Correction to: Comparison of analgesic effect of oxycodone and morphine on patients with moderate and advanced cancer pain: a meta-analysis.

After publication of this article [1], the authors noted that the corresponding email address is incorrect.

Comparison of analgesic effect of oxycodone and morphine on patients with moderate and advanced cancer pain: a meta-analysis.

BACKGROUND: Morphine and oxycodone are considered as wide-spreadly used opioids for moderate/severe cancer pain. However, debate exists about the evidence regarding their relative tolerability and underlying results. METHODS: A systematic search of online electronic databases, including PubMed, Embase, Cochrane library updated on October 2017 were conducted. The meta-analysis was performed including the studies that were designed as randomized controlled trials. RESULTS: In total, seven randomized clinical trials met our inclusion criteria. No statistical differences in analgesic effect between oxycodone and morphine were observed. Both the pooled analysis of API (MD =0.01, 95% CI -0.22 - 0.23; p = 0.96) and WPI (MD = - 0.05, 95% CI -0.21 - 0.30; p = 0.72) demonstrated clinical non-inferiority of the efficacy of morphine compared with oxycodone, respectively. Additionally, no significant difference in PRR response was observed in either oxycodone or morphine that were used in patients (MD =0.99, 95% CI -0.88 - 1.11; p = 0.87). With the pooled result of AEs indicating the comparable safety profiles between the 2 treatment groups, the meta-analysis on the nausea (OR = 1.20, 95% CI 0.90-1.59; p = 0.22), vomiting (OR = 1.33, 95% CI 0.75-2.38; p = 0.33), somnolence (OR = 1.35, 95% CI 0.95-1.93; p = 0.10), diarrhea (OR = 1.01, 95% CI 0.60-1,67; p = 0.98), and constipation (OR = 1.04, 95% CI 0.77-1.41; p = 0.79) was conducted, respectively. CONCLUSIONS: In the current study, no remarkable difference was identified either in analgesic efficacy or in tolerability of oxycodone and morphine as the first-line therapy for patients with moderate to severe cancer pain. Thus, no sufficient clinical evidence on the superior effects of oxycodone to morphine was provided in this experimental hypothesis.

[Effects of Tanshinone IIA on procoagulant activity of human ECV304 cell line induced by NB4 cells].

OBJECTIVE: To investigate the effects of Tanshinone IIA (Tan IIA) on procoagulant activity (PCA) of human ECV304 cells induced by acute promyelocytic leukemia cell line NB4 cells. METHODS: ECV304 monolayers were respectively incubated for different hours at 37 degrees C in the conditioned media (CM) of NB4 cells treated with 0.5 microg/mL Tan IIA(Tan IIA-NB4-CM), 0.3 microg/mL all-trans retinoidic acid (ATRA)(ATRA-NB4-CM), DMSO(DMSO-NB4-CM) or the RPMI1640 medium. ECV304 lysates were tested for PCA using the one-stage clotting assay as well as for tissue factor activity (TF: Act) using the chromogenic substrate assay; ECV304 cell monolayers were incubated for different hours at 37 degrees C in a medium system including 0.5 microg/mL Tan IIA and Tan IIA-NB4-CM, and the ECV304 cell lysates were tested for PCA in the same way as above. Also they were controlled by 0.3 microg/mL ATRA, DMSO or RPMI1640 medium. RESULTS: (1) The conditioned mediums from 0. 5 microg/mL Tan IIA that treated NB4 cells for 24, 72 and 120 hours respectively could elevate PCA of ECV cells, and this capability developed with the time of reaction. ATRA did the same as Tan IIA (P > 0.05). (2) 0.5 microg/mL Tan IIA down-regulated the PCA of ECV304 cells induced by Tan IIA-NB4-CM, and the inhibitory effects increased with time, reaching the highest at 120 hours. (3) Tan IIA120 h-NB4-CM up-regulated TF:Act of ECV304 cells, and the effect increased with time. (4) 0. 5 microg/mL Tan IIA down-regulated PCA and TF: Act of ECV304 cells induced by Tan IIA-NB4-CM, and the inhibitory effect increased with time; simultaneously, the test was controlled with 0.3 microg/mL ATRA, the effects on PCA and TF: Act were not significantly different (P > 0.05). CONCLUSION: Tan IIA-NB4-CM can increase the levels of PCA and TF: Act of ECV304 cells through some unidentified factor; however, Tan IIA can obviously decrease the PCA and TF: Act levels of ECV304 cells induced by Tan IIA-NB4-CM.

[Clinical application of linkage analysis for vWD family].

