[A rare case of deformity of hyoid bone].
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Biomedical subjects
Publications and source records attributed to J S Han.
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Evidence is presented to show a strong and long-lasting analgesic effect after injection of dynorphin into the subarachnoid space of the spinal cord of the rat. Calculating on a molar basis dynorphin was 6-10 times more potent than morphine and 65-100 times more potent than morphiceptin, the specific mu receptor agonist. Dynorphin analgesia was completely reversed by intrathecal injection of anti-dynorphin IgG and partially reversed by naloxone. Acute tolerance to morphine analgesia did not affect the occurrence of dynorphin analgesia. Evidence from different lines of approach suggest that dynorphin may bind with kappa receptors in the spinal cord to exert its analgesic effect.
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An antiserum specific for atriopeptin was used to characterize and localize atriopeptin-like immunoreactive material in rat atrium by radioimmunoassay and immunohistochemical techniques. The antiserum recognizes atriopeptin I, atriopeptin III, and alpha-human atrial natriuretic polypeptide, but does not recognize met-enkephalin, cholecystokinin, dynorphin A, bradykinin, substance P, or beta-endorphin. A high content of atriopeptin was found in crude extracts of rat atria, as compared to ventricles, and the atriopeptin-like immunoreactive material was found to be located exclusively in granules within atrial cardiocytes. Fractionation of the immunoreactive material by gel filtration and reverse-phase HPLC revealed the presence of multiple atriopeptins.
Intrathecal injection of subanalgesic doses of morphine (7.5 nmol) and dynorphin-A-(1-13) (1.25 nmol) in combination resulted in a marked analgesic effect as assessed by tail flick latency in the rat. The analgesic effect of the composite dynorphin/morphine was dose-dependent in serial dilutions so that a composition of 1/8 of the analgesic dose of dynorphin and 1/3 that of morphine produced an analgesic effect equipotent to full dose of either drug applied separately. The analgesic effect induced by dynorphin/morphine mixture was not accompanied by motor dysfunction and was easily reversed by a small dose (0.5 mg/kg) of naloxone. Contrary to the augmentatory effect of dynorphin on morphine analgesia in the spinal cord, intracerevroventricular (ICV) injection of 20 nmol of dynorphin-A-(1-13) exhibited a marked antagonistic effect on the analgesia produced by morphine (120 nmol, ICV). The theoretical considerations and practical implications of the differential interactions between dynorphin-A-(1-13) and morphine in the brain versus spinal cord are discussed.
In lightly pentobarbital-anesthetized and acutely prepared rats, electrical stimulation within the arcuate nucleus of the hypothalamus (ARH) consistently inhibited the tail-flick responses to noxious heating of the tail. The peptide ICI174864, a delta-opioid receptor antagonist applied intrathecally at the lumbar level at a dose of 1 nmol, markedly attenuated this inhibition without affecting the baseline nociceptive threshold. Normal saline injected by the same approach had no effect on the ARH inhibitory modulation. This is the first report showing an involvement of the delta-opioid receptor in the descending inhibition of spinal nociceptive reflex resulting from ARH stimulation.
The working hypothesis that the periaqueductal gray (PAG), N. accumbens and amygdala were connected serially in a unidirectional loop for antinociception, in which Metenkephalin and beta-endorphin were considered to be two important analgesic neurotransmitters, was examined by simultaneously perfusing the PAG and N. accumbens after microinjection of morphine into the amygdala. Intra-amygdaloid injection of morphine increased the release of enkephalins and beta-endorphin in the PAG and N. accumbens. When the perfusion fluid contained 3 microM of naloxone, the release of enkephalins and beta-endorphin was reduced in both the PAG and the N. accumbens. These results do not support the hypothesis of a unidirectional loop and its putative sequence.
Previous studies from this laboratory suggested that the periaqueductal gray (PAG), nucleus accumbens, and amygdala might take part in a serial, unidirectional mesolimbic loop to play their roles in pain modulation. It has been proposed that morphine injected into one of these nuclei would cause the release of opioid peptides in one nucleus after another. This working hypothesis was examined in the present study by perfusing simultaneously the PAG and the amygdala after microinjection of morphine into the N. accumbens. It was found that microinjection of morphine increased the content of immunoreactive enkephalins (ir-ENK) and immunoreactive beta-endorphin (ir-beta-EP) in the perfusate of the PAG and the amygdala. When the perfusion fluid contained 3 microM of naloxone, the increase of ir-ENK and ir-beta-EP was reduced significantly. These results indicate that the three nuclei were not serially connected in a unidirectional loop.
