Biomedical subjects

D Lin

Publications and source records attributed to D Lin.

At least 91 records · Page 5Linked to original sources

PubMed1998

Electrical cardioversion of atrial fibrillation or flutter with conscious sedation in the age of cost containment.

BACKGROUND: The purpose of this study was to compare the safety, efficacy, and cost of conscious sedation administered by electrophysiologists certified in the use of conscious sedation with sedation administered by anesthesiologists during cardioversion of atrial fibrillation or atrial flutter to sinus rhythm. METHODS AND RESULTS: Patients with hemodynamically stable persistent atrial fibrillation and flutter were included in this study. Group 1 patients (n = 33) were sedated by an anesthesiologist and group 2 patients (n = 26) were sedated by an electrophysiologist. Anesthesiologists used propofol and electrophysiologists used midazolam and morphine for sedation. A cost analysis based on professional charges and cost of medications was performed for both groups and compared. Hospital charges were similar for both groups and were excluded from the cost analysis. Although time to sedation in group 1 was shorter than that in group 2, sedation was adequate in both groups such that no patient in group 1 and only 1 patient in group 2 recalled being shocked. There were no complications in either group. The cost incurred in group 2 was less than that in group 1. CONCLUSIONS: Sedation administered by electrophysiologists for cardioversion of atrial arrhythmias is safe and cost effective. Midazolam and morphine, the sedative agents administered by electrophysiologists, were effective and well tolerated by patients.

Aged↗

PubMed1998

Immunologic response to tetanus toxoid in the elderly: one-year follow-up.

STUDY OBJECTIVE: To determine whether elderly patients documented to have nonprotective titers of anti-tetanus antibodies (ATA) are able to achieve and maintain protective ATA titers for at least 1 year after tetanus immunization. METHODS: Thirty-five outpatients aged 65 or older with documented inadequate ATA titers were given 1 tetanus immunization. Repeat titers were obtained 2 months and 12 months after immunization. Titers were measured with an enzyme-linked immunoassay kit (Bindazyme kit). ATA titers in excess of .17 IU were considered protective. The study was conducted at a large urban geriatric center. RESULTS: The mean age of participants was 78.7 years; 86% (24/28) were women. Repeat ATA titers were obtained an average of 122 days and 493 days after immunization. The mean preimmunization ATA titer was .1 IU, (range .04 to .16 IU). After immunization, the 2-month ATA titer rose a mean of .61 (95% confidence interval [CI] .35 to .87) IU, with 86% (30/35) achieving protective titers. After 1 year only 28 of 35 patients were available for follow-up. Protective titers had been present in all 7 patients lost to follow-up. After 1 year, 82% (23/28) patients had protective titers. The mean ATA titer for the 28 patients was .54 (95% CI -.78 to 1.86) IU, a significant increase from preimmunization levels (P=.002). However, ATA titers changed -.18 (95% CI -.98 to .62) IU between 2 months and 1 year (P=.02). There was no correlation between gender, country of birth, and medical history with development or maintenance of protective titers. CONCLUSION: Administration of 1 tetanus toxoid affords protective immunization to a large portion of the elderly population after 1 year.

Aged↗

PubMed1998

Mutations in the human sterol delta7-reductase gene at 11q12-13 cause Smith-Lemli-Opitz syndrome.

