蛛网膜下腔出血患者不同时期脑脊液中一氧化氮浓度的变化

目的：研究动脉瘤性蛛网膜下腔出血后患者不同时期脑脊液中一氧化氮（NO）浓度的动态变化及其与脑血管痉挛的关系。方法：采集52例破裂动脉瘤患者脑脊液标本，采集时间为入院后即刻，出血后第3，5，7，10，14天，采用镉粒还原法检测脑脊液中NO浓度，结果：出血后第3天脑脊液中NO浓度即有明显降低，在出血后第7天达到最低，而后逐渐升高，症状性脑血管痉挛患者NO浓度明显低于未痉挛者及无症状的血管痉挛患者，结论：症状性脑血管痉挛的发生与脑脊液中NO浓度降低有关。     

动脉瘤性蛛网膜下腔出血患者脑脊液中内皮素浓度的动态变化

目的 研究动脉瘤性蛛网膜下腔出血后患者脑脊液中内皮素的动态变化及其与血管痉挛的关系。方法 采集40例破裂动脉瘤患者脑脊液标本,采集时间为入院后即刻、出血后第3、5、7、10、14天,采用放免法检测脑脊液中ET－1浓度。结论 出血后第3天脑脊液中ET－1浓度即有明显升高,在出血后第7天达到高峰,而后逐渐下降。血管痉挛患者ET－1浓度明显高于未痉挛者。结论 脑脊液中ET－1浓度的升高参与蛛网膜下腔出血后脑血管痉挛的发生。     

动脉瘤性蛛网膜下腔出血患者脑脊液垂体激素含量变化的临床研究

目的 研究动脉瘤性蛛网膜下腔出血（SAH）患者脑脊液（CSF）促肾上腺皮质激素（ACTH）、促甲状腺激素（TSH）、卵泡刺激素（FSH）、黄体生成素（LH）、泌乳素（PRL）、生长激素（GH）浓度的动态变化规律。方法对40例动脉瘤性蛛网膜下腔出血患者发病后1～3d、7～9d、13～15d脑脊液ACTH、TSH、FSH、LH、PRL、GH的含量进行动态检测,用TCD检测大脑中动脉血流速度（VMCA）。结果动脉瘤性蛛网膜下腔出血患者CSF中ACTH、TSH、FSH、LH、PRL、GH在发病后1～3d．7～9d各均值明显高于对照组,尤以发病后7—9d变化明显;术前、术后有脑血管痉挛组和非脑血管痉挛组也有明显差异。结论动脉瘤性蛛网膜下腔出血患者脑脊液ACTH、TSH、FSH、LH、GH、PRL含量与病情演变、脑血管痉挛（CVS）程度有关,并可判断预后。     

蛛网膜下腔出血患者的临床治疗研究

脑血管痉挛是蛛网膜下腔出血后严重的并发症，半个世纪以来一直是研究热点。目前，脑血管痉挛发生的病理生理机制仍然很不明确，有关内皮素-1（Endothelin-1，ET-1）的研究较多。作者动态检测脑脊液中ET-1浓度以期进一步探讨血管痉挛的发生机制及ET-1的作用。     

腰大池置管引流蛛网膜下腔出血患者脑脊液中内皮素浓度的动态变化

脑血管痉挛是蛛网膜下腔出血后严重的并发症，半个世纪以来一直是研究热点。目前，脑血管痉挛发生的病理生理机制仍然很不明确，有关内皮素-1（Endothelin-1，ET-1）的研究较多。作者动态检测脑脊液中ET-1浓度以期进一步探讨血管痉挛的发生机制及ET-1的作用。     

蛛网膜下腔出血急性期脑脊液中一氧化氮的变化和意义

目的：探讨一氧化氮（NO）在蛛网膜下腔出血急性期的变化及意义。方法：测定了30例蛛网膜下腔出血患者脑脊液中NO含量和病情、预后的关系和临床意义。结果：和对照组比较，蛛网膜下腔出血急性期NO峰值明显高于对照组。结论：蛛网膜下腔出血急件期NO升高的程度直接和病情、预后、复发的概率有关。NO的测定和临床指标的结合将提高对病情诊断治疗的准确率。     

