PGE1与NO对先天性心脏病术后肺动脉高压疗效的对比研究

目的比较静脉应用前列腺素E1(PGE1)和吸入外源性一氧化氮(NO)对先天性心脏病(先心病)术后中重度肺动脉高压的治疗效果.方法对12例术后存在中重度肺动脉高压的先心病病人,进行前瞻性、交叉、随机试验研究.分别应用PGE1(30ngkg-1min-1)、NO(30ppm)、PGE1+NO,检测用药前后心率(HR)、平均动脉压(mSAP)、平均肺动脉压(mPAP)、中心静脉压(CVP)、肺毛细血管嵌压 (PCWP)、心排指数(CI)、肺血管阻力(PVR)和体血管阻力(SVR)等血液动力学参数.同时检测吸入NO前后二氧化氮(NO2)和高铁血红蛋白(MetHb)的浓度.结果 PGE1和NO在降低mPAP和PVR方面均有非常显著的疗效(P＜0.01),但联合应用(PGE1+NO)并未显示出较单纯应用更明显的效果.对mPAP和PVR降低的幅度比较,PGE1和NO之间差异无显著性(P＞0.05).NO对肺血管有更强的选择性,但PGE1在提高CI方面明显优于NO(P＜0.05).吸入NO后,NO2和MetHb的浓度明显高于吸入前(P＜0.01),但仍在正常范围内.结论 PGE1和NO对先心病合并的中重度肺动脉高压均有显著的治疗作用,二者的作用效果相近.考虑到NO的潜在毒性和PGE1在提高心功能方面的良好效果,在临床上首选合适剂量的PGE1更合理可行.     

前列腺素E1对先天性心脏病合并肺动脉高压的血流动力学效应

为了解前列腺素Ｅ１对先天性心脏病合并肺动脉高压的血流动力学效应，作者对３７例受试患者，在行右心导管（ＣＣ）检查中加用前列腺素Ｅ１（ＰＧＥ１）药物试验。ＰＧＥ１用量为每分钟１００～２００ｎｇ／ｋｇ，连续用药１５分钟。发现在低阻力组中（全肺阻力≤６０ｋＰａ·ｓ／Ｌ），ＰＧＥ１选择性扩张肺动脉作用明显；而高阻力组中（全肺阻力＞６０ｋＰａ·ｓ／Ｌ），ＰＧＥ１则对体循环影响较大。结果提示ＰＧＥ１用药剂量和用药效果与肺血管病变程度呈负效应。     

吸入一氧化氮对心瓣膜置换术后肺动脉高压患者血流动力学的影响

目的：观察吸入一氧化氮（ＮＯ）对心瓣膜置换术后肺动脉高压患者血流动力学的影响。方法：选择９例心瓣膜置换术后伴肺动脉高压的病人，吸入ＮＯ０．００３％，观察三个时象点：吸入ＮＯ前；开始吸入ＮＯ后１５分钟；停止吸入ＮＯ后１５分钟。结果：吸入ＮＯ能显著降低肺动脉压和肺循环阻力指数（Ｐ＜０．０１），停止吸入ＮＯ１５分钟后，肺动脉压和肺循环阻力指数恢复到原有水平。在整个观察过程中，心率、平均动脉压、中心静脉压、肺动脉楔压、体循环阻力指数和心脏指数均无显著变化（Ｐ＞０．０５）。结论：吸入ＮＯ具有选择性肺血管扩张作用，是治疗心瓣膜置换术后肺动脉高压的较理想药物。     

前列腺素E1治疗先心病并肺动脉高压

为了解前列腺素Ｅ１对先天性心脏病合并肺动脉高压的治疗作用。对２９例先天性心脏病（ＣＨＤ）合并肺动脉高压（ＰＨ）病儿，用前列腺素Ｅ１（ＰＧＥ１）进行治疗。用量为每分钟１００～２００ｎｇ／ｋｇ，每天持续治疗４～５小时，连续用药４～７天。结果：用药后肺内核素计数、动脉血氧饱和度、右心射血指数皆有不同程度的改善。结论：ＣＨＤ合并ＰＨ的病儿，其心（主要是右心）、肺功能皆有异常，应用ＰＧＥ１治疗后可明显改善其心、肺功能，而且用药时间越长，这种改善就越明显     

