Biomedical subjects
Publications and source records attributed to X Qin.
The parameters are proposed which can be used in extracting berberine from the rhizoma of Coptis chinensis with ultrasound. Compared with traditional immersing method, ultrasonic extraction is time saving and of higher extraction rate.
This study tested the hypothesis that 1,25-dihydroxyvitamin D3 treatment alters the pattern of protein phosphorylation in rat kidney. Treatment with 1,25-dihydroxyvitamin D3 (100 ng/day s.c. x 7d) in vitamin D-deficient rats markedly decreased phosphorylation of a particulate protein (91 +/- 0.6 kDa, n = 9) and moderately increased phosphorylation of a cytosolic protein (108 +/- 0.8 kDa, n = 9) in the kidney. The decreased phosphorylation of the 91-kDa particulate protein showed a graded dose response (0-200 ng/day), as did the more moderate increase in phosphorylation of the 108-kDa cytosolic protein. In conclusion, this study has provided evidence that 1,25-dihydroxyvitamin D3 plays an important role in the regulation of protein phosphorylation in rat kidney and adds these biochemical events to the growing list of 1,25-dihydroxyvitamin D3 effects in this poorly understood target tissue.
Ultraviolet-induced cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidone (6-4)photoproducts in DNA were quantitatively measured in monkey skin using an immunohistochemical method with two specific monoclonal antibodies. The skins of Cynomolgus monkeys (Macaca fascicularis) were irradiated with UV light and processed for preparation of conventional formalin-fixed, paraffin-embedded histological sections. Both of the photoproducts were detectable in the nuclei of epidermal cells at doses of 500 J/m2 for UVB and 50 J/m2 for UVC, respectively, nuclear staining being clearly dose-dependent. Time course studies also showed a statistically significant decrease in nuclear staining with time after exposure to either UVB or UVC irradiation. Although only 30% of CPDs were removed from DNA in the first 24 h, about half of the (6-4) photoproducts were repaired within 3 h post-UV irradiation. Staining completely disappeared by 48 h in the (6-4) photoproduct case and by 72 h in the case of CPDs. The results suggest that epidermal cells of monkey skin can efficiently repair UV-photoproducts in DNA, but that the capacity is slightly less than in man.
We have characterized the immunobiology of the interaction of intercellular adhesion molecule 3 (ICAM-3; CD50) with its counter-receptor, leukocyte function-associated antigen 1 (LFA-1; CD11a/CD18). Purified ICAM-3 supported LFA-1-dependent adhesion in a temperature- and cation-dependent manner. Activation of cells bearing LFA-1 increased adhesiveness for ICAM-3 in parallel to adhesiveness for ICAM-1. Although CBR-IC3/1 monoclonal antibody (mAb) blocked adhesion of cells to purified LFA-1, when tested alone, neither CBR-IC3/1 nor five novel ICAM-3 mAbs characterized here blocked adhesion of cells to purified ICAM-3 or homotypic adhesion. Two ICAM-3 mAbs, CBR-IC3/1 and CBR-IC3/2, were required to block LFA-1-dependent adhesion to purified ICAM-3- or LFA-1-dependent, ICAM-1-, ICAM-2-independent homotypic adhesion of lymphoid cell lines. Two ICAM-3 mAbs, CBR-IC3/1 and CBR-IC3/6, induced LFA-1-independent aggregation that was temperature and divalent cation dependent and was completely inhibited by ICAM-3 mAb, CBR-IC3/2, recognizing a distinct epitope. Purified ICAM-3 provided a costimulatory signal for proliferation of resting T lymphocytes. mAb to ICAM-3, together with mAbs to ICAM-1 and ICAM-2, inhibited peripheral blood lymphocyte proliferation in response to phytohemagglutinin, allogeneic stimulator cells, and specific antigen. Inhibition was almost complete and to the same level as with mAb to LFA-1, suggesting the most functionally important, and possibly all, of the ligands for LFA-1 have been defined.
