Eosinophil chemotactic activity in Leishmania amazonensis promastigotes

 Tissue eosinophilia was observed in the subcutaneous tissue of mice shortly after their inoculation not only with living but also with lysed promastigotes of Leishmania amazonensis. Intraperitoneal inoculation of lysed promastigotes from five different Leishmania species (L. donovani, L. chagasi, L. tropica, L. amazonensis, and L. braziliensis) induced eosinophil accumulation in the mouse peritoneum. This eosinophil infiltration was also detected in C5-deficient AKR mice, indicating complement independent eosinophil chemotaxis by the parasite. The induced eosinophils were hypodense, suggesting activation of the cells. Finally, we demonstrated in vitro eosinophil chemotactic activity in the promastigote lysates using purified eosinophils and blind well chambers. These results suggest the presence of an eosinophil chemotactic factor in Leishmania, a protozoan parasite. Received: 6 November 1995 / Accepted: 31 January 1996     

Effects of diltiazem on renin-aldosterone and ACTH-adrenocortical function during upper abdominal surgery

Study Objective: To observe the effects of continuous intravenous infusion of diltiazem on the renin-aldosterone system and ACTH-adrenocortical axis responses during surgical stimulation.

Design: Randomized study of intravenous diltiazem.

Setting: Operating room at the Hyogo Medical College Hospital.

Patients: Twenty-three patients undergoing upper abdominal surgery were divided into two groups: the control group (n = 10) and the diltiazem group (n = 13). All the patients were without any complications and classified as ASA physical status I.

Interventions: Patients in the diltiazem group received an infusion of 10 μg/kg/ min for 90 to 120 minutes following skin incision.

Measurements and Main Results: Plasma adrenocorticotropic hormone, plasma aldosterone and cortisol concentrations, and plasma renin activity were determined with radioimmunoassay before the induction of anesthesia at 10, 30, 60, and 90 minutes after skin incision and at the end of anesthesia. Renin activity did not change significantly. Maximal increases in plasma adrenocorticotropic hormone, aldosterone, and cortisol observed 90 minutes after skin incision were 355 ± 95 pg/ml, 118 ± 30 pg/ml, and 14.2 ± 2.3 μg/dl in the control group versus 246 ± 41 pg/ml, 119 ± 25 pg/ml, and 15.0 ± 1.8 μg/dl in the diltiazem group, respectively, and there were no significant differences between these groups. Adrenocorticotropic hormone was significantly lower in the diltiazem group compared with that in the control group 60 minutes after the start of surgery (p < 0.05). There was marked natriuresis (40 ± 25 μEq/min vs 470 ± 147 μEq/min at the 90-minute mark) and diuresis (0.16 ± 0.13 ml/min vs. 2.53 ± 0.88 ml/min) in the diltiazen group.     

Efficacy of Prophylactic Endoscopic Variceal Sclerotherapy in Patients with Hepatocellular Carcinoma

Abstract: A setrospective study to determine the influence of prophylactic endoscopic sclerotherapy on the survival rate of patients with hepatocellular carcinoma complicated by esophageal varices was conducted. The subjects included 132 patients without esophageal varices at the time of diagnosis (NV group), 37 patients with hepatocellular carcinoma for whom prophylactic sclerotherapy had been performed for risky esophageal varices (PS group) and 26 patients with hepatocellular carcinoma and risky varices for whom prophylaxis was not performed (NPS group). Multiple regression analysis was used to identify factors affecting the survival rate of the 132 patients without esophageal varices. A tumor embolus in the primary branch or main trunk of the portal vein adversely affected long-term survival in these patients. The patients were further divided into 2 subgroups, namely those with (Vp3) and without (Vp0-Vp2) tumor emboli in the main trunk and primary branch of the portal vein. In the Vp0– Vp2 emboli subgroup, the patients who received prophylactic sclerotherapy and the patients without varices had similar survival rates. Patients without prophylactic sclerotherapy had a significantly shorter survival rate than the group without varices and the prophylactic sclesotherapy group (p<0.01 and p<0.05). A significant bleeding rate was observed in the group without prophylaxis and not in the group with prophylaxis. However, in the Vp3 subgroup, the survival rate in each group was identical. Thus prophylactic variceal sclerotherapy is indicated for patients with hepatocellular carcinoma who do not have tumor emboli in the main trunk or primary branch of portal vein.     