双心房输注前列腺素E1和去氧肾上腺素对急性肺动脉高压犬血流动力学的影响

目的 观察双心房输注前列腺素E1和去氧肾上腺素对急性肺动脉高压犬血流动力学的影响.方法 15只杂种犬建立急性肺动脉高压模型后,随机均分为三组.A组通过Swan-Ganz导管至右心房给予前列腺素E1 20 ng·kg-1·min-1.通过左心导管至左心房给予去氧肾上腺素2μg·kg-1·min-1;B组经右心房给予和A组同样的两种药物和剂量;C组经右心房给予等容积的生理盐水.记录麻醉前(T0)、建模成功后10 min(T1)、20 min(T2)、给药后10 min(T3)、30 min(T4)、60min(T5)的HR、MAP、SpO2、CVP、平均肺动脉压(MPAP)、肺毛细血管楔压(PCWP)和心输出量(CO),计算心脏指数(CI)、肺循环阻力指数(PVRI)和体循环阻力指数(SVRI).结果 与C组比较,A、B组T3～T5时MPAP降低(P<0.05);与A组比较,B组T3～T5时CI、MAP和SVRI降低(P<0.05).结论 双心房分别输注前列腺素E1和去氧肾上腺素能降低急性肺动脉高压犬的MPAP,改善心功能.     

前列腺素E1与硝普钠控制性降压对犬血流动力学影响的对比研究

对比研究了普鲁卡因复合麻醉下前列腺素Ｅ１（ＰＧＥ１）与硝普钠（ＳＮＰ）控制性降压时犬血流动力学变化。结果表明，ＳＮＰ降压组有显著的反射性心动过速和反跳性高血压，ＰＧＥ；降压组两者均无。ＰＧＥ１降压时心指数、肺动脉压等其它血流动力学参数亦比ＳＮＰ稳定，提示在保证心肌氧供求平衡及防止血管意外方面ＰＧＥ１降压优于ＳＮＰ。     

抑制一氧化氮生物合成对门脉高压鼠血流动力学的影响

目的：研究一氧化氮（ＮＯ）在门脉高压高血流动力学中的作用。方法：用ＳＤ大鼠制备肝内型（ＩＨＰＨ）、肝前型门脉高压（ＰＨＰＨ）和门腔分流（ＰＣＳ）３组模型，并以正常鼠作为对照组。第一组实验动物再分成３个亚组：ＮＯ生物合成抑制剂Ｌ－ＮＭＭＡ组、Ｌ－ＮＭＭＡ＋ＮＯ生物合成底物Ｌ－精氨酸组以及生理盐水安慰组。血流动力学研究帮放射性微球注射技术。结果：ＩＨＰＨ、ＰＨＰＨ和ＰＣＳ鼠均具有心输出量和内压血流量增     

前列腺素E_1在先心病重度肺动脉高压中的应用

对３２例先天性心脏病合并重度肺动脉高压病人术前行前列腺素Ｅ１（ＰＧＥ１）治疗后，根据用药前后其肺动脉平均压、周围动脉血氧分压、血氧饱和度及心率、血压的变化，并结合肺活检指标进行对比研究。结果表明，ＰＧＥ１不但明显改善部分先心病重度肺动脉高压病人的血流动力学指标，而且可使部分病例Ｈｅａｔｈ分级ＩＩ级或ＩＩ级以下的肺血管病变结构趋向好转；ＰＧＥ１不仅有治疗作用，并对手术适应证有重要的参考价值。先天性心脏病合并肺动脉高压，术前应用ＰＧＥ１治疗，可提高手术安全性。     

大剂量肝素对门静脉高压症高血流动力学影响的研究

目的　研究大剂量肝素对门静脉高压症鼠血浆前列环素 (PGI2 )、一氧化氮 (NO)水平及血流动力学的影响。方法　 4 5只雄性 SD大鼠随机分成 IHPH (CCl4 肌肉注射法 )、PHPH (部分门静脉缩窄法 )和 SO(假手术 )三组。动物模型制备后两周 ,三组鼠再随机分成二个亚组 ,即生理盐水对照组和大剂量肝素组。肝素通过鼠尾静脉用微量注射器以 2 0 0 IU / Kg/ m in的速度持续静脉输注 1小时 ,然后用同位素微球技术行血流动力学研究。用放射免疫法测股动脉血浆 6- keto- PGF1α浓度。用还原法测股动脉血浆 NO2 / NO3浓度。结果　与 SO鼠比较 ,IHPH、PHPH两组鼠的 TPR与 SVR均显著降低 (P<0 .0 5 ) ,CI与 PVI均显著升高 (P<0 .0 5 )。应用大剂量肝素后 ,血浆 6- keto- PGF1α浓度 (pg/ m l)在 IHPH、PHPH和 SO鼠分别为 2 3 90 .61± 14 0 0 .3 8、2 766.4 7± 5 0 6.95和 3 965 .96± 976.82 ,均显著地高于生理盐水对照组中三组鼠的浓度 (分别为 112 3 .85± 15 3 .64;891.88± 83 .11;72 5 .5 3± 10 5 .5 4 ) ;相反 ,血浆 NO2 / NO3浓度 (μmol/ L )在 IHPH、PHPH和 SO鼠分别为 5 4 .0 2± 11.89、62 .0 6± 3 .5 6和 4 5 .2 8± 4 .3 9,均显著地低于生理盐水对照组中三组鼠的浓度 (分别为 73 .3 4± 4 .3 1;75 .2 1     

