Beta2-glycoprotein I-dependent anticardiolipin antibody in early recurrent spontaneous abortion

The objective of this study was to assess the clinical significance of autoimmune anticardiolipin antibody that can react with cardiolipin only in the presence of beta2-glycoprotein I (beta2-glycoprotein I- dependent anticardiolipin antibody) in the pathogenesis of early recurrent abortion. A total of 72 early recurrent spontaneous aborters and 175 normal healthy women were analysed for the occurrence of beta2- glycoprotein I-dependent anticardiolipin antibody in serum samples by an enzyme-linked immunosorbent assay specific for the detection of beta2-glycoprotein I-dependent anticardiolipin antibody. The incidence of beta2-glycoprotein I-dependent anticardiolipin antibody in the early recurrent spontaneous aborters was essentially the same as that of normal women. Thus, the beta2-glycoprotein I-dependent anticardiolipin antibody seemed to have little, if any, implication in the pathogenesis of early recurrent spontaneous abortion.      

Five percent, 7.5% or 10% hypertonic saline prevents delayed neuronal death in gerbils

PURPOSE: To clarify the appropriate concentration and dose of hypertonic saline solution (HSS) for preventing delayed neuronal death in the hippocampal CA1 subfield after transient forebrain ischemia in gerbils. METHODS: Thirty gerbils were randomly assigned to five groups: physiological saline solution (PSS) group, ischemia/reperfusion treated with PSS 2 mL x kg(-1); 5% HSS group, treated with 5% HSS 2 mL x kg(-1); 7.5% HSS group, treated with 7.5% HSS 2 mL x kg(-1); 10% HSS group, treated with 10% HSS 2 mL x kg(-1); 20% HSS group, treated with 20% HSS 2 mL x kg(-1). Transient forebrain ischemia was induced by occluding the bilateral common carotid arteries for four minutes. Five days later, histopathological changes in the hippocampal area were examined, and the degenerative ratio of the pyramidal cells were measured according to the following formula: (number of degenerative pyramidal cells/total number of pyramidal cells per 1 mm of hippocampal CA1 subfield) x 100. RESULTS: In PSS and 20% groups, neuronal cell damage was observed five days after ischemia. In the other three groups, these changes were not observed. The degenerative ratios of pyramidal cells were as follows; PSS group: 91.6 +/- 5.6%, 5% HSS group: 7.2 +/- 1.6%, 7.5% group: 8.3 +/- 1.4%, 10% HSS group: 6.2 +/- 1.1%, 20% HSS group: 85.8 +/- 8.7% (P < 0.05; PSS and 20% HSS vs three other groups). CONCLUSION: This study demonstrates that 5, 7.5 or 10% HSS 2 mL x kg(-1) may prevent delayed neuronal death in the hippocampal CA1 subfield after cerebral ischemia/reperfusion in gerbils.     

Approach to early diagnosis of acute mesenteric ischemia: evaluation in canine model

The high mortality rate of patients with acute mesenteric ischemia may be mainly due to the difficulty of making an early diagnosis. Many clinical and experimental studies have been attempted to make an early diagnosis in the view of history, physical examination, laboratory data, X-rays and angiographies. This study was undertaken to estimate the diagnostic value of twenty one laboratory parameters and three clinical parameters measured after superior mesenteric artery occlusion (SMAO) in the mongrel dogs. Consequently, the valuable diagnostic indicators of SMAO that statistically had significant difference were serum CPK isoenzyme-BB, serum CPK isoenzyme-MB, serum inorganic phosphate, serum calcium and base excess of arterial blood gas analysis. In these indicators, serum CPK isoenzyme-BB, serum inorganic phosphate and serum calcium were especially valuable indicators of its early diagnosis, because they showed significant change in the early phase after SMAO. However, other indicators showed significant change within eighteen hours after SMAO. Therefore, if these indicators are able to be examined in a case of abdominal emergency, they are considered to play a valuable role in the diagnosis of acute mesenteric ischemia.     

