Invasive papillary carcinoma in elderly women: sonographic and mammographic features.
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Biomedical subjects
Publications and source records attributed to R Silva.
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We have identified a plasmatic substance, "pepsanurin" (PU) obtained by pepsin hydrolysis which inhibits the renal effects of the atrial natriuretic factor (ANF). To investigate whether patients with congestive heart failure (CHF) have increased plasma levels of PU we prepared PU from 10 patients with CHF class IV (NYHA), 9 patients with CHF class II or III and 16 healthy controls. Anesthetized rats were used to test the effects of ANF, 0.5 ug/100 g body weight i.v., before and following the intraperitoneal injection of 0.5 ml of PU. The inhibition of the diuretic and natriuretic effects of ANF was 40.9 +/- 11.9% and 49.8 +/- 12% respectively for control subjects. Corresponding figures for class IV CHF patients were 62.3 +/- 3.1% and 73.8 +/- 3.5% (p less than 0.02) and for class II-III patients 39.2 +/- 7.0% and 53.1 +/- 8.2% (NS). Accordingly, an increased capacity to generate PU may underlie the decreased sensitivity to ANF in patients with advanced CHF.
Conventional preparation of goitrous hyperthyroid patients using lugol and propranolol may take 2 weeks. This period may be shortened using sodium iopodate and dexamethasone. We used 500 mg of sodium iopodate and 1 mg dexamethasone for 4 days in 34 hyperthyroid patients. Surgical indication derived from failure to medical treatment (68%), large goiter (27%) or adverse reaction to PTU (6%). Clinical euthyroidism was achieved after 4 days in all patients. T3 levels decreased from 482 +/- 26.2 to 137.6 +/- 3.7 ng/dl and T4 from 20.6 +/- 1.04 to 15.2 +/- 0.5 micrograms/dl (p < 0.005). Surgery was uneventful in 33 patients, one subject developed supraventricular tachycardia responsive to verapamil. Electron microscopy of the removed thyroid tissue revealed marked decrease of superficial villi and large phagosomes. Thus, sodium iopodate and dexamethasone are effective and safe for preoperative preparation of hyperthyroid patients.
Radionuclide angiocardiography and left ventricular manometry were performed simultaneously in 12 men undergoing elective coronary artery bypass grafting. Pressure-volume loops constructed from these data allow calculation of stroke work and provide a more complete description of global left ventricular function immediately before cardiopulmonary bypass and at a mean of 18 and 34 minutes after termination of ischemic arrest. Early reperfusion was characterized by significant elevation of end-diastolic pressure (p less than 0.01) without a corresponding increase in end-diastolic volume. With continued reperfusion, end-diastolic volume, calculated stroke work, and cardiac output increased significantly with respect to control (p less than 0.05). Heart rate, ejection fraction, mean arterial pressure, stroke work/end-diastolic volume, and maximal dP/dt remained unchanged during the study period. No new focal abnormalities were detected in regional wall motion. These data indicate that minimal residual impairment of diastolic function exists during the acute recovery from cardioplegic arrest and bypass grafting but improves with further reperfusion. Systolic function appears to normalize more rapidly than diastolic function after ischemic arrest.
Use of 2-nitroimidazole, 5-nitrofuran and 5-nitroimidazole compounds in T. cruzi-infected rabbits resulted in a reduction in duration of parasitaemia in comparison with untreated, infected rabbits. The chronic myocarditis associated with Chagas' disease was not, however, prevented in nitroarene-treated rabbits; lymphocytic infiltrates associated with cardiac cell lysis, in the absence of parasites in situ, were present in both treated and untreated rabbits. The carcinogenic effect of each trypanocidal nitroarene used in this study was also assessed. Administration of nitroarenes to rabbits resulted in the appearance of solid tumours in 37.8 per cent of animals that received drug therapy. Untreated, control rabbits in this series did not show tumour growth. Furthermore, malignant, mixed-cell type, non-Hodgkin's lymphomas were seen in 32.4 per cent of the treated rabbits. It seems that a direct relationship could be present between the presence of the nitro group, the trypanocidal cytotoxicity and the prevalence of tumours. Benznidazole cleared up parasitaemias in the shortest time and was associated with 41.6 per cent of lymphoma growths, whereas MK-436 required twice as much time to clear blood parasites, and showed lymphomas in 25 per cent of experimental rabbits. The demonstration of a high prevalence of malignant tumours in addition to the chronic myocarditis of Chagas' disease in nitroarene-treated rabbits is important since indiscriminate use of such compounds currently used to treat T. cruzi infections in man could increase the risk of lymphoma.
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The polarity of release and activation of renal kallikrein and its regulation by adrenal hormones was studied in isolated perfused rat kidneys. Bilateral adrenalectomy (AX) produced a decrease in kallikrein and prokallikrein excretion into urine and perfusate of isolated kidneys, as well as in active kallikrein excretion in vivo. One-week treatment with deoxycorticosterone acetate (DOCA 2.5 mg/day) or dexamethasone (DEX 0.25 mg/day) increased the urinary output of active and total kallikrein above AX levels but below control. In contrast, neither corticoid increased enzyme secretion to perfusate. Regardless of AX or corticosteroid treatment, the prokallikrein fraction was 90% of total enzyme in perfusate and only 40% in urine. These results confirm that adrenal steroids are necessary for renal kallikrein synthesis and excretion; however, neither DOCA nor DEX appears to be a unique regulator for release or activation of this enzyme. In addition, whereas the processes of secretion and activation toward the urine are regulated in parallel, kallikrein release to the venous effluent seems to be regulated separately.
