Tandem chromosome fusions in karyotypic evolution of Muntiacus: evidence from M. feae and M. gongshanensis

The muntjacs (Muntiacus, Cervidae) are famous for their rapid and radical karyotypic diversification via repeated tandem chromosome fusions, constituting a paradigm for the studies of karyotypic evolution. Of the five muntjac species with defined karyotypes, three species (i.e. Muntiacus reevesi, 2n = 46; M. m. vaginalis, 2n = 6/7; and M. crinifrons, 2n = 8/9) have so far been investigated by a combined approach of comparative chromosome banding, chromosome painting and BAC mapping. The results demonstrated that extensive centromere–telomere fusions and a few centric fusions are the chromosomal mechanisms underlying the karyotypic evolution of muntjacs. Here we have applied the same approach to two additional muntjac species with less well-characterized karyotypes, M. feae (2n = 14♂) and M. gongshanensis (2n = 8♀). High-resolution G-banded karyotypes for M. feae and M. gongshanensis are provided. The integrated analysis of hybridization results led to the establishment of a high-resolution comparative map between M. reevesi, M. feae, and M. gongshanensis, proving that all tandem fusions underpinning the karyotypic evolution of these two muntjac species are also centromere–telomere fusions. Furthermore, the results have improved our understanding of the karyotypic relationships of extant muntjac species and provided compelling cytogenetic evidence that supports the view that M. crinifrons, M. feae, and M. gongshanensis should each be treated as a distinct species.     

Apoptosis, proliferation and gene expression patterns in mouse developing tongue

The Fgf/Fgfr (Fgf receptor) and Bmp signal pathways are critical for embryonic development and postnatal growth. In order to address their roles in tongue development, preliminary study of expression patterns of some important members in the two families, as well as of apoptosis and proliferation, were carried out in mouse developing tongue. Apoptosis in tongue is a very late event in embryogenesis, restricted to the upper layer of the epithelium whereas proliferation is very vigorous at the early stage of tongue development and remains active throughout embryogenesis. Bmp2, −4 and -5 were localized within the mesenchyme at the early embryonic stage of tongue development (E12 to E13), whereas Bmp3 and Bmp7 were mainly expressed in the epithelium. Most of these molecules were also seen in the tongue muscles at postnatal stages. Among Fgfr isoforms, Fgfr1c, −2b, and -2c were detected in embryogenesis with peak expression at E11 to E13. Fgfr1c and Fgfr2c were localized within the mesenchyme, while Fgfr2b was mainly expressed in the epithelium. High expression of Fgf7 and Fgf10 was also detected in the mesenchyme at the early embryonic stage of tongue development, corresponding to the Fgfr expression, suggesting that they are among the principal ligands functioning at the early embryonic expanding stage. Fgf2 was seen in the tongue muscles at the late embryonic and postnatal stages. These results suggest that Bmp and Fgf signalling regulates tongue development at multiple stages, possibly related to proliferation and differentiation.     

Inhibitory effects of rat alpha2 macroferoprotein (alphaMFP), an acute phase globulin, on galactosamine hepatitis.

Refractoriness to Gal N toxicity occurs especially in fetal rats, newborn rats, and in rats after partial hepatectomy. An injury however (laparotomy, incision on the back or ip BaSO₄ suspension), prior to Gal N administration, also inhibits Gal N toxicity. In all these circumstances high levels of rat α₂-macrofetoprotein (α_MFP) occur. This protein is an acute phase reactant and is identical to rat α₂-macroglobulin. α_MFP isolated from the serum of injured rats and then administered to normal rats strongly inhibits Gal N toxicity. When time interval between the preceding injury, provoking α_MFP production and Gal N administration shortens, the inhibiting effects are less and α_MFP production remains low.During resistance to Gal N, the primary and secondary biochemical lesions of Gal N persist and the protecting effect of α_MFP must be due to another mechanism, operating in later phases of cell injury. Very probably this is attributable to the stabilizing effect on membranes of hepatocytic organelles and the plasma membranes. As α_MFP is an acute phase reactant the importance of these proteins to the course of hepatitis must be considered.     

