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Biomedical subjects

A Sebastian

Publications and source records attributed to A Sebastian.

At least 109 records · Page 6Linked to original sources
PubMed1976

Exaggerated phosphaturic response to circulating parathyroid hormone in patients with familial X-linked hypophosphatemic rickets.

To determine whether the phosphaturic response to circulating parathyroid hormone (PTH) is exaggerated in patients with familial x-linked hypophosphatemic vitamin D-resistant rickets (FHR), we examined the phosphaturic response to parathyroid extract (PTE) (administered intravenously in the posthypercalcemic state) in two unrelated adult hemizygotes with FHR. In these two patients whose plasma concentration of PTH was normal (determined by radioimmunoassay). neither vitamin D nor phosphate therapy had been given during the past 10 yr. Two normal men and a hypophosphatemic man with intestinal malabsorption, hypocalcemia, and osteomalacia served as control subjects. In all subjects, calcium gluconate was adminstered intravenously from 6 p.m. to 12 midnight at a rate that maintained the concentration of serum calcium at 13-15 mg/100 ml during the administration of calcium. When normocalcemia had recurred the next morning, and the plasma PTH concentration and urinary excretion of cyclic 3', 5'-AMP were reduced. PTE was administered intravenously at successively increasing rates of 0.1, 0.4, and 0.8 U/kg per h, each rate lasting 90 min. Minutes after the initiation of PTE in the affected hemizygotes, fractional excretion of filtered phosphate increased from negligible values to values strikingly greater than those of similarly studied control subjects and plateaued at strikingly greater values throughout further administration of PTE. This phenomenon of exaggerated phosphaturia could not be attributed to volume expansion, decreases in serum concentration of calcium during the study, differences in percent of administered calcium retained, or hemodynamic changes. Only the phosphaturic response to PTE appeared to be exaggerated. At any cumulative dose of PTE, urinary excretion of cyclic 3', 5'-AMP in the hemizogytes was indistinguishable from that of control subjects. The findings in this study suggest that in patients with FHR, circulating PTH is required for the genetically transmitted abnormality to be physiologically expressed as a reduction in net renal reabsorption of phosphate, and that this physiological expression of the genetic abnormality is expressed fully at normal or nearly normal circulating levels of PTH.

Absorption↗
PubMed1976

Impaired renal conservation of sodium and chloride during sustained correction of systemic acidosis in patients with type 1, classic renal tubular acidosis.

In 10 patients with classic renal tubular acidosis in whom correction of acidosis was sustained with orally administered potassium bicarbonate, renal conservation of sodium was evaluated when dietary intake of sodium was restricted to 9--13 meq/day. In five patients, renal conservation of sodium was impaired by at least one criterion of impairment. In the remaining patients, renal conservation of sodium appeared to be relatively well-maintained, but an impairment could not be excluded. In each of six patients studied during induced water diuresis, including two in whom renal conservation of sodium was not unequivocally impaired, the minimal urinary concentrations of sodium were inappropriately high and the urinary excretion rates of sodium were flow-dependent. These results provide direct evidence that an abnormality in renal transport of sodium can occur in classic renal tubular acidosis, and compel a reconsideration of the pathophysiology of disordered renal transport of sodium in this disorder. The results indicate that in at least some patients with classic renal tubular acidosis impaired renal conservation of sodium is not exclusively a reversible consequence of the renal acidification defect. These findings raise the question whether renal transport of sodium is unimpaired in any patients with classic renal tubular acidosis. In the presently studied patients, the impairment in renal conservation of sodium appeared to be in part the consequence of an impaired ability of the vasopressin-responsive segments of the distal nephron to generate and maintain appropriately steep transepithelial sodium concentration gradients.

Acid-Base Equilibrium↗
PubMed1972

Renal tubular acidosis in infants: the several kinds, including bicarbonate-wasting, classic renal tubular acidosis.

