Ex vivo measurement of postmortem tissue changes in the crystalline lens by Brillouin spectroscopy and confocal reflectance microscopy.

Use of Brillouin spectroscopy in ophthalmology enables noninvasive, spatially resolved determination of the rheological properties of crystalline lens tissue. Furthermore, the Brillouin shift correlates with the protein concentration inside the lens. In vitro measurements on extracted porcine lenses demonstrate that results obtained with Brillouin spectroscopy depend strongly on time after death. The intensity of the Brillouin signal decreases significantly as early as 5 h postmortem. Moreover, the fluctuation of the Brillouin frequency shift inside the lens increases with postmortem time. Images of lens tissue taken with a confocal reflectance microscope between measurements reveal a degenerative aging process. These tissue changes correlate with our results from Brillouin spectroscopy. It is concluded that only in vivo measurements appropriately reflect the rheological properties of the eye lens and its protein concentration.

[Transpalpebral measurement of axial eye length. Use of contact B-scan sonography]. / Transpalpebrale Messung der axialen Bulbuslänge. Nutzung der Kontakt-B-Bild-Sonographie.

PURPOSE: In ophthalmology, it is very often necessary to determine the axial eye length. When standard measuring techniques fail, B-scan sonography may be used. However, coupling problems inhibit exact measurement. The aim of this study was to counter these problems. PATIENTS AND METHODS: Correction values were created for the ultrasonic devices (1) Master-Vu (Sonomed), (2) CineScan (Quantel Medical), and (3) System-ABD (Innovative Imaging), including the position of the coupling layer of the hand pieces and the lid thickness. For evaluation of the method, the axial eye lengths of 35 eyes were measured transpalpebrally. These data were compared to those from the (4) IOL Master (Carl Zeiss Meditec). The usefulness of the developed method was shown by two patients. RESULTS: The correction values were (1) 3.0 mm, (2) 1.5 mm, and (3) 1.5 mm. The medial aberrations to (4) were (1) 0.4+/-0.5 mm, (2) 0.9+/-0.7 mm, and (3) 0.2+/-0.7 mm. CONCLUSIONS: The introduced method enables transpalpebral eye length measurement and is also applicable in cases of missing compliance or in eyes with an obfuscated optical medium.

Response inhibition in borderline personality disorder: event-related potentials in a Go/Nogo task.

Borderline personality disorder (BPD) has been related to a dysfunction of anterior cingulate cortex, amygdala, and prefrontal cortex and has been associated clinically with impulsivity, affective instability, and significant interpersonal distress. We examined 17 patients with BPD and 17 age-, sex-, and education matched control participants with no history of Axis I or II psychopathology using event-related potentials (ERPs). Participants performed a hybrid flanker-Go/Nogo task while multichannel EEG was recorded. Our study focused on two ERP components: the Nogo-N2 and the Nogo-P3, which have been discussed in the context of response inhibition and response conflict. ERPs were computed on correct Go trials (button press) and correct Nogo trials (no button press), separately. Groups did not differ with regard to the Nogo-N2. However, BPD patients showed reduced Nogo-P3 amplitudes. For the entire group (n = 34) we found a negative correlation with the Barratt Impulsiveness Scale (BIS-10) and Becks's depression inventory (BDI). The present study is the first to examine Nogo-N2 and Nogo-P3 in BPD and provides further evidence for impaired response inhibition in BPD patients.

[Brugada or not-Brugada: misdiagnosis of recorder-induced artifact]. / Brugada oder nicht-Brugada: Fehldiagnose durch gerätebedingtes EKG-Artefakt.

The Brugada-Brugada syndrome is a life threatening cardiac arrhythmia that features syncopal events or aborted sudden death in combination with electrocardiographic characteristics (ST-segment elevation of V(1)-V(3) and right bundle branch block). Typical ECG alterations were recorded in a young man who was admitted to our hospital after syncope and a Brugada-Brugada syndrome was suspected. The following days similar pathological ECG recordings of other patients were noticed. The electrocardiographic artifact was diagnosed as being caused by incorrect handling of the ECG recorder.

[A case of malignant neuroleptic syndrome. Case report]. / Ein Fall von malignem neuroleptischem Syndrom (MNS). Eine Kasuistik.