脑脊液置换对蛛网膜下腔出血患者的影响

本文探讨脑脊液置换对蛛网膜下腔出血（SAH）继发性脑血管痉挛（CVS）的影响，并观察治疗前后脑脊液NO浓度的变化。     

1-磷酸鞘胺醇与动脉瘤性蛛网膜下腔出血后脑血管痉挛的相关性研究

目的：探讨1-磷酸鞘胺醇（S1P）与颅内动脉瘤破裂所致的自发性蛛网膜下腔出血（SAH）后脑血管痉 挛的相关性。方法：纳入部分动脉瘤破裂所致自发性SAH患者37例,分别在发病后第3、5、7、10、14天行 TCD检测跟踪血管痉挛程度,其中27例纳入痉挛组,10例纳入无痉挛组。另选取我院收治未破裂颅内动脉 瘤介入栓塞治愈术后半年复诊患者中,未见血管痉挛及血管狭窄的患者12例为对照组。采用高效液相色 谱法测定3组患者血清及脑脊液的S1P 水平。结果：与无痉挛组和对照组相比,痉挛组患者发病后3 d患者 血清和脑脊液中S1P 浓度升高,5 d时显著升高,至第7天达到高峰,至第14天时降至无明显差异。发病后 第7天,痉挛组患者大脑中动脉流速增加与血清和脑脊液中S1P 的浓度呈正相关（P＜0.05）。结论：SAH后 脑血管痉挛患者大脑中动脉流速明显增加,同时其血清及脑脊液中S1P 显著升高。     

蛛网膜下腔出血后血浆NO和ET1浓度变化与发生CVS关系探讨

目的探讨蛛网膜下腔出血（SAH）后不同时期血浆一氧化氮（NO）、内皮素1（ETl）浓度的变化及其与SAH后脑血管痉挛（CVS）发生之间的关系。方法测定SAH患者不同时期ET1和NO的含量,计算ET1／NO值。并与健康对照组血浆ET1和NO的含量相比较。结果SAH后ET1水平显著升高,并在3-4d内维持较高水平;NO在SAH后下降明显。3d后才慢慢回升;ET1／NO值SAH后明显减低,而后慢慢回升。SAH各组ET1、NO、ET1／NO与对照组比较,差异均具有非常显著性（P〈0．01）。结论SAH后ET1／NO动态失衡,这一动态失衡在SAH后发生脑血管痉挛过程中起着非常重要的作用。     

动脉瘤性蛛网膜下腔出血患者脑脊液IL-1β、IL-6及TNFα检测及意义

【目的】探讨动脉瘤性蛛网膜下腔出血（SAH）患者脑脊液白介素-1β（IL-1β）、白介素-6（IL-6）和肿瘤坏死因子d（TNFa）水平及其与脑血管痉挛的关系。【方法】选用双抗体夹心酶联免疫吸附试验（ELISA）检测动脉瘤性SAH患者脑脊液IL-1β、IL-6和TNFa浓度,并将其结果与经颅多普勒（TCD）检查判别的脑血管痉挛与否进行相关分析。【结果】动脉瘤性SAH患者脑脊液中IL-1β、IL-6和TNFa水平均明显升高（P〈0．05）,IL-1β、IL-6水平与脑血管痉挛显著相关（P〈0．05）,TNFa水平与脑血管痉挛无统计学相关（P〉O．05）。【结论】动脉瘤性SAH患者脑脊液IL-1β和IL-6水平增高可能与脑血管痉挛发病有关,检测其患者脑脊液中IL-1β和IL-6有助于脑血管痉挛的预测及治疗。     

Measurement of L-carnitine and acylcarnitines in body fluids and tissues in children and in adults

We have developed a reliable and validated radio-enzymatic method for the assay of L-carnitine and acylcarnitines, using a modification of existing methods. The sensitivity of the assay is 10 mumol/l using 10 microliters of plasma or urine. It is also suitable for measurements of carnitine in a 10 mg sample of liver or muscle obtained by percutaneous biopsy. The use of N-ethylmaleimide in the reaction mixture together with an excess of [1-14C]acetyl CoA ensures that the reaction proceeds to completion and a linear response is obtained. Using this method control ranges have been established for plasma and urine carnitine concentrations in healthy children and adults, and for the carnitine content of liver and muscle in adults. No significant difference was found between fasting and post-prandial plasma carnitine levels. An age-related increase was found in urinary total carnitine and acylcarnitine concentration throughout childhood. These data provide a reliable basis for studies of patients with abnormal carnitine and acylcarnitine metabolism, distribution and excretion.     

Erythropoietin and uremic platelet aggregation in vivo and in vitro

Erythropoietin treatment is known to correct anemia and to improve hemostasis. Since platelets may contribute to thromboembolic complications, we assessed platelet aggregation in whole blood and platelet-rich plasma from chronically hemodialyzed patients treated with erythropoietin and evaluated in vitro effects of this drug on aggregatory responses of uremic and normal platelets. Recombinant human erythropoietin was given to uremic patients at a dose of 2.000 IU subcutaneously three times a week. Platelet aggregation in whole blood and platelet-rich plasma was induced by collagen, ADP, arachidonic acid, and ristocetin. In uremic patients, erythropoietin therapy resulted in an enhancement of platelet sensitivity to various agonists, particularly in platelet-rich plasma, reaching values comparable to those of healthy volunteers. In vitro studies we were unable to show any direct effect of erythropoietin, used at concentrations that occurred post intravenous administration, on platelet aggregation both in whole blood and in platelet-rich plasma.     