The Smith-Lemli-Opitz syndrome (SLOS; also known as "RSH syndrome" [MIM 270400]) is an autosomal recessive multiple malformation syndrome due to a defect in cholesterol biosynthesis. Children with SLOS have elevated serum 7-dehydrocholesterol (7-DHC) levels and typically have low serum cholesterol levels. On the basis of this biochemical abnormality, it has been proposed that mutations in the human sterol Delta7-reductase (7-DHC reductase; E.C.1.3.1.21) gene cause SLOS. However, one could also propose a defect in a gene that encodes a protein necessary for either the expression or normal function of sterol Delta7-reductase. We cloned cDNA encoding a human sterol Delta7-reductase (DHCR7) on the basis of its homology with the sterol Delta7-reductase from Arabidopsis thaliana, and we confirmed the enzymatic function of the human gene product by expression in SLOS fibroblasts. SLOS fibroblasts transfected with human sterol Delta7-reductase cDNA showed a significant reduction in 7-DHC levels, compared with those in SLOS fibroblasts transfected with the vector alone. Using radiation-hybrid mapping, we show that the DHCR7 gene is encoded at chromosome 11q12-13. To establish that defects in this gene cause SLOS, we sequenced cDNA clones from SLOS patients. In three unrelated patients we have identified four different mutant alleles. Our results demonstrate both that the cDNA that we have identified encodes the human sterol Delta7-reductase and that mutations in DHCR7 are responsible for at least some cases of SLOS.

Alleles↗

PubMed1998

[Glutathione S-transferase M1, T1 genotypes and the risk of esophageal cancer: a case-control study].

To examine the association between genetic polymorphisms of glutathione S-transferase (GST) M1 and T1 and susceptibility to esophageal cancer, a multiplex polymerase chain reaction method was used to detect the presence or absence of the GSTM1 and GSTT1 genes in genomic DNA isolated from surgically removed esophageal tissues or scraped esophageal cells from cases with cancer (n = 45), cases with severe hyperplasia (n = 45), and sex/age matched normal controls (n = 45) from a high risk area, Linxian, China. Results showed that the frequency of the GSTM1-null genotype in cancer cases (44.4%) or hyperplasia cases (44.4%) was not significantly different from that in controls (46.7%). Similarly, no statistically significant differences were observed in the frequency of GSTT1-null genotype in cancer cases (40.0%) or hyperplasia cases (37.8%) when compared with the controlled population (51.1%). However, the frequency of combined GSTM1-nonnull and GSTT1-nonnull genotypes in cases with cancer (40.0%) and cases with hyperplasia (37.8%) showed a significant increase compared to that in controls (22.2%). Persons with both GSTM1 and GSTT1 positive genotypes had 4-fold risk in developing esophageal cancer (odds ratio, OR = 4.20; 95% confidence interval, CI = 1.23-14.36) and 2.6-fold risk for hyperplasia (OR = 2.64; 95% CI = 0.84-8.30), respectively. These results suggest that combined GSTM1-nonnull and GSTT1-nonnull genotypes may act as risk factor in the development of esophageal cancer in Linxian population.

Adult↗

PubMed1998

[Chemoprotection by green tea against the formation of food-borne carcinogen 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP)-DNA adducts in rats].

OBJECTIVE: The food-borne mutagen 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP) induces colon and mammary gland tumors in rats and has been implicated in the etiology of human cancer, particularly colorectal cancer. This study was conducted to examine the potential chemopreventive effect of Chinese green tea against PhIP-DNA adduct formation in rats and its possible mechanisms. METHODS: Sprague-Dawley rats were maintained on freshly prepared aqueous extract of Chinese green tea (3%) or tap water as the sole source of drinking fluid for 10 days prior to administration with a single dose of PhIP (10 mg/kg body wt) by oral gavage. Rats were sacrificed at 20 h after PhIP treatment and PhIP-DNA adducts in the colon, heart, lung, and liver were analyzed using 32P-postlabeling technique. The activity of cytosolic glutathione S-transferases (GSTs) in the liver, lung and colon mucosa was also determined using CDNB as substrate. RESULTS: The levels of PhIP-DNA adducts in the four tissues of rats treated with PhIP alone were highest in the colon (53 +/- 9 adducts/10(8) nucleotides), followed by heart (41 +/- 14 adducts/10(8) nucleotides) and lung (22 +/- 5 adducts/10(8) nucleotides), but much lower in the liver (5 +/- 3 adducts/10(8) nucleotides). Rats pre-treated with green tea had significantly reduced levels of PhIP-DNA adducts, with the inhibition rates being 59%-80%, respectively. While the organ distribution profile of the adducts was not altered by tea treatment as compared with controls given PhIP alone. The GST activity towards CDNB in hepatic, colonic and lung cytosols appear not to be modified by drinking green tea. CONCLUSION: These results support a protective role for green tea against PhIP-initiated carcinogenesis in rats and suggest that consumption of green tea may have significant impact in chemoprevontion against human cancer presumably related to PhIP and other heterocyclie amines.