骨水泥强化椎弓根螺钉固定治疗老年退行性腰椎疾病的疗效观察

目的评价骨水泥强化椎弓根螺钉固定治疗老年退行性腰椎疾病的近期临床疗效。方法回顾性分析2011年6月~2013年5月采用聚甲基丙烯酸甲酯(PMMA)骨水泥强化椎弓根螺钉固定结合后路椎体间植入聚醚醚酮(PEEK)材质椎间融合器治疗老年退行性腰椎疾病30例。所有患者术前骨密度检测均符合骨质疏松诊断(超声骨密度值测定-2.5)。结果 30例患者均顺利完成手术,术中无神经及硬膜损伤,骨水泥无严重渗漏,术后复查X线、CT显示骨水泥分布均匀。随访10~21个月,平均(16±2.11)个月,神经受压症状均得到改善。VAS评分术前(7.01±1.44)、术后6个月随访为(3.00±0.57)、末次随访为(2.23±1.19);JOA评分术前为(9.98±5.64)、术后6个月随访为(17.99±1.41)、末次随访为(18.42±1.47);ODI评分术前为(0.64±0.24)、术后6个月为(0.27±0.07)、末次随访为(0.22±0.09)。三项评分术后6个月、末次随访分别与术前对比差异有统计学意义;术后6个月和末次随访对比差异无统计学意义。末次随访时复查X线或CT显示椎弓根螺钉无松动,椎间融合器无下沉,椎间融合满意,融合率为86.7%。结论使用骨水泥强化椎弓根螺钉能够提高螺钉对伴有骨质疏松的椎体的握持力,防止椎弓根螺钉松动,保证较高的椎间融合率,是治疗老年退行性腰椎疾病一种安全而有效的手术方式。     

肾综合征出血热病毒特异性双价纯化免疫血清F（ab）2的制备和临床治疗应用

１９８８年至１９９１年对收治的发病５日以内的肾综合征出血热（ＨＦＲＳ）病人应用姬鼠型ＨＦＲＳＶ陈株及家鼠型ＨＦＲＳＶＲ２２株，免疫猪所制备的特异性双价纯化免疫血清Ｆ（ａｂ）２（称Ｆ（ａｂ）２血清），治疗ＨＦＲＳ病人６５例作为研究组，以４４例作为对照组。治疗结果表明：①球结膜水肿渗出减轻，２４小时出血减轻；②白细胞病毒抗原消失迅速；③研究组出院平均早９．１天；④在洽疗后２、４日，对照组的特异性免疫荧光ＩｇＭ抗体明显高于研究组的。⑤其他实验室检测指标都以研究组为优。提纯后的免疫血清Ｆ（ａｂ）２无抗体－介导反应，无副作用及过敏反应。它含有特异性中和抗体及其他免疫因子，可中和清除体内的病毒抗原，减轻病毒血症及毛细血管壁的损伤，阻断病情发展，促进病情恢复。     

Functional interaction of auxiliary subunits and synaptic proteins with Ca(v)1.3 may impart hair cell Ca2+ current properties

We assessed the functional determinants of the properties of L-type Ca(2+) currents in hair cells by co-expressing the pore-forming Ca(V)1.3alpha(1) subunit with the auxiliary subunits beta(1A) and/or alpha(2delta). Because Ca(2+) channels in hair cells are poised to interact with synaptic proteins, we also co-expressed the Ca(V)1.3alpha(1) subunit with syntaxin, vesicle-associated membrane protein (VAMP), and synaptosome associated protein of 25 kDa (SNAP25). Expression of the Ca(V)1.3alpha(1) subunit in human embryonic kidney cells (HEK 293) produced a dihydropyridine (DHP)-sensitive Ca(2+) current (peak current density -2.0 +/- 0.2 pA/pF; n = 11). Co-expression with beta(1A) and alpha(2delta) subunits enhanced the magnitude of the current (peak current density: Ca(V)1.3alpha(1) + beta(1A) = -4.3 +/- 0.8 pA/pF, n = 10; Ca(V)1.3alpha(1) + beta(1A) + alpha(2delta) = -4.1 +/- 0.6 pA/pF, n = 9) and produced a leftward shift of approximately 9 mV in the voltage-dependent activation of the currents. Furthermore, co-expression of Ca(V)1.3alpha(1) with syntaxin/VAMP/SNAP resulted in at least a twofold increase in the peak current density (-4.7 +/- 0.2 pA/pF; n = 11) and reduced the extent of inactivation of the Ca(2+) currents. Botulinum toxin, an inhibitor of syntaxin, accelerated the inactivation profile of Ca(2+) currents in hair cells. Immunocytochemical data also indicated that the Ca(2+) channels and syntaxin are co-localized in hair cells, suggesting there is functional interaction of the Ca(V)1.3alpha(1) with auxiliary subunits and synaptic proteins, that may contribute to the distinct properties of the DHP-sensitive channels in hair cells.     

