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J Yu

Publications and source records attributed to J Yu.

At least 883 records · Page 49Linked to original sources
PubMed1986

Background activity in pulmonary vagal C-fibers and its effects on breathing.

Vagal cooling experiments suggest that the deep slow breathing observed after vagotomy results not only from loss of pulmonary stretch receptor feedback, but also from loss of some unidentified vagal input. To investigate this possibility we cooled the vagus nerves in anesthetized dogs. In dogs breathing spontaneously, the Hering-Breuer reflex was abolished at 7 degrees C, but average expiratory time was unchanged and lengthened only on cooling below 3 degrees C. In artificially ventilated dogs the pulmonary vagus nerves were cooled in the chest and phrenic activity was recorded. Entrainment of phrenic bursts to the ventilator cycle ceased at 7 degrees C, and expiratory pauses shortened; they lengthened again on cooling below 3 degrees C. Cervical vagotomy did not change breathing pattern after the pulmonary vagus nerves were cut. Recording of afferent impulses during cooling showed that at 5 degrees C or less pulmonary vagal input was confined largely to nonmyelinated fibers; at 3 degrees C, background activity in pulmonary C-fibers was still 78% of control whereas myelinated afferents were virtually silent. We suggest that in eupnea low frequency, background activity in pulmonary afferent C-fibers shortens expiratory time.

Afferent Pathways↗
PubMed1986

The neuroanatomy of mental retardation in the white rat.

A provisional examination of a set of questions pertaining to the neuroanatomical basis of mental retardation was undertaken by assessing the learning ability of 25 different groups of young rats prepared with various cortical and subcortical lesions. The test battery included a visual discrimination, a nonvisual discrimination, a three-cul maze and three separate detour problems. Seven of the 25 groups were impaired in learning all problems (suggestive of a generalized learning impairment) and therefore were viewed as being mentally retarded. One of these groups suffered diffuse multifocal neocortical damage, while the lesions in the remaining six were located either within the parietal cortex, globus pallidus, ventrolateral thalamus, substantia nigra, median raphe or pontine reticular formation. Based upon a variety of observations, it is proposed that the generalized learning impairment seen in our brain-damaged rats, rather than being reducible to a sensory, motor, arousal-motivational-emotional, attentional, inhibitory or recent memory defect, is the product of a defect in "executive" processes.

Animals↗
PubMed1986

ADR1-mediated regulation of ADH2 requires an inverted repeat sequence.

DNA sequence analysis of wild-type and mutant ADH2 loci suggested that two unusual features 5' of the promoter, a 22-base-pair perfect dyad sequence and a (dA)20 tract, were important for regulation of this gene (D. W. Russell, M. Smith, D. Cox, V. M. Williamson, and E. T. Young, Nature [London] 304:652-654, 1983). Oligonucleotide-directed mutagenesis was used to construct ADH2 genes lacking the 22-base-pair dyad or the (dA)20 tract (V.-L. Chan and M. Smith, Nucleic Acids Res. 12:2407-2419, 1984). These mutant genes and other ADH2 deletions constructed by BAL 31 endonuclease digestion were studied after replacing the wild-type chromosomal locus with the altered alleles by the technique of gene transplacement (T. L. Orr-Weaver, J. W. Szostak, and R. S. Rothstein, Proc. Natl. Acad. Sci. USA 78:6354-6358, 1981), using canavanine resistance as the selectable marker. Deletions lacking the dyad failed to derepress normally and did not respond to mutations at the ADR1 locus, which encodes a protein necessary to activate ADH2. Deletions of the (dA)20 tract did not have a detectable phenotype. A small deletion located just 3' to the (dA)20 tract (between positions -164 and -146) had a low amount of ADR1-dependent transcription during repressed growth conditions, indicating that the regulatory protein encoded by ADR1 is present in a potentially active form during repression and that alterations of a DNA sequence in the promoter region can unmask its latent activity.