In four infants with renal tubular acidosis (RTA), including three with apparently classic RTA and one with Fanconi syndrome (FS), the physiologic character of the renal acidification defect was investigated. In two of the infants with apparently classic RTA, the acidification defect was physiologically separable from that described in both adult patients and children with classic RTA (type 1 RTA) in the following ways. (a) The fractional excretion of filtered bicarbonate (C(HCO3)/C(ln)) was not trivial but substantial (6-9%), as well as relatively fixed, over a broad range of plasma bicarbonate concentrations (15-26 mmoles/liter). (b) This value of C(HCO3)/C(ln), combined with a normal or near normal glomerular filtration rate, translated to renal bicarbonate wasting (RBW). (c) RBW at normal plasma bicarbonate concentrations was the major cause of acidosis, and its magnitude was the major determinant of corrective alkali therapy (5-9 mEq/kg per day), just as in the patient with FS, who was found to have type 2 ("proximal") RTA. (d) Persistence of RBW at substantially reduced plasma bicarbonate concentrations, which did not occur in FS, accounted for the spontaneous occurrence of severe acidosis and its rapid recurrence after reduction in alkali therapy. (e) During severe acidosis the urinary pH was >7, a finding reported frequently in infants with apparently classic RTA and "alkali-resistant" acidosis but rarely in adult patients with classic RTA. Continued supplements of potassium were required to maintain normokalemia during sustained correction of acidosis with alkali therapy. Yet, in at least two of the three infants with apparently classic RTA, but in distinction from the patient with FS and other patients with type 2 RTA, fractional excretion of filtered potassium decreased when plasma bicarbonate was experimentally increased to normal values. In one of the two infants with apparently classic RTA and RBW, C(HCO3)/C(ln) and the therapeutic alkali requirement decreased concomitantly and progressively over 2 yr, but RBW continued. Renal tubular acidosis has persisted in all four patients for at least 3 yr, and in three for 4 years.

Acidosis, Renal Tubular↗
PubMed1971

Modulation of experimental renal dysfunction of hereditary fructose intolerance by circulating parathyroid hormone.

In a woman with hereditary fructose intolerance and intact parathyroid function, the experimental administration of fructose at different dosage schedules invariably induced the dose-dependent, complex dysfunction of the proximal renal tubule now recognized as characteristic. But in a woman with hereditary fructose intolerance and hypoparathyroidism given similar amounts of fructose, the experimental dysfunction was strikingly attenuated or nondemonstrable unless or until fructose and parathyroid hormone were administered in sustained combination. Thereupon, a renal dysfunction of characteristic type and severity occurred invariably and almost immediately. Thus, the concentration of circulating parathyroid hormone can modulate the functional expression of the experimental renal disorder. This effect of parathyroid hormone, which appears to involve more than simple physiologic summation, may have important clinical implications.

Adult↗
PubMed1971

On the mechanism of renal potassium wasting in renal tubular acidosis associated with the Fanconi syndrome (type 2 RTA).

The mechanism of renal potassium wasting in renal tubular acidosis associated with the Fanconi syndrome (type 2 RTA) was investigated in 10 patients, each of whom had impaired proximal renal tubular reabsorption of bicarbonate as judged from a greater than 15-20% reduction of renal tubular bicarbonate reabsorption (THCO(3) (-)) at normal plasma bicarbonate concentrations. When the plasma bicarbonate concentration ([HCO(3) (-)]p) was experimentally increased to normal levels in three patients with a fractional potassium excretion (C(K)/C(in)) of less than 1.0 during acidosis, C(K)/C(in) and urinary potassium excretion (U(K)V/C(in)) increased strikingly and concurrently with a striking increase in urinary sodium (U(Na)V/C(in)) and bicarbonate (U(HCO3-)V/C(in)) excretion. When [HCO(3) (-)]p was increased to normal levels in two patients with a C(K)/C(in) of greater than 1.0 during acidosis and in whom U(Na)V/C(in) and U(HCO3-)V/C(in) were already markedly increased, C(K)/C(in) did not increase further. When [HCO(3) (-)]p was decreased to subnormal levels in a patient given ammonium chloride, U(K)V/C(in), C(K)/C(in), and U(HCO3-)V/C(in) decreased concurrently. In the six patients in whom [HCO(3) (-)]p was maintained at normal levels (oral alkali therapy) for 2 months or longer, C(K)/C(in) was directly related to the urinary excretion rates of sodium and bicarbonate, hence was directly related to the magnitude of reduction of THCO(3) (-) at normal [HCO(3) (-)]p; C(K)/C(in) was greater than 0.55 in all six patients and greater than 1.0 in four. In eight patients with classic RTA (type 1 RTA), proximal renal tubular reabsorption of bicarbonate was largely intact as judged from a trivial reduction of THCO(3) (-) at normal [HCO(3) (-)]p. When [HCO(3) (-)]p was either increased from subnormal to normal levels, or decreased from normal to subnormal levels, U(HCO3-)V/C(in) remained essentially constant, and U(K)V/C(in) did not change significantly. When correction of acidosis was sustained, U(HCO3-)V/C(in) remained a trivial fraction of that filtered, and C(K)/C(in) was consistently less than 0.55. These results provide evidence that renal potassium wasting in type 2 RTA is physiologically separable from that in type 1 RTA and in part the result of a reduction in the rate at which the proximal tubule reabsorbs bicarbonate and the distal delivery of supernormal amounts of sodium bicarbonate. With an increased stimulus to distal sodium reabsorption, indicated by the finding of hyperaldosteronism, delivery to the distal nephron of supernormal amounts of sodium with the relatively impermeant bicarbonate anion would be expected to increase intraluminal negativity in the distal nephron, and as a consequence, increase potassium secretion and promote renal potassium wasting.

