重症急性胰腺炎患者早期血液流变学及血管活性指标血栓素A_2、前列环素I_2水平变化

目的观察重症急性胰腺炎(SAP)患者早期血液流变学指标及血栓素A2(TXA2)、前列环素I2(PGI2)的变化。方法2012年1月至2013年9月住院的32例SAP患者为SAP组,30例体检健康人为NC组。于患者入院后治疗前即静脉采血,平行检测血液流变学指标及血浆TXA2、PGI2水平,并计算TXA2、PGI2比值。结果比较进行t检验。结果 SAP组血液流变学中除红细胞变形指数低于NC组(t=2.185,P0.05)外,全血高、中、低切黏度、血浆黏度高于NC组(t=2.820、2.755、2.700、3.622,P0.05),全血高切还原黏度、全血低切还原黏度高于NC组(t=3.391、2.018,P0.05),红细胞压积、红细胞刚性指数、红细胞聚集指数高于NC组(t=2.980、2.209、2.004,P0.05)、全血高切相对指数、全血低切相对指数高于NC组(t=2.630、2.440,P0.05);SAP组TXA2、PGI2、TXA2、PGI2比值高于NC组(t=3.256、2.589、2.640,P0.05)。结论 SAP患者早期即存在血液流变性异常及血管内皮细胞活性增高。     

重症急性胰腺炎患者早期血液流变学及血管活性指标血栓素A2、前例环素I2水平变化

目的：观察重症急性胰腺炎（SAP）患者早期血液流变学指标及血栓素A2（TXA2）、前列环素I2（PGI2）的变化。方法2012年1月至2013年9月住院的32例SAP患者为SAP组,30例体检健康人为NC组。于患者入院后治疗前即静脉采血,平行检测血液流变学指标及血浆TXA2、PGI2水平,并计算TXA2、PGI2比值。结果比较进行t检验。结果 SAP组血液流变学中除红细胞变形指数低于NC组（t＝2．185,P＜0．05）外,全血高、中、低切黏度、血浆黏度高于NC 组（t＝2．820、2．755、2．700、3．622,P＜0.05）,全血高切还原黏度、全血低切还原黏度高于NC组（t＝3．391、2．018,P＜0．05）,红细胞压积、红细胞刚性指数、红细胞聚集指数高于NC组（t＝2．980、2.209、2.004,P＜0．05）、全血高切相对指数、全血低切相对指数高于NC组（t＝2.630、2．440,P＜0．05）;SAP组TXA2、PGI2、TXA2、PGI2比值高于NC组（t＝3．256、2.589、2.640,P＜0．05）。结论 SAP患者早期即存在血液流变性异常及血管内皮细胞活性增高。     

醒脑启智胶囊对血管性痴呆病人血液流变学的影响

目的观察醒脑启智胶囊对血管性痴呆病人血液流变学的影响.方法将血管性痴呆病人随机分为治疗组92例和对照组90例,治疗组服用醒脑启智胶囊,对照组服用舒血宁片(银杏叶提取物),6周为1个疗程,两个疗程后观察病人精神状态简易速检表(MMSE)和日常生活自理能力量表(ADL-R)积分以及血液流变学的变化.结果两组治疗后MMSE评分较治疗前显著升高(P＜0.01),ADL-R评分较治疗前显著降低(P＜0.01),治疗后治疗组MMSE和ADL-R评分与对照组比较有统计学意义(P＜0.05);两组治疗后全血高切黏度、全血低切黏度、纤维蛋白原较治疗前显著降低(P＜0.05或P＜0.01);治疗组还可显著降低血浆黏度、红细胞比容(P＜0.05或P＜0.01),治疗后治疗组全血高切黏度、全血低切黏度、红细胞比容与对照组比较有统计学意义(P＜0.05).结论醒脑启智胶囊不仅可明显改善血管性痴呆病人的认知功能,提高病人的日常生活自理能力,而且可改善病人血液流变学,减少痴呆的危险因素.     

