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Biomedical subjects

E Haase

Publications and source records attributed to E Haase.

At least 19 recordsLinked to original sources

Influence of flight on protein catabolism, especially myofilament breakdown, in homing pigeons.

In order to study protein degradation during flight in homing, a high-performance liquid chromatography technique was developed for the quantitative analysis of N tau-methylhistidine. Secondly, it was necessary to confirm that the excretion of N tau-methylhistidine correlates with myofilament breakdown in homing pigeons. In these experiments, ten birds were subcutaneously injected with N tau-[14C]methylhistidine and the excreta were quantitatively collected for 1 week. Of the 94.5% radioactivity recovered, 87.1% was associated with N tau-[14C]methylhistidine and 6.1% with N-acetyl-N tau-[14C]methylhistidine. This rapid excretion of unmetabolized N tau-[14C]methylhistidine validates the assumption that the amount of N tau-methylhistidine excreted is a measure of myofilament catabolism in homing pigeons. The influence of endurance flight on protein breakdown was determined after flights from release sites 368-646 km away. Immediately after return, plasma urea and uric acid levels were increased, whereas plasma concentration of N tau-methylhistidine remained unchanged compared to unflown control birds. Flown pigeons excreted significantly more urea and N tau-methylhistidine within 24 h and significantly more urea and uric acid within 96 h after flight than unflown controls. Our findings support the hypothesis that in homing pigeons protein catabolism is increased during endurance flight. Elevated N tau-methylhistidine excretion probably results from repair processes in damaged muscle fibers, including breakdown of myofilaments.

Actin Cytoskeleton↗

SNG1--a new gene involved in nitrosoguanidine resistance in Saccharomyces cerevisiae.

We have molecularly characterized the SNG1 gene that confers hyper-resistance to the mutagen N-methyl-N'nitro-N-nitrosoguanidine (MNNG) in Saccharomyces cerevisiae when overexpressed on a multi-copy plasmid. This hyper-resistance to MNNG is not due to depletion of glutathione pools since multi-copy SNG1 containing yeast transformants contain at least wild type levels of glutathione; DNA repair seems unaffected in these transformants as the multi-copy SNG1-mediated MNNG hyper-resistance is also seen in DNA repair mutants belonging to each of the three epistasis groups of yeast repair mutants. It could be shown that SNG1 is not under control of the YAP1 encoded transcription activator that controls expression of at least two genes involved in MNNG metabolism in yeast. sng1 null mutants are viable but exhibit only slight sensitivity to MNNG, indicating that SNG1 does not encode a protein involved in a major detoxification step of this mutagen. Sequencing of the HYR-mediating passenger DNA revealed that SNG1 encodes a 547 a polypeptide containing seven transmembrane-spanning regions that may be membrane-bound. Comparison of the DNA sequence with established gene databanks revealed that SNG1 is a novel yeast gene.

Amino Acid Sequence↗

Influences of sex, castration, and androgens on the eumelanin and pheomelanin contents of different feathers in wild mallards.

In mallards the bright nuptial plumage of the drake represents the neutral, sex hormone-independent coloration of the species that both sexes eventually exhibit after castration. We compared the pheo- and eumelanin contents of feathers from the head, breast, flank, and under-tail coverts in five groups of mallards after the post-nuptial molt in summer: intact hens, intact drakes, castrated drakes, castrated drakes injected with testosterone during the spring, and castrated drakes injected with 5 alpha-dihydrotestosterone during the spring. In the head feathers and under-tail coverts, the gonadal hormones of the intact birds and the testosterone injections into castrates significantly reduced the eumelanin content, tended to increase the pheomelanin content, and, thereby, changed the melanin type from eumelanic in the untreated castrates to mixed melanic in the other three groups. The eumelanin contents of the flank feathers did not differ among the groups, but the pheomelanin contents at this site was significantly elevated in the two intact groups and the testosterone-treated compared to the uninjected castrates. Again, the melanin type changed from eumelanic in the castrates to mixed melanic in the other three groups. The high pheomelanin content of the breast feathers in the castrated birds was significantly reduced in the hens, intact drakes, and testosterone-injected castrates with a concomitant tendency for elevated eumelanin contents. At this site, a change occurred from pheomelanic to mixed melanic. 5 alpha-dihydrotestosterone was clearly less effective than testosterone in affecting the melanin contents in castrates and resulted in an intermediate coloration.(ABSTRACT TRUNCATED AT 250 WORDS)

