Potentiated anti-inflammatory effect of combined 780 nm and 660 nm low level laser therapy on the experimental laryngitis.

Reflux laryngitis is a common clinic complication of nasogastric intubation (NSGI). Since there is no report concerning the effects of low level laser therapy (LLLT) on reflux laryngitis, this study aimed to analyze the protective effect of single and combined therapies with low level laser at the doses of 2.1J and 2.1+1.2 J with a total irradiation time of 30s and 30+30 s, respectively, on a model of neurogenic reflux laryngitis. NSGI was performed in Wistar rats, assigned into groups: NGI (no treatment), NLT17.5 (single therapy), and NLT17.5/10.0 (combined therapy, applied sequentially). Additional non-intubated and non-irradiated rats were use as controls (CTR). Myeloperoxidase (MPO) activity was assessed by colorimetric method after the intubation period (on days 1, 3, 5, and 7), whereas paraffin-embedded laryngeal specimens were used to carry out histopathological analysis of the inflammatory response, granulation tissue, and collagen deposition 7 days after NSGI. Significant reduction in MPO activity (p<0.05) and in the severity of the inflammatory response (p<0.05), and improvement in the granulation tissue (p<0.05) was observed in NLT17.5/10.0 group. Mast cells count was significantly decreased in NGI and NLT17.5 groups (p<0.001), whereas no difference was observed between NLT17.5/10.0 and CTR groups (p>0.05). NLT17.5/10.0 group also showed better collagenization pattern, in comparison to NGI and NLT17.5 groups. This study suggests that the combined therapy successfully modulated the inflammatory response and collagenization in experimental model of NSGI-induced neurogenic laryngitis.

[Detection of serum fucosidase activity].

A procedure has been developed for simultaneous determination of the activity of a-L-fucosidase (EC 3.2.1.5 1) and the beta-D-fucosidase activity caused by beta-D-galactosidase (EC 3.2.1.23, Form IV) in serum. The paper presents data on changes in the above serum enzymatic activities in an experiment, in children with recurrent laryngotracheitis and in pregnant females with gestosis and placental insufficiency.

COX-2 inhibitors celecoxib and rofecoxib prevent oxidative DNA fragmentation.

BACKGROUND: Cyclooxygenase (COX) is the key regulatory enzyme in prostaglandin (PG) synthesis and is up-regulated in many premalignant and malignant lesions. The aim of this study was to investigate the in vitro DNA protective or damaging effects of COX-2 inhibitors using the single-cell gel electrophoresis (Comet) assay. MATERIALS AND METHODS: Cells from miniorgan cultures of pharyngeal mucosa from 30 patients were incubated once or five times with the COX-2 inhibitors celecoxib and rofecoxib. After treatment with H2O2, DNA fragmentation was determined. RESULTS: DNA strand-breaks were significantly reduced in cells pre-incubated with COX-2 inhibitors. Repeated incubation with celecoxib showed the strongest effect. This direct influence on DNA repair could be excluded by implementing DNA repair steps into the Comet assay. CONCLUSION: The findings suggest that, in addition to the known influence of COX-2 inhibitors on immune surveillance, neo-angiogenesis and cell proliferation, these substances may express a direct antimutagenic effect in conditions of oxidative stress.

Elevated creatine phosphokinase and creatine phosphokinase-MB in acute laryngitis.

Elevated creatine phosphokinase (684 mU/ml) and creatine phosphokinase-MB (3.5%, 23.9 mU/ml) were observed in a 66 year old female with acute laryngitis. The patient had received L-thyroxine because of hypothyroidism for 10 years and her T3 and TSH levels were normal. Acute myocardial infarction was denied by repeated EKG findings. The mechanisms of the enzyme abnormality were discussed.

[Smoking and induction of the enzyme aryl hydrocarbon hydroxylase in patients with laryngeal carcinomas and precancerous conditions]. / Rauchen und Induktion des Enzyms Arylhydroxkarbonhydroxylase bei Patienten mit Karzinomen und Präkanzerosen des Larynx.

The risk for a smoker of developing cancer of the larynx depends on the activity of the enzyme arylhydroxcarbonhydroxylase in his cells. The higher the genetically determined arylhydroxcarbonhydroxylase activity, the higher is the probability of developing the disease.