[Squamous cell carcinoma of the chest wall in a patient with chronic empyema].

We report a rare case of squamous cell carcinoma of the chest wall in a patient with chronic empyema. The patient was a 74-year-old male who had been treated by closed chest drainage for empyema for 20 years until the development of carcinoma. He received chest wall resection followed by radiation therapy because of disseminated lesions comfirmed at surgery. However, his condition worsened gradually, and he died 2 months postoperatively. In the treatment of chronic empyema, we must pay attention to the possible association of malignant tumor for treating as early as possible, because the associated malignant tumor usually has a poor prognosis.

Soluble Fas ligand expression in the ocular fluids of uveitis patients.

PURPOSE: The expression of Fas ligand (FasL) in ocular tissues is thought to play a critical role in maintaining immune privilege in the eye. In this study, to clarify the involvement of the Fas-FasL system in inflammatory processes of the eye,we examined soluble FasL (sFasL) in ocular inflammation. METHODS: Using ELISA systems recently developed, sFasL concentrations in aqueous humor (AH) and/or vitreous fluid (VF) were measured. AH was obtained from 17 eyes of 17 uveitis patients and from 12 eyes of 12 non-uveitis (cataract) patients. VF was obtained from 22 eyes of 22 uveitis patients and 7 eyes of 7 non-uveitis (macular hole) patients. Serum levels of sFasL were also determined. RESULTS: sFasL in AH and VF was below the detection limit of the ELISA systems in all non-uveitis eyes. On the other hand, sFasL was detected in AH from uveitis patients where it measured 367.0 +/- 154.7 pg/ml (mean +/- SEM). sFasL was also detected in VF from uveitis patients where it measured 1132.2 +/- 281.7 pg/ml. None of the sera from patients with or without uveitis contained a detectable level of sFas L. CONCLUSIONS: sFasL levels in AH and VF are elevated in the eye during ocular inflammation. Fas-FasL mediated apoptosis may play an important role in the regulation of inflammation during uveitis.

Possible role of herpes simplex virus in the origin of Posner-Schlossman syndrome.

PURPOSE/METHODS: We conducted this study to determine if the herpesviruses are possible etiologic agents in Posner-Schlossman syndrome. We aspirated aqueous humor samples from patients during acute attacks of the syndrome. Ten normal aqueous humor specimens from patients undergoing cataract surgery were used as controls. DNA was extracted and subjected to polymerase chain reaction amplification and Southern blot hybridization. RESULTS/CONCLUSION: All three specimens were positive for amplified genomic fragments of herpes simplex virus and negative for varicella-zoster virus and cytomegalovirus. Ten normal aqueous specimens were negative for all three. Herpes simplex virus may play a role in the origin of Posner-Schlossman syndrome.

Indocyanine green videoangiographic findings in choroidal metastatic tumor.

BACKGROUND: Indocyanine green videoangiography (ICGV) has recently advanced and become widely available as a clinical tool. We tested the efficacy of ICGV in evaluating metastatic choroidal tumors. METHODS: ICGV using Topcon 50-IA was performed in five patients with clinically diagnosed choroidal metastatic tumors. The findings were compared with those of conventional fluorescein angiography (FAG). RESULTS: Compared with FAG, ICGV demonstrated more smooth and regular hypofluorescent lesions, precisely indicating the exact size of the tumor. In all cases, no tumor vessels were found. The choroidal vascular integrity around the tumors was observed. FAG, however, was more sensitive in detecting the tumor development than ICGV when the extent of the hypofluorescent lesion could be seen clearly in the early phase. FAG provided more information regarding retinal pigment epithelial dysfunction in the outer blood retinal barrier overlying the tumor. CONCLUSION: Since ICGV enables visualization of tumors through the retina, it is very useful, particularly in cases of associated secondary retinal detachment around the tumors. ICGV combined with FAG provides more precise assessment of the tumors themselves and their response to treatment than FAG alone.

[Clinical features of uveitis in childhood during the past 20 years].

One hundred and fifty five cases (237 eyes) of children with uveitis were clinically observed in the past 20 years. There was no fluctuation in the number of patients during the period. Concerning the age as the first visit, the smallest group was under 4 years of age and the numbers of patients increased at ages 14 and 15. Chief complaints usually corresponded to the age of the cases. Cases with anterior uveitis accounted for 25% of all cases, intermediate uveitis 12%, posterior uveitis 45% and panuveitis consisted of 17% of all cases, respectively. In the course of treatment, improvement of visual acuity was not statistically significant; the visual prognosis of cases affected under age 7 years was relatively poor. At the time of final observation, the visual acuity of cases, who had first visited during the past 10 years, were better than those who presented during the previous decade. Uveitis had healed or improved in 68% of cases treated in our clinic. As complications, band-shaped keratopathy was seen in 8% of the patients, cataract in 22% and glaucoma in 5%, respectively. Thirty two per cent of the cases received systemic steroid therapy and the average duration was 3.8 months. Fifty two operations were performed in 30 cases (19%), 37 eyes (16%); 16 were cataract operations and 24 were operations for glaucoma.

