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K D Knudsen

Publications and source records attributed to K D Knudsen.

At least 19 recordsLinked to original sources
PubMed2000

Rapid characterization of complex structural phase transitions using powder diffraction and an area detector.

The use of a high-intensity and well collimated X-ray beam from a third-generation synchrotron source, combined with an area detector with online readout capabilities, allows high-quality powder patterns to be obtained with exposure times of only a few seconds. Powder measurements of a rare-earth manganate perovskite (Nd(0.43)Sr(0.57)MnO(3)) were performed in the temperature range 105-200 K, and the data were of sufficient quality to be able to extract, via Rietveld refinement, accurate values for the lattice constants and atomic parameters. The temperature dependence of the Mn-O-Mn bond angles and Mn-O distances obtained in this manner illustrate the well known correlation between the distortion of the MnO(6) octahedra and the onset of orbital ordering. The success of this study, for which only two hours of synchrotron beam time was required, indicates the enormous improvements in efficiency and throughput which area detectors are bringing to powder diffraction experiments.

Journal Article↗
PubMed1993

Temperature-induced conformational transition in xanthans with partially hydrolyzed side chains.

The conformational properties of xanthans with partially hydrolyzed side chains were investigated by optical rotation, CD, and differential scanning calorimetry (DSC). All variants displayed the well-known temperature-driven, cooperative order-disorder transition, and both optical rotation and DSC showed that the transition temperature was essentially independent of the content of terminal beta-mannose. It was found that up to 80% of the changes in the specific optical rotation accompanying the transition reflects conformational changes linked to the terminal beta-mannose in the side chains. Modification of the side chains also affected the CD when xanthan was in the ordered state, but in this case the data suggest that the glucuronic acid is the major component determining the magnitude of the CD signal. DSC measurements showed that the transition enthalpy (delta Hcal) increased linearly with the fraction of beta-mannose, again indicating that a significant part (up to 80%) of delta Hcal reflects conformational changes in the side chains. The conformational transition of the xanthan variants generally showed a higher degree of cooperativity (sharper transition) than unmodified, pyruvated xanthan. Calculation of the cooperativity parameter sigma by means of the Zimm-Bragg theory (OR data) or from the ratio between delta Hcal and the van't Hoff enthalpy (delta HvH) using DSC data showed a correlation between sigma and the content of beta-mannose, but the two methods gave different results when the content of beta-mannose approached 100%. The ionic strength dependence of the transition temperature, expressed as d (log I)/d(T-1m), was nearly identical for intact xanthan and a sample containing only 6% of the terminal beta-mannose. Application of the Manning polyelectrolyte theory does not readily account for the observed delta Hcal values, neither does it provide new information on the nature of the ordered and disordered conformations in xanthan.

Calorimetry, Differential Scanning↗
PubMed1982

Thyroid hypofunction after exposure to fallout from a hydrogen bomb explosion.

Thyroid function was evaluated in the Marshallese who were accidentally exposed to fallout-containing radioiodine isotopes in 1954. Measurements of thyrotrophin (TSH, thyroid-stimulating hormone) levels and free thyroxine (T4) index (FT4I) have revealed that, among 86 persons exposed on Rongelap and Ailingnae atolls, 14 have shown evidence of thyroid hypofunction. This was first noted in some individuals about ten years after exposure. Only two of these showed clinical evidence of hypothyroidism. The most marked TSH elevations were noted in nine persons exposed when younger than 6 years, with estimated doses to the thyroid from 390 to 2,100 rad. Most of this group subsequently had surgery for removal of thyroid nodules. The remaining five cases have been noted more recently among 36 surviving adults exposed at an older age who showed no other detectable thyroid abnormalities. This group had received estimated thyroid doses ranging from 135 to 335 rad and showed modest elevation of serum TSH levels (6 to 9 microU/mL) and a slightly subnormal FT4I. No abnormalities were found in persons on Utirik who received substantially less radiation, and hypothyroidism was present in less than 1% of the control, unexposed Marshallese. The high prevalence of a thyroid hypofunction in these persons indicates that this condition, as well as thyroid nodularity, can be a delayed complication of exposure to early fallout from a nuclear explosion. The fact that a significant fraction of the radiation to the thyroid was from short-lived radioiodine isotopes (132I, 133I, 135I), as opposed to 131I, may account for the severity of the thyroid damage.

