Initial and midterm results for repair of aortic diseases with handmade stent grafts.

BACKGROUND: The purpose of this study was to determine the initial and midterm results for repair of thoracic and abdominal aortic diseases using handmade stent-grafts (SGs). METHODS AND RESULTS: Between 1999 and 2004, 41 consecutive patients (31 patients with thoracic and 10 patients with abdominal aortic disease) underwent endovascular stent-graft repair using handmade SGs. The follow-up averaged 24.8+/-17.6 months. The technical and initial clinical success rates were 82.9% (34/41) and 80.5% (33/41), respectively. Primary type I or III endoleaks occurred in 12.2% (5/41) of the patients. The hospital mortality rate was 4.9% (2/41). Persistent type I or III endoleaks occurred in 9.8% (4/41) and SG migrations occurred in 4.9% (2/41) of the patients. Open surgical conversion was undertaken in 12.2% (5/41) of the patients because of an endoleak and/or migration. The mean change observed in the aneurysm diameter was -6.2+/-10.5 mm, and shrinkage in the diameter occurred in 51.4% (18/35) of the cases. There was 1 patient death because of aneurysm rupture. Neither stent fracture nor graft hole was observed. The overall clinical success rate during follow-up was 78.0% (32/41). CONCLUSION: The initial and midterm results obtained after repair of the aortic diseases using handmade SGs were considered to be satisfactory. More surgical experience and long-term patient follow-up are both required to further reassess the effect of this treatment.     

Effect of phosphatidylcholine, phosphatidylethanolamine and lysophosphatidylcholine on the protein C/protein S anticoagulation system.

Phosphatidylserine is known to significantly accelerate the blood coagulation reaction. In a previous communication submitted for publication, we demonstrated that phosphatidylcholine, phosphatidylethanolamine and lysophosphatidylcholine showed effects on the blood coagulation reaction using the factor Xa-prothrombin reaction system, and discuss a new function of membrane phospholipids. The present study examined the role of phospholipids in the blood coagulation regulatory reaction (anticoagulation system), by studying the effects of phospholipids on the protein C/protein S reaction. We have established quantitative methods for measuring activated protein C activity and protein S activity, and used them to measure their activity after the addition of liposomes with different phospholipid compositions. We found that phosphatidylcholine inhibited activated protein C and protein S activities in a dose-dependent manner, as in the factor Xa-prothrombin reaction system. On the other hand, phosphatidylethanolamine and lysophosphatidylcholine showed no effect on activated protein C activity. Phosphatidylethanolamine inhibited and lysophosphatidylcholine accelerated coagulation activity in the factor Xa-prothrombin system, but such effects were not observed in the protein C/protein S reaction system. The coagulation and anticoagulation reactions are exquisitely balanced by thrombin, with a role both as a procoagulant and anticoagulant. Therefore, it is understandable that phosphatidylethanolamine and lysophosphatidylcholine show different effects in the factor Xa-prothrombin and protein C/protein S reaction systems. It appears that coagulation and anticoagulation reactions are co-ordinated and controlled by changes in phospholipid composition of the cellular membrane where the coagulation reaction takes place.     

An Autopsied Case of Interferon Encephalopathy

Abstract: A 78-year-old male with renal carcinoma was treated with a high dose infusion of interferon-alpha (IFN-alpha) for eight months. The patient had evidence of organlc brain syndrome such 88 : dysfunction of memory, slowing of behavior, and development of mental confusion that appeared eight months after the treatment. MRI at the time of mental confusion revealed difise white matter lesions. Neuropathologic findings were compatible to Binswanger's disease and Senile Dementia of Alzheimer Type (SDAT), Preexisting neurologic abnormalities including intracerebral arteriosclerosis and cerebral atrophy may increase susceptibility to unacceptably severe IFN neurotoxicity.     

