The value of quantitative DNA flow cytometry of testicular fine-needle aspirates in assessment of spermatogenesis: a study of 137 previously maldescended human testes

In order to assess the suitability of DNA flow cytometry of fine-needle aspirates for quantiftring spermatogenesis, the results from DNA flow cytometry were compared to histological evaluation of testicular biopsies taken concomitantly from 171 previously maldescended testes. In 137 of 171 cases, sufficient material for flow cytometric as well as histological evaluation was obtained.
Histological analysis of surgical biopsy specimens revealed spermatogenesis including the spermatid stage in 117 of the 137 gonads. In six of the 117 gonads no haploid cells were found using flow cytometry. On the other hand, surgical biopsies failed to reveal spermatogenesis in five cases in which the corresponding aspirates contained haploid cells. Both methods therefore seem equally sensitive in detection of spermatogenesis.
Other types of histological patterns also corresponded to distinct DNA histograms.
Thus, in 11 of 12 cases with Sertoli-cell-only pattern in all tubules, at least 95% of the cells had a diploid DNA content. Furthermore, predominance of tubules with maturation arrest at the primary spermatocyte level corresponded to an increased proportion of tetraploid cells.
When compared to surgical biopsy, DNA flow cytometry of testiclar fine-needle aspirates is a more objective, easy and rapid method, which is more convenient for the patient. This study has indicatedthat DNA flow cytometry is a suitable method of quantitative assessment of spermatogenesis. One of the first target groups might be men with azoospermia. In such men, DNA flow cytometric analysis of fine-needle aspirates and surgical biopsy are apparently of equal sensitivity in detecting gonads with spermatogenesis. We conclude that DNA flow cytometry may become an alternative method for the quantification of spermatogenesis.     

Conservative treatment for acute rupture of the Achilles tendon

Summary Sixty-six patients with acute ruptures of the Achilles tendon were treated by immobilisation in a plaster cast for 12 weeks. Fifty-seven were followed up for a mean time of 70 months. Four re-ruptures occurred shortly after the initial treatment. Most patients had no or only slight complaints, three had moderate and one severe, problems. The activity level dropped slightly from 5.3 to 5.03 (Tegner score). The results are satisfactory with a low complication rate. The method is an alternative to operative repair, especially in patients declining operation and in those in whom operation or anaesthesia is contraindicated.

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Résumé Soixante-six malades ont fait l'objet d'une étude à long terme concernant le traitement non-chirurgical des ruptures aiguës du tendon d'Achille. Le recul moyen était de 70 mois. Les patients avaient été immobilisés dans un plâtre pendant 12 semaines. 4 ruptures itératives survinrent précocément (6%). La plupart des malades n'avaient pas ou peu de séquelles, trois seulement se plaignaient d'une gêne modérée et 1 d'une gêne importante. Le niveau d'activité avait légérement diminué, de 5.3 à 5.03 (selon le score de Tegner). Les résultats paraissaient satisfaisants dans l'ensemble, avec une taux peu élevé de ruptures itératives ou d'autres complications. La méthode constitue une alternative valable au traitement chirurgical, notamment chez les sujets qui ne veulent pas être opérés ou chez ceux qui présentent des contrindications à l'anesthésie ou à la chirurgie.

     

A simple method of chromosomal analysis for malignant solid tumors.

A case of essential thrombocythemia with a partial deletion of the long arm of chromosome 11, del(11)(q21) as a sole chromosomal anomaly is reported. Rearrangement of chromosome 11 at band 11q21 has been reported in six patients with chronic myeloproliferative disorders: four with post-polycythemic myelofibrosis, one with myelofibrosis with myeloid metaplasia, and one with Ph+ chronic myeloid leukemia in blastic phase. Except for the last patient, all patients had been treated with 32P and/or an alkylating agent prior to cytogenetic examination. This is the first report of the 11q21 abnormality in essential thrombocythemia seen at diagnosis.     

Otitis media in children born to human immunodeficiency virus-infected mothers.

