Volumetric rendering of MR images

The authors developed new techniques for three-dimensional display of magnetic resonance (MR) images that preserve soft-tissue definition, are fully automatic, and work with routinely used section thicknesses. MR images are segmented, selectively enhanced, and displayed by means of a volumetric rendering algorithm. These techniques were used to illustrate normal anatomy of the brain, knee, and liver. Three-dimensional rendering of balanced spin-echo images shows the ventricles and extracerebral veins and of T1-weighted images, the sulci and gyri. The large hepatic and portal vessels can be seen with these enhancement techniques. Three-dimensional views of the knee reveal articular surfaces of the tibia and clearly depict menisci and posterior and anterior cruciate ligaments. These techniques make it possible to image multiple soft tissues simultaneously while preserving the detail contained in the original images. Three-dimensional presentation of complex, overlapping anatomic regions is helpful in surgical planning and should lead to improved diagnosis.     

U-80816: A novel partial muscarinic agonist

U-80816 (1-(4-(5-methyl-1H-imidazol-1-yl)-2-butynyl)-2-pyrrolidinone is an acetylenic amine which has been investigated as a partial agonist of muscarinic receptors. In vitro U-80816 inhibited binding of (³H)-N-methylscopolamine [(³H)-NMS] and (methyl-³H) oxotremorine-M acetate [³H)-Oxo-M] to the cortical membrance preparation with Ki's of 75 and 3.24 nM, respectively. In the M1 cell line, U-80816 increased phosphatidylinositol (Pl) hydrolysis. However, the maximum increase in the Pl hydrolysis was significantly (P < 0.01) less than oxotremorine and RS 86. Intraperitoneal administration of U-80816 dose-dependently increased striatal acetylcholine (ACh) concentration, and the effect was significant (P < 0.01) at 30 mg/kg. In the presence of hemicholinium-3 (HC-3), U-80816 inhibited the release of (³H)-ACh from hippocampal slices. On the other hand, in the presence of eserine, U-80816 increased the release of (³H)-ACh. In in vivo pharmacological tests, U-80816 produced hypothermia and tremors in mice. This compound failed to produce lacrimation or salivation in mice when administered up to 100 mg/kg. U-80816 antagonized oxotremorine-induced salivation. It is bioavailable to the brain in a significant amount after oral administration and has a sufficiently long duration of action. The in vitro and in vivo pharmacological investigations indicate that U-80816 is a partial agonist of muscarinic receptors.     

Mouse macrophages release a neutrophil chemotactic mediator following stimulation by staphylococcal enterotoxin type A

OBJECTIVE AND DESIGN: To examine the role of macrophages in the neutrophil migration induced by staphylococcal enterotoxin type A (SEA) in mice. MATERIALS AND METHODS: Peritoneal macrophages were harvested from male Swiss mice pre-treated with thioglycollate. After adhering to plastic tissue culture dishes, the cells were washed and incubated with RPMI or SEA (0.62-2.5 microg/ml) and washed again prior to further incubation with RPMI alone. The medium was then collected, sterilized and assayed for promigratory activity in the mouse peritoneal cavity. RESULTS: Mouse macrophage monolayers stimulated with SEA secreted a thermolabile neutrophil chemotactic component (MNCC-SEA) with a molecular mass >100 kDa (by ultrafiltration). This release was dose- and time-dependent and was inhibited by dexamethasone but not by indomethacin or BW755C. Dexamethasone, indomethacin, BWA4C, BW755C, BN52021, cimetidine and SR48968 had no effect on the neutrophil migration induced by MNCC-SEA while capsaicin and SR 140333 reduced this phenomenon. CONCLUSIONS: Macrophages play a key role in the neutrophil recruitment induced by SEA probably by releasing an MNCC-SEA that presumably induces neutrophil migration via a mechanism mediated by substance P.     

