Research on tunable distributed SPR sensor based on bimetal film.

In order to overcome the limitations in range of traditional prism structure surface plasmon resonance (SPR) single-point sensor measurement, a symmetric bimetallic film SPR multi-sensor structure is proposed. Based on this, the dual-channel sensing attenuation mechanism of SPR in gold and silver composite film and the improvement of sensing characteristics were studied. By optimizing the characteristics such as material and thickness, a wider range of dual-channel distributed sensing is realized. Using a He-Ne laser (632.8 nm) as the reference light source, prism-excited symmetric SPR sensing was studied theoretically for a symmetrical metal-clad dielectric waveguide using thin-film optics theory. The influence of the angle of incidence of the light source and the thickness of the dielectric layer on the performance of SPR dual formant sensing is explained. The finite-difference time-domain method was used for the simulation calculation for various thicknesses and compositions of the symmetric combined layer, resulting in the choice of silver (30 nm) and gold (10 nm). When the incident angle was 78 deg, the quality factor reached 5960, showing an excellent resonance sensing effect. The sensitivity reached a maximum of 5.25×10-5 RIU when testing the water content of an aqueous solution of honey, which proves the feasibility and practicality of the structure design. The structure improves the theoretical basis for designing an SPR multi-channel distributed sensing system, which can greatly reduce the cost of biochemical detection and significantly increase the detection efficiency.

Lithium Treatment Prevents Apoptosis in Neonatal Rat Hippocampus Resulting from Sevoflurane Exposure.

We aimed to observe the therapeutic effects of lithium on inhalational anesthetic sevoflurane-induced apoptosis in immature brain hippocampus. From postnatal day 5 (P5) to P28, male Sprague-Dawley pups were intraperitoneally injected with lithium chloride or 0.9 % sodium chloride. On P7 after the injection, pups were exposed to 2.3 % sevoflurane or air for 6 h. Brain tissues were harvested 12 h and 3 weeks after exposure. Cleaved caspase-3, nNOS protein, GSK-3ß,p-GSK-3ß were assessed by Western blot, and histopathological changes were assessed using Nissl stain and TUNEL stain. From P28, we used the eight-arm radial maze test and step-through test to evaluate the influence of sevoflurane exposure on the learning and memory of juvenile rats. The results showed that neonatal sevoflurane exposure induced caspase-3 activation and histopathological changes in hippocampus can be attenuated by lithium chloride. Sevoflurane increased GSK-3ß activity while pretreatment of lithium decreased GSK-3ß activity. Moreover, sevoflurane showed possibly slight but temporal influence on the spatial learning and the memory of juvenile rats, and chronic use of lithium chloride might have the therapeutic effect. Our current study suggests that lithium attenuates sevoflurane induced neonatal hippocampual damage by GSK-3ß pathway and might improve learning and memory deficits in rats after neonatal exposure.

Proteomic analysis of intestinal ischemia/reperfusion injury and ischemic preconditioning in rats reveals the protective role of aldose reductase.

Intestinal ischemia/reperfusion (I/R) injury is a critical condition associated with high morbidity and mortality. Studies show that ischemic preconditioning (IPC) can protect the intestine from I/R injury. However, the underlying molecular mechanisms of this event have not been fully elucidated. In the present study, 2-DE combined with MALDI-MS was employed to analyze intestinal mucosa proteomes of rat subjected to I/R injury in the absence or presence of IPC pretreatment. The protein content of 16 proteins in the intestinal mucosa changed more than 1.5-fold following intestinal I/R. These proteins were, respectively, involved in the cellular processes of energy metabolism, anti-oxidation and anti-apoptosis. One of these proteins, aldose reductase (AR), removes reactive oxygen species. In support of the 2-DE results, the mRNA and protein expressions of AR were significantly downregulated upon I/R injury and enhanced by IPC as confirmed by RT-PCR and western blot analysis. Further study showed that AR-selective inhibitor epalrestat totally turned over the protective effect of IPC, indicating that IPC confers protection against intestinal I/R injury primarily by increasing intestinal AR expression. The finding that AR may play a key in intestinal ischemic protection might offer evidences to foster the development of new therapies against intestinal I/R injury.

Gut Barrier Dysfunction Induced by Aggressive Fluid Resuscitation in Severe Acute Pancreatitis is Alleviated by Necroptosis Inhibition in Rats.

Fluid resuscitation is the first-line antishock treatment in severe acute pancreatitis (SAP). Currently, although mentions of complications related to aggressive fluid resuscitation are very frequent, a lack of proper handling of complications remains. One of the most important complications is intestinal barrier injury, including intestinal ischemia-reperfusion injury following aggressive fluid resuscitation. Once injured, the intestinal barrier may serve as the source of additional diseases, including systemic inflammatory response syndrome and multiple organ dysfunction syndrome, which aggravate SAP. This study focused on the underlying mechanisms of gut barrier dysfunction in rats induced by aggressive fluid resuscitation in SAP. This study further indicated the important role of necroptosis in intestinal barrier injury which could be relieved by using necroptosis-specific inhibitor Nec-1 before aggressive fluid resuscitation, thus reducing intestinal barrier damage. We also found pancreas damage after intestinal ischemia/reperfusion challenge and indicated the effects of high mobility group protein B1 in the vicious cycle between SAP and intestinal barrier damage.

[Detecting the haplotype of three Y-STR loci by fluorescent multiplex amplification].

OBJECTIVE: To establish a fluorescent multiplex PCR system for typing Y-STR loci Y-GATA-A7.1, DYS456 and DYS443, and investigate their haplotype frequencies in Chinese Han population. METHODS: 203 unrelated males of Han population living in Zhengzhou were typed by fluorescent multiplex amplification system and ABI 3100 genetic analyzer. RESULTS: In Zhengzhou Han population, 5,6 and 6 different alleles were observed for Y-GATA-A7.1, DYS456 and DYS443 loci, and their gene diversity (GD) were 0.669 2, 0.583 9 and 0.705 3 respectively. A total of 44 different haplotypes formed by these three loci was identified and the haplotype diversity (HD) reached 0.952 3. CONCLUSION: The fluorescent multiplex system for these three Y-STR loci will be very powerful for forensic individual identification and paternity testing in Chinese Han population.

Sevoflurane-induced down-regulation of hippocampal oxytocin and arginine vasopressin impairs juvenile social behavioral abilities.

Cumulative evidence indicates that early childhood anesthesia can alter a child's future behavioral performance. Animal researchers have found that sevoflurane, the most commonly used anesthetic for children, can produce damage in the neonatal brains of rodents. To further investigate this phenomenon, we focused on the influence of sevoflurane anesthesia on the development of juvenile social behavioral abilities and the pro-social proteins oxytocin (OT) and arginine vasopressin (AVP) in the neonatal hippocampus. A single 6-h sevoflurane exposure for postnatal day 5 mice resulted in decreased OT and AVP messenger RNA (mRNA) and protein levels in the hippocampus. OT and AVP proteins became sparsely distributed in the dorsal hippocampus after the exposure to sevoflurane. Compared with the air-treated group, mice in the sevoflurane-treated group showed signs of impairment in social recognition memory formation and social discrimination ability. Sevoflurane anesthesia reduces OT and AVP activities in the neonatal hippocampus and impairs social recognition memory formation and social discrimination ability in juvenile mice.