前列腺素E1控制性降压对血流动力学的影响

选择犬１４只，随机分为硝普钠组（ＳＮＰ组）和前列腺素Ｅ１组（ＰＧＥ１组），输注降压药使平均动脉压降低 ３０％～４０％，于降压前、降压后 １５、３０分钟及停止降压后１５分钟测定血流动力学指标。结果表明，降压期间外周血管阻力指数、肺血管阻力指数、平均肺动脉压、左室每搏功指数、右室每搏功指数两组均显著降低；ＳＮＰ组中心静脉坛显著降低，心率显著增快；ＰＧＥ１组中心静脉压、心率无显著变化。两组每搏指数、心脏指数、肺毛细血管嵌压无显著变化。     

H1N1 infection in emergency surgery: A cautionary tale

Pandemic 2009 influenza A H1N1 has spread rapidly since its first report in Mexico in March 2009. This is the first influenza pandemic in over 40 years and it atypically affects previously healthy young adults, with higher rates of morbidity and mortality. The medical literature has been inundated with reports of H1N1 infection, the majority found in critical care and internal medicine journals with a relative paucity in the surgical literature. Despite this, it remains an important entity that can impact greatly on acute surgical emergencies. We present a case of previously healthy 31-year-old male who underwent open appendectomy. His post-operative recovery was complicated by acute respiratory distress syndrome secondary to H1N1 infection. This case report highlights the impact that H1N1 virus can have on acute surgical emergencies and how it can complicate the post-operative course.     

Estrogen inhibits Dlk1/FA1 production: A potential mechanism for estrogen effects on bone turnover

We have recently identified delta‐like 1/fetal antigen 1 (Dlk1/FA1) as a novel regulator of bone mass that functions to mediate bone loss under estrogen deficiency in mice. In this report, we investigated the effects of estrogen (E) deficiency and E replacement on serum (s) levels of Dlk1/FA1 (s‐Dlk1FA1) and its correlation with bone turnover markers. s‐Dlk1/FA1 and bone turnover markers (serum cross‐linked C‐telopeptide [s‐CTX] and serum osteocalcin) were measured in two cohorts: a group of pre‐ and postmenopausal women (n = 100) and a group of postmenopausal women, where half had received estrogen‐replacement therapy (ERT, n = 166). s‐Dlk1/FA1 and s‐CTX were elevated in postmenopausal E‐deficient women compared with premenopausal E‐replete women (both p < 0.001). s‐Dlk1/FA1 was correlated with s‐CTX (r = 0.30, p < 0.01). ERT in postmenopausal women decreased s‐Dlk1/FA1, as well as s‐CTX and s‐osteoclacin (all p < .0001). Changes in s‐Dlk1 were significantly correlated with those observed in s‐CTX (r = 0.18, p < 0.05) and s‐osteocalcin (r = 0.28, p < 0.001). In conclusion, s‐Dlk1/FA1 is influenced by E‐deficiency and is correlated with bone turnover. Increased levels of s‐Dlk1/FA1 in postmenopausal women may be a mechanism mediating the effects of estrogen deficiency on bone turnover. © 2011 American Society for Bone and Mineral Research     

Differential localization of MT1-MMP in human prostate cancer tissue: role of IGF-1R in MT1-MMP expression

