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PubMed2000

Primary structure of mouse and rat nephrin cDNA and structure and expression of the mouse gene.

Nephrin is a central component of the glomerular podocyte slit diaphragm and is essential for the normal renal filtration process. This study describes the complete structure of the mouse nephrin gene, which was shown to be homologous to the human gene, the major difference being 30 exons in the mouse gene as opposed to 29 in human. The complete primary structure of mouse and rat nephrins was also determined. The sequence identity between the mouse and rat proteins was shown to be 93%, while both rodent proteins have only about 83% sequence identity with human nephrin. The availability of the three mammalian sequences is significant for the interpretation of sequence variants and mutations in the nephrin gene in patients with congenital nephrotic syndrome. In situ hybridization analyses of whole mouse embryos and tissues revealed high expression of nephrin in kidney glomeruli and, surprisingly, an intense and highly restricted expression in a set of cells in hindbrain and spinal cord. No expression was observed elsewhere. This expression pattern may explain occasionally occurring neural symptoms caused by inactivating mutations in the nephrin gene in patients with congenital nephrotic syndrome.

Animals↗
PubMed1992

Activation of mouse oocytes, fertilization and development of mouse embryos in vitro after staining with trypan blue or fluorescein diacetate.

The influence of vital staining with trypan blue or fluorescein diacetate on the fertilization of mouse oocytes and the developmental potential of mouse embryos was assessed. Neither stain induced spontaneous activation in mouse oocytes, nor did they impair the in vitro development and implantation of mouse zygotes, two-cell embryos, stressed morulae or blastocysts. However, fertilization and subsequent development of mouse oocytes have been shown to be reduced by vital staining.

Animals↗
PubMed1991

Binding of mouse and rabbit iron-59 transferrins to lactating mouse mammary epithelial cells.

The binding of mouse and rabbit transferrins to lactating mouse mammary epithelial cells was tested in a 59Fe-protein-binding assay. The homologous and heterologous binding was slow during the first 30 min, after which the uptake steadily increased. In ligand concentration-dependent saturation studies, the heterologous rabbit protein showed a high degree of binding and required approximately 9.7 ng of ligand to saturate approximately 2 x 10(6) cells. The homologous mouse protein demonstrated a low degree of binding and failed to demonstrate saturation at the above ligand concentration. Scatchard plot for homologous binding data was nonlinear and implied a low (1.08 x 10(-10) M) and a high (1.82 x 10(-9) M) affinity interaction mechanism. However, the plot for heterologous binding was linear and characterized by one high affinity (1.0 x 10(-9) M) binding interaction. A total of 11,000 and 19,600 binding sites per cell were estimated for mouse and rabbit proteins, respectively. These data suggest a binding crossreactivity between mouse and rabbit transferrins. A high affinity binding mechanism seems to be conserved in proteins from both species; however, an additional low affinity binding was present only in the homologous system.

Animals↗
PubMed1968

[The Host-Parasite Relations Of Clonorchis Sinensis In The Mouse: Studies On The Development Of C. Sinensis In Mouse]

