PURPOSE:To evaluate the effects of copaiba oil on jaw defects repair in Wistar rats treated with bioglass or adipose tissue. METHODS:A jaw defect was randomly created in forty-two rats and filled with bioglass or adipose tissue. The two groups (Gbio and Gcell) were subdivided in three subgroups with seven animals each according to gavage administration: control (distillated water), oil (copaiba oil) and melox (meloxicam). Euthanasia was performed after forty post-operative days. The bone formation was analyzed regarding the histological aspects. RESULTS:The osteoclasts activity was observed only in four subgroups (p=0.78). Regarding the osteoblasts presence, it was very similar between the subgroups, the difference was due to Gcell-melox (p=0.009) that presented less osteoblastic activity. The inflammatory cells were more evident in Gcell-melox subgroup, however, there was no difference in comparison with the other subgroups (p=0.52).Bone formation was observed in all subgroups, just two animals showed no bone formation even after 40 days. More than 50% of bone matrix mineralization was observed in 56% (23 animals) of the analyzed areas. The bone matrix mineralization was not different between subgroups (p=0.60). CONCLUSIONS:The subgroups that received copaiba oil showed bone repair, although not statistically significant in comparison to subgroups treated whit meloxicam or controls. Copaiba oil administered by gavage had no effect on bone repair in this experimental model.

PURPOSE:To evaluate the effects of copaiba oil as a prophylactic and/or therapeutic substance on survival of rats subjected to cecal ligation and puncture, describing histopathological and oxidative stress findings. METHODS: Forty rats (Ratus RESULTS:Survival analysis demonstrated that animals treated with copaiba oil prior to the execution of the CLP (PreG and Pre/Post groups) had longer survival compared to the sepsis group (p<0.0001) whereas animals receiving copaiba only after the completion of CLP (PostG) showed no statistically significant difference compared to the sepsis group. However, when comparing the two groups in which was administered copaiba previously (PreG and Pre/PostG groups), there was no statistical significance between the groups (p=0.4672). There was no statistical difference between histopathological findings or the levels of oxidative stress. CONCLUSION:Prophylactic subcutaneous administration of copaiba increases survival of rats subjected to severe sepsis by cecal ligation and puncture.

Sex steroids can determine several responses in the clinical evolution of malaria. Seventy Balb-c mice were randomly distributed into 7 groups (10 mice per group): G1 to G6 corresponding to castrated females, castrated females that received estradiol cypionate, uncastrated females, castrated males, castrated males that received intramuscular testosterone decanoate and uncastrated males infected with Plasmodium berghei, and G7, the control group. The mice were evaluated with regard to survival, parasitemia, temperature, body weight, hemoglobin level (anemia) and splenic index. Castrated infected females had lower rates of survival. In the castrated male, the administration of testosterone had a negative influence on survival. There was a progressive increase in parasitemia without repercussions for survival. Castration had a significant influence on weight gain in females. Weight loss was observed in all mice, except those in groups G2 and G5, although this bore no direct relation to parasitemia. A significant and progressive decline in temperature and hemoglobin levels occurred in mice over the course of their infection, which differed from the G7 group. The weight of the spleen in relation to total body weight did not differ among the groups of infected mice, but was significantly higher than it was for the control group.

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e24112 Background: Anticipatory nausea (AN) and vomiting are unpleasant symptoms observed in anticipation of chemotherapy regimens. It is best described as a learned response through classical conditioning when one or more distinctive features of the chemotherapy clinic (conditioned stimuli) associated with the administration of emetogenic chemotherapy (unconditioned stimuli) trigger the emetogenic reflex. Little is known about AN's occurrence after the advent of the new neurokinin-1 antagonist. This prospective study evaluated AN's prevalence in ambulatory breast cancer patients receiving high effective antiemetic prophylaxis and evaluated potential predictors of AN. Methods: This prospective observational study was performed at a single Brazilian Institution. Key inclusion criteria were patients aged 18 years or older with breast cancer scheduled to receive anthracycline chemotherapy with an appropriate antiemetic regimen, including a neurokinin-1 receptor antagonist, a serotonin-3 receptor antagonist, and a corticosteroid. Eligible patients used a diary to record nausea, vomiting, and use of rescue medication in the first 2-cycle of treatment through 120 after infusion. AN was assessed before chemotherapy on day 1 of cycle two. We excluded patients with nausea and vomiting presented 24h before cycle one and patients who did not receive standard antiemetic prophylaxis. Results: Between August 04, 2020, and August 12, 2021, 60 patients were screened, and 52 patients were enrolled. The mean age was 50,8 (28 – 69), the majority had stage III (53,8%) and received chemotherapy with curative intent (94%). During cycle 1, the frequency of overall nausea and vomiting was 67.31%, and severe nausea and vomiting (defined as grade > 4 at a 10-point visual scale or use of rescue medication) was 55.77%. Ten patients had AN (19.23%). The occurrence of nausea and vomiting during cycle one was the only statistically significant predictor of AN (OR = 16, 95% CI 2.4, 670.9, p-value = 0.0003). Conclusions: The prevalence of AN is still high in the era of neurokinin-1 antagonists, and failure of antiemetic control on cycle one remains the main risk factor. All efforts should be made to control chemotherapy-induced nausea or nausea and vomiting on cycle one to avoid AN. Clinical trial information: NCT04785495.