Infections caused by Cunninghamella bertholletiae, an opportunistic fungal organism, have an extremely high mortality rate. A fatal case of C. bertholletiae fungal pneumonia occurred in a man who had received an allogeneic bone marrow transplant. Aggressive debridement and high-dose liposomal amphotericin B failed to eradicate the infection. Right lung tissue samples obtained during lobectomy were assayed for amphotericin B concentrations by high-performance liquid chromatography, and minimum inhibitory concentration (MIC) determinations of amphotericin B against C. bertholletiae were determined by the macrobroth dilution method. The MIC for the isolate of C. bertholletiae was 4 microg/ml. Amphotericin B lung concentrations averaged 9.5 microg/ml (range 3.7-13.8 microg/ml), with a corresponding serum trough concentration of 0.9 microg/ml. To our knowledge, this is the first reported case of amphotericin B concentrations measured at the site of infection in a patient with a pulmonary Cunninghamella infection, together with a corresponding MIC of the organism. The patient's death, which occurred despite aggressive debridement and high amphotericin B lung concentrations, highlights the need for novel strategies to treat infections caused by invasive molds such as C. bertholletiae.
The purpose of this study was to determine the levels of calprotectin and lactoferrin, 2 microbiostatic proteins, in the gingival crevicular fluid (GCF) of normal children. The children represented a population, primarily underprivileged, seeking care at a regional dental health care center. GCF was collected from Ramfjord teeth (or their deciduous equivalent). GCF volume was quantified by conductance. Calprotectin and lactoferrin levels were quantified by sandwich ELISA, and found to have a mean value of 70.8 ± 94.2 μg/mL and 68.2 ± 108.7 μg/mL, respectively. The levels of calprotectin and lactoferrin varied directly with one another and inversely with the amount of fluid obtained in a 20‐second sampling period. The mean levels were at or above the minimum inhibitory concentration determined in vitro. J Periodontol 1998;69:879–883.
Protegrins are broad spectrum antibiotic peptides isolated from porcine leukocytes. In this study, we (i) examine the sensitivity of Gram‐negative, anaerobic periodontal pathogens to synthetic protegrins; (ii) determine the relative potencies of protegrin congeners against these bacteria; and (iii) compare the potency of protegrins with other antibiotic peptides, including magainin MSI‐78, tachyplesin I, cecropin P1, human defensins HNP‐1‐3, and clavanin A. Synthetic l‐ and d‐enantiomers of protegrin 1 (PG‐1 and D‐PG‐1, respectively), and L‐enantiomers of protegrins 2, 3 and 5 (PG‐2, PG‐3 and PG‐5) were tested against Fusobacteriurn nucleatum, and black‐pigmented organisms including Porphyromonas gingivalis and Prevotella intermedia. Strains of both F. nucleatum and the black‐pigmented organisms were sensitive to PG‐1, and exhibited mean ED99 of 2.2‐2.3 μg/ml and 3.4‐9.9 μg/ml, respectively. The D‐form was statistically more potent than the L‐form against these oral anaerobes, and although this difference in potency is unlikely to be of decisive therapeutic significance, the d‐form may be of value given ability to resist microbial and host‐derived proteases. PG‐1 was more potent than magainin, tachyplesin, cecropin, defensins and clavanin under test conditions. Hypertonic saIt concentrations and heat‐inactivated serum were found to be inhibitory to the bactericidal activity of PG‐1. PG‐1 was found to induce morphologic alterations in the ultrastructural appearance of F. nucleatum consistent with damage to the bacterial membranes. We conclude that protegrins may be useful antimicrobial agents in therapy against Gram‐negative anaerobic bacteria believed to be involved in chronic, adult forms of periodontal infections.
The drought and salinity intrusion in the Mekong Delta in the years has become more and more serious, but in this region, the system automatically measures and collects water salinity data at either the river mouths or the canal has not been deployed and used widely due to the high investment cost. The goal of this study is to design a monitoring and data acquisition on river water salinity based on the IoT (Internet of Things) technology. The sensor nodes are designed by using the Texas Instruments MSP432 microcontrollers to read data from sensors such as water level, temperature, and salinity. This information is encapsulated and then send to a gateway via a LoRa network. The gateway uses the Raspberry Pi 3 B+ board allowing to receive the data from the sensor nodes and upload data to the cloud server through the Internet connection. A webpage is designed to offer everyone to observe measured parameters rapidly so that the people can take a proactive plan to take water for domestic use and production activities. An experiment to evaluate the performance of our proposed system was carried out in Soc Trang province, Mekong Delta, Vietnam with initial positive results.
Increasing evidence supports the systemic inflammatory nature of atopic dermatitis (AD), but data has been based on studies in adults with decades of chronic disease. No studies have sought systemic inflammation in early AD, although 85% of cases begin before 5 years of age. Using a high-throughput proteomic platform (OLINK), we assessed 257 inflammatory and cardiovascular risk proteins in the serum of 30 children with moderate-to-severe AD < 5 years of age and within 6 months of disease onset, compared to age-matched controls (n¼20). As in studies of skin mRNA expression, Th2 (CCL13, CCL22, IL-13) and Th17 (PI3, S100A12) markers were increased compared to controls (p < 0.05). We also found increases in markers of tissue remodelling (MMP3/9/10), T-cell activation (CD5, IL2RA), lipid metabolism (FABP4), and growth factors (FGF21, TGF-alpha, PDGF). Positive correlations with disease severity/ SCORAD were detected with inflammatory markers (e.g. vascular activation marker E-selectin, heat shock protein 27, KLK6, IL1RT2; p < 0.05) and inverse correlations with Th1 markers (IFNg, CXCL11). The blood profile of early pediatric AD shows Th2/Th17 proteomic skewing, attesting to systemic alterations within months of onset and suggesting the need for more aggressive intervention before disease chronicity. The negative correlation of severity with Th1 markers may explain the propensity to infections in pediatric AD.
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