维生素D衍生物联合供者骨髓细胞输注诱导异基因大鼠心脏移植免疫耐受

目的 探讨同种异基因心脏移植后免疫耐受的诱导。方法 建立大鼠颈部异位心脏移植模型，按分组分别给予门静脉输注供者骨髓细胞(DBMC)(B组)、骨化三醇灌胃(C组)、输注DBMC及骨化三醇灌胃(D组)以及环孢素A(CsA)灌胃(E组)。观察移植心脏的存活时间及心肌组织病理改变，测定心肌组织中肿瘤坏死因子及细胞间粘附分子-1 mRNA的表达以及血清钙、磷浓度，进行受者与供者及无关第三品系大鼠脾细胞混合淋巴细胞培养(MLR)。结果 D组移植心脏的存活时间较其它各组显著延长(P＜0．05)；术后7d，C组、D组、E组受者脾细胞均能显著抑制供者及第三方无关供者脾细胞作为刺激细胞引起的MLR；D组手术前后血磷、血钙浓度的差异无显著性(P＞0．05)；各组急性排斥反应的程度，D组最轻；D组肿瘤坏死因子及细胞间粘附分子-1 mRNA的表达受到显著抑制，与对照组(A组)、B、C组比较，差异有显著性(P＜0．05)。结论 骨化三醇灌胃联合DBMC输注可显著延长移植心脏的存活时间，二者具有协同作用。     

血细胞彩色图像的微机自动计数方法探讨

目的　探讨血细胞自动计数的方法。方法　采用微机彩色图像处理技术对血液细胞图像进行图像分割和细胞计数。结果　与人工计数相平行 ,相关系数r =0 .96 1～ 0 .997,P >0 .0 5。结论　该方法可行且计数相对精确、迅速、客观     

计算法测定肾小球滤过率的临床应用价值

目的 :探讨采用 WCP公式计算方法测定肾小球滤过率 (GFR)的临床应用价值。方法 :采用 99m Tc DTPA清除率测定 6 6例不同疾病住院患者 GFR(Tc GFR) ,并测血清肌酐 (SCr)及尿素氮 (BU N) ,同时以 WCP公式、Robert公式计算 GFR(WCP GFR,Robert GFR) ,以 Cockcroft/ Gault公式计算内生肌酐清除率 (CG CCr) ,所得数据进行对比研究及相关性分析。结果 :除肾功能正常者 CG CCr与 BU N无显著相关外 ,肾功能不全及肾功能正常者的 WCP GFR、Robert GFR、CG CCr均分别与 Tc GFR呈显著正相关(P均 <0 .0 1) ,与 BU N、SCr呈显著负相关 (P<0 .0 1或 P<0 .0 5 ) ;与 Robert GFR、CG CCr比较 ,WCPGFR始终与 Tc GFR最接近 (P均 >0 .0 5 ) ;WCP GFR、Robert GFR、CG CCr与 Tc GFR的平均差绝对值逐渐增大 ,三者间差异显著 (P均 <0 .0 5 )。结论 :WCP GFR、Robert GFR、CG CCr均能在一定程度上准确反映 GFR,而以 WCP GFR更准确 ,且简便、快速、安全而廉价 ,可代替 Tc GFR应用于临床     

Signal-to-noise ratio effects in quantitative cerebral perfusion using dynamic susceptibility contrast agents.

Theoretical and simulation evidence is presented in support of the idea that the optimal manner of determining blood flow from MR perfusion studies is not necessarily obtained by setting experimental conditions to maximize either the arterial input or the measured tissue concentration level for a particular echo time (TE). The noise power in the contrast concentration curve is associated with its peak because of the nonlinear relationship between the contrast concentration and MR signal intensity curves. The optimum signal-to-noise ratio (SNR), SNR(C), for a particular contrast concentration curve can be obtained when the experimental concentration level and TE are adjusted to produce an MR intensity curve whose signal loss is 63% of the precontrast MR signal intensity. It is demonstrated that the stability of the singular valued decomposition (SVD) deconvolution approach to determine blood flow parameters is increased when the tissue curve maximum signal loss is in the range of 40-80%. The accuracy and stability of the SVD-determined blood flow parameters are affected by deviations from these optimum conditions in a manner that depends on the mean transit time (MTT) associated with the residue function. It is recommended that the experimental TE value be set so that neither the tissue nor the arterial curves are placed a region of rapidly deteriorating SNR(C).     

Functional magnetic resonance imaging based on changes in vascular space occupancy.

