Detection of Chlamydia trachomatis in the prostate by in-situ hybridization and by transmission electron microscopy.

Chlamydia trachomatis infection has been investigated in the prostate gland using in-situ DNA hybridization and transmission electron microscopy. Sixty-four samples of tissue removed by trans-urethral resection or by open surgery from men with benign prostatic hypertrophy (BPH), were examined histologically and 20 of the cases were found to be positive for mononuclear cell infiltration. Some samples were then investigated using in-situ hybridization and transmission electron microscopy. Out of 20 tissue samples with mononuclear cell infiltration, nine were found to be positive for C. trachomatis infection.

[Detection of Chlamydia trachomatis in chronic prostatitis by in situ hybridization (preliminary methodical report)]. / Chlamydia trachomatis kimutatása in situ hibridizációval krónikus prostatitisben (metodikai elözetes közlemény).

(Preliminary methodical report). In situ hybridization of Chlamydia trachomatis in formalin fixed, paraffin embedded specimens from the Urology Clinic were performed in 2nd Department of Pathology Semmelweis University of Medicine by a biotin labelled DNA probe. Chlamydia trachomatis is suspected to be responsible for the chronic abacterial inflammation of the prostate besides Ureaplasma urealyticum and Mycoplasmae. According to our retrospective study out of 79 biopsy specimens 34 had the diagnosis of chronic abacterial prostatitis. We examined 11 specimens of them. Bacteria were not identified. Three specimens were positive for Chlamydia trachomatis which were improved by transmission electron microscope. The age of patients was between 59 and 81 years. The detection of chlamydia infection rises the suspicion of a "healthy" career and especially at younger age could cause Chlamydia trachomatis associated genital disease. The undiagnosed and untreated diseases may lead to infertility.

Ultrastructural study of a black insulinoma.

A case of black insulinoma is reported. The color was due to a cytoplasmic pigment. Immunostaining for neuron-specific enolase and chromogranin was positive in the tumor cells, and the pigment granules themselves reacted with the chromogranin antibody. Numerous beta cell type dense core granules as well as atypical granules were found by electron microscopy. An important finding was that the dense core granules contribute to the lipofuscin pigment formation.

Attachment of ribosomes to endoplasmic membranes in mouse pancreas. Degranulation in vivo caused by the inducers of autophagocytosis neutral red, vinblastine, puromycin, and cadmium ions, and prevention by cycloheximide.

The present investigation was undertaken to discover whether in vivo inducers of autophagocytosis such as neutral red (0.40 mg/g body weight), cadmium chloride (0.15 mg/animal), vinblastine sulfate (7.5 mg/kg b.w.), and puromycin dihydrochloride (0.20 mg/g b.w.) are able to produce degranulation of rough surfaced endoplasmic reticulum (ER) of pancreatic acinar cells as we suggested earlier. Using a modified method of Blobel and Potter about 30% of the total ribosomes of untreated control pancreas were recovered in the free form, and 70% in the membrane-bound form. Cycloheximide (0.20 mg/g body weight) had no effect on this distribution of ribosomes, while neutral red, cadmium ions, vinblastine, and puromycin led to the presence of more free ribosomes: thus up to 70% of the total cytoplasmic ribosomes were recovered in the free form 30 to 60 min after treatments with the autophagic inducers. Pretreatments with cycloheximide prevented this shift and the distribution of ribosomes remained normal. On the basis of these and previous results we conclude that in pancreas an initial degranulation of the ER caused by these agents is a precondition of membrane transformation in autophagocytosis which is preventable by cycloheximide. Confirming the ultrastructural data of Longnecker et al. on rat pancreas, puromycin was shown to cause different forms of cellular injury including autophagocytosis. All forms of cellular injury were also prevented by pretreatment with cycloheximide in mouse pancreas.