Fig. 4 Topical application of SAAP-148 ointment eradicates acute and established infections of MRSA and A. baumannii from the skin. Topical application.

Slides:



Advertisements
Similar presentations
Figure 1. Blue light inactivation of Acinetobacter baumannii and keratinocytes in vitro. Bars denote SDs. From: Antimicrobial Blue Light Therapy for Multidrug-Resistant.
Advertisements

Fig. 1 CSF1 is increased in blood of melanoma patients and correlates with disease progression. CSF1 is increased in blood of melanoma patients and correlates.
Fig. 1. TP is highly expressed in myeloma.
Fig. 2. LUM015 fluorescently labels tumor cells in mouse models of STS and breast cancer. LUM015 fluorescently labels tumor cells in mouse models of STS.
Fig. 6. AZD6738 induces DNA damage and apoptosis and exhibits antitumor efficacy in xenograft models of high-risk medulloblastoma and neuroblastoma. AZD6738.
Fig. 2. Bestatin treatment improves tail anatomy and restores lymphatic function. Bestatin treatment improves tail anatomy and restores lymphatic function.
Fig. 8. Gene and protein changes in ALK-dependent STING pathways in human sepsis. Gene and protein changes in ALK-dependent STING pathways in human sepsis.
Fig. 5. Correlation of tail and long bone growth velocities with Cxm serum concentrations in mice. Correlation of tail and long bone growth velocities.
Fig. 2. VEGF-C/VEGFR-3 signaling increases responsiveness of melanoma to immunotherapy. VEGF-C/VEGFR-3 signaling increases responsiveness of melanoma to.
In vivo prophylactic and therapeutic efficacy of C12G6 in mice
Fig. 6. Combinatorial VCPI and OV M1 treatment is efficacious in vivo and ex vivo. Combinatorial VCPI and OV M1 treatment is efficacious in vivo and ex.
Fig. 6. Treatment with a DLK inhibitor is neuroprotective and reverses stress-induced gene expression changes. Treatment with a DLK inhibitor is neuroprotective.
Fig. 5. Prophylactic treatment with GS-5734 reduces SARS-CoV disease.
Fig. 1. Schematic representation of the MANO method.
Fig. 6. N95BA5 biocompatibility beyond intended use frame.
Fig. 8. In vivo suppression of MM by CMLD
Fig. 1 pDCs infiltrate the skin of SSc patients and spontaneously secrete IFN-α and CXCL4. pDCs infiltrate the skin of SSc patients and spontaneously secrete.
Fig. 4. Prion infectivity of skin samples from sCJD patients.
Fig. 8. mRIPO elicits neutrophil influx followed by DC and T cell infiltration into tumors. mRIPO elicits neutrophil influx followed by DC and T cell infiltration.
Fig. 2. GPC3 expression in normal and tumor tissues.
Fig. 5. Antitumor efficacy of ERY974 in immunocompetent human CD3 transgenic mice. Antitumor efficacy of ERY974 in immunocompetent human CD3 transgenic.
Fig. 3. Paclitaxel promotes TMEM-dependent vascular permeability, cancer cell dissemination, and metastasis in breast cancer. Paclitaxel promotes TMEM-dependent.
Fig. 1. Paclitaxel delays tumor growth and promotes infiltration of TIE2hi/VEGFhi macrophages and TMEM assembly. Paclitaxel delays tumor growth and promotes.
Expression of CD36 and psap in a TMA of human ovarian cancer patients
Fig. 5 A competent Fc is required for the antitumor immune response.
Fig. 4. In vivo analysis of slpA mutant in the Syrian Golden hamster.
Fig. 4. Antitumor efficacy of ERY974 against various cancer types.
Fig. 7 Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors. Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors.
Neutrophil antifungal response in CCR2-depleted mice is rescued by adoptive transfer of CCR2+ monocytes or by treatment with recombinant IFNs. Neutrophil.
Fig. 2 STED microscopy of isolated cardiomyocytes from mice treated with MP-rhodamine–loaded CaPs. STED microscopy of isolated cardiomyocytes from mice.
Fig. 7 pDCs are critical for the maintenance of skin fibrosis and for the presence of CXCL4 in the skin. pDCs are critical for the maintenance of skin.
Fig. 2 L. lactis–derived lactic acid antagonizes V
Fig. 2. Best model fits. Best model fits. Illustration of the best model fits for the (A) basic, (B) continuous, and (C) cluster models. See Table 1 and.
Fig. 8 TLR8 exacerbates disease in the BLM-induced fibrosis model.
Fig. 6 pDCs infiltrate the skin of BLM-treated mice, and their depletion attenuates skin fibrosis. pDCs infiltrate the skin of BLM-treated mice, and their.
Fig. 3 In situ vaccination with CpG and anti-OX40 is therapeutic in a spontaneous tumor model. In situ vaccination with CpG and anti-OX40 is therapeutic.
Fig. 7 BRD0705 impairs colony formation in AML cell lines and patient cells and shows in vivo efficacy in multiple AML mouse models. BRD0705 impairs colony.
Fig. 4 DMF enhances VSVΔ51 therapeutic efficacy in syngeneic and xenograft tumor models. DMF enhances VSVΔ51 therapeutic efficacy in syngeneic and xenograft.
Fig. 5 EGFR mutation status of patients with NSCLC, detected by histological examination and ARMS PCR. EGFR mutation status of patients with NSCLC, detected.
The TGF-β pathway is activated in the skin after C
Fig. 1. Map showing the study catchment area in the East of England.
Fig. 5 Local gel scaffold for T cell memory response.
Fig. 4. Improved tumor response to docetaxel in TNBC and trastuzumab in HER2-amplified PDX models with the addition of S Improved tumor response.
Fig. 8 SQLE inhibitor terbinafine suppresses NAFLD-HCC growth in vitro and in vivo. SQLE inhibitor terbinafine suppresses NAFLD-HCC growth in vitro and.
Comparison of therapeutic efficacies of C12G6 and other bnAbs in mice
HECTD2 knockdown ameliorates Pseudomonas-induced lung injury in vivo
Fig. 2 Analysis of CLL lymph nodes.
PAAND is driven by local inflammasome activation and IL-1β production
Fig. 3. TKI sensitivity assessed by the MANO method.
Fig. 4. The effect of single-dose rozanolixizumab on the concentration of IgG subtypes in healthy subjects. The effect of single-dose rozanolixizumab on.
Fig. 4. Efficacy of C12G6 compared with and in combination with oseltamivir in mice. Efficacy of C12G6 compared with and in combination with oseltamivir.
CD facilitates RCT in vivo and promotes urinary cholesterol excretion
Fig. 3 Agonists of innate immunity are effective only when released locally from the hydrogel. Agonists of innate immunity are effective only when released.
Fig. 4 Surgery initiates a systemic inflammatory response that triggers the outgrowth of distant immunogenic tumors and can be inhibited by perioperative.
Fig. 7 Analysis of the bacterial nidus within tissue abscesses by MALDI IMS demonstrates a paucity of calprotectin signal. Analysis of the bacterial nidus.
Fig. 1. Exposure to P. duboscqi uninfected sand flies (USFs) induces an anti-saliva immunity that protects NHP from vector-transmitted CL. Exposure to.
IIV induces CD21hiCD27+ and CD21loCD27+ influenza-specific B cells
Fig. 4. Clearance of 12-mer-1 from a nonhuman primate model.
Fig. 5 Metarrestin treatment induces nucleolar structure changes.
Fig. 4 cTFH1 cells correlate with a boosting of influenza-specific memory B cells. cTFH1 cells correlate with a boosting of influenza-specific memory B.
Fig. 1 Neutrophils derived from patients with MPNs are associated with an increase in NET formation and a prothrombotic, NET-rich phenotype. Neutrophils.
Fig. 3. Phenotypic characterization of FM2.5.
Fig. 2. CD treatment facilitates regression of murine atherosclerosis.
Fig. 6. Nontaxane chemotherapies induce TMEM-dependent prometastatic changes in the breast cancer microenvironment. Nontaxane chemotherapies induce TMEM-dependent.
Vaccine MN confer protective innate and adaptive immunity.
HECTD2 knockdown ameliorates Pseudomonas-induced lung injury in vivo
Fig. 4. Paclitaxel promotes the expression of invasive isoforms of MENA in the primary breast cancer microenvironment. Paclitaxel promotes the expression.
Neutrophil antifungal response in CCR2-depleted mice is rescued by adoptive transfer of CCR2+ monocytes or by treatment with recombinant IFNs. Neutrophil.
In vivo prophylactic and therapeutic efficacy of C12G6 in mice
Fig. 3. Paclitaxel promotes TMEM-dependent vascular permeability, cancer cell dissemination, and metastasis in breast cancer. Paclitaxel promotes TMEM-dependent.
Presentation transcript:

