Abatement of fluorinated compounds using a 2.45GHz microwave plasma torch with a reverse vortex plasma reactor.

Abatement of fluorinated compounds (FCs) used in semiconductor and display industries has received an attention due to the increasingly stricter regulation on their emission. We have developed a 2.45GHz microwave plasma torch with reverse vortex reactor (RVR). In order to design a reverse vortex plasma reactor, we calculated a volume fraction and temperature distribution of discharge gas and waste gas in RVR by ANSYS CFX of computational fluid dynamics (CFD) simulation code. Abatement experiments have been performed with respect to SF6, NF3 by varying plasma power and N2 flow rates, and FCs concentration. Detailed experiments were conducted on the abatement of NF3 and SF6 in terms of destruction and removal efficiency (DRE) using Fourier transform infrared (FTIR). The DRE of 99.9% for NF3 was achieved without an additive gas at the N2 flow rate of 150 liter per minute (L/min) by applying a microwave power of 6kW with RVR. Also, a DRE of SF6 was 99.99% at the N2 flow rate of 60 L/min using an applied microwave power of 6kW. The performance of reverse vortex reactor increased about 43% of NF3 and 29% of SF6 abatements results definition by decomposition energy per liter more than conventional vortex reactor.

Analysis of S gene mutation of the hepatitis B virus in adult liver transplant recipients showing resistance to hepatitis B immunoglobulin therapy.

BACKGROUND: A considerable proportion of recipients of liver transplantations who are presented hepatitis B immunoglobulin (HBIG) monotherapy for hepatitis B virus (HBV) prophylaxis develop HBIG resistance. In this study, we investigated the mutation patterns in the major hydrophilic region (MHR) of amino acid sequences 100 to 160. METHODS: Using the gene sequence analyzer for amino acid sequences 0 to 226 in the S/pre-S region we analyzed blood samples of 15 patients showing HBIG resistance after high-dose HBIG prophylaxis. RESULTS: Various mutations in the MHR were observed in 14/15 samples: Gly145Arg mutation in 8/13 Adr subtype and 1/2 Ayw subtype samples (60%). The next most common mutation was Gly165Trp in 8/13 Adr subtype but neither of 2 Ayw subtype samples (53.3%). Concurrent antiviral resistance was noted in 5 patients: lamivudine (n = 5), or entecavir (n = 3), but not adefovir, suggesting the occurrence of simultaneous, antiviral cross-resistances. Two patients underwent retransplantation due to the progression of HBV infection despite vigorous antiviral therapy. At diagnosis of HBV recurrence, the mean HBV DNA load was 6.5 × 10(6) copies/mL; 4 patients showed paradoxical coexistence of anti-HBs and HBsAg. Currently, 2 subjects show low-level HBV DNA replication in peripheral blood, although the other 12 had no DNA replication after prolonged antiviral therapy. CONCLUSIONS: This study suggested that various mutations in the "a" determinant were associated with HBIG resistance. Since treatment failure to rescue antiviral therapy was often associated with delayed detection of HBV recurrence rather than concurrent antiviral resistance, frequent HBV surveillance using more sensitive screening tests, such as HBeAg and HBV DNA polymerase chain reaction assay, seems to be mandatory.

Shelf acetabuloplasty for children with Perthes' disease and reducible subluxation of the hip: prognostic factors related to hip remodelling.

We evaluated radiological hip remodelling after shelf acetabuloplasty and sought to identify prognostic factors in 25 patients with a mean age of 8.9 years (7.0 to 12.3) who had unilateral Perthes' disease with reducible subluxation of the hip in the fragmentation stage. At a mean follow-up of 6.7 years (3.2 to 9.0), satisfactory remodelling was observed in 18 hips (72%). The type of labrum in hip abduction, as determined by intra-operative dynamic arthrography, was found to be a statistically significant prognostic factor (p = 0.012). Shelf acetabuloplasty as containment surgery seems to be best indicated for hips in which there is not marked collapse of the epiphysis and in which the extruded epiphyseal segment slips easily underneath the labrum on abduction, without imposing undue pressure on the lateral edge of the acetabulum.

Depression and the vision-related quality of life in patients with retinitis pigmentosa.

