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Biomedical subjects

J L Liu

Publications and source records attributed to J L Liu.

At least 109 records · Page 6Linked to original sources
PubMed1995

[Coagulase type and antimicrobial susceptibility of Staphylococcus aureus isolated from various areas in Taiwan].

A total of 129 strains of Staphylococcus aureus, isolated from clinical specimens in Taiwan between February 1992 and December 1993, were subjected to coagulase typing and susceptibility testing to 21 kinds of antimicrobial agents using Pasco MIC Gram-positive panels. In the determination of minimum inhibition concentration (MIC), there were 94 strains (72.9%) resistant to penicillin and ampicillin, 54 strains (41.9%) resistant to tetracycline and erythromycin, and 21 strains (16.3%) resistant to oxacillin (oxacillin-resistant S. aureus; ORSA), but none of them was resistant to vancomycin or nitrofurantoin. As the susceptibility of the isolates from four different geographic districts was compared, no statistical difference was found except that the resistance rate to penicillin and ampicillin was higher in southern Taiwan, and resistance rate to rifampin and gentamicin was higher in central Taiwan. The ORSA strains were all resistant to penicillin, ampicillin, tetracycline; 95.2% of the strains were resistant to gentamicin, tobramycin and erythromycin. The resistance rates to drugs tested for ORSA strains were statistically higher than those for OSSA strains except vancomycin, nitrofurantoin, trimethoprim/sulfamethoxazole and ampicillin/sulbactam. In the coagulase typing of 127 strains, Type IV, III and VII were most frequently encountered. Among the coagulase types, Type IV was mostly encountered in the North, the South and the East of Taiwan; Type III was mostly encountered in central Taiwan. Among the ORSA strains, coagulase Type III was most predominant (85%). In conclusion, analysis of an antibiogram is easy to perform and the results can provide clinicians not only with correct guides for patient treatment but also with a useful tool for epidemiological studies. However, if antibiogram and coagulase typing are carried out simultaneously, results will be more reliable in epidemiological studies, including nosocomial infection survey.

Coagulase↗
PubMed1994

Sequence analysis of the 5'-flanking promoter region of the human somatostatin receptor 5.

We have determined the sequence of 2.2 kb of 5' flanking promoter region of the human somatostatin receptor 5 (hsstr5) gene. A number of widely distributed promoter elements were identified including AP1, AP2, AP3, E2A, GCF, and SP1 consensus sequences. hsstr5/CAT gene fusions showed that the 0.9 kb of DNA immediately upstream of the ATG functions as a promoter in rat pituitary GH3 but not in CHO ovary cells. Insertion of this hsstr5 fragment in the anti-sense orientation led to a four fold reduction in CAT activity. Dibutyryl cAMP produced a three fold induction of CAT activity whereas estradiol and retinoic acid had no significant effect. These results indicate that we have identified a DNA fragment at the 5' end of the hsstr5 gene which contains both tissue-specific and regulated elements. The absence of CRE consensus sequence suggests that the cAMP effect is mediated by the multiple AP1 and AP2 sites.

Animals↗
PubMed1994

Glucocorticoids activate somatostatin gene transcription through co-operative interaction with the cyclic AMP signalling pathway.

The somatostatin (SS) gene is transcriptionally regulated via the cyclic AMP (cAMP) response element (CRE), located in the proximal promoter (-41 to -48 bp). We have previously reported that glucocorticoids induce dose-dependent cell-specific alterations in the steady-state SS mRNA level. Here we have investigated direct transcriptional control of the SS gene by glucocorticoids. We have examined transcriptional interaction between glucocorticoids and the cAMP signalling pathway and mapped the 5' upstream regulatory region of the SS gene involved in glucocorticoid transactivation. Transcriptional regulation was determined by analysis of chloramphenicol acetyltransferase (CAT) activity in PC12 rat pheochromocytoma cells and A126-1B2 (protein kinase A-deficient mutant PC12) cells, by acute transfection of 5' flanking SS DNA (- 750, -250 and -71 bp) ligated to the reporter (CAT) gene. Dexamethasone (DEX) induced a dose-dependent 2.2-fold stimulation of SS gene transcription in PC12 cells, but not in A126-1B2 cells. Other steroid and thyroid hormones tested, and retinoic acid, were ineffective, while cAMP and forskolin stimulated gene transcription 4-5-fold in PC12 cells but not in A126-1B2 cells. DEX exerted an additive effect on cAMP-induced gene transcription. Deletion of the promoter from -750 to -71 bp (but not from -750 to -250 bp) abolished all stimulatory effects of DEX without affecting cAMP responsiveness. Mutation of the CRE abrogated both DEX- and cAMP-dependent gene enhancement. Gel electrophoretic mobility shift assays confirmed that the -250 to -71 bp region of the SS promoter (but not the -71 to +55 bp domain) binds specifically to a glucocorticoid response element-sensitive nuclear protein(s) from PC12 cells, suggesting a putative glucocorticoid receptor interaction with SS promoter DNA. We conclude that glucocorticoids regulate SS gene transcription positively. Glucocorticoid-induced transactivation shows dependence on protein kinase. A activity, and may be mediated via protein-protein interaction between the glucocorticoid receptor and the CRE binding protein. DNA sequences upstream from the CRE between -250 and -71 bp in the SS promoter appear to be the target of glucocorticoid action.