It is well established that guinea pig, rabbit and rat are equally susceptible to experimental infection with the Chinese liver fluke, Clonorchis sinensis. However, little work has been done on the studies of the host-parasite relationships between the liver fluke and mouse host. The experiments were undertaken to investigate the susceptibility, development and sexual maturity of Clonorchis sinensis in mouse host. The metacercariae of C. sinensis used in these experiments were isolated from the fish, Pseudorasbora parva by digestion technic. And in all these studies the mice weighing around 20 g were commercially purchased and infected with the metacercariae under slightly narcotized condition with ether. The animals were starved overnight before infection. The mature metacercariae, e.g. 5, 10, 20, 30, 50, 200 were given orally into stomach by means of the polyethylene tubing (intramedic, Clay Adams, Inc.PE-90/S12) respectively to each mouse of groups ranging 4 to l5. After various period of infection, the mouse liver was first opened along the common bile duct and cut into small pieces for collecting and counting the worms. For the histopathological examination of the liver, the tissue specimens were fixed in formalin, sectioned and stained with haematoxylin-eosin. Another experiment was separately set up for the study of egg laying capacity of C. sinensis in mice. The following results were obtained: 1)Mice were successfully infected with metacercariae of C. sinensis in all cases of the groups except the group given 5 and 10 metacercariae, in which the infection was not established in one case of each group. Therefore it is assumed that mice are susceptible to infection with this worm. In an earlier period ot infection, the worms were found mostly in common bile duct and intrahepatic biliary passages with same rate, however in later period, they were seen rather in the intrahepatic biliary passages (73 %) than in common bile duct and gall bladder. The recovery rate of fully matured adult worms (less than 10 %) was lower than that of the average recovery rate of the worms in general (22.3 %). 2)Under same age of infection or even in same host, the size of collected worms showed the great variations. Oral sucker was smaller in size than ventral sucker in the early stage of infection. After 11 days of infection it reversed. The posterior part of body length began to elongate since 5 days after infection, and therefore the ratio of antero-posterior part became l to 3. Fully matured adult worms were only collected after 30 days of infection. The first positive appearance of eggs in feces was on the 17th and 18th day after infection. However, the egg-laying capacity in mouse host seemed to be stabilized since 30 days after infection. 3)Histopathologically, the cystic dilatation of medium to small biliary passages was noted and focal but diffusely scattered necrosis of the liver cells with scarce inflammatory cells was also observed as well as the hepatocellular degeneration, diffuse vascular congestions and adenomatous proliferationof bile duct.

Journal Article↗
PubMed1992

Mixed xenogeneic chimeras (rat + mouse to mouse). Evidence of rat stem cell engraftment, strain-specific transplantation tolerance, and skin-specific antigens.

We report the induction of stable and reliably detectable mixed xenogeneic chimerism through the coadministration of a mixture of untreated rat bone marrow plus T cell-depleted mouse bone marrow into B10 recipients conditioned with total body irradiation (TCD B10 mouse + untreated F344 rat----B10 mouse). Recipients repopulated as true mixed lymphopoietic chimeras, with from 1-21.6% rat-derived lymphoid cells in peripheral blood and splenic lymphoid tissue. Production of rat platelets was also demonstrated. Rat platelet and lymphoid chimerism was reliably detectable in chimeras from 1 to 7 months following reconstitution, suggesting engraftment of the rat bone marrow stem cell. Production of each stem cell-derived lineage appeared to be under independent regulation since a significantly greater proportion of platelets were rat-derived (24-81%) than were lymphocytes (1-21.6% rat), while erythrocytes were preferentially syngeneic (less than 2% rat). The tolerance induced by this model was highly donor strain-specific: donor-specific rat and mouse skin grafts were accepted while MHC-disparate third-party mouse (C3H; H-2k) and rat (Wistar Furth; Rt1Au) skin grafts were promptly rejected. Although specifically prolonged xenogeneic donor rat skin grafts underwent a slow chronic rejection, and some totally disappeared. In spite of this, chimeras retained their lymphoid chimerism, suggesting the presence of skin-specific antigens. This model for mixed xenogeneic chimerism with reliably detectable rat lymphoid cells may provide a model to study the existence of tissue-specific antigens across a species barrier, as well as mechanisms responsible for the induction and maintenance of this strain-specific transplantation tolerance.

Animals↗
PubMed2006

Role of the carbohydrate recognition domains of mouse galectin-4 in oligosaccharide binding and epitope recognition and expression of galectin-4 and galectin-6 in mouse cells and tissues.

