Enteral Nutrition: Based on the Combination of Nutrison Fibre and TPF-DM with A Marine Biological-Based Active Polysaccharide Preparation.

Good nutrition is essential for human growth, wound healing, and spiritual vitality. However, some individuals are unable to eat or experience gastrointestinal problems such as severe diarrhea, vomiting, gastric retention, and even gastrointestinal bleeding for a variety of causes. Therefore, it has important clinical significance to provide patients with required nutrients and maintain the integrity of the body's tissues and organs through enteral nutrition. Based on this, this work uses a dual carrier of polylactic acid (PLA) and polyvinyl alcohol (PVA) to carry marine biopolysaccharides combined with sodium alginate (PSS) and successfully obtains the intestinal tract based on marine bioactive polysaccharides. Nutritional oral biological preparations (PSS-PLA/PVA) also cooperate with enteral nutritional suspension (diabetes) (TPF-DM) and Nutrison fibre to provide enteral nutritional support for critically ill patients. PSS-PLA/PVA has been shown in clinical studies to increase the effect of enteral nutrition support, the function of intestinal T lymphatic tissue, and the ability to control immunological function, indicating that it is worthy of further clinical development.

Schisandrin B improves cerebral ischemia and reduces reperfusion injury in rats through TLR4/NF-κB signaling pathway inhibition.

It has been established that poor outcomes in ischemic stroke patients are associated with the post-reperfusion inflammatory response and up-regulation of TLR4. Therefore, suppression of the TLR4 signaling pathway constitutes a potential neuroprotective therapeutic strategy. Schisandrin B, a compound extracted from Schisandra chinensis, has been shown to possess anti-inflammatory and neuroprotective properties. However, the mechanism remains unclear. In the present study, the therapeutic effect of schisandrin B was assessed following cerebral ischemia and reperfusion (I/R) injury in a model of middle cerebral artery occlusion and reperfusion (MCAO/R) in rats. The effects of schisandrin B were investigated with particular emphasis on TLR4 signal transduction and on the inflammatory response. Schisandrin B treatment conferred significant protection against MCAO/R injury, as evidenced by decreases in infarct volume, neurological score, and the number of apoptotic neurons and inflammatory signaling molecules. ABBREVIATIONS: I/R: schemia/reperfusion; IL: interleukin; MCAO/R: middle cerebral artery occlusion and reperfusion; NF-κB: nuclear; TLR4: Toll-like receptor 4; TNF-α: tumor necrosis factor-α.

Lin28 is associated with astrocytic proliferation during intracerebral hemorrhage.

As an evolutionarily conserved RNA-binding protein, LIN28 is known to be involved in the regulation of the translation and stability of a large number of mRNAs and the biogenesis of certain miRNAs. Increasing evidence indicates that LIN28 regulates many cellular processes, such as embryonic stem cell proliferation, cell fate succession, developmental timing, and oncogenesis. However, the expression and function of LIN28 after intracerebral hemorrhage (ICH) are still unclear. In this study, we performed an intracranial hemorrhage model in adult rats and western blot, immunohistochemistry, as well as immunofluorescence showed that LIN28 was obviously up-regulation in neurons adjacent to the hematoma after ICH. Besides, the transitory increase of LIN28 expression was paralleled with the up-regulation of proliferating cell nuclear antigen (PCNA) as well as GFAP. Hence, LIN28 might play an important role in astrocyte proliferation after ICH.

Enhancement of glyoxalase 1, a polyfunctional defense enzyme, by quercetin in the brain in streptozotocin-induced diabetic rats.

