Safety and efficacy evaluation of laparoscopy in colorectal cancer with liver metastasis.

OBJECTIVE: To study the safety and efficacy of simultaneous completion of colorectal cancer resection and liver metastasis resection by total laparoscopy. PATIENTS AND METHODS: In the observation group, 40 patients with colorectal cancer combined with liver metastasis (CRCLM) were selected to receive total laparoscopic surgery. At the same time, 40 cases were selected for laparoscopic resection of colorectal cancer and hepatic resection as control group. RESULTS: The outcomes of the two methods in the treatment of CRCLM were compared. The results showed that the difference in surgery time between the two groups was not statistically significant (p>0.05). The blood loss, drainage tube retention time and anal exhaust recovery time in the observation group were significantly less than those in control group (p<0.05). No significant difference in completion rate was found between the two groups (p>0.05); the prevalence rate of complications in the observation group was significantly lower than that in control group (p<0.05). No significant differences in the median survival period and the survival rate at 1 year, 2 years and 3 years after surgery were found between the two groups (p>0.05). CONCLUSIONS: The outcomes of total laparoscopy in the treatment of CRCLM are not inferior to open surgery.

Rapamycin enhances IFN-γ and IL-4 production in co-culture of gδ T and dendritic cells from mice with lipopolysaccharide-induced acute lung injury.

This study aimed to study the role of rapamycin (RAPA) in modulating the interaction between gδ T cells and dendritic cells (DCs) in a lipopolysaccharide (LPS)-induced acute lung injury mouse model. Mice were injected with LPS to establish the acute lung injury model or LPS + RAPA to assess the role of RAPA in modulating cell interactions. Mice were injected with PBS or RAPA alone as controls. gδ T cells and DCs were isolated from all mice and assessed by flow cytometry and fluorescence microscopy. The isolated gδ T cells and DCs were cultured independently or co-cultured to study their interactions. Enzyme-linked immunosorbent assay was performed to assess the expression of the cytokines, namely, interferon (IFN)-γ, interleukin (IL)-4, tumor necrosis factor (TNF)-α and IL-12 in the individually cultured or co-cultured gδ T cells and DCs, and reverse transcription-polymerase chain reaction (RT-PCR) was employed to investigate the levels of relevant mRNAs. Our study found that co-culture of gδ T cells and DCs from mice treated with LPS + RAPA have reduced expression of IFN-γ and IL-4 (but not TNF-α and IL-12) compared to mice treated with LPS only. These results were confirmed by RT-PCR, where the levels of IFN-γ and IL-4 mRNA were also reduced. This study may provide useful information in understanding the interaction between gδ T cells and DCs in the LPS-induced lung injury model in mice.

[Study on anti-oxidase in smoking-related laryngeal squamous cell carcinoma].

Objective:To investigate the role of oxidative stress in smoking-related laryngeal squamous carcinoma through detecting the expression of antioxidant enzymes in smoking patients. Method:A total of 138 cases with laryngeal squamous cell carcinoma enrolled in the first hospital affiliated the northern he bei college from 2012 to 2015 and forty five volunteers were conducted. All participants were divided into three groups according to smoking index: group A(heavy smoking, 88 cases of laryngeal cancer patients) and group B(no smoking 50 cases of laryngeal cancer patients) and C group(45 heavy smoking volunteers).Catalase(CAT), glutathione peroxidase(GSH-px) and malondialdehyde(MDA) and the expression of NRF2 in serum, tissue adjacent to carcinoma, and carcinoma tissues from each groups were measured, respectively. Result:①the expression of the CAT and GSH-px in group A were significantly lower than that of group B(P <0.05), but higher than that of group C(P <0.05); ②the MDA level of group A is significantly higher than group B(P <0.05) and C group(P <0.01);③NRF2 was highly expressed in carcinoma tissues, and the expression level was negatively correlated with degree of carcinoma differentiation (P <0.05). Conclusion:Compared with nonsmoking patients, heavy smoking patients with laryngeal cancer were under more severe oxidative stress. NRF2 expression level in patients with laryngeal squamous cell carcinomas was associated with pathological stage.

[Investigation of CXCR4 mediated chemoresistance in nasopharyngeal carcinoma cell line CNE2].