Galectin-4 and its homologue galectin-6 are members of the tandem-repeat subfamily of monomer divalent galectins. Expression of mouse galectin-4 and galectin-6 by RT-PCR using primers designed to distinguish both galectin transcripts indicates that both are expressed in the small intestine, colon, liver, kidney, spleen and heart and P19X1 cells while only galectin-4 is expressed in BW-5147 and 3T3 cell lines. In situ hybridization confirmed the presence of galectin-4/-6 transcripts in the liver and small intestine. Galectin-4 is expressed in spermatozoons and oocytes and its expression during early mouse emryogenesis appears in 8-cell embryos and remains in later stages, as tested by RT-PCR. To study the role of carbohydrate recognition domains (CRDs) in oligosaccharide binding and epitope recognition, we cloned mouse full-length galectin-4 and galectin-6 cDNA and constructed bacterial expression vectors producing histidin-tagged recombinant galectin-4 and its truncated CRD1 and CRD2 forms. Oligosaccharide binding profile for all recombinant forms was assessed using Glycan Array available through the Consortium for Functional Glycomics. Acquired data indicate that mGalectin-4 binds to alpha-GalNAc and alpha-Gal A and B type structures with or without fucose. While the CRD2 domain has a high specificity and affinity for A type-2 alpha-GalNAc structures, the CRD1 domain has a broader specificity in correlation to the total binding profile. These data suggest that CRD2 might be the dominant binding domain of mouse galectin-4. Mapping of epitopes reactive for biotinylated his-tagged CRD1, CRD2 and mGalectin-4 performed on mouse cryosections showed that all three forms bind to alveolar macrophages, macrophages of red pulp of the spleen and proximal tubuli of the kidney and this binding was inhibited by 5 mM lactose. Interestingly, mGalectin-4, but not CRD forms, binds to the suprabasal layer of squamous epithelium of the tongue, suggesting that the link region also plays an important role in ligand recognition.

3T3 Cells↗
PubMed1991

cDNA cloning of mouse NKR-P1 and genetic linkage with LY-49. Identification of a natural killer cell gene complex on mouse chromosome 6.

NK cells lyse tumor cells and virally infected cells, but the molecular basis for this phenomenon has not been defined. A mAb specific for the rat cell surface molecule, NKR-P1, stimulates rat NK cell lytic activity and is reactive with all rat NK cells, suggesting that this molecule may play a significant role in NK cell function. We have previously described another NK cell-specific Ag, Ly-49, that belongs to a family of cross-hybridizing genes on distal mouse chromosome 6. The rat NKR-P1 Ag shares several features with the mouse Ly-49 Ag, including selective cell surface expression on NK cells, homology to the C-type lectins, expression as a type II integral membrane protein, and disulfide-linked homodimeric structure. To further examine the relationship of NKR-P1 to Ly-49, we have cloned the cDNA encoding a mouse homologue of NKR-P1 (mNKR-P1). The mouse and rat NKR-P1-deduced polypeptide sequences are highly conserved, suggesting a similar tertiary structure. By examination of DNA from informative recombinant inbred mice with Southern blot analysis, we have determined that mNKR-P1 is encoded by a distinct gene that is genetically linked to the Ly-49 locus, lying within 0.5 centi-Morgan (cM) of Ly-49. Although the deduced amino acid sequences of mNKR-P1 and Ly-49 reveal that these proteins are structurally similar, they are only 24% identical at the amino acid level and the cDNA sequences do not demonstrate significant nucleotide homology. Our studies suggest that we have identified a region on mouse chromosome 6 that includes distinct NK-specific genes that encode structurally related proteins (type II integral membrane proteins, C-type lectin super-gene family) but which demonstrate considerable heterogeneity. We have termed this genetic region the NK complex.

Amino Acid Sequence↗
PubMed2006

[A histological innovative study of Balb/c mouse tooth germ transplanted to nude mouse in vivo].