Animals↗
PubMed1994

Cysteamine-induced reduction in tissue somatostatin immunoreactivity is associated with alterations in somatostatin mRNA.

The drug cysteamine (CHS) induces a profound loss of somatostatin-14 (SS-14) biological and immunological (SS-14 LI) activity from somatostatin cells in vivo and in vitro. The present study was designed to determine (i) whether CHS induced loss of somatostatin is accompanied by secondary increases in SS-mRNA perhaps through loss of autoinhibition of somatostatin cells; (ii) whether CHS exerts additional direct effects on SS gene regulation. CHS was administered to rats in vivo or applied in vitro to primary cultures of rat islet cells, rat islet somatostatin-producing tumor cells (1027 B2), and endogenous or in vitro synthesized SS-mRNA. In vivo administration of CHS led to 80% reduction in tissue SSLI by 4 h. These changes were accompanied by significant alterations in SS-mRNA that were both tissue-specific and time-dependent. The pattern in brain and intestine was typified by a significant 60% increase in SS-mRNA at 2 h followed by a gradual reduction to approximately 55% of control at 8 h. Stomach showed a significant 95% increase in SS-mRNA at 4 h followed by a 37% decrease by 8 h. Pancreatic SS-mRNA displayed a sustained 25-65% reduction for 8 h. Pretreatment of islet cell cultures with CHS reproduced the in vivo findings with pancreas viz. decreased SSLI (80-90% of control) accompanied by a parallel reduction in SS-mRNA (40-50% of control) sustained from 2-72 h. CHS also induced a reduction in immunoreactive insulin and insulin mRNA in cultured islet cells. As with normal islet cells, CHS treatment of 1027 B2 islet tumor cells led to a profound and sustained decrease in SSLI and SS-mRNA. These changes occurred in the absence of any alteration in intracellular cAMP levels. CHS was without effect when incubated directly with SS-mRNA isolated from 1027 B2 cells or with in vitro synthesized SS-mRNA. We conclude that in addition to its effect on SSLI, CHS also induces time- and tissue-dependent alterations in SS-mRNA. The mechanism of CHS action on SS-mRNA is complex and may involve both an indirect effect secondary to loss of somatostatin autoinhibition (to account for SS-mRNA increases) and/or a direct inhibition of SS gene expression (to explain SS-mRNA reduction). The precise site of direct CHS action on SS gene regulation remains to be defined.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Characterization and localization of Schistosoma mansoni calreticulin Sm58.

Recombinant Schistosoma mansoni calreticulin (SmCaR) was expressed in Escherichia coli, using the glutathione S-transferase fusion protein, and its Ca(2+)-binding capacity was determined. Results obtained by a 45Ca2+ overlay technique showed that Ca(2+)-binding site(s) were present in the recombinant CaR indicating that proper folding of the protein was obtained using this system. An antiserum raised against the recombinant SmCaR showed that the native protein (Sm58) was expressed in all stages of the life-cycle from cercariae to the adult worm and in the egg. However, SmCaR seems to be a developmentally regulated protein whose expression can be used to study the post-transformational differentiation of the schistosomulum. Localization of SmCaR demonstrated that the majority of SmCaR was expressed in the epithelia of the digestive duct and in the genital organs. These results suggest that SmCaR, by regulating the Ca2+ concentration, may play an important role during cell proliferation. Finally the presence of SmCaR in miracidia and in the genital organs suggests that the antibody response directed against this protein could interfere in egg production.

