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H Y Lin

Publications and source records attributed to H Y Lin.

At least 91 records · Page 5Linked to original sources
PubMed1996

Potentiation by thyroxine of interferon-gamma-induced HLA-DR expression is protein kinase A- and C-dependent.

L-Thyroxine (T4) and 3,3',5-L-triiodothyronine (T3) potentiate the antiviral state induced by interferon-gamma(IFN-gamma) in homologous cells by a mechanism that is dependent upon calcium/phospholipid-dependent protein kinase (PKC). L-T4 and T3 also potentiate induction by IFN-gamma of MHC class II HLA-DR antigen expression in HeLa cells. In the present studies of HLA-DR expression, the PKC inhibitor staurosporine (0.1-1 nM) enhanced the expression of HLA-DR when the inhibitor was added simultaneously with IFN-gamma, 100 IU/ml. In the presence of IFN-gamma and 10(-7) M T4, the same concentrations of staurosporine inhibited potentiation of HLA-DR expression by thyroid hormone. A more specific PKC inhibitor, CGP41251 (0.5-5 nM), similarly enhanced HLA-DR expression in the presence of IFN-gamma but inhibited thyroid hormone potentiation of antigen expression. Both actions of CGP41251 were suppressed when cells were also treated with phorbol 12-myristate 13-acetate (PMA). A phospholipase C inhibitor, U73122 (1-1000 nM), did not alter the potentiating ability of T4, although it inhibited in a concentration-dependent manner the expression of HLA-DR induced by IFN-gamma. The potentiating effect of T4 was much more sensitive to a cyclic AMP-dependent protein kinase (PKA) inhibitor,KT5720 (1-1000nM), than was the induction of HLA-DR by IFN-gamma. The inhibitory effects of KT5720 were reversed by concurrent 8-bromo-cAMP treatment. The calmodulin antagonist W-7 (5-50 microM) did not alter IFN-gamma induction of HLA-DR in either the presence or absence of T4. HLA-DR expression in HeLa cells appears to be under PKC-associated inhibition; IFN-gamma reverses this inhibition to promote the appearance of the DR antigen. In contrast, potentiation by T4 of induction of HLA-DR by IFN-gamma requires activation of PKC. PKA is involved both in DR induction by IFN-gamma and in potentiation of the latter by T4. Thus, PKA and PKC have discrete roles in IFN-gamma-induced MHC class II antigen expression and its modulation by thyroid hormone.

Antiviral Agents↗
PubMed1996

The relationship of aging to endotoxin shock and to production of TNF-alpha.

BACKGROUND: Aged people are considered prone to gram-negative bacteremia and septic shock. This relationship was tested in murine endotoxin shock. METHODS: Balb/c mice of various ages (1.4-13.4 months) were intraperitoneally injected with lipopolysaccharide (LPS), and rates of survival were observed. The production of TNF-alpha in vivo induced by LPS was measured. RESULTS: The survival rates were the smallest in the oldest and youngest groups. Production of TNF-alpha attained a maximum at 2 h after LPS injection and was smaller in the oldest group; it had a reciprocal relationship to survival rates in each group except the youngest group. CONCLUSION: Old and young mice had smaller rates of survival and greater production of TNF-alpha following endotoxin shock induced by LPS.

Aging↗
PubMed1996

Potentiation by thyroxine of interferon-gamma-induced antiviral state requires PKA and PKC activities.

Added to HeLa cells previously exposed to recombinant human interferon (IFN)-gamma for 20 h, thyroid hormone [L-thyroxine (T4)] in physiological concentrations potentiates the antiviral action of IFN-gamma by more than 100-fold in 4 h. We examined protein kinase activities for their contributions to the mechanism of this posttranslational effect of thyroid hormone. Added concurrently with thyroid hormone, the protein kinase C (PKC) inhibitor CGP-41251 (5 nM) blocked T4 potentiation of IFN-gamma action. Coincubated with CGP-41251, phorbol 12-myristate 13-acetate (PMA) reversed the effect of the inhibitor on thyroid hormone action. U-73122 (10 nM), a phospholipase C inhibitor, also blocked hormone potentiation. KT-5720 (500 nM), a protein kinase A (PKA) inhibitor, completely inhibited the T4 effect, whereas 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) restored hormone action in the presence of KT-5720. In the absence of T4, 8-BrcAMP and PMA, added together to cells in the 4-h paradigm, fully reproduced hormone potentiation of the antiviral effect of IFN-gamma. Incubated individually with IFN-gamma-treated cells, the two agonists had no potentiating action. Thyroid hormone apparently must activate both PKA and PKC in the nongenomic pathway of IFN-gamma action to enhance antiviral activity in HeLa cells.

