[Tuberculosis of pupils as an accident occurring "on the job" II (author's transl)].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to E Jensen.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The estrogen receptor protein content of recurrent breast cancer correlates well with the clinical response of hormonal manipulation. This predictive value of the ER of the primary tumor obtained at the time of mastectomy has not yet been proven. If this predictive capability should hold for primary tumors and eventual endocrine treatment, the ramifications are obvious: endocrine therapy could be offered to patients on a rational basis and adjuvant therapy could be considered on a plausible biochemical basis. This report details our observations as to the ER content of the primary tumor and the eventual result of endocrine therapy. Thirty-seven patients whose tumor ER was determined from the primary tumor eventually underwent some form of endocrine therapy for recurrent disease. Fifteen of the primary tumors had significant ER content and 22 possessed insignificant amounts. Only one of the 22 patients with insignificant ER content was benefited by endocrine treatment. Those patients whose tumors contained low amounts of ER experienced recurrence of their disease more rapidly than did those with higher ER content. There was no correlation of age, cell type of tumor or metastatic site with the ER content of the tumor. There is a positive correlation between response to chemotherapy and ER content of tumor. Measurement of the estrogen receptor protein content of the primary breast tumor is a reliable method for choosing patients for eventual endocrine therapy. Those patients whose tumors contain insignificant estrophilin are not candidates for such attempts at palliation.
It was studied whether treatment with sulphadiazine and trimethoprim for 8 weeks affected the folate status. The therapy did not inhibit the absorption as assessed by the 3H--folic acid absorption (TRIFA) test. Plasma folic acid clearance showed that folate deficiency had not developed. Bone marrow studies revealed that the antifolic action of the drugs did not manifest itself at the cellular level. The Lactobacillus casei method should not be employed in the determinations of the serum folate concentration during the treatment because therapeutic plasma concentrations of the two drugs inhibit the growth of the test bacteria.
The possible existence of circulating pancreatic type glucagon (immunoreactive glucagon as measured with a highly specific antibody) of extrapancreatic origin was investigated in 20-25 kg pigs after pancreatectomy. In intact conscious animals intravenous arginine infusions stimulated glucagon as well as insulin secretion, while blood glucose remained unaffected. Two weeks after pancreatectomy, and 48 hours after insulin withdrawal, basal glucagon and glucose concentrations were elevated (from 22 +/- 3.7 to 55 +/- 9.5 pmol/1 and 5.8 +/- 0.4 to 16.2 +/- 2.0 mmol/l, respectively), (mean +/- SEM), while insulin concentrations were either undetectable or very low. After pancreatectomy, however, glucagon concentrations no longer increased during arginine infusion. Gut type glucagon levels were not affected by pancreatectomy, and did not change during arginine infusion. When examined by gel filtration, plasma from unoperated pigs contained two components of pancreatic type glucagon, one coeluting with the glucagon marker, the other eluting earlier, probably reflecting larger molecular size. After pancreatectomy only this larger component was found in the plasma. The role of this component in the control of blood glucose is unknown.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The effect of physical training on hemodynamic performance was evaluated in a group of patients who had had a myocardial infarction and a group of healthy, age-matched controls. Before training, the patients' mean ventilatory equivalent was significantly less than that of the controls at the lowest workload (300 kpm/min), the mean stroke volume was significantly increased at the highest workload then achieved (600 kpm/min), and the mean arteriovenous oxygen content difference was significantly smaller at the highest workload. The patients had a relative bradycardia before training and there was no significant reduction in mean resting or submaximal heart rate after training. Their mean oxygen uptake was significantly reduced at the lowest exercise workload after training and this response was significantly different from that of the controls after 8 weeks of training. Mean cardiac output during exercise was significantly reduced in the patients after training, but only at the 600-kpm/min workload, the response being blunted at 900 kpm/min; mean stroke volume was also significantly reduced at this workload after training; both these responses were significantly different from those of the controls Mean arteriovenous oxygen content difference at 6oo kpm/min was significantly increased in the patients after training, though the response was not significantly different from that of the controls. Mean ventilatory equivalent was also significantly increased in patients after training, becoming similar to that of the controls.
Explore the source record for details and available documents.