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Biomedical subjects

H Sager

Publications and source records attributed to H Sager.

7 recordsLinked to original sources
PubMed1990

The nigrostriatal dopaminergic system assessed in vivo by positron emission tomography in healthy volunteer subjects and patients with Parkinson's disease.

A group of healthy control subjects and patients with Parkinson's disease were investigated using positron emission tomography and two tracers as indicators of different specific properties of the presynaptic dopaminergic system in caudate nucleus and putamen. The first tracer, 6-L-(18F)-fluorodopa, was used as an analog of levodopa to assess its regional brain uptake, conversion into, and retention as dopamine and further metabolites. The second tracer, (11C)-nomifensine was employed as an indicator of striatal monaminergic reuptake sites that are principally dopaminergic. We have used this tracer to assess dopaminergic nerve terminal density. In patients with Parkinson's disease, striatal uptake of both tracers was decreased, putamen being significantly more affected than caudate. Side-to-side differences of uptake in putamen, but not caudate, correlated with corresponding left-right differences of scored clinical motor performance. Both 6-L(18F)-fluorodopa and (11C)-nomifensine tracer uptake in putamen was decreased on average to 40% of normal values, suggesting that a substantial part of the cellular elements of the dopaminergic nigrostriatal system is still intact in living parkinsonian patients. This is in contrast to the generally extreme depletion of endogenous dopamine in the putamen of patients found at postmortem. Our results lend support to the search for drug treatments that protect against further nigrostriatal cell loss and that could be exhibited as soon as the disease manifests clinically. If successful, a sufficient striatal nerve terminal pool would remain so that the effectiveness of levodopa as a dopamine repletor could persist.

Aged↗
PubMed1988

The effect of hyperthermia on radiation-induced carcinogenesis.

Ten groups of mice were exposed to either a single (30 Gy) or multiple (six fractions of 6 Gy) X-ray doses to the leg. Eight of these groups had the irradiated leg made hyperthermic for 45 min immediately following the X irradiation to temperatures of 37 to 43 degrees C. Eight control groups had their legs made hyperthermic with a single exposure or six exposures to heat as the only treatment. In mice exposed to radiation only, the postexposure subcutaneous temperature was 36.0 +/- 1.1 degrees C. Hyperthermia alone was not carcinogenic. At none of the hyperthermic temperatures was the incidence of tumors in the treated leg different from that induced by X rays alone. The incidence of tumors developing in anatomic sites other than the treated leg was decreased in mice where the leg was exposed to hyperthermia compared to mice where the leg was irradiated. A systemic effect of local hyperthermia is suggested to account for this observation. In mice given single X-ray doses and hyperthermia, temperatures of 37, 39, or 41 degrees C did not influence radiation damage as measured by the acute skin reactions. A hyperthermic temperature of 43 degrees C potentiated the acute radiation reaction (thermal enhancement factor 1.1). In the group subjected to hyperthermic temperatures of 37 or 39 degrees C and X rays given in six fractions, the skin reaction was no different from that of the group receiving X rays alone. Hyperthermic temperatures of 41 and 43 degrees C resulted in a thermal enhancement of 1.16 and 1.36 for the acute skin reactions. From Day 50 to Day 600 after treatment, the skin reactions showed regular fluctuations with a 150-day periodicity. Following a fractionated schedule of combined hyperthermia and X rays, late damage to the leg was less than that following X irradiation alone. Mice subjected to X rays and hyperthermic temperatures of 41 and 43 degrees C had a lower median survival time than the mice treated with hyperthermia alone. This effect was not associated with tumor incidence.

Animals↗
PubMed1986

The influence of levamisole and hyperthermia on the incidence of metastases from an X-irradiated tumor.

Fragments of the KHT sarcoma were transplanted into the right rear legs of C3H/He mice. At 10 days, groups of 16 to 20 mice had the consequent developing tumor treated by local irradiation (40 Gy in 2 fractions), levamisole (5 mg/kg every 2nd day), local hyperthermia, or a combination of these treatments. Local tumor control, the incidence and sites of metastatic spread, and survival times were measured. Radiation alone controlled 25% of the local tumors, but 75% of the treated mice developed metastases. Radiation combined with levamisole increased local control to 31% with a corresponding decrease in the incidence of metastases. Hyperthermia alone prolonged the survival time compared to nontreated mice. This increase in survival time was lost when levamisole was combined with hyperthermia. Combined hyperthermia and irradiation controlled 89% of tumors. This corresponded to a thermal enhancement factor of 3.5. When levamisole was added to hyperthermia and irradiation, local tumor control was decreased and the incidence of metastases was increased compared to the combination treatment of irradiation and hyperthermia. The nonspecific immune stimulant levamisole was antagonistic to the action of hyperthermia on the KHT tumor. An hypothesis to explain this antagonism is proposed.

Animals↗