Functional characterization of CYP4G11-a highly conserved enzyme in the western honey bee Apis mellifera.

Determining the functionality of CYP4G11, the only CYP4G in the genome of the western honey bee Apis mellifera, can provide insight into its reduced CYP4 inventory. Toward this objective, CYP4G11 transcripts were quantified, and CYP4G11 was expressed as a fusion protein with housefly CPR in Sf9 cells. Transcript levels varied with age, task, and tissue type in a manner consistent with the need for cuticular hydrocarbon production to prevent desiccation or with comb wax production. Young larvae, with minimal need for desiccation protection, expressed CYP4G11 at very low levels. Higher levels were observed in nurses, and even higher levels in wax producers and foragers, the latter of which risk desiccation upon leaving the hive. Recombinant CYP4G11 readily converted octadecanal to n-heptadecane in a time-dependent manner, demonstrating its functions as an oxidative decarbonylase. CYP4G11 expression levels are high in antennae; heterologously expressed CYP4G11 converted tetradecanal to n-tridecane, demonstrating that it metabolizes shorter-chain aldehydes. Together, these findings confirm the involvement of CYP4G11 in cuticular hydrocarbon production and suggest a possible role in clearing pheromonal and phytochemical compounds from antennae. This possible dual functionality of CYP4G11, i.e., cuticular hydrocarbon and comb wax production and antennal odorant clearance, may explain how honey bees function with a reduced CYP4G inventory.

High risk of cross-reactivity between vancomycin and sequential teicoplanin therapy.

WHAT IS KNOWN AND OBJECTIVE: Teicoplanin and vancomycin show similar clinical and bacteriological efficacy in clinical trials. Teicoplanin has been reported to have a lower adverse drug reaction (ADR) rate than vancomycin. Cross-reactivity between these two glycopeptides is controversial. Our aim was to study the cross-reactivity between teicoplanin and vancomycin through an assessment of all the reported ADRs of these drugs in our University hospital. METHODS: Over a period of 2 years, 170 cases of vancomycin therapy, which were closely monitored by doctors and clinical pharmacists, were used to analyse ADRs. Teicoplanin therapy was used as an alternative in cases of vancomycin intolerance. When an ADR related to vancomycin or teicoplanin was suspected, specialists were consulted to confirm if these were true ADR and to determine whether the implicated drug should be stopped. All ADRs for the two glycopeptides were assessed for causality using the Naranjo probability scale. RESULTS AND DISCUSSION: Thirty-eight of 170 patients (22·4%) treated with vancomycin developed ADRs. Twenty-four patients were switched to teicoplanin. However, 14 of those 24 patients (58·3%) developed ADRs. The time of onset of ADRs involving vancomycin was 12·7 ± 10·9 days (range, 1-46 days). The time of onset of sequential teicoplanin-induced ADRs was 11·7 ± 4·7 days (range, 2-20 days). Of the 14 patients with ADRs related to sequential teicoplanin therapy, six showed cross-reactivity between vancomycin and teicoplanin. The incidence of vancomycin-induced neutropenia was 4·7% (8/170), whereas the incidence of teicoplanin-induced neutropenia subsequent to vancomycin intolerance was as high as 33·3% (8/24). Furthermore, 71·4% (10/14) of the teicoplanin-induced ADRs were associated with haematological abnormalities such as neutropenia, thrombocytopenia or leucopenia. WHAT IS NEW AND CONCLUSION: Teicoplanin, used as an alternative in cases of vancomycin intolerance, was associated with a high incidence of ADRs and haematological reactions, most notably neutropenia. This high rate of ADRs suggests cross-reactivity between the two glycopeptides.

[Application of single incision plus one port laparoscopic surgery in radical right hemicolon cancer surgery].