Amino Acid Sequence↗
PubMed1994

T cell receptor V alpha gene usage in human T cells stimulated with SEE and SED.

V alpha gene usage in human T cells stimulated with SEE and SED was investigated by using polymerase chain reaction with specific primers. V beta 8 T cells from normal blood donors PBMC were sorted at day 5 after stimulation with SEE and analysed for TCR-V alpha gene usage. Whole T cells stimulated with anti-CD3 MoAb or SED were also analysed and compared at different time points after stimulation. There was no biased V alpha gene usage found as a response to either of the two superantigens. These results show that V alpha gene usage of human T cells stimulated with SEE or SED is normal.

Base Sequence↗
PubMed1994

Identification of mutations in the gene for glucose-6-phosphatase, the enzyme deficient in glycogen storage disease type 1a.

Glycogen storage disease (GSD) type 1a is an autosomal recessive inborn error of metabolism caused by a deficiency in microsomal glucose-6-phosphatase (G6Pase), the key enzyme in glucose homeostasis. Southern blot hybridization analysis using a panel of human-hamster hybrids showed that human G6Pase is a single-copy gene located on chromosome 17. To correlate specific defects with clinical manifestations of this disorder, we identified mutations in the G6Pase gene of GSD type 1a patients. In the G6Pase gene of a compound heterozygous patient (LLP), two mutations in exon 2 of one allele and exon 5 of the other allele were identified. The exon 2 mutation converts an arginine at codon 83 to a cysteine (R83C). This mutation, previously identified by us in another GSD type 1a patient, was shown to have no detectable phosphohydrolase activity. The exon 5 mutation in the G6Pase gene of LLP converts a glutamine codon at 347 to a stop (Q347SP). This Q347SP mutation was also detected in all exon 5 subclones (five for each patient) of two homozygous patients, KB and CB, siblings of the same parents. The predicted Q347SP mutant G6Pase is a truncated protein of 346 amino acids, 11 amino acids shorter than the wild type G6Pase of 357 residues. Site-directed mutagenesis and transient expression assays demonstrated that G6Pase-Q347SP was devoid of G6Pase activity. G6Pase is an endoplasmic reticulum (ER) membrane-associated protein containing an ER retention signal, two lysines (KK), located at residues 354 and 355. We showed that the G6Pase-K355SP mutant containing a lysine-355 to stop codon mutation is enzymatically active. Our data demonstrate that the ER protein retention signal in human G6Pase is not essential for activity. However, residues 347-354 may be required for optimal G6Pase catalysis.

Base Sequence↗
PubMed1994

Glucocorticoids regulate somatostatin peptide and steady state messenger ribonucleic acid levels in normal rat tissues and in a somatostatin-producing islet tumor cell line (1027B2).

Although a number of previous studies have suggested that glucocorticoids influence somatostatin (SS) function at the peptide level in some tissues and SS mRNA levels in thyroid tumor cells, there has been no systematic investigation of the effects of glucocorticoids on SS gene expression in normal tissues. In the present study, we have examined the effect of dexamethasone (DEX) on SS secretion and gene expression in rat tissues using as models DEX-treated rats in vivo, primary cultures of rat islet and cerebrocortical cells, and a SS-producing rat islet tumor cell line (1027B2). In vivo DEX administration (0.5 mg/kg) for 3 or 8 days augmented SS-mRNA 2- to 3-fold in peripheral tissues (stomach, pancreas, and jejunum), but reduced it by 50-60% in brain. The DEX effect was time dependent, being more pronounced after 8 days than after 3 days of treatment. In all tissues, SS mRNA levels returned to control values 2 weeks after cessation of DEX. Changes in tissue content of immunoreactive SS paralleled those in SS mRNA. In cultured rat islet cells, 18-h incubation with DEX induced dose-dependent biphasic effects on immunoreactive SS and SS mRNA; low doses (10(-10) M) were stimulatory, and high doses (10(-8)-10(-5) M) were inhibitory. Insulin secretion displayed dose-dependent stimulation by DEX, whereas glucagon release was inhibited. The effect of DEX on SS mRNA levels in primary cultures of brain cells was solely inhibitory. 1027B2 cells responded to DEX with augmented immunoreactive SS secretion and SS mRNA levels at low concentration (10(-10) M), followed by a dose-dependent inhibition of both parameters with increasing DEX concentrations. We conclude that glucocorticoids exert significant effects on SS peptide production and steady state mRNA levels in normal SS-producing tissues in vivo, in vitro, and in cultured 1027B2 cells. The glucocorticoid effect is time and dose dependent, tissue specific, and at least in part due to a direct action of the steroid hormone on SS-producing cells.