Responses in extracellular and intracellular calcium and magnesium in aldosteronism

We hypothesized the hypercalciuria and hypermagnesuria that accompany aldosteronism could be pharmacologically attenuated to prevent shifts in extracellular and intracellular levels of these divalent cations and the adverse outcomes associated with them. Accordingly, rats administered aldosterone/salt treatment (ALDOST) were cotreated with either hydrochlorothiazide (Hctz), to selectively reabsorb urinary Ca2+, or with Hctz plus spironolactone (Hctz+Spi), where Spi retards the excretion of these cations in both urine and feces. We monitored urinary excretion and responses in extracellular and intracellular Ca2+ and Mg2+, together with indices of oxi/nitrosative stress in plasma and ventricular tissue. At 4 weeks ALDOST we found the following: (1) hypercalciuria was reduced by Hctz and normalized by Hctz+Spi, and this combination, unlike Hctz alone, also rescued hypermagnesuria; (2) the decrease in plasma-ionized [Ca2+]o was not seen with Hctz or Hctz+Spi, whereas Spi cotreatment protected against a decline in [Mg2+]o; (3) the Ca2+ loading of peripheral blood mononuclear cells and cardiac tissue was not seen with Hctz+Spi; and (4) the induction of oxi/nitrosative stress, expressed as reduced plasma alpha1-antiproteinase activity and activation of gp91(phox) subunit of NADPH oxidase in inflammatory cells invading intramural coronary arteries of the right and left ventricles, together with vascular fibrosis, was completely prevented by Spi cotreatment. In rats with aldosteronism, cotreatment with Hctz+Spi more effectively (vis-à-vis Hctz alone) protects against adverse iterations in extracellular and intracellular concentrations of Ca2+ and Mg2+, as well as the appearance of oxi/nitrosative stress to prevent the proinflammatory vascular phenotype.     

Rosamicin in Urethral and Vaginal Secretions and Tissues in Dogs and Rats

In animal studies we investigated the distribution of rosamicin in plasma and urethral and vaginal tissues in rats as well as in urethral and vaginal secretions in dogs. We found concentration ratios between urethral secretion and plasma of 1.9 and between vaginal secretion and plasma of 2.4. The rosamicin concentrations in urethral and vaginal tissue significantly exceeded the levels of all other tissues investigated. Because rosamicin could be valuable for the treatment of bacterial urethritis and the colonization of the vaginal introitus with fecal bacteria in women, it should be investigated clinically in this respect.     

Similarities and differences in clients treated and in medications prescribed by APRNs and psychiatrists in a CMHC

This study is part of a larger study comparing prescribing practices of psychiatrists and advanced practice psychiatric nurses (APRNs) using the following three groups of patients: patients treated by psychiatrists, those treated by APRNs, and those treated by both APRNs and psychiatrists at different times in 1 year. Demographics for 5507 patients were examined. A subsample of APRNs and psychiatrists prescribed similar total numbers of medications. Psychiatrists prescribed more types of antidepressant medications other than the SSRI antidepressants, and they prescribed more than twice the number of benzodiazepines. APRNs prescribed more SSRIs and spent more time with clients during medication visits.     

Racial differences in oxidative stress and inflammation: in vitro and in vivo

African American race is an independent risk factor for enhanced oxidative stress and inflammation. We sought to examine whether oxidative-stress and inflammatory markers that are typically measured in humans also differ by race in cell culture. We compared levels between African American and Caucasian young adults and then separately in human umbilical vein endothelial cells (HUVECs) from both races. We found heightened oxidative stress and inflammation in the African Americans both in vitro and in vivo. African American HUVECs showed higher nitric oxide (NO) levels (10.8 ± 0.4 vs. 8.8 ± 0.7 μmol/L/mg, p = 0.03), Interleukin-6 (IL-6) levels (61.7 ± 4.2 vs. 23.9 ± 9.0 pg/mg, p = 0.02), and lower superoxide dismutase activity (15.6 ± 3.3 vs. 25.4 ± 2.8 U/mg, p = 0.04), and also higher protein expression (p < 0.05) of NADPH oxidase subunit p47phox, isoforms NOX2 and NOX4, endothelial nitric oxide synthase (NOS), inducible NOS, as well as IL-6. African American adults had higher plasma protein carbonyls (1.1 ± 0.1 vs. 0.8 ± 0.1 nmol/mg, p = 0.01) and antioxidant capacity (2.3 ± 0.2 vs. 1.1 ± 0.3 mM, p = 0.01). These preliminary translational data demonstrate a racial difference in HUVECs much like that in humans, but should be interpreted with caution given its preliminary nature. It is known that racial differences exist in how humans respond to development and progression of disease, therefore these data suggest that ethnicity of cell model may be important to consider with in vitro clinical research.