Effects of insecticides on acariasis in mice

1972 ◽  
Vol 6 (3) ◽  
pp. 279-286 ◽  
Author(s):  
M. L. Constantin
Keyword(s):  
Inbred Mice ◽  
Old Mice

Inbred mice of strains CBA/T6T6, A, C57BL/10Sn and B10.LP were found to be infested in ascending order of severity by Myocoptes musculinus or Myobia musculi mites. All of the 4 insecticidal preparations applied to 5-month-old mice killed the adult stages of Myocoptes musculinus within 2-6 hours, but only 1 was active against Myobia musculi. This latter was 100% active in vitro at 0.5%, but 1% was required in vivo. At 3% it killed 2 of 20 mice, but at 1% it did not interfere with insemination and reproduction, neither did it damage newborn young.

scholarly journals Delivery of melittin-loaded niosomes for breast cancer treatment: an in vitro and in vivo evaluation of anti-cancer effect

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Farnaz Dabbagh Moghaddam ◽  
Iman Akbarzadeh ◽  
Ehsan Marzbankia ◽  
Mahsa Farid ◽  
Leila khaledi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Treatment ◽  
Cell Lines ◽  
Encapsulation Efficiency ◽  
Inbred Mice ◽  
Breast Cancer Treatment ◽  
Anticancer Effect ◽  
Anti Cancer

Abstract Background Melittin, a peptide component of honey bee venom, is an appealing candidate for cancer therapy. In the current study, melittin, melittin-loaded niosome, and empty niosome had been optimized and the anticancer effect assessed in vitro on 4T1 and SKBR3 breast cell lines and in vivo on BALB/C inbred mice. "Thin-layer hydration method" was used for preparing the niosomes; different niosomal formulations of melittin were prepared and characterized in terms of morphology, size, polydispersity index, encapsulation efficiency, release kinetics, and stability. A niosome was formulated and loaded with melittin as a promising drug carrier system for chemotherapy of the breast cancer cells. Hemolysis, apoptosis, cell cytotoxicity, invasion and migration of selected concentrations of melittin, and melittin-loaded niosome were evaluated on 4T1 and SKBR3 cells using hemolytic activity assay, flow cytometry, MTT assay, soft agar colony assay, and wound healing assay. Real-time PCR was used to determine the gene expression. 40 BALB/c inbred mice were used; then, the histopathology, P53 immunohistochemical assay and estimate of renal and liver enzyme activity for all groups had been done. Results This study showed melittin-loaded niosome is an excellent substitute in breast cancer treatment due to enhanced targeting, encapsulation efficiency, PDI, and release rate and shows a high anticancer effect on cell lines. The melittin-loaded niosome affects the genes expression by studied cells were higher than other samples; down-regulates the expression of Bcl2, MMP2, and MMP9 genes while they up-regulate the expression of Bax, Caspase3 and Caspase9 genes. They have also enhanced the apoptosis rate and inhibited cell migration, invasion in both cell lines compared to the melittin samples. Results of histopathology showed reduce mitosis index, invasion and pleomorphism in melittin-loaded niosome. Renal and hepatic biomarker activity did not significantly differ in melittin-loaded niosome and melittin compared to healthy control. In immunohistochemistry, P53 expression did not show a significant change in all groups. Conclusions Our study successfully declares that melittin-loaded niosome had more anti-cancer effects than free melittin. This project has demonstrated that niosomes are suitable vesicle carriers for melittin, compare to the free form.

Studies on the functional activity of organotypically cultured mouse ovary

Development ◽  
1966 ◽  
Vol 15 (2) ◽  
pp. 133-141
Author(s):  
T. N. Chapekar ◽  
G. V. Nayak ◽  
Kamal J. Ranadive
Keyword(s):  
Functional Activity ◽  
Synthetic Medium ◽  
Culture Conditions ◽  
Short Term ◽  
Plasma Clot ◽  
Rat Ovary ◽  
Old Mice ◽  
Term Maintenance

Short-term maintenance of mouse and rat ovary in organotypic culture system is no longer a problem (Martinovitch, 1938; Gaillard, 1953; Trowell, 1959). Gaillard (1953) cultivated ovaries from 7- to 8-day-old and 21-day-old mice for a week on the plasma clot. Trowell (1959) maintained ovaries of 8-day-old mice on a synthetic medium in an O2-CO2 atmosphere for 9 days. He observed no histological differentiation in the tissues of the ovary. What needs confirmation and further investigation is the possibility of maintenance of functional activity of the ovary under culture conditions. A study was therefore undertaken to investigate if an ovary, cultivated in vitro for some time, shows hormonal activity when transplanted in vivo. In the present work cultured ovaries were grafted in the anterior eye-chamber of spayed female mice and the development of secondary sex organs such as mammary glands and uterus was studied.

