Assessment of Sea-Surface Wind Retrieval from C-Band Miniaturized SAR Imagery.

Synthetic aperture radar (SAR) has been widely used for observing sea-surface wind fields (SSWFs), with many scholars having evaluated the performance of SAR in SSWF retrieval. Due to the large systems and high costs of traditional SAR, a tendency towards the development of smaller and more cost-effective SAR systems has emerged. However, to date, there has been no evaluation of the SSWF retrieval performance of miniaturized SAR systems. This study utilized 1053 HiSea-1 and Chaohu-1 miniaturized SAR images covering the Southeast China Sea to retrieve SSWFs. After a quality control procedure, the retrieved winds were subsequently compared with ERA5, buoy, and ASCAT data. The retrieved wind speeds demonstrated root mean square errors (RMSEs) of 2.42 m/s, 1.64 m/s, and 3.29 m/s, respectively, while the mean bias errors (MBEs) were found to be -0.44 m/s, 1.08 m/s, and -1.65 m/s, respectively. Furthermore, the retrieved wind directions exhibited RMSEs of 11.5°, 36.8°, and 41.7°, with corresponding MBEs of -1.3°, 2.4°, and -8.8°, respectively. The results indicate that HiSea-1 and Chaohu-1 SAR satellites have the potential and practicality for SSWF retrieval, validating the technical indicators and performance requirements implemented during the satellites' design phase.

Critical role for αvß6 integrin in enamel biomineralization.

Tooth enamel has the highest degree of biomineralization of all vertebrate hard tissues. During the secretory stage of enamel formation, ameloblasts deposit an extracellular matrix that is in direct contact with the ameloblast plasma membrane. Although it is known that integrins mediate cell-matrix adhesion and regulate cell signaling in most cell types, the receptors that regulate ameloblast adhesion and matrix production are not well characterized. We hypothesized that αvß6 integrin is expressed in ameloblasts where it regulates biomineralization of enamel. Human and mouse ameloblasts were found to express both ß6 integrin mRNA and protein. The maxillary incisors of Itgb6(-/-) mice lacked yellow pigment and their mandibular incisors appeared chalky and rounded. Molars of Itgb6(-/-) mice showed signs of reduced mineralization and severe attrition. The mineral-to-protein ratio in the incisors was significantly reduced in Itgb6(-/-) enamel, mimicking hypomineralized amelogenesis imperfecta. Interestingly, amelogenin-rich extracellular matrix abnormally accumulated between the ameloblast layer of Itgb6(-/-) mouse incisors and the forming enamel surface, and also between ameloblasts. This accumulation was related to increased synthesis of amelogenin, rather than to reduced removal of the matrix proteins. This was confirmed in cultured ameloblast-like cells, in which αvß6 integrin was not an endocytosis receptor for amelogenins, although it participated in cell adhesion on this matrix indirectly via endogenously produced matrix proteins. In summary, integrin αvß6 is expressed by ameloblasts and it plays a crucial role in regulating amelogenin deposition and/or turnover and subsequent enamel biomineralization.

Mice lacking beta6 integrin in skin show accelerated wound repair in dexamethasone impaired wound healing model.

Integrin alphavbeta6 is an epithelial-specific receptor that is absent from the healthy epidermis but synthesized de novo during wound repair. However, its function in wound repair is unknown. Integrin-mediated transforming growth factor-beta1 (TGF-beta1) activation is the main activation mechanism of this key cytokine in vivo. Impaired wound healing caused by glucocorticoids is a major clinical problem and is associated with a disturbed balance of TGF-beta1 activity. Therefore, alphavbeta6 integrin-mediated regulation of TGF-beta1 activity may be involved in this process. To determine the function of alphavbeta6 integrin in glucocorticoid-induced impaired wound healing, both beta6 integrin-deficient (beta6-/-) and wild-type mice were exposed to dexamethasone treatment. Multiple wound parameters, keratinocyte proliferation, inflammation, and TGF-beta1 activation were assessed. Wound healing was significantly accelerated in the dexamethasone-treated beta6-/- mice compared with the corresponding wild-type mice. The dexamethasone-treated beta6-/- mice showed enhanced keratinocyte proliferation in both wound epithelium and hair follicles while the production of proinflammatory cytokines and TGF-beta1 activation were reduced. Accelerated wound repair in the dexamethasone-treated beta6-/- mice might be associated with the reduced antiproliferative and proinflammatory effects of TGF-beta1. Inhibition of alphavbeta6 integrin may provide a future target for treatment of impaired wound healing.

Integrin ß6-deficient mice show enhanced keratinocyte proliferation and retarded hair follicle regression after depilation.

Integrin αvß6 is an epithelial-specific receptor that binds and activates latent transforming growth factor-ß1 (TGF-ß1). TGF-ß1 has been implicated as an endogenous inducer of hair follicle (HF) regression during hair cycling. We hypothesized that αvß6 integrin-mediated TGF-ß1 signaling regulates hair regeneration and HF involution. In wild-type (WT) mice, the expression of integrin αvß6 was strongly upregulated in the outer root sheath (ORS) during early hair regeneration, and was specifically enhanced in the HF bulge region. Expression gradually decreased in late anagen and remained restricted to the bulge region in the catagen and telogen stage HFs. The first spontaneous hair cycle was not altered in ß6 integrin knockout (ß6(-/-)) mice. However, after depilation, ß6(-/-) mice exhibited retarded HF regression compared with WT controls. ß6(-/-) follicles contained significantly higher numbers of proliferating Ki67-positive keratinocytes than WT follicles at an identical cycle stage. The ß6(-/-) follicles also demonstrated significantly reduced levels of TGF-ß1 expression and Smad2 phosphorylation during early anagen and anagen-catagen transition. Our study indicates that αvß6 integrin has an important inhibitory role in keratinocyte proliferation in both HFs and interfollicular epidermis. Thus, downregulated TGF-ß1 signaling in ß6(-/-) mice may affect bulge niche stem cell behavior.