A case of acute hepatitis E associated with multidrug hypersensitivity and cytomegalovirus reactivation

A 65-year-old Japanese man was hospitalized because of acute hepatitis and severe cholestasis due to hepatitis E virus (HEV) infection combined with a drug reaction to a cold preparation. He died of disseminated intravascular coagulation and severe intestinal bleeding due to systemic cytomegalovirus reactivation following the development of severe eruptions with marked eosinophilia due to drug hypersensitivity to taurine and ursodeoxycholate preparations. The close interaction between viral infection or reactivation and drug hypersensitivity was considered as a pathophysiology in this case, which emphasizes the need for further study of the immunological mechanism of the interaction.     

Right ventricular thrombosis due to familial heparin cofactor II deficiency

This case report was with regard to familial heparin cofactor II (HC II) deficiency. The patient was a 14-years-old female, having complaints of chest pain, fever and swelling of right lower extremity. Echocardiography and DSA showed a pediculated mass at the right ventricular outflow tract which highly suggested a ventricular myxoma. At surgery, a large pediculated thrombus was removed from the RV conus septum aun pulmonary valve. The mass was identified as thrombus by histological examination. Two months later, the RV thrombi recurred with additional pulmonary embolus to the left lung. HC II was discovered by hemo-coagulation tests. Her HC II antigen value was 48%, and 32% on repeat study. Her brother's HC II antigen value was 53%. At reoperation, small thrombi less than phi 10 mm, were removed from the RV outflow tract and pulmonary valve. Fresh frozen plasma was given and intravenous urokinase therapy was taken. She is doing well with therapy of oral warfarin, aspirin and ticlopidine for anticoagulation.     

Hypoplasia of the humeral trochlea

Radiographic studies of three cases of hypoplasia of the humeral trochlea were done. Several other anomalies were also detected, including a hypoplastic capitellum in case 2, a hyperplastic radial head in cases 2 and 3, and bulging of the loose joint capsule in case 3. Operations in cases 1 and 3, disclosed that ganglions and fibrous septa compressed the ulnar nerve. The cause of ulnar nerve palsy in patients with hypoplasia of the humeral trochlea is thought to be associated with the high incidence of ganglions in hypoplastic elbow joints. The ganglion may play a role.     

Projections of supraspinal structures to the phrenic motor nucleus in cats studied by a horseradish peroxidase microinjection method

The activity of phrenic motor neurons is influenced by the cardiovascular control system of the supraspinal structures. In order to obtain the basic data for analyzing the anatomical relations between the cardiovascular and the pulmonary control system, supraspinal structures projecting to the phrenic motor nucleus of the cat spinal cord were studied using a horseradish peroxidase method. A double-barrel coaxial electrode was employed. To determine the site of the phrenic motor neurons, the inner barrel electrode, filled with 3 M NaCl solution, was used for recording the activity of these neurons. The outer barrel electrode, filled with a 20% HRP solution, was used for injecting HRP iontophoretically into the phrenic motor nucleus. Out of 13 experiments, 5 showed that the HRP-injection sites were centered in and almost confined to the phrenic motor nucleus. Some 1798 HRP-labeled cells were thus identified in the selected 5 experiments. They were distributed in the medulla oblongata (93.5%), pons (6.0%) and midbrain (0.5%). The majority were concentrated in the nucleus para-ambiguus (48.9%), nucleus tractus solitarii (21.5%) and in or around the nucleus retrofacialis (9.8%). A few labeled cells were scattered throughout the nucleus raphe (1.1%) and the parabrachial and Koelliker-Fuse nuclei (0.3%), suggesting that these nuclei may be, if any, only minor sources of input to the phrenic motor nucleus.     

Suppressive effect of LD78 on the proliferation of human hemopoietic progenitors.

LD78 is a cDNA newly isolated from human stimulated tonsillar lymphocytes. The expression of LD78 is related to inflammatory responses and its structure has a homology with macrophage inflammatory protein 1-alpha, which is known to have an inhibitory effect on murine CFU-S. Using a colony assay technique, we examined the effects of LD78 on human hemopoietic progenitors. The addition of doses of 100 ng/ml or more of LD78 suppressed the colony formation of KMT-2, a factor-dependent myelomonocytic cell line established from cord blood cells; this suppressive activity was neutralized by the addition of antibody against LD78. The same doses of LD78 suppressed the formation of neutrophil, macrophage, and megakaryocytic colonies which were supported by human interleukin-3 and erythropoietin; however, LD78 did not affect colony formation by either non-phagocytic mononuclear cells or sorted CD34+ cells. The conditioned medium of KMT-2 cells or peripheral blood mononuclear cells cultured with LD78 suppressed colony formation by CD34+ cells. From these findings, it is suggested that LD78 affects phagocytic cells and induces factors that are inhibitory for hemopoiesis. We consider LD78 to be a new cytokine that plays an inhibitory role in hemopoiesis.     

Preferential inhibitions of hepatic P450IA2 expression and induction by lead nitrate in the rat

Male F344 rats were treated with lead nitrate and changes inthe expression and induction of P450IA subfamily enzymes anda placental form of glutathione-S-transferase (GST-P) in theliver were assessed by means of a bacterial mutation test, immunoblottingwith a monoclonal antibody reactive to P450IA1/IA2 and anti-GST-Psera and Northern blotting with P450IA2 cDNA as a probe. Treatmentof rats with lead nitrate (20, 50 or 100 µmol/kg bodywt) decreased P450IA2 mRNA and protein in the liver in the dose-dependentfashion and also decreased the microsomal activity for P450IA2-dependentmutagenization of aromatic amines. Pretreatment of rats withlead nitrate suppressed the inductions of both P450IA2 mRNAand protein by an inducer of P450IA subfamily enzymes in theliver. In addition, amount of the induced P450IA2 was decreasedalong with increase in that of the induced GST-P.     

Long-term effects of ozone and nitrogen dioxide on the metabolism and population of alveolar macrophages.

To investigate how alveolar macrophages adapt themselves to oxidative pollutants in the long term, rats were exposed to a strong oxidant, ozone (O3), or a weak oxidant, nitrogen dioxide (NO2), for a maximum duration of 12 wk. After exposures, alveolar macrophages were collected by pulmonary lavage. Throughout 11 wk of exposure to 0.2 ppm O3, the specific activities of glucose-6-phosphate dehydrogenase (G6PDH) and glutathione peroxidase of the peroxidative metabolic pathway and pyruvate kinase and hexokinase of the glycolytic pathway were 40-70% elevated over the controls in alveolar macrophages. The population of alveolar macrophages was consistently 60% higher than the controls. The small-sized macrophages, immature macrophages, preferentially increased. To the contrary, the thymidine incorporation per cell was always 20-30% lower than in the controls, although the total incorporation remained unchanged. No infiltration of polymorphonuclear leukocytes occurred. By 12 wk of exposures to 1.2 and 4.0 ppm NO2, the population of alveolar macrophages increased 30% over the control. Among the enzymes examined, however, only the G6PDH activity increased 10% for 4.0 ppm NO2. No increase in the enzyme activities occurred for 1.2 ppm NO2. Based on these results, alveolar macrophages adapt themselves to the long-term exposure of O3 or NO2 by recruiting immature macrophages through an apparent influx of monocytes. During the exposure to O3, the peroxidative metabolic and glycolytic pathways are enhanced persistently in alveolar macrophages, whereas both pathways were not enhanced by the exposures to NO2.