An analysis of baby boom characteristics in China.
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Biomedical subjects
Publications and source records attributed to G Li.
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The effects of methionine-enkephalin (Met-Enk) on mitogenic and mixed lymphocyte culture (MLC) proliferation of splenocytes from Zn-deficient, restricted and control mice were evaluated. The data from this experiment show that Met-Enk can suppress the responses of splenocyte from the 3 groups to concanavalin A (Con A), but less inhibition was observed in the Zn-deficient group. Met-Enk can also enhance the responses to pokeweed mitogen (PWM) and decrease the response to lipopolysaccharide (LPS) in all groups. Alteration of proliferative responses to Con A and PWM were reversible in the presence of naloxone 10 mumol/L indicating that the effect of Met-Enk on cellular proliferation was mediated by the opioid receptor. In the proliferation of MLC, the response of lymphocytes from Zn-deficient mice was increased in the absence of Met-Enk and Met-Enk can suppress this increased response. It is therefore concluded that Met-Enk can modify the pattern of mitogenic responses and the alteration in Con A and MLC responses can be influenced by zinc deficiency.
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Fifty-seven guinea pigs weighting 200-400 g with normal Preyer's reflexes were randomly divided into five groups, one for control and the others studied 8, 48 hours and 7, 30 days after explosion. Cortical response threshold measurement and AchE histochemical observations were made. Histochemical sections were prepared as follows: under anesthesia, blood was washed out with Ringer's solution, then the animals were perfused with ice-cold neutral formol-calcium solution for 10 minutes. Temporal bones were removed and fixed in the same fixative for 24 hours. Fixed specimens were decalcified in 10% EDTA solution at 15 degrees C for one week. Tissue blocks were sectioned serially at 20 microns in a cryostat. Horizontal sections were obtained. Sections were then incubated in a substrate solution prepared according to Tsuji (1983) at 4 degrees C for 50 minutes, washed with 3 changes of distilled water and mounted in 25% gelatin. Inhibitory tests were carried out to non-specified chE or Pseudo-chE activity by using iso-OMPA during incubation. Control sections were incubated without the substrate. The results showed that explosion reduced the AchE activity of the cochlea and elevated cortical response threshold. Both showed a negative correlation. The significance of the results obtained had been discussed.
The number of bovine papillomavirus type 1 (BPV) DNA copies [plasmid pdBPV-1 (142-6)] was examined in transformed C127 cells of an RIII mouse during exposure to all-trans-retinoic acid (RA) and after its withdrawal. RA treatment of a transformed cell line reduced the number from approximately 60 copies to an average of less than one copy per cell within 5 weeks. The composition of the RA-treated cell population was heterogeneous with respect to BPV DNA copies: 89.7% of the cells had no detectable copies, 8.6% had one copy, 1.7% had fewer than five copies, and one in 13,000 cells carried more than 10 copies. The low number of BPV DNA copies in the RA-treated cell population did not increase when the cells were subcultured before reaching confluence. RA-treated cell populations that contained less than one BPV DNA copy lost the transformed phenotype. However, a small fraction of cells (1 in 13,000) with greater than or equal to 10 BPV DNA copies retained the capacity to develop into transformed colonies. The relevance of these results to the regression of papillomavirus, DNA-carrying human lesions after exposure to retinoids and the redevelopment of these lesions after withdrawal of retinoids is discussed.
The addition of 0.5% globulin-free (GF-BSA) or 0.5% delipidated BSA (D-BSA) to short-term murine bone marrow (BM) (cultures) increased the number of plaque-forming cells (PFC) responding to trinitrophenylated lipopolysaccharide (TNP-LPS) 2-5-fold (1.1 X 10(4)-2.7 X 10(4) PFC per 10 X 10(6) nucleated BM cells). Although it was necessary to continue to supplement these cultures with 5% fetal calf serum (FCS), the inclusion of the aforementioned BSA preparations provided enhanced PFC production for all lots of FCS tested. Similarly, these preparations of BSA made it feasible to also culture BM in autologous mouse sera (MS) or in medium without 2-mercaptoethanol (2-ME) if in the latter case the D-BSA was pretreated with 2-ME. Thus, the inclusion of GF-BSA or D-BSA in short term cultures of BM not only substantially increased the number of Ig-secreting B cells produced in response to TNP-LPS but seemed to eliminate the need to screen for supportive batches of FCS or MS. These preparations of BSA also facilitated hapten specific PFC responses of fetal liver cultures.
The effect of all-trans-retinoic acid (RA) was examined on (1) transformation induced in C127 cells by transfection with plasmid pdBPV-1 (142-6), which contains DNA of bovine papillomavirus (BPV), (2) the capacity of transformed BPV DNA-containing clones to form colonies with transformed properties (e.g., piling up into multilayered colonies), and (3) the number of BPV DNA copies in transformed cells. At nontoxic doses ranging from 10(-7) to 10(-5) M, RA reduced the frequency of transformed foci in a dose-dependent manner. The extent of inhibition depended on the length of RA treatment and on the time that elapsed between DNA transfection and RA treatment. RA exerted only a slight inhibitory effect during the first days after transfection. Complete inhibition was observed when the cells were continuously exposed after transfection to RA at doses ranging from 0.5 to 1 X 10(-5) M. The inhibitory effect of RA on transformation was reversible. Transformed foci started to form after withdrawal of RA treatment. In the presence of RA (5 X 10(-6) M), cells from transformed colonies were no longer able to form foci displaying transformed properties. The number of BPV DNA copies gradually decreased when the cells were grown over several generations in the presence of RA (5 X 10(-6) M). After approximately 30 cell generations, the cell cultures appeared to have less than one copy of BPV DNA.