Animals↗
PubMed1996

Clinical significance of complements in ascitic diseases: elevated complement levels disapproving the liver disease origin.

In a two-year period, ascitic fluid concentrations of complement 3c and complement 4 were measured in 110 patients with sterile cirrhotic ascites, 31 patients with spontaneous bacterial peritonitis, 65 patients with hepatocellular carcinoma, 36 patients with peritoneal carcinomatosis and 12 patients with miscellaneous diseases (nephrotic syndrome 4, systemic lupus erythematosus 3, secondary peritonitis 2, cardiac ascites 1, eosinophilic peritonitis 1 and tuberculosis peritonitis 1) to assess the clinical utility of ascitic fluid complements. The ascitic fluid level of complements 3c or C4 was significantly higher in patients with peritoneal carcinomatosis (32.8 +/- 10.2, 13.4 +/- 7.4 mg/dL) than in patients with sterile cirrhotic ascites (9.2 +/- 5.2, 4.5 +/- 3.9 mg/dL, p < 0.001), spontaneous bacterial peritonitis (8.2 +/- 4.1, 3.8 +/- 2.4 mg/dL, p < 0.001) or hepatocellular carcinoma (12.8 +/- 8.3, 5.6 +/- 4.4 mg/dL, p < 0.001). However, it was not significantly different from the miscellaneous disease group. To verify that ascites formation is not related to liver disease origin, diagnostic sensitivity, specificity and accuracy were 83.3%, 92.7% and 90.9%, respectively, by the ascitic fluid level of complement 3c higher than the cut-off value (20 mg/dl); or 60.4%, 89.8% and 84.3%, respectively, by the ascitic fluid level of complement 4 higher than the cut-off value (10 mg/dL). A direct correlation was found between the ascitic fluid protein level and the ascitic fluid complement 3c (r = 0.70) or complement 4 (r = 0.57) level. Based on results in this study, we can conclude that measuring ascitic fluid complements is clinically useful in disapproving the liver disease origin of ascites formation. However, it is of little value in diagnosing spontaneous bacterial peritonitis or hepatocellular carcinoma.

Ascites↗
PubMed1995

Endothelin-induced endocytosis of cell surface ETA receptors. Endothelin remains intact and bound to the ETA receptor.

We demonstrate unusual features of the intracellular processing of endothelin-1 (ET-1) and its receptor ETA, the receptor subtype that mediates contraction of vascular smooth muscle cells. First, we show that in stably transfected CHO cells expressing ETA, binding of an ET-1 ligand induces rapid endocytosis of cell surface ETA. Receptor endocytosis was measured both by immunofluorescence and by radioiodinated antibodies specific for ETA. Second, we demonstrate that ET-1 remains intact for up to 2 h after endocytosis and, as judged by co-immunoprecipitation, internalized 125I-ET-1 remains bound to ETA receptors. We hypothesize that internalized ET-1, bound to ETA receptors, continues to activate a signal-transducing G protein, thus accounting for the prolonged period of contraction induced in smooth muscle cells by a single administration of ET-1.

Animals↗
PubMed1995

The soluble exoplasmic domain of the type II transforming growth factor (TGF)-beta receptor. A heterogeneously glycosylated protein with high affinity and selectivity for TGF-beta ligands.

