Writing Affects the Brain Network of Reading in Chinese: A Functional Magnetic Resonance Imaging Study

We examined the hypothesis that learning to write Chinese characters influences the brain’s reading network for characters. Students from a college Chinese class learned 30 characters in a character-writing condition and 30 characters in a pinyin-writing condition. After learning, functional magnetic resonance imaging collected during passive viewing showed different networks for reading Chinese characters and English words, suggesting accommodation to the demands of the new writing system through short-term learning. Beyond these expected differences, we found specific effects of character writing in greater activation (relative to pinyin writing) in bilateral superior parietal lobules and bilateral lingual gyri in both a lexical decision and an implicit writing task. These findings suggest that character writing establishes a higher quality representation of the visual–spatial structure of the character and its orthography. We found a greater involvement of bilateral sensori-motor cortex (SMC) for character-writing trained characters than pinyin-writing trained characters in the lexical decision task, suggesting that learning by doing invokes greater interaction with sensori-motor information during character recognition. Furthermore, we found a correlation of recognition accuracy with activation in right superior parietal lobule, right lingual gyrus, and left SMC, suggesting that these areas support the facilitative effect character writing has on reading. Finally, consistent with previous behavioral studies, we found character-writing training facilitates connections with semantics by producing greater activation in bilateral middle temporal gyri,whereas pinyin-writing training facilitates connections with phonology by producing greater activation in right inferior frontal gyrus

Early stage visual-orthographic processes predict long-term retention of word form and meaning: A visual encoding training study

Adult learners of Chinese learned new characters through writing, visual chunking or reading-only. Following training, ERPs were recorded during character recognition tasks, first shortly after the training and then three months later. We hypothesized that the character training effects would be seen in ERP components associated with word recognition and episodic memory. Results confirmed a larger N170 for visual chunking training than other training and a larger P600 for learned characters than novel characters. Another result was a training effect on the amplitude of the P100, which was greater following writing training than other training, suggesting that writing training temporarily lead to increased visual attention to the orthographic forms. Furthermore, P100 amplitude at the first post-test was positively correlated with character recall 3 months later. Thus the marker of early visual attention (P100) was predictive of retention of orthographic knowledge acquired in training

Acute Wounding Alters the Beta2-Adrenergic Signaling and Catecholamine Synthetic Pathways in Keratinocytes

Keratinocyte migration is critical for wound re-epithelialization. Previous studies showed that epinephrine activates the beta2-adrenergic receptor (B2AR), impairing keratinocyte migration. Here, we investigated the keratinocyte catecholamine synthetic pathway in response to acute trauma. Cultured keratinocytes were scratch wounded and expression levels of the B2AR and catecholamine synthetic enzymes tyrosine hydroxylase and phenylethanolamine-N-methyltransferase were assayed. The binding affinity of the B2AR was measured. Wounding downregulated B2AR, tyrosine hydroxylase, and phenylethanolamine-N-methyltransferase expression, but pre-exposure to timolol, a beta-adrenergic receptor antagonist, delayed this effect. In wounded keratinocytes, B2AR-binding affinity remained depressed even after its expression returned to prewounding levels. Keratinocyte-derived norepinephrine increased after wounding. Norepinephrine impaired keratinocyte migration; this effect was abrogated with B2AR-selective antagonist ICI-118,551 but not with B1AR-selective antagonist bisoprolol. Finally, for clinical relevance, we determined that norepinephrine was present in freshly wounded skin, thus providing a potential mechanism for impaired healing by local B2AR activation in wound-edge keratinocytes. Taken together, the data show that keratinocytes modulate catecholamine synthetic enzymes and release norepinephrine after scratch wounding. Norepinephrine appears to be a stress-related mediator that impairs keratinocyte migration through activation of the B2AR. Future therapeutic strategies evaluating modulation of norepinephrine-related effects in the wound are warranted

Dynamic modeling of gene expression in prokaryotes: application to glucose-lactose diauxie in Escherichia coli

Coexpression of genes or, more generally, similarity in the expression profiles poses an unsurmountable obstacle to inferring the gene regulatory network (GRN) based solely on data from DNA microarray time series. Clustering of genes with similar expression profiles allows for a course-grained view of the GRN and a probabilistic determination of the connectivity among the clusters. We present a model for the temporal evolution of a gene cluster network which takes into account interactions of gene products with genes and, through a non-constant degradation rate, with other gene products. The number of model parameters is reduced by using polynomial functions to interpolate temporal data points. In this manner, the task of parameter estimation is reduced to a system of linear algebraic equations, thus making the computation time shorter by orders of magnitude. To eliminate irrelevant networks, we test each GRN for stability with respect to parameter variations, and impose restrictions on its behavior near the steady state. We apply our model and methods to DNA microarray time series' data collected on Escherichia coli during glucose-lactose diauxie and infer the most probable cluster network for different phases of the experiment.Comment: 20 pages, 4 figures; Systems and Synthetic Biology 5 (2011

Effect of Penetrating Keratoplasty and Keratoprosthesis Implantation on the Posterior Segment of the Eye