Acidosis, Renal Tubular↗
PubMed1971

Renal potassium wasting in renal tubular acidosis (RTA): its occurrence in types 1 and 2 RTA despite sustained correction of systemic acidosis.

IN TWO PATIENTS WITH CLASSIC RENAL TUBULAR ACIDOSIS (RTA) AND IN TWO PATIENTS WITH RTA ASSOCIATED WITH THE FANCONI SYNDROME, RENAL POTASSIUM WASTING PERSISTED DESPITE SUSTAINED CORRECTION OF ACIDOSIS: (a) during moderate degrees of hypokalemia, daily urinary excretion of potassium exceeded 80 mEq in each patient; (b) during more severe degrees of hypokalemia, daily urinary excretion of potassium exceeded 40 mEq in two patients and 100 mEq in another. These urinary excretion rates of potassium are more than twice those observed in potassium-depleted normal subjects with even minimal degrees of hypokalemia. The persistence of renal potassium wasting may have resulted in part from hyperaldosteronism, since urinary aldosterone was frankly increased in two patients and was probably abnormally high in the others relative to the degree of their potassium depletion. The hyperaldosteronism persisted despite sustained correction of acidosis, a normal sodium intake, and no reduction in measured plasma volume, and was not associated with hypertension; its cause was not defined. In the two patients with classic RTA, neither renal potassium wasting nor hyperaldosteronism could be explained as a consequence of a gradient restriction on renal H(+) - Na(+) exchange because the urinary pH remained greater than, or approximately equal to, the normal arterial pH or considerably greater than the minimal urinary pH attained during acidosis. The findings provide no support for the traditional view that renal potassium wasting in either classic RTA or RTA associated with the Fanconi syndrome is predictably corrected solely by sustained correction of acidosis with alkali therapy.

Acidosis, Renal Tubular↗
PubMed1967

Time of arrival of gravid Culex pipiens fatigans at an oviposition site, the oviposition cycle and the relationship between time of feeding and time of oviposition.

One of the most important activities in a female mosquito's life is the flight to the breeding place and the subsequent deposition of eggs. During this phase, motivated by endogenous and exogenous stimuli, the female is particularly exposed and susceptible to attack. It is therefore important to investigate these episodes in the gravid female's life.The work reported in this paper shows that gravid Culex pipiens fatigans females are easily trapped over breeding-water; there are two peaks in the arrival at a breeding site, one just after sunset and the other at sunrise. The oviposition cycle is biphasic, the two peaks coinciding, in calm weather, with the two arrival peaks; wind and rain cause marked disturbances in the oviposition cycle.The mean duration of the gonotrophic cycle depends on the time of feeding; this finding is of practical importance since the length of the cycle is often used to calculate the daily survival rate of adult mosquitos. It appears that oviposition is stimulated by a change in light: from light to dark for mosquitos ovipositing in the evening and from dark to light for those ovipositing in the morning.Apart from revealing some hitherto unknown behaviour patterns, the techniques evolved could also be used in the assessment of mosquito populations and hence the effects of control measures.