自拟逐痰祛瘀方对脑血管支架术后再狭窄的预防作用研究

目的探讨逐痰祛瘀方对脑血管支架术后再狭窄的预防作用。方法选择2013年1月—2015年2月清远市清城区中医院神经内科收治的脑血管支架术病人50例,随机均分为对照组与观察组,每组25例。对照组采用单纯西药治疗,观察组在对照组基础上给予自拟逐痰祛瘀方治疗,比较两组病人治疗后血液流变学参数及血管再狭窄情况。结果术后6个月,观察组血浆黏度、纤维蛋白浓度、血栓素A_2(TXA_2)/前列环素I2(PGI_2)值均显著低于治疗前,TXA_2、PGI_2浓度则显著升高,差异均有统计学意义(P0.05);与对照组治疗后比较,观察组治疗后血浆黏度、纤维蛋白、TXA_2、PGI_2浓度及TXA_2/PGI_2值均有显著改善,差异有统计学意义(P0.05)。观察组支架段直径显著大于对照组(P0.05),直径减少指数、再狭窄率及再介入率均明显低于对照组,差异均有统计学意义(P0.05)。结论逐痰祛瘀方可改善脑血管状态,有利于降低支架术后再狭窄的发生率。     

体外反搏辅助治疗脑梗死的临床疗效及其对血液流变学指标的影响研究

目的观察体外反搏辅助治疗脑梗死的临床疗效,并探讨其对血液流变学指标的影响。方法选取2014年10月—2015年10中山市东凤人民医院收治的脑梗死患者260例,采用随机数字表法分为对照组和观察组,每组130例。对照组患者采用常规治疗,观察组患者在常规治疗基础上进行体外反搏辅助治疗;12 d为1个疗程,两组患者均连续治疗2个疗程。比较两组患者临床疗效及治疗前后血液流变学指标。结果观察组患者临床疗效优于对照组(P0.05)。治疗前两组患者血浆比黏度、低切变率下全血黏度、高切变率下全血黏度、红细胞聚集指数、红细胞电泳时间、红细胞比容、纤维蛋白原比较,差异无统计学意义(P0.05);治疗后观察组患者血浆比黏度、低切变率下全血黏度、高切变率下全血黏度、红细胞聚集指数、红细胞比容、纤维蛋白原均低于对照组,红细胞电泳时间短于对照组(P0.05)。治疗后,对照组患者血浆比黏度、低切变率下全血黏度、高切变率下全血黏度低于治疗前(P0.05);观察组患者血浆比黏度、低切变率下全血黏度、高切变率下全血黏度、红细胞聚集指数、红细胞比容、纤维蛋白原均低于治疗前,红细胞电泳时间短于治疗前(P0.05)。结论体外反搏辅助治疗脑梗死能有效改善患者的神经功能和血液流变学情况,临床疗效确切。     

丹红注射液对老年高血压血液流变学的影响

目的观察丹红注射液对老年高血压患者血液流变学的影响。方法选择老年高血压患者140例,分成丹红注射液治疗组(72例)和对照组(68例)。治疗组加用丹红注射液30ml加入5%葡萄糖或0.9%氯化钠溶液中静脉滴注,1次/d,疗程12d。对照组不加用丹红注射液,未采取其他干预施。检测两组治疗前后血液流变学指标进行对照分析。结果治疗前后两组的血液流变学指标均有明显改善,差异有统计学意义(P0.01)。治疗后,丹红注射液治疗组全血黏度、血浆黏度、全血还原黏度、血细胞比容、红细胞聚集指数、红细胞刚性指数、红细胞变形指数以及红细胞电泳指数均优于对照组,差异有统计学意义(P0.05)。结论丹红注射液能显著改善高血压患者血液流变学状态,改善微循环,降低血液黏滞度。     