Adenoma, Islet Cell↗
PubMed1994

Immunolocalization of the lactotransferrin receptor on the human T lymphoblastic cell line Jurkat.

Monoclonal antibodies have been raised against the soluble lactotransferrin binding protein purified from the cell culture supernatant of Jurkat cell line, a human T-lymphoblastic cell. All monoclonal antibodies were able to specifically bind to the membrane of Jurkat cells. One of the monoclonal antibodies, DP5B3G10, recognized both the soluble lactotransferrin-binding protein and the membrane lymphocyte lactotransferrin receptor after SDS-PAGE in presence of 2-mercaptoethanol and electrotransfer on nitrocellulose. The monoclonal antibody DP5B3G10 inhibited the binding of lactotransferrin to Jurkat cells and human peripheral activated lymphocytes. In addition, lactotransferrin inhibited the binding of the monoclonal antibody to the cell surface. These results suggest that the 95 kDa lactotransferrin-binding protein isolated from the cell culture medium corresponds to the soluble form of the 105 kDa lymphocyte lactotransferrin receptor. Corresponding proteins of 105 kDa molecular mass were identified in Jurkat and CEM T-cells and Raji B-cells. Finally, the monoclonal antibody DP5B3G10 was used to immunolocalize the lactotransferrin receptor on the Jurkat cells. Using fluorescence and electron microscopy, the receptor was localized both inside and at the cell surface. The cell membrane receptor was associated into clusters. After permeabilization of the plasma membrane, the staining was positive in the peri-membrane area. The region near the nucleus was devoid of receptor.

Antibodies, Monoclonal↗
PubMed1994

A ten-year observation on experimental infection of periodic Brugia malayi in man.

This paper reports the results of 10 years of observations on the clinical manifestations, pathology and immunity to filariasis and aetiological biology of filariae in three volunteers (first author and his family members) who were inoculated experimentally with infective larvae of periodic Brugia malayi in 1981. The changes in clinical symptoms and signs were recorded systematically. Microfilariae were first detected at 41 and 46 weeks after inoculation in two subjects and remained detectable in small numbers until 8-8.5 years after infection. The microfilarial density fluctuated at 1-2 mf 120 microliters-1. Thereafter no microfilariae were detected in 12 blood sample examinations, suggesting that the adult reproductive period of periodic B. malayi could last up to 8-9 years in the human body. Eosinophilia occurred mainly before and at the initial stage of microfilaraemia. An increase in the lymphocytes was observed to some extent at 2-156 weeks after infection. Biopsy at the inoculation site 6 weeks after inoculation showed infiltration of the lymph node by inflammatory cells, mainly eosinocytes, lymphocytes and monocytes. Lymphangiectasis and lymphostasis were observed in both limbs and pelvic regions by lymphangiogram taken 11 weeks after inoculation. Antibodies against B. malayi first appeared at 2-5 weeks after infection, peaked at 12-56 weeks and thereafter declined gradually. Subjects A and C became antibody free but subject B remained positive to antibody against B. malayi 10 years after infection. E-rosette forming lymphocytes became lower than normal at 11 weeks and recovered to normal within 10 years after infection.

Adolescent↗
PubMed1994

[Effects of lowering perilymph calcium concentration on various cochlear potentials].

In the present experiment, changes in compound action potentials of auditory nerve (CAP), cochlear microphonics (CM) and endocochlear potentials were observed when the calcium concentration of perilymph was reduced by means of perilymph perfusion, with the aim of analyzing how calcium was involved. Perfusion with Ca(2+)-free artificial perilymph reversibly suppressed both CAP and CM amplitudes, but did not alter the basic nonlinear properties of CAP I/O curve. Furthermore, the perfusion did not alter the EP and negative EP (n-EP) induced by anoxia but eliminated the fast change of EP with respect to turning on and off of intense sound. The mechanisms underlying the effects of calcium are discussed.

Action Potentials↗
PubMed1993

Characterization of two allelic variants of a human pregnancy-specific glycoprotein gene.

