鹅胃肠内分泌细胞的免疫组织化学定位

应用６种胃肠激素抗血清，对鹅胃肠各段的内分泌细胞分布进行了免疫组织化学定位。腺胃显示有较多促胃泌素释放肽和生长抑素细胞。肌胃有较多促胃泌素释放肽、生长抑素和胃泌素细胞，少量胰多肽细胞。幽门部有大量的生长抑素细胞，密集的胃泌素细胞，偶见胰多肽细胞。小肠内有胃泌素、胰多肽和生长抑素细胞，细胞类型和数量由前段向后段逐渐减少。未检出胃动素和抑胃肽细胞。     

Parental origin and mechanism of formation of X chromosome structural abnormalities: Four cases determined with RFLPs

Parental origin and mechanism of formation of X chromosome structural anbormalities were studied in one each case of dup(X)(pter p11.4::p22.1qter), del(X)(qterp11:), i(X)(qtercenqter), and inv dup(X) (pterq22::q22pter) using various X-linked RFLPs as genetic markers. Segregation and densitometric analyses on polymorphic DNAs revealed that the dup(Xp) and the del(Xp) are both of paternal origin and the i(Xq) and i dic(X) are of maternal origin. The dup(Xp) had arisen by an unequal sister chromatid exchange and the del(Xp) had occurred through an intrachromosomal breakage-reunion mechanism, both in the paternal X chromosome. The i(Xq) had arisen either through centromere fission of a maternal X chromosome, followed by duplication, of its long-arm, or through a translocation between two maternal X chromosomes after meiotic crossing-over. The inv dup(X) arose through sister chromatid breakage and reunion in a maternal X chromosome. These results, together with those of previous studies, suggest that thede novo abnormalities due to events involving centromere disruption arise predominantly during oogenesis, while those due to simple breakage-reunion events occur preferentially during spermatogenesis.     

腺苷对心肌梗死再灌注无复流的保护作用及其对一氧化氮和内皮素影响的实验研究

目的:探讨腺苷对心肌梗死再灌注无复流的保护作用,以及这种保护作用与腺苷对一氧化氮(NO)和内皮素(ET)影响的关系。方法:制作离体兔心急性心肌梗死模型。30只兔心随机分为三组:A:假手术组,B:心肌梗死再灌注组,C:腺苷+心肌梗死再灌注组。分别取灌流开始5min和再灌流90min时冠脉流出液2ml,测定乳酸脱氢酶(LDH)、肌酸激酶(CK)、内皮素(ET)及一氧化氮(NO)含量。灌流结束时,测量无复流区域面积的百分比,并在光镜下观察心肌细胞的变化情况。结果:(1)A组灌流开始与结束时和B组、C组开始灌流时冠脉流出液中LDH、CK含量相比无显著性差异;(2)B组各项化验指标分别进行组内比较其结果有统计学差异。(3)灌流结束时,B组与C组相比NO的降低和ET的升高有统计学差异。(4)C组和B组比较无复流区域面积百分比明显缩小,有统计学差异。结论:腺苷对心肌梗死再灌注无复流具有明显的保护作用。腺苷升高NO和降低ET的作用可能是其发挥保护作用的原因之一。     

Behavioral Characterization of Alcohol-Tolerant and Alcohol-Nontolerant Rat Lines and an F2 Generation