AIMS: To assess the relationship between depression and the vision-related quality of life in patients with retinitis pigmentosa (RP). METHODS: The study included 144 patients diagnosed as having RP. The mean age of the patients was 38.5 (SD 13.3) years, and 42% of the subjects were women. They answered the National Eye Institute Visual Function Questionnaire (NEI-VFQ) to assess the vision-related quality of life and the Beck Depression Inventory (BDI) to assess depressive symptoms. Patients were classified into groups with and without depression according to the BDI score. The NEI-VFQ composite and subscale scores were compared between groups. The correlations between the BDI and the NEI-VFQ, weighted visual acuity (WVA) and functional vision score (FVS) were investigated. RESULTS: The depressed group had significantly less subjective visual function compared with the non-depressed group. A negative correlation was observed between the BDI and the NEI-VFQ scores, while no correlation was found between the BDI score and WVA or FVS. CONCLUSION: The RP patients with depression had poorer vision-related functions compared with those patients without depression, which cannot be explained by the visual acuity. Interventions to diagnose and treat depression are necessary to enhance the overall quality of life in RP patients.

White matter abnormalities in drug-naïve patients with obsessive-compulsive disorder: a diffusion tensor study before and after citalopram treatment.

OBJECTIVE: The aim was to investigate the white matter abnormalities of drug-naïve patients with obsessive-compulsive disorder (OCD) using diffusion tensor-imaging and the white matter changes in the patients after pharmacotherapy. METHOD: Thirteen drug-naïve OCD patients and 13 age- and sex-matched healthy comparison subjects were examined using diffusion tensor-imaging and structural magnetic resonance imaging. Measurements were made in OCD patients before and after 12 weeks of citalopram treatment. RESULTS: Compared with controls, the drug-naïve OCD patients showed significant increases in fractional anisotropy (FA) in the corpus callosum, the internal capsule and white matter in the area superolateral to the right caudate. The increases in FA were mostly no longer observed in patients after 12 weeks of treatment compared with controls. CONCLUSION: Our findings suggest that white matter alterations are associated with the pathophysiology of OCD, and the abnormalities may be partly reversible with pharmacotherapy.

Altered neural circuit for working memory before and after symptom provocation in patients with obsessive-compulsive disorder.

OBJECTIVE: The authors compared the neural circuits recruited for working memory (WM) in obsessive-compulsive disorder (OCD) patients both at a neutral state and at a symptom provoked state. METHOD: Twelve OCD patients, and 12 age-, and sex-matched healthy subjects underwent [(15)O]H(2)O positron emission tomography (PET) scanning, while performing WM task. In the patients, the tasks were performed both in the neutral and in the symptom provoked states. RESULTS: In the OCD patients, the right caudate and the right superior parietal cortex (rSPC) displayed activations for WM at the neutral state, while the right cingulate cortex and rSPC displayed activations for WM at the symptom provoked state. Path analysis revealed that the activity of the caudate and orbitofrontal cortex was altered according to the interaction between WM and symptom provocation. CONCLUSION: The interaction between symptom provocation and WM occurring in the fronto-striatal system may hold the key to the neurobiology of OCD.

Similarity and disparity of obsessive-compulsive disorder and schizophrenia in MR volumetric abnormalities of the hippocampus-amygdala complex.

OBJECTIVES: Given that obsessive-compulsive disorder (OCD) and schizophrenia may share clinical symptoms as well as functional brain abnormalities, this study was designed to clarify common and different morphological abnormalities in OCD and schizophrenia. METHODS: Volumes of the hippocampus, the amygdala, and the thalamus were measured in three age and sex matched groups of 22 patients with OCD, 22 patients with schizophrenia, and 22 normal subjects using three dimensional magnetic resonance imaging. Volume tracing was performed manually on serial coronal slices with the references of sagittal or axial planes using internal landmarks. RESULTS: Hippocampal volume was bilaterally reduced in both OCD and schizophrenic patients versus the normal controls. Left amygdala volume was significantly enlarged in patients with OCD but not in patients with schizophrenia versus the normal controls. The thalamus did not show any volumetric group differences. CONCLUSIONS: Non-specific hippocampal reduction in both the OCD and schizophrenic groups is likely to link to a clinical overlap between the two illnesses, whereas the left amygdala enlargement observed only in the OCD patients seems to be suggestive of a unique role for the amygdala in the pathophysiology of OCD.

Survival and prognostic factors in patients with primary pulmonary hypertension.

OBJECTIVES: Primary pulmonary hypertension (PPH) that affects predominantly young and productive people is a progressive fatal disease of unknown cause. The objectives of this study were to characterize mortality in patients with PPH and to investigate the factors associated with their survival. METHODS: Thirteen patients with PPH were enrolled between 1988 and 1996 and followed-up through July 1999. Measurements at diagnosis included hemodynamic and pulmonary function variables in addition to information on demographic data and medical history. RESULTS: 1) The mean age of the patients with PPH enrolled into the study was 36.1 +/- 9.3 years with female predominance. 2) The estimated median survival was 3.4 +/- 0.6 years. 3) Decreased cardiac index was the only significant predictor of mortality (Cox proportional hazards model). CONCLUSION: Patients with PPH have a poor survival expectancy. In this limited study with a small number of patients, mortality is largely associated with decreased cardiac index.

