A hospital based comprehensive cardiac rehabilitation program.
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Biomedical subjects
Publications and source records attributed to M Garcia.
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We are reporting about an inoperable cell carcinoma of the stomach, which exclusively caused thoracal pains due to metastases into a pleural thickening. First this symptomatology with thoracal pains and recurring pleural effusions was thought to be a pleural mesothelioma. Only the immediate histological examination of the tissue showed the origin of the tumor. Although cancer of stomach appears very commonly, this tumor is often diagnosed too late and in most cases it is already inoperable. Even nowadays more than 75% of the patients with a cancer of the stomach die of their metastases, although diagnosis and therapy have been developed. - Pleural mesotheliomas are rare; nevertheless the possibility of a mesothelioma in connection with all pleural effusions of a vague genesis should be considered. The exposure to asbestos strengthens the suspicion that this tumor is existing. In connection with a pleural mesothelioma an indurative pleurisy, a primary cancer of the lung and - like in our case - pleural metastases of a primary cancer of another site have to be differentiated.
In the MCF7 human breast cancer cell line, estrogens induce a secreted glycoprotein with an Mr of 46 000 (46 000-Mr protein) and the progesterone receptor; they also increase to a lesser extent the secretion of [35S]-methionine-labelled proteins. When the cells are grown in the presence of 5-bromo-2'-deoxyuridine (BrdUrd, 5 microgram/ml for 4 days) these estrogen-induced responses are substantially inhibited while other proteins not regulated by estrogens and cell growth are not affected by BrdUrd. This effect of BrdUrd is not secondary to a decrease in estrogen receptor levels and appears to require incorporation of BrdUrd into DNA for the following reasons. First, there is a lag before any effect of BrdUrd is seen which is similar to the doubling time of the cells. Second, the effect of BrdUrd is not seen when cells are cultured in medium containing BrdUrd and 1-beta-D-arabinofuranosylcytosine, a DNA synthesis inhibitor, or excess thymidine, which blocks the incorporation of BrdUrd into DNA. Finally 2'-deoxycytidine, which reverses the effects of non-incorporated BrdUrd, is without effect on the inhibition of the estrogen-induced 46 000-Mr protein. We conclude that BrdUrd selectively prevents the effects of estrogens in MCF7 cells and that the mechanism of this anti-estrogenic effect of BrdUrd probably requires its incorporation into DNA and occurs beyond the nuclear translocation step of the estrogen receptor. Alterations in the recognition of chromatin effector sites by the estrogen-receptor complex could be involved in preventing hormone action.
Exchangeable sodium (E-Na), plasma volume (PV), and plasma renin activity (PRA) have been studied in 19 patients with essential hypertension and diabetes, and the results compared to those of non-diabetic patients with benign essential hypertension. None of the cases had renal disease or hypertension with systolic predominance. E-Na was 114 +/- 9.74 (SD), significantly superior to that of normal subjects (p less than 0.001). An elevated E-Na was observed in 52.6% of the diabetic group, while PV was normal. PRA levels were normal in most patients, mean 1.28 +/- 1.97 ng ml-1 h-1, only two patients disclosing an elevated PRA (10.5%). No relationship was found between PRA and age, blood pressure, and E-Na. From the comparison of results between diabetic and non-diabetic hypertension patients it appears that: 1) no differences between mean PRA and E-NA exist, although a greater percentage of diabetics have an elevated E-Na, and 2) in the non-diabetic group there is a positive correlation between E-NA and PV, while in the diabetic group such a correlation is negative (p less than 0.05). The finding of an elevated body sodium in patients with essential hypertension and diabetes probably represents a true abnormality in the body composition of these patients, although there is no explanation for the fact that it is unassociated to an increase of the plasma volume, as opposed to essential hypertension in non-diabetics.
