Characterization of surface and resonance phonons for the Ni(001)-c(2 x 2) system.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to K Ho.
Explore the source record for details and available documents.
We describe four patients and review prior reports to clarify the clinical, radiographic, and pathologic findings of intracranial vertebral artery (VA) dissection. A 43-year-old man and a 33-year-old woman had chronic bilateral VA dissecting aneurysms. The man had multiple episodes of subarachnoid hemorrhage (SAH) and necropsy showed multiple dissections and defects in the internal elastica. The woman had many brainstem TIAs and strokes during 3 years. Two other patients had SAH and unilateral dissections. Intracranial VA dissection causes four overlapping syndromes: (1) brainstem infarcts are usually due to subintimal dissection extending into the basilar artery, affect younger patients, and often are single fatal events; (2) SAH is due to subadventitial or transmural dissection; (3) aneurysms cause mass effect on the brainstem and lower cranial nerves; and (4) chronic dissections due to connective tissue defects cause extensive bilateral aneurysms and repeated TIAs, small strokes, and SAH.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Two patients with adrenal carcinoma treated with 2,2-bis (2-chlorophenyl-4-chlorophenyl)-1,1-dichloroethane (o,p'-DDD) as adjuvant therapy were studied. Both patients developed hypoadrenalism while on o,p'-DDD and apparently adequate dexamethasone replacement therapy. The hypoadrenalism was overcome by increasing steroid replacement therapy. Dexamethasone levels were measured in the serum by radioimmunoassay and shown to be lowered by o,p'-DDD therapy. A study of the absorption and disappearance of dexamethasone from the circulation in response to a (1 mg oral dose indicated that the steroid was absorbed normally but was cleared more rapidly from the circulation of these two patients than from normal controls. This may be due to a change in the type of metabolites excreted. It is suggested that many of the reported side-effects of o,p'-DDD may be due to hypoadrenalism and may be controlled by greatly increasing the steroid replacement dose. The adequacy of corticosteroid replacement therapy may best be assessed by monitoring the levels of ACTH.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The purpose of this study was to determine the effects of various programs of physical activity on anxiety-related myocardial damage in rats. The anxiety-producing stress consisted of randomly distributed applications of a disturbing but nonpainful electrical shock. Physical activity consisted of long-duration, low-speed running. Three hundred and seventy-five male albino rats were randomly assigned to five comparison groups. The results show that the anxiety treatment produced marked myocardial damage. Animals preconditioned by eight weeks of exercise prior to the introduction of the anxiety treatment did not suffer as much myocardial damage as did animals that were not preconditioned. However, a group in which exercise and anxiety were introduced simultaneously had the highest incidence of myocardial necrosis. We conclude that aerobic exercise can modify the effects of a subsequent or simultaneous anxiety-producing stressful situation on the myocardium of the laboratory rat. The time at which the exercise is imposed determined the nature of the effect.
Growth hormone-releasing factor (GRF) is found in the highest concentration (albeit lower compared to other hypothalamic regulatory hormones) in the hypothalamus. There is mounting evidence that GRF-like immunoreactivity is found in other sites in the CNS and in the periphery. The role of GRF, other than to stimulate growth hormone secretion by the somatotroph, is unknown. In addition generation of IGF-1 in response to GRF appears to be dependent on an intact pituitary.
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.
A patient with Wilson's disease underwent neuropsychological and electrophysiological examination 4 months following symptom onset. Although motor deficits were more severe, there was considerable impairment of cognitive and intellectual function. Auditory evoked responses were also abnormal in this patient. This case is unusual because of the early severe cognitive deficits.
In vitro studies in this laboratory indicated that at low radiation doses (0-3 Gy), sensitization by misonidazole diminishes. We have suggested that this results from a failure of misonidazole to enhance effectively the single-hit or alpha component of cell inactivation. Our low dose assay uses a partially automated microscopic analysis procedure which scores both surviving and killed cells. If enough cells are scored, this assay provides much better accuracy at low doses than the conventional assay. Recently, we have applied our low dose assay to a study of sensitization by diamide. This was done, in part, as a test of our assay system, since many investigators have shown that diamide substantially reduces the shoulder of the hypoxic cell survival curve. At high doses (D = 6.5 to 10 Gy, S = 0.1 to 0.01) we obtained for 150 microM diamide an enhancement ratio (ER) of 2.6 for hypoxic cells and 1.1 for aerobic cells. At low doses, 0-2.5 Gy, diamide still sensitized hypoxic cells well; with 150 microM diamide, the ER at 1 Gy (S = 0.8) was 2.0, about equal to the oxygen enhancement ratio (OER) at this dose. The fact that diamide shows good sensitization at low doses with our assay adds to the credibility of the assay and reduces the likelihood that our observations with misonidazole are an artifact of our system.
The present study evaluated uptake of phosphate by brush border membrane vesicles (BBMV) and alkaline phosphatase activities in brush border membrane fractions in rats fed a normal (0.6%) or low (0.03%) phosphorus diet for 24 h. After 2 min of incubation, the phosphate uptake by BBMV from rats ingesting normal and low phosphorus diets was 1,531 +/- 98 and 2,112 +/- 183 pmol/mg protein, respectively (p less than 0.025); peak glucose uptake was 226 +/- 17 and 209 +/- 42 pmol/mg protein, respectively. Vmax increased 74% in the 0.03% dietary phosphorus groups (p less than 0.005) while Km was similar between groups. Alkaline phosphatase activities were 824 +/- 48 and 816 +/- 56 nmol/min/mg protein with the respective diets. The earliest detectable increase in phosphate uptake by BBMV occurred within 4 h of dietary phosphorus deprivation while alkaline phosphatase increased 3 days later. Renal adaptation to phosphate deprivation can occur within 4 h, is not due solely to a change in the filtered load of phosphate and occurs before increases in the specific activity of alkaline phosphatase.
Metabolic acidosis produces a phosphaturia which is independent of parathyroid hormone or dietary phosphorus intake. To study the underlying mechanism, inorganic phosphate (Pi) and glucose transport were studied in brush-border membrane vesicles prepared from the renal cortex of parathyroidectomized rats gavaged for three days with either 7.5 ml of 1.6% NaCl (control) or 1.5% NH4Cl (acidosis). At killing, blood pH and plasma bicarbonate were 7.36 +/- 0.01 and 21.8 +/- 0.8 mequiv./l, respectively, in control and 7.12 +/- 0.03 (P less than 0.01) and 11.1 +/- 1.2 (P less than 0.01) in acidotic rats. Serum Pi was similar in both groups, while 24 h urine Pi excretion was higher in the acidotic group (P less than 0.01). Peak sodium-dependent uptake of Pi, measured after 1.5 min of incubation, was higher in controls than acidotic rats (4442 +/- 464 vs. 2412 +/- 259 pmol/mg protein, P less than 0.01), whereas peak glucose uptake at 1.5 min was not significantly different between the groups. Equilibrium values for Pi and glucose uptake were similar in the two groups. Km for Pi uptake in the control and acidotic animals were not different, 0.036 and 0.040 mM, respectively. By contrast, Vmax was higher in controls than in the acidotic group, 3.13 vs. 1.15 nmol/mg protein per 15 s. These results suggest that metabolic acidosis directly inhibits Pi uptake by the brush border of the proximal tubule by decreasing the availability of Pi carriers of the renal brush-border membrane.