骨碱性磷酸酶与碱性磷酸酶在佝偻病诊断中的比较

目的 了解定量骨碱性磷酸酶( BAP-E)、定性骨碱性磷酸酶(BAP-CIT)、血清碱性磷酸酶(AP)三个指标在佝偻病诊断中的意义。方法 检测55例佝偻病患儿、26例对照婴幼儿血清AP、BAP-E、BAP-CIT,BAP-E采用ELISA法,BAP-CIT用全血干化学和免疫浓缩技术。结果 佝偻病患儿的AP和BAP-E较...     

Measurement of bone alkaline phosphatase and relative study with osteosarcoma

The objective of this paper is to explore the value of bone alkaline phosphatase (BALP) for diagnosing osteosarcoma, evaluating the effect of the chemotherapy, judging the prognosis and supervising the relapse and metastasis. The immunoassay was used to check the BALP of the blood serum that was from 42 primary osteosarcoma patients. Alkaline phosphatase (ALP) in blood serum was checked with auto biochemistry equipment. The biopsy tissue and the lesion resected in operation were treated with pathology and histological response was counted. The patients were followed up from five months to 49 months with an average of 24.3 months. Eighteen cases relapsed and transferred, among which, 16 of them were dead, and others were survival to the end of the follow-up. BALP was more sensitive than ALP in diagnosing osteosarcoma (P = 0.015). Fifteen cases decreased to normal value in ALP after preoperative chemotherapy, and 34 cases decreased in BALP. Both ALP and BALP in all cases decreased to normal value in post-operative. There was significant difference in positive correlation between the decrease of BALP and the increase of histological response (P = 0.001, r = 0.642). In the follow-up, there was significant difference in BALP between the group of relapse and transfer and the group of free disease survival (P = 0.000). As a check marker in blood serum, BALP, reflecting the process of ossification, has a higher sensitivity than ALP. It has applied value in the diagnosis of osteosarcoma, reflection of the effect of chemotherapy and forecast the prognosis. Translated from Journal of Shandong University (Health Sciences), 2006, 44(6): 610–613 [译自: 山东大学学报 (医学版)]     

血清总碱性磷酸酶和骨特异性碱性磷酸酶与非小细胞肺癌骨转移的相关性

目的探讨血清总碱性磷酸酶（tALP）和骨特异性碱性磷酸酶（bALP）与非小细胞肺癌（NSCLC）骨转移的相关性。方法分析湖北省新华医院2009年9月至2011年9月收治的30例NSCLC骨转移患者和30例NSCLC无骨转移患者血清标本,分别采用酶免疫荧光法和电化学发光法检测血清tALP和bALP水平。结果NSCLC骨转移组血清tALP和bALP均高于无骨转移组[（158±13）U／L比（69±12）U／L,（34±7）μg／L比（12±4）μg／L]（P〈0。05）。血清tALP水平升高判断NSCLC的灵敏度为63．3％,特异度为70．0％;血清bALP升高判断骨转移的灵敏度为86．7％,特异度为83．3％。结论血清tALP和bALP水平对NSCLC骨转移的诊断具有重要的参考价值。     

Pregnane X receptor-mediated induction of Cyp3a by black cohosh

Black cohosh (BC) has been widely applied for the treatment of menopausal symptoms. However, increasing concerns about herb–drug interactions demand the need for studies on the influence of BC on cytochrome 450. Cyp3a11 in liver was induced by 7-fold in wild-type mice treated with 500?mg/kg black cohosh for 28 days compared with the control group as assessed by quantitative real-time PCR; no difference was found in small intestine and kidney, suggesting that up-regulation of Cyp3a11 by black cohosh was liver-specific. Western blot, activity assays, and pharmacokinetic analyses established dose- and time-dependent induction of Cyp3a11. To determine the mechanism of Cyp3a11 induction, including the role of pregnane X receptor (PXR) in vivo and in vitro, respectively, in Pxr-null, PXR-humanized, and double transgenic CYP3A4/hPXR mice, cell-based luciferase assays were employed revealing that mouse PXR played a direct role in the induction of Cyp3a11; human PXR was not activated by black cohosh. Overall, these findings demonstrate that induction of Cyp3a11 is liver-specific and involved only mouse PXR, not the human counterpart. Thus, the incidence of herb–drug interaction in patients administered black cohosh may not be mediated by human PXR and CYP3A4.     