针灸联合硝苯地平控释片对原发性高血压病人血浆TXA_2/PGI_2平衡及血液流变学的影响

目的探讨针灸联合硝苯地平控释片对原发性高血压病人血浆血栓素A_2(A_2,TXA_2)、前列腺素I_2(PGI_2)平衡以及对血液流变学的影响。方法选择2016年4月—2018年4月于上海中医药大学附属曙光医院接受诊治的原发性高血压病人108例,依据随机数字表法进行分组,每组54例。对照组病人接受硝苯地平控释片治疗,研究组接受针灸与硝苯地平控释片联合治疗。治疗5周后评价两组临床疗效,测定收缩压、舒张压,采用血栓素B_2(TXB_2)与6酮-前列腺素F1α(6-Keto-PGF1α)以及TXA_2/6-Keto-PGF1α比值观察血浆TXA_2/PGI_2平衡情况,观察血液流变学指标,并统计复发率。结果研究组总有效率明显高于对照组(P0.05);治疗后两组收缩压与舒张压水平明显降低(P0.05),且组间比较差异有统计学意义(P0.05);治疗后两组TXB_2及二者比值均明显降低(P0.05),治疗后两组6-Keto-PGF1α明显升高(P0.05),且组间比较差异有统计学意义(P0.05);治疗后两组血液流变学各项观察指标均明显降低(P0.05),且组间比较差异有统计学意义(P0.05);对照组复发率(11.11%)与研究组(0)比较,差异有统计学意义(P0.05)。结论针灸联合硝苯地平控释片可明显提高原发性高血压病人临床疗效,良好控制收缩压与舒张压,维持血浆TXA_2与PGI_2平衡,在改善血液流变学相关指标以及复发率等方面亦具有确切效果。     

丹红注射液对2型糖尿病肾病病人血小板参数及血液流变学指标的影响

目的探讨丹红注射液对2型糖尿病肾病(DN)病人血小板参数及血液流变学的影响。方法选择符合条件的2型糖尿病肾病病人95例,随机分为观察组和对照组。对照组给予常规降糖、降压、降脂药物治疗,观察组在此基础上加用丹红注射液治疗。治疗2周,观察各组治疗前后血小板参数及血液流变学指标的影响。结果两组治疗前血小板参数及血液流变学指标无明显差异;两组治疗后空腹血糖(FPG)、餐后2h血糖(2hPG)均较前明显下降,但观察组糖化血红蛋白(HbA1c)明显改善(P0.01);两组治疗后全血高低切黏度。血浆黏度、红细胞比容、红细胞刚性指数、红细胞变形指数水平均明显改善,观察组疗效好于对照组(P0.05);观察组治疗后总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)明显下降,高密度脂蛋白胆固醇(HDL-C)明显升高,且与对照组相比有统计学意义(P0.05);观察组治疗后血小板计数(PLT)、血小板平均体积(MPV)和血小板分布宽度(PDW)变化明显,疗效优于对照组(P0.05)。结论丹红注射液可明显改善2型糖尿病病人血液流变学指标,纠正糖和脂类代谢紊乱,改善血小板参数。     