Acute otitis media (AOM) is thought to occur frequently in children infected with human immunodeficiency virus (HIV). We compared experience with AOM of 28 HIV-infected children with that of 33 children who seroreverted to HIV antibody negative status by age 18 months. The mean number of episodes/year of AOM for children who seroreverted decreased from 1.33 in the first year of life to 0.13 in the third year, whereas the mean number of episodes/year in HIV-infected children increased from 1.89 to 2.40. By age 3 years, all HIV-infected children had experienced 1 or more episodes of AOM, and 80% had experienced 6 or more, whereas 75% of children who seroreverted had experienced 1 or more episodes, and none had had 6 or more. HIV-infected children with normal T4 lymphocyte counts had a mean of 1.18 episodes of AOM in the first year of life compared with 2.35 episodes in HIV-infected children with decreased counts (P = 0.023). HIV-infected children with low counts had a nearly 3-fold increased risk of recurrent AOM (47% vs. 18%).     

Lack of effect of recombinant human interferon-alpha 2b on expression of 17-1A antigen on human colon cancer cells.

The effects of recombinant human interferon alpha (rHuIFN-alpha 2b) on cell growth, expression of antigenic receptor sites (r) and the affinity constant (Ka) of monoclonal antibody CO 17-1A IgG were studied on two human colorectal cancer cell lines, CX-1 and SW 1116. Cells were incubated with varying concentrations of rHuIFN-alpha 2b prior to exposure to 125I-labeled 17-1A IgG at 37 degrees C following which r and Ka were determined by means of Scatchard plots. Varying concentrations of rHuIFN-alpha 2b had significant growth inhibitory effects on CX-1 and SW 1116 cells, which were time and concentration dependent, but no effects on expression of r and Ka compared to controls. Our data indicate that rHuIFN-alpha 2b does not invariably increase the expression of tumor-associated antigens and that this effect may be independent of its antiproliferative activity. The in vitro response or lack thereof of neoplastic cells to rHuIFN-alpha 2b may be useful to identify those patients who potentially might gain from a clinical course of rHuIFN-alpha 2b for either therapeutic or diagnostic purposes.     

A case of congenital antithrombin II deficiency with pulmonary infarction

A 48-year-old woman was admitted because of increased bloody sputum. Since she had had a history of repeated thrombotic episodes including venous thrombosis in the lower limbs (21 year old) and pulmonary emboli developing into pulmonary infarction (41 years old), the patient was treated with anti-coagulant therapy using Warfarin for 7 years. Warfarin was discontinued after admission and heparin was administered instead at a relatively low dose of 5,000 units daily, resulting in a considerable diminution of hemoptysis. Unfortunately however, it caused a relapse of active thrombosis associated not only with a significant increase of the product of fibrinolysis (FDP), LDH and GOT but with a concomitant decrease of the platelet count. Hematological examinations concerning coagulation and fibrinolysis remained within a normal range except for the serum concentration of antithrombin III (AT III) and its functional property with regard to the heparin cofactor, which were 8.8 mg/dl and 48%, respectively. Since the findings were consistent with congenital deficiency of AT III, some members of her family were also examined. The concentration of AT III and its activity in the patient's son and her daughter deteriorated in a similar manner, indicating that this was a definite case of congenital deficiency of AT III. The clinical manifestations of 87 cases with congenital AT III deficiency, belonging to 24 families reported in Japan were reviewed.     

Hereditary protein C deficiency and portal-vein thrombosis

Inherited defects of the natural coagulation inhibitors predispose patients to thrombosis. These disorders have similar clinical presentations with a strong family history of thrombosis, episodes of recurrent venous thromboembolism, beginning in early adulthood. We report a case of upper gastrointestinal bleeding in a patient with portal hypertension due to portal-vein thrombosis secondary to hereditary protein C deficiency, an association that has seldom been reported.     

Effect of supplementation with water-soluble vitamins on erythrocyte alanine aminotransferase activity of healthy adolescents

The erythrocyte alanine aminotransferase (E-ALAT) activity with and without in vitro stimulation by pyridoxal phosphate of 60 healthy adolescents was measured before and after 6 weeks of supplementation with different water-soluble vitamins. The subjects who were divided into six groups received placebo (lactose tablets), pyridoxine, pyridoxine + ascorbic acid, pyridoxine + iron, pyridoxine + riboflavin and multivitamin supplements, respectively. Presupplementation E-ALAT activity increased significantly (p less than 0.05) for all supplemented subjects after 6 weeks. Deficient subjects (E-ALAT) index less than 1.16) however failed to respond to a combination of pyridoxine + ascorbic acid or multivitamins. It is suggested that pyridoxine in multivitamin preparations must exceed 1 mg to produce any useful improvement in vitamin B6 status of adolescents on suboptimal vitamin B6 intakes.