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BACKGROUND: The incidence of hepatocellular carcinoma (HCC) in southern China, including Guangxi Province, is among the highest in the world. Investigations of the etiology of HCC in this area have focused on hepatitis B virus (HBV) and aflatoxin. However, hepatitis C virus (HCV) has been shown to be a possible pathogenic agent for HCC in a number of countries. METHODS: Antibodies to HCV (anti-HCV), determined by second-generation enzyme immunoassay, and hepatitis B surface antigen (HBsAg) were assayed in the sera of 186 patients with HCC and 48 healthy control subjects from Guangxi Province in southern China. RESULTS: HBsAg was detected in 131 (70.4%) of 186 patients with HCC, whereas only 10 (5.4%) patients were found to be positive for anti-HCV. The prevalence of anti-HCV in patients with HBsAg-positive HCC was 6.9% (9 of 131) and that in patients with HBsAg-negative HCC was 1.8% (1 of 55); there was no significant difference between these two groups. Anti-HCV was not detected in any of the healthy control subjects, in whom the prevalence of HBsAg was 10.4% (5 of 48). CONCLUSIONS: These findings indicate that HCV does not seem to play an important role in the development of HCC in Guangxi Province; however, HBV infection appears to be a major pathogenic factor for HCC in this area.
Incubation of mammalian cells in medium containing low K+ is often associated with an increase in Na,K-ATPase activity and content. In the present studies, we investigated the effect of low K+ on the regulation of Na,K-ATPase alpha 1 and beta 1 gene expression in primary cultures of neonatal rat cardiac myocytes. Northern blot hybridization analysis indicated that exposure of cardiocytes to a medium containing 0.3 mmol/L K+ for 72 h resulted in 1.8- and 3.3-fold increases in the abundance of alpha 1 and beta 1 mRNAs, respectively, compared with control cells exposed to 5.4 mmol/L K+. To investigate the molecular mechanism of the low K effect on beta 1 mRNA content, we constructed chimeric genes with a full-length and deleted portion of the 5' end of the rat beta 1 gene linked to the firefly luciferase gene. Transient transfection experiments using these constructs indicated that beta 1 gene sequences between -102 and +151 base pairs (bp) are required for low K(+)-induced trans-activation of reporter gene expression. Taken together, these results indicate that low K+ induction of beta 1 mRNA abundance in neonatal rat cardiac myocytes is mediated by regulatory DNA sequences in close proximity to the site of transcription initiation of the beta 1 gene.
N-Nitroso-compound DNA adduct formation in vivo and occurrence of aberrant crypt foci (ACF) were studied in the rat colon mucosa after a single, local treatment with a carcinogen, N-methyl-N-nitrosourea (MNU), using a simple surgical approach. A segment of F344 rat colon was ligated to make a pouch and injected with MNU solution. For the study of DNA adduct formation, the solution contained 50 microCi of [3H]MNU. The results demonstrated that similar ranges of carcinogen dose, i.e. 0.15 x 10(-2) - 1.5 x 10(-2) M MNU, could induce both DNA adduct formation and appearance of ACF in the rat colon with both parameters showing a nearly linear dose dependence. HPLC analysis revealed the DNA adducts to include both 7-methylguanine (7-mGua) and O6-methylguanine (O6-mGua) with the 7-mGua/O6-mGua ratio being 8.2-11.3:1 in the system used. Assessment of ACF development from 4 to 16 weeks after MNU treatment at a dose of 7.5 x 10(-2) M showed the numbers to increase up to the 8th week, followed by a decrease at weeks 12 and 16, when 40% of the ACF counted at the peak time point were still present. The percentage of large ACF (> or = 4 crypts/ACF) significantly increased with time. These results indicate a clear relation between DNA adducts and preneoplastic lesions, i.e. ACF. In conclusion, DNA adduct formation and ACF can be efficiently and simply detected in vivo by using the method described in the present paper.
The gene coding for the major carboxysome shell peptide (csoS1) from Thiobacillus neapolitanus has been isolated and sequenced. Oligonucleotide primers for polymerase chain reaction (PCR) amplification of the 5' end of the gene were made possible by amino acid sequencing of the N-terminal residues of the shell peptide. A 41 bp PCR product was used as a probe to isolate the gene. The deduced amino acid composition of the 216 bp gene shows a high degree of hydrophobicity. The gene is located within a series of three repeated regions of DNA and appears to have arisen via gene duplication. The transcript of csoS1 is approximately 400 bases in length. The shell peptide shares significant homology with Synechococcus open reading frames implicated in carboxysome structure/assembly. These open reading frames and csoS1 are related and are probably members of a carboxysome gene family.
