Onset and development of cannibalistic and schooling behavior in the early life stages of Pacific bluefin tuna Thunnus orientalis

Behavioral development was observed in the early life stages of Pacific bluefin tuna in order to provide fundamental information for improving seedling production techniques. Behavioral observations to quantify swimming, schooling and cannibalistic behavior were made at different developmental stages: pre-flexion (5 days after hatching, DAH), flexion (12 DAH), post-flexion (14 DAH) and juvenile (20 DAH). Video recordings of either observation containers or the rearing tank were made to observe swimming and schooling behavior, respectively. Cannibalistic behavior was estimated by frequency of chase behavior. Swimming speed maintained constant values from 6 DAH (9.2 ± 6.0 mm/s, pre-flexion stage) to 20 DAH (22.4 ± 9.0 mm/s, beginning of juvenile stage) and increased rapidly thereafter to 29 DAH (85.2 ± 32.5 mm/s). Schooling behavior was first observed on 25 DAH juveniles (SL 23.5 ± 5.0 mm). Chase behavior was first observed at 14 DAH (standard length, SL 6.1 ± 0.6 mm, transition at flexion to post-flexion stage) and increased thereafter. We propose that a practical developmental stage for size grading to reduce the mortality by cannibalism should be between post-flexion and early juvenile (SL 6-23 mm), when the cannibalistic behavior onsets and swimming speed are relatively low

Exocytosis of Neutrophil Formyl Peptide Receptor-Like 1 (fPRL1) Results in Downregulation of Cytoplasmic fPRL1 in Patients with Purulent Dermatitis▿

N-Formyl peptide receptor-like 1 (fPRL1) is a member of the chemoattractant subfamily of G protein-coupled receptors and plays a key role in inflammation via chemotaxis and the regulation of mediator release from leukocytes. Activated fPRL1 has recently been shown to induce a complicated pattern of cellular signaling in vitro, but the details of the regulation and alteration of leukocyte cellular fPRL1 during inflammation in vivo remain unclear. To clarify the alteration of neutrophil fPRL1 during inflammation in vivo, the immunohistochemical staining of neutrophil fPRL1 in samples from patients with purulent dermatitis was performed. The in vitro morphological alteration of neutrophil fPRL1 on cellular membranes by stimulation with N-formylmethionyl-leucyl-phenylalanine (fMLP) was also examined. Both the cytoplasm and the cellular membranes of blood neutrophils stained strongly for fPRL1. On the other hand, the cellular membranes of neutrophils in dermatitis tissue stained strongly for fPRL1 but the cytoplasm stained weakly. The enhancement of neutrophil fPRL1 on cellular membranes by stimulation with fMLP indicates the exocytosis of neutrophil fPRL1-containing granules. In conclusion, we for the first time confirmed the alteration of neutrophil fPRL1 in clinical cases of purulent dermatitis. Cytoplasm that was weakly stained and cellular membranes that were well stained for fPRL1 were considered to be distinctive features of activated neutrophils in purulent dermatitis tissue

Estrogen is involved in improvement of impaired cardiac glucose uptake in cancer patients

AbstractWe previously demonstrated that inflammatory stress impaired cardiac glucose uptake, using fluorodeoxyglucose positron emission tomography/computed tomography (FDG-PET/CT) by showing that a proportion of patients with subtle FDG signals was remarkably increased compared with that of normal subjects. The current study assessed the inhibitory effects of cancer-associated stress on cardiac glucose uptake in female cancer patients, and compared the results with those obtained for healthy female subjects. Cardiac glucose uptake was decreased in female cancer, as indicated by the significantly higher number of patients with poor FDG uptake and the lower number of patients with high FDG uptake, compared with the number of healthy subjects with poor and high FDG uptake, respectively. These results suggest that cancer-associated stress inhibited cardiac glucose utilization. From the 78 female cancer patients, 13 oophorectomized patients, who underwent repeated postoperative follow-up examinations by FDG-PET/CT before and after receiving hormone replacement therapy (HRT) with estrogen derivatives, were analyzed to determine the effects of estrogen on cardiac glucose uptake. HRT increased a proportion of patients with high FDG signals to comparable in healthy subjects with high FDG uptake, whereas that of patients with poor FDG uptake decreased. These results suggest that estrogen can improve cardiac glucose uptake in cancer-resected and oophorectomized patients.<Learning objective: This study presents us a new point of view, which should be taken into account on the pathophysiology in some cardiovascular diseases, the sex-differences of energy substrates for the heart, i.e., estrogen or its derivatives accelerates the preference of glucose by the heart. Unfortunately, a very few studies have studied on this issue, e.g., effects of sex-steroid on cardiac uptake of energy substrate, and therefore, this suggests that cardiologists do not focus on this issue.

Neutrophil infiltration and oxidant-production in human atherosclerotic carotid plaques

To clarify the clinical implications of neutrophils in vulnerable plaques we evaluated the function and activity of infiltrated neutrophils in an atherosclerotic plaque, focusing on oxidant production. A histopathological investigation was performed using carotid arterial samples obtained from seven patients. The atherosclerotic plaques were examined cytochemically for naphthol-ASD-chloroacetate esterase activity and oxidant-production, and immunohistochemically using N-formyl peptide receptor-like 1 (fPRL1)-, CD66b-, CD68- or p22phox-specific antibodies. The cytoplasmic fPRL1 intensity value of the neutrophils in the plaque was estimated using an activity index. Naphthol-ASD-chloroacetate esterase activity was found in cells located in the atherosclerotic plaque, indicating that the cells were neutrophils. The cytoplasmic fPRL1 intensity value of the neutrophils in the plaque decreased to approximately 60% of the intensity observed in the capillary vessels. Oxidantproduction was also detected in the plaques, and both neutrophils and macrophages were observed at the corresponding oxidant-production sites. p22phox expression was also located in the same areas in which oxidant-production was observed in these plaques. We could not directly evaluate how much ROS generated from the infiltrated neutrophils contributed the plaque vulnerability followed by its rupture. However, the infiltrated neutrophils in the atherosclerotic plaques morphologically appeared activated and were actively generating oxidant, implying that neutrophils, together with macrophages, infiltrate into atherosclerotic plaques and contribute to plaque vulnerability