Feasibility and efficacy of laparoscopic radical right hemicolectomy with complete mesocolic excision using an 'artery-first' approach.

BACKGROUND: According to previous guidelines, the lymph nodes around the right side of the superior mesenteric artery (SMA) should be dissected and removed en bloc. However, due to the technical challenge and the risk of complications, most surgeons perform the dissection along the axis of the superior mesenteric vein (SMV). Herein, we described an 'artery-first' approach for laparoscopic radical extended right hemicolectomy with complete mesocolic excision (CME). METHODS: A total of 22 cases were collected from January to October 2016. The right side of the SMA and SMV were exposed and separated, and the No. 203, No. 213 and No. 223 lymph nodes were dissected en bloc. Toldt's fascia was dissected and expanded laterally to the ascending colon, cranial to the pancreas head. The caudal root of the mesentery and lateral attachments of the ascending colon were completely mobilized. RESULTS: There were 9 male and 13 female patients, with a mean age of 63.1 (range, 39-83) years and the mean body mass index was 24.6 (range, 18.3-37.7) kg/m2. The mean operative time was 192.5 (range, 145-240) minutes and the mean intra-operative blood loss was 55.0 (range, 10-300) ml. The mean number of harvested lymph nodes was 27.0 (range, 13-55) and the time to flatus and hospital stay were 35.0 (range, 26-120) hours and 7.5 (range, 5-20) days, respectively. Minor complications occurred in two patients and no post-operative death was observed. CONCLUSIONS: The preliminary results suggest that the reported approach may be a feasible and safe procedure that is more in accordance with the principles of CME.

Hyperammonaemia induces hepatic injury with alteration of gene expression profiles.

BACKGROUND: Hyperammonaemia is a serious metabolic disorder commonly observed in patients with hepatic failure. However, it is unknown whether hyperammonaemia has a direct adverse effect on the hepatocytes and thereby serves as both a cause and effect of hepatic failure. AIMS: The purposes were to determine whether hepatic injury can be caused by hyperammonaemia, and if so, screen the key genes involved in hyperammonaemia. METHODS: Hyperammonaemic rats were established via intragastric administration of the ammonium chloride solution. The liver tissues were assessed via biochemistry, histology, immunohistochemistry and microarray analysis. Selected genes were confirmed by quantitative RT-PCR. RESULTS: Administration of the ammonium chloride caused the hyperammonaemia, accompanied with the changes of plasma markers indicating hepatic injury. A pathological assessment demonstrated increased apoptosis and higher level of cyclin D1 and cyclin A in hyperammonaemic rat liver. Microarray was performed on the liver samples and 198 differentially expressed genes were identified in hyperammonaemic rats and validated by quantitative RT-PCR. These genes were associated with many vital functional classes and belonged to different signal transduction pathways. CONCLUSIONS: This study demonstrates that hyperammonaemia can directly induce hepatic injury via the hepatocyte apoptosis. Gene expression profile may provide the possible explanations and mechanisms for the hepatic injury induced by hyperammonaemia.

[Quantity and distribution of CD44+/CD24- cells in breast cancer tissue and the cell lines].

OBJECTIVE: To study the distribution and quantity of CD44+/CD24- cells in breast cancer tissue and the cell lines, and as well as its correlation with the expression of various breast cancer markers and molecular subtyping of breast carcinoma. METHODS: The expression of CD44/CD24, estrogen receptor, progesterone receptor, HER2, human estrogen-induced protein PS2, bcl-2 and nm23 in 60 cases of invasive ductal carcinoma of breast were studied by either single or double immunohistochemical staining. The co-expression of CD44 and CD24 in 3 breast cancer cell lines (MCF-7, MDA-MB-468, and MDA-MB-231) was also examined. RESULTS: The quantity and distribution of CD44+/CD24- cells varied greatly and no specific patterns were identified. The percentage of CD44+/CD24- in breast cancer was 65%. The amount of CD44+/CD24- cells did not correlate with the age of patients, lymph node metastasis, tumor size, molecular subtypes and expression of various breast cancer markers in breast carcinoma. The proportion of CD44+/CD24- cells in MCF-7, MDA-MB-468, and MDA-MB-231 cell lines was <1%, 5% and >80%, respectively. CONCLUSIONS: CD44+/CD24- cells are demonstrated in certain breast cancer tissues and cell lines. However, there is no relationship obtained between the quantity or the distribution of these cells and the molecular subtyping or the clinicopathologic parameters in breast cancer.