The role of sympathetic catecholaminergic nerves in wound healing

We postulate that the sympathetic nerve may correlate with the degeneration of regenerated arterial vessels and collagen metabolism during burn wound healing (Kishimoto, Maruo, Ohse et al., 1982). To verify these suggestions, 6-hydroxydopamine, a specific toxin of the sympathetic nerve, was employed in burn wounded animals. The initial degenerative features of regenerated arterial vessels in the sympathectomized animals could be observed about 2 weeks later than in the untreated animals. Moreover, it seemed evident that the decrease in the number of capillaries during wound healing was elicited by the regeneration of sympathetic nerves. Furthermore, severe dilatation of the capillaries as well as the arterial vessels in the granulation tissue was observed only in the sympathectomized animals until the twenty-first day after burning. In addition, morphological appearances of collagen in the sympathectomized animals significantly differed from those in the untreated animals. The collagen in the former was fine fibrous, while thick collagen fibres were seen in the latter.     

Autoradiographic Distribution of 131I-Clioquinol in Canine and Feline

To elucidate the absorption, intracellular location and pathogenicity of clioquinol, micro-autoradiographic studies were done. ¹³¹I-clioquinol was administered under different methods to 6 mongrels, 2 inbred beagles and a cat. Shortly after i.v.- or i.p.-injections of the substance to the mongrels and cat, a high concentration of radioactive grains was seen in the following nervous system: Nerve cells of the spinal root ganglia, spinal grey matter and nuclei in the brain stem; peripheral nerves; capsular cells of the spinal root ganglia; glial cells in the spinal cord, brain stem and periventricular region of the cerebrum. Though in lesser degree, orally administered radioactive clioquinol was also detected in the nervous system of the mongrels. I.p.-injected beagles showed, however, a low concentration of the grains in the nervous system. This may indicate strain-difference of dogs for the neurotoxicity of clioquinol.     

EFFECTS OF PROSTAGLANDIN D2 AND OMEPRAZOLE ON INDOMETHACIN-INDUCED GASTRIC ULCERS IN RATS

1. The mechanism of indomethacin-induced gastric ulcers was investigated by measuring tissue prostaglandins (PG) levels. 2. The effects of PGD2 and omeprazole, an H+ pump inhibitor, were also estimated. 3. Four kinds of PG--6-keto PGF1 alpha, PGF2 alpha, and PGD2--in rat gastric mucosa were measured by high performance liquid chromatography. 4. All PG levels decreased 1 h after oral administration of 2 mg/kg indomethacin, although they recovered considerably 24 h after administration. No gastric ulcers were observed throughout the experiments in rats treated with 2 mg/kg indomethacin. 5. All PG were not detected 1 h, and even 24 h after administration of 12 mg/kg indomethacin. Over 6 h after administration, gastric ulcers were observed. 6. Premedication with omeprazole prevented ulcer formation, although it did not improve gastric mucosal PG levels. Administration of PGD2 also reduced ulcer formation, and considerable amounts of PGD2 in gastric mucosa were detected. 7. It can be concluded that H+ is a determining factor in the genesis of indomethacin-induced gastric ulcers and that persistent decreases in tissue PG levels also participate in ulcer formation.     

Studies on metabolism and disposition of sizofiran (SPG), an anti-tumor polysaccharide. III. Degradation and excretion of SPG in rats

Degradation and excretion of Sizofiran (SPG), an anti-tumor polysaccharide, were studied in rats after a single or multiple administration. After a single intravenous injection of [14C]SPG (3 mg/kg), SPG distributed in the liver was degraded at very slow rate to SPG-like substances (SPGLS) having lower molecular weight than that of SPG, while SPG in the spleen and mesenteric lymph node was metabolized at much slower rate than that in the liver. In the experiment with multiple subcutaneous administration, SPG was also found to be present mainly as SPGLS in the liver, but almost as an unchanged SPG in the spleen. SPG was excreted in the urine mainly as metabolites with a molecular weight of less than 10000. These results indicate that degradation of SPG to lower molecular weight-SPGLS is a prerequisite for efficient urinary excretion and the degradation occurs mainly in the liver.     

Brain abscess secondary to intracranial extradural epidermoid cyst

A case of brain abscess in the right temporal lobe secondary to an intracranial extradural epidermoid cyst in the right parasellar region is reported. The etiology of the brain abscess in this particular case was deduced using the findings of computed tomography, carried out several times over a 3-year period, after an initial operation to remove the epidermoid cyst. One of the scans showed a very-low-density spot in the right parasellar region compatible with air, suggesting a communication between the intracranial space and the paranasal sinuses.