Display and visualization of three-dimensional reconstructed anatomic morphology: experience with the thorax, heart, and coronary vasculature of dogs.

A new method, termed reprojection, is used to visualize anatomic morphology contained within three-dimensional reconstructions made up of images of multiple parallel cross sections. This method involves the projection, either orthographically into a plane or radially onto a cylinder, of the volume picture elements (voxels) of the reconstruction. Orthographic reprojection images, formed by mathematically summing the magnitudes of the voxels along selected parallel paths through the reconstructed volume, are analagous to conventional radiographs formed by the passage of an X-ray beam through the volume. The reprojection image is a two-dimensional array of picture elements that is displayed on a television monitor using a digital-to-video scan converter. Also described are the techniques of noninvasive selective tissue dissolution and numerical dissection, whereby obscuring portions of the reconstructed volume are either partially "dissolved" or totally eliminated before reprojection. Utilizing these methods, anatomic information present in a three-dimensional reconstruction but not clearly seen in a reprojection image is rendered visible after removal of superposed structures. The usefulness of these methods is demonstrated utilizing three-dimensional reconstructions of the thorax, heart, and coronary arteries of dogs.     

Changes in the N- and C-terminal sequences of the murine R7 Gag-tMos protein affect brain lesion induction

Our preliminary studies suggested that the novel gag-truncated mos (tmos) open reading frame (ORF) of R7, a spontaneous deletion mutant of Moloney murine sarcoma virus 124 (MoMuSV124), may be responsible for R7's unique ability to induce brain lesions in all R7-injected mice. However, when we replaced the gag-tmos ORF with either the MoMuSV124 or the homologous myeloproliferative sarcoma virus env-mos gene, we found that both recombinant viruses also induced brain lesions in all injected mice. Although these studies suggested that the critical determinants for brain lesion induction may reside in the tmos sequence common to all three viruses, they did not demonstrate if the N-terminus of Mos was dispensable for this activity. By inserting the FLAG sequence at the 3' end of the R7 gag-tmos ORF, we demonstrated that R7 does synthesize a Gag-tMos fusion protein. Using R7 gag deletion mutants with and without the FLAG sequence, we further demonstrated that (i) deletion of the entire gag sequence abolished R7's transforming activity; (ii) the ability of the virus to transform cultured NIH/3T3 cells was significantly reduced only when most of gag was deleted; (iii) the ability of the virus to induce brain lesions was inversely proportional to the extent of its gag deletions; and (iv) the insertion of FLAG at the Mos C-terminus did not reduce the in vitro transforming activity of the FLAG-tagged viruses but did reduce their ability to induce brain lesions. Thus, we have demonstrated that altering the N- or C-terminus of the R7 Gag-tMos fusion protein can affect disease manifestation.     

3-硝基丙酸预处理诱导沙土鼠脑缺血耐受与海马星形胶质细胞的激活

目的：探讨海马区星形胶质细胞的激活与3－硝基丙酸（3－NPA）预处理诱导脑缺血耐受的关系。方法：阻断沙土鼠双侧颈总动脉造成前脑缺血模型，通过HE染色和免疫组化观察海马锥体细胞死亡和星形胶质细胞的反应。结果：对照组海马CA1区已失去正常结构，锥体细胞大部分丧失，存活神经元计数显低于假手术组。3－NPA预处理组存活神经元减少，但高于对照组，假手术组海马CA1区仅见少量胶质原纤维酸性蛋白（GFAP）阳性细胞，染色较弱，突起不明显，对照组海马CA1区GFAP阳性细胞增多，多为弱阳性。3－NPA预处理组海马CA1区GFAP阳性细胞数目明显增多，染色较深，突起增粗。结论：星形胶质细胞形态和机能的改变可能与3－硝基丙酸预处理诱导脑缺血耐受有关。     

Contradictory effects of chlorpromazine on endothelial cells in a rat model of endotoxic shock in association with its actions on serum TNF-alpha levels and antioxidant enzyme activities.

We examined the effects of the phenothiazine derivative, chlorpromazine on thoracic aortic endothelial cell histology (14 h after LPS challenge) in a model of endotoxic shock in rats. Since excessive formation of tumor necrosis factor-alpha (TNF-alpha) and oxygen-derived free radicals contribute to endothelial injury in endotoxemia, we also evaluated the effect of the drug on the activities of antioxidant enzymes superoxide dismutase (SOD) and catalase in liver tissue in this model and tried to find out whether this possible effect was associated with a change in serum TNF-alpha levels (measured 90 min after chlorpromazine administration). Endotoxemia was induced by a single i.p. injection of lipopolysaccharide (LPS) (5 mg kg(-1) in 1.5 ml of saline; LPS from Escherichia coli serotype 055:B5, L-2880, Sigma Chemical Company). Electron microscopic evaluation of the aortas revealed that chlorpromazine (administered 30 min prior to LPS challenge), in smaller doses (3 mg kg(-1)) ameliorated the endothelial cell injury caused by LPS, whereas it caused deterioration of endothelial cell morphology in higher doses (10 and 25 mg kg(-1)). Chlorpromazine administration caused a significant reduction in serum TNF-alpha levels, which was correlated well with an increase in SOD activity in all drug doses (3, 10 and 25 mg kg(-1)). Catalase activity was increased only in the 25 mg kg(-1) chlorpromazine group.     