The pregnancy-specific glycoproteins (PSGs) of the human placenta are a group of proteins that together with the carcinoembryonic antigens comprise a subfamily within the immunoglobulin superfamily. To study the control of PSG expression, we isolated and characterized PSG genes and identified cis-acting DNA elements in the 5'-flanking gene regions essential for PSG expression. Two overlapping PSG cosmid clones, which contain two allelic variants of a PSG gene (PSG12 and PSG12 psi), were isolated from an unamplified library made from a single individual. Cosmid 1 contains exons 1 (5'/L) and 2 (L/N) of the PSG12 gene located downstream of a previously identified PSG1-I gene. Cosmid 6 contains a portion of the PSG1-I gene lacking exons 1 and 2 upstream of a complete PSG12 psi transcription unit. Sequence comparison indicates that exons 5'/L and L/N in PSG12 and PSG12 psi are 99% identical, except that the L/N exon in the PSG12 psi gene contains a stop codon. Both PSG12 and PSG12 psi transcripts were detected in the human placenta, indicating that both genes are actively transcribed. However, the PSG12 psi gene may represent an allelic pseudogene variant of the PSG12 gene, because all identified PSGs contain a functional N-domain. Primer extension analysis showed that the PSG12 gene starts at a cluster of sites located at -106 to -104 base pairs with respect to the translation start site. In transient transfection assays using a chloramphenicol acetyltransferase reporter gene, we demonstrated that the -835 to -34 DNA region upstream of the translation start site of PSG12 or PSG12 psi contained both positive and negative elements that control PSG expression. Deletion analysis showed that nucleotides -172 to -34 in the PSG12 gene could function as a promoter. Gel retardation analysis showed that protein factors in human placental cell extract formed four complexes (I, II, IIa, and III) with the PSG12(-172/-34) DNA. Site-directed mutagenesis that prevents protein factor binding to the PSG12 promoter resulted in a marked reduction in transcription activation, locating the core enhancers at nucleotides -148 to -141 and -60 to -55. Mutagenesis studies also showed that the ACAGC repeats at nucleotides -84 to -68 in the PSG12 5'-flanking are essential for expression of the PSG12 gene in human placental cells.

Alleles↗
PubMed1993

Molecular structure of a Toxoplasma gondii dense granule antigen (GRA 5) associated with the parasitophorous vacuole membrane.

The P21 antigen of Toxoplasma gondii, defined by the monoclonal antibody TG17-113, has been described as a dense granule component, secreted in the parasitophorous vacuole during host cell invasion. The present work reports the cloning of the gene encoding the P21 antigen, for which we propose the name GRA 5. A cDNA library was screened with a rat antiserum raised against an HPLC fraction enriched in the P21 antigen. cDNA clones encoding GRA 5 were selected by antibody selection on the recombinant proteins. All these clones were incomplete at the 5' end. The 5' fragment of the longest cDNA clone isolated by this first screening was used as a probe in secondary screenings of cDNA and genomic DNA libraries. A genomic fragment containing the P21 gene and nearly full-length cDNAs have been isolated and sequenced. The gene encoding GRA 5 is 834 bp long and does not contain any intron. The deduced amino acid sequence of an open reading frame encoding 133 amino acids perfectly matched that of 5 peptides microsequenced from the native antigen. A N-terminal hydrophobic region was found to possess the characteristics of a signal peptide of 25 amino acids. A second hydrophobic domain, bordered by two hydrophilic regions strongly suggests a transmembrane region. This molecular structure is supported by ultrastructural studies showing the association of the P21 antigen with the parasitophorous vacuole membrane.

Amino Acid Sequence↗
PubMed1993

[Weight-for-length index in evaluation of children's body weight status: a simple and accurate method].

This study examines the weight-for-length index (WLI)--weight/height/the WLI constant, where the WLI constant is the ratio between the 50th percentile weight and height for the age and sex--for its appropriateness in estimating the status of body weight among school children. The WLI constant has been calculated for practical use and rapid calculation. Using the known percentile data in the Taiwan area, this report shows evidence that the WLI constant has changed a little during the past 30 years. On theoretical grounds, it seems that the WLI is a valid index because it is independent of the progressing physical growth of children it Taiwan. Data were obtained for a sample of 5,214 healthy boys and 5,607 healthy girls ages 5 to 14, attending schools in Taipei, Taiwan. The WLI was found to be a satisfactory measure of relative weight as has been generally found for the body mass index (weight/height2) because it has little correlation with age (r = 0.07) and only a fair correlation with height (r = 0.26) for the whole sample of children. In an attempt to offer support for the findings, the relationship between WLI and the overweight index (actual weight/average weight for sex, age and height) were evaluated. The correlations between the WLI and the overweight index were excellent for each sex grouping (r = 0.91 for boys and 0.89 for girls). The results also suggest that the WLI appears to be a very accurate measure of obesity (sensitivity: 88.3-92.1%, specificity: 86.9-89.9%) for all the school children in this sample.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

The role of acetylcholine in the cognitive function of frontal neurons in monkeys.

