Neonatal exposure to a type-I pyrethroid (bioallethrin) induces dose—response changes in brain muscarinic receptors and behaviour in neonatal and adult mice

1994 ◽  
Vol 645 (1-2) ◽  
pp. 318-324 ◽  
Author(s):  
Jonas Ahlbom ◽  
Anders Fredriksson ◽  
Per Eriksson
Keyword(s):  
Muscarinic Receptors ◽  
Dose Response ◽  
Neonatal Exposure ◽  
Type I ◽  
Adult Mice

EVIDENCE FOR AN ABNORMAL EXPRESSION OF THE COLLAGEN BINDING DOMAIN IN VON WILLEBRAND'S DISEASE TYPE II

1987 ◽  
Author(s):  
J Ingerslev ◽  
S Stenbjerg ◽  
A Bukh ◽  
NPH Møller ◽  
J Zeuthen
Keyword(s):  
Polyclonal Antibody ◽  
Dose Response ◽  
Binding Domain ◽  
Molecular Defect ◽  
Type I ◽  
Collagen Binding ◽  
Von Willebrand's Disease ◽  
Von Willebrand’S Disease ◽  
Antibody Elisa ◽  
Von Willebrand

A recently developed new series of monoclonal antibodies (MAbs) against the von Willebrand factor (vWf) included antibodies strongly inhibiting ( Mab vWf-41) and partly inhibiting ( Mab vWf-33) the collagen binding of vWf. We also characterized two Mabs with interacting properties against the ristocetin induced platelet aggregation (MAbs vWf-21 and vWf-39). These antibodies were conjugated with horse-radish peroxidase (HRP) and examined in different constructions forming two-site MAb ELISA's for plasma vWf:Ag and compared with polyclonal antibody ELISA. Symmetrical MAb-ELISA ( i.e. same Mab for extraction and detection) gave practical no dose-response in the standard assay, whereas any different combination of Mabs gave favourable dose-response relationships in sensitive ELISA's for vWf:Ag. Two different sandwiches were chosen using MAb vWf-33 and Mab vWf-41 at either side of the ELISA. These two assay models gave results of plasma from normal persons almost identical to those obtained with polyclonal antibody ELISA. Also in type I von Willebrand's disease these three assays performed very uniformly. In subtypes II plasma ( IIA: n=7; IIB: n=3, IIC: n=l, IID: n=i) . the assay using vWf-33 for coating and vWf-41-HRP for detection measured considerably lower than the polyclonal ELISA and the Mab-ELISA based on the opposite combination. We believe, that our results are indicative of a molecular defect in the collagen binding domain of vWf in subtype II plasma.

scholarly journals Mechanism and Function of Antiviral RNA Interference in Mice

mBio ◽  
2020 ◽  
Vol 11 (4) ◽  
Author(s):  
Qingxia Han ◽  
Gang Chen ◽  
Jinyan Wang ◽  
David Jee ◽  
Wan-Xiang Li ◽  
...  
Keyword(s):  
Rna Interference ◽  
Rna Replication ◽  
Interferon Response ◽  
Type I ◽  
Small Interfering Rnas ◽  
Guide Rna ◽  
Argonaute 2 ◽  
Adult Mice ◽  
And Function ◽  
Nodamura Virus