Cholecystokininergic (CCK) and dopaminergic systems in the midbrain have been implicated in pain modulation. In the present study, Fos immunoreactivity was used as a marker of neuronal activity to investigate if subcutaneous injection of formalin (a model of noxious stimulation) could activate the CCKergic and dopaminergic neurons in the midbrain. Noxious stimulation increased significantly the numbers of Fos-positive CCKergic and dopaminergic neurons in the ventral tegmental area (VTA), whereas no significant changes in the numbers of Fos-positive CCKergic or dopaminergic neurons were observed in other midbrain nuclei. These results indicate that the VTA may play a role in pain modulation.
One hundred sixteen magnetic resonance (MR) imaging studies from 105 pediatric patients with a variety of cerebral abnormalities were reviewed to determine the diagnostic efficacy of MR in the pediatric population. All subjects tolerated the MR procedure well, although sedation was necessary for younger children. Compared with CT, MR proved to be advantageous in detection and characterization of the pathology in 23 of 105 patients, especially when the abnormality was located along the base of the brain and midline, or when it involved primarily the white matter. Intracranial calcification was the one abnormality not detected with MR although dense calcifications could be seen as areas of low signal intensity. Some characteristics of various pathological entities were compared in an attempt to differentiate among abnormalities in the same anatomical location: craniopharyngioma from optic chiasm and hypothalamic glioma, cystic glioma from arachnoid cyst, and chronic subdural hematoma from subdural hygroma. The lack of ionizing radiation in MR is of particular interest in pediatric neuroradiology since radiation is of special concern in the young age group.
Magnetic resonance (MR) and CT examinations of 26 patients with the established or clinically suspected diagnosis of brain stem glioma were reviewed. Eleven tumors were seen on both MR and CT. The entire extent of the abnormality was better outlined on MR, although CT was more advantageous in demonstrating cystic components and calcium deposition. Magnetic resonance and CT depicted focal intratumoral hemorrhage equally. Magnetic resonance was found to be particularly suitable to follow up the progression or regression of the disease. Of particular interest were two patients with evidence of aqueductal obstruction but normal CT appearance of the midbrain; the causative abnormality, believed to be a glioma, was clearly shown by MR imaging. In nine patients the normal appearance was helpful to exclude the possibility of a brain stem glioma. Thus far, results have shown 100% sensitivity (true positive ratio) and specificity (true negative ratio) with MR in the evaluation of brain stem gliomas. It is concluded that MR imaging should be the examination of choice and could be the definitive screening procedure in patients with suspected brain stem glioma.
Contrast-enhanced CT and MR imaging of the kidney were performed in two patients with acute renal failure and severe loin pain following a track race. Prior to the exercise both patients had had flu-like symptoms and took oral medications. There was no evidence of myoglobinuria. Immediate postcontrast CT of the kidney showed multiple patchy areas of poor contrast enhancement; after 24 h, there were multiple patchy enhancing cortical areas on CT without further use of intravenous contrast media. Magnetic resonance imaging of the kidney showed patchy areas of high signal intensity with obliteration of the corticomedullary contrast on T1-weighted images. On T2-weighted images the signal intensity of the lesion was high in one patient and low in the other.
To elucidate the prevalence and clinical implications of antineutrophil cytoplasmic antibody (ANCA) in lupus nephritis (LN), we examined ANCA by indirect immunofluorescence and by ELISA against antilactoferrin (anti-LF) and antimyeloperoxidase (anti-MPO) antibody. To discriminate perinuclear ANCA (pANCA) with antinuclear antibody (ANA), all the ANCA-positive sera were tested again after incubating patients' sera with single-stranded (SS) and double-stranded (ds) DNA. These results were compared with clinicopathologic manifestations and clinical courses of LN. ANCA was positive in 19 (37.3%) of 51 LN patients. Among these LN patients, 3 had cytoplasmic ANCA (cANCA) and 16 had pANCA. ANCA was not found in 8 SLE patients without nephritis and 30 normal controls. The presence of ANCA, particularly pANCA, was associated with the presence of nephritis (18/51 cases vs. 0/8 cases, p < 0.05), especially with diffuse proliferative lupus nephritis, WHO class IV (17/18 cases vs. 21/31 cases, p < 0.05) as well as the presence of anti-dsDNA antibody (17/19 cases vs. 18/30 cases, p < 0.05). Patients with ANCA frequently had deterioration of renal function (3/16 vs. 0/26 cases). Anti-LF antibody was positive in 13 patients. Among those, 12 patients had nephritis. Five patients with anti-LF antibody did not have ANCA, but 7 had pANCA, and 1 had cANCA. Patients with anti-LF antibody had lower initial creatinine levels than those without it [serum creatinine (mg/dl): 0.78 (0.6-1.0) vs. 1.43 (0.5-5.0), p < 0.05]. Anti-MPO antibody was positive in only 1 patient, suggesting that MPO is a rare antigen for ANCA in LN.
