and maturity of the digenean, with infection potentially occurring early in the season, as the snakes emerge from torpor. The need for research on the seasonal dynamics of infection with this parasite is discussed.

Lactoferrin (LF), a sialylated iron-binding glycoprotein, has numerous vital physiological functions including immunomodulation and protection against a large group of microorganisms, improving neurodevelopment, health, growth performance, and milk production. Lactoferrin occurs in human milk at a higher concentration compared with bovine milk, but little information is available on LF concentrations in porcine milk and the effects of sow parity on milk LF concentration. The objective of this study was to quantify the LF concentration in porcine milk and to compare that concentration between gilts and sows during lactation. We also investigated the effect of genetic background and litter size of the female pig on the LF concentration of porcine milk. The milk from 30 gilts and 35 sows was collected at 3 stages of lactation, namely colostrum, transition, and mature milk. Standard and experimental samples were analyzed by ultra-high performance liquid chromatography using a diode array UV detector. The following findings were reported: (1) porcine milk contained significant levels of LF with the highest concentration in colostrum, which decreased by ∼62% and ∼67% in transitional and mature milk, respectively; (2) mature gilt milk contained a 22% higher concentration of LF compared with sow milk, which was statistically significant; (3) breed line had an overall significant effect on the LF content of porcine milk; however, when the breed was considered, no significant difference was observed; and (4) LF concentration of porcine milk was not significantly influenced by the litter size. The presence of LF in a higher concentration in porcine milk suggests that LF is an important constituent of pig milk that might contribute to the optimum growth and development of piglets.

Student engagement is often considered a challenging term to define since it is a complex construct of several factors. Nevertheless, it refers to the degree of interest, motivation, or curiosity students demonstrate in their learning. This chapter explores how student engagement frameworks have evolved from a traditional didactic model (educator focused) to a modern co-created collaborative model (student focused) and has missed some key factors. To fill in the identified gaps on student engagement, a framework of learning stewardship is proposed.

Lactoferrin (LF) is a sialylated iron-binding glycoprotein, occurring in several biological secretions like milk, saliva, and seminal fluids and is a major component of a mammalian innate immune system. It plays multiple protective roles against large group of microorganisms and performs anti-inflammatory and anti-cancer activities. The concentration of serum LF in gilt (primiparous sow) and their piglets remains unknown. We determined serum LF concentration in gilts during gestation and lactation to that of 19-d-old piglets, including sow-fed and formula-fed piglets using enzyme-linked immunosorbent assay (ELISA). We found that the concentration of serum LF in gilts varied during gestation (0.77 ± 0.10 µg/mL) and lactation (0.62 ± 0.11 µg/mL). The mean concentration of serum LF in gilts (0.72 ± 0.06 µg/mL) was significantly higher than that of piglets (0.42 ± 0.07 µg/mL, P = 0.004). Additionally, a marginal significant difference (P =0.06) was observed for serum LF concentration in sow-fed piglets (0.42 ± 0.03 µg/mL) at 19 d old compared to that of formula-fed piglets (0.33 ± 0.04 µg/mL) at 37 d old. This study provides noble information regarding the serum LF concentration in the healthy gilts and piglets and thereby the data can be used as a standard reference point for future studies on the role of LF in pig reproduction.

Oxidative stress is known to modulate insulin secretion and initiate gene alterations resulting in impairment of &beta, cell function and type 2 diabetes mellitus (T2DM). Rice bran (RB) phenolic extracts contain bioactive properties that may target metabolic pathways associated with the pathogenesis of T2DM. This study aimed to examine the effect of stabilized RB phenolic extracts on the expression of genes associated with &beta, cell function such as glucose transporter 2 (Glut2), pancreatic and duodenal homeobox 1 (Pdx1), sirtuin 1 (Sirt1), mitochondrial transcription factor A (Tfam), and insulin 1 (Ins1) in addition to evaluating its impact on glucose-stimulated insulin secretion. It was observed that treatment with different concentrations of RB phenolic extracts (25-250 &micro, g/mL) significantly increased the expression of Glut2, Pdx1, Sirt1, Tfam, and Ins1 genes and glucose-stimulated insulin secretion under both normal and high glucose conditions. RB phenolic extracts favourably modulated the expression of genes involved in &beta, cell dysfunction and insulin secretion via several mechanisms such as synergistic action of polyphenols targeting signalling molecules, decreasing free radical damage by its antioxidant activity, and stimulation of effectors or survival factors of insulin secretion.

