OBJECTIVE: To study the preparation and in vitro release profile of compound vitamin microencapsules using cross-linked gelatin as wall material. METHODS: At the presence of hydrogen peroxide, the cross-linked gelatin was prepared with ferulic acid as the cross-linking agent. During this reaction, horseradish peroxidase was used as the catalyst. Influences of reaction conditions on the cross-linking degree were investigated. Compound vitamin microcapsules were prepared by spray-drying technique using the obtained cross-linked gelatin as wall material. The core material was the mixture of thiamine hydrochloride (vitamin B1), riboflavin (vitamin B2), pyridoxine hydrochloride (vitamin B6), folic acid and nicotinamide. The effect of the ratio of wall material to core material on the encapsulation efficiency and loading of the vitamins were investigated. The size and surface morphology of the compound vitamin microcapsules were characterized. The encapsulation efficiency, loading and in vitro release property of the core material were determined by fluorospectrophotometry. RESULTS: A comparatively high cross-linking degree (ca. 10%) of cross-linked gelatin was obtained under the following reaction conditions:temperature of 40°C, pH value of 8.0, gelatin concentration of 9% (W/V), ferulic acid concentration of 40 mmol·L-1 and reaction time of 24 h. The vitamins were embedded by the cross-linked gelatin and the encapsulation efficiency was more than 85%. Scanning electron microscopy (SEM) study showed that the compound vitamin microcapsules had a regular spherical shape but the majority presented rough surfaces or dents. Particle size analysis indicated that the microcapsules had a mean diameter of 15.27 μm. At the ratio of coating material to core material was 10/1 (W/W), the vitamins encapsulated with the cross-linked gelatin released completely in 30 min in simulated gastric fluid, and they released completely in 16 min in simulated intestinal fluid. They released slower than the vitamins encapsulated with the gelatin accordingly. CONCLUSION: Compound vitamin microencapsules with high encapsulation efficiency and sustained release effect can be obtained by spray-drying using cross-linked gelatin as wall material.

OBJECTIVE: To determine the expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) of peripheral blood monocytes in patients with acute coronary syndromes (ACS),and to further explore the effect of anti-inflammatory factor interleukin-10 (IL-10) on the expression of LOX-1. METHODS: Twenty-eight healthy controls and 28 ACS patients were enrolled in the study. The levels of IL-10 and tumor necrosis factor (TNF-alpha) were determined by enzyme-linked immunosorbnent assay(ELISA). The monocytes of peripheral blood in patients and controls were isolated and incubated with exogenous IL-10 (20 microg/L). The expression of LOX-1 protein and mRNA in the monocytes was examined by Western blot and reverse transcriptase PCR (RT-PCR). RESULTS: Compared with the healthy controls, the levels of serum IL-10 and TNF-alpha were significantly elevated in ACS patients (P<0.01). The expression of LOX-1 protein and mRNA was markedly upregulated in the isolated monocytes from ACS patients, which could be downregulated by IL-10 (20 microg/L, 3 h) (P<0.01). CONCLUSION The effect of anti-inflammatory factor IL-10 on the atherosclerosis may be a new mechanism resulting in plaque stabilization via the decreased LOX-1 expression of peripheral monocytes in ACS patients.
Acute Coronary Syndrome ; blood ; Aged ; Cells, Cultured ; Female ; Humans ; Interleukin-10 ; metabolism ; pharmacology ; Male ; Middle Aged ; Monocytes ; cytology ; metabolism ; RNA, Messenger ; biosynthesis ; genetics ; Scavenger Receptors, Class E ; biosynthesis ; genetics

Bile Duct Neoplasms ; diagnosis ; Bile Ducts, Intrahepatic ; CA-19-9 Antigen ; blood ; Carcinoma, Hepatocellular ; diagnosis ; Cholangiocarcinoma ; diagnosis ; Humans ; Liver Neoplasms ; diagnosis

OBJECTIVE: To investigate the toxic effects of nano-sized neodymium oxide( nano-Nd_2O_3) on the central nervous system in mice. METHODS: Specific pathogen free female ICR mice were randomly divided into control group,lowdose group and high-dose group,with 12 rats in each group. The mice in low-dose group and high-dose group were treated with nano-Nd_2O_3 by nasal drip method at 80 and 160 mg/( kg·d) body weight for 30 days,while the mice in the control group were given 0. 9% sodium chloride solution. The water maze experiment and jump platform experiment were used to evaluate learning and memory ability. Hippocampus was examined using Hematoxylin-Eosin( HE) staining and glial fibrillary acidic protein( GFAP) immunohistochemical staining. The level of malondialdehyde( MDA) and the activity of total superoxide dismutase( T-SOD) in brain tissue were detected by microplate reader. RESULTS: The escape latency increased and the step down latency decreased in the low-dose group and high-dose group compared with the control group(P < 0. 05). No obvious pathological changes were observed by HE staining in brain hippocampus. Immunohistochemistry staining showed that the expression of GFAP protein in the hippocampal astrocytes of the low-and high-dose groups was higher than that in the control group,especially in the high-dose group,when compared with the control group. The MDA level increased and the T-SOD activity decreased in the low-and high-dose groups compared with the control group( P <0. 05). CONCLUSION: nano-Nd2 O3 can reduce the learning and memory ability of mice and increased GFAP expression in hippocampal astrocytes. The mechanism may be related to oxidative stress.

Itch is an unpleasant sensation that provokes the desire to scratch. While acute itch serves as a protective system to warn the body of external irritating agents, chronic itch is a debilitating but poorly-treated clinical disease leading to repetitive scratching and skin lesions. However, the neural mechanisms underlying the pathophysiology of chronic itch remain mysterious. Here, we identified a cell type-dependent role of the anterior cingulate cortex (ACC) in controlling chronic itch-related excessive scratching behaviors in mice. Moreover, we delineated a neural circuit originating from excitatory neurons of the ACC to the ventral tegmental area (VTA) that was critically involved in chronic itch. Furthermore, we demonstrate that the ACC→VTA circuit also selectively modulated histaminergic acute itch. Finally, the ACC neurons were shown to predominantly innervate the non-dopaminergic neurons of the VTA. Taken together, our findings uncover a cortex-midbrain circuit for chronic itch-evoked scratching behaviors and shed novel insights on therapeutic intervention.
Mice ; Animals ; Gyrus Cinguli/physiology* ; Pruritus/pathology* ; Mesencephalon ; Cerebral Cortex/pathology* ; Neurons/pathology*