ABSTRACT Distinct mammalian RNA viruses trigger Dicer-mediated production of virus-derived small-interfering RNAs (vsiRNA) and encode unrelated proteins to suppress vsiRNA biogenesis. However, the mechanism and function of the mammalian RNA interference (RNAi) response are poorly understood. Here, we characterized antiviral RNAi in a mouse model of infection with Nodamura virus (NoV), a mosquito-transmissible positive-strand RNA virus encoding a known double-stranded RNA (dsRNA)-binding viral suppressor of RNAi (VSR), the B2 protein. We show that inhibition of NoV RNA replication by antiviral RNAi in mouse embryonic fibroblasts (MEFs) requires Dicer-dependent vsiRNA biogenesis and Argonaute-2 slicer activity. We found that VSR-B2 of NoV enhances viral RNA replication in wild-type but not RNAi-defective MEFs such as Argonaute-2 catalytic-dead MEFs and Dicer or Argonaute-2 knockout MEFs, indicating that VSR-B2 acts mainly by suppressing antiviral RNAi in the differentiated murine cells. Consistently, VSR-B2 expression in MEFs has no detectable effect on the induction of interferon-stimulated genes or the activation of global RNA cleavages by RNase L. Moreover, we demonstrate that NoV infection of adult mice induces production of abundant vsiRNA active to guide RNA slicing by Argonaute-2. Notably, VSR-B2 suppresses the biogenesis of both vsiRNA and the slicing-competent vsiRNA-Argonaute-2 complex without detectable inhibition of Argonaute-2 slicing guided by endogenous microRNA, which dramatically enhances viral load and promotes lethal NoV infection in adult mice either intact or defective in the signaling by type I, II, and III interferons. Together, our findings suggest that the mouse RNAi response confers essential protective antiviral immunity in both the presence and absence of the interferon response. IMPORTANCE Innate immune sensing of viral nucleic acids in mammals triggers potent antiviral responses regulated by interferons known to antagonize the induction of RNA interference (RNAi) by synthetic long double-stranded RNA (dsRNA). Here, we show that Nodamura virus (NoV) infection in adult mice activates processing of the viral dsRNA replicative intermediates into small interfering RNAs (siRNAs) active to guide RNA slicing by Argonaute-2. Genetic studies demonstrate that NoV RNA replication in mouse embryonic fibroblasts is inhibited by the RNAi pathway and enhanced by the B2 viral RNAi suppressor only in RNAi-competent cells. When B2 is rendered nonexpressing or nonfunctional, the resulting mutant viruses become nonpathogenic and are cleared in adult mice either intact or defective in the signaling by type I, II, and III interferons. Our findings suggest that mouse antiviral RNAi is active and necessary for the in vivo defense against viral infection in both the presence and absence of the interferon response.

scholarly journals Neonatal oxygen adversely affects lung function in adult mice without altering surfactant composition or activity

2009 ◽  
Vol 297 (4) ◽  
pp. L641-L649 ◽  
Author(s):  
Min Yee ◽  
Patricia R. Chess ◽  
Sharon A. McGrath-Morrow ◽  
Zhengdong Wang ◽  
Robert Gelein ◽  
...  
Keyword(s):  
Lung Function ◽  
Bronchoalveolar Lavage ◽  
Protein Content ◽  
Lung Development ◽  
Lung Compliance ◽  
Lung Mechanics ◽  
Type I ◽  
Adult Mice ◽  
Epithelial Development ◽  
Surfactant Composition

Despite its potentially adverse effects on lung development and function, supplemental oxygen is often used to treat premature infants in respiratory distress. To understand how neonatal hyperoxia can permanently disrupt lung development, we previously reported increased lung compliance, greater alveolar simplification, and disrupted epithelial development in adult mice exposed to 100% inspired oxygen fraction between postnatal days 1 and 4. Here, we investigate whether oxygen-induced changes in lung function are attributable to defects in surfactant composition and activity, structural changes in alveolar development, or both. Newborn mice were exposed to room air or 40%, 60%, 80%, or 100% oxygen between postnatal days 1 and 4 and allowed to recover in room air until 8 wk of age. Lung compliance and alveolar size increased, and airway resistance, airway elastance, tissue elastance, and tissue damping decreased, in mice exposed to 60–80% oxygen; changes were even greater in mice exposed to 100% oxygen. These alterations in lung function were not associated with changes in total protein content or surfactant phospholipid composition in bronchoalveolar lavage. Moreover, surface activity and total and hydrophobic protein content were unchanged in large surfactant aggregates centrifuged from bronchoalveolar lavage compared with control. Instead, the number of type II cells progressively declined in 60–100% oxygen, whereas levels of T1α, a protein expressed by type I cells, were comparably increased in mice exposed to 40–100% oxygen. Thickened bundles of elastin fibers were also detected in alveolar walls of mice exposed to ≥60% oxygen. These findings support the hypothesis that changes in lung development, rather than surfactant activity, are the primary causes of oxygen-altered lung function in children who were exposed to oxygen as neonates. Furthermore, the disruptive effects of oxygen on epithelial development and lung mechanics are not equivalently dose dependent.

scholarly journals Role of interferon in the pathogenesis of virus diseases in mice as demonstrated by the use of anti-interferon serum. II. Studies with herpes simplex, Moloney sarcoma, vesicular stomatitis, Newcastle disease, and influenza viruses.

