Fucoxanthin: A Promising Medicinal and Nutritional Ingredient

Fucoxanthin, an allenic carotenoid, can be isolated from edible brown seaweeds. Recent studies have reported that fucoxanthin has many physiological functions and biological properties, such as antiobesity, antitumor, antidiabetes, antioxidant, anti-inflammatory, and hepatoprotective activities, as well as cardiovascular and cerebrovascular protective effects. Therefore, fucoxanthin can be used as both medicinal and nutritional ingredient to prevent and treat chronic diseases. Although fucoxanthin possesses many medicinal ingredient and nutritional qualities, studies indicated that its structure was unstable. In this paper, we consulted the current documents and reviewed structural properties and factors affecting the stability of fucoxanthin. We also reported the metabolism, safety, pharmacological activities, and the methods of improving the bioavailability of fucoxanthin. Based on these studies providing essential background knowledge, fucoxanthin can be developed into marine drugs and nutritional products

RANKL/RANK promotes the migration of gastric cancer cells by interacting with EGFR

BACKGROUND: The incidence and mortality rates of gastric cancer (GC) rank in top five among all malignant tumors. Chemokines and their receptor-signaling pathways reportedly play key roles in the metastasis of malignant tumor cells. Receptor activator of nuclear factor κB ligand (RANKL) is a member of the tumor necrosis factor family, with strong chemokine-like effects. Some studies have pointed out that the RANKL/RANK pathway is vital for the metastasis of cancer cells, but the specific mechanisms in GC remain poorly understood. RESULTS: This study reports original findings in cell culture models and in patients with GC. Flow cytometry and western blotting analyses showed that RANK was expressed in BGC-823 and SGC-7901 cells in particular. Chemotaxis experiments and wound healing assay suggested that RANKL spurred the migration of GC cells. This effect was offset by osteoprotegerin (OPG), a decoy receptor for RANKL. RANKL contributed to the activation of human epidermal growth factor receptor (HER) family pathways. The lipid raft core protein, caveolin 1 (Cav-1), interacted with both RANK and human epidermal growth factor receptor-1(EGFR). Knockdown of Cav-1 blocked the activation of EGFR and cell migration induced by RANKL. Moreover, RANK-positive GC patients who displayed higher levels of EGFR expression had poor overall survival. CONCLUSIONS: In summary, we confirmed that with the promotion of RANKL, RANK and EGFR can form complexes with the lipid raft core protein Cav-1, which together promote GC cell migration. The formation of the RANK-Cav-1-EGFR complex provides a novel mechanism for the metastasis of GC. These observations warrant confirmation in independent studies, in vitro and in vivo. They also inform future drug target discovery research and innovation in the treatment of GC progression

Fucoxanthin: A Promising Medicinal and Nutritional Ingredient

Fucoxanthin, an allenic carotenoid, can be isolated from edible brown seaweeds. Recent studies have reported that fucoxanthin has many physiological functions and biological properties, such as antiobesity, antitumor, antidiabetes, antioxidant, anti-inflammatory, and hepatoprotective activities, as well as cardiovascular and cerebrovascular protective effects. Therefore, fucoxanthin can be used as both medicinal and nutritional ingredient to prevent and treat chronic diseases. Although fucoxanthin possesses many medicinal ingredient and nutritional qualities, studies indicated that its structure was unstable. In this paper, we consulted the current documents and reviewed structural properties and factors affecting the stability of fucoxanthin. We also reported the metabolism, safety, pharmacological activities, and the methods of improving the bioavailability of fucoxanthin. Based on these studies providing essential background knowledge, fucoxanthin can be developed into marine drugs and nutritional products

Wheel Running Improves Motor Function and Spinal Cord Plasticity in Mice With Genetic Absence of the Corticospinal Tract