The transforming growth factor (TGF)-beta type II receptor is a transmembrane serine/threonine kinase which is essential for all TGF-beta-induced signals. In several cell types TGF-beta 2 is as potent as TGF-beta or TGF-beta 3 in inducing cellular responses, yet TGF-beta 2 does not bind to the majority of expressed type II receptors. Here we characterized the properties of the soluble extracellular domain of the human TGF-beta type II receptor synthesized in COS-7 cells. Like the membrane-attached type II receptor, the soluble receptor contains complex N-linked oligosaccharides as well as additional sialic acid residues that cause it to migrate heterogenously upon SDS-polyacrylamide gel electrophoresis. 125I-TGF-beta 1 binds to and is chemically cross-linked to this protein. Unlabeled TGF-beta 1 inhibits the binding of 125I-TGF-beta 1 with an apparent dissociation constant (Kd) of approximately 200 pM, similar to the apparent Kd (approximately 50 pM) of the cell-surface type II receptor. TGF-beta 3 inhibits the binding of 125I-TGF-beta 1 to the soluble type II receptor with a similar dissociation constant, approximately 500 pM. In contrast, 125I-TGF-beta 2 cannot bind and be chemically cross-linked to the soluble type II receptor, nor does as much as a 125-fold excess of unlabeled TGF-beta 2 inhibit the binding of 125I-TGF-beta 1 to the soluble receptor. This is the first demonstration of the binding affinities of the type II receptor in the absence of the other cell-surface molecules known to bind TGF-beta. Expressed alone in COS-7 cells the type II receptor also cannot bind TGF-beta 2; co-expression of type III receptor enables the type II receptor to bind TGF-beta 2. Thus, the type III receptor or some other component is required for transmission of TGF-beta 2-induced signals by the type II receptor.

Animals↗
PubMed1995

GH3 pituitary tumor cells contain heteromeric type I and type II receptor complexes for transforming growth factor beta and activin-A.

Transforming growth factors beta (TGF-beta s) and activins induce and inhibins block secretion of follicle-stimulating hormone by rat GH3 pituitary tumor cells. Cheifetz et al. (Cheifetz, S., Ling, N., Guillemin, R., and Massagué, J. (1988) J. Biol. Chem. 263, 17225-17228) reported that GH3 cells express a approximately 50-kDa surface protein, termed the type IV TGF-beta receptor, that directly binds all of these peptide hormones. Here we show that GH3 cells express the previously identified type I and type II receptors for TGF-beta and activin-A. Immunoprecipitation of affinity-labeled surface binding proteins with antisera specific to known receptors demonstrated independent heteromeric complexes of TGF-beta types I and II receptors and of activin types I and II receptors. As judged by ligand-binding and cross-linking analysis, TGF-beta binding to the TGF-beta receptors is not inhibited by activin-A and activin-A binding to its receptors is not inhibited by TGF-beta. Screening of a cDNA library from GH3 cells for potential receptor serine-threonine kinases yielded the known types I and II TGF-beta and activin receptors. The presumed common intracellular signaling pathway for TGF-beta and activin in GH3 cells appears to be mediated by distinct cell-surface receptors.

Activin Receptors↗
PubMed1995

Molecular characterization of a type I serine-threonine kinase receptor for TGF-beta and activin in the rat pituitary tumor cell line GH3.

GH3 pituitary tumor cells have surface receptors for transforming growth factors-beta (TGF-beta s) and activins/inhibins. GH3 cell mRNA was screened by a novel reverse transcriptase-polymerase chain reaction technique with primers for receptor serine-threonine kinases. We isolated rat homologs of previously identified clones for type I (ALK-2 and ALK-5) and type II (ActRII, TGF-beta RII) activin and TGF-beta receptors, together with a novel clone, whose full-length version was isolated from a GH3 cell cDNA library. Named B1, it encodes a 505-amino-acid protein belonging to the family of type I receptor serine/threonine kinases. The kinase domain of B1 exhibits 90% identity to that of the TGF-beta type I receptor. B1 mRNA is expressed not only in pituitary cells but also in all other cells and tissues examined. B1 protein can be expressed on the cell surface, but cannot bind ligand unless a type II receptor is also present. When coexpressed with the type II receptors specific for TGF-beta or activin, B1 can be efficiently cross-linked to either ligand, suggesting that it can form heteromeric complexes with both type II receptor subunits.

Activin Receptors↗
PubMed1995

Extensive wound excision in the acute shock stage in patients with major burns.