Comparison of postnatal lung growth and development between C3H/HeJ and C57BL/6J mice

2006 ◽  
Vol 100 (5) ◽  
pp. 1577-1583 ◽  
Author(s):  
Shawn E. Soutiere ◽  
Wayne Mitzner
Keyword(s):  
Lung Volume ◽  
Lung Development ◽  
Inbred Mice ◽  
Left Lung ◽  
Transpulmonary Pressure ◽  
Mean Linear Intercept ◽  
Old Mice

Previous work by our group has demonstrated substantial differences in lung volume and morphometric parameters between inbred mice. Specifically, adult C3H/HeJ (C3) have a 50% larger lung volume and 30% greater mean linear intercept than C57BL/6J (B6) mice. Although much of lung development occurs postnatally in rodents, it is uncertain at what age the differences between these strains become manifest. In this study, we performed quasi-static pressure-volume curves and morphometric analysis on neonatal mice. Lungs from anesthetized mice were degassed in vivo using absorption of 100% O2. Pressure-volume curves were then recorded in situ. The lungs were then fixed by instillation of Zenker’s solution at a constant transpulmonary pressure. The left lung from each animal was used for morphometric determination of mean air space chord length ( Lma). We found that the lung volume of C3 mice was substantially greater than that of B6 mice at all ages. In contrast, there was no difference in Lma (62.7 μm in C3 and 58.5 μm in B6) of 3-day-old mice. With increasing age (8 days), there was a progressive decrease in the Lma of both strains, with the magnitude of the decrease in B6 Lma mice exceeding that of C3. C3 lung volume remained 50% larger. The combination of parenchymal architectural similarity with lung air volume differences and different rates of alveolar septation support the hypothesis that lung volume and alveolar dimensions are independently regulated.

scholarly journals Isotypic and allotypic specificity of mouse rheumatoid factors.

1983 ◽  
Vol 157 (3) ◽  
pp. 1006-1019 ◽  
Author(s):  
J L Van Snick ◽  
V Stassin ◽  
B de Lestré
Keyword(s):  
Normal Mouse ◽  
Mouse Strains ◽  
Igg Subclass ◽  
Rheumatoid Factors ◽  
Spleen Cells ◽  
Polyclonal Activation ◽  
Old Mice ◽  
Reactive Antibody

The specificity of polyclonal mouse rheumatoid factors (RF) was analyzed by competition experiments with heat-aggregated mouse IgG subclasses. The RF spontaneously produced by three normal mouse strains (129/Sv, CBA/Ht, and C57Bl/6) and by two strains with autoimmune diseases (MRL/l and NZB) were found to consist of distinct non-cross-reactive antibody subpopulations each specific for one IgG subclass. The sera of the normal strains contained IgG1- and IgG2a-specific RF. The autoimmune strains produced an additional variety of RF that was specific for The autoimmune strains produced an additional variety of RF that was specific for IgG2b. Also, the RF secreted by spleen cells of various normal strains after in vitro polyclonal activation with lipopolysaccharide could be resolved into distinct subpopulations specific for IgG1 or IgG2a. These results were confirmed by the analysis of monoclonal RF derived from BALB/c, C57Bl/6, CBA/Ht, and 129/Sv mice: of 73 hybridomas with RF activity, 71 displayed a strict subclass specificity. The subclass predominantly recognized depended on the origin of the spleen cells used to generate the hybridomas. After polyclonal activation in vitro, a broad spectrum of different specificities was obtained with 16 RF specific for IgG1, 13 for IgG2a, and 4 for IgG2b. In contrast, 27 of 28 monoclonal RF derived from 129/Sv and BALB/c mice without prior polyclonal activation were specific for IgG2a, and of these 75% were allotype specific since they failed to react with IgG2a of the b allotype. These results demonstrate the importance of subclass specificity in the production of RF in vivo. With the exception of the IgG2b-specific clones, all these monoclonal RF reacted preferentially with heat-aggregated or antigen-bound IgG. Among the hybridomas generated by the fusion of in vitro polyclonally activated spleen cells of 4-wk-old mice, the frequency of clones with RF activity was at least 40 times higher than that of clones specific for mouse IgM, human IgG, ovalbumin, and hen lysozyme.

