红外多波长无创人体血糖检测阵列模型的研究

无创血糖监测不仅可以减少患者的痛苦，还能进行连续测量，从而降低并发症的发生，它是一种不需收集血样进行体内血糖浓度测量的新技术。本文根据朗伯-比尔定律(The Lambert—Beer Law)原理，为克服无创血糖检测研究中的难点和缺陷，详细分析了血糖红外光谱的吸收特性，利用阵列技术设计了红外多波长无创血糖检测传感器阵列模型，对关键技术进行了讨论。用ME算法建立了信号检测和标定数学模型，结合了人体各种影响因素，使红外无创血糖检测的精度和稳定性得到了改善。列举了详细的实验实施步骤，同时叙述了系统调试的详细过程，讨论了无创血糖检测中需要注意的问题。     

Retinal dehydrogenase-2 is inhibited by compounds that induce congenital diaphragmatic hernias in rodents

Currently, the etiology of the serious developmental anomaly congenital diaphragmatic hernia (CDH) is unknown. We have used an animal model of CDH to address this issue. We characterized four separate teratogens that produced diaphragmatic defects in embryonic rats that are similar to those in infants with CDH. We then tested the hypothesis that all these agents share the common mechanism of perturbing the retinoid-signaling pathway. Specifically, inhibition of retinal dehydrogenase-2 (RALDH2), a key enzyme necessary for the production of retinoic acid and that is expressed in the developing diaphragm, was assayed by measuring retinoic acid production in cytosolic extracts from an oligodendrocyte cell line. The following compounds all induce posterolateral defects in the rat diaphragm; nitrofen, 4-biphenyl carboxylic acid, bisdiamine, and SB-210661. Importantly, we demonstrate that they all share the common mechanism of inhibiting RALDH2. These data provide an important component of mounting evidence suggesting that the retinoid system warrants consideration in future studies of the etiology of CDH.     

表达鼠精子Cyritestin蛋白的减毒沙门氏菌疫苗株的构建及其鉴定

目的 构建表达鼠精子eyritestin蛋白的可口服减毒沙让氏菌活疫苗株。方法 应用质粒TAZ83／13，将之进行双酶切获得含有成熟cyritestin蛋白cDNA序列的酶切片段。将其插入表达载体yA3149中，构建重组质粒pCFL。将该重组质粒转入鼠沙门氏伤寒杆菌疫苗株X4632和X4550中，以获得重组菌株X4632（pCFL)和X4550（pCFL)。结果 该两种无抗药性的重组菌株在体外营养选择压力下，可较稳定地携带重组质粒传代繁殖。X4550(pCFL)在体内可较稳定地害居于Peyer‘s结，肠系膜淋巴结和脾脏；X4632（pCFL)可较稳定地定居于Peyer‘s结。二者均可表达被抗cyritestin单抗（mAb)识别的重组cyritestin蛋白。口服该疫苗菌株无明显的毒性作用。结论 X4632（pCFL),X4550（pCFL)疫苗株的构建，为研究以cyritestin为靶抗原的精子抗原避孕疫苗打下了基础。     

Connexin26 gene ( GJB2): prevalence of mutations in the Chinese population

The connexin26 gene ( GJB2) has been shown to be responsible for DFNB1 and DFNA3 (Autosomal Recessive Hereditary Nonsyndromic Deafness Locus 1 and Autosomal Dominant Hereditary Nonsyndromic Deafness Locus 3). Two hundred ten independently ascertained Chinese probands with nonsyndromic hearing loss (NSHL) were evaluated for mutations in GJB2, including 43 probands from families with more than one sib with NSHL, likely indicating dominant inheritance, and sporadic cases of NSHL, compatible with recessive inheritance. Of the 210 probands, 43 (20%) were homozygous or heterozygous for mutations in GJB2. Four different mutations were identified: 35delG, 109G-A, 235delC, and 299-300delAT. It was confirmed that GJB2 mutations are an important cause of hearing loss in this population. Of these four mutations, 235delC was the most prevalent at 93%; yet the 35delG mutation, which is the most common GJB2 mutation in Caucasian subjects (Europeans and Americans), was found in low frequency in the present study. It appears from our limited data and reports from other East Asians that 235delC is the most prevalent GJB2 mutation in these populations. GJB2 mutations are consistent with ethnic predilections.     

戊二醛交联甲壳胺膜的制备及其渗透性的研究

本文制备戊二醛交联甲壳胺膜。研究了戊二醛交联对膜的亲水性，结晶性的影响；探讨了交联对肌肝、尿素、尿酸的渗透；测定膜在于干态和湿态下的力学机械性能。     

Reaction of chitosan with genipin and its fluorogenic attributes for potential microcapsule membrane characterization