In order to reduce excessive plasma loss, to alleviate the effects of devitalized tissues on the body, and to shorten the time in hospital, we attempted to perform extensive escharectomy during the shock period in extensively burned patients. Group A consisted of 21 patients, aged 9-45 years, with a mean total burn area of 63.2 +/- 18.1 per cent TBSA, and full-thickness injury involving 35.9 +/- 19.6 per cent TBSA. The first escharectomy was performed at 24.1 +/- 13.9 h postburn. The excision area averaged 32.3 +/- 6.7 per cent TBSA (range 24-96 per cent). In 15 patients a Swan-Ganz catheter was introduced to monitor haemodynamic changes. It was found that RAP, PAP, PAWP, ABP, HR, CO and CI were all stable during and after the operation. Group B consisted of 29 patients, and escharectomy was begun 4-5 days postburn. The mean healing time of the patients in group A was 33.1 days, which was shorter than that in group B (40.1 days). The period of haemoconcentration was shorter in group A and the amount of blood required during the first 2 weeks was almost 700 ml less in group A. There were fewer visceral complications in group A and smaller amounts of antibiotics were required in this group. The authors believe that escharectomy during the shock stage is feasible.

Acute Disease↗
PubMed1995

Comparative studies of types 1 and 2 herpes simplex virus infection of cultured normal keratinocytes.

AIMS: To investigate the differences in biological properties, multiplication patterns, and cytopathic effects between type 1 and type 2 herpes simplex virus (HSV) through the replication of HSV in cultured normal human keratinocytes. METHODS: Keratinocytes were obtained from surgical specimens of normal gingiva, cervix, trunk skin, and newborn foreskin. They were cultured in serum free, chemically defined, culture medium and infected with a pool of HSV collected from clinical specimens. RESULTS: The reproductive patterns of HSV type 1 (HSV-1) and HSV type 2 (HSV-2) differed from each other regardless of the anatomical source of the cultured cells. This was made evident by the dissimilarity of their growth curves and cytopathic effects. The growth curve of HSV-2 showed a more or less continuously rising titre, whereas HSV-1 titres varied substantially at different time intervals. The cytopathic effects induced by HSV-1 infection took 24 more incubation hours than those induced by HSV-2 infection to manifest. During the early stages, the cytopathic changes of the two viruses looked different. However, all cultured cells, whether cultured with HSV-1 or HSV-2, eventually became small and globular in shape. The infective titres of both HSV-1 and HSV-2 were higher in infected cultured cervix than in infected cultured normal gingiva. CONCLUSIONS: These data suggest that each serotype of HSV has its own unique replication pattern in human keratinocytes regardless of the cell origin.

Cells, Cultured↗
PubMed1995

Renal function in gout patients.

Patients with gouty arthritis were examined at Veterans General Hospital to evaluate whether their renal function is impaired and to define the factor(s), if any, of renal function deterioration. A total of 152 cases were included in the study, and the patients were divided into two groups. One group (n = 80) exhibited pure gout without any associated medical problems or preexisting renal disorders. The second group (n = 72) included patients with gout and hypertension. The group with pure gout was further stratified into patients with tophi (n = 21) and those without (n = 59). Seventy-two sex- and age-matched normal adults served as the control group. We found (1) that the renal function was impaired in the pure-gout group when compared with sex- and age-matched normal individuals (serum creatinine 1.56 +/- 0.64 vs. 0.90 +/- 0.16 mg/dl, p = 0.0001; creatinine clearance 59.91 +/- 30.90 vs. 97.10 +/- 27.19 ml/min, p = 0.0001); (2) that the renal function was significantly more aggravated in patients with clinically visible tophi than in those without (gout with tophi vs. gout without tophi: serum creatinine 1.89 +/- 0.90 vs. 1.44 +/- 0.48 mg/dl, p = 0.040; creatinine clearance 47.27 +/- 31.90 vs. 64.40 +/- 29.53 ml/min, p = 0.030), and (3) that a further significant decline of the renal function was noted in gouty patients with an associated medical illness, i.e., hypertension (gout with hypertension vs. pure gout: serum creatinine 2.10 +/- 0.97 vs. 1.56 +/- 0.64 mg/dl, p = 0.0001; creatinine clearance 45.06 +/- 24.69 vs. 59.91 +/- 30.90 ml/min, p = 0.0029).(ABSTRACT TRUNCATED AT 250 WORDS)

Arthritis, Gouty↗
PubMed1995

Prednisolone non-compliance and its related factors in patients with systemic lupus erythematosus.

