Association between tobacco exposure and bladder cancer recurrence: A systematic review and meta-analysis.

BACKGROUND: However, the connection between smoking and the prognosis of patients with bladder cancer remains unclear. AIM: To determine whether smoking is linked to the recurrence and progression of bladder cancer. METHODS: As of July 20, 2022, relevant English-language research was identified by searching PubMed, the Web of Science, and the Cochrane Library. We pooled the available data from the included studies using a random effects model. Subgroup analysis and sensitivity analysis were also conducted. RESULTS: A total of 12 studies were included in this meta-analysis. The combined analysis revealed that tobacco exposure was associated with a significantly greater recurrence rate than nonsmoking status [odd ratios (OR) = 1.76, 95%CI: 1.84-2.93], and the progression of bladder cancer was significantly greater in smokers than in nonsmokers (OR = 1.21, 95%CI: 1.02-1.44). Stratified analysis further revealed that current smokers were more likely to experience relapse than never-smokers were (OR = 1.85, 95%CI: 1.11-3.07). Former smokers also had a greater risk of relapse than did never-smokers (OR = 1.73, 95%CI: 1.09-2.73). Subgroup analysis indicated that non-Caucasians may be more susceptible to bladder cancer recurrence than Caucasians are (OR = 2.13, 95%CI: 1.74-2.61). CONCLUSION: This meta-analysis revealed that tobacco exposure may be a significant risk factor for both the recurrence and progression of bladder cancer.

NPM promotes hepatotoxin-induced fibrosis by inhibiting ROS-induced apoptosis of hepatic stellate cells and upregulating lncMIAT-induced TGF-ß2.

Liver fibrosis is caused by a variety of chronic liver injuries and has caused significant morbidity and mortality in the world with increasing tendency. Elucidation of the molecular mechanism of liver fibrosis is the basis for intervention of this pathological process and drug development. Nucleophosmin (NPM) is a widely expressed nucleolar phosphorylated protein, which is particularly important for cell proliferation, differentiation and survival. The biological role of NPM in liver fibrosis remains unknown. Here we show that NPM promotes liver fibrosis through multiple pathways. Our study found that NPM was up-regulated in cirrhosis tissues and activated in hepatic stellate cells (HSCs). NPM inhibition reduced liver fibrosis markers expression in HSCs and inhibited the HSCs proliferation and migration. In mice model, NPM knockdown in HSCs or application of specific NPM inhibitor can remarkably attenuate hepatic fibrosis. Mechanistic analysis showed that NPM promotes hepatic fibrosis by inhibiting HSCs apoptosis through Akt/ROS pathway and by upregulating TGF-ß2 through Akt-induced lncMIAT. LncMIAT up-regulated TGF-ß2 mRNA by competitively sponging miR-16-5p. In response to liver injury, hepatocytes, Kupffer cells and HSCs up-regulated NPM to increase TGF-ß2 secretion to activate HSCs in a paracrine or autocrine manner, leading to increased liver fibrosis. Our study demonstrated that NPM regulated hepatotoxin-induced fibrosis through Akt/ROS-induced apoptosis of HSCs and via the Akt/lncMIAT-up-regulated TGF-ß2. Inhibition of NPM or application of NPM inhibitor CIGB300 remarkably attenuated liver fibrosis. NPM serves a potential new drug target for liver fibrosis.

Colitis and colorectal tumors should be further explored and differentiated.

The original article by Yuichi et al explored whether the Japan Narrow-Band Imaging Expert Team classification and the pit pattern classification are suitable for diagnosing neoplastic lesions in patients with ulcerative colitis. In this letter, we offer some other perspectives. Risk factors for colorectal tumors include type 2 diabetes. Among genetic factors, the deletion or mutation of some genes, such as the p53 gene, can lead to colorectal tumors. There are significant gender differences in the occurrence and development of colorectal tumors. Some non-genetic factors, such as smoking, are also associated with the development of colorectal tumors. These all suggest that colorectal tumors are not only caused by ulcerative colitis, and we suggest further exploration and differentiation between colitis and colorectal tumors.

Application of the descending branch of the lateral circumflex femoral artery in coronary artery bypass grafting.

