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Biomedical subjects

H Sachs

Publications and source records attributed to H Sachs.

At least 37 records · Page 2Linked to original sources
PubMed1993

Hair analysis as evidence in forensic cases.

Because hair analysis can be used for the determination of drug use months after drug consumption, hair analysis data can often act as important and even decisive evidence in the courtroom. More recently developed GC/MS methods offer excellent sensitivity and can make the distinction between chronic heroin and codeine use, which was not possible earlier with radioimmunoassay techniques. From more than a thousand hair analyses, the morphine/codeine ratios necessary to determine heroin use were set at 5:1 for low morphine concentrations (< 1 ng/mg hair) and 2:1 for concentrations above 1 ng/mg hair. The distinction can be further focused with the additional analysis of the metabolite monoacetylmorphine (MAM). As can be seen from several case examples, hair analysis cannot pinpoint an exact date of opiate use, but it can be used to validate or invalidate a subject's statement concerning his/her drug consumption. Interpretations should always be made cautiously. Ranges, means and medians are also listed for amphetamine, cocaine and cannabis and work is under way to draw similar safety guidelines for these drugs.

Codeine↗
PubMed1993

Comparison of quantitative results of drugs in human hair by GC/MS.

Until the first determination of opiates in human hair by GC/MS in 1985, radioimmunological results of hair examinations met with opposition. Since then, further GC/MS methods have been developed that have led not only to considerably increased sensitivity, but can also be used in hair analysis for screening purposes and can detect substances for which RIA kits are not available. In the present study different extraction methods were used along with two GC/MS processes which back-up each other. These methods include the enzymatic dissolution of the hair, incubation with a buffer solution followed by a solid-phase extraction and incubation with methanol without a further extraction. The GC/MS examination for heroin, cocaine, hashish and selected pharmaceuticals was carried out after derivatization with pentafluoropropionic acid anhydride or pentafluoro-1-propanol. Because of the higher sensitivity and versatility of GC/MS, two GC/MS processes were used to confirm each other instead of backing-up radioimmunological measurements with GC/MS.

Child↗
PubMed1991

[Does the 3d decimal number of single values have significance for calculating average blood alcohol content?].

Judgement of driving capability bases on determination of alcohol concentration in blood. This is carried out by two different methods, whereby the mean value is taken out of four test results. The mean value may very slightly taking either two or three decimal places. We suggest not to abandon the third decimal place. Due to German jurisdiction absolute incapability to drive is given when alcohol concentration in blood reaches 1.3 g Promille. An example shows that in a forensic case the limit of 1.3 g Promille was not reached if only two instead of three decimal places were taken.

Alcohol Drinking↗
PubMed1990

[The detection of codeine abuse by hair analysis].

For the purpose of assessing possible opiate dependence (question of culpability) toxicological tests (gas chromatography; mass-spectrometry) were performed on cuttings of hair of a 30-year-old man who had within a short period committed several punishable offences 8 months previously. It was thus possible to determine opiate intake over a period of time corresponding to the length of hair. About 20 micrograms/g codeine and up to 4 micrograms/g morphine were demonstrated, in addition also 30 micrograms/g bromazepam. These results proved that amounts exceeding therapeutic levels of bromazepam and codeine-containing drugs had been taken during the period in question.

Adult↗
PubMed1989

Results of comparative determination of morphine in human hair using RIA and GC/MS.

Results of radioimmunological and mass-spectrometric tests for morphine in human hair samples, conducted independently in two separate laboratories, were compared. A large degree of qualitative and quantitative parity was observed for the two methods at morphine levels above 1000 micrograms/kg. Due to the variation of results at levels below 1000 micrograms/kg, more GC-MS tests are necessary as a safeguard. Additional GC/MS analyses of the same samples showed that discrepancies between the results of the two methods are not necessarily due to a variable response to the analyte. The results of the GC/MS examinations showed that it is also possible to distinguish between heroin and codeine addicts.

Codeine↗
PubMed1987

Mapping human brain monoamine oxidase A and B with 11C-labeled suicide inactivators and PET.

The regional distributions of monoamine oxidase (MAO) types A and B have been identified in human brain in vivo with intravenously injected 11C-labeled suicide enzyme inactivators, clorgyline and L-deprenyl, and positron emission tomography. The rapid brain uptake and retention of radioactivity for both 11C tracers indicated irreversible trapping. The anatomical distribution of 11C paralleled the distribution of MAO A and MAO B in human brain in autopsy material. The corpus striatum, thalamus, and brainstem contained high MAO activity. The magnitudes of uptake of both [11C]clorgyline and L-[11C]deprenyl were markedly reduced in one subject treated with the antidepressant MAO inhibitor phenelzine. A comparison of the brain uptake and retention of the 11C-labeled inactive (D-) and active (L-) enantiomers of deprenyl showed rapid clearance of the inactive enantiomer and retention of the active enantiomer within MAO B-rich brain structures, in agreement with the known stereoselectivity of MAO B for L-deprenyl. Prior treatment with unlabeled L-deprenyl prevented retention of L-[11C]deprenyl. Thus, suicide enzyme inactivators labeled with positron emitters can be used to quantitate the distribution and kinetic characteristics of MAO in human brain structures.

Adult↗
PubMed1987

Alteration of regional cerebral glucose metabolic rate in non-Korsakoff chronic alcoholism.