1976 ◽  
Vol 144 (5) ◽  
pp. 1316-1323 ◽  
Author(s):  
I Gresser ◽  
M G Tovey ◽  
C Maury ◽  
M T Bandu
Keyword(s):  
Herpes Simplex ◽  
Influenza Virus Infection ◽  
Rapid Onset ◽  
Subsequent Treatment ◽  
Influenza Viruses ◽  
Type I ◽  
Virus Diseases ◽  
Newborn Mice ◽  
Infected Control ◽  
Adult Mice

The effect of potent sheep anti-mouse interferon globulin was investigated in several different experimental virus diseases of mice. In anti-interferon globulin-treated mice infected intraperitoneally with herpes simplex virus (HSV) type I, the latent period was shortened, and the overall LD50 was increased several hundredfold compared to virus-infected control mice. When HSV was inoculated subcutaneously all anti-interferon globulin-treated mice died, whereas only 5% of virus-infected control mice died. Subsequent treatment with anti-interferon globulin of previously HSV-infected mice did not result in reactivation of HSV. Treatment of adult mice with anti-interferon globulin resulted in an earlier appearance of MSV-induced tumors, a greater number of mice bearing tumors, an increase in tumor size, and an increase in the duration of tumors. All tumors eventually regressed despite reinjection of anti-interferon globulin. Anti-interferon globulin treatment resulted in a rapid onset of disease and death in adult mice inoculated (intranasal) with VSV and in newborn mice infected with NDV. Anti-interferon globulin exerted no effect on the course of influenza virus infection of mice. We conclude that the early production of interferon is an importane element in the response of the mouse to several viruses exhibiting different pathogeneses.

scholarly journals Heterogeneity in Biodistribution and Cytotoxicity of Silver Nanoparticles in Pulmonary Adenocarcinoma Human Cells

Nanomaterials ◽  
2019 ◽  
Vol 10 (1) ◽  
pp. 36 ◽  
Author(s):  
My Kieu Ha ◽  
Kyung Hwun Chung ◽  
Tae Hyun Yoon
Keyword(s):  
Silver Nanoparticles ◽  
Single Cell ◽  
Dose Response ◽  
A549 Cells ◽  
In Vitro Assays ◽  
Response Analysis ◽  
Complex Nature ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii

Cellular association of nanoparticles (NPs) and their resultant cytotoxicity are heterogeneous in nature and can be influenced by the variances in NPs’ properties, cell types, and status. However, conventional in vitro assays typically consider the administered NP dose and the averaged cellular responses based on the assumption of a uniform distribution of monodisperse NPs in homogeneous cells, which might be insufficient to describe the complex nature of cell–NP interactions. Here, using flow cytometry, we report observations of the heterogeneity in the cellular association of silver nanoparticles (AgNPs) in A549 cells, which resulted in distinct dose-response relationships and cytotoxicity. Type I and Type II cells were moderately associated with AgNPs but as the cellular AgNP dose increased, Type I cells remained viable while Type II cells became less viable. Type III cells did not have high affinity with AgNPs but were, however, the least viable. Transmission electron microscopic images revealed that the biodistribution and the released Ag+ ions contributed to the distinct toxic effects of AgNPs in different populations. This single-cell dose-response analysis approach enabled the examination of how differently individual cells responded to different cellular NP doses and provided insights into nanotoxicity pathways at a single-cell level.

Muscle-specific and inducible expression of 293-base pair beta-myosin heavy chain promoter in transgenic mice

1996 ◽  
Vol 271 (3) ◽  
pp. R688-R695 ◽  
Author(s):  
J. L. Wiedenman ◽  
G. L. Tsika ◽  
L. Gao ◽  
J. J. McCarthy ◽  
I. D. Rivera-Rivera ◽  
...  
Keyword(s):  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Specific Activity ◽  
Fiber Type ◽  
Regulatory Element ◽  
Histochemical Staining ◽  
Regulatory Sequences ◽  
Type I ◽  
Adult Mice ◽  
Mechanical Overload