Adolescent↗
PubMed1975

Role of the gonads in hypertension-prone rats.

In a genetically hypertension-prone (S) strain of rats it was observed previously that males generally developed hypertension more rapidly on a high salt diet than did females although final pressure ultimately were similar in both sexes. A genetic study had shown that there was no sex-linkage involved in setting blood pressure levels, so it was thought that the gonads might be involved. In the present work, castration of males had no effect on blood pressure but in the females it caused a rise in pressure that could not be distinguished from that in males, both on a high and low salt diet. Castration resulted in greater growth in females than in controls, whereas it had the opposite effect in males. It was speculated that these changes were due to influences on pituitary growth hormone with castration increasing the net output of growth hormone (or enhancing receptor sensitivity to it) in the female and the opposite in the male. From the work of others, there are some data compatible with such an interpretation. Experimentally, growth hormone will induce hypertension in rats. Therefore, it is conceivable that growth hormone is involved in the increment in hypertension observed in these castrate females. Because the effect on blood pressure was observed in castrate females on both high and low NaCl diets, it was considered unlikely that the blood pressure effect was simply due to increased NaCl intake in the food associated with greater growth. It was suggested that this rise in blood pressure with cessation of ovarian function might bear on the unsettled question of "menopausal" hypertension in women: in the genetically susceptible individual an increase in growth hormone associated with declining ovarian funtion in the menopause could provide the stimulus for the appearance of hypertension some years earlier than would otherwise have been the case.

Animals↗
PubMed1970

Genetic influence on the renin-angiotensin system. Evidence for a renin inhibitor in hypertension-prone rats.

TWO STRAINS OF RATS WITH OPPOSITE GENETIC PROPENSITY FOR HYPERTENSION WERE TESTED FOR: (a) the sensitivity to injections of angiotensin and renin, and (b) the influence of their plasma on the reaction velocity of renin and its substrate in vitro. Intact hypertension-prone (S) rats on low salt had higher sensitivity to angiotensin and a lower sensitivity to renin than hypertension-resistant (R) rats. High NaCl diet did not change the response of the R rats to these injections, but increased the response to renin and angiotensin in intact S rats. Bilateral nephrectomy caused increased response to renin and a decreased response to angiotensin in the S rats, so that both strains were equivalent after bilateral nephrectomy. In vitro, plasma from intact S rats inhibited the activity of hog renin. Plasma from R rats showed no inhibition. The inhibitor disappeared after bilateral nephrectomy. It was speculated that renin inhibitor may be involved in the development of hypertension by increasing sensitivity to angiotensin and other hypertensinogenic stimuli.

Angiotensin II↗
PubMed1970

Effects of chronic excess salt ingestion. Inheritance of hypertension in the rat.

TWO STRAINS OF RAT HAVE BEEN DEVELOPED BY SELECTIVE BREEDING: one strain (R rats) is resistant to salt hypertension, the other strain (S rats) is highly susceptible. The inheritance of these traits has been explored in the first (F(1)) and second (F(2)) generation of crossbred rats and in backcrosses between parent and first filial (F(1) x R, F(1) x S) generations. Male F(1) rats had an average blood pressure close to the mid-parental (R and S) values, and the average of F(2) males was equivalent to that of F(1). Male offspring of F(1) with R, or F(1) with S also showed averages close to the respective mid-parental values. Female offspring showed deviations from this linear relationship, indicating a significant dominance in the female for the genes of normal blood pressure. A model of two autosomal, nonlinked diallelic loci, with a dominance deviation at one locus in the female, gave predictions with a reasonable agreement to the observed values. The same model also appeared compatible with human data if we assume a gene frequency of 0.13 for the hypertensinogenic allele on both loci. Random fluctuations in blood pressure, and incomplete homogeneity of parental strains permit several alternative models. The major conclusions are: that more than one locus is needed to explain the findings though as few as two loci may possibly suffice; the allelic effect seems additive in males, but there is a sex-determined influence on the expression in females; there is no consistent evidence for sex-linked inheritance. Furthermore, this model developed from the study of rats may provide a framework for analysis of human data.

Analysis of Variance↗
PubMed1969

Genetic influence on the development of renoprival hypertension in parabiotic rats. Evidence that a humoral hypertensinogenic factor is produced in kidney tissue of hypertension-prone rats.