Early microsurgical reconstruction in birth palsy.

Most patients with birth palsy can be expected to recover spontaneously. But in some patients the recovery is unsatisfactory and the functional results are disappointing. One possible way to improve the prognosis for such patients is early surgical nerve reconstruction. In six infants, exploration of the brachial plexus was carried out at about six months after delivery, when there were no signs of recovery in shoulder and elbow joint movements. Preoperative metrizamide myelography, computerized tomography with intrathecal metrizamide (CT myelography), and axon reflex test (histamine test) were followed by intraoperative electrophysiologic examinations of root sensory evoked potential (SEP), nerve action potential (NAP), and evoked muscle response (M-response). Microsurgical nerve repair was performed on the basis of intraoperative diagnosis. Metrizamide myelography showed 13% false-positive root avulsion. Reliability of the histamine test was 80%. The intraoperative electro-diagnosis is essential for understanding the actual condition of the brachial plexus lesion and obtaining better results from microsurgical reconstruction in birth palsy. The surgical results, with an average follow-up evaluation of two years and four months, have been encouraging enough to continue this diagnostic and therapeutic program, though its superiority to natural recovery has not yet been clarified.

Activation of glycogenolysis by the reduction in the extracellular calcium concentration in verapamil-perfused rat liver.

In an attempt to elucidate the role of Ca2+ flux in the initial events of hepatic glycogenolysis, extracellular Ca2+ concentration was manipulated in rat liver perfused with Ca2+ antagonistic drugs. After the liver had been perfused with a buffer containing verapamil and 1 mM CaCl2, either the addition of ethyleneglycol-bis-(beta-aminoethyl ether)-N,N'-tetraacetic acid to the perfusate or the replacement of the perfusate with Ca2+-free buffer caused a rapid increase in glucose output as well as 45Ca2+ efflux. Substitution of diltiazem, but not 5-20 mM LaCl2, for verapamil also stimulated glucose output and 45Ca2+ efflux. However, when Ca+-free buffer was used throughout the experiment, any modes of verapamil or diltiazem perfusion were without significant effects on glucose output or Ca2+ efflux. The increases in glucose output and 45Ca2+ efflux were not affected by either 20 microM phentolamine or 300 microM ouabain, but they were inhibited significantly by 10-100 microM trifluoperazine. These results indicate that rapid decline in the extracellular Ca2+ concentration in verapamil- or diltiazem-perfused liver initiates the change in Ca2+ equilibrium on or across plasma membrane and activates glycogenolysis through a Ca2+-dependent mechanism.

Inhibition by trifluoperazine of glycogenolytic effects of phenylephrine, vasopressin, and angiotensin II.

The effects of trifluoperazine on the activation of glycogenolysis by various hormones were studied in perfused rat liver. Trifluoperazine significantly inhibited glycogenolytic effect of phenylephrine and angiotensin II by lowering maximal response, and that of vasopressin by shifting the dose-response curve to the right, while alpha-antagonist phentolamine was inhibitory only to phenylephrine. Phosphorylase activation of phenylephrine was inhibited by trifluoperazine in parallel with glycogenolytic response. The increase in 45Ca2+ efflux induced by phenylephrine, angiotensin II, and vasopressin was also inhibited by the agent. These inhibitory effects of trifluoperazine were not related to the change in tissue cyclic AMP or cyclic GMP levels. On the other hand, neither the glycogenolytic effect of glucagon, cyclic AMP, and N6,O2-dibutyryl cyclic AMP nor phosphorylase activation by glucagon was affected by trifluoperazine. Thus, trifluoperazine specifically inhibits the activation of glycogenolysis by Ca2+-dependent hormones.

[Seven-year follow-up studies on asymptomatic HBs Ag carriers].