Histopathology of BALB/c mice infected with the D variant of encephalomyocarditis virus

BALB/c mice infected with 10(5) pfu of the D variant of encephalomyocarditis virus were examined histopathologically during the subacute stage of infection. Main pathologic changes were observed in the brain, heart (massive myocardial necrosis with subsequent organization (i.e., replacement of necrotic myocardium by connective tissue) and congestion and dilatation of the right ventricle) and pancreas (moderate degranulation of beta-cells resulting in elevation of blood glucose level). The brain lesions were found most frequently in the pyramidal layer of the hippocampus and the granular layer of the cerebellum and were characterized by degeneration of neurons containing virus antigens. Perivascular mononuclear cell infiltration, spreading to the adjacent brain tissue, and thrombosis in small vessels were also frequently seen. Focal loss of neurons and gliosis developed later in these lesions.     

Independent association of antibodies against human papillomavirus type 16 and E7 proteins with cervical cancer

The E4 open reading frame (ORF) of human papillomaviruses (HPVs) is transcribed in abundant mRNAs encoding an fusion gene during the productive infection, and the HPV 16 E7 ORF encodes an oncoprotein detectable in the cell lines derived from cervical carcinoma. We examined 421 human sera, which included 108 samples from the patients with cervical carcinoma, for the presence of IgG antibodies against the HPV 16 E4 and E7 proteins by enzyme-linked immunosorbent assay. Bacterially expressed fusion protein lac- and nonfusion protein E7 were purified and used as antigens. All of the 22 serum samples positive for anti-E7 antibody and the 11 out of 15 samples positive for anti- antibody were from the patients with cervical carcinoma, but only one sample was found to contain both anti- and anti-E7 antibodies. These findings show specific and independent association of these antibodies with cervical carcinoma.     

Treatment of tardive dyskinesia with ceruletide

1. Seven patients with TD were treated with a single dose of ceruletide 0.8 microgram/kg i.m. 2. EMG and MV were recorded, and the average power spectrum was computed. 3. Effect of ceruletide on TD within 2 hr after injection was varied (3 cases: inhibitory, 2 cases: facilitatory, 2 cases: no effect). 4. Two patients with severe TD, who showed improvement after a single administration, received repeated administration of ceruletide (0.6 microgram/kg i.m.) and their TD symptoms were recorded on videotape for blind consensus ratings. In both patients ceruletide caused a marked decrease in severity of TD, and the effects lasted for several weeks. 5. The present findings might contribute to further understanding of the role of CCK in the brain and to the treatment of TD.     

Effects of angiotensin II on behavioral responses of defensive burying paradigm in rats.

The effects of angiotensin II (ATII) administered intracerebroventricularly in male Wistar rats in doses of 0.1, 0.5, and 1.0 micrograms, as well as of ATII (1.0 micrograms) + saralasin (SAR, an analog ATII) (5.0 micrograms), on behavioral responses of the defensive burying paradigm were studied. ATII-treated animals displayed significantly less defensive burying behavior (less time spent in defensive burying and less frequent burying than in vehicle-treated rats) in a dose-dependent manner. SAR at a dose of 5 micrograms did not affect burying behavior significantly; it also did not modify the inhibition effects of ATII on behavioral responses of the defensive burying test. These results provide evidence that ATII can exert anxiolytic actions on central transmitter systems mediating conditioned fear-related behaviors (i.e., defensive burying). The present study suggests that the defensive burying animal model is a rather sensitive test fulfilling the pharmacological criteria of dose-dependent sensitivity for studying the central effects of neuropeptides (e.g., ATII).     

3D kinematic analysis of the acromioclavicular joint during arm abduction using vertically open MRI.