Fig. 4 Topical application of SAAP-148 ointment eradicates acute and established infections of MRSA and A. baumannii from the skin. Topical application of SAAP-148 ointment eradicates acute and established infections of MRSA and A. baumannii from the skin. (A to F) Ex vivo wounded human skin (A to C) and in vivo abraded murine skin (D to F) were inoculated with MRSA LUH14616 (gray circles) or A. baumannii RUH875 (black circles). Ten minutes after inoculation (D) or 1 hour (A), 24 hours (C and E), or 48 hours (F) after inoculation, the skin was treated with ointments containing no peptide (vehicle) or 0.125, 0.5, or 2% (w/w) SAAP-148 ointment. Results are expressed as the numbers of viable bacteria (in log10 CFU) per skin model of three to six donors and of 16 skin samples for each group of mice (eight mice per group and two skin samples per mouse). Each circle represents one skin sample, and bars indicate medians. *, significantly different (*P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001) as compared to the vehicle, as calculated using the Mann-Whitney rank sum test. (B) Light micrographs of hematoxylin and eosin–stained skin biopsies 24 hours after inoculation with MRSA and A. baumannii and subsequent vehicle treatment. Arrows indicate biofilm formation, which is shown at a higher magnification in the inset. Anna de Breij et al., Sci Transl Med 2018;10:eaan4044 Published by AAAS