Surfactant Protein A Enhances the Degradation of LPS-Induced TLR4 in Primary Alveolar Macrophages Involving Rab7, β-arrestin2, and mTORC1.

Respiratory infections by Gram-negative bacteria are a major cause of global morbidity and mortality. Alveolar macrophages (AMs) play a central role in maintaining lung immune homeostasis and host defense by sensing pathogens via pattern recognition receptors (PRR). The PRR Toll-like receptor (TLR) 4 is a key sensor of lipopolysaccharide (LPS) from Gram-negative bacteria.

Surfactant Protein A Enhances Constitutive Immune Functions of Clathrin Heavy Chain and Clathrin Adaptor Protein 2.

NF-κB transcription factors are key regulators of pulmonary inflammatory disorders and repair. Constitutive lung cell type- and microenvironment-specific NF-κB/inhibitor κBα (IκB-α) regulation, however, is poorly understood. Surfactant protein (SP)-A provides both a critical homeostatic and lung defense control, in part by immune instruction of alveolar macrophages (AMs) via clathrin-mediated endocytosis.

Dose escalation for metastatic spinal cord compression in patients with relatively radioresistant tumors.

Purpose: Radiotherapy alone is the most common treatment for metastatic spinal cord compression (MSCC) from relatively radioresistant tumors such as renal cell carcinoma, colorectal cancer, and malignant melanoma. However, the results of the "standard" regimen 30 Gy/10 fractions need to be improved with respect to functional outcome. This study investigated whether a dose escalation beyond 30 Gy can improve treatment outcomes.

Radiotherapy for oligometastatic disease in patients with spinal cord compression (MSCC) from relatively radioresistant tumors.

Background: Radiotherapy alone is the most common treatment for metastatic spinal cord compression (MSCC). Patients with relatively radioresistant tumors and oligometastatic disease may benefit from more intensive therapies (surgery, high-precision radiotherapy). If such therapies are not available, one can speculate whether patients benefit from dose escalation beyond the standard regimen 30 Gy in ten fractions.

Inhaled tert-butyl acetate and its metabolite tert-butyl alcohol accumulate in the blood during exposure.

1. A continuous 5 h-exposure to approximately 440 ppm tert-butyl acetate in air (via a tracheal canule) resulted in continuously increasing concentrations of tert-butyl acetate and tert-butyl alcohol (metabolite of tert-butyl acetate) in the blood of rats. 2.

Effects of N,N-dimethylformamide and its degradation products in zebrafish embryos.

The response of zebrafish (Brachydanio rerio) embryos, cultured in reconstituted water, to continuous treatment with N,N-dimethylformamide (DMF) or its degradation products until hatching, was investigated. The embryos were distinctly susceptible to DMF, N-(hydroxymethyl)-N-methylformamide (DMF-OH), N-methylformamide (NMF), N-acetyl-S-(N-methylcarbamoyl)cysteine (AMCC), and formamide (FA). Concentrations of 18 (DMF-OH), 121 (DMF), 163 (AMCC), 186 (NMF) and 203 (FA) mmol/litre produced 50% embryo lethality (LC(50)).

The karyotype of the zebrafish (Brachydanio rerio).

Fertilized eggs of the age of 24 hr from the zebrafish (Brachydanio rerio) were examined. The number of chromosomes is 2n = 50. The size of a metaphase chromosome is 1.

[Blood alcohol in relation to the presence of n-butyl acetate].

Adult female SPF rats (strain: Sprague-Dawley) were treated with 790 mg ethanol/kg body weight by intraperitoneal injection 30 minutes after the beginning of a 5-hr-inhalation of about 1,000 ppm n-butyl acetate in air via a tracheotomy tube (under urethane anesthesia). The elimination of the ethanol from blood which was increased to about 24 mmol/l (1.1%, g/v) was not delayed during the initial linear phase as compared to control (ethanol treatment without inhalation of n-butyl acetate).

Ferrous sulfate combined with ascorbic acid does not significantly reduce acetaldehyde accumulation in the blood of alcoholized rats treated with disulfiram or betalactam antibiotics.

Adult female SPF Sprague-Dawley rats treated orally by gavage with disulfiram (1 g/kg b.wt.) or betalactam antibiotics (3.

Growth of rats during a subchronic intake of the heavy metals Pb, Cd, Zn, Mn, Cu, Hg, and Be.

