Orthopaedic metallic artefact reduction algorithm facilitates CT evaluation of the urinary tract after hip prosthesis.

AIM: To examine the improvement in the visualisation of bladder and ureteric pathologies next to a hip prosthesis with metallic artefact reduction for orthopaedic implants (O-MAR). MATERIALS AND METHODS: Thirty-four patients who underwent pelvic computed tomography (CT) for non-prosthesis-related causes were enrolled retrospectively. Portal venous phase scans were reconstructed both with standard iterative reconstruction (ITR) and with O-MAR. The density of the ureters and the bladder was measured at both sides in the plane of the prosthesis. A semi-quantitative score was also used to assess visibility. The R (version 3.4.1) package was used for statistical analysis. RESULTS: The average (µ) density of the 41 prosthesis side ureters was significantly lower on ITR images (µ=-94.76±150.48 [±SD] HU) than on O-MAR images (µ=-13.40±36.37 HU; p<0.0004). The difference between the ITR and O-MAR (µ=-138.62±182.64 versus -35.55±40.21 HU; p<0.0003) was also significant at the prosthesis side of the bladder. The visibility of the prosthesis side ureters was improved: 53.7% was obscured on ITR series compared to 4.9% on O-MAR. The visibility score was also better across all levels (p<0.001) with O-MAR. In four cases (13%), the O-MAR images significantly changed the diagnosis: in two cases ureteric stones, in one case each a bladder stone and a bladder tumour were discovered. CONCLUSIONS: O-MAR reconstruction of CT images significantly improves the visibility of the urinary tract adjacent to metallic hip implants. Thus, O-MAR is essential for detecting ureteric and bladder pathologies in patients with a hip prosthesis.

Different pattern of carotid and myocardial changes according to left ventricular geometry in hypertensive patients.

The relation between left ventricular (LV) hypertrophy and LV function is well known. However, less is known about the vascular changes influenced by LV geometry. We sought to investigate the relationship of LV geometry to carotid arterial and LV function. A total of 476 hypertensive patients were prospectively recruited. All subjects underwent echocardiography and carotid ultrasound. LV geometry is categorized into four groups according to relative wall thickness (RWT) and LV mass index (LVMI). Concentric LV geometry was associated with increased carotid intima-media thickness (IMT), ß-stiffness, and lower strain. All of the carotid parameters showed a stepwise change according to RWT of LV, whereas LV function was worse in hypertrophic geometry, as reflected by significantly lower systolic mitral annular velocity, higher left atrial volume index and E/E' ratio (P<0.001). By multivariate analysis after adjustment for clinical and laboratory parameters, IMT was independently associated with RWT, whereas myocardial function was independently associated with LVMI. Carotid arterial function and IMT showed worse values in concentric geometry, whereas LV systolic and diastolic function were worse in hypertrophic geometry, suggesting a discrepancy between carotid arterial and LV function in hypertensive patients.

The prevalence of metabolic syndrome and its association with alanine aminotransferase in clozapine-treated Korean patients with schizophrenia.

Widely ranging prevalence rates for metabolic syndrome (MetS) in patients taking clozapine have been reported on the basis of various criteria, and most studies have been carried out in non-Asian countries. Therefore, we examined the prevalence of MetS in Korean patients using three commonly applied criteria with two waist-circumference cutoff values. The indirectly standardized prevalence ratio (ISPR) was estimated using data from the Fourth Korean National Health and Nutrition Examination Survey (KNHNES, 2007) to compare the prevalence of MetS in patients with that in the general population. In addition, we also examined whether serum alanine aminotransferase (ALT) and aspartate aminotransferase levels serve as biochemical markers for the identification of MetS. We reviewed the electromedical records of patients with schizophrenia who had taken clozapine as the sole antipsychotic for 3 months or more. The prevalence of MetS ranged from 34.5 to 46.9%, and the ISPR ranged from 2.4 to 2.8, given the three definitions of MetS and the two waist-circumference cutoff points for women. The ISPR for MetS among those aged 18-30 years was the highest and decreased with age in both men and women. After adjusting for age, patients with normal serum ALT levels who were in the top third were significantly more likely to have MetS compared with those who were in the bottom third. Logistic regression analysis showed that serum ALT levels and use of antidepressants were significantly related to the presence of MetS. Korean patients with schizophrenia who were receiving clozapine as the sole antipsychotic showed a high prevalence of MetS. Although we found substantial differences in the prevalence according to criteria, the ISPR indicated significantly higher rates of MetS in this group than in the general population. In the general population, younger patients had a much higher risk for MetS than older patients. Elevated levels of serum ALT that were in the normal range were associated with the presence of MetS, which suggests the possibility of using serum ALT level as an early indicator for MetS in patients treated with clozapine.