Ultrasonographic study on kidneys in patients with acute renal failure]

Ultrasonotomograms of 22 kidneys were obtained in 11 patients with renal-acute renal failure (renal-ARF). The underlying diseases of renal-ARF were acute tubular necrosis in 8 patients and acute on-set chronic glomerulonephritis in 3 patients. They were treated by hemodialysis in 10 patients and intermittent peritoneal dialysis in 1 patient. Ultrasonic measurement of the size of kidneys revealed that the thickness (anterior-posterior diameter) and the ratio of thickness to length (T/L) were greater in patients with ARF than in those with chronic renal failure and normal renal function. The patients with a low value of T/L (under 0.60) had a significantly greater urine volume than those with high a value of T/L (0.60 or more). The sonographic features of renal-ARF kidneys were marked increase in parenchymal echogenicity and appearance of hypoechoic swollen renal pyramids with sharpness of the corticomedullary border. In the course of ARF, these sonographic changes gradually disappeared when the patients had recovered from ARF. However, the prognosis was poor in patients with severer sonographic findings. We believe that repeated ultrasonic examination of the kidneys in patients with renal-ARF is useful for not only differential diagnosis of post-renal urinary obstruction but evaluating the course of ARF.     

Myocardial 11C-diacylglycerol accumulation and left ventricular remodeling in patients after myocardial infarction.

Left ventricular (LV) remodeling after myocardial infarction (MI) is a maladaptive process that increases the risk of heart failure and death. The myocardial phosphoinositide cycle, which is located downstream from several neurohumoral factors, plays a crucial role in LV remodeling. Our animal studies demonstrated that 1-[1-11C]butyryl-2-palmitoyl-rac-glycerol (11C-DAG) can be used to visualize regions with an activated phosphoinositide cycle. Therefore, we examined whether myocardial 11C-DAG accumulation assessed by PET is relevant to LV enlargement and systolic dysfunction in post-MI patients. METHODS: We performed PET with 11C-DAG in 13 post-anteroseptal MI patients and 4 healthy volunteers. We placed regions of interest on the noninfarcted myocardium and calculated the myocardium-to-left atrial (LA) chamber ratio of 11C-DAG accumulation. RESULTS: The myocardium-to-LA chamber ratio of 11C-DAG was significantly higher in the post-MI patients (mean +/- SD, 1.73 +/- 0.35) compared with that of the healthy volunteers (mean +/- SD, 1.25 +/- 0.13; P < 0.05). In the post-MI patients, the myocardium-to-LA chamber ratio of (11)C-DAG was significantly correlated with the LV end-diastolic volume index (r = 0.79, P < 0.01) and the plasma concentration of brain natriuretic peptide (r = 0.85, P < 0.001) and negatively correlated with the LV ejection fraction (r = -0.69, P < 0.01). CONCLUSION: These findings suggest that the myocardial 11C-DAG accumulation assessed by PET is relevant to LV enlargement, LV systolic dysfunction, and humoral activation in post-MI patients. This new imaging strategy based on intracellular signaling may contribute to the assessment and treatment of post-MI patients.     

Successful treatment of a patient with penetrating injury of the esophagus and brachiocephalic artery due to migration of Kirschner wires.

Pins and wires offer the simplest and most effective tools for managing bone fractures and dislocations. Migration of these devices within the chest is rare, but can cause serious problems. The spontaneous migration of Kirschner wires from the right clavicle to the mediastinum resulted in penetrating injury of the esophagus and pseudo-aneurysm of the brachiocephalic artery in an 84-year-old patient. Two Kirschner wires were removed via a vertical incision on the right shoulder without thoracotomy and the brachiocephalic artery was replaced with a Dacron graft.     

Epinephrine is an enhancer of rat intestinal absorption.

Some physiological substances, including acetylcholine and nitric oxide, are useful candidates for stimulation of intestinal absorption of drugs. In the present study, we elucidated the ability of epinephrine (Epi) to stimulate the intestinal absorption of drugs. We evaluated the ability of Epi to enhance absorption of macromolecules using dextran (Mw 4000 Da), which is poorly absorbed from the intestine, as a model compound in situ in a closed loop of the rat jejunum. Treatment of the jejunum with Epi resulted in significant increase in absorption of dextran in a dose-dependent fashion. The area under the curve (AUC) from 0 to 4 h in the Epi-treated jejunum was 13-fold higher than that in the vehicle-treated jejunum. The absorption-enhancing activity of Epi was 40-fold higher than that of caprate, a clinically used absorption-enhancer of drugs. In the experimental conditions used in this study, histological injury of the mucosa and perturbation of the mucosal membrane were not observed in the Epi-treated jejunum. Treatment with an antagonist of alpha-adrenergic receptors attenuated the stimulation of intestinal absorption by Epi, and treatment with an agonist of alpha-adrenergic receptors resulted in enhancement of intestinal absorption. While an antagonist of beta-adrenergic receptors enhanced the absorption-enhancing effect of Epi, an agonist of beta-adrenergic receptors stimulated intestinal absorption. These results indicate that stimulation of adrenergic receptors may be a novel strategy for intestinal absorption of drugs.