A novel serine protease of the mammalian HtrA family is up-regulated in mouse uterus coinciding with placentation

This paper characterizes a novel gene, previously identified as uniquely regulated at implantation in mouse uterus. We cloned its full mRNA sequence encoding a serine protease possessing an IGF-binding domain and named it pregnancy-related serine protease (PRSP). PRSP is structurally similar to mammalian HtrA1 (56% amino acid similarity). Northern analysis revealed that the expression of PRSP mRNA was low before pregnancy, but it was increased at implantation and markedly up-regulated post-implantation. In-situ hybridization localized low levels of mRNA expression to the epithelium and stroma during very early pregnancy, but high expression to the decidual cells on day 8.5, primarily at the mesometrial pole where the placenta was forming. By day 10.5, PRSP mRNA was detected in the placenta. We also cloned an alternatively spliced PRSP mRNA that is expressed at a very low level. We located PRSP gene on chromosome 5 and established its intron/exon structure, which unambiguously explains how the two mRNA variants are produced through alternative splicing. Based on PRSP protein domain structure and its unique expression during pregnancy, we propose that PRSP plays an important role in the formation/function of the placenta.     

Myosin VIIA gene: heterogeneity of the mutations responsible for Usher syndrome type IB

Usher syndrome is recognized as the most frequent cause of hereditary deaf-blindness. Usher syndrome type I (USH1), the most severe form of the disease, is characterized by profound congenital sensorineural deafness, constant vestibular dysfunction, and retinitis pigmentosa of prepubertal onset. This form is genetically heterogeneous and five loci (USH1A-E) have been mapped thusfar. However, only the gene responsible for USH1 B (which accounts for approximately 75% of USH1 cases) has been characterized. It encodes a long-tailed unconventional myosin, myosin VIIA, with a predicted 2215 amino acid sequence. Primers covering the complete myosin VIIA coding sequence as well as the 3' non coding sequence were designed, allowing direct sequence analysis of each of the 48 coding exons and flanking splice sites in seven patients affected by USH1. Four novel mutations were thereby identified. The possibility should now be considered of a sequence-based prenatal diagnosis in some of the families affected by this very severe form of Usher syndrome.      

Recurrent genetic alterations in 26 colorectal carcinomas and 21 adenomas from Chinese patients

Colorectal cancer (CRC) is one of the most common malignancies worldwide. The incidence of CRC in the Chinese population has increased dramatically during the last two decades; however, nonrandom chromosomal alterations in Chinese patients have not been described. In the present study, comparative genomic hybridization (CGH) was applied to detect recurrent chromosome alterations in 26 primary colorectal carcinomas and 21 colorectal adenomas from Chinese patients. In CRC, several recurrent chromosomal changes were found, including gains of 8q (14/26 cases, 54%), 20q (54%), 3q (50%), 13q (50%), 5p (46%), 7p (42%), 7q (42%), and 12p (38%) and losses of 18q (65%) and 17p (42%). From comparison with previous CGH studies, the frequent gains of 3q and 12p might be distinctive occurrences in Chinese patients. The distribution of frequently found chromosomal alterations in different locations was studied. The gain of 20q was more frequently found in colon cancer (P<0.01) and the gain of 12p was more frequently found in rectal cancer. Chromosomal alterations were found in 19/21 of adenomas; the most frequent chromosomal alteration was the loss of 18q (9/21 cases, 43%). These recurrent alterations provide several starting points for the isolation of candidate oncogenes and tumor suppressor genes.     

单侧外周伤害性刺激诱发大鼠脊髓中转录因子CREB的双侧磷酸化(英文)

c AMP反应成分结合蛋白 (c AMP response elem ent-binding protein,CREB)是一种转录因子 ,它在磷酸化之后可调节靶基因的转录。 CREB在 13 3位置的丝氨酸的磷酸化 ,与脊髓中伤害性传入的处理有关 ,本文作者等用特殊抗体对此进行了免疫细胞化学研究。在正常大鼠 ,虽然几乎所有脊髓神经元的核中都可见 CREB的轻度着色 ,但磷酸化的 CREB仅见于双侧腰段脊髓的 ～ 层 (75± 15 vs60± 18)和 层 (9± 3 )。用福尔马林注射引起一侧后脚掌出现炎症时 ,可在双侧腰段脊髓看到磷酸化CREB细胞核的快速 (小于 5 min)和节段性的显著增多 ;它们主要分布在双侧背角表层 ～ 层 (2 5 4± 2 0 vs 2 62± 2 3 )、 层(115± 13 )和双侧 ～ 层 (3 46± 2 0 vs3 2 8± 2 6) ;而在对照和炎症组大鼠的胸段脊髓中均未见磷酸化 CREB的增加。在注射CFA诱发一侧炎症或切断一侧坐骨神经的实验组大鼠 ,也可看到至少延续到第三天的强而双侧性的 CREB的磷酸化。这种由一侧后肢伤害性传入引致腰段脊髓中镜像式双侧 CREB磷酸化的出现 ,与一般看到的损伤传入只在同侧脊髓背角引起某些神经化学改变的结果不同 ,可能是人神经损伤后或在实验动物中出现对侧镜像式疼痛过敏现象的基础