Animals↗
PubMed1967

Outdoor resting of Culex pipiens fatigans in Rangoon, Burma.

The sites occupied by resting adult mosquitos are of importance, since they may be accessible to treatment with insecticide. It has usually been assumed that Culex pipiens fatigans feeds and rests indoors, thus making itself vulnerable to indoor spraying. However, work in the Kemmendine Experimental Area of Rangoon, Burma, has now shown that many C. p. fatigans rest out of doors in a variety of shelters. The lower parous rate in outside catches as compared with indoor catches tends to confirm the view that newly hatched C. p. fatigans rest out of doors for some time before setting off to feed. The percentage of infected mosquitos is remarkably constant from site to site and from month to month and does not differ significantly from that obtained in indoor resting catches or on bait out of doors. It appears that the possibility of acquiring infection out of doors will have to be seriously considered in any anti-filariasis campaign.

Animals↗
PubMed1967

Qualitative and quantitative characteristics adult Culex pipiens fatigans populations according to time, site and place of capture.

The composition of a vector population is largely influenced by the pressures and modifying effects of the environment. Changes in the latter, whether natural or induced (e.g., by insecticides) will be reflected in the former. Thus if the existing characteristics of a vector population are determined, the parameters can subsequently be used to assess the effect of control measures.The effect of environmental conditions on the density and parity of Culex pipiens fatigans in catches in Burma is illustrated by a comparison of results obtained in Kemmendine, which is served by a bucket system for the removal of night-soil, with those from South Okkalapa, which has pit latrines; in the latter area there is a large preponderance of young mosquitos in the monsoon period, in contrast to the situation in Kemmendine.In Kemmendine, the inside-biting catch is reduced by about one-half if an inside-resting catch is made simultaneously. This suggests that C. p. fatigans rests indoors before biting indoors and that an efficient insecticide for inside application would markedly reduce the mosquito population. When a correction is made for the inside-resting catch it is shown that there is little to choose between inside- and outside-biting catches as measures of the activity of C. p. fatigans. The chances of acquiring infection are at least as great out of doors as indoors and this may account for differences in infectivity among different ethnic groups, according to the extent that they sleep out of doors.Differences in parity and in the state of infection of mosquitos according to the type of catch and the time of catching are discussed. Finally, it is noted that, although most male mosquitos are obtained in inside-resting catches, a considerable number, surprisingly, are taken on bait; the reason for this is not yet known.

Adaptation, Biological↗
PubMed1967

The duration of egg, larval and pupal stages of Culex pipiens fatigans in Rangoon, Burma.

Laboratory experiments to determine the duration of the immature stages of Culex pipiens fatigans were carried out because such information is important from the point of view of control by larvicides. At a temperature of 25.1 degrees C+/-0.7 degrees C the mean incubation period is 27.11+/-0.57 hours. Females spend a longer time in the pupal stage than males (34.16+/-0.74 hours and 32.95+/-0.75 hours, respectively, at 28.6 degrees C+/-0.8 degrees C; there is no 24-hour pupating or emerging rhythm. The duration of larval life is longer for the female (135.3+/-4.4 hours) than for the male (118.4+/-2.4 hours). Larvae that take a long time to pupate also take a long time to emerge. Withholding of food for a few hours from first-stage larvae increases the duration of larval life but does not affect that of pupal life. These observations on the differences between the sexes in the duration of larval and pupal life are in agreement with observations made on Aedes aegypti in Uganda.

Animals↗
PubMed1967

Evaluation of Wuchereria bancrofti infection in Culex pipiens fatigans in Rangoon, Burma.

In the past, several indices have been proposed to evaluate the threat of vectors to the community. Such indices, if accurately determined, could serve to assess the effectiveness of vector control campaigns. In this paper, a "risk of infection" index is introduced for the case of urban filariasis transmitted by Culex pipiens fatigans in Rangoon, Burma. This index is directly proportional to the three principal parameters that determine the extent of transmission-namely, the biting density of the vector, the proportion parous to total biting, and the proportion infective to total parous; all these parameters are easily determined from biting catches. Examples of the use of the index are given and it is noted that, in areas where conditions are not favourable to the vector throughout the year, or where the speed of development of the parasite in the vector may not be constant, these variables must be taken into account in calculating the index.

Animals↗