Animals↗

PubMed1998

[Direct detoxification of N-acetoxy-PhIP by tea polyphenols: a possible mechanism for chemoprevention against PhIP-DNA adduct formation in vivo].

OBJECTIVE: We have shown that green tea inhibited food-borne carcinogen 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP)-induced carcinogen-DNA adduct formation in rats, and this protective effect of tea appears not relote to the modifications of metabolic enzymes involved in PhIP metabolism. The aim of this study was to explore the direct reaction of tea and tea polyphenols with N-acetoxy-PhIP, an ultimate carcinogen of PhIP formed via metabolic activation. METHODS: DNA binding assays were conducted to examine the effect of aqueous extract of tea and tea polyphenols on the reaction of [3H]N-acetoxy-PhIP with DNA. The reaction mixtures were analyzed by HPLC for the possible product (s) formed by the reaction of [3H]N-acetoxy-PhIP with tea polyphenols. RESULTS: It was found that agueous extract of tea and tea polyphenols strongly inhibited covalent binding of [3H]N-acetoxy-PhIP to DNA, and the inhibition was concentration-dependent with respect to inhibitors. HPLC analyses of reaction mixture containing [3H]N-acetoxy-PhIP and tea polyphenols revealed the production of the parent amine, PhIP, indicating a redox mechanism. CONCLUSION: In view of the presence of tea polyphenols in rat and human plasma after ingestion of tea, these results suggest that direct reduction of ultimate carcinogen N-acetoxy-PhIP by tea polyphenols is likely to be involved in the mechanism of chemoprevention of tea against PhIP-DNA adduct formation in vivo.

Animals↗

PubMed1998

[Relationship between tumor cell proliferating activity and biological behavior, prognosis in laryngeal carcinoma].

Using PC 10, an antibody to proliferating cell nuclear antigen (PCNA) and a standard immunohistochemical staining the authors examined 11 cases of simple hyperplasia of epithelium (SHE), 32 cases of atypical hyperplasia of epithelium (AHE) and 42 cases of laryngeal squamous cell carcinoma (LSCC) for expression of PCNA, a protein associated with DNA polymerase dalta and DNA replication, a marker for tumor cell proliferation. The results revealed that PCNA indices in SHE, AHE and LSCC were 9.5%, 27.33% and 68.05%, respectively. The PCNA indices were 63.68%, 69.57%, 71.18% in the well, moderately and poorly differentiated LSCC, respectively, there were significant differences. The PCNA indices were 63.88%, 70.82%, 66.20% and 69.04%, respectively in stages I, II, III, and IV of LSCC; no significance was found. There was a strong negative correlation betwee survival time and the tumor cell proliferative activity (r = 0.6243). PCNA might provide a useful tool for studying cell proliferation in situ under normal and pathological condition.

Adult↗

PubMed1998

[Chemoprevention of 2-amino-1-methyl-6-phenylimidazo[4,5-b] pyridine-induced carcinogen-DNA adducts by Chinese cabbage in rats].

