The prognosis of LCNEC is poor. To improve the outcome, we must evaluate the effectiveness of adjuvant or neoadjuvant therapy in patients with resectable disease. In addition, the evaluation of systemic and multimodality treatment strategies similar as in small cell lung cancer is worthy of consideration.

No abstract

No abstract

Effect of L-5-HTP (L-5-hydroxytryptophane) on the release of human growth hormone (HGH), thyroid stimulating hormone (TSH) and immunoreactive insulin (IRI) was investigated in 7 normal subjects and 25 patients with endocrine disorders. A single oral dose of 200mg of L-5-HTP showed the elevation of HGH in plasma; however, no release of TSH and insulin in plasma of normal subjects. HGH response to L-5-HTP administration was less in quantity as compared with HGH respone to insulin hypoglycemia or arginine infusion. The timing of HGH respone to L-5-HTP was quite variable (between 30 and 120min) in an oral dose of L-5-HTP. No release of HGH by L-5-HTP administration was observed in each of the patients with primodial dwarfism, panhypopituitarism, pituitary dwarfism, and some cases of hypothyroidism. The effect of hyperglycemia or sedative on the release of HGH induced by L-5-HTP was observed. HGH release by L-5-HTP was not observed in these treatments of glucose or diazepam, therefore it might suggest that HGH release by L-5-HTP was inhibited by hyperglycemia or diazepam administration. Suppression of TSH release by L-5-HTP dose was noticed in some patients with hypothyroidism; however no effect in normal subjects. Neither elevation nor reduction of IRI was observed by the L-5-HTP oral dose in normal subjects. These findings suggested that L-5-HTP might induce the release of HGH from normal pituitary gland, that the release of TSH might be reduced by the dose of L-5-HTP in the patients with hypothyroidism, but not in normal subjects, and that IRI was not affected by the dose of L-5-HTP in normal subjects.

We estimated defensins, antimicrobial and cytotoxic peptides localized in azurophil granules of neutrophils, in bronchoalveolar lavage fluid (BALF) in patients with diffuse panbronchiolitis (DPB). BALF from DPB patients contained a higher concentration of defensins than those from patients with idiopathic pulmonary fibrosis and healthy volunteers. A significant correlation was observed between the concentration of defensins and the number of neutrophils, the concentration of interleukin-8 or neutrophil elastase in BALF of DPB patients. An immunohistochemical defensins in neutrophils and mucinous exudates in the airways and in the surface of bronchiolar epithelial cells. After treatment with macrolide antibiotics, significant reductions in the concentrations of defensins, IL-8 and neutrophil numbers in BALF of DPB patients were observed. These findings suggest that the lung injury in DPB could be caused by defensins released by neutrophils accumulated in the airways.