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At least 109 records · Page 6Linked to original sources
PubMed1977

Vertical eye movement related unit activity in the rostral mesencephalic reticular formation of the alert monkey.

Eye movement related unit activity was recorded in the rostral mesencephalic reticular formation (MRF) of the alert monkey. Most units (78 out of 117) were activated with a short activity burst starting before the eye movement and were otherwise silent. The activity was the same whether movements occurred spontaneously in the light or dark, or were fast phases of vestibular or optokinetic nystagmus, and could be related to parameters of a vector representing the eye movement such as amplitude, position changes along certain planes or direction of movements. Units coding position changes or direction of movement had their preferred direction always close to the vertical. Other units (18 out of 117) showed some tonic activity, which was also only related to vertical eye position. It is suggested that this region of the rostral MRF acts an an immediate supranuclear structure, mediating eye movements in the vertical plane.

Action Potentials↗
PubMed1985

The use of comparability ratios to adjust hospital trend data.

Hospital trend data may be affected by changes in diagnostic coding schemes. We studied the change from ICDA-8 (I-8) to ICD-9-CM (I-9) in a sample of roughly 13,600 double-coded Veterans Administration hospital diagnoses. Comparability ratios were computed and used to adjust trend data which overlap the time period when the shift from I-8 to I-9 occurred. With this adjustment for change in diagnostic coding scheme, apparent diagnostic trends are substantially altered.

Diagnosis↗
PubMed1967

Frequency sensitivity of single auditory neurons in the gecko Coleonyx variegatus.

Although acoustic communication is not pronounced in reptiles, analysis of single auditory neurons in the medulla oblongata shows that the cochlea is a frequency analyser. Auditory neurons of the lizard Coleonyx variegatus respond to acoustic stimuli over a range of less than 0.1 to 17 kilohertz and are maximally responsive between 0.8 and 2.0 kilohertz. The frequencies to which they are most sensitive differ from neuron to neuron, ranging from 0.11 to 4 kilohertz. Some neurons have an inhibitory area which greatly overlaps the response area, so that inhibitory areas do not seem to sharply tune the response area at this level of the auditory tract. The inhibitory area is responsible for producing in some neurons a phasic response and nonmonotonic relation between sound intensity and number of impulses. The response pattern shows a tendency to change from tonic to phasic in more advanced auditory centers. This may serve to code rapid changes in the acoustic stimuli.

Animals↗
PubMed1991

A quantitative measure of error minimization in the genetic code.

We have calculated the average effect of changing a codon by a single base for all possible single-base changes in the genetic code and for changes in the first, second, and third codon positions separately. Such values were calculated for an amino acid's polar requirement, hydropathy, molecular volume, and isoelectric point. For each attribute the average effect of single-base changes was also calculated for a large number of randomly generated codes that retained the same level of redundancy as the natural code. Amino acids whose codons differed by a single base in the first and third codon positions were very similar with respect to polar requirement and hydropathy. The major differences between amino acids were specified by the second codon position. Codons with U in the second position are hydrophobic, whereas most codons with A in the second position are hydrophilic. This accounts for the observation of complementary hydropathy. Single-base changes in the natural code had a smaller average effect on polar requirement than all but 0.02% of random codes. This result is most easily explained by selection to minimize deleterious effects of translation errors during the early evolution of the code.

Amino Acids↗
PubMed1987

Estimation of myocardial infarction mortality from routinely collected data in Western Australia.

The accuracy of routinely collected mortality data for ischemic heart disease (IHD) as indicators of death from acute myocardial infarction (AMI) was assessed in ages 25-64 years, according to the WHO criteria defined in 1983. Cases were identified from computer records (linked for individuals) of all death certificates and hospital discharges in Western Australia between 1971 and 1982. Where the official cause was IHD about 90% of deaths fulfilled the WHO criteria for definite or possible AMI. Up to 10% of fatal cases of definite or possible AMI were coded to other causes in the official death statistics, however it appeared that variations in this figure with changes in coding practices could cause appreciable bias in the estimation of secular trends in IHD mortality. This problem could largely be overcome by reviewing fatal events where the death certificate was coded to one of a limited number of other ICD rubrics.

Adult↗
PubMed1989

A new epidemiologic classification system for interim myocardial infarction from serial electrocardiographic changes.

Many clinical trials or population studies have used change in Minnesota Q code, ST-segment depression code or T-wave inversion code as evidence of new myocardial infarction or new coronary heart disease event. Direct electrocardiogram (ECG) waveform comparison is a new standardized procedure for diagnosing interim myocardial infarction from ECGs classified according to the Minnesota code (serial Q-wave pattern change). This procedure was investigated for its application in epidemiologic studies. Use of this procedure in the Multiple Risk Factor Intervention Trial resulted in a 50% increase in the positive predictive accuracy, improved agreement with clinically defined myocardial infarction and a strong independent prognostic association with total and coronary heart disease mortality. Among those with major Minnesota Q-code findings, there was substantial variation in mortality. The 5-year coronary heart disease death rates estimated by life table analysis were 8.5% for those with major serial Q-wave pattern change, 5.1% for those with minor serial Q-wave pattern change and 1.5 to 2.6% for those with major or minor Minnesota Q-code change not substantiated by direct waveform comparison, compared with 2.4% for those with no Minnesota Q-code findings. The coronary heart disease death rate for those with major serial Q-wave pattern change was greater than that for the other ECG groups (p less than 0.01). Adjustment for age and other risk factors did not qualitatively alter these findings. This new approach is eminently suitable for export to other investigators, for incorporation into computer analysis programs and for statistical analysis.