Our previous studies showed that mutant mice with congenital absence of the corticospinal tract (CST) undergo spontaneous remodeling of motor networks to partially compensate for absent CST function. Here, we asked whether voluntary wheel running could further improve locomotor plasticity in CST-deficient mice. Adult mutant mice were randomly allocated to a “runners” group with free access to a wheel, or a “non-runners” group with no access to a wheel. In comparison with non-runners, there was a significant motor improvement including fine movement, grip strength, decreased footslip errors in runners after 8-week training, which was supported by the elevated amplitude of electromyography recording and increased neuromuscular junctions in the biceps. In runners, terminal ramifications of monoaminergic and rubrospinal descending axons were significantly increased in spinal segments after 12 weeks of exercise compared to non-runners. 5-ethynyl-2′-deoxyuridine (EDU) labeling showed that proliferating cells, 90% of which were Olig2-positive oligodendrocyte progenitors, were 4.8-fold more abundant in runners than in non-runners. In 8-week runners, RNAseq analysis of spinal samples identified 404 genes up-regulated and 398 genes down-regulated, and 69 differently expressed genes involved in signal transduction, among which the NF-κB, PI3K-Akt and cyclic AMP (cAMP) signaling were three top pathways. Twelve-week training induced a significant elevation of postsynaptic density protein 95 (PSD95), synaptophysin 38 and myelin basic protein (MBP), but not of brain derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF) and insulin like growth factor-1 (IGF-1). Thus, locomotor training activates multiple signaling pathways, contributes to neural plasticity and functional improvement, and might palliate locomotor deficits in patients

Robust estimation of bacterial cell count from optical density

Optical density (OD) is widely used to estimate the density of cells in liquid culture, but cannot be compared between instruments without a standardized calibration protocol and is challenging to relate to actual cell count. We address this with an interlaboratory study comparing three simple, low-cost, and highly accessible OD calibration protocols across 244 laboratories, applied to eight strains of constitutive GFP-expressing E. coli. Based on our results, we recommend calibrating OD to estimated cell count using serial dilution of silica microspheres, which produces highly precise calibration (95.5% of residuals <1.2-fold), is easily assessed for quality control, also assesses instrument effective linear range, and can be combined with fluorescence calibration to obtain units of Molecules of Equivalent Fluorescein (MEFL) per cell, allowing direct comparison and data fusion with flow cytometry measurements: in our study, fluorescence per cell measurements showed only a 1.07-fold mean difference between plate reader and flow cytometry data

Role of planar polarity proteins Celsr1-3 in neuronal migration and ciliogenesis

Celsr1-3 (for Cadherin EGF Laminin Seven Pass Receptor), the mammalian orthologs of Drosophila Flamingo/starry night, encode proteins of the cadherin superfamily. Celsr1-3 belong to a group named ‘core PCP (Planar Cell Polarity) genes’. All three Celsr genes are expressed in the developing Central nervous system (CNS) in mice. Our lab is interested in studying their functions in mouse CNS development. In this program, I specifically addressed two issues, namely facial branchiomotor neuron (FBM neuron) migration and ependymal ciliogenesis. During development, neurons are generated in ventricular zones, and postmitotic neurons usually need to migrate over variable distances to reach their final destination. Among the many neuronal migration events, that of FBM neuron in the hindbrain is unique and complex. In zebrafish, mutations in PCP genes such as van gogh-like2, celsr2, frizzled3a, prickle1a and prickle1b are known to affect normal FBM neuron caudal migration. This prompted us to investigate the role of Celsr1-3, and Fzd3 in FBM neuron migration in mice. During mouse hindbrain development, FBM neurons migrate caudally from medial rhombomere (r) 4 to lateral r6. Celsr1 is expressed in FBM neuron precursors and the floor plate, but not in FBM neurons themselves. In Celsr1 constitutive mutants, caudal migration was compromised and neurons often migrated rostrally into r2 and r3, as well as laterally. Consistent with the expression profile, when we specially deleted Celsr1 in FBM neurons using Isl1- Cre, no rostral migration stream was observed. In contrast, when Celsr1 was deleted in FBM neuron precursors by Nkx6.2-Cre, abnormal rostral migration was seen in Celsr1|Nkx6.2 mutants. Thus, Celsr1 regulates FBM neuron migration direction in a non-FBM neuron-autonomous manner. In Celsr2 mutants, FBM neurons initiated caudal migration but moved prematurely into lateral r4 and r5. This phenotype was enhanced by inactivation of Celsr3 in FBM neurons and mimicked by inactivation of Fzd3. Celsr2 and Celsr3 act in a FBM neuron autonomous manner. Furthermore, Celsr2 is epistatic to Celsr1. All these phenotypes were not caused by defects in hindbrain patterning or neuronal specification. These data indicate that Celsr1-3 differentially regulate FBM neuron migration. Celsr1 helps to specify the direction of FBM neuron migration, whereas Celsr2 and 3 control its ability to migrate. Studies in Xenopus indicate that there is a link between PCP signaling and ciliogenesis. In our mouse colony, I noticed that Celsr2 and Celsr3 double mutant mice developed huge hydrocephalus, and we decided to investigate the role of cilia in this phenotype. Ependymal cells form the epithelial lining of cerebral ventricles. Their apical surface is covered by cilia that beat in a coordinated fashion to facilitate circulation of the cerebrospinal fluid (CSF), and abnormal CSF circulation leads to hydrocephalus. In Celsr2 mutant mice, the development and planar organization of ependymal cilia were compromised, leading to defective CSF dynamics and hydrocephalus. In Celsr2 and Celsr3 double mutant ependyma, ciliogenesis was markedly impaired, resulting in lethal hydrocephalus. The membrane distribution of Vangl2 and Fzd3, two key planar cell polarity proteins, was disturbed in Celsr2 mutants, and even more so in Celsr2 and Celsr3 double mutants. Our findings suggest that planar cell polarity signaling is involved in ependymal cilia development and in the pathophysiology of hydrocephalus.(SBIM 3) -- UCL, 201