Androgens↗

Gene SNQ2 of Saccharomyces cerevisiae, which confers resistance to 4-nitroquinoline-N-oxide and other chemicals, encodes a 169 kDa protein homologous to ATP-dependent permeases.

The yeast gene SNQ2 confers hyper-resistance to the mutagens 4-nitroquinoline-N-oxide (4-NQO) and Triaziquone, as well as to the chemicals sulphomethuron methyl and phenanthroline when present in multiple copies in transformants of Saccharomyces cerevisiae. Subcloning and sequencing of a 5.5 kb yeast DNA fragment revealed that SNQ2 has an open reading frame of 4.5 kb. The putative encoded polypeptide of 1501 amino acids has a predicted molecular weight of 169 kDa and has several hydrophobic regions. Northern analysis showed a transcript of 5.5 kb. Haploid cells with a disrupted SNQ2 reading frame are viable. The SNQ2-encoded protein has domains believed to be involved in ATP binding and is likely to be membrane associated. It most probably serves as an ATP-dependent permease.

4-Nitroquinoline-1-oxide↗

Isolation and characterization of additional genes influencing resistance to various mutagens in the yeast Saccharomyces cerevisiae.

Screening of a multi-copy vector-based yeast genomic library in haploid cells of wild-type Saccharomyces cerevisiae yielded transformants hyper-resistant to various chemical mutagens. Genetical analysis of the yeast insert DNAs revealed three genes SNG1, SNQ2, and SNQ3 that confer the phenotype hyper-resistance to MNNG, to 4-NQO and triaziquone, and to mutagens 4-NQO, MNNG, and triaziquone, respectively. Integration of the gene disruption-constructs into the haploid yeast genome yielded viable null-mutants with a mutagen-sensitive phenotype. Thus, copy number of these non-essential yeast genes determines the relative resistance to certain chemical mutagens, with zero copies yielding a phenotype of mutagen sensitivity and multiple copies one of mutagen hyper-resistance, respectively.

4-Nitroquinoline-1-oxide↗

Systemic responses to carotid occlusion in the anesthetized rat.

We evaluated the effects of four standard anesthetization regimens on the systemic cardiovascular responses to bilateral common carotid artery occlusion in 28 adult male rats. Rats were randomly assigned to anesthesia groups: thiopental sodium (PT; 100 mg/kg ip), alpha-chloralose (CH; 100 mg/kg iv), ketamine hydrochloride plus acepromazine (KA; 135 mg/kg and 1.5 mg/kg sc), and pentobarbital sodium (PB; 50 mg/kg ip). PT and PB animals had similar baseline heart rates (HR; 333 and 345 beats/min, respectively) and arterial pressures (MAP; 126 and 118 mmHg, respectively), whereas both were lower in CH and KA (314 and 288 beats/min, 92 and 85 mmHg). During bilateral carotid occlusion, PT demonstrated the largest change in MAP (dMAP; +27 mmHg) but the smallest change in HR (dHR; +8 beats/min). CH and PB demonstrated similar dHR (+24 and +16 beats/min) and dMAP (+20 and +19 mmHg). KA demonstrated a significant dHR (+14 beats/min), but the average dMAP was not statistically significant (+3 mmHg). Therefore, carotid occlusion in rats anesthetized with PT, PB, or CH consistently elicits a systemic arterial pressor response comparable with that reported for conscious animals. When the magnitude and stability of baseline HR and MAP are also considered, PT and PB anesthetization seem to be the most reliable for evaluation of the carotid occlusion pressor response in rats.