Glyoxalase 1 (Glo-1) is an ubiquitous cellular enzyme that participates in the detoxification of methylglyoxal (MG), a cytotoxic byproduct of glycolysis that induces protein modification (advanced glycation end products [AGEs]), oxidative stress, and inflammation. The concentration of MG is elevated under high-glucose conditions, such as diabetes. Therefore, Glo-1 and MG have been implicated in the pathogenesis of diabetic encephalopathy. We investigated the effect of quercetin on brain damage that was caused by diabetes in rats and the mechanisms associated with Glo-1. Streptozotocin-induced diabetic rats were treated orally with quercetin (30, 60, and 90 mg/kg) or distilled water for 14 weeks. The temporal cortex and hippocampus were harvested and analyzed for different indices assays. Quercetin, especially at a high dose, increased the levels of reduced glutathione and the activity of superoxide dismutase and decreased the levels of AGEs, the receptor for AGEs (RAGE), and malondialdehyde in the diabetic brain. Quercetin also significantly decreased the levels of inflammatory markers (cyclooxygenase-2, interleukin-1ß, and tumor necrosis factor α) in diabetic brains. Most importantly, Glo-1 activity and protein expression were increased in quercetin-treated diabetic rat brains compared with untreated diabetic brains. These results indicate that quercetin exerts beneficial effects by decreasing protein glycation, oxidative stress, and inflammation through the upregulation of Glo-1, which may ameliorate diabetic encephalopathy.

Normal anatomy and variations in the confluence of sinuses using digital subtraction angiography.

OBJECTIVES: The configuration of the confluence of sinuses differs not only between individuals, but also between the two brain hemispheres, making the anatomical classification of this region difficult. In this study, we evaluated the anatomy of the confluence of sinuses and ascertained the accuracy and usefulness of digital subtraction angiography (DSA) in the evaluation of cerebral veins. METHODS: Bilateral carotid and vertebral artery angiographies were performed in 500 adult patients to evaluate the anatomy of the confluence of sinuses and contributory venous sinuses. We appraised the anatomy of the sinuses adjacent to the confluence, the lateralization of venous draining into the transverse sinuses (TSs), the communications between the TSs, and the presentation of the occipital sinus (OS). RESULTS: Based on the anatomical descriptions of Osborn's Brain (Diagnostic Cerebral Angiography, 2nd edition), we delineated 10 different configurations of the confluence of sinuses that showed connections among the superior sagittal sinus, the straight sinus, and the left and right TSs. Right side dominant transverse sinus accounted for 49% of the cases. Direct communication between the TSs accounted for 46.4% of the cases. Indirect communication accounted for 51.6% of the case, and absence of communication between the left and the right TS accounted for 2%. Lastly, the presence of OS was observed in 6% of the cases. CONCLUSION: DSA promises to be an effective technique for studying the anatomy and normal variations of the confluence of sinuses, providing useful information for the diagnosis of cerebral venous diseases, and ensuring safer surgical procedures.

Mangiferin Upregulates Glyoxalase 1 Through Activation of Nrf2/ARE Signaling in Central Neurons Cultured with High Glucose.

Mangiferin, a natural C-glucoside xanthone, has anti-inflammatory, anti-oxidative, neuroprotective actions. Our previous study showed that mangiferin could attenuate diabetes-associated cognitive impairment of rats by enhancing the function of glyoxalase 1 (Glo-1) in brain. The aim of this study was to investigate whether Glo-1 upregulation by mangiferin in central neurons exposed to chronic high glucose may be related to activation of Nrf2/ARE pathway. Compared with normal glucose (25 mmol/L) culture, Glo-1 protein, mRNA, and activity levels were markedly decreased in primary hippocampal and cerebral cortical neurons cultured with high glucose (50 mmol/L) for 72 h, accompanied by the declined Nrf2 nuclear translocation and protein expression of Nrf2 in cell nucleus, as well as protein expression and mRNA level of γ-glutamylcysteine synthetase (γ-GCS) and superoxide dismutase activity, target genes of Nrf2/ARE signaling. Nonetheless, high glucose cotreating with mangiferin or sulforaphane, a typical inducer of Nrf2 activation, attenuated the above changes in both central neurons. In addition, mangiferin and sulforaphane significantly prevented the formation of advanced glycation end-products (AGEs) reflecting Glo-1 activity, while elevated the level of glutathione, a cofactor of Glo-1 activity and production of γ-GCS, in high glucose cultured central neurons. These findings demonstrated that Glo-1 was greatly downregulated in central neurons exposed to chronic high glucose, which is expected to lead the formation of AGEs and oxidative stress damages. We also proved that mangiferin enhanced the function of Glo-1 under high glucose condition by inducing activation of Nrf2/ARE signaling pathway.

