颅底胆脂瘤的MRI特征

目的探讨颅底胆脂瘤MRI分型的意义及其MRI诊断特征。方法观察15例颅底胆脂瘤的CT、MRI与病理学资料，根据肿瘤T1WI信号的不同，将颅底胆脂瘤分为Ⅰ型和Ⅱ型，分析两型胆脂瘤在CT、MRI征象和颅底骨质侵犯等方面的差异。结果15例颅底胆脂瘤T2WI显著高信号，肿瘤实质无强化。15例中，Ⅰ型，6例，肿瘤位于桥前池和桥小脑角区，CT均匀低密度，T1WI均匀低信号，包膜不强化，颅底骨质改变轻微，肿瘤实质为胆固醇结晶；Ⅱ型，9例，肿瘤位于一侧中、后颅窝底，CT呈混杂密度，T1WI呈混杂信号，其中4例为低信号中夹杂少量高信号，另5例以高信号为主，包膜强化，颅底骨质呈显著外压性改变，肿瘤实质为角化上皮和蛋白。结论颅底胆脂瘤分为Ⅰ型和Ⅱ型是合理的，体现了两型颅底胆脂瘤组织病理和生物学行为的差异，对指导MRI诊断有积极意义。T1WI信号多样性、T1WI显著高信号、肿瘤实质不强化以及与MRI分型相关的颅底骨质侵犯是颅底胆脂瘤的MRI诊断特征。     

试尖对根管充填质量影响的研究

目的：了解试尖对侧向加压法根管充填质量的影响因素。方法：随机提取我院1998年10月至2004年12月所完成的根管充填病例的X线片1000例，按试尖与未试尖，分别对前牙、前磨牙和磨牙根管充填质量进行分析。结果：在482例未试尖根管充填病例中，前牙、前磨牙和磨牙的适充比例分别为46％、37％和23％，欠充为20％、29％和47％。超充为34％、33％和29％：在518例试尖病例中，前牙、前磨牙和磨牙的适充比例分别为68％、62％和51％，欠充为6％、12％和13％，超充为25％、24％和36％。结论：在侧向加压法根管充填中，试尖可明显改善充填质量。     

多层螺旋CT和MRI测量肩胛盂斜倾角的互补性初探

目的 探讨多层螺旋CT(MSCT)多平面重组(MPR)及MRI测量肩胛盂斜倾角的互补性.方法 收集成人肩胛骨干标本22侧及肩关节防腐湿标本24侧,用16层螺旋CT扫描仪扫描,多平面重组重建肩胛骨并测量肩胛盂斜倾角,得数据A组.收集MRI检查正常的肩关节病例50侧,取其斜冠状位T1WI显示肩锁关节的层面测量肩胛盂斜倾角,得数据B组.进行统计学处理.结果 肩胛盂斜倾角最小值91.10°,最大值118.50°,A、B 2组肩胛盂斜倾角数据分别为101.14°±4.66°和104.05°±7.72°.2种测量方法肩胛盂斜倾角值统计学上有显著性差异(P＜0.05).结论 MSCT的MPR法测量肩胛盂斜倾角与MRI测量值不同,前者略小于后者;MSCT和MRI 2种测量肩胛盂斜倾角方法结合具有重要的应用价值.     

川芎嗪对P2X3受体介导的大鼠伤害性兴奋传入的作用

通过动物痛行为反应(缩足反射)确定局部和鞘内应用川芎嗪(TMP)对ATP等P2X受体激动剂所致大鼠足底急性伤害性行为反应的影响。P2X3受体拮抗剂TNP-ATP(0．3μmol／L)明显抑制P2X受体激动剂ATP(1μmol／L)或α，β-meATP(0．6μmol／L)引起的大鼠足底急性伤害性反应。大鼠足底局部应用TMP(0．1-10mmol／L)剂量依赖性地对ATP(1μmol／L)或α，β-meATP(0．6μmol／L)引起的伤害性反应具有抑制作用。鞘内应用TMP(50mmol／L)对ATP(1μmol／L)或α，β-meATP(0．6μmol／L)引起的伤害性反应具有抑制作用。结果表明，TMP可通过阻断P2X3受体介导的伤害性兴奋传入抑制P2X受体激动剂引起的大鼠足底急性伤害性反应。     

阻塞性肺病呼气末肺残气量的CT评价

目的:探讨呼气末高分辨率CT(HRCT)对阻塞性肺病(OLD)患者的肺残气量的评估价值.方法:对有肺功能检测结果的13名健康志愿者与14例OLD患者行吸气与呼气末HRCT扫描,测量吸气与呼气状态下肺CT值,并目测呼气末HRCT扫描时肺残气量的范围.结果:所有的OLD与8名健康志愿者都有肺内空气残余,但OLD的范围明显增大.OLD患者在吸气与呼气时肺CT值变化及残气量分数与健康者明显不同,且与肺功能密切相关(P＜0.01).结论:呼气末HRCT可用于评估OLD患者肺残气量并可诊断这类疾病.肺CT值的测量与肺残气量的评估是两种有价值的分析方法.     