The DNA regulatory element(s) involved in beta-myosin heavy chain (beta-MHC) induction by the physiological stimulus of mechanical overload have not been identified as yet. To delineate regulatory sequences that are required for mechanical overload induction of the beta-MHC gene, transgenic mouse lines were generated that harbor transgenes containing serial deletions of the human beta-MHC promoter to nucleotides -293 (beta 293), -201 (beta 201), and -141 (beta 141) from the transcription start site (+1). Mechanically overloaded adult plantaris and soleus muscles contained 11- and 1.9-fold increases, respectively, in endogenous beta-MHC-specific mRNA transcripts (Northern blot) compared with sham-operated controls. Expression assays (chloramphenicol acetyltransferase specific activity) revealed that only transgene beta 293 expression was muscle specific in both fetal and adult mice and was induced in the plantaris (10- to 27-fold) and soleus (2- to 2.5-fold) muscles by mechanical overload. Histochemical staining for myosin adenosinetriphosphatase activity revealed a fiber-type transition of type II to type I in the overloaded plantaris and soleus muscles. These transgenic data suggest that sequences located between nucleotides -293 and +120 may be sufficient to regulate the endogenous beta-MHC gene in response to developmental signals and to the physiological signals generated by mechanical overload in fast- and slow-twitch muscles.

scholarly journals Posttranslational regulation of keratins: degradation of mouse and human keratins 18 and 8.

1989 ◽  
Vol 9 (4) ◽  
pp. 1553-1565 ◽  
Author(s):  
D A Kulesh ◽  
G Ceceña ◽  
Y M Darmon ◽  
M Vasseur ◽  
R G Oshima
Keyword(s):  
Cell Types ◽  
Immunofluorescent Staining ◽  
Type I ◽  
Type Ii ◽  
Tail Domain ◽  
Proteolytic System ◽  
L Cells ◽  
Adult Mice ◽  
3T3 Fibroblasts ◽  
Keratin Filament

Human keratin 18 (K18) and keratin 8 (K8) and their mouse homologs, Endo B and Endo A, respectively, are expressed in adult mice primarily in a variety of simple epithelial cell types in which they are normally found in equal amounts within the intermediate filament cytoskeleton. Expression of K18 alone in mouse L cells or NIH 3T3 fibroblasts from either the gene or a cDNA expression vector results in K18 protein which is degraded relatively rapidly without the formation of filaments. A K8 cDNA containing all coding sequences was isolated and expressed in mouse fibroblasts either singly or in combination with K18. Immunoprecipitation of stably transfected L cells revealed that when K8 was expressed alone, it was degraded in a fashion similar to that seen previously for K18. However, expression of K8 in fibroblasts that also expressed K18 resulted in stabilization of both K18 and K8. Immunofluorescent staining revealed typical keratin filament organization in such cells. Thus, expression of a type I and a type II keratin was found to be both necessary and sufficient for formation of keratin filaments within fibroblasts. To determine whether a similar proteolytic system responsible for the degradation of K18 in fibroblasts also exists in simple epithelial cells which normally express a type I and a type II keratin, a mutant, truncated K18 protein missing the carboxy-terminal tail domain and a conserved region of the central, alpha-helical rod domain was expressed in mouse parietal endodermal cells. This resulted in destabilization of endogenous Endo A and Endo B and inhibition of the formation of typical keratin filament structures. Therefore, cells that normally express keratins contain a proteolytic system similar to that found in experimentally manipulated fibroblasts which degrades keratin proteins not found in their normal polymerized state.

Lack of expression of the mRNA encoding a major protein of the mouse vas deferens after neonatal exposure to oestrogens

1991 ◽  
Vol 7 (1) ◽  
pp. 63-69 ◽  
Author(s):  
E. Pailhoux ◽  
A. Martinez ◽  
Ch. Jean-Faucher ◽  
G. Veyssière ◽  
Cl. Jean
Keyword(s):  
Gene Expression ◽  
Western Blot ◽  
Blot Analysis ◽  
Northern Blot Analysis ◽  
Vas Deferens ◽  
Secretory Protein ◽  
Neonatal Exposure ◽  
Major Protein ◽  
Mouse Vas Deferens ◽  
Adult Mice

ABSTRACT We have previously characterized an androgen-inducible secretory protein from the mouse vas deferens (MVDP), and a cDNA to its mRNA has been obtained. This report describes altered MVDP gene expression after neonatal exposure to oestrogens. As shown by immunohistochemistry and Western blot analysis, MVDP was missing in the vas deferens from adult mice neonatally exposed to oestrogens. Northern blot analysis showed that the expression of MVDP mRNA was also suppressed. Exogenous testosterone was unable to stimulate MVDP production (either message or protein) in neonatally oestrogenized males. The results suggest that the alterations in gene expression in the oestrogen-exposed vas deferens reflect changes in the programme of differentiation of the organ itself.

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