Ibuprofen attenuates nephropathy in streptozotocin­induced diabetic rats.

Ibuprofen, a commonly administered nonsteroidal anti­inflammatory therapeutic agent, is also a partial agonist of peroxisome proliferator­activated receptor Î³ (PPARγ). The present study investigated the effects of ibuprofen on type 1 diabetic nephropathy (DN) in rats, and the potential mechanisms associated with the activation of PPARγ. Diabetic rats were induced through a single intraperitoneal injection of streptozotocin before oral treatment with ibuprofen or pioglitazone for 8 weeks. The 24­h urine collection was performed for measurement of total protein content. The kidney was fixed in 10% formalin for periodic acid­Schiff and Masson's trichrome staining. Blood and residual kidney tissue samples were collected to measure the associated biochemical parameters. Chronic ibuprofen treatment decreased urinary protein excretion, blood urea nitrogen, glomerular basement membrane thickening and renal fibrosis, which were accompanied by increases in PPARγ protein expression, glutathione (GSH) level, and superoxide dismutase (SOD) activity, decreases in cyclooxygenase 2 and inducible nitric oxide synthase protein expressions, as well as a decreased interleukin 1ß (IL­1ß) level in the renal cortex of DN rats. Furthermore, the reduced IL­1ß level, increased GSH quantities and stronger SOD activity in the rat serum were evaluated in ibuprofen­treated diabetic rats and were compared with untreated diabetic rats. Regarding GSH and IL­1ß levels, ibuprofen was identified to be superior to the positive control, pioglitazone, while levels of the other indices were identified to be similar. Thus, ibuprofen was observed to prevent the development of DN, caused by type 1 diabetes, by anti­inflammatory and anti­oxidative action, potentially via PPARγ activation.

Activation of mTOR signaling mediates the increased expression of AChE in high glucose condition: in vitro and in vivo evidences.

Acetylcholinesterase (AChE) is impaired in brain of diabetic animals, which may be one of the reasons for diabetes-associated cognitive decline. However, the mechanism is still unknown. The present study was designed to investigate whether the increased expression of AChE in central neurons under high glucose (HG) condition was due to activation of mammalian target of rapamycin (mTOR) signaling. It was found that more production of reactive oxygen species, and higher levels of phospho-Akt, phospho-mTOR, phospho-p70S6K, and AChE were detected in HT-22 cells in HG group than normal glucose group after culture for 24 h, which were all attenuated by an antioxidant N-acetyl-L-cysteine. A PI3K inhibitor LY294002 significantly decreased the levels of phospho-Akt, phospho-mTOR, phospho-p70S6K, and AChE protein expression in HG-cultured HT-22 cells, and an mTOR inhibitor rapamycin markedly reduced the levels of phospho-mTOR, phospho-p70S6K, and AChE expression. Furthermore, compared with normal rats, diabetic rats showed remarkable increases in levels of AChE activity and expression, malondialdehyde, phospho-mTOR, phospho-p70S6K, and a significant decrease in total superoxide dismutase activity in both hippocampus and cerebral cortex. However, much lower levels of phospho-mTOR, phospho-p70S6K, and AChE expression occurred in both brain regions of diabetic rats treated with rapamycin when compared with untreated ones. These results indicated that mTOR signaling was activated through the activation of PI3K/Akt pathway mediated by oxidative stress in HG-cultured HT-22 cells and diabetic rat brains, which contributed to the elevated protein expression of AChE in central neurons under the condition of HG.

