CRC (colorectal cancer) is one of the most malignant tumours in both developing and developed countries. It is estimated that 60% of CRC patients have liver metastasis. In the present study, we show that miR-30b is an important regulator in human CRC migration and invasion, which are vital steps in CRC liver metastasis. miR-30b was significantly down-regulated in primary CRC specimens compared with normal tissues. Furthermore, miR-30b was much lower in liver metastasis tissues than in CRCs. We validated SIX1 (SIX homeobox 1), a member of the SIX homeodomain family of transcription factors and an EMT (epithelial-mesenchymal transition)-promoting gene, as the direct target of miR-30b. Forced expression of miR-30b inhibited CRC cell migration and invasion in vitro via its target gene SIX1. Furthermore, an inverse correlation between expression of SIX1 and miR-30b has been observed both in primary CRC specimens and liver metastasis. Taken together, miR-30b plays an important role in mediating metastatic related behaviour in CRC. miR-30b may serve as a potential diagnostic marker and therapeutic target for patients with CRC in the future.

Previous studies have indicated that high expression of lactate dehydrogenase A (LDHA) exists in many human cancers. Recently, several reports showed that silencing or inhibition of LDHA could suppress metastasis of human cancer including renal cell carcinoma (RCC). However, the mechanism remains unknown. The role of LDHA in RCC migration and invasion was investigated using immunohistochemistry, western blotting, Transwell and scratch assays, and in vivo experiment. The influence of LDHA on the Warburg effect was also investigated by LDHA activity and lactate production assay. LDHA was overexpressed in RCC tissues and predicted a worse survival following renal resection. Correlation analysis demonstrated that LDHA was negatively correlated with E‑cadherin and positively with N‑cadherin. Experimentally, both in vivo and in vitro experiments found downregulation of LDHA suppressed RCC cells migration and invasion by inhibiting EMT. In addition, results indicated LDHA could promote the Warburg effect. Further research presented that the LDHA inhibitor, oxamate, suppressed tumor metastasis by inhibiting LDHA activity and EMT. These results demonstrated that LDHA mediates tumor metastasis by promoting EMT in RCC, suggesting that LDHA could be a promising therapeutic target for RCC therapy.

Recent studies have found that propofol may protect brain from cerebral ischemic-reperfusion injury. However, the underlying mechanism remains unclear. The effects of propofol were evaluated in HBVSMC after hypoxia/reoxygenation (H/R). Cell viability and levels of SOD, LDH, and MDA were measured. Apoptosis was detected by flow cytometry. The levels of Bax, Bcl-2, Caspase3, Sur2b, Kir6.1, JNK, p-JNK, mTOR, and p-mTOR proteins were measured by western blotting. H/R decreased cell viability and SOD activity and increased LDH leakage and MDA content in HBVSMC, all of which were significantly reversed by propofol. Propofol suppressed the levels of H/R-induced apoptosis. The expression of Bcl-2 and p-mTOR was significantly downregulated and the expression levels of Bax, Caspase3, Kir6.1, and p-JNK were upregulated following H/R injury. The ratio of p-JNK/JNK was increased; however, that of p-mTOR/mTOR decreased correspondingly. The effects on the expression of these proteins were reversed by propofol treatment. SP600125 enhanced and Everolimus attenuated the effect of propofol. These findings suggested that the protective effect of propofol against H/R injury in the HBVSMC was through the inhibition of apoptosis by inducing the expression of Bcl-2 and p-mTOR as well as inhibiting the expression levels of Bax, Caspase3, Kir6.1, and p-JNK.

Our study demonstrated that baseline toe PIs were inversely associated with the incidence of postspinal hypotension during cesarean delivery. Continuous monitoring of toe PIs during induction of spinal anesthesia might help to predict the development of postspinal hypotension and reflect the aortocaval compression by the gravid uterus.

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Colorectal cancer (CRC) is the third most common form of cancer, and the incidence of sporadic young-onset colorectal cancer (yCRC) has been increasing. Microbiota residing in the tumor microenvironment are emerging tumor components. The colonic microbiome differs between patients with CRC and healthy controls; however, few studies have investigated the role of the tumor microbiota in disease diagnosis and tumorigenesis of yCRC. We performed 16S rRNA sequencing analysis to identify the microbiome in CRC and found that tumor microbial diversity decreased in yCRC. Proteobacteria and Firmicutes were the most abundant phyla in all CRC samples, and Actinomyces and Schaalia cardiffensis were the key microbiota in the yCRC group. Correlation analysis revealed that Actinomyces co-occurred with various pro-tumor microbial taxa, including Bacteroidia, Gammaproteobacteria, and Pseudomonas. An independent cohort was used to validate the results. The Actinomyces in CRC was co-localized with cancer-associated fibroblasts and activated the TLR2/NF-κB pathway and reduces CD8+ T lymphocyte infiltration in CRC microenvironment. This study suggests that tumoral microbiota plays an important role in promoting tumorigenesis and therefore has potential as a promising non-invasive tool and intervention target for anti-tumor therapy.

Whether pulse oximeter perfusion index (PI) may be applied to detect the onset of caudal block in pediatric patients under ketamine intravenous basal anesthesia is investigated. 40 ASA I, 2–8-year-old boys scheduled for elective circumcision surgery were randomized into two groups. Group I: 20 patients were anesthetized by 2 mg·kg−1 ketamine intravenous injection (IV) followed by caudal block using 1 mL·kg−1 lidocaine (1%); Group II: 20 patients were anesthetized by 2 mg·kg−1 ketamine IV only. PI on the toe in Group II decreased by 33 ± 12%, 71 ± 9% and 65 ± 8% at 1 min, 15 min, and 30 min after ketamine injection. The maximum increase in MAP and HR after ketamine IV was 11 ± 6% at 3 min and 10 ± 6% at 2 min. Compared to the PI value before caudal injection of lidocaine, PI in Group I increased by 363 ± 318% and 778 ± 578% at 5 min and 20 min after caudal block, while no significant changes in MAP and HR were found compared to the baseline before caudal block. Thus, PI provides an earlier, more objective, and more sensitive indicator to assess the early onset of caudal block under basal ketamine anesthesia.

Background and Objectives: There is controversy regarding whether the inferior mesenteric artery (IMA) should be ligated at its origin from the aorta (high ligation, HL) or below the branch of the left colic artery (low ligation, LL) during surgery for rectal cancer.Methods: This prospective study randomized 95 patients with histologically proven rectal cancer (clinical stages I-III based on the 8th American Joint Committee on Cancer guidelines) to undergo HL (n = 47) or LL with lymph node dissection at the root of the IMA (n = 48).Results: Only two intraoperative adverse events were observed (two HL patients experienced anastomotic ischemia and underwent extended bowel excision and splenic flexure mobilization). The LL group had a significantly shorter time to first flatus (p < .0001). No significant differences were observed in operative time (p = .14), intraoperative blood loss (p = .21), distance from the upper margin (p = .77), distance from the lower margin (p = .35), harvested lymph nodes (p = .33), or anastomotic leakage (p = .44), 2-year overall survival (p = .97), or 2-year disease-free survival (p = .42). Conclusion:During laparoscopic low anterior resection, a combination of LL at the IMA and vascular root lymph node dissection may help protect the blood supply of the anastomosis, reduce postoperative complications, and enhance recovery, without compromising radical excision.