Curr Probl Pediatr Adolesc Health Care
August 2020
Motility of the gut is affected by the nervous system, the endocrine system, smooth muscle cells, interstitial cells of Cajal, secretory mucosal cells, the immune system, and gut flora. Abnormal gastrointestinal motility can generate nonspecific symptom complaints that are refractory to standard treatment approaches. It is important to exclude anatomical obstruction or other causes for patients' symptoms prior to proceeding with motility evaluation.
View Article and Find Full Text PDFAntimicrobial peptides (AMPs) are short, amphipathic peptides that are typically cationic in sequence and display broad-spectrum activity against bacteria, fungi, and protists. Herein, we report the effect of appending the amino terminal copper and nickel binding motif (ATCUN) to Sub5. The Cu-ATCUN derivatives show a two- to three-fold increase in antimicrobial activity for a variety of microbes, relative to Sub5, with MICs as low as 0.
View Article and Find Full Text PDFAntimicrobial peptides are short amphipathic peptides that are produced by the innate immune system in order to protect a host from pathogens. They have been shown to have broad-spectrum antimicrobial activity toward Gram-positive and Gram-negative bacteria, as well as antifungal, antiprotozoan, and antiviral activity. These peptides are able to exert their activity through a variety of mechanisms that include inhibiting DNA and RNA replication, inhibiting protein synthesis, permeabilizing the cell membrane, disrupting proton and ion transmembrane gradients, and inhibiting cell wall biosynthesis.
View Article and Find Full Text PDFAntimicrobial peptides are short peptides secreted by the innate immune system to protect the host from pathogens. We have investigated the influence of the amino terminal copper and nickel binding (ATCUN) motif on derivatives of ovispirin-3 (OV-3), an α-helical peptide from the cathelicidin family, demonstrating an increased antimicrobial activity toward a broad range of bacteria, relative to OV-3, with MICs as low as 1.3 ± 0.
View Article and Find Full Text PDFReplication forks encounter obstacles that must be repaired or bypassed to complete chromosome duplication before cell division. Proteomic analysis of replication forks suggests that the checkpoint and repair machinery travels with unperturbed forks, implying that they are poised to respond to stalling and collapse. However, impaired fork progression still generates aberrations, including repeat copy number instability and chromosome rearrangements.
View Article and Find Full Text PDFRereplication generates double-strand breaks (DSBs) at sites of fork collisions and causes genomic damage, including repeat instability and chromosomal aberrations. However, the primary mechanism used to repair rereplication DSBs varies across different experimental systems. In Drosophila follicle cells, developmentally regulated rereplication is used to amplify six genomic regions, two of which contain genes encoding eggshell proteins.
View Article and Find Full Text PDFReplication origins are under tight regulation to ensure activation occurs only once per cell cycle [1, 2]. Origin re-firing in a single S phase leads to the generation of DNA double-strand breaks (DSBs) and activation of the DNA damage checkpoint [2-7]. If the checkpoint is blocked, cells enter mitosis with partially re-replicated DNA that generates chromosome breaks and fusions [5].
View Article and Find Full Text PDFPyoderma gangrenosum may occur in unusual sites and not be readily recognized. Delays in diagnosis and appropriate treatment may result in extensive ulcerations and scarring. We present two patients with pyoderma gangrenosum involving the breasts after breast operation.
View Article and Find Full Text PDFBackground: Urticarial vasculitis is a form of cutaneous leukocytoclastic vasculitis clinically characterized by persistent and often painful urticarial lesions. Numerous systemic diseases have been associated with urticarial vasculitis, including certain hematologic disorders. This distinctive form of cutaneous necrotizing vasculitis can be resistant to standard therapeutic modalities, necessitating more aggressive intervention.
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