马来酸桂哌齐特联合尤瑞克林治疗急性脑梗死的疗效及对血液流变学和血清IL-10、TNF-α、hs-CRP的影响

目的探讨急性脑梗死应用马来酸桂哌齐特(CM)联合尤瑞克林治疗的临床效果及对血液流变学和血清白细胞介素(IL)-10、肿瘤坏死因子(TNF)-α、超敏C反应蛋白(hs-CRP)水平的影响。方法选取我院2015年3月—2017年3月收治的114例急性脑梗死病人,采取随机数字表法均分为两组。对照组(57例)采取尤瑞克林治疗,观察组(57例)在此基础上加用CM治疗。记录比较两组临床疗效,治疗前后血液流变学及血清指标水平变化、不良反应发生情况。结果治疗2周后,观察组总有效率达91.2%,较对照组(71.9%)显著升高(P0.01)。与对照组同期对比,观察组治疗2周后全血高切黏度、全血低切黏度、血浆黏度、纤维蛋白原值均显著降低(P0.01)。与治疗前相比,两组治疗2周后血清TNF-α、hs-CRP水平均显著降低(P0.01),血清IL-10水平均显著升高(P0.01);且观察组以上指标改善较对照组更显著(P0.01)。观察组不良反应率为7.0%,与对照组(5.3%)比较,差异无统计学意义(P0.05)。结论 CM联合尤瑞克林治疗急性脑梗死能有效减轻病人神经功能损伤,疗效更优,可能与其显著调节病人血液流变学状态和血清IL-10、TNF-α、hs-CRP水平有关。     

红花黄色素联合阿加曲班治疗急性脑梗死的疗效及对血清IL-8、ET-1、NO水平和血液流变学的影响

目的探究红花黄色素(SY)联合阿加曲班(Arg)治疗急性脑梗死(ACI)的临床疗效及对病人血清白细胞介素(IL)-8、内皮素(ET)-1、一氧化氮(NO)水平和血液流变学的影响。方法选取中国医科大学附属第一医院2015年3月—2017年3月收治的108例ACI病人,采用随机数字表法分为两组,各54例。所有病人均采取相同的基础治疗,对照组加用Arg治疗,观察组在对照组基础上联合SY治疗。比较两组临床疗效,治疗前后血清指标及血液流变学指标变化,不良反应发生情况。结果治疗1个月后,观察组总有效率达90.7%,较对照组明显升高(75.9%,P0.05)。与治疗前比较,两组治疗2周后血清IL-8、ET-1水平均显著降低(P0.01),NO水平显著升高(P0.01),且观察组改善较对照组更显著(P0.01)。与治疗前比较,两组治疗2周后红细胞聚集指数(RCAI)、红细胞比容(HCT)、全血黏度(WBV)和血浆黏度(PV)均显著降低(P0.01),且观察组下降较对照组更显著(P0.01)。对照组与观察组不良反应发生率比较差异无统计学意义(9.3%vs 3.7%,P0.05)。结论红花黄色素联合阿加曲班治疗急性脑梗死更能有效保护病人神经功能,改善预后,疗效显著且安全可靠,可能与其显著改善血清中IL-8、ET-1、NO水平及血液流变学状态有关。     

The Prevalence of CYP2C8, 2C9, 2J2, and soluble epoxide hydrolase polymorphisms in African Americans with hypertension

BACKGROUND: The cytochrome P450 (CYP) epoxygenase pathway produces arachidonic acid metabolites that are vasoactive, that affect renal sodium handling, and that have been proposed to play a mechanistic role in hypertension. Multiple single nucleotide polymorphisms (SNP) in CYP2C8, 2C9, 2J2 and soluble epoxide hydrolase (sEH) have been identified, many of which have altered functional activity in vitro. We performed a case-control study to determine the prevalence of epoxygenase-related SNP in African American individuals and to evaluate whether these SNP are associated with increased risk of hypertension. METHODS: Normotensive African American individuals (N = 107) and African American patients with hypertension (N = 108) were recruited. DNA was extracted from a venous blood sample and genotyped for CYP2C8*2,*3, CYP2C9*2-*5,*8,*11, CYP2J2 *2-*7, L50L, R49S, V113M, N124S, sEH R287Q, and sEH 403Rins variant alleles by allelic discrimination using real-time polymerase chain reaction. Genotype and allele frequencies were calculated and associations with hypertension were estimated using unconditional logistic regression, adjusting for age and sex. RESULTS: No association was found between any of the variant alleles and hypertension. We did find that only the CYP2C8*3and CYP2C9*2 alleles were in strong linkage disequilibrium in both the hypertensive and healthy African American groups, a finding that was reported previously in healthy individuals of white ethnicity. CONCLUSIONS: These results suggest that these epoxygenase-related SNP are not associated with increased risk of hypertension in the African American population. There was significant linkage disequilibrium between CYP2C8*3 and CYP2C9*2 alleles that was not associated with hypertension.     