OBJECTIVE: To investigate a technical method for harvesting and using the descending branch of the lateral circumflex femoral artery (DLCFA) in coronary artery bypass grafting (CABG). METHODS: Between January 2017 and January 2019, 40 patients (36 in the planed selection group and 4 in the temporary decision group) with mean age of 49.1 ± 7.5 years received DLCFA as an arterial conduit in CABG. In all patients, the DLCFA was successfully harvested via an anterior thigh incision. Depending on the location of the target vessel, the DLCFA was used as a free graft or a composite graft. RESULTS: Of the 44 patients in the planned selection group, DLCFA harvesting was abandoned in 8 patients because computed tomographic angiography revealed anatomical variation or stenosis of the superficial femoral artery. Of the 5 patients in the temporary decision group, harvesting was abandoned in 1 because of short length and thin caliber. On an average, 3.7 ± 0.9 distal anastomoses were created during CABG, with no adverse effects. The length of the harvested DLCFA was 9.9 ± 1.7 cm, with an average proximal lumen diameter of 3.4 ± 0.7 mm. The DLCFA was used as a free graft in 26 patients and as a "Y"-shape composite graft in 14 patients. Total arterial CABG was performed in 75% of the patients. CONCLUSIONS: The DLCFA is an alternative conduit for CABG. It can be harvested easily and safely. However, preoperative computed tomographic angiography examination is necessary for the smooth application of the DLCFA, and an appropriate strategy for graft establishment should be considered.

Heterogeneous nuclear ribonucleoprotein A2/B1 is a negative regulator of human breast cancer metastasis by maintaining the balance of multiple genes and pathways.

BACKGROUND: Heterogeneous nuclear ribonucleoprotein (hnRNP) A2/B1 is an important RNA-binding protein that affects the RNA processing, splicing, transport and stability of many genes. hnRNPA2/B1 is expressed during proliferation and metastasis of various cancer types and promotes such processes. However, the precise role and mechanism of hnRNPA2/B1 in breast cancer remain unclear. METHODS: The association of hnRNPA2/B1 with breast cancer metastasis was assessed using tissue chips, mouse models and publicly available data. The role and mechanism of hnRNPA2/B1 in breast cancer metastasis were studied in cell lines and mouse models. FINDINGS: In contrast to other cancer research findings, hnRNPA2/B1 expression was negatively correlated with breast cancer metastasis. hnRNPA2/B1 inhibited MDA-MB-231 triple-negative breast cancer (TNBC) cell metastasis in vitro and in vivo. hnRNPA2/B1 knockout activated ERK-MAPK/Twist and GR-beta/TCF4 pathways but inhibited STAT3 and WNT/TCF4 signalling pathways. Profilin 2 (PFN2) promoted breast cancer cell migration and invasion, whereas hnRNPA2/B1 bound directly to the UAGGG locus in the 3'-untranslated region of PFN2 mRNA and reduced the stability of PFN2 mRNA. INTERPRETATION: Our data supported the role of hnRNPA2/B1 in tumour metastasis risk and survival prediction in patients with breast cancer. The inhibitory role of hnRNPA2/B1 in metastasis was a balance of downstream multiple genes and signalling pathways. PFN2 downregulation by hnRNPA2/B1 might partly explain the inhibitory mechanism of hnRNPA2/B1 in breast cancer metastasis. Therefore, hnRNPA2/B1 might be used as a new prognostic biomarker and valuable molecular target for breast cancer treatments.

Retracted: Long noncoding RNA MEG3 inhibits proliferation and migration but induces autophagy by regulation of Sirt7 and PI3K/AKT/mTOR pathway in glioma cells.

