Biomedical subjects
Publications and source records attributed to Y Yin.
The following case is presented to illustrate the roentgenographic and clinical findings of a condition of interest to the orthopaedic surgeon. The initial history, physical findings, and roentgenographic examinations are found on this page. The final clinical and roentgenographic differential diagnosis is then presented.
The following case is presented to illustrate the roentgenographic and clinical findings of a condition of interest to the orthopaedic surgeon. Initial history, physical findings, and roentgenographic examinations are presented along with the final histologic and differential diagnoses.
The following case is presented to illustrate the roentgenographic and clinical findings of a condition of interest to the orthopaedic surgeon. Initial history, physical findings, and roentgenographic examinations are found on the first two pages. The final clinical and roentgenographic differential diagnoses are presented on the following pages.
Loss of cell cycle control and acquisition of chromosomal rearrangements such as gene amplification often occur during tumor progression, suggesting that they may be correlated. We show here that the wild-type p53 allele is lost when fibroblasts from patients with the Li-Fraumeni syndrome (LFS) are passaged in vitro. Normal and LFS cells containing wild-type p53 arrested in G1 when challenged with the uridine biosynthesis inhibitor PALA and did not undergo PALA-selected gene amplification. The converse occurred in cells lacking wild-type p53 expression. Expression of wild-type p53 in transformants of immortal and tumor cells containing mutant p53 alleles restored G1 control and reduced the frequency of gene amplification to undetectable levels. These studies reveal that p53 contributes to a metabolically regulated G1 check-point, and they provide a model for understanding how abnormal cell cycle progression leads to the genetic rearrangements involved in tumor progression.
Dgp1, a circular 4.4-kb plasmid found in the nuclei of Dictyostelium giganteum strain DG61, is a member of the same plasmid family as plasmids Ddp2 and pDG1. Dgp1 has sequence similarity to a conserved region of the Ddp2 and pDG1 open reading frames. As with Ddp2 and pDG1, a single large RNA is transcribed from Dgp1. This 3.3-kb transcript is present at about 350 copies per vegetative cell. The transcript abundance decreased about 10-fold in early aggregation and continued at this lower level until late culmination when it returned to the level seen in vegetative cells. Dgp1 has a repeat of several hundred base pairs in a location, relative to the transcribed region, similar to the inverted repeats found in Ddp2 and pDG1. Dgp1 cannot be maintained as a plasmid in Dictyostelium discoideum AX4 cells, suggesting that Dgp1 carries species-specific maintenance elements.
The effects of germanium oxide on the genotoxicity of cadmium chloride were investigated. The incorporation of [3H]thymidine into testicular DNA was inhibited in mice injected ip with 1.35, 1.80 or 2.70 mg cadmium chloride/kg body weight. Germanium oxide (0.05 or 0.1 mg/kg body weight, sc) alone did not affect [3H]thymidine incorporation into testicular DNA but 0.05 mg germanium oxide/kg antagonized the inhibitory effect of 1.35 mg cadmium chloride/kg. However, combinations of the other doses of the two compounds did not show statistically significant antagonistic effects. Cadmium chloride significantly increased the frequencies of micronucleus formation in polychromatic erythrocytes, and of chromosome aberrations in the bone marrow of mice treated with 0.7, 1.4 or 2.7 mg/kg body weight, in a dose-related manner. These effects were inhibited by germanium oxide at doses of 0.1 or 0.5 mg/kg body weight, although germanium oxide alone did not affect micronucleus formation or the chromosome aberration rate. Cadmium chloride produced a dose-related increase in the frequency of sister chromatid exchanges in cultured human lymphocytes at concentrations of 5, 10 or 50 mumol. This effect was also inhibited by germanium oxide (0.05 or 0.1 mumol), although germanium oxide alone had no effect. There was a dose-related increase in the frequency of sperms with abnormal head morphologies from mice treated with 0.6, 1.1 or 2.2 mg cadmium chloride/kg body weight and this too was antagonized by the injection of germanium oxide (0.1 or 0.5 mg/kg body weight). Germanium oxide alone did not affect the frequency of sperm-head abnormalities.
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The following is presented to illustrate the roentgenographic and clinical findings of a condition of interest to the orthopaedic surgeon. The initial history, physical findings, and roentgenographic examinations are found on this page. The final clinical and roentgenographic differential diagnoses are presented on the following pages.
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Explore the source record for details and available documents.
A disease with main symptoms of fever, headache, malaise, profuse sweating and diarrhoea occurred as an outbreak in a few villages at suburb of Hengyang City from March to July 1987. It was diagnosed as Type B paratyphoid fever by laboratory examinations. The number of cases occurred in this outbreak was 59 in total. All of them recovered after isolation and proper-treatment.
When stimulation of DLF at cervical cord, a train of evoked potentials are recorded with a microelectrode at lumber level in rat. The longer slow positive potential wave, latency 7.22 +/- 1.41 ms, peak time 15 +/ 12 +/- 5.58 ms, duration 93 +/ 92 +/- 9.06 ms, is called DLF-FP. The negative center of the isopotential map of DLF-FP is located at 1.0-1.3 mm below the dorsal surface nearly in coincidence with that of the P1-FP evoked by the sural nerve stimulation. The amplitude of DLF-FP was decreased by picrotoxin and increased by strychnine. Both summation and inhibition can be observed between the potentials evoked by stimulation of the sural nerve and DLF. The results mentioned above show that DLF-FP is the reflection of primary afferent depolarization probably by the same spinal circuit underlying P1-FP.
In order to determine a suitable indicator for estimating the exposure levels of the dietary carcinogen 2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (Glu-P-1), a carcinogenic glutamic acid pyrolysis product, the levels of Glu-P-1 bound to blood components were monitored for 8 weeks by a high-performance liquid chromatography method after the dietary carcinogen was administered as single oral doses (0.2-50 mg) to rabbits. In all rabbits dosed with Glu-P-1, Glu-P-1 in erythrocytes was detectable even on day 42 after administration. Glu-P-1 in plasma disappeared faster than did Glu-P-1 in erythrocytes. Glu-P-1 levels in rabbit hemoglobin were linearly related to administered doses at all points of time investigated. The results suggest that Glu-P-1 covalently bound to hemoglobin is very suitable for monitoring long-term exposure levels.
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From 1965 to 1968, the Honolulu Heart Program began following 8006 men of Japanese ancestry in a prospective study of cardiovascular disease. Of the subjects who had not had a stroke by the time of study entry, 3435 were cigarette smokers and 4437 were nonsmokers. In 12 years of follow-up, 171 smokers and 117 nonsmokers had a stroke. As compared with nonsmokers, cigarette smokers had two to three times the risk of thromboembolic or hemorrhagic stroke, after control for age, diastolic blood pressure, coronary heart disease, and other risk factors (P less than 0.001). Subjects who continued to smoke in the course of follow-up had the highest risk of stroke. When these subjects were compared with those who never smoked, their risk of hemorrhagic events was increased four- to six-fold (P less than 0.001). Subjects who were smokers at study entry but stopped smoking in the course of follow-up had a slight excess risk of stroke. When these subjects were compared with those who continued to smoke, however, their risk was reduced by more than half after adjustment for risk factors (P less than 0.05), indicating that stopping smoking had significant benefits.
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