Distribution and induction of CYP3A1 and CYP3A2 in rat liver and extrahepatic tissues

Previously, we have shown that highly specific antibodies against cytochrome P450 enzymes can be produced by targeting a 5-amino acid sequence at the C-terminus. Although rat CYP3A1 and CYP3A2 share 89% amino acid sequence similarity, they differ by 3 out of 5 of their C-terminal residues. In an effort to produce antibodies specific to each form, rabbits were immunised with the peptides IITGS and VINGA, corresponding to the C-termini of CYP3A1 and CYP3A2, respectively. Both antibodies bound strongly to hepatic microsomal fraction from rats treated with pregnenolone 16α-carbonitrile (PCN) in enzyme-linked immunosorbent assay. Binding of the anti-IITGS antibody was strongly inhibited by incubation with IITGS, but VINGA was 60 times less effective. Conversely, binding of the anti-VINGA antibody was inhibited by VINGA 100 times more effectively than IITGS. Similar inhibition of antibody binding was also found using immunoblotting. Immujnoadsorption using the anti-IITGS antibody yielded a single protein from solubilised hepatic microsomal fraction from PCN-treated rats, which was recognised only by the anti-IITGS antibody. Both antibodies bound to single proteins in the liver which were increased following treatment with PCN, but only the anti-IITGS antibody recognised protein in the lung, small intestine, and kidney of untreated and PCN-treated rats. Also, the binding of the two antibodies to hepatic and extrahepatic microsomal fractions from uninduced and induced rats showed differences in the expression of proteins recognised by the two antibodies, providing further evidence of antibody specificity. Thus, the binding of anti-IITGS and anti-VINGA antibodies is mutually exclusive and consistent with specific binding to their target antigens, CYP3A1 and CYP3A2, respectively. Immunocytochemistry was used to determine the distribution of CYP3A1 and CYP3A2. In the liver of untreated animals, both CYP3A1 and CYP3A2 were found to be expressed in the centrilobular region. However, some CYP3A1 immunoreactivity was also detected in many, but not all, hepatocytes throughout the lobule. However, following treatment of rats with PCN, both CYP3A1 and CYP3A2 were found to be strongly expressed in hepatocytes throughout the lobule, although CYP3A2 showed greater expression in the centrilobular region. PCN treatment was also found to result in induction of CYP3A1 in specific regions of the small intestine, lung, and kidney.     

不同年龄儿童血清骨碱性磷酸酶的水平分布及其临床应用观察

目的 了解各年龄段(0～ 12岁)儿童血清中骨源性碱性磷酸酶(Bone alkaline phosphatase,BALP)的水平,并观察其在维生素D缺乏性佝偻病诊断中的应用,为合理防治儿童维生素D缺乏性佝偻病提供科学依据.方法 回顾性分析2013年至2014年6月在我院儿保科就诊的0～ 12岁儿童的资料,选取2825例健康体检儿童作为研究对象,2084例确诊佝偻病或有临床表现儿童作为病例组,血清中BALP水平采用酶联免疫法定量检测.结果 健康体检组0～1岁婴幼儿血清BALP水平较高[(108.27±31.93)μg/L],随着年龄的增长,BALP水平呈递减趋势,至9～ 12岁,儿童血清BALP水平为(86.82±29.74)μg/L,组间差异有统计学意义(P＜0.05);健康男、女儿童血清BALP水平分别为(96.4±30.6)μ g/L、(98.2±32.0) μg/L,病例组男、女儿童血清BALP水平分别为(111.7±38.3)μg/L、(114.2±40.8).μg/L,不同性别儿童血清BALP水平差异无统计学意义(P＞0.05),但病例组儿童血清BALP水平高于健康儿童,差异有统计学意义(P＜0.05);各年龄段患病儿童血清BALP水平都高于健康儿童,差异有统计学意义(P＜0.05).结论 儿童血清骨碱性磷酸酶的浓度变化与年龄有关,制定不同年龄段儿童血清骨碱性磷酸酶的参考范围,可为临床诊断儿童维生素D缺乏性佝偻病提供更可靠的依据.     