Digital learning has gained a lot of attention over the recent years and is increasingly being utilised as a substitute for both distance education and face-to face learning activities. This chapter initially defines and briefly discusses the advantages and disadvantages of digital learning. With the advancement in technology, there are various digital tools that are now available to enhance the effectiveness of digital learning experience, and some of the major innovative digital tools are detailed in the chapter.

Activation of protease-activated receptor-2 (PAR2) expressed by T cells has been linked to the bone loss associated with periodontitis. We generated PAR2 conditional-null mice and crossed these with mice expressing Cre recombinase under control of the Lck proximal promoter, to produce T cell-specific PAR2-null mice in order to further study the cellular mechanism involved in periodontitis. Here we report that efficient deletion of PAR2 in thymocytes isolated from T cell-specific PAR2-null mice resulted in thymic and splenic hypoplasia and a reduction in the cells of the cortex and a loss of distinction between the cortex and the medulla of the thymus. FACS analysis confirmed significant reductions in CD4 and CD8 double negative (DN3 and DN4) sub-populations, as well as double positive and single positive T cells, in T cell-specific PAR2-null mice compared to Cre expressing PAR2 wild-type mice. The proportion of annexin V positive and propidium iodide negative cells was increased in CD4 and CD8 double negative, double positive and single positive T cells from T cell-specific PAR2-null mice. No change in the proportion of Ki67 positive cells was observed in sections of thymus from T cell-specific PAR2-null mice, suggesting that the depletion of T cell sub-populations in T cell-specific PAR2-null mice resulted from increased apoptosis rather than reduced proliferation. Together, these results demonstrate that PAR2 plays an important and previously unrecognised anti-apoptotic role in T cell development and suggest that the PAR2 conditional-null mouse will be an important resource for determining tissue and cell specific effects of PAR2.

Inflammation and oxidative stress are the primary underlying causes of several chronic inflammatory diseases. Dietary polyphenols have been demonstrated to possess anti-inflammatory and antioxidant potential. This study aims to determine if chickpea hull phenolic extracts (CHPE) can modulate biomarkers of inflammation and oxidative stress in RAW 264.7 murine macrophage cells. Cells were pre-treated with varying concentrations of CHPE (20, 50, 100, 250, and 500 μg/mL) before inducing inflammatory conditions using lipopolysaccharide (LPS). The antioxidant and anti-inflammatory properties of CHPE was determined by measuring the activity of antioxidant enzymes and the expression of inflammatory mediators. CHPE pre-treatment significantly increased the activity of catalase and glutathione peroxidase (GPx). Pre-treatment with CHPE also significantly reduced the production of inflammatory markers such as nitric oxide (NO) and interleukin-6 (IL-6). Results obtained from this study suggest that CHPE may alleviate oxidative stress and inflammation by regulating pro-inflammatory markers and antioxidant enzymes associated with chronic inflammation.

Type 2 diabetes mellitus (T2DM) is a complex metabolic disorder with various contributing factors including genetics, epigenetics, environment and lifestyle such as diet. The hallmarks of T2DM are insulin deficiency (also referred to as β-cell dysfunction) and insulin resistance. Robust evidence suggests that the major mechanism driving impaired β-cell function and insulin signalling is through the action of intracellular reactive oxygen species (ROS)-induced stress. Chronic high blood glucose (hyperglycaemia) and hyperlipidaemia appear to be the primary activators of these pathways. Reactive oxygen species can disrupt intracellular signalling pathways, thereby dysregulating the expression of genes associated with insulin secretion and signalling. Plant-based diets, containing phenolic compounds, have been shown to exhibit remedial benefits by ameliorating insulin secretion and insulin resistance. The literature also provides evidence that polyphenol-rich diets can modulate the expression of genes involved in insulin secretion, insulin signalling, and liver gluconeogenesis pathways. However, whether various polyphenols and phenolic compounds can target specific cellular signalling pathways involved in the pathogenesis of T2DM has not been elucidated. This review aims to evaluate the modulating effects of various polyphenols and phenolic compounds on genes involved in cellular signalling pathways (both in vitro and in vivo from human, animal and cell models) leading to the pathogenesis of T2DM.

Oxidative stress is one of the primary factors leading to endothelial dysfunction, a major underlying cause of vascular disorders. This study aims to understand the key signalling pathways regulated by sorghum (Shawaya short black 1 variety, characterised to be very high in its antioxidant activity) under oxidative stress in endothelial cells. Human umbilical vein endothelial cells (HUVECs) were pre-treated with non-cytotoxic concentrations of phenolic-rich black sorghum extract (BSE) prior to induction of oxidative stress using hydrogen peroxide (H2O2). Treatment with BSE upregulated the expression of heme oxygenase 1 (HO1) and endothelial nitric oxide synthase (eNOS) and downregulated the levels of NADPH oxidase 4 (NOX4). BSE treatment significantly reduced the expression of pro-inflammatory mediators such as monocyte chemoattractant protein 1 (MCP1) and intracellular adhesion molecule 1 (ICAM1). Results from this study suggest that phenolic-rich BSE may reduce oxidative stress by regulating pro- and antioxidant signalling pathways and the expression of inflammatory mediators linked to endothelial dysfunction under oxidative stress.