Intravenous,Intratracheal, and Intranasal Inoculation of Swine with SARS-CoV-2

Since the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the susceptibility of animals and their potential to act as reservoirs or intermediate hosts for the virus has been of significant interest. Pigs are susceptible to multiple coronaviruses and have been used as an animal model for other human infectious diseases. Research groups have experimentally challenged swine with human SARS-CoV-2 isolates with results suggesting limited to no viral replication. For this study, a SARS-CoV-2 isolate obtained from a tiger which is identical to human SARS-CoV-2 isolates detected in New York City and contains the D614G S mutation was utilized for inoculation. Pigs were challenged via intravenous, intratracheal, or intranasal routes of inoculation (n = 4/route). No pigs developed clinical signs, but at least one pig in each group had one or more PCR positive nasal/oral swabs or rectal swabs after inoculation. All pigs in the intravenous group developed a transient neutralizing antibody titer, but only three other challenged pigs developed titers greater than 1:8. No gross or histologic changes were observed in tissue samples collected at necropsy. In addition, no PCR positive samples were positive by virus isolation. Inoculated animals were unable to transmit virus to naïve contact animals. The data from this experiment as well as from other laboratories supports that swine are not likely to play a role in the epidemiology and spread of SARS-CoV-2.     

Classification and characterization of hereditary types 2A, 2B, 2C, 2D, 2E, 2M, 2N, and 2U (unclassifiable) von Willebrand disease.

All variants of type 2 von Willebrand disease (VWD) patients, except 2N, show a defective von Willebrand factor (VWF) protein (on cross immunoelectrophoresis or multimeric analysis), decreased ratios for VWF:RCo/Ag and VWF:CB/Ag and prolonged bleeding time. The bleeding time is normal and FVIII:C levels are clearly lower than VWF:Ag in type 2N VWD. High resolution multimeric analysis of VWF in plasma demonstrates that proteolysis of VWF is increased in type 2A and 2B VWD with increased triplet structure of each visuable band (not present in types 2M and 2U), and that proteolysis of VWF is minimal in type 2C, 2D, and 2E variants that show aberrant multimeric structure of individual oligomers. VWD 2B differs from 2A by normal VWF in platelets, and increased ristocetine-induced platelet aggregation (RIPA). RIPA, which very likely reflects the VWF content of platelets, is normal in mild, decreased in moderate, and absent in severe type 2A VWD. RIPA is decreased or absent in 2M, 2U, 2C, and 2D, variable in 2E, and normal in 2N. VWD 2M is usually mild and characterized by decreased VWF:RCo and RIPA, a normal or near normal VWF multimeric pattern in a low resolution agarose gel. VWD 2A-like or unclassifiable (2U) is distinct from 2A and 2B and typically featured by low VWF:RCo and RIPA with the relative lack of high large VWF multimers. VWD type 2C is recessive and shows a characteristic multimeric pattern with a lack of high molecular weight multimers, the presence of one single-banded multimers instead of triplets caused by homozygosity or double hereozygosity for a mutation in the multimerization part of VWF gene. Autosomal dominant type 2D is rare and characterized by the lack of high molecular weight multimers and the presence of a characteristic intervening subband between individual oligimers due to mutation in the dimerization part of the VWF gene. In VWD type 2E, the large VWF multimers are missing and the pattern of the individual multimers shows only one clearly identifiable band, and there is no intervening band and no marked increase in the smallest oligomer. 2E appears to be less well defined, is usually autosomal dominant, and accounts for about one third of patients with 2A in a large cohort of VWD patients.     