Glioma is a common primary brain tumor with high mortality rate and poor prognosis. Long noncoding RNA maternally expressed gene 3 (MEG3) is a tumor suppressor in diverse cancer types. However, the role of MEG3 in glioma remains unclear. We aimed to explore the effects of MEG3 on U251 cells as well as the underlying mechanisms. U251 cells were stably transfected with different recombined plasmids to overexpress or silence MEG3. Effects of aberrantly expressed MEG3 on cell viability, migration, apoptosis, expressions of apoptosis-associated and autophagy-associated proteins, and phosphorylated levels of key kinases in the PI3K/AKT/mTOR pathway were all evaluated. Then, messenger RNA (mRNA) and protein expression of Sirt7 in cells abnormally expressing MEG3 were estimated. In addition, effects of abnormally expressed MEG3 and Sirt7 on U251 cells were determined to reveal the underlying mechanism of MEG3-associated modulation. Cell viability and migration were significantly reduced by MEG3 overexpression whereas cell apoptosis as well as Bax and cleaved caspase-3/-9 proteins were obviously induced. Beclin-1 and LC3-II/LC3-I were upregulated and p62 was downregulated in MEG3 overexpressed cells. In addition, the autophagy pharmacological inhibitor (3-methyladenine, 3-MA) affected the effect of MEG3 overexpression on cell proliferation. Furthermore, the phosphorylated levels of key kinases in the PI3K/AKT/mTOR pathway were all reduced by MEG3 overexpression. Sirt7 was positively regulated by MEG3 expression, and effects of MEG3 overexpression on U251 cells were ameliorated by Sirt7 silence. MEG3 suppressed cell proliferation and migration but promoted autophagy in U251 cells through positively regulating Sirt7, involving in the inhibition of the PI3K/AKT/mTOR pathway.

Detoxification and immunoprotection of Zn(II)-curcumin in juvenile Pacific white shrimp (Litopenaeus vannamei) feed with aflatoxin B1.

Aflatoxins, which was produced by Aspergillus flavus or Aspergillus parasiticus fungi during grain and feed processing or storage, could cause severe health problems and reduction of yield during shrimp cultures. To evaluate toxic effects of aflatoxin B1 (AFB1) in juvenile Pacific white shrimp (Litopenaeus vannamei) and potential protective effect of Zn(II)-curcumin (Zn-CM), four experimental diets (control, 500 µg/kg AFB1, 500 µg/kg AFB1+100 mg/kg Zn-CM, 500 µg/kg AFB1+200 mg/kg Zn-CM) were formulated in quadruplicate to feed the shrimp for 8 weeks. The results revealed that AFB1 could induce significant decrease in final body weight (FBW), weight gain (WG, %) and visible variations of the hepatopancreas structures in L.vannamei. Compared with AFB1 group, AFB1+100 mg/kg Zn-CM group significantly ameliorated the toxic effects of AFB1 on growth performance, while AFB1+100 mg/kg Zn-CM group had no effect on growth performance. Dietary AFB1+100 mg/kg Zn-CM enhanced phenoloxidase (PO) (P < 0.05) activity. Both dietary AFB1+100 mg/kg Zn-CM and AFB1+200 mg/kg Zn-CM reduced inducible nitric oxide synthase (iNOS) activity and glutathione (GSH) level, decreased the content of malondialdehyde (MDA) (P < 0.05) in hepatopancreas compared with AFB1 group. Transmission electron microscopy (TEM) analysis demonstrated that Zn-CM could relieve the microvilli transformation and mitochondria accumulation reduction caused by AFB1. Consequently, the results demonstrated that suitable Zn-CM could mitigate the AFB1-induced hepatotoxicity and immunotoxicity effects on L.vannamei.

Relocation of NPM Affects the Malignant Phenotypes of Hepatoma SMMC-7721 Cells.

Nucleophosmin(NPM), heavily implicated in diverse solid tumors, is an important multifunctional protein mainly located in the nucleolus. Our previous study confirmed that NPM can also localize and accumulate in the cytoplasm of liver cancer cells. However, the role of cytoplasmic NPM (NPMc +) is unclear. Here, we showed that both nucleolar NPM and NPMc+ could promote cell proliferation, although the effect of NPMc+ was weaker than that of NPM. Cell adhesion ability of hepatoma cells was significantly reduced to a greater extent by NPMc+ expression. Nucleolar NPM enhanced cell migration and invasion, whereas NPMc+ impeded cell migration and invasion. The investigation of NPM interactional proteins by proteomic method demonstrated that the NPM was involved in multiple biological processes. By contrast, the interactional proteins of NPMc+ were mainly implicated in tRNA amino acylation regulation. The interactional network of NPMc+ was significantly small and simple. These results suggested that relocation of NPM altered its interactional network and consequently disturbed the primary functions, including cell proliferation, adhesion, migration, and invasion. NPM plays a promotional role in cancer and the reducing relocation may be a potential therapeutic target for hepatocellular carcinoma. J. Cell. Biochem. 118: 3225-3236, 2017. © 2017 Wiley Periodicals, Inc.