Rats from two strains with opposite constitutional predisposition to hypertension were joined in parabiosis and one partner was nephrectomized. The influence of genetic factors and of diet on the blood pressures of the two classes of parabionts, operated and intact, indicated that renoprival hypertension occurred with equal frequency in rats from both strains; that the development of renoprival hypertension depended on the influence from an intact S partner, or on a high salt intake, or on both. A nephrectomized S rat developing renoprival hypertension did not induce high blood pressure in its intact R partner. In this respect renoprival hypertension differs from salt and renal hypertension. The findings are interpreted to mean that the hypertensinogenic agent specific for S rats is produced by S kidneys.

Analysis of Variance↗
PubMed1969

Effects of adrenalectomy on blood pressure in salt-fed, hypertension-prone rats. Failure of hypertension to develop in absence of evidence of adrenal cortical tissue.

In adrenalectomized, genetically hypertension-prone rats, a high degree of correlation was found between evidence of functioning adrenal tissue and the development of salt hypertension. There is considerable evidence that some rats have the capacity to regenerate functioning adrenal cortical tissue from accessory glands and microscopic rests, sometimes in remote locations. Therefore, the criteria for continued absence of adrenal function after surgical adrenalectomy are critical. In this study we used three tests to validate the presence, or absence, of adrenal function: (a) a biochemical test, the quantitative, serial measurement of plasma glucocorticoids in individual rats; (b) a physiological test, the ability to survive a virtually sodium-free diet; and (c) the anatomical search for histological evidence of adrenal cortical tissue. Among those animals that developed hypertension after adrenalectomy, the correlation between plasma steroid concentration and blood pressure was statistically significant. We suspect that this correlation exists only during the period when cortical tissue is regenerating; it does not exist among intact animals with and without hypertension induced by salt. It was concluded that some adrenocortical function is necessary for salt hypertension to develop. The evidence was insufficient to settle the question whether the action of corticosteroids is causative, or whether they play a supporting, although necessary, role for an extraadrenal hypertensinogenic factor to become manifest.

Adrenal Glands↗
PubMed1969

Genetic influence on the development of renal hypertension in parabiotic rats. Evidence for a humoral factor.

The effects of several renal manipulations including uninephrectomy, unilateral renal artery constriction, and a combination of these two (Goldblatt procedure) were studied in two strains of rats with opposite constitutional predispositions to experimental hypertension. The protective value of intact renal tissue to protect against hypertension was shown to be genetically determined. The Goldblatt procedure carried out on only one member of a parabiotic pair induced hypertension in this operated rat but significant hypertension developed in the intact partner only when the operated animal belonged to the strain predisposed to hypertension. It was speculated that there were qualitative differences in the pressor signals of the two strains of rats. In the strain genetically predisposed to hypertension there are at least two pressor principles: (a) one which is common to both strains, not transmittable via the parabiosis junction and presumably related to the renin-angiotensin system; and (b) a second which is specific for the hypertension-prone strain and can be transmitted through the parabiosis junction. This transmittable agent is probably identical with the factor that produces salt hypertension and is associated with the salt-excreting mechanism.

Angiotensin II↗
PubMed1967

Effects of chronic excess salt ingestion. Genetic influence on the development of salt hypertension in parabiotic rats: evidence for a humoral factor.

Parabiosis has been found to modify the expected blood pressure response of rats from two strains with opposite genetic propensities for experimental hypertension. When a member from one strain was united in parabiosis with a member from the other and both were maintained on high NaCl diet, the rat from the strain ordinarily resistant to it rapidly developed hypertension, in contrast to appropriate controls from this strain. The development of hypertension in this resistant animal preceded that in its mate from the strain highly sensitive to hypertension. In the latter, both the level of hypertension and mortality were significantly less than in its control. It seems likely that the hypertension observed is the resistant parabiont was initiated in its partner from the sensitive strain. This modification in blood pressures was not observed in the absence of a high NaCl diet. Parabiosis between animals from the same strain did not alter their response. Thus, as in earlier experiences (1-4) the interaction of a nongenetic factor (NaCl) with the appropriate genetic substrate appeared to be necessary for the development of hypertension. The findings are interpreted as evidence that a transmittable humoral influence plays an important role in the pathogenesis of rat hypertension. The presence of this agent is genetically determined but, under the conditions of these experiments, it took the added stimulus of dietary NaCl to demonstrate its existence.

Animals↗