Yolk utilization and growth during the early larval life of the Silver Perch, Bidyanus bidyanus (Mitchell, 1838)

The aim of this research was to investigate the yolk sac and oil globule utilization by silver perch (Bidyanus bidyanus) larvae produced from domesticated broodfish. The larvae were kept unfed in the holding tank, sampled, and investigated by image analysis software to determine various characteristics, such as the diameters of ova, water-hardened eggs, yolk-sac, oil globules, and the total length of larvae. The research illustrated that, with the exception of oil globule diameter, all other morphometric parameters were significantly lower (P < 0.05) when compared to the larvae from the wild broodfish. The yolk sac was completely absorbed at 96 h post-hatching (hph) and the oil globule was visible until 240 hph. The larvae exhibited predatory movements and tried to catch rotifer at 4 days post hatching (dph). However, the onset of feeding took place at 5 dph, while 100% of feeding occurred at 6 dph. During the first 96 h (h), larvae grew significantly faster than the next 144 h. Larvae encountered low mortalities (<10%) during the first 96 hph, before increasing significantly in the next 24 h and no unfed larvae survived post 240 h. The results also suggested that the exogenous feed should be available at 96 hph, which is well after the yolk sac is completely depleted. In addition, although most of eggs and larval performance from domesticated broodfish were inferior compared to the wild one, it has larger oil globule that could make longer of its mixed feeding period and therefore could have better in viability

The epithelial cholinergic system of the airways

Acetylcholine (ACh), a classical transmitter of parasympathetic nerve fibres in the airways, is also synthesized by a large number of non-neuronal cells, including airway surface epithelial cells. Strongest expression of cholinergic traits is observed in neuroendocrine and brush cells but other epithelial cell types—ciliated, basal and secretory—are cholinergic as well. There is cell type-specific expression of the molecular pathways of ACh release, including both the vesicular storage and exocytotic release known from neurons, and transmembrane release from the cytosol via organic cation transporters. The subcellular distribution of the ACh release machineries suggests luminal release from ciliated and secretory cells, and basolateral release from neuroendocrine cells. The scenario as known so far strongly suggests a local auto-/paracrine role of epithelial ACh in regulating various aspects on the innate mucosal defence mechanisms, including mucociliary clearance, regulation of macrophage function and modulation of sensory nerve fibre activity. The proliferative effects of ACh gain importance in recently identified ACh receptor disorders conferring susceptibility to lung cancer. The cell type-specific molecular diversity of the epithelial ACh synthesis and release machinery implies that it is differently regulated than neuronal ACh release and can be specifically targeted by appropriate drugs

Early immune anergy towards recall antigens and mitogens in patients at onset of septic shock

Abstract The pathology of sepsis is typically characterized by an infection and excessive initial inflammation including a cytokine storm, followed by a state of immune suppression or paralysis. This classical view of a two peak kinetic immune response is currently controversially discussed. This study was a sub-study of the randomized clinical Trial SISPCT registered with www.clinicaltrials.gov (NCT00832039, Registration date: 29/01/2009). Blood samples from 76 patients with severe sepsis and septic shock were incubated for 48 h at 37 °C in vitro with bacterial or fungal recall-antigens or specific mitogen antigens within 24 hours of sepsis onset. Recall-antigen stimulation led to a severe dampening of normal cytokine release. This immunologic anergy was similarly observed after mitogen stimulation. Moreover, patients under hydrocortisone therapy or with lowered arterial oxygen tension had further reductions in cytokine levels upon B- and T-cell mitogen stimulation. This investigation reveals an early onset of immunoparalysis during sepsis. This immune incompetence in mounting an adequate response to further infections includes previously sensitized pathogens, as seen with recall-antigens. Also, the immune-suppressive role of hydrocortisone and low PaO2 is highlighted. Aside from early broad-spectrum antimicrobial therapy, our findings reinforce the need for maximal immunological support and protection against further infections at the onset of sepsis