Effect of cadmium-polluted diet on growth, salinity stress, hepatotoxicity of juvenile Pacific white shrimp (Litopenaeus vannamei): Protective effect of Zn(II)-curcumin.

Cadmium (Cd) is one of the major transitional metals that have toxic effects on aquatic organisms. To investigate the effects of dietary cadmium on growth, salinity stress, hepatotoxicity in juvenile Pacific white shrimp (L. vannamei) and potential protective effect of Zn(II)-curcumin, five experimental diets (control, 100mg/kg Zn(II)-curcumin, 30mg/kg Cd, 30mg/kg Cd+100mg/kg Zn(II)-curcumin, 30mg/kg Cd+200mg/kg Zn(II)-curcumin) were formulated. The results showed that Cd at 30mg/kg induced significant increase in weight gain, specific growth rate and visible alterations to the hepatopancreas structures of L. vannamei. Compared with control diet, 100mg/kg Zn(II)-curcumin added diet had no effect on growth performance or feed utilization, while healthier hepatopancreas and less plasma ALT, AST production was found. Moreover, 200mg/kg dietary Zn(II)-curcumin significantly ameliorated the Cd induced hepatotoxicity while 100mg/kg dietary Zn(II)-curcumin slightly ameliorated. Cd accumulation in the whole body was decreasing and Metallothioneins like was increasing in hepatopancreas with increasing dietary Zn(II)-curcumin level. The shrimp fed with dietary Zn(II)-curcumin showed higher survival rate after acute salinity change. Therefore, it can be demonstrated that hepatotoxicity and hormesis could be induced by Cd when Cd levels were 30mg/kg, Zn(II)-curcumin could mitigate the effects of dietary Cd on L. vannamei.

Zn(II)-curcumin protects against oxidative stress, deleterious changes in sperm parameters and histological alterations in a male mouse model of cyclophosphamide-induced reproductive damage.

The poor bioavailability and stability of curcumin limit its clinical application. A novel Zn(II)-curcumin complex was synthesized and its effects against cyclophosphamide (CP)-induced reproductive damage were compared with curcumin. Oral administration of Zn(II)-curcumin significantly prevented CP-induced elevation of malondialdehyde (MDA) level and reductions in superoxide dismutase (SOD) activity and glutathione (GSH) content in mouse testis. Zn(II)-curcumin significantly ameliorated CP-induced reductions in body and reproductive organs weights. Zn(II)-curcumin dose-dependently ameliorated CP-induced reproductive system impairments, by improving sperm parameters (sperm count, viability, motility) and reducing serum testosterone and histological alterations. Compared to curcumin at the same dose, Zn(II)-curcumin more effectively alleviated CP-induced reproductive injury, leading to a reduced severity of testicular pathologic changes, lower MDA level, elevated SOD activity and GSH content, and increased sperm parameters and serum testosterone. These results suggest Zn(II)-curcumin more effectively protects against CP-induced reproductive damage than curcumin alone due to a synergistic reduction in oxidative stress.

Gastroprotective effect of taurine zinc solid dispersions against absolute ethanol-induced gastric lesions is mediated by enhancement of antioxidant activity and endogenous PGE2 production and attenuation of NO production.