Many researchers have evaluated the motions of the shoulder girdle, especially scapular and humeral motion. However, few reports exist that describe motions of the acromioclavicular joint. The purpose of the present study was to analyze the 3D kinematics of the acromioclavicular joint during arm abduction using 3D MR images obtained by a vertically open MRI. Fourteen shoulders of seven volunteers were examined in seven static positions from 0 degrees to the maximum abduction in a seated position. 3D surface models of the clavicle and scapula were created, and the movements of the acromioclavicular joint from 0 degrees to each position were calculated using the volume-based registration technique. From these calculations, the translations were evaluated and the rotational motions were analyzed using the concept of the screw axis. In the anteroposterior direction, the clavicle translated most posteriorly (-1.9 +/- 1.3 mm) at 90 degrees of abduction and most anteriorly (1.6 +/- 2.7 mm) at maximum abduction. In the superoinferior direction, the clavicle translated slightly superiorly (0.9 +/- 1.9 mm). When analyzing relative motion of the scapula with respect to the clavicle, the scapula generally rotated about a specific screw axis passing through the insertions of both the acromioclavicular and the coracoclavicular ligaments on the coracoid process. The average rotation was 34.9 +/- 8.4 degrees.     

Mild Hypercapnia Induces Vasodilation via Adenosine Triphosphate-sensitive K+ Channels in Parenchymal Microvessels of the Rat Cerebral Cortex

Background: Carbon dioxide is an important vasodilator of cerebral blood vessels. Cerebral vasodilation mediated by adenosine triphosphate (ATP)-sensitive K+ channels has not been demonstrated in precapillary microvessel levels. Therefore, the current study was designed to examine whether ATP-sensitive K+ channels play a role in vasodilation induced by mild hypercapnia in precapillary arterioles of the rat cerebral cortex.

Methods: Brain slices from rat cerebral cortex were prepared and superfused with artificial cerebrospinal fluid, including normal (Pco2 = 40 mmHg; pH = 7.4), hypercapnic (Pco2 = 50 mmHg; pH = 7.3), and hypercapnic normal pH (Pco2 = 50 mmHg; pH = 7.4) solutions. The ID of a cerebral parenchymal arteriole (5-9.5 [mu]m) was monitored using computerized videomicroscopy.

Results: During contraction to prostaglandin F2[alpha] (5 x 10-7 m), hypercapnia, but not hypercapnia under normal pH, induced marked vasodilation, which was completely abolished by the selective ATP-sensitive K+ channel antagonist glibenclamide (5 x 10-6 m). However, the selective Ca2+-dependent K+ channel antagonist iberiotoxin (10-7 m) as well as the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester (10-4 m) did not alter vasodilation. A selective ATP-sensitive K+ channel opener, levcromakalim (3 x 10-8 to 3 x 10-7 m), induced vasodilation, whereas this vasodilation was abolished by glibenclamide.     

Pharmacologic preconditioning effects: Prostaglandin E1 induces heat-shock proteins immediately after ischemia/reperfusion of the mouse liver

Prostaglandin E1 (PGE1) has several potential therapeutic effects, including cytoprotection, vasodilation, and inhibition of platelet aggregation. This study investigates the protective action of PGE1 against hepatic ischemia/reperfusion injury in vivo using a complementary DNA microarray. PGE1 or saline was continuously administered intravenously to mice in which the left lobe of the liver was made ischemic for 30 minutes and then reperfused. Livers were harvested 0, 10, and 30 minutes postreperfusion. Messenger RNA was extracted, and the samples were labeled with two different fluorescent dyes and hybridized to the RIKEN set of 18,816 full-length enriched mouse complementary DNA microarrays. Serum alanine aminotransferase and aspartate aminotransferase levels at 180 minutes postreperfusion were significantly lower in the PGE1-treated group than in the saline-treated group. The cDNA microarray analysis revealed that the genes encoding heat-shock protein (HSP) 70, glucose-regulated protein 78, HSP86, and glutathione S-transferase were upregulated at the end of the ischemic period (0 minutes postreperfusion) in the PGE1 group. Our results suggested that PGE1 induces HSPs immediately after ischemia reperfusion. HSPs might therefore play an important role in the protective effects of PGE1 against ischemia/reperfusion injury of the liver.