Cranial Suture Regeneration Mitigates Skull and Neurocognitive Defects in Craniosynostosis

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Noncanonical Transforming Growth Factor β (TGFβ) Signaling in Cranial Neural Crest Cells Causes Tongue Muscle Developmental Defects

Microglossia is a congenital birth defect in humans and adversely impacts quality of life. In vertebrates, tongue muscle derives from the cranial mesoderm, whereas tendons and connective tissues in the craniofacial region originate from cranial neural crest (CNC) cells. Loss of transforming growth factor β (TGFβ) type II receptor in CNC cells in mice (Tgfbr2^fl/fl;Wnt1-Cre) causes microglossia due to a failure of cell-cell communication between cranial mesoderm and CNC cells during tongue development. However, it is still unclear how TGFβ signaling in CNC cells regulates the fate of mesoderm-derived myoblasts during tongue development. Here we show that activation of the cytoplasmic and nuclear tyrosine kinase 1 (ABL1) cascade in Tgfbr2^fl/fl;Wnt1-Cre mice results in a failure of CNC-derived cell differentiation followed by a disruption of TGFβ-mediated induction of growth factors and reduction of myogenic cell proliferation and differentiation activities. Among the affected growth factors, the addition of fibroblast growth factor 4 (FGF4) and neutralizing antibody for follistatin (FST; an antagonist of bone morphogenetic protein (BMP)) could most efficiently restore cell proliferation, differentiation, and organization of muscle cells in the tongue of Tgfbr2^fl/fl;Wnt1-Cre mice. Thus, our data indicate that CNC-derived fibroblasts regulate the fate of mesoderm-derived myoblasts through TGFβ-mediated regulation of FGF and BMP signaling during tongue development.     

Analysis of palm dermatoglyphics in Taiwan indigenous populations

An analysis of a-b and a-d palm ridge counts was made from samples of people in eight indigenous Taiwan populations. Differences between hands, sexes, and populations were all significant. Bimanual differences for both counts were large, and right hand counts were consistently smaller than those for the left hand in all the populations. This is believed to be a consequence of the evolution of development, reflecting some inborn bilateral differences in function and anatomy. Sex differences, although small, were noticed. Variations between populations, ranging from approximately 7 to 19% of the total, were assumed to be genetic. The population relationships, based on dermatoglyphics, partially resembled those based on anthropometric measurements; and some aspects of their evolutionary significance were discussed.     

Iron modulates the activity of monoamine oxidase B in SH-SY5Y cells

Both monoamine oxidase B (MAO-B) and iron accumulation are associated with neurologic diseases including Parkinson’s disease. However, the association of iron with MAO-B activity was poorly understood. Here we took advantage of highly sensitive and specific fluorescence probes to examine the change in MAO-B activity in human dopaminergic neuroblastoma (SH-SY5Y) cells upon iron exposure. Both ferric and ferrous ions could significantly enhance the activity of MAO-B, instead of MAO-A, in SH-SY5Y cells. In addition, iron-induced increase in MAO-B probe fluorescence could be prevented by pargyline and other newly developed MAO-B inhibitors, suggesting that it was MAO-B activity-dependent. These findings may suggest MAO-B is an important sensor in iron-stressed neuronal cells.     

基于“心与小肠相表里”理论探讨肠道微生态与骨质疏松症的关系

近年来相关研究显示,肠道微生态在骨质疏松症的发生发展中起着重要作用。中医脏腑理论密切关注脏腑之间的生理病理关系,以中医经典《内经》“心与小肠相表里”理论为基础,探讨心、小肠、肠道微生态与骨质疏松症之间的关系。研究发现肠道微生态可能是心系疾病导致骨质疏松症的途径之一,这一发现可能为骨质疏松症的研究与防治提供一定的理论依据。     

Glucose biosensor based on electrodeposited platinum nanoparticles and three-dimensional porous chitosan membranes

The chitosan with three-dimensional porous structure greatly increased the effective electrode surface for loading of platinum nanoparticles and promoted efficient electron transfer. The resulting biosensor had a response time (within 5 s) and a linear response from 6 μM to 4.2 mM glucose with a detection limit of 2 μM (S/N = 3). Moreover, the methodology can be applied for the immobilization of other enzymes.     

D-β-Hydroxybutyrate Prevents MPP+-Induced Neurotoxicity in PC12 Cells

Numerous studies show that D-β-Hydroxybutyrate (DβHB) is neuroprotective. The present study was to explore the neuroprotective effects of DβHB against the cell death and apoptosis induced by 1-methyl-4-phenylpyridinium ion (MPP+) in PC12 cells. PC12 cells were pretreated with DβHB and followed by MPP+ exposure. The cell viability was determined by MTT assay. The morphological characteristics of apoptosis was observed by Acridine Orange (AO) staining and apoptotic rates were measured by flow cytometer. The product of lipid peroxidation, malondialdehyde (MDA), was measured using thiobarbituric acid method. The mitochondrial membrane potential (MMP), intracellular ROS and total glutathione were detected by microplate reader. In PC12 cells, pretreatment with DβHB significantly reduced MPP+-induced the decrease of cell viability. AO staining and flow cytometric analysis found DβHB inhibited MPP+-induced apoptosis. The measurement of MDA formation showed that DβHB alleviated lipid peroxidation induced by MPP+. The loss of MMP induced by MPP+ was preventive by DβHB. The changes of intracellular ROS and total glutathione induced by MPP+ were reversed by DβHB. DβHB protected PC12 cells against MPP+-induced death and apoptosis.