Assessment of the effect of the Aquamantys® system on local recurrence after hepatectomy for hepatocellular carcinoma through propensity score matching.

OBJECTIVE: To assess the effect of the intraoperative application of the Aquamantys® system to treat the hepatic resection margin on local and overall recurrence of HCC. METHODS: We retrospectively analyzed 101 patients admitted from November 2016 to June 2018 who underwent hepatectomy using the Aquamantys® as hemostatic device, who were matched with 101 patients (control group) using conventional hemostatic devices through PSM. Univariate and multivariate analyses of recurrence-free survival (RFS) and local recurrence-free survival (LRFS) were performed using the Cox proportional hazard model. RESULTS: There were no significant differences in baseline data and surgical procedures between the two groups. The Aquamantys® group showed less blood loss (P = 0.005) and a lower blood transfusion rate (P = 0.036), while the incidences of postoperative complications of the two groups showed no difference (P = 0.266). OS rates of the Aquamantys® group and the control group were 82.6% and 84.2%, respectively (P = 0. 446), and RFS rates were 65.5% and 58.2%, respectively (P = 0.153), with no significant differences. The Aquamantys® group and the control group had two cases and 11 cases of local recurrence, respectively, with LRFS rates of 98% and 87.9%, respectively, in the follow-up period, corresponding to a significant difference (P = 0.011). Multivariate analysis showed that microvascular invasion (MVI), tumor diameter > 5 cm, and the control group were independent risk factors for LRFS. CONCLUSION: Our results indicate that application of the Aquamantys® system in hepatectomy can reduce local recurrence, but it can neither reduce overall recurrence nor improve OS.

Immune strategies using single-component LipL32 and multi-component recombinant LipL32-41-OmpL1 vaccines against leptospira

Genes encoding lipoproteins LipL32, LipL41 and the outer-membrane protein OmpL1 of leptospira were recombined and cloned into a pVAX1 plasmid. BALB/c mice were immunized with LipL32 and recombined LipL32-41-OmpL1 using DNA-DNA, DNA-protein and protein-protein strategies, respectively. Prime immunization was on day 1, boost immunizations were on day 11 and day 21. Sera were collected from each mouse on day 35 for antibody, cytokine detection and microscopic agglutination test while spleen cells were collected for splenocyte proliferation assay. All experimental groups (N = 10 mice per group) showed statistically significant increases in antigen-specific antibodies, in cytokines IL-4 and IL-10, as well as in the microscopic agglutination test and splenocyte proliferation compared with the pVAX1 control group. The groups receiving the recombined LipL32-41-OmpL1 vaccine induced anti-LipL41 and anti-OmpL1 antibodies and yielded better splenocyte proliferation values than the groups receiving LipL32. DNA prime and protein boost immune strategies stimulated more antibodies than a DNA-DNA immune strategy and yielded greater cytokine and splenocyte proliferation than a protein-protein immune strategy. It is clear from these results that recombination of protective antigen genes lipL32, lipL41, and ompL1 and a DNA-protein immune strategy resulted in better immune responses against leptospira than single-component, LipL32, or single DNA or protein immunization.

Immune strategies using single-component LipL32 and multi-component recombinant LipL32-41-OmpL1 vaccines against leptospira.

Genes encoding lipoproteins LipL32, LipL41 and the outer-membrane protein OmpL1 of leptospira were recombined and cloned into a pVAX1 plasmid. BALB/c mice were immunized with LipL32 and recombined LipL32-41-OmpL1 using DNA-DNA, DNA-protein and protein-protein strategies, respectively. Prime immunization was on day 1, boost immunizations were on day 11 and day 21. Sera were collected from each mouse on day 35 for antibody, cytokine detection and microscopic agglutination test while spleen cells were collected for splenocyte proliferation assay. All experimental groups (N = 10 mice per group) showed statistically significant increases in antigen-specific antibodies, in cytokines IL-4 and IL-10, as well as in the microscopic agglutination test and splenocyte proliferation compared with the pVAX1 control group. The groups receiving the recombined LipL32-41-OmpL1 vaccine induced anti-LipL41 and anti-OmpL1 antibodies and yielded better splenocyte proliferation values than the groups receiving LipL32. DNA prime and protein boost immune strategies stimulated more antibodies than a DNA-DNA immune strategy and yielded greater cytokine and splenocyte proliferation than a protein-protein immune strategy. It is clear from these results that recombination of protective antigen genes lipL32, lipL41, and ompL1 and a DNA-protein immune strategy resulted in better immune responses against leptospira than single-component, LipL32, or single DNA or protein immunization.

First Report of Zonate Leaf Spot of Artocarpus altilis Caused by Cristulariella moricola in Taiwan.

Breadfruit (Artocarpus altilis (Parkinson) Fosberg) is an important landscape and garden tree in Taiwan. During the spring of 2002, zonate leaf spots of breadfruit were observed at a Taipei nursery in northern Taiwan. Initially, several small, brown, zonate lesions developed on leaves. As lesions enlarged, they coalesced, leading to blighting of leaves and premature defoliation. Sporophores on the host were generally hypophyllous but sometimes amphigenous, solitary, erect, easily detachable, and as much as 850 µm long. The upper portion of the sporophore is considered an individual conidium and consisted of a pyramidal head that was fusiform to ventricose and cristulate, 495 to 534 µm long and 210 to 290 µm wide at the broadest point. Branches within the pyramidal head were short and compact, and dichotomously or trichotomously branched. The conidia were hyaline, broad, septate, tapering toward an acute apex, and sometimes constricted at the basal septum. Conidiophores were 400 to 680 × 20 to 100 µm. The fungus was isolated from infected tissue and maintained on potato dextrose agar (PDA). Sclerotia were produced on PDA after 4 to 5 weeks at 20°C without light, but conidia were not observed in culture. The fungus was identified as Cristulariella moricola (Hino) Redhead based on morphological characteristics (1,2). To complete Koch's postulates, three sporophores from infected leaves or three sclerotia from cultures were placed individually on each of 10 breadfruit leaves. The plants were placed in plastic bags and incubated at 16 to 20°C. Symptoms were observed after 2 to 3 days on 100% of plants inoculated with sporophores and after 6 days on 50% of plants inoculated with sclerotia. The pathogen was reisolated from lesions on plants inoculated with sporophores and sclerotia. No symptoms were observed on the control plants. C. moricola has been known to cause a bull's eye or zonate leaf spot and defoliation on woody and annual plants, including at least 51 host species and 36 families distributed in the central and eastern United States (1). To our knowledge, this is the first report of zonate leaf spot and defoliation of breadfruit caused by C. moricola. References: (1) T. T. Chang. Bull. Taiwan For. Res. Inst. New Ser. 10 (2):235, 1995. (2) S. A. Redhead. Can. J. Bot. 53:700, 1975.

[Study on the influence of enzymatic digestion upon tumor-infiltrating lymphocytes].

To get a long-term culture of tumor-infiltrating lymphocytes (TILs) is very difficult. The authors have investigated some suitable enzymes, their digestive conditions such as time and temperature, which may influence the viability and cytotoxicity of TILs. The results showed that collagenase II and IV could keep viability of TILs much longer than those treated with trypsin or hyaluronidase. The digestion with collagenase II or IV at 4 degrees C for 24 hours was much less damage to viability of TILs than those treated at 37 degrees C for one hour. The TILs, which digested at 4 degrees C for 24 hours, still had cytotoxicity against autologous tumor cells as long as sixty to seventy-five days.