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.

Isoflurane inhibits occludin expression via up-regulation of hypoxia-inducible factor 1α.

UNLABELLED: The blood-brain barrier (BBB) is a functional structure which regulates and restricts the transfer of circulating molecules and immune cells into the central nervous system. The barrier is formed by the presence of tight junctions (TJ) between the specialized brain endothelial cells. The volatile anesthetic isoflurane may affect the permeability of the BBB. Previous studies have proven that isoflurane alters hypoxia-inducible factor-1α (HIF-1α) expression, which may affect the TJ proteins; however, the mechanism of how TJ proteins are affected by isoflurane is still unclear. Primary human brain vascular endothelial cells (HBVEC) were exposed to isoflurane at various concentrations (0-2.5%) and different time periods (0-6 h). The cell viability, occludin expression, paracellular permeability, VEGF expression, TGF-ß3 expression and occludin protein endocytosis were quantified. Isoflurane treatment induced a time- and concentration-dependent decrease in occludin mRNA and protein levels in HBVEC. This effect was partially abrogated by silencing the HIF-1α expression. Isoflurane could activate HIF-1α, and the overexpression HIF-1α up-regulated the level of VEGF and TGF-ß3, VEGF decreased the expression of occludin and TGF-ß3 accelerated the endocytosis of occludin. RNA interference targeting HIF-1α reduced both VEGF and TGF-ß3 expression after isoflurane treatment. CONCLUSION: This study provides direct evidence in vitro that exposing isoflurane to HBVECs can trigger HIF-1α activation, leading to lower protein levels of occludin, and increased permeability of the BBB.

[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.

[The variation of Caspase3 activity in tanshinone induced NB4 cells apoptosis].

OBJECTIVE: To study the variation and role of Caspase3 activity in the process of Tanshinone (Tan II A) induced NB4 cells apoptosis. METHODS: NB4 cell apoptosis induced by Tan II A was demonstrated by cell morphology, DNA content analysis and DNA fragmentation assay. Caspase3 activity was determined by spectrofluorometry, and its inhibitory assay was performed using N-acetyl-Asp-Glu-Val-Asp-aldehyde(AC-DEVD-CHO). RESULTS: Tan II A could induce NB4 cell apoptosis accompanied with increase of caspase3 activity. The induction of NB4 cell apoptosis by use of Tan II A could be partially inhibited by AC-DEVD-CHO. CONCLUSION: The induction of NB4 cell apoptosis by Tan II A could be fulfilled by activating Caspase3.

Study on the relationship between NB4 cell apoptosis induced by tanshinone IIA and the cell mitochondrial transmembrane potential.

OBJECTIVE: To explore the relationship between NB4 cell apoptosis induced by tanshinone IIA (TanIIA) and the cell mitochondrial transmembrane potential (DeltaPsim). METHODS: NB4 cells were treated with TanIIA, As(2)O(3), TanIIA plus 1.0 micro g/ml CsA and As(2)O(3) plus 1.0 micro g/ml CsA, respectively. Morphological changes were observed under light microscope and transmission electron microscope. The percentages of sub-G(1) cells and DeltaPsim of cells doublely stained with PI and Rh123 were assayed by flow cytometry. RESULTS: The percentages of sub-G(1) cells after treatment with 1.0 micro g/ml and 2.0 micro g/ml TanIIA had no significant difference but was higher than that of 0.5 micro g/ml. After treatment with TanIIA, NB4 cells appeared the classical apoptotic morphology. The percentages of sub-G(1) cells were increased, while the DeltaPsim reduced (P < 0.01) and there was a linear correlation between them. The increment of sub-G(1) cell percentages and decrement of DeltaPsim induced by TanIIA were partly inhibited by CsA (P < 0.01). CONCLUSIONS: TanIIA can induce NB4 cells apoptosis through opening the mitochondrial permeability transition pore and reducing DeltaPSgr;m, and this effect could be inhibited by CsA.

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.

[Disseminated Penicillium marneffei infection associated with AIDS, report of a case].

OBJECTIVE: To explore the clinical and laboratory features of disseminated Penicillium marneffei infection in patients with AIDS. METHODS: The HIV antibody in serum was assayed by both enzyme immunoassay (EIA) and Western immunoblot (WIB) methods. Morphology of the pathogenic fungus in smear and biopsy specimens of bone marrow was observed. The fungus was isolated from the patient's skin lesion and inoculated into the abdominal cavities of 2 rats and 2 mice. Twenty days later the rats and mice were killed and their viscera were taken out. Blood from the organs were cultured in Sabourand glucose agar at 25 degrees C and 37 degrees C. The colonies were observed. The morphology of the fungus was observed by microscopy and scanning electron microscopy. RESULTS: The most common clinical manifestations of Penicilium marneffei infection were fever, weight loss, anemia, papular skin lesion, hepatosplenomegaly, and lymphadenectasis. Yeast-like cells were found in the culture at 37 degrees C or in tissues. The fungi outside the host cells were elongated, often curved, sausage-like and with clear central septi. When cultured at 25 degrees C, the fungus was mycelia-like and produced a characteristic red pigment, diffusing into the medium. CONCLUSION: Disseminated Penicilliosis marneffei is one of the most important opportunistic infections in patients with AIDS in Southeast Asia and the southern part of China. Since there is no specific clinical manifestation for Penicillium marneffei infection, it is often misdiagnosed. Definite diagnosis requires culture of the pathogenic fungus from clinical specimens. The fungus is thermally dimorphic, produces red pigment, and is sausage-form with clear central septum outside the host cell. Amphotericin B and itraconazole are effective in treating Penicilliosis marneffei.