金枪鱼骨胶原蛋白肽螯合钙制备工艺及对MG-63细胞碱性磷酸酶分泌的影响

目的 为获得一种能够增加人成骨细胞碱性磷酸酶生成量的金枪鱼骨胶原蛋白肽螯合钙(collagen peptide from tuna bone chelated calcium, TCP-Ca)的工艺方法。方法 本文利用正交实验优化蛋白酶酶解法制备金枪鱼骨胶原蛋白肽的工艺,利用正交实验优化金枪鱼骨胶原蛋白肽和柠檬酸钙进行螯合反应的工艺,然后利用傅里叶变换红外光谱对TCP-Ca进行定性分析,同时检测TCP-Ca对MG-63细胞碱性磷酸酶生成量的影响。结果 金枪鱼骨胶原蛋白肽制备的最佳工艺为pH 9.0、酶解时间180 min、加酶量5000 U/g、酶解温度45 ℃;TCP-Ca制备的最佳工艺为温度35 ℃、pH 7.5、肽钙质量比6:1、时间40 min;金枪鱼骨胶原蛋白肽的氨基和羟基均参预了钙螯合反应;TCP-Ca比金枪鱼骨胶原蛋白肽更有利于增加MG-63细胞分泌碱性磷酸酶。结论 本文优化了TCP-Ca的制备工艺,发现其具有增加成骨细胞分泌碱性磷酸酶的生物活性。     

Significance of elevated urinary human intestinal alkaline phosphatase in Japanese people exposed to environmental cadmium

Urinary human intestinal alkaline phosphatase (IAP),β₂-microglobulin (β₂-MG) and N-acetyl-β-d-glucosaminidase (NAG) were analyzed in 40 Japanese environmental-cadmium (Cd)-exposed and 40 non-exposed subjects to evaluate early biological markers for Cd-induced renal damage. All urinary indicators were significantly higher in the Cdexposed subjects than non-exposed subjects. A fourth-order function was fitted for the relationship between β₂-MG and IAP or NAG. The β₂-MG concentration corresponding to the inflexion point for IAP was smaller than that for NAG. This result may support the contention that the cells containing IAP are damaged earlier than those containing NAG, and that IAP is a useful marker for detecting renal tubular dysfunction in people moderately exposed to Cd. However, in the stage of severe renal damage, the combination of IAP and β₂-MG is considered to be more useful.     

骨碱性磷酸酶在佝偻病早期诊断中的应用

目的分析研究骨碱性磷酸酶(BALP)测定对维生素D缺乏性佝偻病早期诊断的临床意义。方法收集体检诊断为维生素D缺乏性佝偻病的0～3岁儿童520例,采用骨碱性磷酸酶(BALP)试剂盒进行检测,对比分析其中部分病例的血清钙磷及碱性磷酸酶含量。结果骨碱性磷酸酶早期诊断佝偻病阳性率达90.8%,与血清钙磷、ALP检测差异有统计学意义(P<0.01)。结论 BALP检测简便、快捷、特异性高、结果可靠、可减少漏诊率,对佝偻病早期诊断具有重要的指导价值,基层医院应推广。     

骨源性碱性磷酸酶与小儿佝偻病的早期诊断

目的：探讨骨源性碱性磷酸酶（BAP）测定对小儿佝偻病的早期诊断价值。方法：对2008年10月～2009年4月儿童保健门诊体检的487例3个月～2岁小儿进行末梢血小儿骨源性碱性磷酸酶（NBAP）活性检测,并按卫生部颁发的婴幼儿佝偻病预防方案对487例小儿进行佝偻病临床筛查。结果：487例3个月～2岁小儿中NBAP阳性率为34．91％,而临床筛查佝偻病患儿为65例,阳性率为13．35％。结论：NBAP检测方法简单,灵敏度高,对小儿佝偻病早期诊断、预防具有较好的临床意义。     

