One-Month-Old Rabbits Exhibit a Longer Postoperative Remodeling in Extraocular Muscles Compared to 3-Month-Old Rabbits.

Purpose: To explore whether there is a difference in postoperative extraocular muscle (EOM) remodeling between 1-month-old and 3-month-old rabbits.

Methods: Recession (n = 16) and resection (n = 16) were performed on the right superior rectus (SR) muscles of 1-month-old and 3-month-old rabbits. SR tissues were harvested 1 and 4 weeks post-surgery (n = 4 for each group), and mid-belly sections were used to assess myosin heavy chain (MyHC) isoform expression (fast 2X, embryonic, and neonatal MyHCs), activated satellite cells (SCs), and centrally nucleated myofibers.

Ocular trauma from Lawn mower accidents: Clinical insights, visual outcomes and microbial profiles.

Aims: To characterize the clinical features of ocular trauma resulting from lawn mower, identify determinants of unfavorable final visual acuity (FVA), and assess the spectrum of microbial in posttraumatic endophthalmitis.

Methods: This retrospective study enrolled patients who experienced ocular trauma due to lawn mower at Zhongshan Ophthalmic Center from January 2013 to August 2021. Demographics, clinical features, isolated microorganisms, risk factors influencing reduced visual acuity, treatment regimens, and utilization of eyewear were collected.

Effect of Kaempferol on the Biological Behavior of Human Colon Cancer via Regulating MMP1, MMP2, and MMP9.

Kaempferol is a kind of flavonoid, which has a significant anticancer effect. MMPs were discovered with the function of cleaving the extracellular matrix. We utilized bioinformatics to analyze the association and bonding mode between the traditional Chinese medicine (TCM) monomer composition (i.

Simple and rapid determination of homozygous transgenic mice via in vivo fluorescence imaging.

Setting up breeding programs for transgenic mouse strains require to distinguish homozygous from the heterozygous transgenic animals. The combinational use of the fluorescence reporter transgene and small animal in-vivo imaging system might allow us to rapidly and visually determine the transgenic mice homozygous for transgene(s) by the in vivo fluorescence imaging. RLG, RCLG or Rm17LG transgenic mice ubiquitously express red fluorescent protein (RFP).

Plasma arginine metabolites reflect airway dysfunction in a murine model of allergic airway inflammation.

L-arginine metabolism is important in the maintenance of airway tone. Shift of metabolism from the nitric oxide synthase to arginase pathways contributes to the increased airway responsiveness in asthma. We tested the hypothesis that systemic levels of L-arginine metabolites are biomarkers reflective of airway dysfunction.

Multitracer stable isotope quantification of arginase and nitric oxide synthase activity in a mouse model of pseudomonas lung infection.

Cystic fibrosis airways are deficient for L-arginine, a substrate for nitric oxide synthases (NOSs) and arginases. The rationale for this study was to quantify NOS and arginase activity in the mouse lung. Anesthetized unventilated mice received a primed constant stable isotope intravenous infusion containing labeled L-arginine, ornithine, and citrulline.

Lung arginase expression and activity is increased in cystic fibrosis mouse models.

The activity of arginase is increased in airway secretions of patients with cystic fibrosis (CF). Downstream products of arginase activity may contribute to CF lung disease. We hypothesized that pulmonary arginase expression and activity would be increased in mouse models of CF and disproportionally increased in CF mice with Pseudomonas aeruginosa pneumonia.

Effect of arginase inhibition on pulmonary L-arginine metabolism in murine Pseudomonas pneumonia.

Rationale: Infection of the lung with Pseudomonas aeruginosa results in upregulation of nitric oxide synthases (NOS) and arginase expression, and both enzymes compete for L-arginine as substrate. Nitric oxide (NO) production may be regulated by arginase as it controls L-arginine availability for NOS. We here studied the effect of systemic arginase inhibition on pulmonary L-arginine metabolism in Pseudomonas pneumonia in the mouse.

Asymmetric dimethylarginine is increased in asthma.

Rationale: Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase (NOS) inhibitor that competes with L-arginine for binding to NOS. It has been suggested that ADMA contributes to inflammation, collagen deposition, nitrosative stress, and lung function in murine models.

Objectives: To test the hypothesis that ADMA is increased in asthma and that NOS inhibition by ADMA contributes to airways obstruction.

Fog2 is required for normal diaphragm and lung development in mice and humans.

Congenital diaphragmatic hernia and other congenital diaphragmatic defects are associated with significant mortality and morbidity in neonates; however, the molecular basis of these developmental anomalies is unknown. In an analysis of E18.5 embryos derived from mice treated with N-ethyl-N-nitrosourea, we identified a mutation that causes pulmonary hypoplasia and abnormal diaphragmatic development.

Interacting genetic loci cause airway hyperresponsiveness.

Airway hyperresponsiveness (AHR) is a key physiological component of asthma, and the genetic basis of this complex trait has remained elusive. We created recombinant congenic mice with increased naive AHR by serially backcrossing A/J mice (which have elevated naive AHR) with C57BL/6J mice and selecting for mice with an elevated naive AHR phenotype. The seventh backcross-generation hyperresponsive mice retained A/J loci in three regions.

Modulation of inducible nitric oxide synthase by hypoxia in pulmonary artery endothelial cells.

The effects of hypoxia on the regulation of inducible nitric oxide synthase (NOS) 2 expression were examined in cultured rat pulmonary microvascular endothelial cells (EC). EC did not express NOS 2 mRNA or protein when exposed to normoxia or hypoxia unless they were pretreated with interleukin (IL)-1beta and/or tumor necrosis factor (TNF)-alpha for 24 h. Induction of NOS 2 by IL-1beta+TNF-alpha was significantly attenuated by concomitant exposure of EC to hypoxia or treatment of EC with antioxidants such as tiron, diphenyliodonium, and catalase, suggesting that NOS 2 expression is dependent on the production of reactive oxygen species.