Alcohol Dehydrogenase↗
PubMed1986

Comparison of Doppler and strain-gauge plethysmography to detect vasculogenic impotence.

Doppler penile-pressure determinations to diagnose vasculogenic impotence require an experienced technician, can be time-consuming, yield inconsistent results and require much penile manipulation. Therefore the authors assessed and compared strain-gauge plethysmography as an alternative noninvasive procedure. Sixty-one patients with erectile failure had penile blood pressure determined by Doppler and indium-gallium alloy in Silastic strain-gauge plethysmography. Penile brachial indices were calculated. Strain-gauge results agreed with the Doppler measurements in all but three patients whose indices were found to be normal by Doppler and borderline by strain-gauge plethysmography. The sensitivity, accuracy and specificity of strain-gauge plethysmography were 93%, 95% and 100% respectively. Doppler determinations required an average of 20 minutes to perform, strain-gauge measurements only 4. The authors conclude from this study that strain-gauge plethysmography is a rapid, reliable, accurate method of determining penile blood pressures.

Blood Pressure↗
PubMed1986

Anomalous clustering of underglycosylated band 3 in erythrocytes and their precursor cells in congenital dyserythropoietic anemia type II.

Congenital dyserythropoietic anemia type II (CDA II or HEMPAS) is a genetic anemia caused by membrane abnormality. Our previous studies indicated that in HEMPAS, erythrocytes band 3 and band 4.5 are not glycosylated by polylactosaminoglycans. The present study was aimed at determining how such underglycosylated band 3 behaves in erythrocyte membranes. By using anti-band 3 antibodies, immunogold electron microscopy revealed that band 3s are clustered in HEMPAS erythrocyte membranes. By freeze-fracture electron microscopy, band 3s were also seen as lightly clumped intramembrane particles on a protoplasmic fracture face. Erythrocyte precursor cells stained by anti-band 3 antibodies showed that band 3s are present in the cytoplasmic area of the reticulocytes as scattered single particles. However, in young erythrocytes in which intracellular membranes are almost degenerated, band 3s were clustered in the cytoplasmic area of the cell. These observations suggest that band 3s cluster before they are incorporated into the plasma membranes of HEMPAS erythrocytes. In contrast to band 3, glycophorin A detected by anti-glycophorin A antibodies did not show a noticeable difference between normal and HEMPAS. Such a clustering of band 3 may cause abnormal localization of band 3-associated proteins and may thus result in the macroscopic membrane abnormality seen in HEMPAS erythrocytes.

Anemia, Dyserythropoietic, Congenital↗
PubMed1985

Sequential alterations in globin gene chromatin structure during erythroleukemia cell differentiation.

During differentiation of murine erythroleukemia cells, adult beta-globin gene chromatin acquires site-specific, DNase I hypersensitivity and an increased sensitivity in the globin gene region toward micrococcal nuclease (MNase) digestion. The relationship of these changes in chromatin structure to globin gene activation and to cellular commitment events has been studied. Imidazole, which blocks globin gene transcription during induction does not affect the terminal differentiation of the cells nor does it prevent the acquisition of DNAse I hypersensitivity. The formation of the inducible DNase I-hypersensitive site near the globin gene accompanies the developmental events which lead to cellular differentiation independent of the transcription process. The increased MNase sensitivity of the adult beta-globin gene region, normally preceded by the acquisition of 5' DNase I hypersensitivity, was blocked by the addition of imidazole prior to but not after globin gene activation. The enhanced MNase sensitivity was not abolished by the addition of actinomycin D and, thus, reflects a part of chromatin alterations that define potential for transcription. Therefore, there is a sequential series of chromatin alterations in the globin gene region associated with murine erythroleukemia cell differentiation. The appearance of the inducible 5' DNase I-hypersensitive site precedes the onset of globin gene transcription and is strongly correlated with commitment events. The enhanced MNase sensitivity is closely related to globin gene transcription, but it is not a consequence of the transcription process. In addition, the commitment of cells to terminal differentiation is dissociable from the stimulation of globin gene transcription.