Objective:Since nasopharyngeal carcinoma is easy to develop resistance during cisplatin-based chemotherapy,CXCR4 expression levels were elevated in mang tumors,and the factor to do with tumor metastasis and chemotherapy drug resistance,and so on has a very important link.We established cisplatin-resistant nasopharyngeal carcinoma cell line, named as CNE2/DDP, and investigated the function of CXCR4 in molecular mechanism behind this resistance.Method:CNE2/DDP was firstly build up by increasing concentration of cisplatin. And then afterwards,MTT assay, RNA interference techniques, microRNA overexpresion techniques, quantative PCR and western blotting were applied to analyze the function of CXCR4 and its downstream effectors.Result:①the expression of CXCR4 was increased in CNE2/DDP and downregulation of CXCR4 with CXCR4 siRNA was able to decrease the resistance of CNE/DDP to cisplatin; ②the expression of let-7a was decrease in CNE2/DDP, while the expression of bcl-2 was increased. Upregulation of let-7a via transfection of let-7a mimics could downregulate the expression of bcl-2 and damage the resistance of CNE2/DDP to cisplation;③downregulation of CXCR4 through CXCR4 siRNA transfection was capable of improving the expression of let-7a. Conclusion:We were the first to found that CXCR4 was related to chemoresistance of CNE2/DPP to cisplatin. Meanwhile, we confirmed that CXCR4 affected the expression of bcl-2 through regulating the expression of let-7a to modulate the chemoresistance of CNE2/DPP to cisplatin.

Three branches of phospholipase C signaling pathway promote hepatocyte growth in rat liver regeneration.

In general, the phospholipase C (PLC) signaling pathway is involved in many physiological activities, including cell growth. However, little is known regarding how the PLC signaling pathway participates in regulating hepatocyte (HC) growth during liver regeneration (LR). To further explore the influence of the PLC signaling pathway on HCs at the cellular level, HCs of high purity and vitality were isolated using Percoll density-gradient centrifugation after partial hepatectomy. The genes of the PLC signaling pathway and target genes of transcription factors in the pathway were obtained by searching the pathways and transcription factor databases, and changes in gene expression of isolated HCs were examined using the Rat Genome 230 2.0 Microarray. The results suggested that various genes involved in the pathway (including 151 known genes and 39 homologous genes) and cell growth (including 262 known genes and 37 homologous genes) were associated with LR. Subsequently, the synergetic effect of these genes in LR was analyzed using a mathematical model (Et) according to their expression profiles. The results showed that the Et values of G protein-coupled receptor/PLC, integrin/PLC, and growth factor receptor/PLC branches of the PLC pathway were all significantly strengthened during the progression and termination phases of LR. The synergetic effect of target genes, in parallel with target gene-related cell growth, was also enhanced during whole rat LR, suggesting the potential positive effect of PLC on HC growth. The present data indicate that the PLC signaling pathway may promote HC growth through 3 mechanisms during rat LR after partial hepatectomy.

Gluteal compartment syndrome following abdominal aortic aneurysm repair: a case report.

Compartment syndromes occur when the elevated tissue pressure within a confined limb's myofascial compartment exceeds capillary pressure, with subsequent neurovascular compromise. In order to reduce disability and the consequences of ensuring ischemia, it is essential for early recognition and intervention. This is more commonly recognized in the calf. We report an unusual case of gluteal compartment syndrome after abdominal aortic aneurysm (AAA) repair.

A review of clinical pathway data of 1,663 total knee arthroplasties in a tertiary institution in Singapore.

INTRODUCTION AND OBJECTIVES: A total knee arthroplasty (TKA) clinical pathway database has been used in our institution since the year 2000. The primary aim of this study was to review the patient epidemiology, postoperative complications and factors influencing hospital length of stay following TKA. The clinical outcomes and cost-savings between elective and same day admissions for TKA patients were also reviewed. MATERIALS AND METHODS: The study cohort retrieved from the database comprised 1,371 patients (1,663 knees) who underwent total knee replacement over a 6-year time period. The following variables were reviewed: epidemiological data, admission data (elective admission [EA] versus same day admission [SDA]), hospital length of stay (LOS), and complication rates. RESULTS: The mean age of patients undergoing TKA is 65.2 years (range, 22 to 90). Osteoarthritis was the main surgical indication in 96% of the study cohort. Overall, there was a gradual decline in the hospital length of stay for the study cohort for the 6-year time period. The overall complication rate was 2% and the 3 most common complications were deep vein thrombosis, pulmonary embolism and urinary tract infection. CONCLUSION: With an increasing elderly population there will be an annual increase in the number of TKAs. In our local population TKAs are performed primarily for the Chinese female in the 7th decade. The overall complication rate of TKA remains low with a mortality rate of <1%.

Clear cell sarcoma of the rectus sheath.

We report a 35-year-old Chinese woman with clear cell sarcoma of the rectus sheath aponeurosis presenting as a tender anterior abdominal mass. She was treated with wide local excision. Local recurrence and distant metastasis occurred within two months of the onset of the complaint. Clear cell sarcoma is a rare cancer with a propensity for slow progressive invasion. They occur most commonly in the extremities, and the majority of patients are young adults. This case report demonstrates an unusual site of occurrence for clear cell sarcoma.