BACKGROUND: MT1-MMP is a metalloproteinase involved in prostate cancer metastasis. The IGF-1R is a tyrosine kinase receptor involved with tumor progression and metastasis. The purpose of this investigation was to examine MT1-MMP and IGF-1R expression and localization in prostate cancer tissues and explore the role of IGF-1R in regulating MT1-MMP in prostate cancer cell lines. METHODS: Immunohistochemistry was utilized to study MT1-MMP and IGF-1R expression in human prostate tissues. IGF-1R regulation of MT1-MMP expression was determined by gene promoter analysis, quantitative RT-PCR and Western blot analysis following pharmacological inhibition of the receptor in PC-3N cells and treatment of LNCaP cells with androgen and IGF-1. RESULTS: MT1-MMP expression was high in the apical regions of the luminal cells in PIN and prostate cancer and less intense in the basalateral regions of benign tissues. IGF-1R was expressed primarily in the basal cells of normal glands and highly expressed in prostate cancer. Inhibition of IGF-1R in PC-3N cells decreased MT1-MMP expression and treatment of LNCaP cells with a synthetic androgen and IGF-1 increased MT1-MMP expression. CONCLUSIONS: These data demonstrate that MT1-MMP is highly expressed in the apical cytoplasmic regions of the luminal cells in PIN and prostate cancer when compared to basalateral cytoplasmic membrane staining in benign glands. Additionally, we demonstrate that IGF-1R is highly expressed in human prostate carcinoma. These findings suggest that MT1-MMP localization and IGF-1R expression in prostate carcinoma could be predictive biomarkers for aggressive disease and support IGF-1R as a promising therapeutic target to decrease processes of prostate cancer metastasis.     

Genetic polymorphisms of CYP1A1, CYP2E1, GSTM1, and GSTT1 associated with head and neck cancer

BACKGROUND: Alcohol intake and tobacco smoke, in addition to other environmental and genetic factors, have been associated with head and neck cancer. We evaluated the role of metabolic enzyme polymorphisms on the risk of head and neck cancer in a hospital-based case-control study. METHODS: CYP1A1MspI, CYP2E1PstI, GSTM1, and GSTT1polymorphisms were evaluated in 103 histologically confirmed head and neck cancer cases and 102 controls by means of polymerase chain reaction-restriction fragment length polymorphism methods. RESULTS: GSTM1null increased the risk of head and neck cancer (odds ratio [OR], 2.2; 95% confidence interval [95% CI], 1.24-3.79), oral cancer (OR, 2.8; 95% CI, 1.28-5.98), and pharyngeal cancer (OR, 2.2; 95% CI, 1.08-4.63). CYP2E1PstI polymorphism indicated a risk for oral cancer (OR, 3.6; 95% CI, 1.29-11.56). The joint effect of GSTM1 null and CYP1A1 polymorphism increased the risk of head and neck cancer (OR, 2.4; 95% CI, 1.13-5.10). CONCLUSIONS: GSTM1 null alone or associated with CYP1A1 increased the risk of head and neck cancer; the CYP2E1PstI mutated allele increased the risk for only oral cancer.     

T1 Radiculopathy: Electrodiagnostic Evaluation

Electromyography (EMG) studies are useful in the anatomical localization of nerve injuries and, in most cases, isolating lesions to a single nerve root level. Their utility is important in identifying specific nerve-root-level injuries where surgical or interventional procedures may be warranted. In this case report, an individual presented with right upper extremity radicular symptoms consistent with a clinical diagnosis of cervical radiculopathy. EMG studies revealed that the lesion could be more specifically isolated to the T1 nerve root and, furthermore, provided evidence that the abductor pollicis brevis receives predominantly T1 innervation.     

An updating meta‐analysis of the GSTM1, GSTT1, and GSTP1 polymorphisms and prostate cancer: A HuGE Review

It has been postulated that individuals with GSTM1, GSTT1 deficiency and, GSTP1 (105Ile/Val transition) have increased susceptibility to carcinogens and are more likely to develop prostate cancer. In recent years, GST status has been extensively studied as a prostate cancer risk factor; however, the results are inconsistent. To re‐examine this controversy, we have undertaken an updating meta‐analysis of 29 studies with GSTM1 genotyping (4,564 prostate cancer cases and 5,464 controls), 22 studies with GSTT1 genotyping (3,837 cases and 4,552 controls), and 24 studies with GSTP1 genotyping (5,301 cases and 5,621 controls). The random effects odds ratio was 1.33 [95% confidence interval (95% CI): 1.15, 1.55; I² = 68.9%, P for heterogeneity = 0.00] for the GSTM1 null versus present genotype and 1.05 (95% CI: 0.86, 1.27; I² = 68.2%, P for heterogeneity = 0.00) for the GSTT1 null versus present genotype, and 1.06 (95% CI: 0.91, 1.24; I² = 71.5%, P for heterogeneity = 0.00) for the GSTP1‐Val versus GSTP1‐Ile allele. For GSTM1 polymorphism, similar results reached in Caucasians and Asians, with exception for Africans. No association between GSTT1 or GSTP1 polymorphisms and prostate cancer risk was detected in different racial. In conclusion, the major finding of our study suggested that GSTM1 polymorphism conferred an increasing risk of prostate cancer on a wide population basis, however, no relationship was found between GSTT1 and GSTP1 status and the risk of prostate cancer. Prostate 69:662–688, 2009. © 2009 Wiley‐Liss, Inc.     