Adult female SPF Sprague-Dawley rats were given 100 ppm Pb (CH3COO)2, CdCl2, MnCl2, ZnSO4, CuCl, Hg2(NO3)2, or BeSO4 for 91 days with their drinking water. The body weight gain of the rats changed during the 91 days of continuous inclusion of the heavy metal salts. During examination, body weights increased after the daily intake of MnCl2, ZnSO4 or BeSO4, but the other salts of Pb, Cd, Cu, Hg decreased the body weights, each compared with the controls.

Transient renal impairment in rats after oral exposure to diethylene glycol.

Volume, specific gravity, creatinine, lactate dehydrogenase (LDH), leucine aminopeptidase (LAP), beta-galactosidase (GAL), leucocytes, erythrocytes, nitrite, protein (albumin), glucose, ketone, urobilinogen, bilirubin and pH were estimated in urine of rats after single (by gavage) or repeated (via drinking water) oral administration of diethylene glycol (DEG). Following single or repetitive doses (daily over 90 days) of 0.2 g DEG kg-1 body weight, no change in renal function was observed (no effect level).

Stability of isolated hepatic aldehyde dehydrogenases from rats in vitro.

Aldehyde dehydrogenases (ALDH) isolated from livers of adult female SPF Sprague-Dawley rats were rapidly (within hours) inactivated by oxygen (7.8 ppm, from air) and simultaneous exposure to light energy (subdued daylight, 5000 lx; direct sunlight, 66,000 lx) at 22 degrees C. Oxygen withdrawal (e.

Non-competitive inhibition of the alcohol dehydrogenase activity in rat liver by latamoxef, cefamandole or cefoperazone.

High concentrations of 1 or 10 mmol/l latamoxef (LMOX), cefamandole (CMD) or cefoperazone (CPZ) in vitro non-competitively inhibit to a small extent the alcohol dehydrogenase isolated from rat liver in the presence of ethanol as a substrate, as is shown by enzyme-kinetic data evaluated in a Lineweaver-Burk diagram. This observation may serve as an approach to partially explain a possible delay of ethanol elimination from the blood after pretreatment with these beta-lactam antibiotics.

Activities of hepatic epoxide hydrolase and glutathione S-transferase in rats under the influence of tetramethyl thiuramdisulfide, tetramethyl thiurammonosulfide or dimethyl dithiocarbamate.

The epoxide hydrolase (EH) activity in the liver of adult female Wistar rats significantly increased 18 h after the administration by gavage of tetramethyl thiuramdisulfide (TMTD, 1 mmol/kg) or tetramethyl thiurammonosulfide (TMTM, 2 mmol/kg). No increase was observed 5 h after administration of Na-dimethyl dithiocarbamate (Na-DMDTC, 4 mmol/kg). The glutathione S-transferase (GST) activity in the cytosol and microsomes of the liver was slightly enhanced after oral (gavage) administration of TMTD, TMTM or Na-DMDTC (doses up to 4 mmol/kg).

Ethanol-induced accumulation of ethylene glycol monoalkyl ethers in rats.

In adult female SPF Sprague-Dawley rats, exposed for 2 hours to 2-methoxy-ethanol (ME, 1600 ppm), 1-acetoxy-2-methoxy-ethane (AME, 800 ppm), 2-ethoxy-ethanol (EE, 420 ppm), or 1-acetoxy-2-ethoxy-ethane (AEE, 170 ppm) the blood level of ME (after ME or AME) or EE (after EE or AEE) was considerably increased after pretreatment with ethanol (20 mmol/kg b.w. i.

Concentrations of D-glucaric acid in human urine after repeated administration of pyrithioxine.

The urinary excretion of D-glucaric acid in 16 healthy male volunteers, 24 to 66 years of age, was 44 +/- 3 mumol/24 h (25 +/- 2 mumol D-glucaric acid/g creatinine/24 h). Six healthy female volunteers aged 25 to 60 years excreted 42 +/- 5 mumol D-glucaric acid/24 h (30 +/- 3 mumol D-glucaric acid/g creatinine/24 h) in the urine. (The values given are means +/- s.

Delayed ethanol elimination in rats after application of cefamandole or cefoperazone.

Adult female Sprague-Dawley rats received ethanol (2 g/kg b.w., i.