A 58-year-old male patient had secondary polycythemia associated with idiopathic nephrotic syndrome. The renal biopsy revealed membranous nephropathy, and the bone marrow biopsy disclosed hypercellular marrow with mild panhyperplasia. The concentration of serum erythropoietin was 8.5 mU/ml. The erythrocytosis was characterized by an increased red cell volume (40.2 ml/kg) and normal arterial oxygen saturation. There were no associated lesions that could induce secondary polycythemia, except the biopsy-proven membranous nephropathy. He was treated with prednisolone and cyclophosphamide, and the nephrotic syndrome was partially remitted after 6 weeks. With partial remission of nephrotic syndrome, the erythrocytosis was resolved. This case illustrates the rarely reported association of the nephrotic syndrome and erythrocytosis, and the resolution of erythrocytosis with improvement of nephrotic syndrome.
It has been proposed that the FOS protein encoded by c-fos protooncogene functions as a nuclear "third messenger" molecule that couples short-term extracellular signals to long-term alterations in cell function, by regulating the expression of specific target genes. In the present study, immunocytochemical double staining technique was used to investigate the effects of electroacupuncture on the expression of c-fos oncogene in the serotonergic neurons in the nucleus raphe dorsalis (NRD) that has been known to play an important role in the endogenous analgesic system of the brain. The number of FOS positive serotonergic cells in the NRD increased significantly after the electroacupuncture stimulation. These results indicate that electroacupuncture can activate central serotonergic neurons at gene expression level.
Recently a "medium frequency" electric stimulator (LIKON) was marketed, which delivers 2000-5000 Hz square waves and was claimed to induce a strong clinical analgesic effect. The aim of this study was to clarify whether electric stimulation over 1000 Hz would induce any antinociceptive effect in the rat. Tail flick latency (TFL) was taken as the nociceptive index. Electrical stimulation was applied via stainless steel pins inserted into the acupoint ST 36 located near the knee joint and SP 6 located near ankle joint on both hind legs. Significant increase of TFL (ANOVA, p < .01) was obtained after 2 or 5 kHz stimulation for 10 min, and lasted for the whole stimulation period of 30 min. No significant difference was observed whether the amplitude remained constant (5 V) or was modulated at 5 or 100 cycles/s. Opioid antagonist naloxone (20 but not 10 mg/kg, sc) produced a 50% blockade of the antinociception induced by 2 kHz, but not 5 kHz stimulation. The results suggest that 2 kHz peripheral stimulation was capable of inducing an opioid mediated antinociception in the rat, whereas a less marked antinociception induced by 5 kHz stimulation was nonopioid in nature.
The analgesic effects induced by two different kinds of peripheral conditioning stimulations, electroacupuncture (EA) and transcutaneous electrical nerve stimulation (TENS), were compared in the rat using the latency of radiant heat-evoked tail flick reflex as nociceptive index. The parallel elevations of withdrawal latency of tail flick were produced by EA and TENS administrations at the acupoints of S36 and Sp6 with low intensity (1-2-3 mA) and one of three different frequencies (2, 15 and 100 Hz). Analgesic effects of EA or TENS were characterized by slow-on and slow-off nature, and a significant linear correlation was found between both at any one of three frequencies. Systemic naloxone hydrochloride (2 mg/kg) almost completely and partially antagonized 2 and 15 Hz EA- or TENS-induced analgesia, respectively, but failed to affect those induced by 100 Hz EA or TENS. Tolerance to EA stimulation with one of three frequencies reduced the corresponding frequency TENS-induced analgesia and vice versa. These data indicate that: (a) there is no significant difference in producing antinociception for two different peripheral conditioning stimulations when applied at the same sites and (b) the common neural mechanisms most likely process the analgesic effects of EA and TENS. The involvement of (an) endogenous opiate mechanism in the management of different frequency EA and TENS analgesia is discussed in detail.
Antibody microinjection has been widely used to investigate the function of neuropeptides, but the capability of antibody to diffuse in the brain tissue has not been well characterized. The present study was conducted with an immunohistochemical method to determine if the anti-enkephalin serum injected intrathecally could diffuse into the spinal cord. Enkephalin immunoreactivity was observed in laminae I and II in slight amounts after 10 min, in moderate amounts after 30 minutes and very clearly after 60 min of the intrathecal injection of enkephalin antiserum. In addition, marked nonspecific staining was observed in the dorsal part but not in the ventral part of the white matter. These results indicate that antibodies injected intrathecally are capable of diffusing into the spinal cord within a time period of 10-60 min.