Relationship between GSTM1/GSTT1 Null Genotypes and Renal Cell Carcinoma Risk: A Meta-Analysis

The results from the published studies on the relationship between GSTM1/GSTT1 null genotypes and renal cell carcinoma (RCC) risk are still conflicting. This meta-analysis was performed to evaluate the relationship between GSTM1/GSTT1 null genotypes and RCC susceptibility. Association studies were identified from the databases of PubMed, Embase, Cochrane Library, and CBM-disc (China Biological Medicine Database) on 1 February 2012, and eligible investigations from 1950 to 2012 were synthesized using meta-analysis method. Results were expressed as odds ratios (ORs) for dichotomous data, and 95% confidence intervals (CIs) were also calculated. Six studies were identified for the analysis of association between polymorphic deletion of GSTM1/GSTT1 and RCC risk. There was no association between GSTM1/GSTT1 null genotype and RCC susceptibility (GSTM1: N = 6, p-heterogeneity = 0.07, OR = 1.07, 95% CI: 0.85–1.35, p = 0.57; GSTT1: N = 6, p-heterogeneity < 0.00001, OR = 0.98, 95% CI: 0.58–1.65, p = 0.94). Interestingly, null genotype of GSTT1 was associated with RCC risk in Caucasians and Asians (Caucasians: N = 4, p-heterogeneity = 0.38, OR = 0.76, 95% CI: 0.61–0.95, p = 0.01; Asians: N = 1, OR = 2.39, 95% CI: 1.63–3.51, p < 0.00001). For the GSTM1–GSTT1 interaction analysis, the dual null genotype of GSTM1/GSTT1 was not significantly associated with RCC susceptibility (N = 4, p-heterogeneity = 0.006, OR = 1.17, 95% CI: 0.98–1.39, p = 0.09). However, the dual null genotype of GSTM1–GSTT1 was associated with RCC risk in Asians (N = 1, OR = 2.06, 95% CI: 1.36–3.13, p = 0.007). In conclusion, our study results suggest that GSTT1 null genotype is associated with the RCC susceptibility in Caucasians and Asians, and the dual null genotype of GSTM1–GSTT1 is associated with RCC risk in Asians. However, more genetic epidemiological investigations are required to further explore this relationship.     

SMARCB1/INI1 Deficient Sino-Nasal Carcinoma: Extending the Histomorphological Features

SMARCB1/INI1 deficient sinonasal carcinoma is a variant of sinonasal undifferentiated carcinoma (SNUC). There is a paucity of literature describing the histomorphological features of this relatively new entity. Herein we describe the histomorphological features of three such cases and review the literature. We retrospectively reviewed the cases of SNUC diagnosed in our institute in the last 6 years. Immunohistochemistry for INI1, NUT & p16 were performed on these cases. Three cases showed loss of INI1. The histomorphology and clinicopathological features of these cases were studied and compared with non INI1 deficient SNUC. A total of 9 cases of SNUC were identified. Three of these cases showed loss of INI1. These three cases had presented with large sinonasal mass and with intracranial extension. Histopathology of these cases showed a diffuse infiltrative pattern, nest, and islands of predominantly basaloid cells with focal rhabdoid morphology. Additional features like small cell carcinoma like pattern, pseudoalveolar and pseudoglandular patterns, clear vacuoles and pseudopapillary appearance were also noted. We conclude that in presence of a mixed pattern of cells with a predominance of basaloid morphology, the possibility of SMARCB1/INI1 deficient sinonasal carcinoma must be strongly suspected and immunohistochemistry for INI1 must be performed.Electronic supplementary materialThe online version of this article (10.1007/s12105-020-01246-9) contains supplementary material, which is available to authorized users.