PURPOSE: To observed the changes of the developed mouse's dental germs after transplanting into nude mouse and find some theoretical foundation for establishing an innovative experimental model. METHODS: Eight tooth germs from four 5th day postnatal Balb/c mice were transplanted to the back muscles of the adult nude mice. At seventh and fourteenth day after grafting, the germs were collected, fixed, demineralized, dehydrated, and embedded in wax. Serial sections of 5 microm thick were made following the routine methods, stained with haematoxylin-eosin dying solution, and observed under a light microscope. The mandibular first molars were taken out from the 12th and 19th day postnatal mouse. Serial sections of 5 microm thick were made following the routine methods, then compared with the germs after graft. RESULTS: All implantations were located in the superficial muscles with abundant capillary vessels. The dental germs could further developed after grafting under the microscope, but slower than dental germs self-development. The layer of dentin was thin, plenty of dentin with disorganized dentin tubule formed after grafting. Although the location of Hertwig's epithelial root sheath hardly moved, the roots developed further. The floor of pulp chamber could form and the pulp chambers were shrinking. The degree of calcification in the area of root increased very clearly. The inflammatory reaction was found at 7th day while hardly noted at 14th day after grafting. CONCLUSIONS: It suggests that late development of mouse tooth germs could further develop after heterotopic transplantation within the superficial muscles of the nude mouse. This model is useful for study of tooth root development in short time.

Animals↗
PubMed1990

Interference by human anti-mouse antibodies in CA 125 assay after immunoscintigraphy: anti-idiotypic antibodies not neutralized by mouse IgG but removed by chromatography.

Falsely increased concentrations of the ovarian carcinoma-associated antigen, CA 125, were measured by a monoclonal antibody (MAb)-based double determinant immunoradiometric assay (IRMA) in patients who developed antibodies to mouse immunoglobulins (IgGs) after receiving injections of the same MAb as is used in the CA 125 IRMA. Addition of undiluted mouse serum or purified mouse IgG to the assay mixture failed to eliminate the falsely increased CA 125 concentrations in most of the samples, owing to the presence of anti-idiotype antibody. Because of their anti-idiotypic nature, the human anti-mouse antibodies (HAMAS) had only little effect on other immunometric assays, and this effect could be completely eliminated by addition of mouse IgG. To eliminate the effect of HAMA on the CA 125 assay, we studied the ability of various chromatographic methods to separate the interfering HAMA from CA 125. For measuring HAMA in serum and chromatographic fractions we developed a time-resolved fluoroimmunoassay. Adequate separation of CA 125 and HAMA was achieved by affinity chromatography of patients' sera with solid-phase Protein A, Protein G, cation-exchange chromatography on Mono S, and gel filtration on Superose 6. These results demonstrate that the interference can effectively be removed by rather simple chromatographic procedures.

Animals↗
PubMed1990

Endogenously secreted IL-4 is required for mouse thymocytes to become cytotoxic. Human, but not mouse, IL-2 induces a functionally immature thymic subset to secrete IL-4 and become CTL.

Experiments described here demonstrate that the differentiation of mouse thymocytes into cytotoxic T lymphocytes (CTL) requires interleukin-4 (IL-4). To reach this conclusion, we took advantage of our discovery that human and mouse IL-2 have very different effects on the development of CTL from a functionally immature subset of thymocytes. The lobster agglutinin 1 (LAg1)-negative subpopulation of thymocytes proliferated when cultured with concanavalin A (Con A)+ human or mouse IL-2, but these cells became CTL only when cultured with Con A+ human IL-2. Furthermore, Con A+ human IL-2, but not mouse IL-2, stimulated IL-4 production by cells within this population. Con A-induced cytotoxicity by mature LAg1-positive thymocytes and normal thymocytes was also accompanied by secretion of IL-4. The anti-IL-4 mAb 11B11 inhibited induction of cytotoxicity by all thymocyte populations tested. Taken together these experiments indicate that stimuli which induce cytotoxicity by mouse thymocytes also induce the secretion of IL-4, which is necessary for the differentiation of thymocyte CTL precursors into CTL.