Effects of rifampicin on porphyrin metabolism in healthy volunteers

Pregnane X receptor (PXR) is known to stimulate haem synthesis, but detailed knowledge on the effects of PXR activation on porphyrin metabolism in humans is lacking. We utilized a randomized, crossover, open (blinded laboratory) and placebo-controlled trial with 600-mg rifampicin or placebo dosed for a week to investigate the effects of PXR activation on erythrocyte, plasma, faecal and urine porphyrins. Sixteen healthy volunteers participated on the trial, but the number of volunteers for blood and urine porphyrin analyses was 15 while the number of samples for faecal analyses was 14. Rifampicin increased urine pentaporphyrin concentration 3.7-fold (mean 1.80 ± 0.6 vs. 6.73 ± 4.4 nmol/L, p = 0.003) in comparison with placebo. Urine coproporphyrin I increased 23% (p = 0.036). Faecal protoporphyrin IX decreased (mean 31.6 ± 23.5 vs. 19.2 ± 27.8 nmol/g, p = 0.023). The number of blood erythrocytes was slightly elevated, and plasma bilirubin, catabolic metabolite of haem, was decreased. In conclusion, rifampicin dosing elevated the excretion of certain urinary porphyrin metabolites and decreased faecal protoporphyrin IX excretion. As urine pentaporphyrin and coproporphyrin I are not precursors in haem biosynthesis, increased excretion may serve as a hepatoprotective shunt when haem synthesis or porphyrin levels are increased.     

The effect of atorvastatin treatment on serum oxysterol concentrations and cytochrome P450 3A4 activity

Aims

Atorvastatin is known to both inhibit and induce the cytochrome P450 3A4 (CYP3A4) enzyme in vitro. Some clinical studies indicate that atorvastatin inhibits CYP3A4 but there are no well-controlled longer term studies that could evaluate the inducing effect of atorvastatin. We aimed to determine if atorvastatin induces or inhibits CYP3A4 activity as measured by the 4β-hydroxycholesterol to cholesterol ratio (4βHC : C).

Methods

In this randomized, double-blind, placebo-controlled 6 month study we evaluated the effects of atorvastatin 20 mg day⁻¹ (n = 15) and placebo (n = 14) on oxysterol concentrations and determined if atorvastatin induces or inhibits CYP3A4 activity as assessed by the 4βHC : C index. The respective 25-hydroxycholesterol and 5α,6α-epoxycholesterol ratios were used as negative controls.

Results

Treatment with atorvastatin decreased 4βHC and 5α,6α-epoxycholesterol concentrations by 40% and 23%, respectively. The mean 4βHC : C ratio decreased by 13% (0.214 ± 0.04 to 0.182 ± 0.04, P = 0.024, 95% confidence interval (CI) of the difference –0.0595, –0.00483) in the atorvastatin group while no significant change occurred in the placebo group. The difference in change of 4βHC : C between study arms was statistically significant (atorvastatin –0.032, placebo 0.0055, P = 0.020, 95% CI of the difference –0.069, –0.0067). The ratios of 25-hydroxycholesterol and 5α,6α-epoxycholesterol to cholesterol did not change.

Conclusions

The results establish atorvastatin as an inhibitor of CYP3A4 activity. Furthermore, 4βHC : C is a useful index of CYP3A4 activity, including the conditions with altered cholesterol concentrations.     

Comparison of the hepatic and thyroid gland effects of sodium phenobarbital and pregnenolone-16α-carbonitrile in wild-type and constitutive androstane receptor (CAR)/pregnane X receptor (PXR) knockout rats

1. The hepatic and thyroid gland effects of the constitutive androstane receptor (CAR) activator sodium phenobarbital (NaPB) and the pregnane X receptor (PXR) activator pregnenolone-16α-carbonitrile (PCN) were examined in male Sprague-Dawley wild-type (WT) and knockout (KO) rats lacking both hepatic CAR and PXR receptors (CAR KO/PXR KO rats).

