[Stress and fertility].

In Western countries, sperm quality and fertility of men significantly worsened. Female infertility does not show a better trend either. Subtle defects in the reproductive functions can not be explained by the current methods, and "unexplained infertility" is becoming a more common diagnosis.

Inappropriate angiogenic response as a novel mechanism of duodenal ulceration and impaired healing.

Background: Despite recent advances and better understanding of the etiology and the pathogenesis of gastrointestinal ulcer diseases, e.g., duodenal ulcer, the molecular events leading to ulcer development, delayed healing, and recurrence remain poorly elucidated.

Cosegregation of gastrointestinal ulcers and schizophrenia in a large national inpatient discharge database: revisiting the "brain-gut axis" hypothesis in ulcer pathogenesis.

The lifetime prevalence of duodenal ulcer in the United States is 8 to 10%, whereas another 1% of the population is affected by gastric ulcer. Both central and peripheral dopamine pathways may influence ulcer pathogenesis. Dopamine agonists prevent whereas antagonists augment stress- and chemically induced gastrointestinal ulcers in preclinical models.

New molecular mechanisms of duodenal ulceration.

Stress is a major etiologic factor in the pathogenesis of gastric and duodenal ulceration, as first described in rats by Hans Selye. In patients with "peptic ulcers" duodenal ulcers are more frequent than gastric ulcers (except in Japan). Thus, our research during the last three decades focused on the molecular mechanisms of duodenal ulcer in rodent models of chemically induced duodenal ulceration, and here we review our three recent findings: Endothelins (ET-1), the immediate early gene egr-1 and imbalance of angiogenic/antiangiogenic molecules.

Suppression of early growth response factor-1 with egr-1 antisense oligodeoxynucleotide aggravates experimental duodenal ulcers.

Previously, we demonstrated that cysteamine releases endothelin-1 in the rat duodenal mucosa, followed by increased expression of early growth response factor-1 (egr-1). We hypothesized that egr-1 is a key mediator gene in the multifactorial mechanisms of duodenal ulcer development and healing because its protein, transcription factor product Egr-1, regulates the expression of angiogenic growth factors. We wanted to determine the effect of egr-1 antisense oligonucleotide on cysteamine-induced duodenal ulcers as well as on the expression of bFGF, PDGF, and VEGF, of which synthesis is modulated by Egr-1.