Animals↗
PubMed1988

Monoclonal antibodies to mouse complement receptor type 1 (CR1). Their use in a distribution study showing that mouse erythrocytes and platelets are CR1-negative.

mAb to murine C receptor type 1 (CR1) were produced and three of them were characterized. One antibody, designated as 8C12, immunoprecipitated a protein of 190,000 Mr from a detergent extract of surface-labeled spleen cells and stained spleen B but not T lymphocytes in fluorescent flow cytometry. It inhibited both CR1-mediated rosette formation and the cofactor activity of CR1 for factor I-mediated cleavage of C3b, suggesting that it recognizes the ligand-binding site of CR1. The two other antibodies, designated as 7G6 and 7E9, recognized different epitopes from that recognized by 8C12, and they cross-reacted with a protein of 150,000 Mr that is present in a spleen extract. The distribution of CR1 in murine hemopoietic cells was studied by binding experiments with radiolabeled 8C12 and fluorescent flow cytometry. When CR1 was not detected by 8C12 alone, the two other antibodies were used in combination with 8C12 to confirm the negative results. Almost all B lymphocytes from the spleen, lymph nodes, and peripheral blood were CR1 positive. Most of the Thy-1-positive lymphocytes from these tissues were CR1 negative. Thymus lymphocytes were also CR1 negative. Peritoneal macrophages and chemotactic factor stimulated but not unstimulated peripheral blood granulocytes were CR1 positive. In contrast to human E, mouse E were CR1 negative. This pattern of distribution was consistent with previous results obtained by rosette assays. Although mouse platelets cause immune adherence hemagglutination with C3b-bearing SRBC, they are CR1 negative. Three other lines of evidence also indicated that platelets are CR1 negative. First, no band of CR1 was demonstrated by immunoprecipitation with 8C12 of an extract of surface-labeled platelets. Second, 8C12, which inhibited rosette formation by lymphocytes, alone or in combination with 7G6 and 7E9, did not inhibit immune adherence between platelets and C3b-bearing SRBC. Third, polyclonal rabbit IgG prepared from anti-mouse CR1 antiserum did not inhibit immune adherence by platelets. These results strongly suggest that the C3b-binding factor(s) on mouse platelets is different from CR1 and that processing of C3b-bearing immune complexes in mouse blood may be mediated by a new and as yet unidentified C3b-binding factor(s).

Animals↗
PubMed1977

Humoral primary immune response in vitro in a homologous mouse system: replacement of fetal calf serum by a 2-mercaptoethanol or macrophage-activated fraction of mouse serum.

The primary immune response in mouse spleen cell cultures against heterologous red cell antigens is dependent on the medium being supplemented with selected batches of fetal calf serum. Mouse serum itself is not able to support this response. The active immune response-supporting component in fetal calf serum seems to be a distinct factor (s), which has been partially purified by Sephadex G-100 filtration and termed MaSF-2-mercaptoethanol-activated serum factor. In this report it is demonstrated that MaSF is also present in mouse serum. For functional detection, mouse MaSF has to be separated from higher m.w. inhibitors, and has to be activated by 2-ME. After separation and activation mouse MaSF can support the primary immune response in a completely homologous in vitro culture system. Evidence is presented that MaSF can also be activated by macrophages. It is concluded that macrophages and 2-ME have the same mode of action in the primary immune response in vitro, i.e., induction of lymphocyte competence by activation of a serum factor.

Animals↗
PubMed1987

Mapping the mouse X chromosome: possible symmetry in the location of a family of sequences on the mouse X and Y chromosomes.

Major advances in our knowledge of the genetic organization of the mouse X chromosome have been obtained by the use of interspecific crosses involving Mus spretus-derived strains. This system has been used to study sequences detected by three probes 80Y/B, 302Y/B and 371Y/B isolated from a mouse Y-chromosome library which have been shown to recognize both male-female common and male-female differential sequences. These patterns are due to the presence of a family of cross-reacting sequences on the mouse X and Y chromosomes. Detailed genetic analysis of the localization of the X-chromosome-specific sequences using both a somatic cell hybrid panel and an interspecific mouse cross has revealed the presence of at least three discrete clusters of loci (X-Y)A, (X-Y)B and (X-Y)C. Two of these clusters, (X-Y)B and (X-Y)C, lie distally on the mouse X chromosome, the other cluster (X-Y)A being situated close to the centromere. In situ hybridization shows a striking symmetry in the localization of the major sequences on both the X and Y chromosomes detected by these probes, hybridization being preferentially localized to a subcentromeric and subtelomeric region on each chromosome. This striking localization symmetry between the X and Y chromosome sequences is discussed in terms of the extensive pairing of the X-Y chromosomes noted during meiosis.