BACKGROUND: The combination of western medicine and traditional Chinese medicine is still exerting a pervading influence on symptom relief in Chinese society. The Medical behavior pattern may influence medication non-compliance by patients with chronic illness. METHODS: The study was designed to investigate prednisolone non-compliance and its related factors for patients with systemic lupus erythematosus (SLE) under giving patients' health beliefs, the influence of prednisolone and Chinese culture. All patients of the SLE Mutual Aid Group (N=570) participated in this study. A questionnaire which included medical behavior and individual attitudes was sent each by mail. The response rate was 63.7% (N=363); 329 responses were useable in the study. RESULTS: Of the 329 patients, 27.9% had taken traditional medicine or a combination of traditional medicine with western medicine within the past month; 25.4% patients were non-compliant with prescribed prednisolone during the past week. The important reasons for non-compliance were feeling better, fearing side effects and treatment by Chinese medicine. The predicting factors for prednisolone non-compliance were the effects of the prednisolone, medical feasibility, patterns of medical behavior and perceived seriousness of the disease. Physician-patient relationship served as modifying factors which influenced individual attitudes toward prednisolone non-compliance and choice of medical behavior. Traditional beliefs, influenced by Chinese culture, indirectly affected prednisolone non-compliance, but through medical behavior patterns. CONCLUSIONS: Predisolone non-compliance is quite essential for SLE patients. Findings suggested that the attributes of prednisolone and the influences of Chinese traditional medicine should be considered as well as a health belief model, when trying to improve prednisolone compliance for SLE patients in Taiwan society.

Adult↗
PubMed1995

Genetic analysis of the HPRT mutation of Lesch-Nyhan syndrome in a Chinese family.

BACKGROUND: The Lesch-Nyhan syndrome is an X-linked recessive inherited disease caused by a complete deficiency of hypoxanthine guanine phosphoribosyl-transferase (HPRT) activity. Many different mutations throughout the HPRT coding region of Lesch-Nyhan patients have been described, including single base substitutions, partial or entire gene deletions, gene insertions or endoduplication of exons. However, study of gene mutation in Chinese patients has rarely been reported in Taiwan. METHODS: Polymerase chain reaction (PCR) and nucleotide sequence analysis were used to identify the location and the nature of the mutation at the HPRT locus in two brothers affected with Lesch-Nyhan syndrome. The HPRT cDNA, amplified from total RNA of patient's peripheral blood by reverse transcription-polymerase chain reaction, was cloned into a pGEM-3Zf(-) vector and then sequenced. Family study involved initial screening using single-strand conformation polymorphism, and further confirmation by direct sequencing of the exon encompassing the mutation. RESULTS: The mutation identified in these two affected siblings was a single nucleotide substitution, from cytosine to guanine, in exon 3 of the HPRT coding region. This transversion putatively caused a single amino acid substitution from phenylalanine to leucine at codon 74 in the translated protein. This base change was further confirmed by direct sequencing of both the HPRT cDNA fragment and the exon 3 of HPRT gene amplified from genomic DNA. The family study revealed that the patient's mother was a heterozygous carrier, and the mutation seemed to have occurred de novo in a germinal cell from one of the maternal grandparents. CONCLUSIONS: This is the first family study on Chinese patients with Lesch-Nyhan syndrome identified by molecular analysis in Taiwan. The mutation described herein is a novel substitution which occurs in a suggested "hotspot" of mutation (exon 3) of the HPRT gene. The application of molecular analysis of HPRT-gene allows not only DNA diagnosis by directly detecting the mutant alleles, but also prenatal diagnosis and carrier identification within individual families affected by Lesch-Nyhan syndrome.

Base Sequence↗
PubMed1994

Isolation, characterization, and chromosomal localization of the porcine calcitonin receptor gene. Identification of two variants of the receptor generated by alternative splicing.

The gene encoding the calcitonin receptor (CTR) was isolated from a porcine kidney epithelial cell line (LLC-PK1) genomic library and found to span approximately 70 kilobases. Analysis of the gene sequence revealed that the CTR mRNA encompasses 14 exons with 12 exons encoding the protein. Two splicing acceptor sites separated by 48 nucleotides were found in intron 7. The expression of two mRNA species in LLC-PK1 cells was subsequently confirmed by reverse transcription-polymerase chain reaction (RT-PCR) and DNA sequencing. In LLC-PK1 cells the mRNA encoding the shorter CTR (CTR-1a) is approximately 1,000 times more abundant than the longer variant (CTR-1b), as estimated by the competitive RT-PCR. The transcription initiation site of the CTR gene was mapped by primer extension, S1 nuclease, and RT-PCR analysis. The proximal promoter region of 500 base pair is GC-rich (66%) and CpG-rich (CpG/GpC ratio 0.71). Transient transfection of CTR gene promoter-luciferase chimeras in LLC-PK1 cells led to the expression of luciferase activity. The CTR gene was mapped to chromosome band 9q11-q12.