That chronic alcoholism yields devastating effects to the central nervous systems of its victims is well known, but the actual physiologic mechanisms underlying that deterioration have yet to be completely identified. What is also known is that many chronic alcoholics seem to recover brain function after a protracted period of abstinence, but the actual mechanisms of that restoration are also not well understood. Using positron emission tomography with the tracer 11C-2-deoxy-D-glucose as a probe to measure regional cerebral metabolic rate of glucose (RCMRGlu), we compared the magnitudes of glucose consumption in 44 brain regions between a group of newly abstinent chronic alcoholics without Korsakoff's psychosis and a control group of normal nonalcoholic subjects whose range of age was that of the alcoholic group. We found that RCMRGlu measurements in the brains of alcoholics were significantly lower than in the brains of the control group, and that there were many fewer significant interregional correlations in the brains of the alcoholics than in the brains of the control group. We also found no significant correlation between age and global metabolic rate of glucose in either group. However, even though the number of alcoholic subjects was too few to allow a reliable statistical comparison, the measurements suggest that chronic alcoholics over the age of 50 years suffer a greater decrease of RCMRGlu values than do their counterparts under the age of 50 years. While resting in a bland environment, neither alcoholic nor control subjects were found to have significant differences in RCMRGlu values between their brain hemispheres. In contrast to this similarity, normal dextrous subjects responded to a nonverbal auditory stimulus by increasing the metabolic rate of glucose in their right hemispheres while eight of nine chronic alcoholics did not. The results of this pilot study point to arguments that the alcoholic brain metabolizes glucose at a lower rate than do normal brains, that there are fewer region-to-region functional relationships in the alcoholic brain than in the normal brain, and that alcoholics may be impaired in right hemispheric processing. In subsequent investigations, we will measure the metabolic changes that follow abstinence, if any, by tracking subjects throughout an interval of rehabilitation. Also, we intend to test the findings of this study by measuring greater numbers of alcoholic subjects to separate the consequences of measurement variability, age, and chance from the underlying biologic processes that seem to be affected by chronic alcoholism.

Adult↗
PubMed1986

Effect of reserpine on regional cerebral glucose metabolism in control and migraine subjects.

The regional cerebral metabolic rate of glucose metabolism (RCMRGlu) in five headache and six control subjects was measured with positron emission tomography (PET) using the tracer 2-deoxy-D-[1-11C] glucose before and after the administration of reserpine. The short half-life of the carbon 11 tracer made possible a test-retest paradigm wherein each subject served as his own control in assessing the effect of reserpine on RCMRGlu. Thus, measurements were first performed with subjects at rest and subsequently at 1 1/2 hours after the parenteral administration of reserpine (rest-reserpine). In control subjects without history of migraine, reserpine did not induce headache, and, furthermore, PET measurements 1 1/2 hours after drug administration consistently showed a global increase in RCMRGlu over resting values similar to that observed in a normal control (rest-rest) group not receiving reserpine. By contrast, four of the five subjects with migraine began to experience a mild unilateral headache or visual disturbances 1 1/2 hours after reserpine, at which time PET scanning showed a 5% to 30% decline in RCMRGlu below the values that had been measured before reserpine injection, all well outside of the 99% confidence limits of normal variation separately determined on 25 control subjects (rest-rest). There was no apparent laterality, and subjects with a history of either common or classic migraine responded in a similar manner. The difference in percent change in RCMRGlu following administration of reserpine observed in these four subjects with migraine headaches was significantly different over all regions of interest as compared with all six control subjects receiving the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

[Effect of various types of artificial respiration on raised intracranial pressure, associated with acute alcoholic intoxication].

The effects of spontaneous respiration and mechanical ventilation on ICP were examined by investigating the interaction between elevated pressure and alcohol intoxication. 200 ml ethanol 48% were infused in 11 young pigs with elevated cerebral pressure during mechanical ventilation (Group 1), 7 young pigs with elevated intracranial pressure during spontaneous respiration (Group 2), and 4 young pigs without elevated intracranial pressure during spontaneous respiration (Group 3). While the behaviour of intracranial pressure during mechanical ventilation in the animals from Group 1 was inhomogeneous with a tendency to rise (29 mmHg to 34 mmHg), intracranial pressure (28 mmHg to 55 mmHg) increased dramatically in Group 2. This increase was associated with a sharp rise of paCO2 (37.6 mmHg to 73.3 mmHg) and a decline of paO2 (74 mmHg to 13 mmHg). None of the animals in Group 2 survived. paCO2 also rose in alcoholized animals without elevated ICP (Group 3) (41.9 mmHg to 63.9 mmHg); intracranial pressure, however, remained within the normal range. All animals in Group 3 survived. Our findings indicate that elevated intracranial pressure and alcohol intoxication have a cumulative or potentiating effect on depression of the respiratory centre. Respiratory depression can be prevented by mechanical ventilation and, therefore, a further rise of intracranial pressure can be generally avoided.

Alcoholic Intoxication↗
PubMed1985

[Fatal poisoning by the retard form of verapamil. Therapeutic considerations].

A 60-year-old woman swallowed 2.4 g verapamil in a retard form (Isoptin retard). Depsite intensive efforts she died 44 hours later in a coma due to circulatory collapse. In contrast to other reported cases of poisoning, the verapamil concentration in plasma continued to rise. This atypical course with continuing absorption of verapamil was due to small-intestinal deposits of the drug, found at autopsy.

Coma↗