Anesthetics↗

[Chemical sensors in medical use: ion-selective electrodes, limitations and potentials].

The electrolyte concentrations of potassium and sodium, for example, are routinely analyzed in diluted serum and plasma. In contrast, electrolyte activities are quantified by ISEs directly in undiluted whole blood and plasma and promise to be highly informative. Nevertheless, some drawbacks, such as the interaction between the biological matrix and the ISE surface, limit the accuracy of measurements. A symmetrical measuring arrangement allows one to localize and quantify the known sources of errors. These are minimized by adequate techniques. The membrane composition for sodium selective electrodes is optimized in particular. The interpretation of ISE values as compared to FAES (flame atomic emission spectroscopy) is closely related to the water concentration of the samples. Comparisons between ISE and FAES results obviously allow one to evaluate the water concentration of samples, as is shown by a linear regression plot.

Calibration↗

Hyper-resistance to nitrogen mustard in Saccharomyces cerevisiae is caused by defective choline transport.

The recessive hnm1 mutant allele is responsible for hyper-resistance to nitrogen mustard in Saccharomyces cerevisiae. Transformation with a single-copy HNM1 wild-type allele of such hyper-resistant mutants will restore wild-type sensitivity to nitrogen mustard. By contrast the presence of multi-copy vectors containing HNM1, in either a hyper-resistant hnm1 mutant or an HNM1 wild-type, will lead to a novel, mustard-sensitive phenotype unrelated to defects in DNA repair genes. Gene disruption of HNM1 revealed that this gene is non-essential for cells prototrophic for choline (CHO1) but lethal for cells with a cho1 genotype. Sensitivity to nitrogen mustard of wild-type HNM1, but not of hnm1 mutants, depends on the choline content of the growth medium, with cells grown in choline-free medium exhibiting the highest sensitivity. Sequencing of a 300 bp DNA fragment of HNM1 revealed the identity of this gene with the CTR locus, which is responsible for choline transport in Saccharomyces cerevisiae.

Alleles↗

The SNQ3 gene of Saccharomyces cerevisiae confers hyper-resistance to several functionally unrelated chemicals.

A multi-copy plasmid containing the SNQ3 gene confers hyper-resistance to 4-nitroquinoline-N-oxide (4NQO), Trenimon, MNNG, cycloheximide, and to sulfometuron methyl in yeast transformants. Restriction analysis, subcloning, and DNA sequencing revealed an open reading frame of 1,950 bp on the SNQ3-containing insert DNA. Gene disruption and transplacement into chromosomal DNA yielded 4NQO-sensitive null mutants which were also more sensitive than the wild-type to Trenimon, cycloheximide, sulfometuron methyl, and MNNG. Hydropathic analysis showed that the SNQ3-encoded protein is most likely not membrane-bound, while the codon bias index points to low expression of the gene.

Amino Acid Sequence↗

A recessive mutant allele of the HNM1 gene of Saccharomyces cerevisiae is responsible for hyper-resistance to nitrogen mustard.

A screening of haploid yeast strains for enhanced resistance to nitrogen mustard (HN2) yielded a recessive mutant allele, hnm1, that conferred hyper-resistance (HYR) to HN2. Diploids, homo- or heterozygous for the HNM1 locus, exhibit normal wild-type like resistance while homozygosity for hnm1 leads to the phenotype HYR to HN2. The hnm1 mutation could be found in yeast strains proficient or deficient in different DNA repair systems. In these mostly HN2-sensitive haploid repair-deficient mutants, hnm1 acted as a partial suppressor of HN2 sensitivity. All isolated recessive mutations conferring hyper-resistance belonged to a single complementation group. The HYR to HN2 phenotype was maximally expressed in growing cells and was associated with reduced mutability by HN2. HNM1 most probably controls uptake of HN2 which would be impaired in the hnm1 mutants.

Alleles↗

Molecular cloning of SNM1, a yeast gene responsible for a specific step in the repair of cross-linked DNA.