Acetamides↗
PubMed1985

Deficits in response inhibition and attention in rats rendered mentally retarded by early subcortical brain damage.

Young rats with lesions to either the globus pallidus, substantia nigra, median raphe, or pontine reticular formation have previously been reported to be deficient in learning a wide variety of laboratory tasks. In the current study, weanling rats subjected to one of these lesions were rested for three weeks, then examined for acquisition and extinction of a water-motivated straight alley task, and finally tested on luminous flux discriminations of increasing difficulty. All brain-damaged groups were slower than the controls in extinguishing the alley task and only the median raphe group failed to show an impairment on the discrimination problems. These results and others suggest that the foregoing lesions produce deficits in inhibitory and attentional processes. The possibility is discussed that young rats bearing these lesions might serve as a model for the investigation of the neurobiological and cognitive disturbances underlying certain classes of mental retardation in children.

Animals↗
PubMed1985

The comparative effects of frontal, parietal, occipitotemporal, and limbic forebrain lesions in weanling rats on learning.

Young rats prepared with discrete bilateral lesions to the cerebral cortex, cingulate cortex, or dorsal hippocampus were required to learn a white-black discrimination, a 3-cul maze, and a nonvisual inclined plane discrimination. Only those rats with parietal lesions were impaired in acquiring all three habits. Those with occipitotemporal, frontocingulate, or posterior cingulate lesions were impaired on two habits, those with dorsal hippocampal lesions were impaired on one habit, and those with frontal (motor) cortical lesions failed to show any impairment. These results coupled with others suggest that the parietal cortex is unsurpassed in the wide range of learning and retention deficits which follows restricted neopallial lesions.

Animals↗
PubMed1985

Effects of thoracic spinal cord transection on colonic motor activity in rats.

The resting colonic motor activity before and consecutively after spinal cord transection was recorded in male Sprague-Dawley rats. Recording probes were anchored surgically in the ascending and descending colon. Pressure changes were recorded on a dynograph using a low compliance perfusion system. A motility index took into account the amplitude, duration and frequency of contractions. Following a baseline recording animals were subjected either to spinal cord transection at T4 level or a sham operation. The recording sessions continued regularly on alternate days for the observation period of 3 weeks. Transection of the thoracic spinal cord markedly reduced the motility index of the distal colon on the first postoperative day. However, the motor activity gradually returned to pre-operative values after 7 days. Sham surgery did not influence the motor activity. These findings suggest that colonic motor activity is influenced by spinal shock and probably by different neural mechanisms mediating proximal and distal activities of the colon in rats.

Animals↗
PubMed1985

Morphological changes in leukemic lymphoblasts and normal lymphocytes treated with deoxyadenosine plus deoxycoformycin.

It remains unclear how lympholysis occurs in children with an inherited deficiency of adenosine deaminase (ADA) and in leukemic patients undergoing treatment with an inhibitor of ADA, deoxycoformycin. Adenosine deaminase deficiency with subsequent lympholysis can be simulated in vitro by treatment of lymphoid cells with deoxyadenosine plus deoxycoformycin. We found that such in vitro treatment caused fragmentation of the nucleus, disintegration of nuclear chromatin, and the formation of cytoplasmic blebs in T-lymphoblast lines, but not in B-lymphoblast lines. For all but one of the cell lines tested, the extent of morphological changes paralleled the sensitivity to growth inhibition by deoxyadenosine plus deoxycoformycin. Similar morphological changes were observed in normal peripheral blood lymphocytes treated with deoxyadenosine plus deoxycoformycin. These morphological changes were energy-dependent processes. They were preceded by inhibition of DNA synthesis and deoxyadenosine triphosphate (dATP) accumulation, but followed by depletion of adenosine triphosphate (ATP) and cell lysis. These changes may represent an intermediate step between metabolic alterations and lympholysis.

Adenosine Triphosphate↗