A 51 year old nurse had a long complicated medical history with repeated medical and surgical interventions. Her condition fits the clinical description of the Münchausen syndrome. She presented to the hospital with hyperabsorptive hypercalcemia of over 20 mg/100 ml. Many diagnostic studies and intriguing detective investigations were undertaken before the cause of the extreme hypercalcemia was determined. The patient had been secretly ingesting between 20 and 30 Os-Cal 500 tablets daily which she repeatedly denied and which eventually were found in a false compartment of her purse. This is thought to be the highest recorded serum calcium level observed following the clandestine ingestion of excessive amounts of oral calcium.
Hemangioma calcificans is a rare condition that may be regarded as a calcified cerebral cavernous angioma. The clinical presentation is usually that of epilepsy in an adult. A calcified nodule is visible on radiographs of the skull or computed tomographic (CT) scans. Angiography does not demonstrate vascularity. It is usually a solitary subcortical lesion that is surgically removable. Because of the favorable results from treatment of this lesion, this report reviews the clinical and radiological features described in the literature and includes an additional case.
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5-Androstene-3 beta, 17 beta-diol (ADIOL) has previously been shown to have a high affinity for the estrogen receptor and to translocate it to the nucleus in vitro and in vivo. This compound and related C19 delta 5-steroids of adrenal origin have now been examined for their ability to induce the synthesis in MCF7 cells of an estrogen-dependent secreted glycoprotein (M.W. 46,000). Concentrations required for half-maximum induction were 2 nM for ADIOL and 500 nM for dehydroepiandrosterone (DHEA). Dehydroepiandrosterone sulfate showed weak inducing ability at concentrations of 1 microM or greater. The induction by ADIOL was unaffected by the presence of an aromatase inhibitor, and 5 alpha-androstane-3 beta, 17 beta-diol, which cannot be aromatized, also induced the M.W. 46,000 protein at low concentrations. When cells were exposed to 10 nM [3H]ADIOL, the cytosol and nuclear fractions contained [3H]ADIOL resistant to charcoal adsorption. The bound [3H]ADIOL in the cytosol and nucleus was displaceable by 17 beta-estradiol and tamoxifen, suggesting that it was binding to the estrogen receptor. [3H]ADIOL was metabolized to its 3 beta-sulfate, which was excreted into the medium, and to [3H]DHEA, which was found in the cells and the medium as free DHEA and its 3 beta-sulfate. [3H]DHEA was also metabolized by the cells to its 3 beta-sulfate, to free ADIOL, and to the 3 beta-sulfate of adiol. We conclude that: (a) ADIOL is effective as an estrogen in MCF7 cells at a concentration of 2 nM, which is within the range found in the blood of normal women; and (b) sulfurylation is a major route of inactivation of 3 beta-hydroxy delta 5-steroids in MCF7 cells.
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From 1975 to 1978, ten patients were on long-term hemodialysis due to acute barbiturate intoxication. Duration of hemodialysis varied from 16 to 40 hours (mean 23 +/- 9.4 hours). Phenobarbital was the most common type of barbiturate ingested (6 out of 10 patients), and diazepam the drug most frequently taken in association with barbiturates (3 out of 10 patients). All patients were in a state of deep unconsciousness (coma II: 1 case; coma III: 5 cases; coma IV: 4 cases), and all of them required endotracheal intubation. Seven patients needed the assistance of automatic intermittent positive-pressure respirator. Two patients presented hypothermia, and another a peripheral collapse. Long-term hemodialysis was well tolerated without major complications. Significant decreases of barbiturate levels were obtained in all cases (before hemodialysis: 7.3 +/- 1.9 mg/dl, after hemodialysis: 1.8 +/- 1.2 md/dl, corresponding to the pattern of secobarbital used to refer the results). No correlation was observed between initial levels of barbiturates and number of hours of long-term hemodialysis required. Neurologic symptoms improved in all cases. Eight patients were conscious after hemodialysis had been discontinued, and only two patients remained unconscious (coma I). Intratracheal tube could be removed in six patients, but positive-pressure respirator could be took away from all cases. Complete recovery was achieved in eight patients. Two patients died on the 2nd. and 8th. postdialysis days due to respiratory distress. Long-term hemodialysis has proven of value in the treatment of severe barbiturate intoxication, particularly better to conventional hemodialysis.
