Wireless-capsule diagnostic endoscopy for recurrent small-bowel bleeding.
Explore the source record for details and available documents.
Adolescent↗
Biomedical subjects
A Glukhovsky
Publications and source records attributed to A Glukhovsky.
A randomized trial comparing wireless capsule endoscopy with push enteroscopy for the detection of small-bowel lesions.
BACKGROUND & AIMS: Wireless capsule endoscopy is a new, painless method of imaging the entire small bowel. It has not been compared with push enteroscopy. We compared the sensitivity, specificity, and safety of capsule and push enteroscopy in detecting small-bowel lesions. METHODS: Nine to 13 radiopaque, colored beads (3-6 mm diameter) were sewn in random order inside 9 canine small bowels, half within the first meter, and confirmed on x-ray. After recovery, the number, order, and color of beads were assessed in 23 capsule enteroscopies and 9 push enteroscopies in a random order. The surgeons, push enteroscopists, capsule video interpreters, and pathologist were blinded to the others' findings. RESULTS: The capsules identified more beads than push enteroscopy (median, 6 [range, 2-9] vs. 3 [range, 2-6 beads]; P < 0.001). The sensitivity of the capsule was 64% compared with 37% for push enteroscopy. The specificity was 92% for capsule enteroscopy and 97% for push enteroscopy. The capsules identified significantly more beads beyond the reach of the push enteroscope (median, 4 [range, 2-7] vs. 0; P < 0.0001). Hair, ingested plastic, ulceration, submucosal swelling, and worms were clearly identified by the capsule. The capsules passed safely through the animals with no significant histologic findings. CONCLUSIONS: Wireless capsule endoscopy detected more abnormalities in the small bowel than push enteroscopy.
Animals↗
A model of Ca2+ release from the sarcoplasmic reticulum.
Various functions in the myocyte depend on Ca2+ transport, yet the control of these processes is still obscure. In order to better understand the intracellular Ca2+ processes, a model of Ca2+ release from the cardiac sarcoplasmic reticulum (SR) is suggested, in which the release of Ca2+ from the SR is mainly regulated by the kinetics of Ca2+ channels within the SR membrane. These kinetics are controlled by changes in the concentration of free Ca2+ near the openings of Ca2+ channels, and are affected by Ca2+ competitors, e.g., ryanodine. The control mechanism is based on a combination of positive and negative control loops, associated with two respective types of Ca2+ binding sites located on the SR membrane: 1) activating sites with low affinity to Ca2+ and high binding rate, and 2) inactivating sites with high affinity but low binding rate. The model also assumes that the activation of the Ca2+ channels depends on the preceding stimulation pattern (short term memory), an additional activation mechanism which is Ca2+ independent. This report describes the cytoplasmatic Ca2+ concentration in response to Ca2+ release from the SR, including the dependence on the beat intervals, either in the steady state or during response to premature and delayed beats. The analysis of ryanodine intervention supports a control mechanism based on two feedback loops, and available interval-dependent data favors inclusion of the short-term memory mechanism in the proposed model.
Animals↗
Comparison between single signed integral pulse frequency and sine wave crossing modulation techniques.
The single signed integral pulse frequency modulation (SS-IPFM) is used in modeling neural communication processes. The reference signal crossing and in particular sine wave crossings (SWC) are used to describe physiological processes like vision. Under some restrictions upon the input signal it is possible to define SS-IPFM and SWC systems with identical output for the same modulation input. These restrictions and the exact compositions of the encoders are examined by comparison of both SS-IPFM and SWC to general form of Pulse Position Modulation (PPM) technique.
Cybernetics↗
Mechanism of Ca++ release from the sarcoplasmic reticulum: a computer model.
The proposed model describes myocyte calcium (Ca++) cycling, emphasizing the kinetics of sarcoplasmic reticulum (SR) Ca++ release channels. The suggested SR channel regulating mechanism includes two types of Ca++ binding sites: (1) low affinity sites with high binding rates, regulating the opening of Ca++ channels and (2) high affinity sites with low binding rates, which regulate their closing. The amount of Ca++ released from the SR and the peak value of Ca++ ion concentration [Ca++] in the cytoplasm were found to depend on the rate of the increase of [Ca++], similar to Ca++ induced Ca++ release experiments. The model describes spontaneous release of Ca++ from overloaded SR. The dependence of the control mechanism on the activating and inactivating sites is substantiated by simulations of ryanodine intervention, providing results similar to experimental results. Simulations under conditions of isolated SR vesicles produced Ca++ release results similar to measured data. Consequently, it is suggested that the recovery of Ca++ release channels represents the rate limiting factor in the process of mechanical restitution.
Animals↗