2. The treatment of WT rats for 7?d with 500?ppm NaPB in the diet and 100?mg/kg/d PCN by gavage resulted in increased relative liver weight, hepatocyte hypertrophy, increased hepatocyte replicative DNA synthesis (RDS) and induction of cytochrome P450 CYP2B and CYP3A subfamily enzymes. NaPB and PCN also induced thyroid gland follicular cell RDS and hepatic microsomal UDP-glucuronosyltransferase activity towards thyroxine as substrate. These effects were not observed in the liver and thyroid gland of CAR KO/PXR KO rats.

3. Male C57BL/6?J (WT) and CAR KO/PXR KO mice were given 1000?ppm NaPB in the diet for 7?d. In WT, but not in CAR KO/PXR KO, mice NaPB treatment resulted in liver hypertrophy and induction of hepatocyte RDS and Cyp2b enzymes.

4. These results suggest that the CAR KO/PXR KO rat and mouse models are useful experimental models for mode of action studies with rodent CAR activators.

     

Pharmacological antagonism of α-adrenergic agonist induced increases in canine intraurethral pressure in vivo

Treatment with α₁ antagonists represents a pharmacological alternative to surgery for the treatment of urinary obstruction associated with benign prostatic hyperplasia (BPH). A minimally invasive method to measure elevation of prostatic urethral tone through a urethral catheter was used to study the effects of α-adrenoceptor agonists and antagonists on canine intraurethral pressure (IUP). α₁-adrenoceptor agonists, but not α₂ agonists, elicited elevations in IUP. The contractile response was primarily the result of prostatic smooth muscle contraction, since it was of smaller magnitude in female dogs or in male dogs outside of the prostatic urethra. The contractile responses to epinephrine obtained in the absence of antagonist on the same or different test dates were highly reproducible in dogs greater than 2 years of age. The increase in IUP caused by epinephrine was specifically antagonized by α₁-adrenoceptor antagonists, in direct proportion to their potency in isolated canine prostatic strips in vitro and in proportion to their affinity at receptors determined in radioligand binding assays in vitro. These data confirm the role of α₁-adrenoceptors in canine prostatic smooth muscle contraction and this relatively non-invasive in vivo model will allow the study of novel compounds for their effects on canine prostatic tone. © 1995 Wiley-Liss, Inc.     

Identification of Genes Controlled by the Pregnane X Receptor by Microarray Analysis of mRNAs from Pregnenolone 16{alpha}-Carbonitrile-Treated Rats

Mammalian liver contains a pregnane X receptor (PXR, NR1I2),which binds drugs and other xenobiotics, and stimulates (orsuppresses) expression of numerous genes involved in the metabolicelimination of foreign compounds and some toxic endogenous substances.In the present study, we used microarray analysis to identifygenes whose expression in rat liver was significantly alteredby pregnenolone 16-carbonitrile (PCN) treatment. PCN is a syntheticsteroid that induces cytochrome P4503A expression and is hepatoprotectiveby increasing resistance to subsequent stressful insults. Significantinduction was seen for 138 genes while expression of 82 geneswas significantly repressed. We found induction of genes knownto be induced by PCN, such as enzymes involved in drug metabolismand transport. In addition, many genes were differentially expressedwhose functions concerned intracellular metabolism, transportof essential small molecules, cell cycle, and redox balance.Our results support the idea that the domain of PXR-controlledgene networks may be even more extensive than currently thoughtand may extend to functions apart from xenobiotic metabolism.     

Effect of prototypical inducers on ligand activated nuclear receptor regulated drug disposition genes in rodent hepatic and intestinal cells

Aim:

The aim of this study was to investigate the impact on expression of mRNA and protein by paradigm inducers/activators of nuclear receptors and their target genes in rat hepatic and intestinal cells. Furthermore, assess marked inter laboratory conflicting reports regarding species and tissue differences in expression to gain further insight and rationalise previously observed species differences between rodent and human based systems.