The Alcohol Tolerant (AT) and Alcohol Nontolerant (ANT) rats, selectively bred for ethanol-induced ataxia on the inclined plane at ALKO in Finland, were moved to the University of Colorado in 1998. The selection phenotype was tested on generation 60 animals in Colorado. In week one, ataxia was measured on the inclined plane 30 minutes after an intraperitoneal dose of 2 g/kg 15% w/v ethanol. Differences in ethanol-induced ataxia between the AT and ANT lines at the University of Colorado were similar to those in the original lines in Finland. In week two, ataxia was measured on the inclined plane at 5 and 30 minutes, and tolerance was measured as the time to regain the original angle of sliding. The AT rats rapidly developed tolerance to 2 g/kg ethanol on the inclined plane; tolerance development was significantly slower in the ANT rats. In week three, the animals were tested for the duration of loss of righting reflex (LORR) and blood ethanol concentration at regain of the righting reflex (BEC_RRR) following a dose of 3.5 g/kg. The AT rats had a significantly higher BEC_RRR than did the ANT rats, but did not differ in LORR. A separate experiment with previously untreated rats demonstrated that naïve animals of the two lines did not differ in BEC_RRR or LORR. AT and ANT rats were genotyped for the mutation that occurs in the gene for the α6 subunit of the GABA_A receptor, a natural mutation that is known to affect benzodiazepine responses. All ANT animals tested carried the mutant allele, whereas some AT families carried the mutation and others were wild type. There was no effect of the mutation in AT rats for any of the phenotypes that were tested. After several generations of brother–sister mating, the AT and ANT lines were more than 90% inbred as determined by genotyping. One AT (wild-type) line and one ANT (mutant) line were selected for breeding an F₂ intercross generation of 1200 animals. They were phenotyped for sensitivity and tolerance to ethanol on each of three consecutive weeks. Order of testing had a modest effect on some of the phenotypes: when tested during the third week as compared to weeks one or two, BEC_RRR was increased, 30-minute sensitivity was increased, and development of acute tolerance was increased. Statistically significant correlations were found between tolerance and sensitivity at both 5 and 30 minutes, and between LORR and BEC_RRR. The smaller (or absence of) significant correlations between others of the phenotypes indicate(s) that they are most likely controlled by different sets of genes.     

Preparation of graded porous titanium coatings on titanium implant materials by plasma spraying

Graded porous titanium coatings have been deposited on titanium substrates for dental implants by plasma spraying in an argon atmosphere. X-ray diffraction (XRD), scanning electron microscopy (SEM), surface roughness measurement, and tensile strength tests were performed on graded porous coatings. The results showed that Ti(3)O(5) was formed in the outermost surface of the porous coatings due to oxidation. The graded porous coatings consisted of three layers. The outer layer was full of macropores with a surface roughness of approximately 100 microm. The diameter of many macropores reached and even surpassed 150 microm, which could be beneficial for tissue to grow into the coating. The middle layer consisted of a mixture of micropores and macropores. The inner layer was a very dense and tight interface layer that included mechanical, physical, and metallurgical bonding. In tensile strength tests, testing bars peeled off the coatings, because the adhesive agent fractured, but the coatings remained intact.     

A Ser(365)-->Cys mutation of fibroblast growth factor receptor 3 in mouse downregulates Ihh/PTHrP signals and causes severe achondroplasia

Missense mutations in fibroblast growth factor receptor 3 (FGFR3) result in several types of human skeletal dysplasia, including the neonatally lethal dwarfism known as thanatophoric dysplasia. An engineered Ser(365)-->Cys substitution in mouse FGFR3, which is equivalent to a mutation associated with thanatophoric dysplasia-I in humans, has now been shown to cause severe dwarfism but not neonatal death. The mutant mice exhibit shortened limbs as a result of markedly reduced proliferation and impaired differentiation of growth plate chondrocytes. The receptor-activating mutation also resulted in downregulation of expression of the Indian hedgehog (IHH) and parathyroid hormone-related protein (PTHrP) receptor genes, both of which are important for bone growth. Interactions between FGFR3- and PTHrP-receptor-mediated signals during endochondral ossification were examined with embryonic metatarsal bones maintained in culture under defined conditions. Consistent with the in vivo observations, FGF2 inhibited bone growth in culture and induced downregulation of IHH and PTHrP receptor gene expression. Furthermore, PTHrP partially reversed the inhibition of long bone growth caused by activation of FGFR3; however, it impaired the differentiation of chondrocytes in an FGFR3-independent manner. These observations suggest that FGFR3 and IHH-PTHrP signals are transmitted by two interacting parallel pathways that mediate both overlapping and distinct functions during endochondral ossification.     

Molecular cloning and nucleotide sequence of a pestivirus genome, noncytopathic bovine viral diarrhea virus strain SD-1.