scholarly journals Enhancement of coxsackievirus B3 infection by antibody to a different coxsackievirus strain

2002 ◽  
Vol 83 (2) ◽  
pp. 351-358 ◽  
Author(s):  
Jaskamal Girn ◽  
Mojgan Kavoosi ◽  
Janet Chantler
Keyword(s):  
Viral Myocarditis ◽  
Neutralizing Antibody ◽  
Inbred Strains ◽  
Inbred Strains Of Mice ◽  
Infected Cells ◽  
Group B ◽  
Multiple Strains ◽  
Old Mice

Group B coxsackieviruses (CVBs) are a major cause of viral myocarditis and pancreatitis in humans and produce a similar pattern of disease in inbred strains of mice. As there are six strains of CVBs, individuals can be infected with multiple serotypes. This raises the possibility of antibody enhancement of infectivity (AEI) by cross-reactive but non-neutralizing antibody to a different strain from a prior infection. To determine whether AEI plays a role in coxsackievirus pathogenesis, an in vitro system using the murine macrophage cell line J774.1 was tested for enhanced infection when incubated with CVB3 plus anti-CVB2 antibody. Yields of virus were found to increase by 10–50-fold and the percentage of infected cells increased proportionately. The effect was Fc-mediated as F(ab′)2 fragments of the antibody could not mediate the effect. To determine whether AEI could also be demonstrated in vivo CVB3 was injected into 5-week-old mice together with mouse polyclonal anti-CVB2. Controls included mice injected with PBS or CVB3 alone. Results showed that the titres of virus in tissues of animals injected with virus plus antibody were 1–2 logs higher than when virus was injected alone. This was accompanied by greater histopathological damage, particularly in the heart. These results have implications for human disease as infection with multiple strains likely occurs during the lifetime of an individual.

scholarly journals Enhanced VWF biosynthesis and elevated plasma VWF due to a natural variant in the murine Vwf gene

Blood ◽  
2006 ◽  
Vol 108 (9) ◽  
pp. 3061-3067 ◽  
Author(s):  
Heidi L. Lemmerhirt ◽  
Jordan A. Shavit ◽  
Gallia G. Levy ◽  
Suzanne M. Cole ◽  
Jeffrey C. Long ◽  
...  
Keyword(s):  
Genetic Variation ◽  
Inbred Mice ◽  
Inbred Mouse ◽  
Mouse Strains ◽  
Genetic Modifiers ◽  
Wide Range ◽  
Natural Variant ◽  
Vitro Analysis

Abstract Both genetic and environmental influences contribute to the wide variation in plasma von Willebrand factor (VWF) levels observed in humans. Inbred mouse strains also have highly variable plasma VWF levels, providing a convenient model in which to study genetic modifiers of VWF. Previously, we identified a major modifier of VWF levels in the mouse (Mvwf1) as a regulatory mutation in murine Galgt2. We now report the identification of an additional murine VWF modifier (Mvwf2). Mvwf2 accounts for approximately 16% of the 8-fold plasma VWF variation (or ∼ 25% of the genetic variation) observed between the A/J and CASA/RkJ strains and maps to the murine Vwf gene itself. Twenty SNPs were identified within the coding regions of the A/J and CASA/RkJ Vwf alleles, and in vitro analysis of recombinant VWF demonstrated that a single SNP (+7970G>A) and the associated nonsynonymous amino acid change (R2657Q) confers a significant increase in VWF biosynthesis from the CASA/RkJ Vwf allele. This change appears to represent a unique gain of function that likely explains the mechanism of Mvwf2 in vivo. The identification of a natural Vwf gene variant among inbred mice affecting biosynthesis suggests that similar genetic variation may contribute to the wide range of VWF levels observed in humans.

scholarly journals P0913HYPERPHOSPHATEMIA INCREASE INFLAMMATION PROMOTING SENESCENCE AND MUSCLE DYSFUNCTION

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Patricia Sosa ◽  
Elena Alcalde-Estévez ◽  
Ana Asenjo-Bueno ◽  
Patricia Plaza ◽  
Gemma Olmos ◽  
...  
Keyword(s):  
Muscle Function ◽  
Strength Test ◽  
Normal Diet ◽  
Serum Phosphate ◽  
Phosphate Concentration ◽  
The Other ◽  
Old Mice ◽  
Pro Inflammatory Cytokines