OBJECTIVES: To examine the preventive effect of Chinese cabbage (Brassica chinensis) against colon carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-induced PhIP-DNA adduct formation in rats and its possible mechanism. METHODS: Sprague-Dawley rats were maintained for 10 days on lab chow or chow containing 20% (w/w) freeze-dried cabbage powder prior to administration of a single dose of PhIP (10 mg/kg) by oral gavage. Rats were sacrificed at 20 h after PhIP treatment and PhIP-DNA adducts in the colon, heart, lung, and liver were analyzed using 32P-postlabeling technique. Levels of hepatic cytochrome P450 (CYP) 1A1 and 1A2, as indicated by 7-ethoxyresorufin O-deethylase and 7-methoxyresorufin O-demethylase activity, and cytosolic glutathione S-transferases (GST) towards CDNB in the liver, lung and colon mucosa were measured. RESULTS: Rats pre-treated with Chinese cabbage and given a single dose of PhIP had reduced levels of PhIP-DNA adducts in the colon, heart, lung and liver, with an inhibition rate of 82.3, 60.6, 48.4 and 48.9%, respectively (P < 0.01). Enzyme assays revealed that both CYP1A1 and 1A2 were induced by cabbage, but the induction was preferential for CYP1A1 over 1A2 (80.6% vs 50.2%). GST activity towards CDNB in the liver and lung, but not colon, was also significantly induced by the cabbage. CONCLUSION: The results indicate a preventive effect of Chinese cabbage against PhIP-initiated carcinogenesis in rats and the mechanism is likely to involve induction of detoxification enzymes.

Animals↗

PubMed1998

[Genetic polymorphisms of cytochrome P450 2E1 and glutathione S-transferase P1 and susceptibility to esophageal cancer].

OBJECTIVES: To study the association between genetic polymorphisms of cytochrome P4502E1 (CYP2E1) and/or glutathione S-transferase P1 (GSTP1) and susceptibility to esophageal cancer. METHODS: Genotyping of CYP2E1 and GSTP1 was performed using PCR-based RFLP analysis on DNA isolated from surgically removed esophageal tissues or scraped esophageal epithelium from cancer cases (n = 45), severe epithelial hyperplasia cases (n = 45), and normal controls (n = 45). RESULTS: The variant genotypes (c1/c2 and c2/c2) detected by RsaI digestion was found in 17% of epithelial hyperplasia cases, 20.0% of esophageal cancer cases and 55.6% of controls, with the differences being statistically significant (P < 0.001). Subjects carrying wild-type genotype of CYP2E1 had more than 5-fold risk for developing severe epithelial hyperplasia (odds ratio, OR = 5.78; 95% confidence interval, CI = 2.2-15.2) and esophageal cancer (OR = 5.00; 95% CI = 2.0-12.8). No association with the risk of severe epithelial hyperplasia and esophageal cancer was observed for the DraI polymorphism of CYP2E1 or for the Awl26I polymorphism of GSTP1. CONCLUSION: CYP2E1 is a genetic susceptibility factor involved in the early events for esophageal carcinogenesis.

Adult↗

PubMed1998

Quantitative anatomy of the transverse foramen and pedicle of the axis.

Forty dry C2 cervical vertebrae were obtained to evaluate quantitatively the anatomy of the C2 transverse foramen and pedicle. Computed tomography (CT) scans and plain radiographs were also obtained of 20 specimens to evaluate the internal structure of the transverse foramen and pedicle. The results of the measurements showed that differences between male and female specimens were found to be significant for four of seven linear parameters and for one of the two angular parameters. With regard to the sides, differences were found to be significant for two of the seven linear parameters and both of the angular parameters between right and left measurements. The variation of the foramen size between sexes was more significant than that between sides, and a remarkable variation between sides and between sexes was found in the transverse foramen horizontal angle and the pedicle width. The inferior pedicle width was approximately 3 mm less than the superior pedicle width. CT scans revealed that the lateral wall of the pedicle is very thin compared with the medial wall. Considering the greater variation of the C2 foramen orientation, smaller inferior pedicle dimension, and thinner lateral pedicle wall, a screw placement as close as possible to the mediosuperior cortex is recommended to avoid violation of the transverse foramen if transpedicular screw fixation in C2 is intended.

Adult↗

PubMed1997

Use of low-dose oral contraceptives and stroke in young women.

