Feasibility and efficacy of transthoracic single-port assisted laparoscopic esophagogastrectomy for Siewert type II adenocarcinoma of the esophagogastric junction.

BACKGROUND: The surgical treatment of Siewert type II adenocarcinoma of the esophagogastric junction (AEG) is controversial, and no systematic technology has been established. The aim of this retrospective study is to introduce the technology of transthoracic single-port assisted laparoscopic esophagogastrectomy. METHODS: Data from patients with Siewert type II AEG who underwent transthoracic single-port assisted laparoscopic esophagogastrectomy in Guangdong Provincial Hospital of Chinese Medicine from May 2017 to December 2020 were analyzed. RESULTS: A total of 35 patients, including 30 males and 5 females, were enrolled in this study. Eight patients underwent proximal gastrectomy while the other 27 patients underwent total gastrectomy. The median operative times were 247.5 (195.0-275.0) min and 290.0 (173.0-530.0) min for proximal and total gastrectomy, respectively. The median lower mediastinal lymph node dissection (LMLD) time was 41.5 (20.0-57.0) min and the median estimated blood loss was 100.0 (20.0-200.0) mL. The median number of harvested mediastinal lymph nodes was 5 [2-13]. Lower mediastinal lymph node metastasis occurred in 9 patients (25.7%). The lower mediastinal lymph node metastasis rate was significantly higher in patients with esophageal involvement exceeding 2 cm [>2 vs. ≤2 cm: 55.6% (5/9) vs. 15.4% (4/26), P=0.03]. The median postoperative hospital stay was 10 [6-73] days. Overall morbidity was 11.8% (4 patients), including 2 cases of pleural effusion, 1 case of pancreatic fistula, and 1 case of anastomotic leakage. CONCLUSIONS: Transthoracic single-port assisted laparoscopic esophagogastrectomy is safe and feasible. It has the advantages of reducing the difficulty of LMLD and digestive tract reconstruction.

Genistein inhibits Aß25₋35 -induced neurotoxicity in PC12 cells via PKC signaling pathway.

Protein kinase C (PKC) signaling pathway is recognized as an important molecular mechanism of Alzheimer's disease (AD) in the regulation of neuronal plasticity and survival. Genistein, the most active molecule of soy isoflavones, exerts neuroprotective roles in AD. However, the detailed mechanism has not been fully understood yet. The present study aimed to investigate whether the neuroprotective effects of genistein against amyloid ß (Aß)-induced toxicity in cultured rat pheochromocytoma (PC12) cells is involved in PKC signaling pathway. PC12 cells were pretreated with genistein for 2 h following incubation with Aß(25-35) for additional 24 h. Cell viability was assessed by MTT. Hoechst33342/PI staining was applied to determine the apoptotic cells. PKC activity, intracellular calcium level and caspase-3 activity were analyzed by assay kits. The results showed that pretreatment with genistein significantly increased cell viability and PKC activity, decreased the levels of intracellular calcium, attenuated Hoechst/PI staining and blocked caspase-3 activity in Aß(25-35)-treated PC12 cells. Pretreatment of Myr, a general PKC inhibitor, significantly attenuated the neuroprotective effect of genistein against Aß(25-35)-treated PC12 cells. The present study indicates that PKC signaling pathway is involved in the neuroprotective action of genistein against Aß(25-35)-induced toxicity in PC12 cells.

Mechanism of isoflavone aglycone's effect on cognitive performance of senescence-accelerated mice.

This study investigated the effect of isoflavone aglycone (IA) on the learning and memory performance of senescence-accelerated mice, and explored its neural protective mechanism. Results showed that SAM-P/8 senescence-accelerated mice treated with IA performed significantly better in the Y-maze cognitive test than the no treatment control (P<0.05). The cortex AchE activity, serum SOD and GSH-Px activities were notably higher (P<0.05). MDA concentration and the ß-secretase activity in the hippocampal tissue were both lower (P<0.05). Additionally, the number of hippocampal neurons was increased and cell morphology was significantly improved. Data suggested that IA could indirectly increase concentration of the cholinergic neural transmitter Ach through regulation of AchE, therefore improving the central cholinergic function and enhancing the learning and memory ability. By reducing the ß-secretase activity, IA could decrease the formation and deposition of insoluble Adebris, relieve the resulted toxicity and damage to neurons, and thereby effectively protect the nervous system.