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While heavy exposure to inorganic lead is capable of inducing symptomatic neuropathy in man, the subclinical neuropathy due to low levels of occupational lead exposure remains to be proved. The reported results of electroneurographic studies on lead workers, however, have been controversial. In this study, 40 lead smeltery workers and 50 non-exposed referents were investigated. The air concentrations of lead at worksites were 0.25 to 42.5 mg/m3. The geometric means of PbB, PbU and delta-ALAU in lead exposed group were 40.03 micrograms/dl, 71 micrograms/l and 4.68 mg/l respectively, which were significantly higher (P less than 0.001) than those (7.01 micrograms/dl, 6.0 micrograms/l and 1.81 mg/l respectively) in the reference group. There were no clinical symptoms or signs of nerve damage in either group. Alcoholism and diabetes were excluded in both groups. Nerve conduction velocity was measured by a DISA 1500 electromyograph in both groups. Eleven electroneurographic parameters, including motor nerve conduction velocity (MCV) and distal latency (DML) of median, ulnar and peroneal nerves as well as sensory nerve conduction velocity (SCV) and distal latency (DSL) of median, ulnar and sural nerves, showed statistically significant differences between the two groups. However, the results of electroneurographic measurements of each individual in the lead-exposed group were all within the normal range. There was no correlation between the blood-lead levels and the neurophysiological measurements except for the median MCV. No correlation was seen between the median MCV and the exposure duration.(ABSTRACT TRUNCATED AT 250 WORDS)
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The effects of high-dose irradiation on the biomechanical and morphological properties of cortical bone and their time-related changes were studied in male Sprague-Dawley rats. A single fraction of 3500 rads was applied to the middle part of the right thigh. Age and sex-matched control rats that did not receive radiation were used for comparison. Two weeks after irradiation, the animals had lost weight and disappearance of bone cells, shrunken osteocytes, and significantly decreased bone-turnover activities were noted. The bone marrow showed reduced hematopoietic elements and sinusoids with increased fat. No change in the torsional strength and geometric properties of bone was noted at this time. Six to ten weeks after irradiation, histopathological abnormalities of the bone persisted, and there was an accelerated resorption process. However, significant increases in the strength and cortical area of bone appeared only in the non-irradiated, contralateral femur. On the irradiated side, decreased cortical area and increased porosity of bone were found at fourteen to eighteen weeks when compared with the control rats. Other histomorphological properties, such as bone porosity, osteocyte count, and periosteal new-bone formation, appeared to recover eighteen weeks after irradiation, as they became similar to the values for the age-matched normal control rats.
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We have measured endogenous and induced rates of 70-kD, 89-kD, and 110-kD heat shock proteins in highly pure G1-, S-, or G2-M phase fractions of Chinese hamster fibroblasts (CHO) separated by fluorescence-activated cell sorting (FACS). Relative rates of synthesis of all three polypeptides as measured by two-dimensional gel electrophoresis were similar throughout the cell cycle, and therefore, endogenous levels were unlikely to explain the thermal sensitivity of S-phase cells. Distinct heterogeneity in induced rates of these polypeptides was noted in all phase fractions. Enhanced rates of 70-kD polypeptide were measured in S and G2-M as compared to G1 following heat shock. Little increase in either the 89-kD or 110k-kD heat shock proteins was observed in heated G1 cells. This heterogeneity in induced rates of synthesis was in contrast to the similarity in thermal tolerance expression kinetics between each phase. Finally, enhanced synthesis of these polypeptides appeared unrelated to regulation of either heat-induced cell cycle delay or to the resumption of phase-specific progression after heat shock as measured by simultaneous flow cytometric measurement of incorporated BrdUrd and DNA content.
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The kinetics of calcium (Ca2+) uptake have been studied in mitochondria isolated from the different types of skeletal muscle. These studies demonstrate that the Ca2+ uptake properties of skeletal mitochondria are similar to those from liver and cardiac mitochondria. The Ca2+ carriers apparently have a high affinity for Ca2+ (Michaelis constants in the microM range). The relationship between Ca2+ uptake and initial Ca2+ concentration (10(-5) to 10(-7) M) is sigmoid in all mitochondria from the different skeletal muscle types suggesting that the uptake process is cooperative. Hill plots reveal coefficients of approximately 2 for mitochondria from fast-twitch muscle and 3.5 for slow-twitch muscle, adding further evidence to the concept that the uptake process is cooperative. An analysis of the potential role of mitochondria in the sequestration of Ca2+ during muscular contraction demonstrated that mitochondria from slow-twitch muscle of both rats and rabbits can potentially account for 100% of the relaxation rate at a low frequency of stimulation (5 Hz). In fast-twitch muscle, the mitochondria appear unable to play a significant role in muscle relaxation, particularly at stimulation frequencies that are considered in the normal physiological range. In summary, it appears that Ca2+ uptake by mitochondria from slow-twitch skeletal muscle has kinetic characteristics which make it important as a potential regulator of Ca2+ within the muscle cell under normal physiological conditions.