Pulmonic stenosis caused by a malignant tumore of the heart.
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Biomedical subjects
Publications and source records attributed to J de Koning.
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Ten patients with chronic Yersinia enterocolitica infections are described. The initial diagnosis was made by culture, significant agglutinin titres and indirect immunofluorescence (IF) on biopsies. During the chronic phase, culture and agglutinin titres were negative, but specific serum IgA and IgG antibodies reactive with at least two, i.e. the 36 kDa and the 46 kDa, virulence-associated released proteins were demonstrated in nine patients by immunoblot techniques. One patient had only IgG antibodies. The chronically elevated IgA production was the result of chronic stimulation of the gut-associated lymphoid tissue by virulent persistent Yersinia antigen, which was identified by IF with O-specific antiserum and monospecific antiserum to the 46 kDa released protein in biopsies. Virulent Yersinia bacilli were demonstrated in the intestinal mucosa and in the lymphoid tissue of the submucosa associated with macrophages in patients with chronic ileitis and arthritis, in granulomatous centres of lymph nodes in patients with chronic lymphadenopathy and in portal infiltrates in a patient with chronic hepatitis. Recognition of persistent Yersinia infections may have therapeutic implications.
The IgA and IgG antibody response to plasmid-encoded outer membrane proteins was studied in 59 patients with yersinia-associated spondylarthropathy during 15 months of follow-up. Initially, all patients had specific IgA and IgG antibodies to the 36 and 46 kDa and 30% also to the 26 and 58 kDa released proteins, which correlated with the finding of virulent Yersinia bacilli in intestinal biopsies. IgA disappeared in 69% of untreated patients after nine months and persisted in 31% after one year. IgA disappeared within three to six months in 81% of the patients treated with antibiotics for four to six weeks and persisted in 6% after one year (p less than 0.002). IgG antibodies to the 36 and 46 kDa outer membrane proteins persisted in 80% of all patients. Disappearance of IgA was coupled with disappearance of yersinia from intestinal biopsies.
Anterior pituitary glands of intact diestrous and gonadectomized female rats were incubated with a supramaximally active dose of LH-RH. Puromycin (P) and cycloheximide (C) did not consistently affect the LH release from glands of ovariectomized rats. In intact rats, LH release induced by LH-RH occurred in two phases, an initial one (relatively slow rate of release) and a secondary one (high rate of release). P and C had no effect on the initial phase, but prevented the secondary one. Pre-incubation with LH-RH prevented the effect of P and C added after 4 hours. Since P and C did not affect the total amount of LH present in media and hypophyses, the LH-released during the P- and C-sensitive phase is not newly formed LH. It is concluded that LH-RH induces the synthesis of protein which is necessary for LH-RH-induced LH release. The initial phase of LH release is made possible by protein already present in the glands at the beginning of the experiment.
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