Zinc plays a key role in maintaining gastric mucosal integrity, while alcohol dependency can lead to low zinc status. Complexes containing zinc have been reported to have better ability to protect gastric mucosa than the compounds alone. In this study, taurine zinc [Zn(NH3CH2CH2SO3)2] solid dispersions (SDs) were synthesized and investigated in an ethanol-induced ulcer model in rats. Gastric ulcer index; gastric mucosa malondialdehyde (MDA) level, glutathione (GSH) content, superoxide dismutase (SOD) activity and prostaglandin E2 (PGE2) production; and serum nitric oxide (NO) were assessed and histological analysis of the gastric mucosa tissue was performed. Taurine zinc (100, 200 mg/kg) SDs protected rat gastric mucosa from ethanol-induced injury. Moreover, the gastroprotective effect of taurine zinc SDs was accompanied by a decrease in serum NO and significant increase in gastric prostaglandin E2 (PGE2). When indomethacin, a non-selective COX inhibitor was administered before the last dose of taurine zinc, the gastroprotective effect of taurine zinc was weakened. Furthermore, taurine zinc (200 mg/kg) SDs protected against ulceration more significantly than the same dose of taurine alone, suggesting a synergistic effect between taurine and zinc. These results indicate taurine zinc protects the gastric mucosa against ethanol-induced damage by elevating antioxidants, decreasing lipid peroxidation and inhibiting the production of nitric oxide. The gastroprotective effect of taurine zinc was also partially mediated by endogenous PGE2 production.

Regulatory role of nucleophosmin during the differentiation of human liver cancer cells.

Nucleophosmin (NPM, also known as B23), mainly localized in the nucleolus, has been reported to be overexpressed in many types of human cancer, including colon, ovarian, prostate and gastric cancer. NPM was identified while screening the differential nuclear matrix proteins during HMBA-induced differentiation of human liver cancer cells. We investigated the aberrant expression and subcellular localization of NPM in clinical liver cancer tissues and a cell line with the aim of providing more evidence for revealing the roles of NPM on regulating liver cancer cell proliferation and differentiation. In addition, we studied the potential interaction between NPM and several important proteins. Our results revealed that NPM protein was overexpressed in cancer cells, which was in accordance with the overexpressed mRNA in cancer tissues compared to the corresponding non-cancer tissues. We also found a decrease of NPM in protein and mRNA levels upon treatment with the differentiation reagent HMBA. We focused on the aberrant localization of NPM. Immunochemistry and immunofluorescence revealed aberrant cytoplasmic and nucleoplasm localization of NPM in liver cancer tissues and its colocalization with c-Myc, c-Fos, P53 and Rb in the SMMC-7721 cell line. The interactions between NPM and the above proteins were confirmed by GST pull-down assay and co-immunoprecipitation assay. These findings indicate that NPM plays a regulatory role in liver cancer, which deserves in-depth investigation.

Protective effects of seahorse extracts in a rat castration and testosterone-induced benign prostatic hyperplasia model and mouse oligospermatism model.

This study investigated the effects of seahorse (Hippocampus spp.) extracts in a rat model of benign prostatic hyperplasia (BPH) and mouse model of oligospermatism. Compared to the sham operated group, castration and testosterone induced BPH, indicated by increased penile erection latency; decreased penis nitric oxide synthase (NOS) activity; reduced serum acid phosphatase (ACP) activity; increased prostate index; and epithelial thickening, increased glandular perimeter, increased proliferating cell nuclear antigen (PCNA) index and upregulation of basic fibroblast growth factor (bFGF) in the prostate. Seahorse extracts significantly ameliorated the histopathological changes associated with BPH, reduced the latency of penile erection and increased penile NOS activity. Administration of seahorse extracts also reversed epididymal sperm viability and motility in mice treated with cyclophosphamide (CP). Seahorse extracts have potential as a candidate marine drug for treating BPH without inducing the side effects of erectile dysfunction (ED) or oligospermatism associated with the BPH drug finasteride.

Zn(II)-curcumin protects against hemorheological alterations, oxidative stress and liver injury in a rat model of acute alcoholism.

Curcumin can chelate metal ions, forming metallocomplexes. We compared the effects of Zn(II)-curcumin with curcumin against hemorheological alterations, oxidative stress and liver injury in a rat model of acute alcoholism. Oral administration of Zn(II)-curcumin dose-dependently prevented the ethanol-induced elevation of serum malondialdehyde (MDA) content and reductions in glutathione level and superoxide dismutase (SOD) activity. Zn(II)-curcumin also inhibited ethanol-induced liver injury. Additionally, Zn(II)-curcumin dose-dependently inhibited hemorheological abnormalities, including the ethanol-induced elevation of whole blood viscosity, plasma viscosity, blood viscosity at corrected hematocrit (45%), erythrocyte aggregation index, erythrocyte rigidity index and hematocrit. Compared to curcumin at the same dose, Zn(II)-curcumin more effectively elevated SOD activity, ameliorated liver injury and improved hemorheological variables. These results suggest that Zn(II)-curcumin protected the rats from ethanol-induced liver injury and hemorheological abnormalities via the synergistic effect of curcumin and zinc.

