Triamcinolone impairs the synthesis of collagen and noncollagen proteins in condylar cartilage of newborn mice

1988 ◽  
Vol 42 (1) ◽  
pp. 63-69 ◽  
Author(s):  
Anna Weiss ◽  
Erella Livne ◽  
Esther Brandeis ◽  
Michael Silbermann
Keyword(s):  
Condylar Cartilage ◽  
Newborn Mice ◽  
Noncollagen Proteins

Growth and repair of cartilage: Organ culture system utilizing chondroprogenitor cells of condylar cartilage in newborn mice

2009 ◽  
Vol 3 (1) ◽  
pp. 93-100 ◽  
Author(s):  
Anna Weiss ◽  
Erella Livne ◽  
Klaus von der Mark ◽  
Dick Heinegard ◽  
Michael Silbermann
Keyword(s):  
Organ Culture ◽  
Culture System ◽  
Condylar Cartilage ◽  
Newborn Mice ◽  
Organ Culture System ◽  
Chondroprogenitor Cells

Altered thymic epithelial cells may be decisive for Moloney virus-induced lymphoma development

1983 ◽  
Vol 41 ◽  
pp. 784-785
Author(s):  
U.I. Heine ◽  
G.R.F. Krueger ◽  
E. Munoz ◽  
A. Karpinski
Keyword(s):  
Epithelial Cells ◽  
Leukemia Virus ◽  
Light And Electron Microscopy ◽  
Tumor Development ◽  
Current Evidence ◽  
Thymic Epithelial Cells ◽  
Thymic Tissue ◽  
Newborn Mice ◽  
Moloney Leukemia Virus ◽  
Differentiation Block

Infection of newborn mice with Moloney leukemia virus (M-MuLV) causes a T-cell differentiation block in the thymic cortex accompanied by proliferation and accumulation of prethymic lymphoblasts in the thymus and subsequent spreading of these cells to generate systemic lymphoma. Current evidence shows that thymic reticular epithelial cells (REC) provide a microenvironment necessary for the maturation of prethymic lymphoblasts to mature T-lymphocytes by secretion of various thymic factors. A change in that environment due to infection of REC by virus could be decisive for the failure of lymphoblasts to mature and thus contribute to lymphoma development.We have studied the morphology and distribution of the major thymic cell populations at different stages of tumorigenesis in Balb/c mice infected when newborn with 0.2ml M-MuLV suspension, 6.8 log FFU/ml. Thymic tissue taken at 1-2 weekly intervals up to tumor development was processed for light and electron microscopy, using glutaraldehyde-OsO4fixation and Epon-Araldite embedding.

Reversal of cardiomyopathy resulting from prenatal exposure to ethanol

1984 ◽  
Vol 42 ◽  
pp. 716-717
Author(s):  
C. Uphoff ◽  
C. Nyquist-Battie
Keyword(s):  
Prenatal Exposure ◽  
Heart Development ◽  
Membrane Integrity ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Pathological Changes ◽  
Prenatally Exposed ◽  
Inner Mitochondrial Membrane ◽  
Fetal Alcohol ◽  
Newborn Mice

Fetal Alcohol Syndrone (FAS) is a syndrome with characteristic abnormalities resulting from prenatal exposure to ethanol. In many children with FAS syndrome gross pathological changes in the heart are seen with septal defects the most prevalent abnormality recorded. Few studies in animal models have been performed on the effects of ethanol on heart development. In our laboratory, it has been observed that prenatal ethanol exposure of Swiss albino mice results in abnormal cardiac muscle ultrastructure when mice were examined at birth and compared to pairfed and normal controls. Fig. 1 is an example of the changes that are seen in the ethanol-exposed animals. These changes include enlarged mitochondria with loss of inner mitochondrial membrane integrity and loss of myofibrils. Morphometric analysis substantiated the presence of these alterations from normal cardiac ultrastructure. The present work was undertaken to determine if the pathological changes seen in the newborn mice prenatally exposed to ethanol could be reversed with age and abstinence.

