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Biomedical subjects

C Mohn

Publications and source records attributed to C Mohn.

7 recordsLinked to original sources
PubMed2003

Interaction among beta-endorphin, nitric oxide and prostaglandins during ovulation in rats.

The aim of this study was to investigate the relationship between beta-endorphin and nitric oxide (NO) during the ovulatory process in rats. Immature rats were treated with equine chorionic gonadotrophin-hCG to induce ovulation. An intrabursal injection of beta-endorphin stimulated nitric oxide synthase (NOS) activity. This effect was completely reversed when naltrexone was co-injected with beta-endorphin. The stimulatory action of beta-endorphin on NOS activity was studied to determine whether it was exerted via prostaglandins. Treatment with prostaglandin E(2) (PGE(2)) completely reversed the beta-endorphin-induced stimulation of NOS activity. Moreover, intrabursal injection of meloxicam, an inhibitor of cyclooxygenase 2, increased NOS activity, but this effect was not altered by co-injection with beta-endorphin. The presence of both endothelial NOS (eNOS) and inducible NOS (iNOS) in the ovary at 10 h after hCG treatment was studied by western blot analysis. Local administration of beta-endorphin inhibited the expression of eNOS protein, whereas expression of iNOS protein was not detectable. Ovarian beta-endorphin content was diminished at 10 h after hCG injection. Treatment with prostaglandin synthesis inhibitors in vivo augmented the ovarian beta-endorphin content. In conclusion, these results indicate that beta-endorphin stimulates the activity of ovarian NOS indirectly by inhibiting prostaglandin production.

Animals↗
PubMed2001

Inhibition of salivary secretion by lipopolysaccharide: possible role of prostaglandins.

Inducible (calcium-independent) nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) are important in the regulation of the function of different organs during infection. A single dose of lipopolysaccharide (LPS; 5 mg/kg ip) within 6 h increased NOS activity (20%) and prostaglandin E (PGE) content (100%) in submandibular glands (SMG) and blocked stimulated salivary secretion in adult male rats. The administration of an iNOS synthesis inhibitor, aminoguanidine (AG), with LPS decreased NOS activity and PGE content. Furthermore, the administration of meloxicam (MLX), an inhibitor of COX-2, blocked the increase in PGE and the production of NO. The incubation of slices of SMG in the presence of 3-morpholinosydnonimine, a donor of NO, increased the release of PGE highly significantly. The incubation of SMG in the presence of a PGE(1) analog (alprostadil) increased the production of NO. These results indicate that LPS activates NOS, leading to NO release, which activates COX, generating PGEs that act back to further activate NOS, causing further generation of PGEs by activation of COX. Because the alprostadil administration inhibited stimulated salivation, LPS-induced inhibition of salivation appears to be caused by increased PGE production. Diminished salivary secretion produces poor oral health; thus the use of COX-2 inhibitors to counteract the effects of inhibited salivation should be considered.

Alprostadil↗
PubMed2001

Effects of aminoguanidine and meloxicam on nitric oxide and prostaglandin E production induced by lipopolysaccharide in the hypothalamus and anterior pituitary of the rat.

BACKGROUND/OBJECTIVE: Injection of bacterial lipopolysaccharide (LPS) into male rats activates genes that in turn induce many enzymes that participate in the animals' response to LPS. There is induction of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) in many tissues. This induction could result from combination with cell surface LPS receptors that directly induce both genes, or the nitric oxide (NO) released as a result of iNOS induction could induce COX-2. METHODS: To distinguish between these two possibilities, specific inhibitors of iNOS and COX-2 activity, aminoguanidine (AG) and meloxicam (MLX), respectively, were injected either peripherally or intracerebroventricularly (i.c.v.), and their effect on NO and prostaglandin E (PGE) production induced by LPS in the medial basal hypothalamus (MBH) and anterior pituitary gland (AP) were determined. RESULTS: Peripheral injection of AG blocked iNOS-derived NO production in the AP but not in the MBH. When AG was injected i.c.v., iNOS-derived NO production in the MBH was blocked. MLX injected peripherally blocked COX-2-derived PGE(2) production in the MBH and AP, whereas AG injected peripherally or i.c.v. was ineffective. Since AG was only effective in blocking iNOS-derived NO production in the MBH when injected i.c.v., AG apparently does not effectively cross the blood brain barrier, whereas MLX injected peripherally inhibited PGE production, probably by inhibiting COX-2 activity in both the MBH and AP. AG was ineffective in preventing the increase in PGE derived from COX-2 in either the MBH or AP. CONCLUSION: LPS directly induces both enzymes, iNOS and COX-2, in the hypothalamus and AP.

Animals↗
PubMed1999

[Secondary longitudinal melanonychia secondary to onychophagia].

BACKGROUND: Melanonychia of the toenails sometimes results from repeated trauma. This etiology is rarely put forward in lesions affecting the fingernails. CASE REPORT: A 44-year-old woman developed melanonychia affecting 9 fingernails. Genetic predisposition and drug, hormonal or infectious causes were ruled out and we postulated that the lesions were induced by nail biting. DISCUSSION: Nail biting is known to lead to several types of lesions, including melanonychia. The lesions may sometimes disappear several months after stopping this habit.

Adult↗
PubMed1998

[Chronic depigmentation due to positive patch tests for methacryate derivatives].

INTRODUCTION: Many chemical products are known to induce depigmentation. This phenomenon was never reported with methacrylates which are components of acrylic resine. CASE REPORT: A female patient with artificial nails developed contact dermatitis. Localized depigmentation at the site of positive patch tests to methacrylates derivatives was observed. DISCUSSION: The chemical substance could have a direct influence either by its toxic effect or by the induced inflammatory reaction.

Adult↗
PubMed1997

Bilateral condylar movement patterns in adult subjects.

The purpose of this study was to determine if there was a difference between the temporomandibular condylar movement patterns of a symptomatic adult population and those of an asymptomatic adult population. Thirty-five volunteers who were not seeking treatment for TMD underwent two different assessments for TMD signs and symptoms: (1) a self-administered questionnaire and (2) a clinical examination. Based on the information obtained from the questionnaires, subjects were divided into "reported-symptomatic" and "reported-asymptomatic" groups. Based on the investigator's clinically evaluation of the same subjects, subjects were divided into "clinically symptomatic" and "clinically asymptomatic" groups. To compare condylar movement patterns, both groups of subjects then had their mandibular border condylar movements measured bilaterally using a sagittal recording device during maximum opening, maximum protrusion, and maximum left and right excursion movements. The patterns were separated into two broad groups, "symmetric" and "asymmetric." Symmetric gliding movements were defined as uninterrupted bilaterally mirror-like patterns of each condyle with a difference between left and right total length excursion not exceeding 2 mm during opening in the sagittal plane or horizontal plane. Our results show that 63% of the subjects who reported clinically asymptomatic for TMD demonstrated asymmetric condylar movements. However, 100% of the patients (n = 5) who reported clinically symptomatic for TMD exhibited asymmetric condylar movements. This finding suggests that, while a very high percentage of TMD subjects will have asymmetric condylar movements, condylar movements alone are not necessarily diagnostic of TMD, and the sagittal recording device may alert the clinician to abnormal movements.

Adult↗