Role of the Atypical Cadherin Celsr3 during Development of the Internal Capsule.

The development of axonal tracts requires interactions between growth cones and the environment. Major bundles, particularly in the internal capsule, are completely defective in mice with constitutive mutation of Celsr3. In order to understand better how Celsr3 controls axonal tract formation, we generated a conditional allele that allowed inactivation of Celsr3 in different sectors of the forebrain. Effects of Celsr3 inactivation specifically in the telencephalon, in the ventral forebrain, or in the cortex, demonstrate essential roles for the gene, both in the neurons that project their axons to subcerebral targets such as the spinal cord, as well as in cells that guide projecting axons through the ventral forebrain. These observations provide unequivocal in vivo evidence that heterotypic interactions between axons and guidepost cells govern axonal path formation in mammals, and that Celsr3 plays a key role in this process. In absence of cortico-subcortical connections, mice can survive up to P20, allowing studies of behavior and cortical maturation. Mutant mice with defective corticospinal tracts survive normally and provide a model to evaluate in vivo the role of this tract in motor function in rodents

Prediction of strata behaviors law based on GRU and XGBoost

In the process of using optical fiber frequency shift value monitored by optical fiber sensor to characterize the strata behaviors law, the data collected by the sensor is missing, and the strata behaviors law can not be accurately predicted. In order to solve this problem, taking Qianqiu Coal Mine as the engineering background, under the premise of partial data loss of the lower half of the optical fiber, two prediction models, GRU (Gated Recurrent Unit) and LSTM (Long Short-Term Memory), are introduced to compare and predict the missing optical fiber frequency shift value. The convergence speed of the GRU model is better than that of the LSTM model, which shows that the missing value processing method based on the GRU model is better. The original and complete optical fiber frequency shift value is converted into the average optical fiber frequency shift change which can characterize the strata behaviors position, and the XGBoost (eXtreme Gradient Boosting) model and the BP neural network model are introduced for comparative prediction. The XGBoost model can predict all the 'peak' positions in the test set accurately. However, the BP neural network model can only predict two 'peak' positions, which shows that the prediction effect of the XGBoost model is better than that of the BP neural network model. The predicted optical fiber frequency shift missing value is replaced to the missing position to form 'complete' optical fiber frequency shift value data. The data is converted into the average optical fiber frequency shift change and then the XGBoost model is used for prediction. The results show that both the LSTM model and the GRU model can predict the data of the lower half of the optical fiber accurately, and the GRU model has higher accuracy than the LSTM model. The XGBoost model can predict the periodic pressure in the test set accurately. After the missing data predicted by the GRU model is integrated into the missing position, the XGBoost model can still predict the strata behaviors effectively