Histological Comparative of Kidney of Neonatal Mice Exposed to Silver Nanoparticles During Fetal Development

2019 ◽  
Vol 10 (01) ◽  
Author(s):  
Najat F. Mohammed Salih ◽  
Gazwa D. Al-Nakeeb
Keyword(s):  
Silver Nanoparticles ◽  
Fetal Development ◽  
High Dose ◽  
Histopathological Analysis ◽  
Histological Changes ◽  
Newborn Mice ◽  
The Third ◽  
Tubular Necrosis ◽  
Neonatal Kidney ◽  
Glomerular Tuft

This study aimed to compare the histological changes in the neonatal kidney after their mothers exposed to different doses of silver nanoparticles colloidal solution (AgNPs) during the three stages of pregnancy. Pregnant Swiss albino mice (n=60) were randomly divided into three treated groups. They were intraperitoneally injected with AgNPs for 7 days during each stage of the gestational period. The newborn mice were sacrificed immediately after the birth, and the kidneys were being collected for histopathological analysis. The results showed that the AgNPs caused histological changes in the neonatal kidneys; vacuolation of some renal vesicles and cortical tubules, cystic tubular dilation, glomerular tuft shrinkage, and focal tubular necrosis in the first week-dose exposed pregnant. Disintegrating of immature glomeruli, distention of Bowman’s space of mature glomeruli, tubular necrosis, loss of renal parenchyma, medullar tubules containing hyaline casts, and subcapsular haemorrhage in the second week-dose exposed pregnant. Massive hypercellularity in the deeper part of the renal cortex, cortical and medullary tubules dilation, atrophy of subcapsular immature tubules, cortical cyst formation, glomerular tuft necrosis, dilation of Bowman’s space with evidence of crescent formation, and medullar portion replaced by scant loose connective tissue containing few numbers of tubules the third week-dose exposed pregnant. The results showed that the AgNPs has more negative effects on the kidney development at the third week-high dose and comparing the histological changes in the neonatal kidney were appeared in a time-depended manner and in a dosedepended manner. More researches must be carried out to obtain better understanding of AgNPs toxicity on fetal development and its ability as a teratogenic agent to induce external and internal abnormalities in the fetus.

Chelidonine Attenuates Sepsis-Induced Acute Lung Injury via Suppressing Toll-like Receptor 4/Myeloid Differentiation Factor 88/Nuclear Factor-॔B Signaling Pathway in Newborn Mice

2020 ◽  
Vol 19 (1) ◽  
pp. 120-126
Author(s):  
Ayinuerguli Adili ◽  
Adilijiang Kari ◽  
Chuanlong Song ◽  
Abulaiti Abuduhaer
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Nuclear Factor Kappa B ◽  
Myeloid Differentiation ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Inflammatory Infiltration ◽  
Newborn Mice ◽  
Myeloid Differentiation Factor

We have examined the mechanism underlying amelioration of sepsis-induced acute lung injury by chelidonine in newborn mice. To this end, a sepsis model was established using cecal ligation and puncture in newborn mice. The sepsis-induced acute lung injury was associated with an increased inflammatory infiltration and pulmonary congestion, as well as abnormal alveolar morphology. The lung injury-associated increased tumor necrosis factor-α and interleukin-1β in bronchoalveolar lavage fluid and lung, the markers of inflammatory infiltration and pulmonary congestion, diminished by chelidonine treatment. Chelidonine administration also downregulated protein levels of toll-like receptor 4, myeloid differentiation factor 88, phosphorylated nuclear factor-kappa B, and nuclear factor-kappa B that are elevated in response to sepsis. In conclusion, chelidonine provides a potential therapeutic strategy for newborn mice with acute lung injury.