BACKGROUND: Low-dose oral contraceptives are widely used, but there are limited data on the cerebrovascular risks associated with these medications. OBJECTIVE: To determine whether use of low-dose oral contraceptives influences the risk for stroke. DESIGN: Population-based case-control study. SETTING: Women 18-44 years of age who resided in western Washington State between 1991 and 1995. PARTICIPANTS: Patients with ischemic stroke (n = 60), hemorrhagic stroke (n = 102), and other types of stroke (n = 11) and controls identified through random-digit dialing (n = 485). MEASUREMENTS: Details about oral contraceptive use and other risk factors for stroke were obtained through in-person interviews. RESULTS: The estimated incidences of hemorrhagic stroke and ischemic stroke were 6.4 and 4.3 per 100,000 women-years, respectively. Compared with women who had never used oral contraceptives (after adjustment for risk factors for stroke), current users of low-dose oral contraceptives had estimated odds ratios of 0.93 (95% CI, 0.37 to 2.31) for hemorrhagic stroke and 0.89 (CI, 0.27 to 2.94) for ischemic stroke. Compared with past users of oral contraceptives, current users had odds ratios of 1.41 (CI, 0.67 to 2.96) for hemorrhagic stroke and 1.37 (CI, 0.49 to 3.81) for ischemic stroke. For past users compared with never users, the odds ratios were 0.59 (CI, 0.30 to 1.18) for hemorrhagic stroke and 0.57 (CI, 0.25 to 1.32) for ischemic stroke. The odds ratio for hemorrhagic stroke in current users of low-dose oral contraceptives containing norgestrel or levonorgestrel was elevated (3.23 [CI, 1.24 to 8.41]). Among patients with hemorrhagic stroke, the odds ratio for aneurysmal bleeding associated with current use of low-dose oral contraceptives containing norgestrel or levonorgestrel was 4.46 (CI, 1.58 to 12.53). CONCLUSION: The overall risk for stroke and type of stroke was not increased among current users of low-dose oral contraceptives in the study population. Larger studies are needed to clarify both the relation of risk for stroke to past use of oral contraceptives and the possible association between current use of norgestrel-containing oral contraceptives and hemorrhagic stroke.

Adolescent↗

PubMed1997

beta2-adrenergic receptor desensitization, internalization, and phosphorylation in response to full and partial agonists.

Previous studies indicated that partial agonists cause less desensitization of the beta2-adrenergic receptor (betaAR) than full agonists; however, the molecular basis for this in intact cells has not been investigated. In the present work, we have determined the rates of desensitization, internalization, and phosphorylation caused by a series of betaAR agonists displaying a 95-fold range of coupling efficiencies. These studies were performed with HEK-293 cells overexpressing the betaAR with hemagglutinin and 6-histidine epitopes introduced into the N and C termini, respectively. This modified betaAR behaved identically to the wild type receptor with regard to agonist Kd, coupling efficiency, and desensitization. The coupling efficiencies for betaAR agonist activation of adenylyl cyclase relative to epinephrine (100%) were 42% for fenoterol, 4.9% for albuterol, 2.5% for dobutamine, and 1.1% for ephedrine. At concentrations of these agonists yielding >90% receptor occupancy, the rate and extent (0-30 min) of agonist-induced desensitization of betaAR activation of adenylyl cyclase followed the same order as coupling efficiency, i.e. epinephrine >/= fenoterol > albuterol > dobutamine > ephedrine. The rate of internalization of the betaAR with respect to these agonists also followed the same order as the desensitization and exhibited a slight lag. Like internalization and desensitization, betaAR phosphorylation exhibited a dependence on agonist strength. The two strongest agonists, epinephrine and fenoterol, provoked 11-13-fold increases in the level of betaAR phosphorylation after just 1 min, whereas the weak agonists dobutamine and ephedrine caused only 3-4-fold increases, similar to levels induced by cAMP-dependent protein kinase activation with forskolin. With longer treatment times, the level of betaAR phosphorylation declined with strong agonists, but it progressively increased with the weaker partial agonists, such that after 30 min the -fold elevation with epinephrine (6.2 +/- 0.82) was not appreciably different from ephedrine (5.0 +/- 0.96) and significantly less than that caused by albuterol (10.4 +/- 1.7). In summary, our results demonstrate an excellent proportionality between the agonist strength and agonist-induced desensitization, internalization, and the rapid initial phase of phosphorylation. The data support the hypothesis that increasing agonist-coupling efficiency primarily affects desensitization by increasing the rate of betaARK phosphorylation of the betaAR.

