Nonopioid analgesics shorten the duration of postoperative ileus

Morphine inhibits propagating and stimulates nonpropagating colon contractions in monkeys and humans. The use of morphine or other opioids that inhibit propulsive contractions prolongs postoperative ileus. In contrast, ketorolac tromethamine, a nonsteroidal analgesic, has no effect on colon contractions in monkeys. In 14 patients having elective abdominal operations, bipolar electrodes were implanted on the right (n = 13) and left (n = 10) colon. Group A (n = 8) received ketorolac, 30 mg IM q6h, for pain relief. Group B (n = 6) needed supplemental morphine, 2-10 mg IV or IM, plus ketorolac to control their pain. Myoelectric activity was recorded from each subject on postop Days 1-5 and analyzed by computer for electrical control activity (ECA), short and long electrical response activity (ERA), and propagation of long ERA. There was a difference between the two groups in return of propagated long ERA bursts that correlated with clinical recovery from postoperative ileus. Postoperative analgesia with ketorolac resulted in faster resolution of ileus compared to morphine plus ketorolac because opioid-induced motor abnormalities in the colon were avoided.     

Time reversal terahertz imaging

We describe a technique for imaging in the terahertz regime using time reversal of single-cycle pulses. Specifically, the time-reversal symmetry of Maxwell's wave equation is exploited to reconstruct the transmission function of a diffracting aperture by inverting the diffracted fields. After deriving a time-reversed form of the Huygens-Fresnel diffraction integral, we demonstrate through simulation and experiment the reconstruction of one-dimensional and two-dimensional (2-D) objects. A means to obtain data efficiently for reconstruction of 2-D apertures is described. The spatial resolution determined by the Sparrow criterion is found to correspond to approximately 30% of the peak wavelength and 85% of the mean wavelength of the power spectrum of the single-cycle waveform. Finally, the modulation transfer function for the imaging method is simulated and is shown to be nearly diffraction-limited when compared to an ideal imaging system.     

In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces genital dysmorphogenesis in the female rat

Recently, Gray and Ostby (Toxicol. Appl. Pharmacol. 133, 285-294, 1995) reported that in utero and lactational TCDD exposure causes striking abnormalities in the rat female reproductive system, including reduced fecundity and vaginal threads. The mechanism by which TCDD induces such abnormalities is unknown. Thus, we sought to determine: (1) whether TCDD reduced fecundity by destroying ovarian follicles and (2) whether the vaginal threads resulted from a TCDD-induced developmental defect during embryogenesis or abnormal vaginal opening at puberty. Pregnant Holtzman rats were treated with 1.0 microgram TCDD/kg or vehicle by a single oral dose on gestation day (GD) 11, 15, or 18. Female offspring were monitored for vaginal opening and terminated on postnatal days 2, 21, and 42. The reproductive tract was removed and evaluated for structural abnormalities. The number of primordial follicles also was determined for each ovary. TCDD exposure on GD 11, 15, or 18 did not change the day of vaginal opening, affect ovarian morphology, or reduce the number of primordial follicles. However, this exposure induced the cleft clitoris and vaginal thread originally described by Gray and Ostby (1995) in approximately 55-96% and 36-44% of the litters in our study, respectively. Histologically the thread presented as a thick cord of mesenchyme surrounded by epithelial cells. This defect was clearly visible in histological sections at birth and was noted in the closed vaginas of prepubertal animals. These data suggest that in utero and lactational exposure to TCDD does not reduce the size of the primordial follicle pool; however, it induces developmental abnormalities in the vaginal canal.     

Diagnosing neurofibromatosis type I in children

Neurofibromatosis is the single most common genetic disease of the neurologic system. Because neurofibromatosis type 1 (NF-1) is often diagnosed early in life, it is essential that health care providers deepen their understanding of this common genetic disorder. Children who meet particular criteria, as formulated by the National Institutes of Health, must be worked-up for NF-1 in order to initiate appropriate treatment implementation and evaluation. This article provides a review of the literature regarding the pathophysiology, clinical manifestations, and plan of treatment related to NF-1, specifically as it affects children. Clear guidelines for health care providers in primary care are outlined.     

Extent of radial sarcomere coupling revealed in passively stretched cardiac myocytes

We report a simple method, the PinPoint assay, for detecting and identifying single-base variations (polymorphisms) at specific locations within DNA sequences. An oligonucleotide primer is annealed to the target DNA immediately upstream of the polymorphic site and is extended by a single base in the presence of all four dideoxynucleotide triphosphates and a thermostable DNA polymerase. The extension products are desalted, concentrated, and subjected to delayed-extraction MALDI-TOF mass spectrometry. The base at the polymorphic site is identified by the mass added onto the primer. Heterozygous targets produce two mass-resolved species that represent the addition of both bases complementary to those at the polymorphic site. The assay is suitable for double-stranded PCR products without purification or strand separation. More than one primer can be simultaneously extended and then mass-analyzed. The mass spectrometric method thus shows promise for high-volume diagnostic or genotyping applications.