V. The epithelial sodium channel and its implication in human diseases

1999 ◽  
Vol 276 (3) ◽  
pp. G567-G571 ◽  
Author(s):  
Edith Hummler ◽  
Jean-Daniel Horisberger
Keyword(s):  
Distal Colon ◽  
Loss Of Function ◽  
Newborn Mice ◽  
Α Subunit ◽  
Salt Wasting ◽  
Lung Fluid ◽  
Wasting Syndrome ◽  
Rate Limiting Step ◽  
Γ Subunit ◽  
Rate Limiting

The epithelial Na+ channel (ENaC) controls the rate-limiting step in the process of transepithelial Na+ reabsorption in the distal nephron, the distal colon, and the airways. Hereditary salt-losing syndromes have been ascribed to loss of function mutations in the α-, β-, or γ-ENaC subunit genes, whereas gain of function mutations (located in the COOH terminus of the β- or γ-subunit) result in hypertension due to Na+ retention (Liddle’s syndrome). In mice, gene-targeting experiments have shown that, in addition to the kidney salt-wasting phenotype, ENaC was essential for lung fluid clearance in newborn mice. Disruption of the α-subunit resulted in a complete abolition of ENaC-mediated Na+ transport, whereas knockout of the β- or γ-subunit had only minor effects on fluid clearance in lung. Disruption of each of the three subunits resulted in a salt-wasting syndrome similar to that observed in humans.

scholarly journals Bv8-Like Toxin from the Frog Venom of Amolops jingdongensis Promotes Wound Healing via the Interleukin-1 Signaling Pathway

Toxins ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 15 ◽  
Author(s):  
Jiajia Chang ◽  
Xiaoqin He ◽  
Jingmei Hu ◽  
Peter Muiruri Kamau ◽  
Ren Lai ◽  
...  
Keyword(s):  
Wound Healing ◽  
Signaling Pathway ◽  
Wide Spectrum ◽  
Interleukin 1 ◽  
Full Thickness ◽  
Mice Model ◽  
Small Peptides ◽  
Newborn Mice ◽  
Proliferative Effect ◽  
Inflammatory Phase

Prokineticins are highly conserved small peptides family expressed in all vertebrates, which contain a wide spectrum of functions. In this study, a prokineticin homolog (Bv8-AJ) isolated from the venom of frog Amolops jingdongensis was fully characterized. Bv8-AJ accelerated full-thickness wounds healing of mice model by promoting the initiation and the termination of inflammatory phase. Moreover, Bv8-AJ exerted strong proliferative effect on fibroblasts and keratinocytes isolated from newborn mice by activating interleukin (IL)-1 production. Our findings indicate that Bv8 is a potent wound healing regulator and may reveal the mechanism of rapid wound-healing in amphibian skins.

scholarly journals Intermittent hypoxia inhibits mandibular cartilage growth with reduced TGF-β and SOX9 expressions in neonatal rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kochakorn Lekvijittada ◽  
Jun Hosomichi ◽  
Hideyuki Maeda ◽  
Haixin Hong ◽  
Chidsanu Changsiripun ◽  
...  
Keyword(s):  
Bone Mineral ◽  
Intermittent Hypoxia ◽  
Hyaline Cartilage ◽  
Body Weight Gain ◽  
Mandibular Condyle ◽  
Neonatal Rats ◽  
Sprague Dawley ◽  
Cartilage Growth ◽  
Condylar Cartilage ◽  
Sprague Dawley Rats

AbstractIntermittent hypoxia (IH) has been associated with skeletal growth. However, the influence of IH on cartilage growth and metabolism is unknown. We compared the effects of IH on chondrocyte proliferation and maturation in the mandibular condyle fibrocartilage and tibial hyaline cartilage of 1-week-old male Sprague–Dawley rats. The rats were exposed to normoxic air (n = 9) or IH at 20 cycles/h (nadir, 4% O2; peak, 21% O2; 0% CO2) (n = 9) for 8 h each day. IH impeded body weight gain, but not tibial elongation. IH also increased cancellous bone mineral and volumetric bone mineral densities in the mandibular condylar head. The mandibular condylar became thinner, but the tibial cartilage did not. IH reduced maturative and increased hypertrophic chondrocytic layers of the middle and posterior mandibular cartilage. PCR showed that IH shifted proliferation and maturation in mandibular condyle fibrocartilage toward hypertrophic differentiation and ossification by downregulating TGF-β and SOX9, and upregulating collagen X. These effects were absent in the tibial growth plate hyaline cartilage. Our results showed that neonatal rats exposed to IH displayed underdeveloped mandibular ramus/condyles, while suppression of chondrogenesis marker expression was detected in the growth-restricted condylar cartilage.

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