We report on a woman patient with organophosphate poisoning resulting from a psychotically motivated suicide attempt. After detoxification and during treatment with haloperidol and levomepromazine, she developed acute malignant neuroleptic syndrome (MNS) in which dyspnea requiring assisted ventilation was the main symptom. Discontinuation of the neuroleptics was enough to effect sufficient recovery. With this case report, we would first like to emphasize that MNS can evolve within a very short time into a severe and life-threatening situation requiring intensive medical care, and secondly to illustrate the implications of organophosphate poisoning and the consequent cholinesterase blocking far the differential diagnosis of MNS.

Myocardial infarction in rats: effects of metabolic and pharmacologic interventions.

Myocardial infarction was induced in rats by ligation of the descending branch of the left coronary artery. The time course of changes in heart function was recorded within the first nine days. There was a progressive decline in LVSP, in LV dP/dtmax and in the pressure-rate-product. LVEDP was elevated. Cardiac output and stroke volume index were depressed after two days. The ATP content in the nonischemic region was lower than control, but recovered spontaneously toward the normal value within the first four days. Three metabolic and pharmacologic interventions known to affect cardiac adenine nucleotide metabolism were applied. Continuous i.v. administration of ribose which stimulates further adenine nucleotide biosynthesis attenuated the fall and promoted the restoration of ATP in the nonischemic myocardium within four days after coronary artery ligation. The elevation of LVEDP was attenuated with ribose after two and four days. The calcium antagonist gallopamil administered as i.v. infusion for two days led to a further reduction of all parameters of left heart function, but did not influence the increase in adenine nucleotide and protein synthesis that occurred in the nonischemic heart. Coenzyme Q10 had only slight effects on LVSP, LVEDP, and LV dP/dtmax, but attenuated significantly the fall in cardiac output and stroke volume index after two days following coronary artery ligation. Thus, all interventions affected differently the infarct-induced changes in heart and circulatory function. An improvement was observed with ribose and with coenzyme Q10.

Function and distribution of three types of rectifying channel in rat spinal root myelinated axons.

1. The nature, distribution and function of rectifying channels in rat spinal root myelinated axons has been assessed with selective blocking agents and a variety of intracellular and extracellular recording techniques. 2. The electrotonic responses of roots poisoned with tetrodotoxin (TTX) to constant current pulses had fast (rise time much less than 1 ms) and slow components, which were interpreted in terms of Barrett & Barrett's (1982) revised cable model for myelinated nerve. Depolarization evoked a rapid outward rectification (time constant, tau approximately 0.5 ms), selectively blocked by 4-aminopyridine (4AP, 1 mM), and a slow outward rectification (tau approximately 15 ms), selectively blocked by tetraethylammonium (TEA, 1 mM) or Ba2+ (0.5 mM). Hyperpolarization evoked an even slower inward rectification, selectively blocked by Cs+ (3 mM) but not by Ba2+. 3. From the different effects of the blocking agents on the fast and slow components of electrotonus, it was deduced (a) that the inward rectification is a property of the internodal axon, (b) that the slow outward rectifier is present at the nodes, and probably the internodes as well, and (c) that the 4AP-sensitive channels have a minor nodal and a major internodal representation. 4. TEA and Ba2+ reduced the accommodation of roots and fibres not poisoned with TTX to long current pulses, whereas 4AP facilitated short bursts of impulses in response to a single brief stimulus. 5. TEA and Ba2+ also abolished a late hyperpolarizing after-potential (peaking at 20-80 ms), while 4AP enhanced the depolarizing after-potential in normal fibres, and abolished an early hyperpolarizing after-potential (peaking at 1-3 ms) in depolarized fibres. Corresponding to the later after-potentials were post-spike changes in excitability and conduction velocity, which were affected similarly by the blocking agents. Cs+ increased the post-tetanic depression attributable to electrogenic hyperpolarization. 6. The physiological roles of the three different rectifying conductances are discussed. It is also argued that the prominent ohmic 'leak conductance', usually ascribed to the nodal axon, must arise in an extracellular pathway in series with the rectifying internodal axon.

Threshold tracking provides a rapid indication of ischaemic resistance in motor axons of diabetic subjects.

An early abnormality in the peripheral nerves of patients with diabetes mellitus is that it takes a long period of limb ischaemia to block conduction. As a diagnostic test, however, the procedure is time consuming (30 min of ischaemia). We have now used an electronic feedback system to track threshold changes in human motor axons during and after a short period of ischemia (10 min) induced by a pressure cuff. The strength of stimulus current applied over an appropriate nerve was adjusted to maintain a constant amplitude of muscle action potential. This method reveals an increase in excitability during the first few minutes of ischaemia, and a post-ischaemic depression. Both changes in excitability were consistently much reduced in diabetic subjects compared with normal controls.