We have isolated yeast gene SNM1 via complementation of sensitivity towards bi- and tri-functional alkylating agents in haploid and diploid yeast DNA repair-deficient snm1-1 mutants. Four independent clones of plasmid DNA containing the SNM1 locus were isolated after transformation with a YEp24-based yeast gene bank. Subcloned SNM1-containing DNA showed (i) complementation of the repair-deficiency phenotype caused by either one of the two different mutant alleles snm1-1 and snm1-2ts; (ii) complementation in haploid and diploid yeast snm1-1 mutants by either single or multiple copies of the SNM1 locus; and (iii) that the SNM1 gene is at most 2.4 kb in size. Expression of SNM1 on the smallest subclone, however, was under the control of the GAL1 promotor. Gene size and direction of transcription was further verified by mutagenesis of SNM1 by Tn10-LUK transposon insertion. Five plasmids containing Tn10-LUK insertions at different sites of the SNM1-containing DNA were able to disrupt the function of genomic SNM1 after gene transplacement. Correct integration of the disrupted SNM1::Tn10-LUK at the genomic site of SNM1 was verified via tetrad analysis of the sporulated diploid obtained after mating of the SNM1::Tn10-LUK transformant to a haploid strain containing the URA3 SNM1 wild-type alleles. The size of the poly(A)+ RNA transcript of the SNM1 gene is 1.1 kb as determined by Northern analysis.

Blotting, Northern↗

Genetic characterization of hyperresistance to formaldehyde and 4-nitroquinoline-N-oxide in the yeast Saccharomyces cerevisiae.

The hyperresistance to 4-nitroquinoline-N-oxide (4-NQO) and formaldehyde (FA) of yeast strains transformed with the multi-copy plasmids pAR172 and pAR184, respectively, is due to the two genes, SNQ and SFA, which are present on these plasmids. Restriction analysis revealed the maximal size of SFA as 2.7 kb and of SNQ as 2.2 kb, including transcription control elements. The presence of the smallest 2.7 kb subclone carrying SFA increased hyperresistance to formaldehyde fivefold over that of the original pAR184 isolate. No such increase in hyperresistance to 4-NQO was seen with the smaller subclones of the pAR172 isolate. Disruption of the SFA gene led to a threefold increase in sensitivity to FA as compared with the wild type. Expression of gene SNQ introduced on a multi-copy vector into haploid yeast mutants rad2, rad3, and snm1 did not complement these mutations that block excision repair.

4-Nitroquinoline-1-oxide↗

Environmental and hormonal factors in seasonal breeding in free-living male Indian rose-ringed parakeets (Psittacula krameri).

Seasonal changes in testicular activity, plasma luteinizing hormone (LH), estradiol (E2), testosterone (T), and 5 alpha-dihydrotestosterone (5 alpha-DHT) were related to pair bond formation, nest building, nest defense, and parental behavior in free-living Indian rose-ringed parakeets (Psittacula krameri) in northwest India. Spermatozoa production occurred between January and March when daylengths were short (10-12 hr) and ambient temperature was seasonally low (8-20 degrees C). At other times of the year the testes were regressed. Plasma LH levels increased during the prebreeding period (September-December) when the birds were forming pairs and selecting or defending nest sites. Plasma LH levels increased further between January and March and decreased to seasonal low values during the post breeding period between April and June when the birds were caring for young. Concentrations of plasma androgens and estrogens were similar during the prebreeding and postbreeding phases of the breeding cycle. During the breeding period, the ratios between plasma 5 alpha-DHT and testosterone and between plasma estradiol and testosterone increased. It is proposed that the absence of marked seasonal changes in plasma steroid levels is related to nest defense behavior which occurs during the prebreeding, breeding, and postbreeding phases of the breeding cycle. Winter breeding makes it possible for the parakeets to avoid competition with other birds for nesting sites, to avoid fledging young during the monsoon period, and to take advantage of the winter pea crop which provides the female with extra nutrients for egg production.

Animals↗

Environmental, dietary, and hormonal factors in the regulation of seasonal breeding in free-living female Indian rose-ringed parakeets (Psittacula krameri).