Frequency and prognostic impact of mutations in SRSF2, U2AF1, and ZRSR2 in patients with myelodysplastic syndromes

Mutations in genes of the splicing machinery have been described recently in myelodysplastic syndromes (MDS). In the present study, we examined a cohort of 193 MDS patients for mutations in SRSF2, U2AF1 (synonym U2AF35), ZRSR2, and, as described previously, SF3B1, in the context of other molecular markers, including mutations in ASXL1, RUNX1, NRAS, TP53, IDH1, IDH2, NPM1, and DNMT3A. Mutations in SRSF2, U2AF1, ZRSR2, and SF3B1 were found in 24 (12.4%), 14 (7.3%), 6 (3.1%), and 28 (14.5%) patients, respectively, corresponding to a total of 67 of 193 MDS patients (34.7%). SRSF2 mutations were associated with RUNX1 (P < .001) and IDH1 (P = .013) mutations, whereas U2AF1 mutations were associated with ASXL1 (P = .005) and DNMT3A (P = .004) mutations. In univariate analysis, mutated SRSF2 predicted shorter overall survival and more frequent acute myeloid leukemia progression compared with wild-type SRSF2, whereas mutated U2AF1, ZRSR2, and SF3B1 had no impact on patient outcome. In multivariate analysis, SRSF2 remained an independent poor risk marker for overall survival (hazard ratio = 2.3; 95% confidence interval, 1.28-4.13; P = .017) and acute myeloid leukemia progression (hazard ratio = 2.83; 95% confidence interval, 1.31-6.12; P = .008). These results show a negative prognostic impact of SRSF2 mutations in MDS. SRSF2 mutations may become useful for clinical risk stratification and treatment decisions in the future.     

Clinical features,management, and outcome of hemodialysis patients with SARS-CoV-2

The aim of the study was to evaluate the clinical features of the patients on HD with COVID-19 and determine the prognostic factors. In this single-center prospective study, a total of 58 chronic renal failure patients on HD and diagnosed COVID-19 infection were enrolled in the study. The patients were divided into two groups according to their need for intensive care unit referral. Demographic features of the patients, clinical manifestations, laboratory data, treatments, and clinical outcome were evaluated. The mean age of 58 HD patients was 63.2 ± 13.8 (30–93) years and female–male ratio was 0.34. SARS-CoV2-PCR positivity rate was 32.8%. 85.2% of patients (n = 46) had bilateral lesions and 14.8% (n = 8) had unilateral one lesion in chest CT. The most common symptoms were fatigue (in 44 patients, 80%) and dyspnea (in 31 patients, 56.4%). The most common comorbidity was HT (in 37 patients, 67.3%). The patients who need intensive care and died were older (p = 0.015). We observed lower platelet and eosinophil counts, potassium levels, higher AST, troponin and CRP levels in the group of patients who need intensive care and died than the group who survived (p = 0.043, 0.005, 0.033, 0.007, 0.001, <0.001, respectively). 15.5% of the patients (n = 9) were transferred to intensive care unit. Among them, two were discharged with cure and seven patients died. Mortality rate was 12.1%. Older age, lower platelet and eosinophil counts and higher AST, troponin and CRP levels were prognostic risk factors in our HD patients who needed intensive care.     

MMP-2, MMP-9, TIMP-1 and TIMP-2 levels in patients with rheumatoid arthritis and psoriatic arthritis