Actuarial Analysis↗
PubMed1990

How the visual system detects changes in the direction of moving targets.

To determine how the visual system represents information about change in target direction, we studied the detection of such change under conditions of varying stimulus certainty. Target direction was either held constant over trials or was allowed to vary randomly. When target direction was constant the observer could be certain about that stimulus characteristic; randomizing the target direction rendered the observer uncertain. We measured response times (RTs) to changes in target direction following initial trajectories of varying time and distance. In different conditions, the observer was uncertain about either the direction of the initial trajectory, or the direction of change or both. With brief initial trajectories in random directions, uncertainty about initial direction elevated RTs by 50 ms or more. When the initial trajectories were at least 500 ms, this directional uncertainty ceased to affect RTs; then, only uncertainty about the direction of change affected RTs. We discuss the implications of these results for (i) schemes by which the visual system might code directional change; (ii) the visual integration time for directional information; and (iii) adaptational processes in motion perception.

Attention↗
PubMed1982

The ovalbumin gene family: complete sequence and structure of the Y gene.

The "ovalbumin Y" gene, one of three which constitute the ovalbumin gene family in chicken has been completely sequenced. The exact location of exons can be derived from the comparison with the ovalbumin gene sequence and from the map previously established by electron microscopy analysis. During evolution of the Y gene, selective pressure has operated to retain a sequence coding for an ovalbumin-like protein. The location of splice junctions, the length of protein coding exons and the reading phase are as in the ovalbumin gene. The overall homology between the Y and ovalbumin protein coding sequences is 72.6% (resulting in a 58% homology for the amino acid sequences). A significantly high number of base changes within coding sequences are present in clusters, which appear in several cases to be correlated with the occurrence of direct repeats. The 3' untranslated sequences of the Y and ovalbumin mRNAs have diverged much more, and the Y sequence contains a peculiar U(T) rich region. Corresponding introns of the ovalbumin and Y genes differ extensively both in sequence and in length. They share however characteristic biases in their base distribution.

Animals↗
PubMed1987

Beta-thalassemia syndromes.

In summary, the beta-thalassemias are due to defects in or around the structural beta-globin gene. In some Indian patients, there is deletion of sequence at the 3' end of the beta-globin gene. Most commonly, single nucleotide mutations cause beta(+)- and beta(0) -thalassemia. More than 30 such mutations have been identified. Defects in the promoter region 5' to the gene as far 5' as -87 and closer to the gene at -27 and -28 in the ATA sequence can cause beta (+)-thalassemia. Single nucleotide changes in coding regions leading to termination or nonsense codons commonly cause beta (0)-thalassemia. In addition, beta(0)-thalassemia can be due to single nucleotide changes in the invariant GT at the 5' splice junction in IVS 1 and 2 and in the AG at the 3' end of IVS 2. Additionally, single nucleotide mutations can occur within IVS that result in both beta(+)- and beta(0)-thalassemia. New splice sites are usually the result of these single nucleotide mutations, and they lead to new, abnormal splicing patterns. In some instances, beta (+)-thalassemia results when a new splice signal created within IVS is still associated with some continued normal splicing as well as with abnormal splicing. The abnormal splicing leads to abnormal mRNA, while the normal splicing leads to some normal mRNA and the beta (+)-pheno-single In other cases, such as with the defect as position 705 of IVS 2, the single nucleotide change within the IVS allows only abnormal mRNA splicing, and it results in beta (0)-thalassemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Base Sequence↗
PubMedDate not supplied

A history of nursing's code of ethics.

This article has focused on the history of the code of ethics for nurses. The changes in the code intertwine with nursing's journey toward professionalism and reflect changes in nursing, society and health care. Over the years, however, the code has remained relatively stable. Six of the statements can be traced back to the 1926 code and five others to the revision of the code in 1960. The code of ethics has provided guidance for the profession, and has helped determine nursing's position as a profession in society.

Codes of Ethics↗
PubMed1988

Complementary DNA clones of chicken proto-oncogene c-ets: sequence divergence from the viral oncogene v-ets.