The roles of environmental, dietary, and hormonal factors in the timing of seasonal breeding were assessed in free-living female Indian rose-ringed parakeets, Psittacula krameri, in northwest India (22 degrees 2'N, 73 degrees E). The ovaries and oviducts began to enlarge in January, were fully developed in February, and began to regress in March. During this time there was no significant change in the concentration of plasma luteinizing hormone (LH) or estradiol. The concentration of plasma LH decreased (P less than 0.01) at the end of the breeding season. Pair bond formation occurred between September and December and was associated with an increase in levels of plasma LH but no change in plasma estradiol. Concentrations of plasma testosterone (T) and 5 alpha-dihydrotestosterone (5 alpha-DHT) did not vary significantly during the year and were similar to those in males except for higher values of 5 alpha-DHT and lower values of T during the pre- and postbreeding periods, respectively. The similar levels of plasma androgens in both sexes may be related to the equal roles that both sexes play in the defence of their nest holes. An analysis of crop sac contents showed that the birds fed chiefly on pigeon peas (Cajanus cajan) during the breeding season and on cereal grains at other times of the year. It is suggested that pigeon peas provide the extra nutrients, including calcium, required for egg production. Since pigeon peas ripen between November and March, the production of the crop may play a role in the timing of seasonal breeding. A further factor appears to be competition for nest sites. By breeding in winter, the parakeet avoids competing with other species which nest in holes.

Animals↗

Allometric comparison of brain weight and brain structure volumes in different breeds of the domestic pigeon, Columba livia f.d. (fantails, homing pigeons, strassers).

In three breeds of domestic pigeons (fantails, homing pigeons, and strassers) the volumes of fresh, i.e. unfixed tissue of 14 brain structures were determined (telencephalon, diencephalon, nervus opticus, tectum, cerebellum, tegmentum and hyperstriatum accessorium, hyperstriatum ventrale, neostriatum, paleostriatum, hippocampus, septum, regio praepiriformis, bulbus olfactorius). Allometric comparisons that take into account differences in body weight and size were made among these three breeds. The tectum, hippocampus, paleostriatum and especially the neostriatum and olfactory bulb are remarkably larger in homing pigeons. These data are discussed in a functional context, in which the homing ability of homing pigeons is considered.

Animals↗

Flight stimulates adrenocortical activity in pigeons (Columba livia).

The influence of long-distance flight on corticosterone secretion has been examined in trained racing pigeons. Flights of 315-561 min from release sites 115-557 km from the home loft greatly increased the circulating corticosterone concentration in comparison with the levels in nonexercised controls sampled before release or bled in the loft at the times of release or arrival. The increase in corticosterone concentration was unrelated to the distance flown or duration of flight. Flights of less than 1 min duration (from release sites 100 m from the loft) increased the corticosterone concentration, in comparison with that in the loft controls, but to levels much lower (P less than 0.001) than those following long-distance flights and to concentrations similar to those in birds that were returned to the loft by hand.

Animals↗

Seasonal changes in the concentrations of plasma gonadotropins and prolactin in wild mallard drakes.

Seasonal changes in the concentrations of plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH), and prolactin were measured in serial samples taken from seven captive wild mallard drakes exposed to natural lighting and temperature in Kiel, West Germany (54 degrees N), for 20 months. The seasonal pattern of plasma LH levels was characterized by high titers during the reproductive phase in the spring, a steep decrease toward the end of this phase (May/June), low levels during the summer, and a second annual peak in the fall. Plasma FSH levels increased during February and March, the period of rapid testicular growth, and reached the highest values at the end of March/beginning of April. Later in the spring FSH levels decreased and remained low for the rest of the year. The concentrations of plasma prolactin increased progressively during April and May, reaching their highest values at the end of the breeding season, coinciding with the steep fall in the levels of plasma gonadotropins. Prolactin concentrations fell during July and August and were at their lowest level in the autumn. It is concluded that the development of photorefractoriness is associated with an increase in the concentrations of plasma prolactin.

Animals↗