OBJECTIVE: To explore the application of amplified fragment length polymorphism (amp-FLP) of short tandem repeat (STR) within intron 40 of vWF gene in the gene diagnosis and genetic consulting service for von Willebrand disease (vWD). METHODS: We isolated DNA from the blood of members in 8 families with vWD, measured the relative parameters of vWD simultaneously; and amplified the fragment length polymorphism of two loci (nt1890-1990 and nt2215-2380) within intron 40 of vWF gene using PCR. The RCR products were analyzed by means of polyacrylamide gel electrophoresis (PAGE) and silver staining. RESULTS: Five types of amp-FLP were identified on nt1890-1990 and nt2215-2380 respectively. Haplotypes could be identified to link with defective vWF gene in these families. CONCLUSION: Combination of PCR and PAGE is a fast and practical method for carrying out family analysis of inherited disease; nt1980-1990 and nt2215-2380 of vWF gene are two ideal genetic labels in linkage analysis and hereditary consultation of vWD family.

[Application of collagen-binding assay for von Willebrand disease].

OBJECTIVE: To explore the application of collagen-binding assay for von Willebrand disease (vWD). METHODS: We investigated the sensitivity and reproducibility of collagen-binding assays (CBA) of vWF using the enzyme-linked immunosorbent assay (ELISA) technique and compared CBA with 3 other assays for their ability to detect vWD. RESULTS: It was found that the vWF: CBA level of plasma from patients with different types of vWD is lower than that from healthy donors, hemophilia and other bleeding disorders (P < 0.001). In general, the four assays have the capability to identify vWD from normal and other bleeding disorders, and can be used for diagnosing vWD. The concordance rates of the four assays on vWD are vWF: Ag 85.7%, vWF: Rcof 76.2%, RIPA 80.9%, vWF: CBA 95.2% respectively. CONCLUSION: vWF: CBA measured by ELISA is highly sensitive, specific and reproducible, and easy to operate. The measurement of the functional activity of vWF by vWF: Rcof or RIPA can be replaced by the more reliable vWF: CBA.

Comparison of Pgp- and MRP-mediated multidrug resistance in leukemia cell lines.

Drug resistance is a major cause of the failure of anticancer chemotherapy. Multidrug resistance is often caused by overexpression of the P-glycoprotein (Pgp) or the multidrug resistance-related protein (MRP). In the present study, we compared daunorubicin (DNR) accumulation, subcellular distribution, and the effect of modulators on drug accumulation and subcellular distribution in the Pgp-expressing K562 cell line and the MRP-expressing HL60 cell line using reverse-transcriptase polymerase chain reaction, MTT (3-[4, 5-dimethylthiazol-z-yl]-2,5-diphenyltetrazolium bromide) drug cytotoxicity assay, fluorocytometry, and confocal laser scanning microscopy. The 2 resistant cell lines exhibit similar levels of resistance to DNR and decreased drug accumulation. Altered drug subcellular distribution in the resistant cell lines compared to that in the sensitive cell lines was shown and, moreover, differences in drug distributions between the 2 resistant cell lines were found. DNR fluorescence in the resistant HL60 cell line was distributed into punctate regions in the cytoplasm; the nucleus and other cytoplasm were almost negative. In contrast, the resistant K562 cells showed a bright fluorescent signal located in the peripheral cytoplasm and perinuclear region; the nucleus and other cytoplasmic regions showed no signal. Use of the modulator verapamil increased drug accumulation and restored the altered subcellular distribution of the drug in the 2 resistant cell lines. The Golgi apparatus inhibitor brefeldin A had similar action in the resistant HL60 line but had little effect in the resistant K562 line. Therefore, our study suggested that there were differences between the 2 resistant cell lines in the compartments sequestering DNR.

[Study on Growth and Maturation of Megakaryocyte Progenitors In Vitro in Patients with Chronic Idiopathic Thrombocytopenic Purpura]

To investigate the growth and maturation of megakaryocyte progenitors in patients with chronic idiopathic thrombocytopenic purpura (CITP), plasma clot culture and GPIIIa monoclonal antibody and ABC immuno- histochemical kit were used to assay CFU-Meg and BFU-Meg, and the area and diameter of GPIIIa(+) cells were determined by image analyzer in 33 CITP cases. It was found that CFU-Meg and BFU-Meg were 39.27 +/- 21.44 and 5.62 +/- 3.93 per 2 x 10(5) MNC, respectively, in CITP patients, there were no significant differences with those in control group. While the area of GPIIIa(+) cells was (134.90 +/- 6.08) micro m(2) and diameter was (12.89 +/- 3.66) micro m, those were lower than those in control group. In patients with normal number of megakaryocytes on marrow smears, CFU-Meg and BFU-Meg were 19.43 +/- 7.28 and 4.67 +/- 1.53, respectively, the values were lower as compared to control group. The positive correlation was showed between the total megakaryocytic colonies and the number of megakaryocytes on marrow smears, r = 0.6503, and there was no correlation with blood platelet counts and course of disease. The results suggest that there was a maturation disturbance of megakaryocyte progenitor in CITP patients and lower proliferative potential in patients with normal megakaryocyte counts on marrow smears.