OBJECTIVE: Rheumatoid arthritis (RA) and psoriatic arthritis (PA) are both chronic rheumatic inflammatory diseases characterized by disruption of the extra-cellular matrix (ECM) protein of the cartilage, likely induced by proteolytic enzymes such as matrix metalloproteases (MMPs). The goal of this study was to quantify the expression of MMPs such as MMP-2 and MMP-9, and their physiological tissue inhibitors TIMP-2 and TIMP-1, respectively, in serum and synovial fluid. METHODS: Serum and synovial fluid from 24 RA patients and 17 PA patients were studied to determine the levels of MMP-2 and MMP-9 proteolytic activity using a modified gelatin zymography procedure. TIMP-1 and TIMP-2 were measured by a commercially available ELISA kit. RESULTS: Our results show that MMP-2 was detected in the latent form only, while MMP-9 was present in latent and active form. Both gelatinases were more concentrated in synovial fluid than in serum, and TIMP-1 and TIMP-2 concentrations were also more elevated in synovial fluid than in serum. CONCLUSIONS: To investigate the remodelling of cartilage ECM proteins, the evaluation of synovial fluid concentrations of MMP-2, MMP-9, TIMP-1 and TIMP-2 is more reliable than that determined in serum. In view of these data, MMPs inhibitors might represent a possible target for new therapies delivered directly in the joint space.     

Cyclooxygenase products and cyclic nucleotide levels with infusion of arachidonic acid, PGI2, PGE2, PGF2, and 6-keto-PGF1 in an isolated dog lung

Arachidonic acid (AA) was infused into the pulmonary artery of an isolated dog lung perfused with a physiologic salt solution. This led to elevations in pulmonary cyclic AMP and prostaglandins (PGs) including PGE2, PGF2 alpha, TXB2 (a metabolite of TXA2), and 6-keto-PGF1 alpha (a metabolite of PGI2). The elevations were prevented by PG synthesis inhibitors. A dose of PGI2 comparable to that produced from AA led to elevations in cyclic AMP. These elevations were not reduced by PG synthesis inhibitors; this indicated that the inhibitors did not reduce cyclic AMP except by inhibiting metabolism of AA. The PGE2 led to lesser elevations in cyclic AMP than did PGI2; PGF2 alpha and 6-keto-PGF1 alpha did not increase cyclic AMP. Levels of cyclic AMP were not elevated. We conclude that some of the elevation in cyclic AMP from AA was most likely from production of PGs since elevations in both were prevented by the inhibitors. However, the possibility remains that AA metabolites other than PGs also contributed to elevations in cyclic AMP. We also conclude that PGI2 most likely accounted for some of the cyclic AMP elevation from AA since PGI2 could be readily produced in amounts that elevate cyclic AMP. However, the possibility remains that PGE2, the less consistent cyclic AMP stimulators (l.e., PGF2 alpha and 6-keto-PGF1 alpha), TXA2 or TXB2, or PGs not measured in this study also contributed to the elevations in cyclic AMP from AA.     

Inhibition of growth of human endometrial adenocarcinoma cells in vitro treated with prostaglandin F2 alpha, E2, D2 and J2

Effects of prostaglandin F2 alpha, E2, D2 and J2 on the DNA and RNA contents of a human endometrial cancer cell lines (SNG and Ishikawa) were studied using flow cytometry. Cytotoxic effects of various prostaglandins on SNG and Ishikawa cell lines were examined and PG J2 and PG D2 were found most active. Among other prostaglandins PG E2 showed a comparable inhibitory activity to cellular growth but PG F2 alpha didn't. In SNG and Ishikawa cell lines after RNase treatment, PG J2, PG D2 and PG E2 caused a decrease of the S-phase and G2 + M-phase cell population in cell cycle. On the other hand, PG F2 alpha caused a increase of the S-phase cell population in cell cycle PG J2, PG D2 and PG E2 after DNase treatment caused a decrease of the relative RNA content in both of cell lines. On the other hand, PG F2 alpha caused a increase of the relative RNA content. It is a noteworthy that PG J2 and PG D2 were remarkably recognized delay of doubling time and decrease of survival fraction under the time and dose dependence. These effects occur not only by direct lethal influence of the prostaglandins, but also by substantially inhibit RNA and DNA synthesis with a delay of the cell cycle. These results might be suggested a role for prostaglandin J2 and D2 in the regulation of growth of endometrial adenocarcinoma cells.