Objective: To investigate the feasibility and advantages of the SILS+1 technique in the radical right hemicolectomy, by comparing the short-term efficacy, postoperative recovery of intestinal function, and stress and inflammatory response of patients with right-sided colon cancer undergoing the conventional 5-hole laparoscopic technique or the single incision plus one port laparoscopic surgery (SILS+1). Methods: A retrospective cohort study was performed. Thirty-five patients with right-sided colon cancer undergoing SILS+1 surgery at Department of Gastrointestinal Surgery of Fujian Cancer Hospital from January 2018 to September 2020 were enrolled in the SILS+1 group. Then a total of 44 patients who underwent completely 5-hole laparoscopic right hemicolectomy at the same time were selected as the conventional laparoscopic surgery (CLS) group. The intraoperative observation indexes (operative time, intraoperative blood loss, and incision length) and postoperative observation indexes (time to ambulation after surgery, time to flatus, pain score in the first 3 days after surgery, hospitalization days, number of lymph node dissections, postoperative complication morbidity, and postoperative total protein, albumin and C-reaction protein) were compared between the two groups. Results: There was no conversion to laparotomy or laparoscopic-assisted surgery in both groups. All the patients successfully completed radical right hemicolectomy under total laparoscopy. There were no statistically significant differences in gender, age, body mass index or tumor stage between the two groups (all P>0.05). Compared with the CLS group, the SILS+1 group had shorter incision length [(5.1±0.6) cm vs. (8.5±4.1) cm, t=4.124, P=0.012], shorter time to the first ambulation (median: 27.6 h vs. 49.3 h, Z=4.386, P=0.026), and shorter time to the first flatus (median:42.8 h vs. 63.2 h, Z=13.086, P=0.012), lower postoperative pain score [postoperative 1-d: 2.0 ± 1.1 vs. 3.6 ± 0.9; postoperative 2-d: 1.4 ± 0.2 vs. 2.9±1.4; postoperative 3-d: 1.1 ± 0.1 vs. 2.3±0.3, F=49.128, P=0.003), shorter postoperative hospital stay [(9.1 ± 2.7) d vs. (11.2 ± 2.2) d, t=3.267,P=0.001], which were all statistically significant (all P<0.05). On the second day after surgery, as compared to CLS group, SILS+1 group had higher total protein level [(59.7±18.2) g/L vs. (43.0±12.3) g/L, t=2.214, P=0.003], higher albumin level [(33.6±7.3) g/L vs. (23.7±5.4) g/L, t=5.845, P<0.001], but lower C-reactive protein level [(16.3 ± 3.1) g/L vs. (63.3 ± 4.5) g/L, t=4.961, P<0.001], which were all statistically significant. There were no significant differences in the operative time, intraoperative blood loss, number of harvested lymph node, number of metastatic lymph node, and postoperative complication morbidity (all P>0.05). Conclusions: The SILS+1 technique has good operability and potential for popularization. Under the premise of radical resection, this technology not only reduces incision number and postoperative physical pain, but also speeds up postoperative recovery and shortens hospital stay.

Promotion of LncRNA HOXA11-AS on the proliferation of hepatocellular carcinoma by regulating the expression of LATS1.

OBJECTIVE: To investigate the expression levels of lncRNA HOXA11-AS in HCC tissues and cells, and to explore its biological role in the development and progression of HCC. PATIENTS AND METHODS: We detected the relative expression level of HOXA11-AS in 72 HCC tissues and cells by the real-time quantitative PCR (qRT-PCR) assay. After interference with HOXA11-AS expression in HCC cells, 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), clone formation, flow cytometry and an established nude mice transplanted tumor model were used to detect the biological behavior of HCC cells. qRT-PCR and Western blotting assays were used to detect the expression level of large tumor suppressor kinases 1 (LATS1). The subcellular localization of HOXA11-AS in HCC was detected by separating nuclei from the cytoplasm. The molecular mechanism of HOXA11-AS was regulated by ribonucleoprotein immunoprecipitation-microarray (RIP-Chip) experiments. RESULTS: qRT-PCR assays showed that HOXA11-AS was relatively highly expressed in HCC tissues and cells. In vivo and in vitro experiments showed that HOXA11-AS could inhibit the proliferation of HCC cells, promote their apoptosis and retard the cell cycle progression from G1 to G0 phase. qRT-PCR and Western blotting assays results showed that LATS1 genes were the downstream target genes of HOXA11-AS. RIP and CHIP experiments showed that HOXA11-AS inhibited the expression of LATS1 genes by binding enhancer of zeste homolog 2 (EZH2) proteins. CONCLUSIONS: HOXA11-AS inhibited the malignant transcription of the LATS1 genes and promoted the malignant proliferation of HCC cells. Interactions among HOXA11-AS, PRC2, and LATS1 may provide a new target for the treatment of HCC.