Methods:

Quantitative real time-polymerase chain reaction (QRT-PCR) and immunoblots were used to assess messenger RNA (mRNA) and protein expression for CYP2B2, CYP3A1, CYP3A2, CYP3A9, ABCB1a, ABCB1b, ABCC1, ABCC2, pregnane X receptor (PXR), farnesoid X receptor (FXR) and constituitive androstane receptor (CAR) in rat hepatoma cell line H411E, intestinal cells, Iec-6, and rat primary hepatocytes, in response to exposure for 18 h with prototypical inducers.

Results:

Dexamethasone (DEX) and pregnenolone 16α carbonitrile (PCN) significantly induced PXR, CYP3A9, ABCB1a and ABCB1b. However, when co-incubated, DEX appeared to restrict PCN-dependent induction. Chenodeoxycholic acid (CDCA) was the only ligand to induce FXR in all three cell types. Despite previously reported species differences between PCN and rifampicin (RIF), both compounds exhibited a similar profile of induction.

Conclusion:

Data presented herein may explain some of the discrepancies previously reported with respect to species differences from different laboratories and have important implications for study design.     

Leptin induces hypertrophy through activating the peroxisome proliferator‐activated receptor α pathway in cultured neonatal rat cardiomyocytes

1. Our previous study has shown that leptin induces cardiomyocyte hypertrophy; however, the mechanisms are poorly understood. Recent studies have shown that peroxisome proliferator‐activated receptor α (PPARα) activation might be responsible for pathological remodeling and severe cardiomyopathy. Leptin, as an endogenous activator of PPARα, regulates energy metabolism through activating PPARα in many cells. Therefore, we hypothesized that leptin induces cardiomyocyte hypertrophy through activating the cardiac PPARα pathway. 2. Cultured neonatal rat cardiomyocytes were used to evaluate the effects of PPARα on hypertrophy. The selective PPARα antagonist GW6471 concentration‐dependently decreased atrial natriuretic factor mRNA expression by 23%, 36%, 44% and 59%, and significantly decreased total RNA levels, protein synthesis and cell surface areas, all of which were elevated by 72 h of leptin treatment. The augmentation of reactive oxygen species levels in leptin treated cardiomyocytes was reversed by 0.1–10 μmol/L GW6471 (40%, 52% and 58%). After 24 h of treatment, leptin concentration‐dependently enhanced mRNA expression by 7%, 93%, 100% and 256%, and protein expression by 31.2%, 64.2%, 143% and 199%, and the activity of PPARα. Meanwhile, cardiomycytes receiving 72 h of treatment with the PPARα agonist, fenofibrate, concentration‐dependently increased total RNA levels, atrial natriuretic factor mRNA expression, protein synthesis and cell surface area. Treatment of fenofibrate for 4 h also elevated oxygen species levels in a concentration‐dependent manner. 3. In conclusion, these findings show that leptin induces hypertrophy through the activation of the PPARα pathway in cultured neonatal rat cardiomyocytes.     

Bisphenol a induces steatosis in HepaRG cells using a model of perinatal exposure

Human exposure to bisphenol A (BPA) could favor obesity and related metabolic disorders such as hepatic steatosis. Investigations in rodents have shown that these deleterious effects are observed not only when BPA is administered during the adult life but also with different protocols of perinatal exposure. Whether perinatal BPA exposure could pose a risk in human is currently unknown, and thus appropriate in vitro models could be important to tackle this major issue. Accordingly, we determined whether long‐term BPA treatment could induce steatosis in human HepaRG cells by using a protocol mimicking perinatal exposure. To this end, the kinetics of expression of seven proteins differentially expressed during liver development was determined during a 4‐week period of cell culture required for proliferation and differentiation. By analogy with data reported in rodents and humans, our results indicated that the period of cell culture around day 15 and day 18 after seeding could be considered as the “natal” period. Consequently, HepaRG cells were treated for 3 weeks with BPA (from 0.2 to 2000 nM), with a treatment starting during the proliferating period. BPA was able to induce steatosis with a nonmonotonic dose response profile, with significant effects on neutral lipids and triglycerides observed for the 2 nM concentration. However, the expression of many enzymes involved in lipid and carbohydrate homeostasis was unchanged in exposed HepaRG cells. The expression of other potential BPA targets and enzymes involved in BPA biotransformation was also determined, giving answers as well as new questions regarding the mechanisms of action of BPA. Hence, HepaRG cells provide a valuable model that can prove useful for the toxicological assessment of endocrine disruptors on hepatic metabolisms, in particular in the developing liver. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1024–1036, 2017.     