Abstract Background and Aims Hyperphosphatemia has been associated with aging and chronic kidney disease (CKD). Sarcopenia, which is a related condition of these pathologies, is defined by loss of force and muscular mass. During aging, chronic systemic inflammation appears, termed inflammaging, due to changes in immune system function. Inflammaging has been associated with many age-related diseases including Sarcopenia and CKD. The work aimed to evaluate the effect of hyperphosphatemia on proinflammatory profile of cultured myoblast cells and to analyze, in old mice, the effect of a dietary restriction in the phosphate intake on the aging-related sarcopenia. Methods Culture murine myoblast C2C12 cells were used for in vitro experiments. Cells were treated with 10 mM beta-glycerophosphate (BGP) as phosphate donor for 24, 48 or 72h. Inflammation was assessed through IL6, TNFα and MCP-1 expression by RT-qPCR. Twenty-four months old, C57BL6 mice were used for in vivo studies. Mice were fed with a normal diet containing 0.6% of phosphate until 21 months, after that, one group of mice continued with a normal diet and the other group was fed with a hypophosphatemic diet, containing a 0.2% of phosphate, for the following 3 months. Old mice were compared with 5 months old mice. Muscle force was measured by a grip strength test. Serum phosphate concentration was evaluated with a commercial kit and inflammation was assessed through IL-1β expression levels by RT-qPCR. Results Results showed that BGP treatment augmented pro-inflammatory cytokines levels, in myoblast, at 72h. On the other hand, old mice had a 40% increase in serum phosphate concentration regarding young mice, and, in parallel, they showed a reduction in forelimb strength. Old animals feeding with a hypophosphatemic diet showed a decreased level of phosphate serum linked to a better muscle function. Pro-inflammatory cytokines expression was higher in old mice compared to young mice; those values were reduced in 24-month-mice fed with a low phosphate diet. Furthermore, there was a positive correlation between IL-1β expression levels and serum phosphate levels, suggesting that high levels of serum phosphate were increasing inflammation in vivo and a negative correlation between IL-1β and grip strength test, which shows that high levels of inflammation decrease muscular function Conclusion In this work, we propose that high levels of phosphate are related to inflammation in vitro and in vivo. This increase of proinflammatory cytokines decreases muscle function whereas dietary restriction of phosphate decreases inflammation and improves muscle function. These results could point to a direct link between elevated serum phosphate levels and inflammaging presented in sarcopenic people such as CKD patients and aged people.

scholarly journals Asc-1 regulates white versus beige adipocyte fate in a subcutaneous stromal cell population

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Lisa Suwandhi ◽  
Irem Altun ◽  
Ruth Karlina ◽  
Viktorian Miok ◽  
Tobias Wiedemann ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Stromal Vascular Fraction ◽  
Tissue Expansion ◽  
White Adipocyte ◽  
The Metabolic Syndrome ◽  
Beige Adipocytes ◽  
Subcutaneous Adipose ◽  
Old Mice

AbstractAdipose tissue expansion, as seen in obesity, is often metabolically detrimental causing insulin resistance and the metabolic syndrome. However, white adipose tissue expansion at early ages is essential to establish a functional metabolism. To understand the differences between adolescent and adult adipose tissue expansion, we studied the cellular composition of the stromal vascular fraction of subcutaneous adipose tissue of two and eight weeks old mice using single cell RNA sequencing. We identified a subset of adolescent preadipocytes expressing the mature white adipocyte marker Asc-1 that showed a low ability to differentiate into beige adipocytes compared to Asc-1 negative cells in vitro. Loss of Asc-1 in subcutaneous preadipocytes resulted in spontaneous differentiation of beige adipocytes in vitro and in vivo. Mechanistically, this was mediated by a function of the amino acid transporter ASC-1 specifically in proliferating preadipocytes involving the intracellular accumulation of the ASC-1 cargo D-serine.

scholarly journals HDAC6 inactivates Runx2 promoter to block osteogenesis of bone marrow stromal cells in age-related bone loss of mice

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Chao Ma ◽  
Juan Gao ◽  
Jun Liang ◽  
Weixiang Dai ◽  
Zhenfei Wang ◽  
...  
Keyword(s):  
Bone Loss ◽  
Bone Formation ◽  
Osteogenic Differentiation ◽  
Differentiation Potential ◽  
Runx2 Expression ◽  
Aged Mice ◽  
Age Related ◽  
Old Mice