Adenylyl Cyclases↗

PubMed1997

Duration of estrogen replacement therapy in relation to the risk of incident myocardial infarction in postmenopausal women.

BACKGROUND: There is little information about whether an increasing duration of estrogen replacement therapy is associated with a declining risk for myocardial infarction in postmenopausal women. OBJECTIVE: To conduct a population-based, case-control study among enrollees of the Group Health Cooperative (GHC) of Puget Sound, Seattle, Wash. SUBJECTS AND METHODS: Case subjects were all post-menopausal women who were enrolled in the GHC with an incident fatal or nonfatal myocardial infarction from July 1986 through December 1993. Control subjects were a stratified random sample of postmenopausal women who were enrolled in the GHC without myocardial infarction and matched to case subjects by age and calendar year. We reviewed the medical records of the 850 case subjects and 1974 control subjects and conducted telephone interviews with consenting survivors. Use of estrogen or estrogen and progestin was assessed using GHC's computerized pharmacy database. RESULTS: Among women who were currently using estrogen, a longer duration of use was inversely associated with a risk for myocardial infarction after adjustment for age, year of identification, diabetes mellitus, angina, and smoking. For categories of increasing duration of estrogen use (never, > 0-< 1.8 years, 1.8-< 4.2 years, 4.2-< 8.2 years, and > or = 8.2 years), the odds ratios for myocardial infarction were 1.00 (reference), 0.91, 0.70, 0.65, and 0.55 (for trend among the current users, P = .05). Among women who had used estrogen in the past, there was no evidence of decreasing risk with increasing duration of estrogen use. CONCLUSION: In this study, a long duration of hormone replacement therapy among women currently using estrogen was associated with a reduced risk for first myocardial infarction.

Adult↗

PubMed1997

The nucleotide sequence of Saccharomyces cerevisiae chromosome V.

Here we report the sequence of 569,202 base pairs of Saccharomyces cerevisiae chromosome V. Analysis of the sequence revealed a centromere, two telomeres and 271 open reading frames (ORFs) plus 13 tRNAs and four small nuclear RNAs. There are two Tyl transposable elements, each of which contains an ORF (included in the count of 271). Of the ORFs, 78 (29%) are new, 81 (30%) have potential homologues in the public databases, and 112 (41%) are previously characterized yeast genes.

Base Sequence↗

PubMed1997

Cyclosporine or cyclosporine plus methylprednisolone for prophylaxis of graft-versus-host disease: a prospective, randomized trial.

Patients with a lymphohematopoietic malignancy considered to be at high risk for posttransplant relapse were enrolled in a study to compare the use of cyclosporine (CSP) as a single agent with a combination of methylprednisolone (MP) and CSP for graft-versus-host disease (GVHD) prophylaxis after marrow transplantation from an HLA-identical sibling donor. Sixty patients were randomized to receive CSP only and 62 were randomized to receive CSP plus MP. Daily CSP was started on day -1 (5 mg/kg/d intravenously) and administered at gradually reduced doses until day 180. MP was started on day 7 at 0.5 mg/kg/d, increased to 1.0 mg/kg/d on day 15, started on a taper schedule on day 29, and discontinued on day 72. All 104 evaluable patients (surviving > or =28 days) had sustained engraftment. The incidence rates of grades II-IV acute GVHD were 73% and 60% for patients receiving CSP and CSP plus MP, respectively (P = .01). No difference was seen for grades III-IV GVHD. However, chronic GVHD occurred somewhat more frequently in patients receiving CSP plus MP (44%) than in patients receiving only CSP (21%; P = .02). The incidence of de novo chronic GVHD was marginally higher in patients receiving CSP plus MP (P = .08). No significant differences in the risk of infections were observed. There was a suggestion that the risk of relapse was lower in patients receiving CSP plus MP (P = .10) and, although the overall survival in the two groups was not different (P = .44), there was a slight advantage in favor of CSP plus MP-treated patients for relapse-free survival (P = .07). These results suggest that prophylactic MP, when combined with CSP, has only limited efficacy in acute GVHD prevention and may increase the probability of chronic GVHD.