Correlation of cytochrome P450 (CYP) 1A2 activity using caffeine phenotyping and olanzapine disposition in healthy volunteers.

Olanzapine has previously been shown to have predominant metabolism by cytochrome (CYP) P450 1A2. Caffeine has been shown to provide an accurate phenotypic probe for measuring CYP1A2 activity. The purpose of this study is to determine if a significant correlation exists between olanzapine disposition and caffeine metabolic ratios. Subjects were phenotyped for CYP1A2 activity with caffeine probe methodology. After 200-mg caffeine administration, blood (4 h), saliva (6 and 10 h), and urine (8 h total) were collected for high-performance liquid chromatography (HPLC) analysis of caffeine and its metabolites.CYP1A2 activity was measured as plasma (PMR(4 h)), saliva (SMR(6 h) and SMR(10 h)), and three urinary metabolic (UMR1(8 h), UMR2(8 h), and UMR3(8 h)) ratios. Each of the 14 healthy nonsmokers (13 male) received a single 10 mg olanzapine dose after which blood was collected for HPLC determination of olanzapine concentrations at predose and at 0.5, 1, 1.5, 2, 2.5, 3, 4, 5, 6, 8, 10, 12, 24, 48, 72, 96, and 120 h postdose. Olanzapine pharmacokinetic parameters in this study were similar to those previously published. All caffeine metabolic ratios (PMR(4 h), SMR(6 h), SMR(10 h), UMR1(8 h), and UMR2(8 h)) significantly correlated with each other (p <0.001) except for UMR3(8 h), which did not correlate. A significant correlation (p <0.05) was also found between olanzapine clearance and PMR(4 h) (r=0.701), SMR(6 h) (r=0.644), SMR(10 h) (r=0.701), UMR1(8 h) (r=0.745), and UMR2(8 h) (r=0.710). A negative correlation was observed between olanzapine clearance and UMR3(8 h) (r=-0.029, p=NS). A significant correlation was found between olanzapine clearance and various caffeine metabolic ratios. Interpatient variability in CYP1A2 activity may explain the wide interpatient variability in olanzapine disposition. Compounds that modulate CYP1A2 activity may be expected to alter olanzapine pharmacokinetics accordingly.     

O-羧甲基N-半乳糖化壳聚糖衍生物的设计、合成和表征

目的：合成和表征O-羧甲基-N-半乳糖化壳聚糖衍生物作为潜在的肝靶向基因载体。方法：以天然聚合物壳聚糖为原料，首先制备得O-羧甲基壳聚糖，然后在其2-NH2上和乳糖酸反应，制得O-羧甲基-N-乳糖酰化壳聚糖；或与乳糖反应，用KB}14还原，制得O-羧甲基-N-乳糖胺化壳聚糖。结果与结论：分别用VF-IR、^1H NMR、^13C NMR和元素分析对其进行了表征。用粉末X-衍射、DSC、TG对其物理性质进行了分析。制得的O-羧甲基-N-乳糖酰化壳聚糖O-羧甲基-N-乳糖胺化壳聚糖有望作为潜在的肝靶向基因载体。     

Spontaneously relapsing clonal, mucosal cytotoxic T-cell lymphoproliferative disorder: case report and review of the literature

Primary T-cell lymphoma of the gastrointestinal tract is a rare and usually aggressive disorder that may be associated with celiac disease. The authors describe a unique case of a clonal proliferation of CD8+ T cells involving the oral mucosa, ileum, and colon of a 35-year-old man that has regressed spontaneously and recurred numerous times over a 9-year period without treatment. The patient's symptoms were limited to occasional rectal bleeding and recurring painful oral ulcers. Within the intestine, these collections of small T cells induced minimal architectural distortions and did not show extensive epitheliotrophism. Polymerase chain reaction and sequencing analyses revealed that the identical T-cell clone has been present for more than 9 years and in different mucosal locations in this patient. This may represent a unique T-cell lymphoproliferative process akin to a mucosal counterpart of lymphomatoid papulosis of the skin.     

Clinical study on therapeutic mechanism of Sini Decoction in treating post-percutaneous transluminal coronary angioplasty ischemia-reperfusion injury in terms of syndrome typing of TCMin treating post-percutaneous transluminal coronary angioplasty ischemia-reperfusion injury in terms of syndrome typing of TCM

Objective: To study the mechanism of Sini Decoction (SND) in prevention and treatment of post-percutaneous transluminal coronary angioplasty (PTCA) ischemia-reperfusion injury with different Syndrome typing of TCM.Methods: Forty patients who received PTCA were randomly divided equally into the SND group and the control group, there were 10 of Excess Syndrome (ES) and 10 of Deficiency Syndrome (DS)in each group. 25 ml SND was given daily to the SND group from 3 days before operation to the third day after operation. The blood Superoxide dismutase (SOD) activity, malondialdehyde (MDA) and nitric oxide (NO) content of patients were determined before PTCA, and 1 hr, 12 hrs, 24 hrs, 48 hrs and 72 hrs after PTCA.Results: Before PTCA, the cases with DS were characterized by low SOD activity and high MDA content, as compared with the patients with ES, P<0.05. SND could relieve the post-PTCA deprivation of SOD activity and NO content and the elevation of MDA level in both ES and DS patients, the amplitude of elevation of SOD activity in DS patients was higher than that in ES patients (P<0.05).Conclusion: SND has antagonizing effect on post-PTCA ischemia-reperfusion injury, which is more effective in treating patients with DS.