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Biomedical subjects

S Ritter

Publications and source records attributed to S Ritter.

At least 127 records · Page 7Linked to original sources
PubMed1985

Intraventricular alloxan impairs feeding to both central and systemic glucoprivation.

Fourth ventricular alloxan injections impair the feeding response to systemically induced glucoprivation. However, the effect of alloxan on responses to centrally administered glucoprivic agents has not been assessed. Therefore, rats implanted with fourth ventricular cannulas were tested for feeding and glycemic responses to centrally administered 5-thioglucose (5TG, 120 micrograms/5 microliter) and subcutaneously administered 2-deoxy-D-glucose (2DG, 250 mg/kg, IP). Subsequently, alloxan (200 micrograms in 5 microliter), alloxan plus 3 M D-glucose, or the saline vehicle solution was injected into the fourth ventricle and the animals were then retested with systemic 2DG and intraventricular 5TG. Feeding responses to both centrally and systemically induced glucoprivic challenge were greatly impaired by alloxan treatment. Thus, feeding elicited by both centrally and systemically induced glucoprivation appears to be mediated by the same central neural substrate. The possibility that the alloxan-damaged cells are glucoreceptors is discussed. In contrast to glucoprivic feeding, the hyperglycemic response to glucoprivation was not impaired by alloxan. Therefore, the neural elements controlling this response may differ biochemically from those controlling feeding.

Alloxan↗
PubMed1985

Alloxan-induced glucoprivic feeding deficits are blocked by D-glucose and amygdalin.

Intracerebroventricular injection of alloxan, a pancreatic beta (B) cell cytotoxin, impairs glucoprivic feeding in rats. The goal of this experiment was to determine whether alloxan-induced impairment of glucoprivic feeding can be attenuated by agents which antagonize alloxan's toxicity in the B cell. Therefore, alloxan was co-administered into the fourth ventricle alone or in combination with D-glucose, L-glutamine, or amygdalin, all known antagonists of alloxan's B cell toxicity, or with L-glucose, which does not antagonize B cell toxicity. We found that alloxan produced deficits in glucoprivic feeding which were not attenuated by co-administration with L-glucose or L-glutamine. Alloxan/L-glucose treated rats ate 11% and 14% of control intake, respectively, after systemic administration of 2-deoxy-D-glucose (2DG, 250 mg/kg) and fourth ventricular 5-thioglucose (5TG, 120 micrograms/5 microliter). Alloxan/L-glutamine rats ate 20% and 22% of control intake after 2DG and 5TG, respectively. In contrast, D-glucose and amygdalin (15 mM) completely blocked alloxan-induced impairment of glucoprivic feeding and amygdalin (10 mM) exerted a partial protective effect. These behavioral results may indicate that in the brain, susceptibility to alloxan toxicity depends upon cellular characteristics shared with the B cell.

Alloxan↗
PubMed1983

Remission of rapidly growing desmoid tumors after tamoxifen therapy.

A patient is described with Gardner's syndrome manifested initially by an extra-abdominal desmoid which was resected. The case was complicated by metastatic adenocarcinoma of the colon and recurrence of several large painful desmoid lesions. In view of the predilection of desmoids to occur in women in their childbearing years, it was decided to treat these painful lesions with an anti-estrogen, tamoxifen (20 mg orally, four times daily). This therapy led to a complete relief of pain within 1 week and a progressive decrease in the size of the desmoid tumors to less than 50% of their initial volume by the end of the second week. Unfortunately, the patient's metastatic adenocarcinoma progressed and was complicated by sepsis leading to her death. This case suggests that the growth of desmoid tumors is under hormonal influence, a suggestion which deserves further investigation.

Adenocarcinoma↗
PubMed1983

Plasma catecholamines in fasted and sucrose supplemented rats.

Rats were food deprived or given a sucrose supplemented diet for 3 days. Resting plasma catecholamine levels measured remotely from undisturbed rats were not altered by either dietary treatment. However, food deprivation did result in decreases in resting mean arterial blood pressure, heart rate, plasma volume and plasma Na+ concentration. After one minute of intermittent footshock food deprived and sucrose fed rats did not differ from controls with respect to blood pressure, heart rate or plasma catecholamine levels but food deprived rats were less active during footshock and had lower levels of plasma glucose immediately after footshock when compared to controls or sucrose fed rats. Food deprivation and dietary sucrose supplementation have been shown to alter norepinephrine (NE) turnover in specific sympathetic target tissues. Our data indicate that these changes in turnover are not reflected by changes in plasma NE. Therefore, NE turnover rates and plasma NE concentration may not be equivalent indices of sympathetic activity.

Adrenal Medulla↗
PubMed1983

Kinetics, subtype specificity and immunoglobulin class of anti-HBs induced by hepatitis B vaccine.

The protective effect of anti-HBs against hepatitis B virus is proven only for the common antibody anti-HBs/a but not for subtype specific antibody. Using subtype specific radioimmunoassays, anti-HBs/a and anti-HBs/d were quantitated in recipients of an HBsAg/ad vaccine. All persons developed anti-HBs/a. The relative proportion of anti-HBs/d was variable and very high at the beginning of the immune response. At this time the anti-HBs was predominantly in the IgM class. IgM-anti-HBs disappeared rapidly after its peak value and was more slowly replaced by IgG-anti-HBs. Persons who had only anti-HBs or anti-HBc as the only antibody did usually not react with an anamnestic booster response and developed IgM- anti-HBs after vaccination. An injection schedule of 0, 1, 4 months produced ten times higher titers than a 0, 1.5, 3 months schedule 4 weeks after the third injection. However, 6 months later titers were essentially identical. Nine of ten "non-responders" became positive after a fourth injection.