Two cases of chronic pancreatitis with pseudocyst complicated by obstructive jaundice.

We recently treated two cases of chronic pancreatitis with obstructive jaundice due to compression of the common bile duct by pancreatic pseudocyst. The two cases were males admitted with the complaint of icteric skin color. The first, a 46-year-old male, admitted with the complaint of icteric skin color. He was treated by operative cystojejunostomy after percutaneous drainage of the pseudocyst and percutaneous transhepatic biliary drainage. The other case was a 58 year-old male who admitted with the complaint of icteric skin color. He had an infected pseudocyst in the pancreas and was endoscopically treated. Both of them were discharged with favorable clinical course and normal laboratory findings after the treatment. The former patient remained well 11 months after treatment, but the latter patient died from necrotizing pancreatitis and septic shock 6 months after treatment. Most cases of obstructive jaundice associated with pseudocysts appear to be due to fibrotic stricture of the intrapancreatic portion of the common bile duct rather than due to compression of the bile duct by the pseudocyst. In a patient with secondary pancreatic infection or obstructive jaundice following pancreatic disease, differentiating between these two conditions is an important aspect of accurate diagnosis and therapy. Herein we report two unusual cases of chronic pancreatitis with pseudocyst complicated by obstructive jaundice.

Role of adenosine A(2B) receptors in vasodilation of rat pial artery and cerebral blood flow autoregulation.

This study was aimed to investigate the underlying mechanism of vasodilation induced by the activation of A(2B) adenosine receptors in relation to cerebral blood flow (CBF) autoregulation. Changes in pial arterial diameters were observed directly through a closed cranial window. N(omega)-nitro-L-arginine methyl ester (L-NAME, nitric oxide synthase inhibitor) significantly suppressed the concentration-dependent vasodilations induced by adenosine and 5'-N-ethylcarboxamido-adenosine (NECA) but not the vasodilation by CGS-21680 (A(2A)-receptor agonist). Moreover, NECA-induced vasodilation was suppressed by alloxazine (1 micromol/l) but not by ZM-241385 (1 micromol/l, A(2A) antagonist), which suggests mediation by A(2B)- receptor activation. Otherwise, the level of nitrite/nitrate was concentration dependently increased in the artificial cerebrospinal fluid (CSF) when adenosine and NECA were suffused over the cortical surface. L-NAME and alloxazine, but not ZM-241385, largely inhibited their releases. The lower limit of CBF autoregulation was little affected following pretreatment with L-NAME or alloxazine. Thus it is suggested that adenosine-induced vasodilation via activation of A(2B)-adenosine receptors of the rat pial artery is coupled to the production of nitric oxide, which contributes little to CBF autoregulation.

Hypocholesterolemic effect of naringin associated with hepatic cholesterol regulating enzyme changes in rats.

The effects of the citrus bioflavonoid naringin were tested by using it as a supplement in a high-cholesterol diet. Male rats were fed for 42 days with a 1% (wt/wt) high cholesterol diet either with or without naringin-supplementation (0.1%, wt/wt) to study the effect on plasma lipid levels, hepatic lipid contents, hepatic enzyme activity, and the excretion of fecal neutral sterols. Naringin did not significantly alter the levels of plasma triglycerides, however, the levels of plasma cholesterol (3.80 +/- 0.31 mmol/L vs. 2.61 +/- 0.30 mmol/L, mean +/- SE; p < 0.05) and hepatic cholesterol (70.3 +/- 4.3 mg/g vs. 54.3 +/- 3.8 mg/g, mean +/- SD; p < 0.05) were significantly lowered compared to those of the control. HMG-CoA reductase (2487.0 +/- 210.0 pmole/min/mg vs. 1879.0 +/- 236.0 pmole/min/mg, mean +/- SE; p < 0.05) and ACAT (806.0 +/- 105.0 pmole/min/mg vs. 643.0 +/- 80.0 pmole/min/mg, mean +/- SE; p < 0.05) activities were both substantially lower in the naringin-supplemented group than in the control. The naringin supplementation markedly decreased the excretion of fecal neutral sterols (204.7 +/- 28.5 mg/day) compared to the control (521.9 +/- 53.9 mg/day). The combination of the inhibited HMG-CoA reductase (-24.4%) and ACAT (-20.2%) activities as a result of naringin supplementation could account for the decrease of fecal neutral sterols.