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In twelve patients with primary hyperparathyroidism the raised parathyroid hormone (PTH) levels consistently returned to normal with cimetidine ("Tagamet"), 300 mg four times a day, orally. As PTH levels returned to normal, signs and symptoms improved. Reduction of hypercalcaemia varied with the time, dose, and route of administration of cimetidine. Whenever cimetidine was discontinued, there was a rebound of PTH levels to approximately twice the initial value, which suggests that cimetidine blocks the synthesis and/or secretion of parathyroid hormone, so that parathyroid hormone or its precursor accumulates in the gland. A solitary parathyroid adenoma has been confirmed surgically in the five patients so far operated on. In all surgical patients the PTH levels were brought to normal by cimetidine preoperatively; these levels were maintained postoperatively. The adenomas were unusually large, firm, and congested; there was no atrophy of the rest of the glands. These last two observations further support our hypothesis that cimetidine blocks the synthesis or release of parathyroid hormone; they also support the concept that in primary hyperparathyroidism the parathyroid adenoma becomes autonomous or there is an abnormal hormone.
We have investigated the action of high doses of androgens in Gobius niger L., a marine teleostean fish, by characterizing specific steroid receptors in liver and by assaying the plasma vitellogenin concentration under different hormonal treatments. Estrogen and androgen receptors were characterized in the liver nuclear extracts according to their binding specificity. The maximum binding capacity was 25 fmoles/mg protein for the estrogen and androgen receptors. In vivo, high doses of DHT()increased the concentration of plasmatic vitellogenin as assayed by immunodiffusion while low doses were inefficient. In spite of a similar number of estrogen and androgen nuclear receptor sites (25 fmoles/mg protein), DHT was at least 70 fold less active than E2 on yolk protein and vitellogenin induction both in male and female Gobius niger. In addition, the antiestrogen tamoxifen, which was inactive by itself, inhibited the E2 and the DHT induced accumulation of vitellogenin. Progesterone (2 mg/fish) was also totally inactive in inducing vitellogenin. We conclude that the induction of vitellogenin by DHT is mediated by the estrogen receptor rather than by the androgen receptor. In addition to the estradiol induced protein in rat uterus and to other estrogenic responses obtained by androgens in mammary cancer, fish vitellogenin is another estrogen regulated protein which can be induced by high doses of androgens.
The effect of estradiol on chromatin ultrastructure in interphase nuclei was studied in immature rat and lamb endometrium. Physiological doses of estradiol within the first hour transformed the condensed chromatin into dispersed chromatin both in vivo and in vitro. These ultrastructural modifications were specifically induced by hormones translocating the estrogen receptor to the nucleus of estrogen-responsive tissues. Conversely, the antiestrogen tamoxifen gave a hypercondensation of chromatin. The addition of actinomycin D, cordycepin or alpha-amanitin, but not of cycloheximide, prevented the effect of estradiol both on the ultrastructural change and on [3H]uridine incorporation, suggesting that chromatin decondensation was closely related to transcriptional activity. These results indicate that in endometrium, estrogen rapidly provokes a large and extended modification of chromatin ultrastructure, which suggest a general effect on chromatin function rather than a selective activation of a limited number of genes.
A case of fibromuscular dysplasia (FMD) with involvement of the aorta is described in a 44-year-old woman. So far only 3 cases of aortal FMD have been mentioned, all in female patients. Our observation is characterized by a solitary stenosis of the lower abdominal aorta and it resembles histologically the "intimal fibroplasia" type of renal FMD. The review of the literature about FMD in general reveals that mostly the renal arteries are affected, followed by cervical artery FMD with only rare occurrence in other vessels. Though the etiology is basically unknown several factors have been made responsible, namely hereditary disposition, congenital rubella infection, female hormones, paucity of the vasa vasorum, and stretch-traction-stress. The disease has been classified into several histological subgroups and also according to the roentgenologic form which typically shows a "string of beads" appearance. There is a definitive female sex preponderance of 5:1, which is the same for all affected vessels; whereas in respect to age there is a marked distinction in so far that renal FMD patients on average are 11 years younger than patients with the cervicocephalic form of the disease.
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