Zinc(II)-curcumin accelerates the healing of acetic acid-induced chronic gastric ulcers in rats by decreasing oxidative stress and downregulation of matrix metalloproteinase-9.

Gastric ulcers form as a result of a multifaceted process which includes acid secretion, reactive oxygen species generation and extracellular matrix (ECM) degradation. The aim of this study was to investigate the possible mechanisms underlying the anti-ulcerogenic effects of the Zn(II)-curcumin complex, a curcumin derivative, on the healing of acetic acid-induced gastric ulcers in rats. The severely ulcerated gastric mucosa of control animals had a lower glutathione level (GSH) and superoxide dismutase activity (SOD), and increased malondialdehyde (MDA) content compared to sham operated rats (P<0.001). Zn(II)-curcumin solid dispersions (equivalent to 12, 24 and 48 mg/kg) dose-dependently reduced the gastric ulcer index, significantly increased SOD activity and GSH levels, and reduced the MDA content and matrix metalloproteinase-9 (MMP-9) mRNA expression in the gastric mucosa (P<0.05, compared to control animals). Zn(II)-curcumin exerted a greater anti-ulcerogenic effect than curcumin at the same dose (24 mg/kg), leading to a reduced severity of gastric ulcers, lower MDA content, and increased SOD activity and GSH levels (P<0.05). In conclusion, these results confirm that the Zn(II)-curcumin complex possesses an enhanced mucosal barrier defense activity compared to curcumin alone, due to its synergistic ability to decrease oxidative stress and attenuate MMP-9-mediated inflammation.

Single-incision versus conventional laparoscopy for colorectal disease: a meta-analysis.

BACKGROUND: Single-incision laparoscopic surgery (SILS) was developed as a novel minimally invasive surgical approach. AIMS: The aim of this meta-analysis was to compare SILS and conventional laparoscopy (CL) for colorectal diseases with respect to perioperative and oncologic outcomes. METHODS: An electronic search was performed to retrieve all relevant articles published in the English language between 2008 and 2012 comparing SILS and CL for colorectal diseases. The data were analyzed with fixed-effect or random-effects models using review manager version 5.0. RESULTS: A total of 14 studies (one randomized controlled trial and 13 nonrandomized controlled trials) were found to be eligible and reported on 1,155 subjects, of whom 521 underwent SILS and 634 underwent CL for colorectal diseases. Concerning the perioperative outcomes, no differences were observed in conversion rate, operating time, and postoperative adverse events; however, patients who underwent SILS had lower blood loss, decreased blood transfusion requirement, shorter time to flatus, shorter hospital stay, and smaller incision. Concerning the oncologic outcomes, length of resected specimens, number of harvested lymph nodes, proximal margin, and distal margin, were comparable between two groups. CONCLUSIONS: Single-incision laparoscopic surgery (SILS) is a safe, feasible, and oncological efficient alternative to CL for colorectal diseases. Further larger, multi-centred, randomised controlled trial is indicated.

[Pharmacological researches of curcumin solid dispersions in treatment of cancer].

OBJECTIVE: To investigate the anticancer effect of curcumin Solid Dispersions (SDs). METHODS: Curcumin SDs were prepared by patent technology. The anticancer effect of curcumin SDs were investigated by vivo and vitro tests of SCG-7901, BEL-7402, S-180 and Ehrlich ascites tumor models. RESULTS: The results showed that Curcumin SDs had markedly anticancer effect and could improve the anticancer effect of cisplatin. CONCLUSION: Curcumin SDs could be developed into one kind of adjuvant drug for anticancer, as it has markedly anticancer effect, and could improve the anticancer effects of cisplatin.

