Visual perception in a snapshot.
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Biomedical subjects
Publications and source records attributed to Michael Herzog.
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STUDY OBJECTIVE: A clinical examination of the upper airway in patients with suspected sleep-disordered breathing (SDB) is frequently performed before nighttime polysomnography. In recent years, the findings of "static" examinations, such as dorsalization of the tongue base, the Malampatti index, and Mueller maneuver, have been determined to be of low predictive value. DESIGN: We developed a new method of "dynamic" examination of the upper airway during simulated snoring in awake patients and analyzed the method in terms of the predictive value for suspected SDB. SETTING: N/A PATIENTS: One hundred thirty-one patients were examined prior to night-time polysomnography, and the results were correlated with the apneahypopnea-index (AHI). INTERVENTIONS: N/A RESULTS: A significant correlation was detected between an increased dorsal movement of the tongue base, as well as with pharyngeal collapse at the level of the tongue base and the AHI. Pharyngeal collapse at the level of the velum did not correlate with the AHI. The patient's body position during simulated snoring did not influence the results. The "static" examinations, such as the dorsalization of the tongue base, tonsil size, Malampatti index, and Mueller maneuver, did not correlate with the AHI. Patients with a high degree of pharyngeal collapse at the level of the tongue base, in combination with dorsal movement of the tongue base during simulated snoring, revealed a probability of 75% to have an AHI more than 10 and of 92% for an AHI more than 5. CONCLUSION: The "dynamic" examination of the upper airway under simulated snoring in awake patients is an easy-to-perform method to predict the probability of SDB prior to nighttime polysomnography.
Temperature-controlled radiofrequency reduction (TCRF) of the tongue base has been developed as an alternative option for the treatment of patients with obstructive sleep apnea syndrome. The technique is propagated as an easy and safe surgical method. The case of a 34-year-old male patient with obstructive sleep apnea syndrome who underwent TCRF is reported. Fourteen days after surgery was performed, heavy bleeding at the base of the tongue occurred. Computed tomography and digital subtraction angiography imaging revealed a pseudoaneurysm of the lingual artery, which was treated endovascularly by detachable and free platinum coils during the same session. The article reports the first case of pseudoaneurysm under TCRF of the tongue base and discusses the diagnostic and therapeutic procedure to handle and avoid life-threatening complications under this method of treatment.
How the various features of an object are bound to a unified percept is one of the most fundamental problems the human brain has to solve. Whereas healthy observers usually do not reveal binding errors, it has been proposed that schizophrenic patients suffer from binding deficits. To elucidate such deficits, we investigated one of the most basic binding or integration paradigms: feature fusion. In feature fusion, two stimuli are presented in rapid succession. Using a vernier paradigm, we could, recently, show that the second stimulus determines feature fusion more strongly than the first one (Herzog et al. 2003). However, the first presented stimulus determines feature fusion when a grating follows the two stimuli. Reversal of dominance has occurred. In this study, we show that schizophrenic patients reveal qualitatively the same integration characteristics in feature fusion as healthy controls do. Hence, although some aspects of visual processing are strongly disturbed in schizophrenia as revealed by masking studies, feature fusion appears to be, at least qualitatively, spared. Our fusion paradigm allows one to investigate intact and deficient visual processing in schizophrenic patients with great detail and to elucidate the nature of deficits of visual processing in schizophrenia.
Night time alcohol ingestion influences nocturnal breathing in patients with sleep apnea syndrome or respiratory diseases. To evaluate the influence of nocturnal alcohol ingestion on the cardio-respiratory activity of healthy men, 8 snoring and 13 non-snoring male subjects were measured for 3 nights after alcohol ingestion. Blood alcohol concentration was 0.0, 0.5 and 0.8%, respectively. During each night polysomnographic data were obtained and analyzed. The apnea-hypopnea index was significantly higher in snoring than in non-snoring participants and increased in both groups under the influence of alcohol. Non-snoring males showed a significant increase of hypopneas under nocturnal alcohol ingestion (0.96-1.65-2.06). Mean oxygen saturation (SAO(2)) was significantly higher in non-snoring compared to snoring males, and both groups showed a significant decrease (non-snoring: 96.06%-95.7%-95.52%; snoring: 95.54%-94.74%-94.53%). Snoring individuals had a significant decrease in SAO(2) during NREM4, whereas SAO(2) was reduced significantly in REM and NREM3 in non-snoring subjects. The nocturnal heart rate was significantly increased in both groups under the influence of alcohol. The study proves that snoring and non-snoring healthy males are affected by nocturnal alcohol ingestion. Under the effect of alcohol, these patients can develop signs of a sleep apnea syndrome, which should be considered clinically.
The ductal epithelium of the semicircular canal forms much of the boundary between the K+-rich luminal fluid and the Na+-rich abluminal fluid. We sought to determine whether the net ion flux producing the apical-to-basal short-circuit current (I(sc)) in primary cultures was due to anion secretion and/or cation absorption and under control of receptor agonists. Net fluxes of 22Na, 86Rb, and 36Cl demonstrated a basal-to-apical Cl- secretion that was stimulated by isoproterenol. Isoproterenol and norepinephrine increased I(sc) with an EC50 of 3 and 15 nM, respectively, and isoproterenol increased tissue cAMP of native canals with an EC50 of 5 nM. Agonists for adenosine, histamine, and vasopressin receptors had no effect on I(sc). Isoproterenol stimulation of I(sc) and cAMP was inhibited by ICI-118551 (IC50 = 6 microM for I(sc)) but not by CGP-20712A (1 microM) in primary cultures, and similar results were found in native epithelium. I(sc) was partially inhibited by basolateral Ba2+ (IC50 = 0.27 mM) and ouabain, whereas responses to genistein, glibenclamide, and DIDS did not fully fit the profile for CFTR. Our findings show that the canal epithelium contributes to endolymph homeostasis by secretion of Cl- under beta 2 adrenergic control with cAMP as second messenger, a process that parallels the adrenergic control of K+ secretion by vestibular dark cells. The current work points to one possible etiology of endolymphatic hydrops in Meniere's disease and may provide a basis for intervention.
