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.

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.

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.