The effect of 17 beta-estradiol (E2) on Ca-, Mg-, and Ca-Mg-ATPase activity was investigated in the shell gland of 6-week-old chicks. In the first study, each of 42 birds was implanted with three E2 (Compudose-200) pellets. An additional 6 sham-implanted birds served as controls for measurements of body weight and concentrations of E2 and Ca in plasma. The activities of Mg-, Ca-, and Ca-Mg-ATPase peaked coincident with maximum plasma E2 concentrations 8 days after implantation and then progressively declined in concert with the decline in plasma E2. By 29 days after implantation, the ATPase activities were similar to those measured in birds whose E2 pellets had been removed for 11 days. Concentrations of plasma E2 dropped from peak values of 1676 +/- 317 at Day 8 to 611 +/- 180 pg/ml at Day 29. When birds whose E2 pellets had been removed were reimplanted with three pellets per bird, plasma E2 again increased to 1637 +/- 227 pg/ml. ATPase activity in these reimplanted birds also was greater (P < 0.05) than activities measured in E2-removed or E2-maintained birds. In a second study the Ca-ATPase Km and Vmax were determined in E2-implanted chicks (three pellets per bird) and compared to E2-withdrawn chicks. Five days after reimplantation of chicks with E2, there was a significant increase in both Vmax (3.38 +/- 0.21 vs 2.37 +/- 0.28 micrograms Pi/mg protein/min; P < 0.05) and Km (0.31 +/- 0.02 vs 0.25 +/- 0.01 mM Ca; P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)
The interaction between 17 beta-estradiol (E2), vitamin D3 (D3), and dietary Ca on the activities of Ca-ATPase and alkaline phosphatase (AP) was determined in the intestine of young female chicks. Chicks (n = 36) were assigned to two groups, one of which was transferred to a low Ca (0.2%) diet and the other maintained on a regular diet. One week later, each group was further divided into three subgroups and given daily injections of 0(oil), 0.25, or 0.5 mg E2/kg body wt for 14 days. E2 treatment as well as low dietary Ca significantly increased AP activity (P < 0.05), whereas the highest E2 dose decreased jejunal Ca-ATPase (P < 0.05). In a separate study, day-old chicks (n = 40) fed a purified diet supplemented with or without D3 for 24 days were divided into two subgroups and administered daily injections of either 0 or 0.25 mg estrogen 3-benzoate/kg body wt for 5 days. E2 alone or in combination with D3 failed to change Ca-ATPase activity in either the duodenum or the jejunum. However, E2 enhanced the D3-stimulated AP activity measured in the supernatant of duodenum (D3, P < 0.001; E2, P > 0.05; E2 x D3, P < 0.05) and jejunum (D3, P < 0.001; E2, P > 0.05; E2 x D3, P = 0.06). Daily injections of 0.5 mg E2/kg body wt for 6 days to 6-week-old D3-adequate chicks (n = 16) significantly increased AP activity in jejunum but not in liver and kidney (P < 0.05). In conclusion, E2 treatment enhanced the activity of intestinal AP but not Ca-ATPase. This enhancement was independent of dietary Ca, but was D3-dependent and tissue specific. The results suggest that the pubertal increase in plasma E2 can affect Ca absorption from the intestine by increasing the activity of AP.
The retinoblastoma gene product (RB) contributes to normal cell growth control. One of its functions is manifest as a block to exit from G1, which is carried out by an RB subspecies which is un- or underphosphorylated. After RB phosphorylation, a process which occurs towards the end of G1 in cycling cells, the block is lifted allowing a cell to enter S. Here, we review a series of results which speak to the elements of RB structure which contribute to this activity. Included is its internal colinear protein receptor domain (i.e. the 'pocket').