Safety and efficacy of partial hepatectomy for huge (≥10 cm) hepatocellular carcinoma: a systematic review.

Huge (≥10 cm) hepatocellular carcinoma (HCC) is not uncommon at clinical presentation, and the surgical outcomes of such tumors are poor. This systematic review aimed to assess the safety and efficacy of partial hepatectomy for huge HCC. We performed a search on Medline and PubMed databases for all relevant studies published prior to December 2009. After exclusions, 21 studies remained for appraisal and data extraction. All studies were classified as level-4 evidence. The median overall perioperative morbidity and mortality rates were 29.2% (range: 13.6-72%) and 3.5% (range: 0-18.2%), respectively. The overall median survival since the partial hepatectomy was 20.7 months (range: 10.1-32 months), with median 1-, 3- and 5-year survival of 60.7% (range: 41-72.2%), 34% (range: 0-60.3%) and 28.6% (range: 0-54%), respectively. The median disease-free survival since the partial hepatectomy was 11.3 months (range: 5.5-32 months), with median 1-, 3- and 5-year disease-free survival rates of 48.7% (range: 32-65.4%), 27.5% (range: 14.1-49%) and 20.7% (range: 9.5-43%), respectively. Partial hepatectomy can be performed safely and is associated with long-term survival in a subset of patients with huge HCC, but the evidence of benefit is currently weak.

Meta-analysis of laparoscopic versus open resection for hepatocellular carcinoma.

BACKGROUND: Laparoscopic liver resection (LLR) remains to be established as a safe and effective alternative to open liver resection (OLR) for hepatocellular carcinoma (HCC). AIMS: The aim of this meta-analysis is to compare laparoscopic versus open resection for HCC with regard to perioperative and oncologic outcomes. METHODS: A literature search was performed to identify comparative studies reporting outcomes for both laparoscopic and open resection for HCC. Pooled odds ratios (OR) and weighted mean differences (WMD with 95% confidence intervals (95% CI) were calculated using either the fixed effects model or random effects model. RESULTS: Ten nonrandomized controlled studies matched the selection criteria and reported on 494 subjects, of whom 213 underwent LLR and 281 underwent OLR for HCC. Compared with the perioperative results of open surgery, reports on laparoscopic resection indicate potentially favourable outcomes in terms of operative blood loss (WMD: -160.57, 95% CI: -246.49 to -74.66), blood transfusion requirement (OR: 0.39, 95% CI: 0.18 to 0.86), postoperative morbidity (OR: 0.48, 95% CI: 0.29 to 0.78), and length of hospital stay (WMD: -5.53, 95% CI: -7.89 to -3.16). Concerning the oncologic outcomes, there was no difference between groups in surgical margin, overall survival and disease-free survival. CONCLUSIONS: LLR for HCC is superior to the OLR in terms of its perioperative results and does not compromise the oncological outcomes. Therefore, LLR may be an alternative choice for treatment of HCC.

Localization of prohibitin in the nuclear matrix and alteration of its expression during differentiation of human neuroblastoma SK-N-SH cells induced by retinoic acid.

The nuclear matrix-intermediate filament system of human neuroblastoma SK-N-SH cells before and after retinoic acid (RA) treatment was selectively extracted and the distribution of prohibitin (PHB) in the nuclear matrix, as well as its colocalization with related genes, was observed. Results of two-dimensional gel electrophoresis (2-DE), mass spectrometry (MS) identification, and protein immunoblotting all confirm that PHB was present in the components of SK-N-SH nuclear matrix proteins and was down-regulated after RA treatment. Immunofluorescence microscopy observations show that PHB was localized in the nuclear matrix and its distribution was altered due to RA treatment. Laser confocal microscopy results reveal that PHB colocalized with the expression products of c-myc, c-fos, p53, and Rb, but the colocalization region was altered after RA treatment. Our results prove that PHB is a nuclear matrix protein and is localized in nuclear matrix fibers. The distribution of PHB in SK-N-SH cells and its colocalization with related proto-oncogenes and tumor suppressor genes suggest that PHB plays pivotal roles in the differentiation of SK-N-SH cells and deserves further study.