Purpose To compare the effects of post-penetrating keratoplasty (PK) and post-keratoprosthesis (KPro) surgery-related inflammation on the posterior segment of the eye and to assess inhibition of tumor necrosis factor alpha (TNFα) and interleukin-1 beta (IL-1β) on these effects. Methods: BALB/C (syngeneic) or C57BL/6 (allogeneic) corneas were transplanted onto BALB/C host beds as part of PK or miniature KPro (m-KPro) implantation. Intraocular pressure (IOP) was measured via an intracameral pressure sensor; tissues were harvested and analyzed 8 weeks after surgery. Expression of TNFα and IL-1β in the retina was analyzed using real-time quantitative (q)PCR. Optic nerve degeneration (axon count, circularity, and area) was assessed quantitatively using ImageJ software. After m-KPro implantation, mice were treated with saline, anti-TNFα, or anti-IL-1β antibody, and axonal loss was assessed after 10 weeks. Results: Mean IOP was within normal limits in the operated and fellow eyes in all groups. The mRNA expression of TNFα and IL-1β was highest in m-KPro groups with either syngeneic or an allogeneic carrier. We observed optic nerve degeneration in both allogeneic PK and m-KPro implanted eyes with an allogeneic carrier. However, TNFα blockade significantly reduced axonal loss by 35%. Conclusions: Allogeneic PK and m-KPro implants with an allogeneic carrier lead to chronic inflammation in the posterior segment of the eye, resulting in optic nerve degeneration. In addition, blockade of TNFα prevents axonal degeneration in this preclinical model of allogeneic m-KPro (alloKPro) implantation

Effect of Penetrating Keratoplasty and Keratoprosthesis Implantation on the Posterior Segment of the Eye

Citation:Črnej A, Omoto M, Dohlman TH, et al. Effect of penetrating keratoplasty and keratoprosthesis implantation on the posterior segment of the eye. Invest Ophthalmol Vis Sci. 2016;57:164357: -164857: . DOI:10.1167 PURPOSE. To compare the effects of post-penetrating keratoplasty (PK) and post-keratoprosthesis (KPro) surgery-related inflammation on the posterior segment of the eye and to assess inhibition of tumor necrosis factor alpha (TNFa) and interleukin-1 beta (IL-1b) on these effects. METHODS. BALB/C (syngeneic) or C57BL/6 (allogeneic) corneas were transplanted onto BALB/ C host beds as part of PK or miniature KPro (m-KPro) implantation. Intraocular pressure (IOP) was measured via an intracameral pressure sensor; tissues were harvested and analyzed 8 weeks after surgery. Expression of TNFa and IL-1b in the retina was analyzed using real-time quantitative (q)PCR. Optic nerve degeneration (axon count, circularity, and area) was assessed quantitatively using ImageJ software. After m-KPro implantation, mice were treated with saline, anti-TNFa, or anti-IL-1b antibody, and axonal loss was assessed after 10 weeks. RESULTS. Mean IOP was within normal limits in the operated and fellow eyes in all groups. The mRNA expression of TNFa and IL-1b was highest in m-KPro groups with either syngeneic or an allogeneic carrier. We observed optic nerve degeneration in both allogeneic PK and mKPro implanted eyes with an allogeneic carrier. However, TNFa blockade significantly reduced axonal loss by 35%. CONCLUSIONS. Allogeneic PK and m-KPro implants with an allogeneic carrier lead to chronic inflammation in the posterior segment of the eye, resulting in optic nerve degeneration. In addition, blockade of TNFa prevents axonal degeneration in this preclinical model of allogeneic m-KPro (alloKPro) implantation

A role for CD47 in the development of experimental colitis mediated by SIRPα+CD103− dendritic cells

Mesenteric lymph node (mLN) CD103 (αE integrin)+ dendritic cells (DCs) induce regulatory T cells and gut tolerance. However, the function of intestinal CD103− DCs remains to be clarified. CD47 is the ligand of signal regulatory protein α (SIRPα) and promotes SIRPα+ myeloid cell migration. We first show that mucosal CD103− DCs selectively express SIRPα and that their frequency was augmented in the lamina propria and mLNs of mice that developed Th17-biased colitis in response to trinitrobenzene sulfonic acid. In contrast, the percentage of SIRPα+CD103− DCs and Th17 responses were decreased in CD47-deficient (CD47 knockout [KO]) mice, which remained protected from colitis. We next demonstrate that transferring wild-type (WT), but not CD47 KO, SIRPα+CD103− DCs in CD47 KO mice elicited severe Th17-associated wasting disease. CD47 expression was required on the SIRPα+CD103− DCs for efficient trafficking to mLNs in vivo, whereas it was dispensable on both DCs and T cells for Th17 polarization in vitro. Finally, administration of a CD47-Fc molecule resulted in reduced SIRPα+CD103− DC–mediated Th17 responses and the protection of WT mice from colitis. We thus propose SIRPα+CD103− DCs as a pathogenic DC subset that drives Th17-biased responses and colitis, and the CD47–SIRPα axis as a potential therapeutic target for inflammatory bowel disease