Fecapentaenes are a group of fecal mutagens produced by anaerobic microflora of the colon. The potential of fecapentaene-12 (FP-12) to promote tumor development was tested in a rat colon carcinogenesis model using N-methyl-N-nitrosourea (MNU) as the initiating agent. Two groups of female F-344 rats were initiated by intrarectal instillations of MNU (2 mg in 0.5 ml H2O, 3 times a week, for 3 weeks; MNU and MNU + FP-12 groups). Two additional groups (FP-12 and Control) were given H2O without carcinogen. In the post-initiation phase, rats of the MNU + FP-12 and FP-12 groups were intrarectally administered 400 ng of FP-12 in 0.5 ml T-E buffer, twice a week, for 24 weeks, whereas the MNU and Control groups received the vehicle only. Tumors were found only in the MNU and MNU + FP-12 groups, their number being higher in the latter. The number of carcinoma bearing rats as well as the average number of carcinomas per rat were significantly higher (P < 0.05) in the MNU + FP-12 group as compared to the MNU-alone values. Aberrant crypt foci (ACF) were found in all carcinogen-treated rats, including those that did not contain tumors, whereas none were observed in the FP-12 and Control groups. The average number of ACF/cm2 was also significantly higher in the MNU+FP-12 group, as was the case for the average number of ACF containing > 10 aberrant crypts per focus. These findings suggest that FP-12 can express promoting activity in chemical induced colon carcinogenesis.
The effect of estradiol-17 beta (E2) given as a sustained-release implant (Compudose 200) on concentrations of plasma calcium (Ca) and the development of the chick shell gland has been investigated in food-restricted and thyroid hormone-treated 6- to 8-week-old broiler breeder pullets. Chicks implanted with 0, 0.5, 1.0, 1.5, 2.0, and 3.0 Compudose pellets for 24 days (n = 6/group) revealed a dose-response relationship between plasma E2 and Ca and on oviduct growth. Plasma E2 concentrations were characterized by an initial burst phase for approximately 17 days, followed by a constant release phase. Histologic examination of shell gland tissue confirmed the dose related E2-induced development of microvilliated epithelium and tubular glands over time. Feed restriction initiated at 2 weeks of age markedly increased the response to the E2 implants. Birds (n = 8/group) implanted with 2 pellets and feed restricted had increased plasma concentrations of E2 and Ca, and increased growth of the oviduct (P less than 0.01) as compared to ad libitum implanted birds. In a separate study birds (n = 6/group) had restricted access to feed from 8 weeks of age and were implanted with 0, 2, 4, or 8 pellets. At intervals from 9 to 45 days after implantation one bird from each group was killed. Although concentrations of plasma Ca were significantly greater in feed-restricted birds (P less than 0.01), oviduct growth was only marginally increased by the food restriction program. Plasma Ca concentrations in broiler breeder pullets (n = 8/group) implanted with 1 or 3 pellets and injected with T3/T4 (100 micrograms/day) were significantly decreased (P less than 0.05). Injection of thyroid hormone also marginally decreased shell gland epithelial cell height (P less than 0.05) and development of microvilli (P less than 0.05). There was no effect of the administration of the goitrogen, propylthiouracil (10 micrograms/day im), on the E2 induced development of the shell gland.
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Three experiments were conducted using aged broiler breeder hens (greater than 60 wk) to investigate the effects of supplemental B on egg production (EP), shell quality, and Ca metabolism. Experiment 1 had a 2 x 2 factorial arrangement of treatments: 1) high Ca (3.5%); 2) high Ca plus B; 3) low Ca (1.5%); and 4) low Ca plus B; using 32 60-wk-old hens. The B levels were basal and 100 ppm supplemental for the first 2 wk of the experiment and reduced to 60 ppm for the remaining 3 wk. Egg production, shell thickness (ST), and egg specific gravity (SG) were recorded weekly. In Experiment 2, 40 60-wk-old hens were divided into two groups: high and low shell quality. Each group was further divided into two subgroups and fed a low-Ca basal diet with or without supplemental B. The level of B supplementation and the experimental period was the same as in Experiment 1. In Experiment 3, 52 75-wk-old hens were force-molted. After molting, 36 hens were fed a commercial layer diet with the remaining 16 hens fed the control diet supplemented with 100 ppm B. Blood samples were taken during the nonlaying and laying periods, respectively. The results showed that B significantly (P less than .05) depressed EP in Experiment 1 but not in Experiments 2 and 3. Supplemental B decreased plasma Ca when hens were fed a diet containing high Ca levels (3.5%). Supplemental B did not affect SG, ST, or Ca retention, but did significantly increase tibial bone ash percentage (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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