Glandular kallikrein (a trypsin-like serine protease) is an estrogen-induced and dopamine-repressed protein in the rat anterior pituitary which predominantly exists as a latent zymogen (prokallikrein). Its regulation, presence in estrogen-induced pituitary tumors in F344 rats, and expression in GH3 cells has suggested a localization in lactotrophs (prolactin-producing cells). This study examined the cellular origin of glandular kallikrein using immunocytochemical techniques. Anterior pituitaries from estrogen-treated rats were fixed and embedded in paraffin (for preparation of semi thick sections; 5 microns) or methacrylate (for preparation of thin sections; 1 micron). Glandular kallikrein immunostaining was readily detected in the perinuclear (Golgi) region of parenchymal cells of the anterior pituitary in both thin and semi thick sections. Two-color double immunoperoxidase staining of thin and semi thick sections indicated that glandular kallikrein was localized in cells containing prolactin (PRL) but not other pituitary hormones. Immunoperoxidase staining of consecutive serial thin sections with alternating antisera confirmed a localization of glandular kallikrein in lactotrophs. The results establish that glandular kallikrein is colocalized with PRL in lactotrophs of the rat anterior pituitary. This is consistent with the hypothesis that the function of anterior pituitary glandular kallikrein is linked to PRL in some fashion--possibly as a PRL-processing protease.
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The major chicken vitellogenin gene (VTGII) has previously been cloned and sequenced. We now report the isolation of genomic clones that encompass a minor chicken vitellogenin gene (VTGIII) which is also expressed in the liver in response to estradiol. Our analysis reveals that a pseudogene for VTGII (psi VTGII) lies 1,426 base pairs upstream of this VTGIII gene. A reevaluation of published sequence data reveals that the converse is also true, namely, that a pseudogene for VTGIII (psi VTGIII) lies 1,345 base pairs downstream of the VTGII gene. Our results show that a 335-base-pair deletion has removed the psi VTGIII promoter and cap site but left residual estrogen response element in a region where nuclease-hypersensitive sites have been reported to be induced in response to estradiol.
We report the first precise delineation of a chicken CR1 element and show that it is flanked by a 6-base-pair target site duplication that occurred when this repetitive element transposed. The 3' end of this CR1 element is defined by an 8-base-pair imperfect direct repeat, and we infer that this sequence represents the 3' end of all intact CR1 elements. In contrast, the 5' ends are not unique, and we argue that this variation existed at the time each element transposed. We also provide evidence that CR1 elements transposed into preferred target sites. CR1 elements therefore appear to represent a novel class of passive retroposons.
The effect of intravenous (IV) nitroglycerin (NTG) on perioperative myocardial ischemia as detected by single pass radionuclide angiocardiography was studied in 20 patients scheduled for elective coronary artery bypass grafting (CABG). Ten patients, selected at random, received IV NTG 1 microgram.kg-1.min-1 (NTG group) and 10 others, IV saline (control group). Anesthetic induction consisted of midazolam 0.2 mg.kg-1, vecuronium 0.1 mg.kg-1, and 50% N2O in O2. ECG leads I, II, and V5 were monitored for ST segment changes. Single pass radionuclide angiocardiography (RNA) was performed at 5 times: prior to induction, prior to tracheal intubation, and at 1, 3.5, and 6 min following intubation. The presence of new regional wall motion abnormalities (RWMA) was determined from each RNA study as compared with the preinduction measurement. Apart from one patient in the control group who developed a new "v" wave after intubation, there was no evidence of ischemia by pulmonary capillary wedge pressure. No ECG evidence of ischemia was detected in any patient. Despite this, new regional wall motion abnormalities were observed in 3 patients in the control group and 1 patient in the NTG group. Blood pressure and heart rate responses of patients with new RWMA were not significantly different from other patients. The low incidence of ischemia in this population precludes a definitive statement regarding the efficacy of IV NTG, but the lower incidence of RWMA in the NTG group suggests a protective effect.
Two sibs with partial trisomy-5p are reported. Their father is the carrier of a balanced translocation 46,XY,t(4q+;5p-). Twelve cases of partial trisomy-5p--including our two patients--have been reported. The most common abnormalities found were mental retardation, short stature, dolichocephaly, prominent nasal bridge, prognathism, seizures, hypotonia, ear abnormalities, increased ulnar loops on the fingertips, and cryptorchidism in affected males.
A non-fluorescent Y chromosome was observed in a phenotypic male with 45,X/46,XYq-mosaicism and mixed gonadal dysgenesis. Q-banding of the father's chromosomes showed a normally fluorescent Y. Measurements of the Y chromosomes in the father and the patient showed a significant difference in length. Evidence for translocation of the Y fluorescent segment to another chromosome was lacking in the present case.
A stillborn male fetus having a trisomy of the short arm of chromosome No 10 is described. The father is a carrier of the reciprocal translocation 46XY,t(10;21) (10pter leads to 10p11::21p11 leads to 21qter). The clinical picture included growth retardation, bilateral cleft lip and palate, micrognathia, short neck, microphalus and bilateral clubbed feet. The long bones were markedly thinned with spontaneous fractures. Autopsy findings included pulmonary hypoplasia and renal dysplasia. Previous reports of trisomy 10 and trisomy of the short arm of chromosome 10 are discussed.
This histological study reports the pathological findings in mice deficient in essential fatty acids (EFAD). As shown by others, hyperplasia and hyperkeratosis were observed in skin. In addition, we reported hyperkeratosis of the esophagus and forestomach, severe degrees of atrophy of the seminal epithelium of testes, and diminution of the luminal content of epididymis, and the formation of clusters of lipid-laden macrophages in lungs. Hyperemia was also a systemic change in many organs. These alterations have not been reported in EFAD mice previously.