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Extensive research on marine algae, especially on their health-promoting properties, has been conducted. Various ingredients with potential biomedical applications have been discovered and extracted from marine algae. Alginate oligosaccharides are low molecular weight alginate polysaccharides present in cell walls of brown algae. They exhibit various health benefits such as anti-inflammatory, anti-microbial, anti-oxidant, anti-tumor and immunomodulation. Their low-toxicity, non-immunogenicity, and biodegradability make them an excellent material in biomedicine. Alginate oligosaccharides can be chemically or biochemically modified to enhance their biological activity and potential in pharmaceutical applications. This paper provides a brief overview on alginate oligosaccharides characteristics, modification patterns and highlights their vital health promoting properties.

Background Although drug addiction studies have shown that females are more likely to become addicted and sensitive to drug cues, this feature seems reversed in Internet gaming disorder (IGD), of which males are more likely to be sufferers. Given the prevalence of IGD in the male population, the current study was set to examine the potential effect of sex on IGD’s craving using a cue reactivity task. Methods Sixty-five (32 males) IGD subjects underwent fMRI scanning during exposure to visual gaming cues and neutral cues. Brain responses to gaming cues relative to neutral cues were examined within two groups separately. In addition, Granger causal analysis (GCA) was conducted to investigate how the effective connectivity patterns were altered in male and female IGD subjects. Results When facing gaming cues, lower regions of brain activation were observed in males compared to females, including the left anterior cingulate cortex (ACC), the superior frontal gyrus and the posterior cingulate cortex (PCC); GCA results, using the PCC as the ROI, showed higher middle temporal gyrus-PCC-right ACC/parahippocampal gyrus effective connectivity in males as compared with females, when exposed to gaming cues. Conclusion The results indicate that gaming cues could more severely disturb male IGD subjects’ inhibition control function over game-elicited cravings compared to females, which might make it hard for males to control their game cravings and stop their gaming behaviors. This conclusion is valuable in understanding why males are more vulnerable to IGD than females.

Perineuronal nets (PNNs) are specialized extracellular matrix structures that primarily surround fast-spiking parvalbumin (PV)-containing interneurons within the PFC. They regulate PV neuron function and plasticity to maintain cortical excitatory/inhibitory balance. For example, reductions in PNN intensity are associated with reduced local inhibition and enhanced pyramidal neuron firing. We previously found that exposure to dietary high fat reduced PNN intensity within the PFC of male Sprague-Dawley (SD) rats. However, how high fat affects PNNs in the PFC of females or in obesity-vulnerable vs. -resistant models is unknown. Therefore, we gave male and female SD, selectively bred obesity-prone (OP), and obesity-resistant rats (OR) free access to standard lab chow or 60% high fat for 21 days. We then measured the number of PNN positive cells and PNN intensity (determined by Wisteria floribunda agglutinin [WFA] staining) as well as the number of PV positive neurons using immunohistochemistry. We found sex and region-specific effects of dietary high fat on PNN intensity, in the absence of robust changes in cell number. Effects were comparable in SD and OP but differed in OR rats. Specifically, high fat reduced PNN intensities in male SD and OP rats but increased PNN intensities in female SD and OP rats. In contrast, effects in ORs were opposite, with males showing increases in PNN intensity and females showing a reduction in intensity. Finally, these effects were also region specific, with diet-induced reductions in PNN intensity found in the prelimbic PFC (PL-PFC) and ventral medial orbital frontal cortex (vmOFC) of SD and OP males in the absence of changes in the infralimbic PFC (IL-PFC), and increases in PNN intensity in the IL-PFC of SD and OP females in the absence of changes in other regions. These results are discussed in light of roles PNNs may play in influencing PFC neuronal activity and the differential role of these sub-regions in food-seeking and motivation.

We report here the successful synthesis of CaSiO3:Eu3+ spheres using the reverse micelles soft template. The influence of the calcination temperature on the shape, crystallization and photoluminescence properties of the prepared spheres was investigated by DTA–TG, XRD, IR, SEM and PL. The results showed that the temperature of crystallization (from amorphous phase to β-CaSiO3) is 668 °C. The temperature of phase transition (from β-CaSiO3 to α-CaSiO3) is 790 °C. The average size of CaSiO3:Eu3+ spheres calcined at 700 °C was about 350 nm. The radiation was dominated by the red emission peak at 613 nm and the highest emission intensity was observed when the spheres were calcined at 700 °C. When calcined at 800 °C, the spheres are almost cracked and melted down, due to the high temperature.

Tachykinin neurokinin 3 receptor (NK3R) is a G-protein (GTP binding protein) -coupled receptor that is heavily expressed by magnocellular neurons of the paraventricular nucleus of the hypothalamus (PVN). Osmotic challenge is reported to activate NK3R expressed by magnocellular neurons and cause the NK3R to be internalized to the cytoplasm and perhaps the cell nucleus. In this study we show using immuno-electron microscopy that isolated nuclei from neurons in the PVN of osmotic challenged animals (rats) show a robust labeling for the NK3R. NK3R immunoreactivity was detected by Western blot in isolated nuclei of PVN neurons following the 2 M NaCl injection. No nuclear NK3R immunoreactivity was detected in control animals. NK3R antibody specificity was confirmed by small interfering (SI) RNA technology. This study establishes that the NK3R is trafficked to the nucleus of PVN neurons following a peripheral osmotic challenge.

Acetaldehyde, the major ethanol metabolite that is far more toxic and reactive than ethanol, has been postulated to be responsible for alcohol-induced tissue and cell injury. This study was to examine whether facilitated acetaldehyde metabolism affects acetaldehyde-induced oxidative stress and apoptosis. Transgene-encoding human aldehyde dehydrogenase-2 (ALDH2), which converts acetaldehyde into acetate, was constructed under chicken beta-actin promoter and transfected into human umbilical vein endothelial cells (HUVECs). Efficacy of ALDH2 transfection was verified using green fluorescent protein and ALDH2 enzymatic assay. Generation of reactive oxygen species (ROS) was measured using chloromethyl-2',7'-dichlorodihydrofluorescein diacetate. Apoptosis was evaluated by 4',6'-diamidino-2'-phenylindoladihydrochloride fluorescence microscopy, quantitative DNA fragmentation, and caspase-3 assay. Acetaldehyde (0-200 microm) elicited ROS generation and apoptosis in HUVECs in a time- and concentration-dependent manner, associated with activation of the stress signal molecules ERK1/2 and p38 mitogen-activated protein (MAP) kinase. A close liner correlation was observed between the acetaldehyde-induced ROS generation and apoptosis. Interestingly, the acetaldehyde-induced ROS generation, apoptosis, activation of ERK1/2, and p38 MAP kinase were prevented by the ALDH2 transgene or antioxidant alpha-tocopherol. The involvement of ERK1/2 and p38 MAP kinase in acetaldehyde-induced apoptosis was confirmed by selective kinase inhibitors U0126, SB203580, and SB202190. Collectively, our data revealed that facilitation of acetaldehyde metabolism by ALDH2 transgene overexpression may prevent acetaldehyde-induced cell injury and activation of stress signals. These results indicated therapeutic potential of ALDH2 enzyme in the prevention and detoxification of acetaldehyde or alcohol-induced cell injury.