Publications by authors named "T L B G Lins"

Aims: Carotenoids are a class of hydrophobic substances that are important as food and feed colorants and as antioxidants. The pathway for β-carotene synthesis has been expressed in various yeast species, albeit with rather low yields and titers. The inefficient conversion of phytoene to lycopene is often regarded as a bottleneck in the pathway.

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Pulmonary fibrosis (PF) can be a fatal disease characterized by progressive lung scarring. It is still poorly understood how the pulmonary endothelium is involved in the disease pathogenesis. Differences of the pulmonary vasculature between patients and donors were analyzed using transmission electron microscopy, immunohistochemistry, and single-cell RNA sequencing.

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Studying the complex web of interactions in biological communities requires large multifactorial experiments with sufficient statistical power. Automation tools reduce the time and labor associated with setup, data collection, and analysis in experiments that untangle these webs. We developed tools for high-throughput experimentation (HTE) in duckweeds, small aquatic plants that are amenable to autonomous experimental preparation and image-based phenotyping.

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This study evaluated the effect of reduced water intake on survival, apoptosis and immunoexpression of leptin in sheep preantral follicles, activation of primordial follicles, serum levels of leptin, estradiol (E2) and progesterone (P4), and in vitro maturation (IVM) of oocytes antral follicles, as well evaluated the effects of leptin on in vitro culture of secondary follicles isolated these animals. Ewes (n = 32) were divided into four groups: water ad libitum (Control - 100%), 80%; 60% and 40% of ad libitum intake. Blood was collected to determine, leptin, E2 and P4, before and after experiment.

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Pulmonary fibrosis (PF) is a progressive chronic lung disease characterized by excessive deposition of extracellular matrix (ECM) and structural destruction, associated with a severe 5-year mortality rate. The onset of the disease is thought to be triggered by chronic damage to the alveolar epithelium. Since the pulmonary endothelium is an important component of the alveolar-capillary niche, it is also affected by the initial injury.

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