Pharmacological profiles of SKP-450 and its family, a K+ channel opener, in comparison with levcromakalim.

This study was carried out to characterise the vasodepressor and vasorelaxant actions of a benzopyran derivative, SKP-450 and its family, (+/-)-racemate SKP-411, (+)-enantiomer SKP-451, and the metabolites of SKP-450 (SKP-818 and SKP-310) in comparison with levcromakalim (LCRK) in the canine coronary, rabbit basilar and vertebral arterial segments. SKP-450, its family (SKP-411 and SKP-451) and the metabolite of SKP-450 (SKP-818) caused concentration-dependent relaxations as well as LCRK in the canine coronary artery and rabbit basilar and vertebral arteries. The relaxant potency of SKP-450 was significantly higher than that of LCRK in the three arteries in terms of EC50 values. SKP-450- and LCRK-induced vasorelaxations were competitively antagonised by glibenclamide with pA2 values of 7.60 (slope 1.22) and 7.99 (slope, 1.00), respectively. SKP-450 (0.1 and 1.0 microM) caused a significant stimulation of the 86Rb efflux from canine coronary arteries in a concentration-dependent manner as well as LCRK (1 and 10 microM), and their effects were antagonised by glibenclamide (10 microM). SKP-450 as well as LCRK produced long-lasting decreases in mean arterial pressure in the spontaneously hypertensive rats (SHR). These results suggest that SKP-450 has a significantly higher potency than LCRK in in vitro vasorelaxation, and it exerts potent and long-lasting vasodepressor effects with its active metabolite (SKP-818).

Decreased CGRP level with increased sensitivity to CGRP in the pial arteries of spontaneously hypertensive rats.

It was aimed to investigate the importance of calcitonin gene-related peptide (CGRP) in maintenance of normal cerebral microcirculation. We examined both the functional (in vivo) and biochemical effects (in vitro) of CGRP on the pial arteries of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). When mock cerebrospinal fluid containing capsaicin (3 x 10(-7) M) was suffused over the cortical surface, the diameter of pial arteries of SHR was transiently increased and rapidly returned to the baseline level, while the capsaicin-induced increase in pial arterial diameters of WKY was large and sustained for a longer duration (> 10 min). Capsaicin-induced vasodilation was significantly attenuated by pretreatment with CGRP8-37, a CGRP1, receptor antagonist, in both WKY and SHR. On the other hand, cortical suffusion with CGRP (10(-9) approximately 10(-6) M) exerted a larger enhancement in the vasodilation of pial artery of SHR than WKY. The CGRP-induced vasodilation was significantly antagonized by CGRP8-37 in both WKY and SHR. The released level of CGRP-like immunoreactivity (CGRP-LI) from the pial artery was significantly lower in SHR (12.3 +/- 1.2 fmol/mm2/hr) than that in WKY (24.5 +/- 3.9 fmol/mm2/hr). CGRP (10(-6) M)-induced stimulation of cyclic AMP formation was rather larger in the pial arteries from SHR (50.2 +/- 5.8 fmol/mm2/30 min, p < 0.05) than those from WKY (34.5 +/- 3.8 fmol/mm2/30 min). These data suggest that, in the pial arteries of SHR, the transient vasodilation to capsaicin and enhanced vasodilation to CGRP are related to the decreased CGRP level in the cerebral microvascular beds, consequently leading to increased sensitivity of the CGRP receptors to CGRP.

Characterization of PD 121981- and CGP 42112-induced unmasking of low concentration effects of angiotensin II in rabbit abdominal aorta.

The unmasking of the low concentration effect of angiotensin II (AII) was identified within the concentration ranges of 10(-13) to 10(-11) M of AII by PD 121981 (5-diphenylacetyl-1-(4-methoxy-3-methylbenzyl)- 4,5,6,7-tetrahydro-1H-imidazo[4,5-c]-pyridine-6-carboxylic acid) and 10(-12) to 3 x 10(-10) M of AII by CGP 42112 (nicotinic acid-Tyr-(N alpha-benzyl-oxycarbonyl-Arg)Lys-His-Pro-IIe-OH), AT2 antagonists, in association with the ordinary contraction curve, i.e., high concentration effect (at 3 x 10(-10)-10(-6) M of AII), in the rabbit abdominal aorta. Thus, they showed clear biphasic features of AII-induced contraction curves. However, this was not the case for angiotensin I and angiotensin III. This PD 121981-evoked low concentration effect of AII was selectively inhibited by DuP 753 (0.01-1 nM), dithiothreitol (10 and 100 microM), pertussis toxin (50 and 300 ng/ml, for 2 hr), nifedipine (1 and 10 microM) and 8-(diethylamino)octyl 3,4,5-trimethoxybenzoate hydrochloride (1 and 3 microM), which suggests the receptors were the AT1 subtype. However, the high concentration effect of AII was not affected by these drugs within the concentration ranges used in the present studies. These myographic results were almost consistent with the features of the intracellular Ca++ changes. Thus, it was concluded that the receptors that mediate the low concentration effect of AII belong to the AT1 subtype. However, the current study did not determine the mechanism by which PD 121981 and CGP 42112 evoked the up-regulation of the AT1 receptors.