Coregulator proteins play key roles in transcriptional control by members of the nuclear receptor superfamily. Previously, we demonstrated that tumor necrosis factor α (TNFα)-induced protein 3-interacting protein 1 (TNIP1) is a corepressor of agonist-bound retinoic acid receptors (RARs). Additionally, TNIP1 has been shown to repress peroxisome proliferator-activated receptors (PPAR) and NF-κB activity and interact with HIV proteins nef and matrix. TNIP1 transcriptional regulation, however, is under studied. Here we show that under permissive epigenetic conditions, TNIP1 expression is induced by all trans retinoic acid (ATRA). Within a 6000 bp region of the human TNIP1 promoter we cloned, both proximal and distal promoter regions are RAR responsive with the latter having RA response elements (RAREs) recognizable by their sequence and functionality in native promoter and synthetic RARE luciferase constructs, EMSA, and ChIP assays. These findings suggest a feedback loop whereby RARs activate expression of TNIP1, which then attenuates their activity. Together with anticipated constitutive transcription factors and the previously described NF-κB-responsiveness of the proximal TNIP1 promoter, the expected combinatorial control of TNIP1 expression could likely modulate TNIP1's impact in any of its target pathways. The degree of control by RARs or other transcription factors would in turn depend on their cell-specific level of expression and/or activation from signals in the environment such as ATRA and TNFα.

Chronic periodontitis is characterised by gingival inflammation and alveolar bone loss. A major aetiological agent is Porphyromonas gingivalis, which secretes proteases that activate protease-activated receptor 2 (PAR2 ). PAR2 expressed on oral keratinocytes is activated by proteases released by P. gingivalis, inducing secretion of interleukin 6 (IL-6), and global knockout of PAR2 prevents bone loss and inflammation in a periodontal disease model in mice. To test the hypothesis that PAR2 expressed on gingival keratinocytes is required for periodontal disease pathology, keratinocyte-specific PAR2 -null mice were generated using K14-Cre targeted deletion of the PAR2 gene (F2rl1). These mice were subjected to a model of periodontitis involving placement of a ligature around a tooth, combined with P. gingivalis infection ("Lig + Inf"). The intervention caused a significant 44% decrease in alveolar bone volume (assessed by microcomputed tomography) in wildtype (K14-Cre:F2rl1wt/wt ), but not littermate keratinocyte-specific PAR2 -null (K14-Cre:F2rl1fl/fl ) mice. Keratinocyte-specific ablation of PAR2 prevented the significant Lig + Inf-induced increase (2.8-fold) in the number of osteoclasts in alveolar bone and the significant up-regulation (2.4-4-fold) of the inflammatory markers IL-6, IL-1β, interferon-γ, myeloperoxidase, and CD11b in gingival tissue. These data suggest that PAR2 expressed on oral epithelial cells is a critical regulator of periodontitis-induced bone loss and will help in designing novel therapies with which to treat the disease.

An increasingly wide range of functions, from repression of NF-κB signaling to protection from apoptosis, is being recognized for tumor necrosis factor α–induced protein 3-interacting protein 1 (TNIP1). The authors recently demonstrated TNIP1 interaction with and repression of liganded retinoic acid receptors, distinguishing it from the more typical NCoR and SMRT corepressors, which function only in the absence of ligand. To improve their understanding of TNIP1’s roles in physiologic and pathologic events, the authors examined its distribution in normal and malignant human tissues and cultured cells. They found cytoplasmic and nuclear TNIP1 in normal skin keratinocytes as it colocalized with retinoic acid receptor α, one of the nuclear receptors it corepresses. Nuclear and cytoplasmic TNIP1 was also found in the malignant keratinocytes of squamous cell carcinomas. Compared to adjacent normal tissues of other organs, TNIP1 staining and distribution varied with increased levels in esophageal cancer and marked decreases in prostate cancer. The varying levels and distribution of TNIP1 in normal and disease state tissues could be expected to affect processes in which TNIP1 is involved, such as NF-κB and nuclear receptor signaling, possibly contributing to the disease course or response to therapies targeting these key players of cell growth and differentiation.