Animals↗
PubMed1987

Enhancing effect of a bay region methyl group on tumorigenicity in newborn mice and mouse skin of enantiomeric bay region diol epoxides formed stereoselectively from methylchrysenes in mouse epidermis.

The stereochemistry of diol epoxide formation in mouse epidermis upon topical application of [3H]-1R,2R-dihydroxy-1,2-dihydro-5-methylchrysene ([3H]-5-MeC-1R,2R-diol) and [3H]-6-MeC-1R,2R-diol, and the tumorigenicity in mouse skin and in newborn mice of the R,S,S,R and S,R,R,S enantiomers of 1,2-dihydroxy-3,4-epoxy-1,2,3,4-tetrahydro-5-methylchrysene (5-MeC-1,2-diol-3,4-epoxide), 5-MeC-7,8-diol-9,10-epoxide, and 6-MeC-1,2-diol-3,4-epoxide were examined. Analysis of tetraols and their derived tetraacetates present in mouse epidermis, 2 h after application of [3H]-5-MeC-1R,2R-diol or [3H]-6-MeC-1R,2R-diol, demonstrated greater than 90% stereoselectivity in formation of 5-MeC-1R,2S-diol-3S,4R-epoxide and 6-MeC-1R,2S-diol-3S,4R-epoxide. Taken together with previous data, these results demonstrate that there is a high degree of stereoselectivity for formation of R,S,S,R enantiomers of 5-MeC- and 6-MeC-1,2-diol-3,4-epoxides in mouse skin. The results of the tumorigenicity studies in mouse skin and in newborn mice clearly demonstrated that 5-MeC-1R,2S-diol-3S,4R-epoxide was the most tumorigenic of the diol epoxide enantiomers tested; 6-MeC-1R,2S-diol-3S,4R-epoxide was inactive. The results of this study show that the high tumorigenicity of 5-MeC compared to 6-MeC is due to the remarkable tumorigenic activity of 5-MeC-1R,2S-diol-3S,4R-epoxide which, in contrast to 6-MeC-1R,2S-diol-3S,4R-epoxide, has a methyl group in the same bay region as the epoxide ring. We propose that such methyl bay region diol epoxides of other carcinogenic methylated polynuclear aromatic hydrocarbons will also show unique tumorigenic properties.

Animals↗
PubMed1982

Effect of mouse type I interferon on mouse bone marrow cells and peritoneal exudate cells cultured in vitro.

Type I mouse interferon significantly reduces macrophage colony formation from mouse bone marrow cells or mouse peritoneal exudate cells when cultured in vitro in the presence of colony-stimulating factors (CSF) derived from either pregnant mouse uterus (CSFPMUE or LCM (CSFLCM) (concanavalin-A purified preparation from endotoxin-shocked mouse long-conditioned medium). The effect of interferon on granulocyte (G-CFU) or granulocyte-macrophage-mixed (GM-CFU) colonies depended on the CSF used. G-CFU and GM-CFU were somewhat elevated in interferon-treated cells stimulated by CSFPMUE whereas G-CFU and GM-CFU were slightly inhibited in interferon-treated cells stimulated by CSFLCM. The most dramatic effect of interferon was observed in the macrophage population. We conclude that interferon affects differentiation preferentially at the macrophage progenitor cell level.

Animals↗
PubMed1983

Effect of mouse interferon on growth and differentiation of mouse bone marrow cells stimulated by two different types of colony-stimulating factor.