Effect of ouabain on relaxation induced by cromakalim in human and canine mesenteric arteries.

We investigated the effect of cromakalim, a K+ channel opener, that activates indirectly the Na(+)-K+ pump, in association with increased K+ conductance in the mesenteric arteries. In 65% of human mesenteric arteries tested, the concentration-dependent relaxation curves for cromakalim were biphasic: the low concentration (< 10(-7) M) effect was preferentially inhibited by ouabain, whereas the higher concentration effect was significantly inhibited by glibenclamide. In branches of canine mesenteric artery, the cromakalim-induced relaxation was inhibited by pretreatment with ouabain (1 microM) as well as by glibenclamide (1 microM). The reduction in contraction of human and canine mesenteric arterial strips caused by cromakalim was totally reversed by pretreatment with ouabain (1 microM) or glibenclamide (1 microM). On the other hand, in canine mesenteric artery, cromakalim caused a significant stimulation of 22Na+ influx and ouabain-sensitive 86Rb+ uptake in association with increased 86Rb+ efflux, all of which were inhibited by glibenclamide (1 microM). Thus, it is suggested that cromakalim possesses the additional property to stimulate the Na(+)-K+ pump through an elevation in intracellular Na+, resulting in strong relaxation of blood vessels.

Release of superoxide-dependent relaxing factor(s) from endothelial cells.

In the present work, an experimental system was designed to study superoxide anion radical, implicated as the cause of vascular dilatation. To circumvent its direct effect, we employed a two-bath system. When the endothelial cells (EC) were exposed to electrical field stimulation (EFS) or to a hypoxanthine-xanthine oxidase system in bath A plus its physiological buffer solution suffused on a helical strip of cat basilar artery in bath B, the contraction to 5-hydroxytryptamine (5-HT) was depressed to approximately 40-50% of the control value. The reduction was not elicited on EFS in a state of calcium deficiency or in the absence of EC. The depression could be prevented by pretreatment with superoxide dismutase (SOD), but not with an effective dose of catalase, dimethyl sulfoxide (DMSO), mannitol, or indomethacin. The percent depression of contraction was paralleled by an increase in SOD-inhibitable cytochrome c reduction, which was not associated with cyclic guanosine 3',5'-monophosphate formation. These results suggest that superoxide-dependent relaxing factor is released from EC differently than the endothelium-derived relaxing factor mediated by acetylcholine.

Assessment of superoxide-mediated release of vascular-inhibitory factor(s) from endothelial cells by using a two-bath system.

Release of a vascular-inhibitory factor from endothelial cells (EC), different from endothelium-derived relaxant factor (EDRF), was identified through use of a two-bath system. This two-bath system precluded the effects of oxygen-free radicals that appear when electrical field stimulation (EFS) is directly imposed on detector muscle.

Technetium-99m pyrophosphate scintigraphy for the detection of acute myocardial infarction. How useful is it?

To evaluate the contribution of Tc-99m pyrophosphate scintigraphy (TPS) on the overall management of patients suspected of having acute myocardial infarction (AMI), hospital records of 58 consecutive patients who underwent TPS, were evaluated in depth. The results indicate that TPS was essential for the diagnosis of AMI in 16% of the patients. TPS was most rewarding in perioperative patients and in patients with borderline or uninterpretable electrocardiographic and enzyme changes. Also, in some cases, TPS was able to confirm or exclude the diagnosis of AMI prior to the confirmation by serial electrocardiograms (ECG) and serial enzyme changes. TPS was less rewarding in patients with clinically low index of suspicion for AMI. It may also be confusing in patients with high clinical likelihood of AMI and a history of prior myocardial infarction because of the possibility of persistently positive TPS in some of these patients. Considering the limitations of ECGs, the cardiac enzymes, and atypical clinical presentations in the patient population we evaluated, TPS appears to be fairly accurate when the scintigraphic findings are compared with the final diagnosis at the time of discharge from the hospital.