This report covers 7-year follow-up studies on 35 HBs Ag carriers whose anti-HBc titer levels were 10 (log 2) or more and who had normal liver functions at the start of the studies, when 9 of them (25.7%) were HBe Ag positive, 24 (68.6%) anti-HBe positive and 2 (5.7%) negative to both. 1. There was no significant difference in the incidence of abnormal SGPT levels as a whole between HBe Ag positives and anti-HBe positives. But abnormally high SGPT levels of 100 KU or more were observed at a higher percentage among HBe Ag positives (4/9. 44.4%) than among anti-HBe positives (1/24. 4.2%. p less than 0.02). 2. Based on the results of the 7-year studies, all cases were classified into six clinical stages. HBe Ag positives were divided into three groups by the stage with different SGPT levels: 5 cases (15.2%) whose SGPT leves never rose above 50 KU were classified as Stage 1; 3 cases with chronic active hepatitis (9.6%) whose highest SGPT levels were over 200 KU (2 new cases and 1 case with a relapse of chronic inactive hepatitis) as Stage 2 and 1 case (3.0%) seroconverted to anti-HBe positive following an acute relapse of chronic inactive hepatitis as Stage 3. Anti-HBe positives were divided into another three groups similarly according to their mean HBs Ag titer levels: 6 cases (18.2%) whose mean HBs Ag titer levels ranged from 10 to 13 (log 2) were classified as Stage 4; 13 cases (39.4%) whose mean HBs Ag titer levels ranged from 6 to 9 as Stage 5 and 5 cases (15.2%), including 2 cases turned negative to HBs Ag, whose mean HBs Ag titer levels were below 5 as Stage 6. The average age of each group increased wth its clinical stage, namely, 32.6 in Stage 1, 34.3 in Stage 2, 33.0 in Stage 3, 34.5 in Stage 4 and 37.0 in Stage 5, but the average age in Stage 6 was 29.0. 3. All HBe Ag positives showed fluctuations in HBs Ag titer levels. The fluctuations were particularly noteworthy among cases with chronic active hepatitis in Stage 2 during an acute relapse. The HBs Ag titers rose just before the acute relapses in a case of chronic active hepatitis when SGPT levels went over 200 KU. This suggested a proliferation of the virus. On the other hand, in anti-HBe positives, a decrement of the virus was suggested by the fact that an increasing proportion of cases showed their HBs Ag titer levels to fluctuate or to become lower with the progress of stages (p less than 0.05) and two cases turned negative to HBs Ag as plotted in Stage 6. And the proportion of cases with abnormal SGPT levels decreased with the progress of stages (p less than 0.05). One case whose SGPT level was 125 KU, highest among anti-HBe positives, followed the clinical course of chronic inactive hepatitis and lowered in HBs Ag titer. 4. Between HBe Ag and anti-HBe cases, there were considerable differences in the occurrence of liver disturbances and their clinical courses...

Inhibition by calcium channel blockers of the glycogenolytic effect of glucagon in perfused rat liver.

Verapamil and diltiazem, calcium channel blockers, inhibited significantly the glucagon-induced glucose output and 45Ca efflux from perfused rat liver at concentrations higher than 50 microM when the perfusate contained calcium. Although the blockers partially interfered with glucagon-induced elevation of cyclic AMP in the tissue, they also inhibited the effects of cyclic AMP. The blockers did not show the inhibitory effects in the absence of perfusate calcium. However, the inhibition of calcium influx into hepatocytes by omission of extracellular calcium or addition of EGTA did not interfere with these effects of glucagon and cyclic AMP. In the presence of extracellular calcium, the blockers did not inhibit cyanide-induced glucose output, indicating that the activity of glycogen phosphorylase and later processes leading to glucose output were not affected by the blockers. These data suggest that, in the presence of calcium, the blockers inhibit the effect of glucagon also at a step (or steps) subsequent to cyclic AMP production and before the activation of phosphorylase b, probably by inhibiting glucagon-induced mobilization of calcium from intracellular calcium pools rather than inhibiting calcium influx into hepatocytes.

Sources of calcium mobilized by alpha-adrenergic stimulation in perfused rat liver.

The glycogenolytic effect of catecholamine has been proposed to be mediated by calcium ions mobilized mainly from mitochondria. In this study, the contribution of mitochondria as a source of the mobilized calcium was evaluated by use of perfused rat livers. Phenylephrine-induced efflux of 45Ca from 45Ca preloaded liver was abrupt and transient, and almost ceased within 5 min. The perfusion with 5 microM phenylephrine for 5 min caused a significant decline in the content of 45Ca retained in the liver homogenate; control, 0.97 +/- 0.11 nmol of 45Ca/mg protein (mean +/- SEM) and phenylephrine, 0.41 +/- 0.08 nmol of 45Ca/mg protein (P less than 0.01), when calculated from the specific radioactivity of calcium in the perfusate used for loading perfusion. The contents of 45Ca in mitochondria isolated subsequently from the homogenate were 0.43 +/- 0.07 nmol/mg protein in controls and 0.22 +/- 0.03 nmol/mg protein (p less than 0.05) when phenylephrine was administered. Taking into consideration that mitochondrial protein is a fraction of homogenate protein, it is obvious that the decline in mitochondrial 45Ca represents only a small portion of the total reduction of radioactivity in the homogenate. In a series of experiments in which various perfusion periods were employed for 45Ca loading and for washing-out, it was found that phenylephrine induced 45Ca efflux also from a pool with a calcium turnover rate slower than that if mitochondria. These results suggest that alpha-adrenergic stimulation enhances release of calcium not only from mitochondria but also from other compartments with a slower turnover rate. The probability of plasma membrane is proposed as the other source of calcium released in response to alpha-adrenergic stimulation.