Mangiferin attenuates renal fibrosis through down-regulation of osteopontin in diabetic rats.

This study was designed to investigate the effects of mangiferin on renal fibrosis, osteopontin production, and inflammation in the kidney of diabetic rats. Diabetes was induced through the single administration of streptozotocin (55 mg/kg, i.p.). Diabetic rats were treated with mangiferin (15, 30, and 60 mg/kg/day, i.g.) for 9 weeks. The kidney was fixed in 10% formalin for glomerulus fibrosis examination using Masson trichrome staining. Kidney and blood were obtained for assays of the associated biochemical parameters. Chronic mangiferin treatment prevented renal glomerulus fibrosis evidenced by decreases in Mason-stained positive area of glomeruli, protein expression of type IV collagen, and α-smooth muscle actin in the kidney of diabetic rats, in comparison with decreases in mRNA and protein expression of osteopontin as well as protein expression of cyclooxygenase 2 and NF-кB p65 subunit in the renal cortex of diabetic rats. Moreover, mangiferin reduced the levels of interleukin 1ß in both the serum and the kidney of diabetic rats. Our findings demonstrate that mangiferin prevents the renal glomerulus fibrosis of diabetic rats, which is realized through the suppression of osteopontin overproduction and inflammation likely via inactivation of NF-кB.

[Microstructure and mechanical property of a new IPS-Empress 2 dental glass-ceramic].

OBJECTIVE: To investigate the microstructure and mechanical properties of a new IPS-Empress 2 dental glass-ceramic. METHODS: AFM, SEM and XRD were used to analyze the microstructure and crystal phase of IPS-Empress 2 glass-ceramic. The flexural strength and fracture toughness were tested using 3-point bending method and indentation method respectively. RESULTS: IPS-Empress 2 glass-ceramic mainly consisted of lithium disilicate crystal, lithium phosphate and glass matrix, which formed a continuous interlocking structure. The crystal phases were not changed before and after hot-pressed treatment. AFM showed nucleating agent particles of different sizes distributed on the highly polished ceramic surface. The strength and fracture toughness were 300 MPa and 3.1 MPam(1/2). CONCLUSION: The high strength and fracture toughness of IPS-Empress 2 glass ceramic are attributed to the fine lithium disilicate crystalline, interlocking microstructure and crack deflection.

[Characterization of N-glycan mapping of bioengineering recombinant erythropoietin by capillary electrophoresis with laser-induced fluorescence].

AIM: N-Glycans in recombinant human erythropoietin (EPO) are essential to in vivo biological activity. This paper is to develop a method for mapping sialyated or asialyated N-glycans of EPO. METHODS: At first, N-glycans linked to asparagines in glycoprotein EPO were released by peptide N-glycosidase F. To map asialyated N-glycans, sialic acid in N-glycans were removed by incubating N-glycans with sialidase. Oligosaccharides were labeled with a sensitive fluorescent dye 8-aminopyrene-1,3,6-trisulfonate (APTS), and all of the labeled oligosaccharides released from EPO were mapped by capillary gel electrophoresis with laser-induced fluorescence. The relationship between N-glycans and bioactivity of EPO was investigated on the basis of N-glycan mapping spectra. RESULTS: N-Glycans of seven different batches of EPO were mapped. Each sample was analysed twice, with and without sialidase treatment. The results showed that N-glycans of each sample were approximately the same. But when the expression vector was different, the types of N-glycans and their relative content were quite different. In case of asialyated N-glycan mapping, the retention time of each oligosaccharide delayed greatly, and most importantly, the resulted sialic acid peak can be used as a quantitative standard to determine sialic acid content in N-glycans of EPO. In addition, the difference of N-glycan mapping was observed when the in vivo biological activity of EPO was different. CONCLUSION: The approach in this article for determining N-glycan mapping can be applied to determine the source of EPO and the difference between each batch. It is also a suitable tool for routinely controlling the inner quality of EPO by coupled with peptide mapping.