Preaxial acrofacial dysostosis (Nager syndrome) associated with an inherited and apparently balanced X;9 translocation: Prenatal and postnatal late replication studies

We report on an infant with preaxial acrofacial dysostosis (Nager syndrome) who was diagnosed prenatally as having an apparently balanced X/autosome translocation [46,X,t(X;9)(p22.1;q32)mat] inherited from a previously diagnosed mosaic translocation carrier mother [46,XX/46,X,t(X;9)(p22.1;q32)]. Replication studies on amniocytes showed the normal X chromosome to be late replicating while the same studies repeated on the infant's lymphocytes showed the translocated X chromosome to be late replicating in most cells. Late replication studies of the mother's lymphocytes demonstrated that the normal X chromosome was late replicating in most cells. The presence of Nager syndrome in this infant may be the result of critical break-points and/or position effects on chromosome 9, inducing expression of a gene responsible for the syndrome. © 1993 Wiley-Liss, Inc.     

The search for a marsupial XIC reveals a break with vertebrate synteny

X-chromosome inactivation (XCI) evolved in mammals to deal with X-chromosome dosage imbalance between the XX female and the XY male. In eutherian mammals, random XCI of the soma requires a master regulatory locus known as the ‘X-inactivation center’ (XIC/Xic), wherein lies the noncoding XIST/Xist silencer RNA and its regulatory antisense Tsix gene. By contrast, marsupial XCI is imprinted to occur on the paternal X chromosome. To determine whether marsupials and eutherians share the XIC-driven mechanism, we search for the sequence equivalents in the genome of the South American opossum, Monodelphis domestica. Positional cloning and bioinformatic analysis reveal several interesting findings. First, protein-coding genes that flank the eutherian XIC are well-conserved in M. domestica, as well as in chicken, frog, and pufferfish. However, in M. domestica we fail to identify any recognizable XIST or TSIX equivalents. Moreover, cytogenetic mapping shows a surprising break in synteny with eutherian mammals and other vertebrates. Therefore, during the evolution of the marsupial X chromosome, one or more rearrangements broke up an otherwise evolutionarily conserved block of vertebrate genes. The failure to find XIST/TSIX in M. domestica may suggest that the ancestral XIC is too divergent to allow for detection by current methods. Alternatively, the XIC may have arisen relatively late in mammalian evolution, possibly in eutherians with the emergence of random XCI. The latter argues that marsupial XCI does not require XIST and opens the search for alternative mechanisms of dosage compensation.     

The innate immune response under the control of the LXR pathway

Macrophages play essential roles in infection and resolution of inflammation. This review summarizes recent findings that suggest a relevant role for the nuclear receptor liver X receptor (LXR) in the evolution of immune responses. By exerting both positive and negative regulation of specific macrophage gene expression networks, LXRs display anti-inflammatory activities and promote macrophage survival in bacterial infection settings. Agonists that activate the LXR pathway may be used to enhance innate immunity to highly virulent pathogens that otherwise induce macrophage apoptosis as a means to subvert host immune defense.     

结核性脑膜炎的CT诊断(附16例分析)

目的：通过分析16例结核性脑膜炎的CT表现及其产生的病理基础，提高对本病的认识和诊断水平。方法：16例结核性脑膜炎病人采用常规头颅CT扫描，对其影像及临床资料进行回顾性分析。结果：脑基底池、侧裂池变窄12例(75％)，合并密度增高8例(50％)；不同程度的脑积水14例(88％)；脑梗塞8例(50％)；结核瘤1例(6％)。结论：结核性脑膜炎的主要CT征象是脑基底池、侧裂池变窄，同时有不同程度的脑积水。如同时伴有脑结核瘤，可作出诊断。     

H-Y antigen expression in patients with X-autosomal translocations and gonadal dysgenesis

Cells from three patients with early gonadal failure and a balanced reciprocal translocation involving the long arm of the X chromosome and an autosome were studied. Fibroblasts from a patient with a similar balanced reciprocal translocation but normal reproductive capabilities were also studied. Two of the four patients were found to have serologically detectable H-Y antigen on their cells. Since H-Y antigen has been found on the cells of other patients with X chromosome abnormalities but without a Y chromosome, it is thought that the X chromosome plays a role in the regulation of H-Y antigen expression. This study suggests that the long arm of the X chromosome may be involved but the location of a regulatory gene cannot be identified in these studies. These cases do not permit us to implicate H-Y antigen as a cause of gonadal dysgenesis and early gonadal failure in females who have structurally abnormal X chromosomes.