Adolescent↗

PubMed1997

Cloning of human 25-hydroxyvitamin D-1 alpha-hydroxylase and mutations causing vitamin D-dependent rickets type 1.

The secosteroid hormone, 1,25-dihydroxyvitamin D [1,25(OH)2D], plays a crucial role in normal bone growth, calcium metabolism, and tissue differentiation. The key step in the biosynthesis of 1,25(OH)2D is its 1 alpha-hydroxylation from 25-hydroxyvitamin D (25-OHD) in the kidney. Because its expression in the kidney is very low, we cloned and sequenced cDNA for 25-OHD-1 alpha-hydroxylase (P450c1 alpha) from human keratinocytes, in which 1 alpha-hydroxylase activity and mRNA expression can be induced to be much greater. P450c1 alpha mRNA was expressed at much lower levels in human kidney, brain, and testis. Mammalian cells transfected with the cloned P450c1 alpha cDNA exhibit robust 1 alpha-hydroxylase activity. The identity of the 1,25(OH)2D3 product synthesized in transfected cells was confirmed by HPLC and gas chromatography-mass spectrometry. The gene encoding P450c1 alpha was localized to chromosome 12, where the 1 alpha-hydroxylase deficiency syndrome, vitamin D-dependent rickets type 1 (VDDR-1), has been localized. Primary cultures of human adult and neonatal keratinocytes exhibit abundant 1 alpha-hydroxylase activity, whereas those from a patient with VDDR-1 lacked detectable activity. Keratinocyte P450c1 alpha cDNA from the patient with VDDR-1 contained deletion/frameshift mutations either at codon 211 or at codon 231, indicating that the patient was a compound heterozygote for two null mutations. These findings establish the molecular genetic basis of VDDR-1, establish a novel means for its study in keratinocytes, and provide the sequence of the key enzyme in the biological activation of vitamin D.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗

PubMed1997

Distributions of the cardiac plexuses and ganglia in the Beijing duck.

Distributions of the cardiac plexuses and cardiac ganglia were gross-anatomically and histologically studied in eight Beijing ducks. The cardiac plexuses consisted of two components, the cardiac nerve arising from the sympathetic trunk and the cranial and caudal cardiac nerves arising from the vagus. Branches of these nerves made the cardiac plexuses on the epicardium. The cardiac plexuses could be divided into the six plexuses, that is, the right and left coronary plexuses, pericardiac transverse sinus plexus, caudal cardiac plexus, and right and left superior cardiac plexuses. There were small ganglia in the caudal cardiac plexus and the right and left coronary plexuses. These ganglia containing multipolar neurons were found like a linking chain in a single nerve.

Animals↗

PubMed1997

[Differentiation-inducing effect of stepholidine and retinoic acid on human head and neck carcinoma].

To observe the differentiation-inducing effect of Stepholidine (ST) and Retinoic Acid (RA) on laryngeal and nasopharyngeal carcinoma, the expression of oncogene (C-myc, bcl-2) protein and tumor suppressor gene (p53) was done by using flow cytometry and ABC immunohistochemical methods combined with image analysis technique. The results indicated that after treated with ST and RA, the cells became well-differentiated, the cell growth was suppressed, contact suppress was partially recovered, colony forming was decreased, protooncogenes (C-myc bcl-2) protein was decreased, tumor suppressor gene (p53) protein was increased. No significant difference was observed between the cells treated with ST and TA. We believed that the Chinese medicine-Stephania might be expected to become a new prospective differentiation inducer in carcinoma of head and neck.

Berberine↗