Objective To explore features and clinic values of LNR anatomy with multiple planar reconstruction techniques with 16-slice spiral CT at the same slice.Methods The lumbar vertebrae with normal adults of 55 cases and 23 cases with abnormal ENR caused by 8 cases with protrusion of lumbar disc, 5 cases with spinal stenosis,4 cases with malignant tumor,5 cases with trauma and 1 case with lumbar TB confirmed by operation were scanned with 16-slice spiral CT made in American GE company in routine posture of the lumbar vertebrae,reconstructed LNR with UNIX system in workstation (ADW 4.1),and analyzed their normal and abnormal anatomic manifestations at the same slice.Results All of LNR can symmetrically showed on oblique and coronal planes according to different segments:one segment from L1 to L5(55,100% ),two segments: from L1 to L2,L2 to L3 and L3 to L4(55,100% ),three segments: from L1 to L3 (49,88%),from L2to L4(46,84% )and from L3 to L5(20,36% ),four segments: from L1 to L4 (15,27% )and five segments:(8,15% ),respectively.Each LNR,including their whole shapes of passage from starting to end,direction,size,shape,tension and peripheral relationship and so on can showed clearly on oblique and coronal planes and on other planes. However,the later planes can increase LNR but decreasing numbers of LNR and especially increase very long one LNR reconstruction.Primary manifestation of all diseases can be showed on oppressing along its walking line,meanwhile,20 cases with adhesion, 14 cases with displacement,13 cases atrophy and 9 cases with increasing diameter.Conclusions Image anatomy features of full LNR with 16-slice spiral CT with the multiple plane reconstruction techniques is very ideal ways at the same slice.It is a very valuable way to make diagnosis and treatment of LNR diseases.The concept of"road sing"and showing"at the same slice"of LNR are tried to rise from in order to make foundation for studying their image.

染色质许可和DNA复制因子1（Cdt1）是复制起始许可的主要调控因子，也是组成复制前复合物的核心成员。细胞通过依赖Cdt1的波动水平，且在每个周期中通过调节其总量以确保DNA仅复制一次。Cdt1功能缺陷会造成DNA过度复制，最终导致基因组不稳定。虽然酵母中cdt1和人类Meier-Gorlin综合征（MGS）患者中的CDT1已被广泛研究，但缺乏脊椎动物模型。我们发现在硬骨鱼类分支的几个鲤形目物种（包括斑马鱼）中，Cdt1蛋白在其N末端插入一段其他脊椎动物中没有的独特无序序列。通过分析在cdt1基因中携带移码缺失的遗传性斑马鱼突变体（命名为cdt1^zju1 ），我们发现突变胚胎虽然几乎无任何早期胚胎表型异常，但成年突变斑马鱼却表现出侏儒症、生存能力降低的症状，以及性腺发育不全且不育。此外，我们同样发现除转录本cdt1-201外，斑马鱼还存在第二个cdt1转录本——cdt1-202，它是通过跳过外显子2产生，这在其他生物中暂无报道。有意思的是cdt1-202在cdt1-201纯合突变体中显著上调。上述研究结果表明，cdt1-202转录本可能可以补偿cdt1-201在早期发育过程中的功能损失，但不能补偿后期生长，这可支持斑马鱼作为研究人类MGS的遗传模型。
Animals ; Humans ; Zebrafish ; Growth Disorders ; Cell Cycle Proteins ; Gonads

Adipose tissue is a promising target for treating obesity and metabolic diseases. However, pharmacological agents usually fail to effectively engage adipocytes due to their extraordinarily large size and insufficient vascularization, especially in obese subjects. We have previously shown that during cold exposure, connexin43 (Cx43) gap junctions are induced and activated to connect neighboring adipocytes to share limited sympathetic neuronal input amongst multiple cells. We reason the same mechanism may be leveraged to improve the efficacy of various pharmacological agents that target adipose tissue. Using an adipose tissue-specific Cx43 overexpression mouse model, we demonstrate effectiveness in connecting adipocytes to augment metabolic efficacy of the β ₃-adrenergic receptor agonist Mirabegron and FGF21. Additionally, combing those molecules with the Cx43 gap junction channel activator danegaptide shows a similar enhanced efficacy. In light of these findings, we propose a model in which connecting adipocytes via Cx43 gap junction channels primes adipose tissue to pharmacological agents designed to engage it. Thus, Cx43 gap junction activators hold great potential for combination with additional agents targeting adipose tissue.