003 胺碘酮可作为心房纤颤转复为窦性心律的首选药物

在美国，胺碘酮仅被批准用于治疗致命性室性心律失常，而在其他国家，尤其是南欧，也被广泛用于心房纤颤(Af)的治疗。然而有关胺碘酮复律效果报道不一，其成功率在16％～92％。本文前瞻性随机对照研究胺碘酮作为Af复律的首选药物的疗效及安全性。 连续208例症状性Af，男性102例，女性106例，年龄27～78(65±10)岁。将受试者随机分为胺碘酮治疗组与安慰剂组。胺碘酮用法：300mg静脉注射，持续1小时，然后以20mg/kg静脉滴注，持续24小时，继之口服200mg，tid，共1周，400mg/d共3周。如果受试者此前未用地高辛，则给予地高辛0.5mg静脉注射，2小时后再静脉注射0.25mg，继之静脉注射0.25mg，q6h，共24小时，此后调整地高辛剂量以维持治疗剂量的血清浓度，对Af持续48小时以上或持续时间不明、未用抗凝药物者均应用醋硝香豆素(acenocoumaro1)，至少21天，复律成功者继续用药21天，未成功者用药时间不定。本研究将Af持续1个月以上者定义为慢性Af，＜24小时者定义为新近发作Af，其余定义为持续性Af。     

Biochemical events associated with pulmonary failure in shock and trauma

Evidence obtained by biochemical analysis of BAL fluids from patients with ARDS indicates that at least 2 important pathogenic events take place in the pulmonary tissues. These are the release of neutrophil elastase and the generation of oxidants. Both events can lead to severe pulmonary injury as has been demonstrated in experimental animals. To better understand the mechanisms of oxidant damaged cells, H2O2 was added to cultured cells. H2O2 compromises a multitude of cellular functions, the combination of which leads to cell death. DNA is an important target for oxidant-induced injury. The formation of DNA strand breaks leads to activation of pADP-RP which in turn causes depletion of NAD and ATP, followed by Ca++ influx and eventually cell lysis. Inhibition of pADP-RP prevented cell lysis, but not DNA damage. A similar sequence of events has been described for cell injury following DNA damage induced by gamma-irradiation and alkylating agents and was proposed to be a suicide mechanism for cells with irreversibly damaged DNA. Sublethal doses of H2O2 will delay cell replication, but not necessarily prevent it.     

Polymorphisms in adenosine receptor genes are associated with infarct size in patients with ischemic cardiomyopathy

The goal of this experiment was to identify the presence of genetic variants in the adenosine receptor genes and assess their relationship to infarct size in a population of patients with ischemic cardiomyopathy. Adenosine receptors play an important role in protecting the heart during ischemia and in mediating the effects of ischemic preconditioning. We sequenced DNA samples from 273 individuals with ischemic cardiomyopathy and from 203 normal controls to identify the presence of genetic variants in the adenosine receptor genes. Subsequently, we analyzed the relationship between the identified genetic variants and infarct size, left ventricular size, and left ventricular function. Three variants in the 3'-untranslated region of the A(1)-adenosine gene (nt 1689 C/A, nt 2206 Tdel, nt 2683del36) and an informative polymorphism in the coding region of the A3-adenosine gene (nt 1509 A/C I248L) were associated with changes in infarct size. These results suggest that genetic variants in the adenosine receptor genes may predict the heart's response to ischemia or injury and might also influence an individual's response to adenosine therapy.     

Future horizons in MR imaging

In this article, we defined the major areas of active research in clinical MR imaging. Further increases in the number of parallel coils within an imaging array and in advances in parallel imaging pulse sequences and postprocessing will lead to further reductions in imaging time analogous to the impact of multidetector CT on helical CT. The synergism between parallel and high-field imaging will aid the development of high-field imaging. The combined dynamic and hepatic parenchymal enhancement of new contrast agents that have or may soon receive FDA approval will enable improved detection and characterization of liver lesions. The lymphotropic SPIO agents will remain an active area of clinical research to further assess their role in oncologic staging. Molecular imaging contrast research using magnetic particles and MR microscopy will continue to flourish. Screening examinations by MR imaging will re-main an area of research for the short- and intermediate term, with the final outcome dependent more on socioeconomic costs than the underlying capability of achieving high-quality screening studies.