The avian acute leukemia virus E26 induces erythroblastosis and myeloblastosis in chickens. The oncogene of this virus includes sequences derived from the cellular gene designated c-ets, which is normally expressed in lymphoid cells and whose product is a protein of apparent molecular weight ca. 54,000 daltons. Complementary DNA clones representing the major transcript of the chicken c-ets proto-oncogene were isolated from a spleen cell library. Sequence analysis of the cDNA revealed that it contains an open reading frame encoding a polypeptide of 441 amino acids with a molecular weight of 49,932 daltons. This open reading frame can be transcribed and translated in vitro into a 50 kd protein that is specifically immunoprecipitated with antiserum to the v-ets oncogene product. Within the central region of homology between c-ets and v-ets, there are only 5 nucleotide substitutions resulting in 4 amino acid changes. However, coding sequences at the 5' and 3' ends of the v-ets oncogene and the chicken c-ets cDNA differ from one another. These changes may be responsible for the differential functions of c-ets and v-ets in cells of different hematopoietic lineages and may account for the pathogenic properties of the v-ets oncogene.

Amino Acid Sequence↗
PubMed1981

Amino acid codes in mitochondria as possible clues to primitive codes.

Differences between mitochondrial codes and the universal code indicate that an evolutionary simplification has taken place, rather than a return to a more primitive code. However, these differences make it evident that the universal code is not the only code possible, and therefore earlier codes may have differed markedly from the previous code. The present universal code is probably a "frozen accident." The change in CUN codons from leucine to threonine (Neurospora vs. yeast mitochondria) indicates that neutral or near-neutral changes occurred in the corresponding proteins when this code change took change took place, caused presumably by a mutation in a tRNA gene.

Amino Acids↗
PubMed1992

[Blood cholesterol in women].

The distribution of blood lipids is described and their role as cardiovascular risk factors in women is discussed. The determinants of serum cholesterol levels are identified in genes, in particular in changes of codes for LDL and HDL; in habitual food intake as polyunsaturated and saturated fats. Obesity, jointed by atherogenic lipoproteins as total and LDL-cholesterol, is considered a risk factor independently on smoking habit or age. Finally the role of menopause in changing lipoprotein levels and in increasing cardiovascular risk is reported.

Adult↗
PubMed1990

Rising asthma mortality in young males in Hong Kong, 1976-85.

The trend in asthma mortality in Hong Kong was estimated from published statistics for the years 1976-85. To avoid coding errors in death certifications, only asthma deaths in the age group 5-34 years were analysed. Mortality rose annually by an average of 10.5% in male (P less than 0.02), but not female asthmatics. Such an increase was not due to a change in coding as a result of the revision of the International Classification of Diseases in 1979, or an exchange of diagnostic labelling from other respiratory diseases. The exact causes for the increase in asthma mortality have yet to be determined.

Adolescent↗
PubMed1989

Declining trends in mortality from cerebrovascular disease at ages 10-65 years: a test of validity.

Recent reports of declining trends in mortality rates from cerebrovascular disease are based on underlying cause of death as stated on the death certificate, and may contain inaccuracies because death certificates are often completed without reference to all information in medical records, and because of changes in coding conventions and diagnostic fashion. This is a report of trends in mortality rates from cerebrovascular disease in Baltimore, Md., during 1950-1970 using data validated by reference to individual medical records from 19 hospitals. Overall accuracy of death certificate diagnoses did not change markedly during the study period. Death rates from subarachnoid hemorrhage increased in white women, but decreased in white men and in nonwhites of both sexes. Death rates from other cerebrovascular diseases declined in most sex and color groups, a result which cannot be attributed to errors in death certificate diagnoses. The increasing rates of subarachnoid hemorrhage observed in white women deserve further attention.

Adolescent↗
PubMed1983

The neural signal for skin indentation depth. I. Changing indentations.

Psychophysical tests on human subjects showed that judgments of skin indentation depth made when the fingertip was indented at rates from 0.2 to 16 mm/sec were quite insensitive to changes in indentation velocity. Similar results were obtained on the forearm at indentation velocities of 0.4 to 16 mm/sec. Recordings were made from mechanoreceptors in the monkey's hand that were able to respond over the same range of velocities and at comparable depths to determine how skin indentation depth might be signaled (coded) at the receptor level and to examine the rate sensitivity of the possible depth codes. It was found that most of the receptors with foci under the stimulator were recruited relatively early during an indentation, especially at velocities of 1.6 mm/sec and higher, making it improbable that the full range of indentation depths is signaled by the "subsurface" recruitment of different receptors at different indentation depths. A subsurface recruitment code involving subcutaneous receptors is not likely since subjects could feel virtually none of the stimuli after skin anesthesia. Progressive recruitment with depth of receptors whose foci lie further and further away from the stimulator ("lateral" recruitment) was considered an unlikely depth code because changing the area of the stimulator had little effect on its perceived depth. Also, it was shown that subjects could sense the curvature of the indentation (the profile of the depth at right angles to the skin surface), which requires information about the depth of individual patches of skin beneath the stimulator. There is no obvious way that a lateral recruitment code can provide this information. Thus it is probable that the discharge rate of some or all of the receptors excited by the indentation is involved in indicating its depth. Both impulse frequency and receptor recruitment at any given depth increased as the velocity of the indentation increased. The demonstrated reliability of information about skin indentation depth in humans indicates that the central neural circuitry responsible for judgments of skin indentation depth is able to compensate for the rate-sensitive receptor signals.

Adult↗