术前血清白蛋白-碱性磷酸酶比值在胃癌预后评估中的价值

目的探讨术前血清白蛋白-碱性磷酸酶比值(AAPR)在胃癌预后评估中的临床价值。方法选取2016年3月至2019年12月在徐州医科大学附属医院接受根治性手术切除治疗的胃腺癌病人396例。通过5年时依性ROC曲线分析最佳截断值,将AAPR分为升高组和降低组,比较两组临床病理特征的关系;通过Kaplan Meier法和Log-rank检验进行单因素分析,将差异有统计学意义的因素引入Cox回归模型,从而得出影响胃癌病人生存预后的独立危险因素;通过5年时依性ROC曲线比较AAPR、血小板与淋巴细胞之比(PLR)、中性白细胞与淋巴细胞比率(NLR)以及联合诊断评估胃癌预后的价值。结果AAPR的截断值为0.586。AAPR与胃癌病人的肿瘤浸润程度、淋巴结转移、TNM分期、神经或脉管侵犯、肿瘤长径、年龄、白蛋白、碱性磷酸酶、中性粒细胞、淋巴细胞、血小板、NLR、PLR 均有关(χ2=19.68、9.96、15.03、12.76、18.81、11.06、13.91、137.02、7.03、10.81、8.90、16.87、5.21,均P<0.05)。多因素分析结果显示术后有无化疗、手术方式、TNM分期、肿瘤浸润程度、PLR、AAPR均是影响胃癌病人预后生存的独立危险因素(均P<0.05)。AAPR≥0.586的病人5年累积生存率高于AAPR<0.586的病人(86.7%比41.7%),差异有统计学意义(χ2=47.57,P<0.05),AAPR预测胃癌的AUC值为0.637,PLR预测胃癌的AUC值为0.584,NLR预测胃癌的AUC值为0.554,AAPR预测胃癌的AUC值高于PLR与NLR,同时将AAPR、PLR、NLR综合成为联合指标时,联合诊断的AUC值为0.645。结论术前AAPR有助于预测胃癌病人预后,且AAPR对胃癌生存结果的评估价值高于PLR与NLR。     

葛根素对UMR106细胞增殖及碱性磷酸酶活性的影响

目的:研究葛根素对UMR106细胞增殖及碱性磷酸酶活性的影响.方法:UMR106细胞培养于α-MEM培养基中,葛根素处理后光学显微镜下观察其形态学变化,绘制细胞生长曲线,并采用对硝基苯磷酸钠基质动力学法测定UMR106细胞内、外碱性磷酸酶活性.结果:UMR106细胞经葛根素和10-8mol·L-1雌二醇处理后d1,d2和d3,与空白对照组相比,增殖速度均加快,d2差异最显著.与对照组相比,10-8,10-7,10-6mol·L-1葛根素组的增殖率分别为9.3%,23.3%和40.9%,10-8mol·L-1雌二醇组增殖率为49.7%.与对照组相比,细胞经10-6mol·L-1葛根素处理后1 d和2 d时,细胞内ALP活性显著增加(P＜0.01);细胞经10-6mol·L-1葛根素处理1 d后,细胞外ALP活性显著增加(P＜0.05).结论:葛根素可以促进成骨样细胞UMR106细胞合成和分泌ALP,提示其具有促进成骨细胞增殖和分化的作用.