A peptidic network antibody inhibits both angiogenesis and inflammatory response.

Corneal neovascularization (CNV) is a global threat to human health. Traditional anti-angiogenesis agent may have therapy effect, while the inflammation in disease area remains unsolved. Herein, we reported two binding-induced fibrillogenesis (BIF) peptides as peptidic network antibodies for high-efficient and long-lasting anti-angiogenesis with reduced inflammatory response. BIF peptides could self-assemble into nanoparticles and further perform BIF behavior through binding Ca2+. In vitro, the migration of integrin αvß3 highly expressed endothelial cells was inhibited by BIF peptides. In vivo, one BIF peptide (0.012 mg/Kg) exhibited higher anti-angiogenesis effect than monoclonal antibody bevacizumab (0.96 mg/Kg) in a CNV rabbit model on day 14, despite that the dose of BIF was only 1.3% of bevacizumab. Meanwhile, the inflammatory response, such as PI3 kinase/Akt pathway in CNV was successfully inhibited as well. The peptidic network antibody could block integrin αvß3 via a long-term retention mode, which led to long-term therapeutic effect. The study provides BIF peptides as promising therapeutic agents for both anti-angiogenesis and reduced inflammatory response.

An intelligent peptide recognizes and traps Mycobacterium tuberculosis to inhibit macrophage phagocytosis.

Tuberculosis is a major public health concern worldwide, and it is a serious threat to human health for a long period. Macrophage phagocytosis of Mycobacterium tuberculosis (M. tuberculosis) is a crucial process for granuloma formation, which shelters the bacteria and gives them an opportunity for re-activation and spread. Herein, we report an intelligent anti-microbial peptide that can recognize and trap the M. tuberculosis, inhibiting the macrophage phagocytosis process. The peptide (Bis-Pyrene-KLVFF-WHSGTPH, in abbreviation as BFH) first self-assembles into nanoparticles, and then forms nanofibers upon recognizing and binding M. tuberculosis. Subsequently, BFH traps M. tuberculosis by the in situ formed nanofibrous networks and the trapped M. tuberculosis are unable to invade host cells (macrophages). The intelligent anti-microbial peptide can significantly inhibit the phagocytosis of M. tuberculosis by macrophages, thereby providing a favorable theoretical basis for inhibiting the formation of tuberculosis granulomas.

Smart Peptide Defense Web In Situ Connects for Continuous Interception of IgE against Allergic Rhinitis.

Allergic rhinitis (AR) is a chronic inflammatory reaction by immunoglobulin E (IgE) mediators after individual contact with allergens. It affects 10-40% of the world's population and reduces the quality of life. Long-term symptoms of rhinitis can cause inflammation to spread and trigger asthma, which can harm human health. Herein, we develop a Smart PeptIde defeNse (SPIN) web technique, which in situ constructs a peptide web, trapping IgE against AR. Two candidate SPINs, SPIN-1 and SPIN-2, are designed with different IgE-binding sequences. The SPIN-1 or SPIN-2 is able to bind to IgE and transform from nanoparticles into entangled nanofibers. In turn, the web of SPIN-1 or SPIN-2 acts as a long-term trap of IgE to prevent the IgE from binding to mast cells. SPIN-1 or SPIN-2 (10 mg/kg) is able to treat AR model Balb/c mice with high efficiency and reduced symptoms of rhinitis and inflammatory factors, even better than a first-line clinical drug, cetirizine (10 mg/kg). For example, the amount of IL-4 released in the AR group (185.5 ± 6.8 pg/mL) is significantly reduced after the treatment with SPIN-1 (70.4 ± 14.1 pg/mL), SPIN-2 (86.0 ± 9.3 pg/mL), or cetirizine (112.8 ± 19.3 pg/mL). More importantly, compared with the cetirizine group (1 day), the SPIN-1 or SPIN-2 group shows long-term therapeutic effects (1 week). The SPIN web technique shows the great potential for blocking IgE binding to mast cells in vivo, attenuating AR or other allergic reactions.

[Functional activity mapping during anticipation of dental pain].

OBJECTIVE: To reveal functional activity mapping during anticipation of dental pain with non-invasive fMRI technique, and to offer therapeutic possibilities for treating chronic oral facial pain psychologically. METHODS: 8 right handed patients with dentinalgia of the right maxillary bicuspid were included in this study. Block design was adopted, BOLD level during anticipation epoch (on) was contrasted with that of rest (off). Functional MRI scan covering the whole brain was carried out. The fMRI data were analyzed by SPM2 software with t-test to generate the activation map. RESULTS: Increased BOLD signals during dental pain anticipation were found dominantly on the left side in inferior, middle frontal gyrus/BA10,46, postcentral gyrus/BA2,3, middle frontal gyrus/BA8, precentral gyrus/BA44 and cerebellum. CONCLUSION: Anticipation of dental pain by itself can activate brain regions, especially prefrontal areas, SI, SMA and cerebellum. The results of pain anticipation are consisted with previous studies except that there is no activation in insula and cingulate cortex. Sensory, motor, cognitive and emotional activation in dental pain anticipation may indicate that brain nociceptive network can be affected by hint.

[Neuronal activities related to right-sided mastication detected with functional magnetic resonance imaging].

OBJECTIVE: To observe neuronal activities related to right-sided mastication in cortex and to explore the effect of mastication on brain function. METHODS: Neuronal activities related to right-sided mastication were detected with functional magnetic resonance imaging in 10 healthy volunteers. Image data was analyzed by SPM99 software with the use of t test. RESULTS: Localization of activation in brain was different among subjects. Brain activation during mastication included left basal ganglion, Broca's area, angular gyrus and right supramarginal gyrus. CONCLUSIONS: The functional areas related to right-sided mastication and speech were closely connected, which indicated close relationship between mastication and speech. The central control of mastication might share part of common neural mechanism with that of speech. The roles of activated brain regions in mastication still remained to be elucidated.