Adult↗
PubMed1983

Safety and potency aspects in the preparation of an experimental HBsAg vaccine.

No experimental setting is available to exclude residual infectivity in HBsAg vaccines derived from human plasma. Thus, safety can be achieved only by means of their preparation. To reduce infectivity of the starting material, only plasma from healthy anti-HBe positive donors was used. In the FRG, 50% of all healthy HBsAg carriers with anti-HBe have a suitable serum level of 5 to 20 micrograms/ml. The purification procedure removed hepatitis B virus by a factor greater than 10(4). The purified product contained only the HBsAg proteins and no serum protein, as shown by SDS gel electrophoresis. The pure HBsAg was treated with formalin 1:500 at 37 degrees C for 4 days. A loss of 30 to 50% antigenicity was tolerated to achieve the highest possible destruction of known and unknown infectious agents. After inactivation, the HBsAg was bound to aluminium hydroxide gel. The gel was washed repeatedly to remove the formalin. Doses of 40 micrograms or 20 micrograms absorbed HBsAg protein were given to greater than 2500 persons without serious side effects. In greater than 97% anti-HBs was formed with a median titer of 1900 I.U./ml.

Follow-Up Studies↗
PubMed1983

[Kidney load in spleen irradiation in lymphogranulomatosis patients].

Within the period of 1972 to 1982, 35 patients suffering from lymphogranulomatosis had to be treated by para-aortal pendulum therapy and irradiation of the spleen or spleen pedicle. Some of these patients received an additional polychemotherapy. All of these 35 patients were regularly checked-up by clinical and laboratory examinations in oncologic departments. There were no signs of radiogenic lesions of the kidney. In spite of this, the urines of these patients were examined by discelectrophoresis. Eight patients had a pathologic protein spectrum which was a symptom of other diseases in two cases and did not appear again in four cases, when control examinations were performed. One patient refused the control examination, but this one had no pathologic modifications in abdominal CT. Just one female patient showed in three control examinations protein spectra resembling to those of a proliferating glomerular lesion and a tubular lesion. All the other parameters, including a functional scintigraphy of the kidney, were normal. The patient felt well and had no clinical signs of disease. A functional damage of the kidney after irradiation of the spleen cannot be identified by current clinical and laboratory methods.

Adolescent↗
PubMed1982

Glucoprivic feeding is impaired by lateral or fourth ventricular alloxan injection.

Feeding and blood glucose responses to insulin and 2-deoxy-D-glucose (2-DG) were examined in rats previously given lateral or fourth ventricular injections of the diabetogenic agents, alloxan and streptozotocin. Although streptozotocin (120, 200, and 400 micrograms) was ineffective, lateral ventricular alloxan injections (40 micrograms in 5 microliters) reduced feeding to 45% of control after 350 mg/kg 2-DG (sc), 33% of control after 150 mg/kg 2-DG, and 65% of control after insulin (2 U/kg). Fourth ventricular alloxan injections produced greater deficits, reducing feeding to 19, 7, and 46% of control, respectively. The sympathoadrenal response to glucoprivic agents was normal after alloxan treatment; however, blood glucose levels fell more rapidly during fasting than in controls. Alloxan-induced deficits did not appear to result from damage to catecholamine neurons, since neither regional concentrations nor glucoprivation-induced elevation of catecholamine turnover was altered by alloxan pretreatment. We conclude that cells involved in the glucoprivic control of feeding can be selectively and permanently damaged by intracerebroventricular alloxan administration. Such cells appear to reside in the hindbrain, to be noncatecholaminergic, and to function independently of glucoreceptors mediating sympathodrenal discharge.

Alloxan↗
PubMed1981

Insulin-induced elevation of hypothalamic norepinephrine turnover persists after glucorestoration unless feeding occurs.

We employed a delayed feeding paradigm to assess regional brain catecholamine changes associated with insulin-elicited glucoprivic feeding. This paradigm makes use of the recent discovery that glucoprivic challenges significantly enhance food intake even when food is withheld until other signs of glucoprivation have abated. Using this paradigm we attempted to temporally dissociate the neurochemical events associated with the ingestive response from other potentially confounding consequences of insulin or glucoprivation. We found a high degree of congruence between elevated hypothalamic norepinephrine (NE) turnover (estimated by the change in transmitter concentration after synthesis inhibition) and the persistence of hunger, both during and after apparent glucoprivation. In the absence of food, hypothalamic NE turnover was enhanced during insulin-induced glucoprivation and this increase persisted into the postglucoprivic period. A brief feeding bout, either during glucoprivation or postglucoprivically, rapidly normalized NE turnover rates. Moreover, brief access (30 min) to a limited quantity of food (2.5 g) during glucoprivation abolished both the elevated turnover and the feeding response otherwise observed postglucoprivically. Turnover of catecholamines in the telencephalon was also enhanced after insulin, but the increased activity did not persist into the postglucoprivic period and, in addition, was not altered in any consistent manner by food intake. These findings strengthen the view that hypothalamic NE neurons are involved in the mediation of glucoprivic feeding.

Animals↗