The effects of mouse L-cell interferon (IFN) on growth of mouse bone marrow cells and their differentiation into macrophages and granulocytes were investigated in a liquid suspension culture system with two different types of colony-stimulating factor (CSF). Within 7 days, most bone marrow cells differentiated into macrophages in the presence of macrophage colony-stimulating factor (M-CSF) derived from mouse fibroblast L929 cells, but into both granulocytes (40%) and macrophages (23%) in the presence of a granulocyte-macrophage colony-stimulating factor (GM-CSF) from mouse lung tissue. IFN inhibited growth of bone marrow cells with both M-CSF and GM-CSF, but had 20 times more effect on bone marrow cells stimulated with M-CSF than on those stimulated with GM-CSF. A low concentration of IFN (50 IU/ml) stimulated production of macrophages by GM-CSF in liquid culture medium, whereas it selectively inhibited colony formation of macrophages in semisolid agar culture. IFN caused no detectable block of late stages of differentiation; mature macrophages and granulocytes were produced even when cell proliferation was inhibited by IFN. These results indicate that IFN preferentially affects growth and differentiation of the cell lineage of macrophages among mouse bone marrow cells.

Animals↗
PubMed1980

Metabolic studies of N-bases of phospholipids and long chain bases of sphingolipids in two-weeks-old mouse brain tissue in comparison with one-month-old mouse visceral tissues.

After intraperitoneal administration of 15N-labeled serine, ethanolamine and choline to young mice showing active myelination, the incorporation of 15N-atom into N-bases of phospholipids and long chain bases of sphingolipids in brain tissue was particularly investigated in comparison with those in visceral tissues of adult mouse. After intraperitoneal injection of DL-[15N]-serine into mice, it was found that the 15N-atom was obviously incorporated into phosphatidylserine, phosphatidylethanolamine, ethanolamine-plasmalogen and long chain bases of cerebroside, sphingomyelin and gangliosides, but not significantly into phosphatidylcholine. The apparent maximum rates of the incorporation were also calculated. After administration of [15N]-ethanolamine, the 15N-atom was predominantly incorporated into phosphatidylethanolamine and next into ethanolamine-plasmalogen, but also not significantly into phosphatidylcholine. After administration of [15N]-choline chloride, the 15N-atom was incorporated into phosphatidylcholine and sphingomyelin, but not into other phospholipids and sphingolipids. These results suggested that serine, ethanolamine and choline are available for the biosynthesis of the N-bases of phospholipids in the brain tissue of young mouse and that serine is also utilized for the biosynthesis of long chain bases of sphingolipids. However, neither biosynthesis of choline from ethanolamine nor of phosphatidylcholine from phosphatidylethanolamine by methylation seemed to take place even in the brain tissue of young mouse, while the decarboxylation of phosphatidylserine into phosphatidylethanolamine was obviously observed. The decarboxylation rate of phosphatidylserine into phosphatidylethanolamine in the brain tissue of young mouse seemed to be approximately at the same level with the other tissues like liver, lung spleen and kidney of adult mouse.

Aging↗
PubMed1981

Some characteristics of mouse platelet aggregation and a comparison of the activity of a range of compounds in mouse and human platelet-rich plasma in vitro.

Collegan-induced platelet aggregation in mouse citrated platelet-rich (PRP) was associated with 5-hydroxytryptamine (5-HT) release and degranulation. Adenosine 5'-diphosphate (ADP) induced monophasic and reversible aggregation with no degranulation. Mouse platelets gave no response to adrenaline but changed shape and sometimes aggregated in response to 5-HT. Both amines potentiated the effect of ADP. The respective potencies of prostaglandin E1, papaverine, VK 774, BL 3459 and adenosine as inhibitors of ADP-induced aggregation were similar in mous and human PRP. Although ticlopidine had similar activity in the two species, aspirin and flurbiprofen were considerably less potent in mouse than human PRP as inhibitors of collagen-induced aggregation. It is suggested that collagen-induced aggregation of mouse platelets in vitro occurs by a mechanism largely independent of arachidonic acid metabolites.

Adenosine Diphosphate↗