This study investigates the fluorogenic characteristics of the chitosan-genipin reaction for applications in microencapsulation research. Results showed that the chitosan-genipin reaction generated a colored and fluorescent product, with optimal excitation and emission wavelengths at 369 and 470 nm, respectively. Furthermore, it was found that reaction conditions affected the fluorescence intensity of the product. Mixture at the ratio of 4:1 (chitosan: genipin by weight) fluoresced the most. It also fluoresced stronger if the reaction occurred at higher temperature, with the intensity of 10.4 x 10(5) CPS at 37 degrees C, 5.9 x 10(5) CPS at 20 degrees C, and 2.5 x 10(5) CPS at 4 degrees C. As well, the fluorescence of the mixture developed gradually over time, attaining the emission maxima of 2.9 x 10(5), 7.6 x 10(5), and 10.0 x 10(5) CPS in 1, 6, and 18 h, respectively. Chitosan-coated alginate microcapsules were prepared without prior labeling, to which subsequent genipin treatment was applied in order to examine the potential of using genipin in microcapsule characterization. Chitosan bound to the alginate beads interacted with genipin, from which the resultant fluorescent signals allowed for clear visualization of the chitosan coating under confocal laser scanning microscopy. The relative fluorescence intensity across the chitosan membrane was found to be considerably higher than the controls (175 vs. 50). The membrane thickness measured was 29.2 +/- 7.3 microm. These findings demonstrate a convenient and effective way of characterizing chitosan-based microcapsules using genipin as a fluorogenic marker, a technique that will be useful in microcapsule research and other biomedical applications.     

Reactive Compatibilization of PA6/LDPE Blends with Glycidyl Methacrylate Functionalized Polyolefins

Summary: Blends of polyamide‐6 (PA6) and low density polyethylene (LDPE) were compatibilized by melt mixing with various polyolefins functionalized with glycidyl methacrylate (GMA), i.e., GMA grafted LDPE (LDPE‐g‐GMA), GMA grafted styrene‐ethylene/butylene‐styrene block copolymer (SEBS‐g‐GMA) and ethylene‐co‐glycidyl methacrylate copolymer (E‐GMA). Blends with PA6/LDPE composition ratios of 25/75 and 75/25 wt.‐%/wt.‐% were prepared in a Brabender internal mixer and their properties were evaluated by SEM, rheological measurements and DSC. Morphological investigation by SEM showed a neat improvement of phase dispersion and interfacial adhesion in all compatibilized blends when compared to PA6/LDPE binary blends. The variation of the dispersed phase size was analyzed as a function of blend composition, compatibilizer concentration and GMA content. The emulsification curves of compatibilized blends showed that the equilibrium size of dispersed particles at the saturation concentration of copolymer was lower when PA6 was the major component. The finest dispersion of the LDPE phase (<0.25 μm) was observed in the presence of SEBS‐g‐GMA copolymer. LDPE‐g‐GMA and E‐GMA displayed a similar compatibilizing efficiency. In all cases, the blends with a polyamide matrix presented a marked rise in torque and melt viscosity with increasing compatibilizer content. These effects were accounted for by a reaction between the epoxide groups of LDPE‐g‐GMA and the carboxyl/amine end‐groups of PA6, leading to the formation of an interchain graft copolymer. The phase transition processes of PA6 in the blends were influenced by the compatibilizer content and the interfacial interactions between the polymer components, suggesting a different role for the compatibilizer at the PA6/LDPE interface.

SEM micrograph of PA6/LDPE 25/75 blend compatibilized with 2.5 phr SEBS‐g‐GMA.     

Effects of ammonium metavanadate treatment upon macrophage glutathione redox cycle activity, superoxide production, and intracellular glutathione status

Female B6C3F1 mice were given intraperitoneal injections of ammonium metavanadate (2.5 or 10 mg V/Kg), ammonium chloride, or sodium phosphate buffer every 3 days for 6 weeks. Resident peritoneal macrophages were harvested, lysed by freeze-thawing, and the resulting cytolysate was assayed for total protein content and enzyme activities of glutathione reductase, glutathione peroxidase, and glucose-6-phosphate dehydrogenase. In addition, peritoneal macrophages were assayed for superoxide production using nitroblue tetrazolium reduction, as well as for intracellular levels of oxidized and reduced glutathione. Exposure of mice to vanadium resulted in a dose-trend depression in the three macrophage enzyme activities as compared with the controls. Vanadium treatment resulted in a similar decrease in the production of superoxide anion, and an increase in levels of oxidized glutathione; however, the total glutathione pool (reduced plus oxidized forms) was not affected.     

Immunochemical data suggesting a pattern for the evolution of human placental alkaline phosphatase

Hyperimmune absorbed rabbit antisera which were reactive with epitopes specific for individual variants of human placental alkaline phosphatase were tested for their reactivity with primate placental alkaline phosphatases. Using the three epitope-specific reactivities defined previously, we found that: epitope I is present in the S-, D- and I-variants of human placental phosphatase, and in the chimpanzee and pygmy chimpanzee placentae; epitope II is present in the F- and 17-variants, and in the Nagao isoenzyme of human placental alkaline phosphatase, and in some orangutan placentae and all spider monkey placentae tested; epitope III is present in the F- and 17-variants, and the Nagao isoenzyme of human placental alkaline phosphatase, and in all the spider monkey placentae and the single squirrel monkey placenta examined. The binding assay was complemented by a competitive radioimmunoassay, which confirmed that the spider monkey placental samples were binding to the same antibody population which bound the human enzymes. The presence of epitopes characteristic of rare human placental phosphatase variants in these remote primate relatives suggests that the rare variants in the current human population have been present during the entire course of evolution. The presence of both epitopes characteristic of the Nagao isoenzyme in spider monkeys suggests that this variant isoenzyme is closely related to the enzyme present in the primate placenta at the time of species divergence (humans and New World monkeys). A hypothetical scheme for this divergence is proposed.