Insulin regulation of beta-cell function involves a feedback loop on SERCA gene expression, Ca(2+) homeostasis, and insulin expression and secretion.

The insulin receptor signaling pathway is present in beta-cells and is believed to be important in beta-cell function. We show here that insulin directly regulates beta-cell function in isolated rodent islets. Long-term insulin treatment caused a sustained increase in [Ca(2+)](i) and enhanced glucose-stimulated insulin secretion in rat islets, but failed to increase insulin content. Chronic activation of insulin receptor signaling by IRS-1 overexpression in the beta-cell inhibited gene expression of SERCA3, an endoplasmic reticulum Ca(2+)-ATPase. Insulin gene transcription was stimulated by insulin receptor signaling and insulin mimetic compound (L-783 281) in a glucose- and Grb2-dependent manner. Thus, beta-cell SERCA3 is a target for insulin regulation, which implies that beta-cell Ca(2+) homeostasis is regulated in an autocrine feedback loop by insulin. This study identifies a novel regulatory pathway of insulin secretion at the molecular level with two main components: (1) regulation of intracellular Ca(2+) homeostasis via SERCA3 and (2) regulation of insulin gene expression.

Insulin receptor substrate 1-induced inhibition of endoplasmic reticulum Ca2+ uptake in beta-cells. Autocrine regulation of intracellular ca2+ homeostasis and insulin secretion.

To understand the role of the insulin receptor pathway in beta-cell function, we have generated stable beta-cells (betaIRS1-A) that overexpress by 2-fold the insulin receptor substrate-1 (IRS-1) and compared them to vector-expressing controls. IRS-1 overexpression dramatically increased basal cytosolic Ca2+ levels from 81 to 278 nM, but it did not affect Ca2+ response to glucose. Overexpression of the insulin receptor also caused an increase in cytosolic Ca2+. Increased cytosolic Ca2+ was due to inhibition of Ca2+ uptake by the endoplasmic reticulum, because endoplasmic reticulum Ca2+ uptake and content were reduced in betaIRS1-A cells. Fractional insulin secretion was significantly increased 2-fold, and there was a decrease in betaIRS1-A insulin content and insulin biosynthesis. Steady-state insulin mRNA levels and glucose-stimulated ATP were unchanged. High IRS-1 levels also reduced beta-cell proliferation. These data demonstrate a direct link between the insulin receptor signaling pathway and the Ca2+-dependent pathways regulating insulin secretion of beta-cells. We postulate that during regulated insulin secretion, released insulin binds the beta-cell insulin receptor and activates IRS-1, thus further increasing cytosolic Ca2+ by reducing Ca2+ uptake. We suggest the existence of a novel pathway of autocrine regulation of intracellular Ca2+ homeostasis and insulin secretion in the beta-cell of the endocrine pancreas.

Insulin receptor signaling in the beta-cell influences insulin gene expression and insulin content: evidence for autocrine beta-cell regulation.

The insulin receptor (IR) is expressed by insulin-secreting beta-cells, but its cellular function is unknown. We transfected betaTC6-F7 beta-cells with cDNAs encoding either wild-type or mutant kinase-inactive (A/K1018) IRs, and by fluorescence-activated cell sorting generated polyclonal beta-cell lines that overexpressed each receptor type at levels two- to fourfold higher than the parental cells. Beta-cells overexpressing wild-type IRs had a proportional increase in insulin-stimulated tyrosine kinase activity; no change occurred in beta-cells expressing the mutant IR. We observed a threefold increase in cellular insulin content in beta-cells that overexpressed the wild-type IR, as determined by radioimmunoassay. This increase occurred despite a fivefold elevated rate of both basal and 10 mmol/l glucose-induced insulin secretion. Fractional insulin secretion (percentage of total cell insulin releasable at 10 mmol/l glucose) was unchanged in beta-cells overexpressing the wild-type IR compared with the parental beta-cell line. Insulin content and insulin secretion were unaffected by overexpression of kinase-inactive IRs. Steady-state insulin mRNA levels were elevated twofold in the beta-cells overexpressing the wild-type IR and unchanged in the beta-cells expressing the kinase-inactive receptor, as determined by Northern blot analysis. The rate of insulin mRNA degradation measured in the presence of 5 microg/ml actinomycin D was not significantly affected in either cell line. In the absence of glucose, the basal level of (pro)insulin biosynthesis in the beta-cells overexpressing the wild-type IR increased significantly (61%) compared with the beta-cells transfected with the kinase-inactive IR. These data indicate that IR signaling can regulate insulin gene transcription and can modulate the steady-state insulin content of beta-cells.