Alternative Splicing↗
PubMed1994

Cloning and developmental expression of the chick type II and type III TGF beta receptors.

To address the role of peptide growth factors in chick organogenesis, we have focused on TGF beta 2 and have cloned the chick Type II and Type III TGF beta receptors. The chick Type II receptor is a serine/threonine kinase with a ligand binding profile identical to the human receptor and a divergent N-terminus when compared to the mammalian receptors. The chick Type III receptor is a beta-glycan that demonstrates a binding profile identical to the rat receptor and contains a single transmembrane spanning domain and short cytoplasmic tail that are highly conserved when compared to the mammalian receptors. Both the Type II and Type III TGF beta receptors are coexpressed during chick embryogenesis in the developing heart, lung, and eye, and are developmentally upregulated in parallel in the heart and lung. Levels of both receptor proteins and mRNAs also increase in cardiocytes cultured from different developmental stages, in agreement with the increase in Type II and Type III receptor mRNA levels observed in the developing heart. Although exhibiting different temporal or spatial profiles from the receptors, TGF beta 2 is also expressed in the developing heart, lung, and eye. These findings are consistent with recent data indicating that co-expression of both the Type II and Type III TGF beta receptors is required for high affinity binding of TGF beta 2 by the Type II receptor and suggest that TGF beta 2 and the Type II and Type III TGF beta receptors participate in heart, lung, and eye development.

Amino Acid Sequence↗
PubMed1994

Analysis of neuropeptides by perfusion liquid chromatography/electrospray ion-trap mass spectrometry.

Perfusion high-performance liquid chromatography (HPLC) combined with electrospray ion trap mass spectrometry (ITMS) was evaluated for the determination of neuropeptides in plasma. Perfusion HPLC offers the capability of resolving neuropeptides spiked into plasma in 5 min compared to the 30-60 min separations performed on packed capillary C18 columns. Electrospray combined with the ITMS provides the ability to ionize these neuropeptides and mass analyze them with high sensitivity and specificity. Sub-picomole quantities of neuropeptides injected on-column could be specifically detected in a plasma matrix. The electrospray-ITMS mass spectrum of each neuropeptide showed multiply charged ions which could be used to determine or confirm their molecular weights.

Chromatography, High Pressure Liquid↗
PubMed1994

Expression of TGF-beta s and their receptors during implantation and organogenesis of the mouse embryo.

The spatial and temporal expression of the transforming growth factor beta (TGF-beta) receptors type III, type II, and two types I (ALK-5 and Tsk 7L) and their ligands TGF-beta 1 and TGF-beta 2 in postimplantation mouse development were examined using the reverse transcription polymerase chain reaction (RT-PCR), in situ hybridization, and immunohistochemistry. With RT-PCR, expression of the signaling TGF-beta receptors (types II and ALK-5) was shown to be absent in isolated germ layers of 6.0-7.5 days postcoitum (dpc) embryos, whereas the type III receptor and Tsk 7L were differentially expressed at these stages. In contrast, all TGF-beta receptor types were expressed at these stages in the pregnant uterus and decidua. TGF-beta 1 and TGF-beta 2 transcripts were detected before gastrulation at 6.5 dpc only in the visceral embryonic endoderm, whereas during gastrulation, at 7.5 dpc TGF-beta 1 and TGF-beta 2 mRNA was detected in all three germ layers. In situ hybridization and immunohistochemistry of the expression of the TGF-beta type II receptor confirmed the data obtained by RT-PCR. Furthermore, the type II receptor was detected in the extraembryonic ectoderm of 7.5 dpc embryos. In the embryo proper, TGF-beta type II receptor expression was detected only later in differentiating tissues and developing organs, but not in the brain and neural tube. Since the expression of the type II receptor may essentially determine whether a cell is able to respond to TGF-beta, the results are consistent with the view that TGF-beta s might be implicated in embryo implantation and organogenesis, but are not involved in gastrulation of the embryo.

Animals↗