Automated Algorithm for GI Spike Burst Detection and Demonstration of Efficacy in Ischemic Small Intestine

We present a novel, fully-automated gastrointestinal spike burst detection algorithm. Following pre-processing with SALPA (Wagenaar and Potter, J. Neurosci. Methods 120:113–120, 2002) and a Savitzky–Golay filter to remove unwanted low and high frequency components, candidate spike waveforms are detected utilizing the non-linear energy operator. Candidate waveforms are classified as spikes or artifact by a support vector machine. The new method achieves highly satisfactory performance with >90% sensitivity and positive prediction value. We also demonstrate an application of the new method to detect changes in spike rate and spatial propagation patterns upon induction of mesenteric ischemia in the small intestine. Spike rates were observed to transiently increase 10–20 fold for a duration of ≈600 s, relative to baseline conditions. In ischemic conditions, spike activity propagation patterns included retrograde-longitudinal wavefronts with occasional spontaneous conduction blocks, as well as self-terminating concentric-circumferential wavefronts. Longitudinal and circumferential velocities were 6.8–8.0 cm/s and 18.7 cm/s, respectively.     

Biofilm and cell adhesion strength on dental implant surfaces via the laser spallation technique

ObjectiveThe aims of this study are to quantify the adhesion strength differential between an oral bacterial biofilm and an osteoblast-like cell monolayer to a dental implant-simulant surface and develop a metric that quantifies the biocompatible effect of implant surfaces on bacterial and cell adhesion.MethodsHigh-amplitude short-duration stress waves generated by laser pulse absorption are used to spall bacteria and cells from titanium substrates. By carefully controlling laser fluence and calibration of laser fluence with applied stress, the adhesion difference between Streptococcus mutans biofilms and MG 63 osteoblast-like cell monolayers on smooth and rough titanium substrates is obtained. The ratio of cell adhesion strength to biofilm adhesion strength (i.e., Adhesion Index) is determined as a nondimensionalized parameter for biocompatibility assessment.ResultsAdhesion strength of 143 MPa, with a 95% C.I. (114, 176), is measured for MG 63 cells on smooth titanium and 292 MPa, with a 95% C.I. (267, 306), on roughened titanium. Adhesion strength for S. mutans on smooth titanium is 320 MPa, with a 95% C.I. (304, 333), and remained relatively constant at 332 MPa, with a 95% C.I. (324, 343), on roughened titanium. The calculated Adhesion Index for smooth titanium is 0.451, with a 95% C.I. (0.267, 0.622), which increased to 0.876, with a 95% C.I. (0.780, 0.932), on roughened titanium.SignificanceThe laser spallation technique provides a platform to examine the tradeoffs of adhesion modulators on both biofilm and cell adhesion. This tradeoff is characterized by the Adhesion Index, which is proposed to aid biocompatibility screening and could help improve implantation outcomes. The Adhesion Index is implemented to determine surface factors that promote favorable adhesion of cells greater than biofilms. Here, an Adhesion Index ? 1 suggests favorable biocompatibility.     

Comparison of filtering methods for extracellular gastric slow wave recordings

Background  Extracellular recordings are used to define gastric slow wave propagation. Signal filtering is a key step in the analysis and interpretation of extracellular slow wave data; however, there is controversy and uncertainty regarding the appropriate filtering settings. This study investigated the effect of various standard filters on the morphology and measurement of extracellular gastric slow waves. Methods  Experimental extracellular gastric slow waves were recorded from the serosal surface of the stomach from pigs and humans. Four digital filters: finite impulse response filter (0.05–1 Hz); Savitzky‐Golay filter (0–1.98 Hz); Bessel filter (2–100 Hz); and Butterworth filter (5–100 Hz); were applied on extracellular gastric slow wave signals to compare the changes temporally (morphology of the signal) and spectrally (signals in the frequency domain). Key Results  The extracellular slow wave activity is represented in the frequency domain by a dominant frequency and its associated harmonics in diminishing power. Optimal filters apply cutoff frequencies consistent with the dominant slow wave frequency (3–5 cpm) and main harmonics (up to ～2 Hz). Applying filters with cutoff frequencies above or below the dominant and harmonic frequencies was found to distort or eliminate slow wave signal content. Conclusions & Inferences  Investigators must be cognizant of these optimal filtering practices when detecting, analyzing, and interpreting extracellular slow wave recordings. The use of frequency domain analysis is important for identifying the dominant and harmonics of the signal of interest. Capturing the dominant frequency and major harmonics of slow wave is crucial for accurate representation of slow wave activity in the time domain. Standardized filter settings should be determined.     

Estradiol activates mast cells via a non-genomic estrogen receptor-alpha and calcium influx

BACKGROUND: Allergic airway diseases are more common in females than in males during early adulthood. A relationship between female hormones and asthma prevalence and severity has been suggested, but the cellular and molecular mechanisms are not understood. OBJECTIVE: To elucidate the mechanism(s) by which estrogens enhance the synthesis and release of mediators of acute hypersensitivity. METHODS: Two mast cell/basophil cell lines (RBL-2H3 and HMC-1) and primary cultures of bone marrow derived mast cells, all of which naturally express estrogen receptor-alpha, were examined. Cells were incubated with physiological concentrations of 17-beta-estradiol with and without IgE and allergens. Intracellular Ca(2+) concentrations and the release of beta-hexosaminidase and leukotriene C(4) were quantified. RESULTS: Estradiol alone induced partial release of the preformed, granular protein beta-hexosaminidase from RBL-2H3, BMMC and HMC-1, but not from BMMC derived from estrogen receptor-alpha knock-out mice. The newly synthesized LTC(4) was also released from RBL-2H3. Estradiol also enhanced IgE-induced degranulation and potentiated LTC(4) production. Intracellular Ca(2+) concentration increased prior to and in parallel with mediator release. Estrogen receptor antagonists or Ca(2+) chelation inhibited these estrogenic effects. CONCLUSION: Binding of physiological concentrations of estradiol to a membrane estrogen receptor-alpha initiates a rapid onset and progressive influx of extracellular Ca(2+), which supports the synthesis and release of allergic mediators. Estradiol also enhances IgE-dependent mast cell activation, resulting in a shift of the allergen dose response.