Abstract Background Senile osteoporosis can cause bone fragility and increased risk for fractures and has been one of the most prevalent and severe diseases affecting the elderly population worldwidely. The underlying mechanisms are currently intensive areas of investigation. In age-related bone loss, decreased bone formation overweighs increased bone resorption. The molecular mechanisms underlying defective bone formation in age-related bone loss are not completely understood. In particular, the specific role of histone acetylation in age-related bone loss has not been examined thoroughly. Methods We employed 6- and 18-month-old mice to investigate the mechanisms of defective bone formation in age-related bone loss. Bone marrow stromal cells (BMSCs) were induced to undergo in vitro osteogenic differentiation. Chromatin immunoprecipitation (ChIP) was used to investigate the binding of histone deacetylases (HDACs) on Runx2 promoter in BMSCs. Luciferase reporter and transient transfection assay were employed to study Runx2 gene expression modulation by HDAC and androgen receptor (AR). siRNA and HDAC6 inhibitor, Tubastatin A, were used to inhibit HDAC6 in vitro. And systemic administration of Tubastatin A was used to block HDAC6 in vivo. Results Age-related trabecular bone loss was observed in 18-month-old mice compared with 6-month-old mice. In vitro osteogenic differentiation potential of BMSCs from 18-month-old mice was weaker than 6-month-old mice, in which there was Runx2 expression inactivation in BMSCs of 18-month-old mice compared with 6-month-old mice, which was attributable to HDAC6-mediated histone hypoacetylation in Runx2 promoter. There was competitive binding of HDAC6 and AR on Runx2 promoter to modulate Runx2 expression in BMSCs. More importantly, through siRNA- or specific inhibitor-mediated HDAC6 inhibition, we could activate Runx2 expression, rescue in vitro osteogenesis potential of BMSCs, and alleviate in vivo age-related bone loss of mice. Conclusion HDAC6 accumulation and histone hypoacetylation on Runx2 promoter contributed to the attenuation of in vitro osteogenic differentiation potential of BMSCs from aged mice. Through HDAC6 inhibition, we could activate Runx2 expression and osteogenic differentiation potential of BMSCs from aged mice and alleviate the age-related bone loss of aged mice. Our study will benefit not only for understanding the age-related bone loss, but also for finding new therapies to treat senile osteoporosis.

scholarly journals In vitro and in vivo CRISPR-Cas9 screens reveal drivers of aging in neural stem cells of the brain

2021 ◽  
Author(s):  
Tyson J Ruetz ◽  
Chloe M Kashiwagi ◽  
Bhek Morton ◽  
Robin W Yeo ◽  
Dena S Leeman ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Neural Stem Cells ◽  
Primary Cultures ◽  
Mammalian Brain ◽  
Aging Brain ◽  
Gene Knockouts ◽  
Old Mice

Aging impairs the ability of neural stem cells to transition from quiescence to activation (proliferation) in the adult mammalian brain. Neural stem cell (NSC) functional decline results in decreased production of new neurons and defective regeneration upon injury during aging, and this is exacerbated in Alzheimer's disease. Many genes are upregulated with age in NSCs, and the knockout of some of these boosts old NSC activation and rejuvenates aspects of old brain function. But systematic functional testing of genes in old NSCs - and more generally in old cells - has not been done. This has been a major limiting factor in identifying the most promising rejuvenation interventions. Here we develop in vitro and in vivo high-throughput CRISPR-Cas9 screening platforms to systematically uncover gene knockouts that boost NSC activation in old mice. Our genome-wide screening pipeline in primary cultures of young and old NSCs identifies over 300 gene knockouts that specifically restore old NSC activation. Interestingly, the top gene knockouts are involved in glucose import, cilium organization and ribonucleoprotein structures. To determine which gene knockouts have a rejuvenating effect for the aging brain, we establish a scalable CRISPR-Cas9 screening platform in vivo in old mice. Of the 50 gene knockouts we tested in vivo, 23 boost old NSC activation and production of new neurons in old brains. Notably, the knockout of Slc2a4, which encodes for the GLUT4 glucose transporter, is a top rejuvenating intervention for old NSCs. GLUT4 protein expression increases in the stem cell niche during aging, and we show that old NSCs indeed uptake ~2-fold more glucose than their young counterparts. Transient glucose starvation increases the ability of old NSCs to activate, which is not further improved by knockout of Slc2a4/GLUT4. Together, these results indicate that a shift in glucose uptake contributes to the decline in NSC activation with age, but that it can be reversed by genetic or external interventions. Importantly, our work provides scalable platforms to systematically identify genetic interventions that boost old NSC function, including in vivo in old brains, with important implications for regenerative and cognitive decline during aging.

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