Genomic RNA of noncytopathic (NCP) bovine viral diarrhea virus (BVDV) strain SD-1 was extracted directly from serum obtained from a persistently infected animal. cDNA was synthesized and amplified by polymerase chain reaction (PCR) before cloning. The complete genomic nucleotide sequence was determined by sequencing at least two different clones from independent PCR reactions. The 5' and 3' end sequences of the SD-1 genome was determined from 5'-3' ligation clones. The complete genome sequence was comprised of 12,308 nucleotides containing one large open reading frame which encodes an amino acid sequence of 3898 residues with a calculated molecular weight of 438 kDa. In contrast to cytopathic (CP) BVDV strain NADL, which contains a cellular RNA insert of 270 nucleotides and CP BVDV strain Osloss, which has an inserted ubiquitin RNA sequence of 228 nucleotides, the NCP strain SD-1 had no insertion along the genome. Sequence comparison with other pestiviruses revealed that the overall nucleotide sequence homologies of SD-1 are 88.6% with NADL, 78.3% with Osloss, 67.1% with HoCV Alfort, and 67.2% with HoCV Brescia. The overall deduced amino acid sequence homologies of SD-1 are 92.7% with NADL, 86.2% with Osloss, 72.5% with HoCV Alfort, and 71.2% with HoCV Brescia. The most conserved nucleotide and amino acid sequences are located in the 5' untranslated region (5'UTR) and nonstructural protein p80 region, respectively. The viral glycoproteins, particularly gp53, and nonstructural proteins p54 and p58 have the lowest homology comparing both nucleotide and amino acid sequences between SD-1 and other pestiviruses. Extensive analyses of amino acid sequences for the viral structural proteins and nonstructural protein p54 regions from five pestiviruses led to the identification of four conserved domains (designated as C1, C2, C3, C4) and three highly variable domains (designated as V1, V2, V3) within this region. The C1, C2, and C3 domains are located in the capsid protein p14, glycoprotein gp48, and gp25, respectively. The C4 domain is located in the junction between gp53 and p54. Interestingly, out of three variable domains, two (V1, V2) are located in the same glycoprotein gp53. The third variable domain is located in the nonstructural protein p54.     

Detecting DNA repair capacity of peripheral lymphocytes from cancer patients with UVC challenge test and bleomycin challenge test

The objective of this study was to evaluate DNA repair capacity of cancer patients with the bleomycin (BLM) challenge test and the UVC challenge test. The human peripheral lymphocytes were collected from 33 patients with different kinds of cancers and 33 controls in the same hospital. The lymphocytes of each subject were divided into two groups: (1) In the BLM challenge test, the lymphocytes were treated with BLM (20 microgml(-1)) for 30 min, and repaired for 15 min. The DNA damage before and after BLM exposure was detected with comet assay to assess DNA repair capacity. (2) In the UVC challenge test, the lymphocytes were exposed to UVC (254 nm) at the dose of 1.5 Jm(-2). DNA damage of lymphocytes was measured before UVC exposure and at 90 and 240 min after UVC exposure using comet assay, then DNA repair percentage (DRP) was calculated. The results of this study indicate that the average DRPs of cancer patients were 75.63 +/- 3.11 and 68.98 +/- 4.19% calculated with tail length (TL) and tail moment (TM), respectively, in the BLM challenge test, which were significantly lower than those (91.11 +/- 1.09 and 88.19 +/- 1.71%) of controls (P < 0.01). Also, the mean DRPs of cancer patients were 49.19 +/- 3.47 and 58.27 +/- 3.64% calculated with TL and TM, respectively, in the UVC test, which were significantly lower than those (77.52 +/- 2.06 and 83.12 +/- 2.36%) of controls (P < 0.01). The correlation between the DRPs (%) drawn with TL and TM in the BLM test or between the DRPs (%) drawn with mean TL and mean TM in the UVC challenge test were significant (P < 0.05). The DNA repair capacity measured with the BLM and UVC challenge tests in 33 cancer patients was significantly lower than that in controls.