During brain activation, local control of oxygen delivery is facilitated through microvascular dilatation and constriction. A new functional MRI (fMRI) methodology is reported that is sensitive to these microvascular adjustments. This contrast is accomplished by eliminating the blood signal in a manner that is independent of blood oxygenation and flow. As a consequence, changes in cerebral blood volume (CBV) can be assessed through changes in the remaining extravascular water signal (i.e., that of parenchymal tissue) without need for exogenous contrast agents or any other invasive procedures. The feasibility of this vascular space occupancy (VASO)-dependent functional MRI (fMRI) approach is demonstrated for visual stimulation, breath-hold (hypercapnia), and hyperventilation (hypocapnia). During visual stimulation and breath-hold, the VASO signal shows an inverse correlation with the stimulus paradigm, consistent with local vasodilatation. This effect is reversed during hyperventilation. Comparison of the hemodynamic responses of VASO-fMRI, cerebral blood flow (CBF)-based fMRI, and blood oxygenation level-dependent (BOLD) fMRI indicates both arteriolar and venular temporal characteristics in VASO. The effect of changes in water exchange rate and partial volume contamination with CSF were calculated to be negligible. At the commonly-used fMRI resolution of 3.75 x 3.75 x 5 mm(3), the contrast-to-noise-ratio (CNR) of VASO-fMRI was comparable to that of CBF-based fMRI, but a factor of 3 lower than for BOLD-fMRI. Arguments supporting a better gray matter localization for the VASO-fMRI approach compared to BOLD are provided.     

Effects of low-dose transdermal scopolamine on autonomic cardiovascular control in healthy young subjects

We studied how posture influences the effects of transdermal scopolamine on autonomic cardiovascular regulation in a randomized, double-blind, placebo-controlled crossover study of 10 healthy young volunteers. We recorded the electrocardiogram and auscultatory sphygmomanometric and continuous non-invasive finger arterial pressure (Finapres device) to obtain signals for the beat-by-beat R–R interval and systolic, mean and diastolic pressures. R–R interval and arterial pressure variabilities were characterized by power spectral analysis. Scopolamine increased the mean R–R intervals and reduced arterial pressure in both the supine and the standing positions, but did not affect blood pressure variability. Scopolamine increased the total variability of R–R interval and its mid- (0·07–0·15 Hz) and high- (0·15–0·40 Hz) frequency band power in the standing position during controlled breathing at 0·25 Hz. In the supine position, scopolamine did not affect R–R interval variability. In the deep breathing test, scopolamine increased the maximal expiratory–inspiratory R–R interval ratio. This study showed that low-dose scopolamine increases vagal cardiac inhibition in both supine and standing positions in healthy volunteers. However, scopolamine increases heart rate variability only in the standing position during partial vagal withdrawal. The study also demonstrates that transdermal scopolamine decreases blood pressure in healthy young subjects.     

Association of angiotensin II type 1 receptor gene polymorphism with essential hypertension

The renin-angiotensin system is involved in control of blood pressure and salt and fluid homeostasis. Genes for components of this system have been of major focus in research on the causation of the common, complex, polygenic trait, essential hypertension (HT). Association of an A→C variant at nucleotide 1166 of the angiotensin II type 1 receptor (AT₁R) gene with HT, but an absence of linkage of this locus with this disease, has been reported recently. Since confirmation in a different setting is imperative, we performed a cross-sectional case-control study of the A1166C variant in a well-characterized group of 108 Caucasian HT subjects with a strong family history (two affected parents) and early onset disease. Genotyping was by mismatch polymerase chain reaction/ Bfr I restriction fragment length polymorphism analysis. Frequency of the C¹¹⁶⁶allele was 0.40 in HTs and 0.29 in normotensives. The difference in genotype (χ²= 13, P = 0.0015) and allele (χ²= 5.3, P = 0.02) frequencies between the two groups was significant (odds ratio for CC vs AA+AC = 7.3 [95% CI, 1.9–31.9). The present results implicate the AT₁R gene, or a locus in linkage disequilibrium with the variant tested, in the causation of essential HT.     

Epidural blood patch illustrated by CT-epidurography

Four patients, who received epidural blood patch to treat postdural puncture headache, were examined with computed tomography in order to demonstrate the distribution of the injected blood. Blood alone could not be identified, but adding 2 ml contrast agent Iohexol 180 mg J/ ml (Omnipaque®, Nycomed Imaging) to 18 ml blood gave an excellent demonstration of the distribution of the blood in the epidural space, both cranio-caudally (7–14 segments) and spatially in relation to the epidural septae. The blood-contrast media had a strong affinity to the dural sac. There was no support of the spacefilling effect of blood patch.     

Hydrops Fetalis Caused by Fetal Kasabach-Merritt Syndrome

There have been only 2 previous reports of nonimmunologic hydrops fetalis (NIHF) caused by fetal Kasabach-Merritt syndrome, both of which were pathological studies. This is the first clinical case report of NIHF due to fetal Kasabach-Merritt syndrome that was prenatally diagnosed by sonography, computerized tomography, and percutaneous umbilical blood sampling.