BACKGROUND: The metastasis of prostate cancer to bone is associated with a substantial increase in bone matrix turnover. Matrix metalloproteinases (MMPs) play roles in both normal bone remodeling and invasion and metastasis of prostate cancer. This study was designed to determine the role of MMP activity in prostate cancer that has metastasized to bone. METHODS: Single human fetal bone fragments were implanted subcutaneously in immunodeficient mice. Four weeks later, PC3 human prostate cancer cells were injected directly into some of the implants, and daily treatment was begun with batimastat (a broad-spectrum MMP inhibitor). There were six mice (i.e., six implants) in each of four experimental arms: bone alone with and without batimastat and bone injected with PC3 cells with and without batimastat. Bone implants were harvested after 14 days of treatment and analyzed for MMP expression, bone histomorphometry, osteoclast counts, blood vessel density, and tumor cell proliferation and apoptosis. Complementary data were obtained from bone biopsy samples from patients and a bone organ coculture system. All statistical tests were two-sided. RESULTS: MMPs were detected in tumor and stromal cells of clinical specimens and experimental bone implants. In vivo, MMP inhibition reduced the number of osteoclasts per millimeter in PC3-injected implants-from 8.2 (95% confidence interval [CI] = 7.9 to 8.5) to 3.0 (95% CI = 2.3 to 3.7) (P =.006). In addition, it prevented degradation of marrow trabeculae within the bone implants (cross-sectional area of implant occupied by mineralized trabeculae: untreated implant = 29.1% [95% CI = 27.1% to 31.1%], PC3-injected implant = 14.0% [95% CI = 10.9% to 17.1%] [P =.005 versus untreated], and batimastat-treated PC3-injected implant = 27.2% [95% CI = 22.4% to 32.0%] [P =.03 versus PC3 injected alone]). MMP inhibition reduced proliferating tumor cells from 20.8% (95% CI = 19.9% to 21.7%) to 7.4% (95% CI = 5.2% to 9.6%) (P =.006), without affecting angiogenesis or apoptosis. In vitro, MMP inhibition had no toxic effect on PC3 cells but prevented calcium release from bone fragments cocultured with PC3 cells. CONCLUSIONS: MMP activity appears to play an important role in bone matrix turnover when prostate cancer cells are present in bone. Bone matrix turnover and metastatic tumor growth appear to be involved in a mutually supportive cycle that is disrupted by MMP inhibition.
BACKGROUND AND PURPOSE: Vasospasms of the spiral modiolar artery may cause an ischemic stroke of the inner ear that manifests itself by a sudden hearing loss. Previously we have shown that endothelin-1 (ET-1) induces vasospasms of the spiral modiolar artery. Here we tested the hypotheses that ET-1-induced vasospasms are (1) reversible by ET(A) receptor antagonists; (2) mediated by a Ca(2+) sensitization of the contractile apparatus via a Rho-kinase-induced inhibition of myosin light chain phosphatase; and (3) reversible by the vasodilator calcitonin gene-related peptide (CGRP). METHODS: The Ca(2+) sensitivity of the contractile apparatus was evaluated by correlation between the smooth muscle cell Ca(2+) concentration and the vascular diameter, which were measured by microfluorometry with the fluorescent dye fluo-4 and videomicroscopy, respectively. RESULTS: ET-1-induced vasospasms were prevented but not reversed by the ET(A) receptor antagonists BQ-123 and BMS-182874. The Ca(2+) sensitivity of the contractile apparatus was increased by ET-1 and by inhibition of myosin light chain phosphatase with calyculin A and was decreased by CGRP. ET-1-induced vasospasms and Ca(2+) sensitization were prevented and reversed by the Rho-kinase antagonist Y-27632 and by CGRP. CONCLUSIONS: ET-1 induces vasospasms of the spiral modiolar artery via ET(A) receptor-mediated activation of Rho-kinase, inhibition of myosin light chain phosphatase, and an increase in Ca(2+) sensitivity, which is reversed by CGRP. The observation that vasospasms were reversed by Y-27632 but not by BQ-123 or BMS-182874 suggests that Rho-kinase, rather than the ET(A) receptor, is the most promising pharmacological target for the treatment of ET-1-induced vasospasms, ischemic strokes, and sudden hearing loss.
High transforming growth factor-beta1 (TGF-beta1) expression in combination with fibrotic scar was observed in human tympanic membranes containing a chronic perforation. The purpose of this study was to investigate whether application of exogenous TGF-beta1 to experimentally created tympanic membrane perforations might induce a nonhealing tympanic membrane perforation. Bilateral myringotomies were performed in 20 rats. In 10 animals, a single dose of TGF-beta1 (0.1 microg) was topically applied to the left tympanic membrane after perforation. In the second part of the study with 10 animals, repeated applications of TGF-beta1 at a higher concentration were tested. In both groups, the opposite ears received vehicle alone. Tympanic membranes were observed for a total of 5 weeks. The effect of TGF-beta1 on the healing of the tympanic membranes was evaluated by closure rates and histology. In the single application group, the healing process was not delayed. Repeated applications of TGF-beta1 did cause a faster perforation closure and a thicker tympanic membrane. Topical TGF-beta1 applied to a traumatic tympanic membrane perforation does not create a chronic perforation at the concentrations and modes of application used in this study.