To study the role of acetylcholine (ACh) in the cognitive function of frontal lobes, ACh and atropine were applied iontophoretically to the task-related neurons recorded from an area around the superior ramus of arcuate sulcus in the frontal cortex of 4 rhesus monkeys during the performance of two tasks. The spontaneous discharges and task-related responses of most of the neurons which increased their discharge rate in the delay and differentiation periods of the discrimination response go/no-go task and in the cue and delay periods of the delayed discrimination go/no-go task, were further increased during the application of ACh and suppressed during atropine. These results suggest that ACh may be involved in the excitatory process of the activity of the neurons in the above-mentioned area of frontal cortex to play an important role in the cognitive functions of attention, discrimination and short-term memory.

Acetylcholine↗
PubMed1993

[Hemodynamic actions of N-nitro-L-arginine and its effect on renal sympathetic nerve activity in anesthetized rats].

The hemodynamic actions of N-nitro-L-arginine (L-NNA), a novel NO synthesis inhibitor, and its effect on renal sympathetic nerve activity (RSNA) were examined in anesthetized rats to define the possible role of L-NNA in the regulation of blood pressure and the underlying mechanism(s). The results obtained were as follows. (1) Following intravenous bolus injection of L-NNA (15 mg/kg), MAP was changed from 9.87 +/- 0.80 to 14.67 +/- 0.53 kPa (P < 0.001), HR from 317 +/- 13 to 303 +/- 14 bpm, CI from 9.79 +/- 0.83 to 7.04 +/- 0.41 ml/min.100 g-1 (P < 0.05), and TPRI from 1.04 +/- 0.10 to 2.15 +/- 0.18 u/100 g (P < 0.001), all lasting for more than 30 min. The above-mentioned actions of L-NNA could be inhibited by prior administration of L-arginine (200 mg/kg). (2) In rats with sinoaortic denervation (SAD), i.v. L-NNA might induce an increase in HR, indicating that L-NNA-induced bradycardia was resulted from a baroreceptive activation. (3) In rats with buffer nerves intact, i.v. L-NNA failed to induce a significant change in RSNA, though an increase in MAP accompanied by bradycardia was observed. (4) With i.v. L-NNA for SAD rats, MAP, HR and RSNA were markedly increased by 55.6%, 5.1% and 34.3%, respectively. The results implied that L-NNA was able to activate sympathetic center, and L-NNA-induced change of RSNA could be masked by baroreflex. Prior administration of L-arg was capable of inhibiting the effect of L-NNA on RSNA in SAD rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Nylestriol replacement therapy in postmenopausal women. A three-year prospective study.

A three-year prospective study was carried out in 283 postmenopausal women to evaluate the effects of a long-acting estriol derivative-nylestriol. The women were randomly assigned into 3 groups: group A (136 cases, nylestriol 2 mg/2 wk), group B (97, nylestriol 1 mg/2 wk) and group C (50, placebo/2wk). LDL-C decreased and HDL-C increased after 3 months of medication (P < 0.05), but TC and TG not significantly changed in any group (P > 0.05). No changes of lipids were found in group C (P > 0.05). Serum ALP, Ca/Cr and Hpr/Cr in fasting urine decreased in 3 months in both group A and B (P < 0.05), but not in group C (P > 0.05). Forearm bone mineral content loss was restrained in groups A and B (P > 0.05), but decreased markedly in group C (P < 0.01). The Kupperman index scores decreased by about 50% after 3 months and 80% in 12 months in groups A and B. Nylestriol induced mild stimulatory effect on the uterine endometrium, and addition of 6 mg of provera daily for 7-10 days every 6 months is recommended. Nylestriol exhibited no obvious effect on the breast. This study demonstrated that nylestriol can be used as an effective and acceptable estrogen replacement therapy for postmenopausal women.

Aged↗