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.

Brain glucose metabolic changes associated with neuropsychological improvements after 4 months of treatment in patients with obsessive-compulsive disorder.

OBJECTIVE: The study was designed to elucidate regional brain metabolic changes according to a treatment and their relationship with neuropsychological performance changes in obsessive-compulsive disorder (OCD). METHOD: Cerebral glucose metabolic rates were repeatedly measured before and after treatment in 10 patients with OCD using [18F]-2-fluoro-deoxyglucose positron emission tomography (PET). They were compared on a voxel-basis, and the correlations were counted between the regional metabolic changes and the degree to improvement on the neuropsychological assessments. RESULTS: After treatment, the patients showed significant (P < 0.005, two-tailed) regional metabolic changes in multiple brain areas involving frontal-subcortical circuits and parietal-cerebellar networks. Especially, the metabolic changes of the putamen, the cerebellum, and the hippocampus were significantly correlated with the improvement of the immediate- and delayed-recall scores of the Rey-Osterrieth Complex Figure Test (RCFT). CONCLUSION: These results suggest a possibility that metabolic changes of frontal-subcortical and parietal-cerebellar circuit changes may underlie cognitive improvements in patients with OCD.

Inhibition of nitric oxide synthesis increases apoptotic cardiomyocyte death and myocardial angiotensin-converting enzyme gene expression in ischemia/reperfusion-injured myocardium of rats.

Cardiomyocyte apoptosis is an important pathogenic mechanism in myocardial ischemia/reperfusion (I/R) injury. It has been shown that nitric oxide (NO) and the renin-angiotensin system (RAS) are closely related, and both systems regulate apoptotic cell death. However, the effects of NO modulation on myocardial apoptotic cell death and changes in the RAS in the I/R-injured myocardium have not been studied. Female Sprague-Dawley rats were randomized into three groups: NO synthesis inhibitor, N(G)-nitro-L-arginine-methyl ester (L-NAME, 10mg/kg); NO precursor, L-arginine (540mg/kg); and vehicle. The rats were then subjected to 45 min coronary occlusion followed by 4 h reperfusion. The TdT-mediated in situ nick and labeling (TUNEL) indices were 39.9%+/-0.8% at the border and 30.9%+/-1.2% at the center of the I/R area in the vehicle group. L-NAME administration significantly increased these TUNEL-positive cells to 45.3%+/-1.9% and 37.9%+/-1.3%, respectively (P < 0.05 each). L-arginine administration reduced the TUNEL index at the border zone with marginal significance (P = 0.08 vs vehicle group). I/R injury significantly reduced the angiotensin-converting enzyme (ACE) mRNA expression in the left (ventricular) free wall of vehicle group rats. However, ACE mRNA expression was 1.9 times greater in the L-NAME group than that in the vehicle group (P < 0.05). This study showed that the inhibition of NO synthesis increased apoptotic cardiomyocyte death and local ACE mRNA expression in the I/R-injured myocardium. Our observations indicate that NO, ACE, and apoptotic cardiomyocyte death are related to each other during I/R injury.

Ventricular remodeling and transforming growth factor-beta 1 mRNA expression after nontransmural myocardial infarction in rats: effects of angiotensin converting enzyme inhibition and angiotensin II type 1 receptor blockade.

With the application of early reperfusion therapy after acute MI, the incidence and importance of nontransmural infarction is increasing. In a rat model with nontransmural infarction, we evaluated 1) the changes of LV dimension, LV interstitial fibrosis and transforming growth factor-beta1 (TGF-beta1) mRNA expression and 2) the effects of angiotensin converting enzyme (ACE) inhibitor and angiotensin II type 1 (AT1) receptor antagonist treatment. Female Sprague-Dawley rats were subjected to 45 min of coronary occlusion followed by reperfusion, and five days after the operation the animals were randomized to untreated (n = 19), captopril-treated (n = 15) and losartan-treated (n = 14) groups. Twenty-six days after MI, echocardiographic examination revealed a remarkable dilatation of LV. Captopril or losartan treatment reduced the extent of LV cavity dilatation. Collagen volume fractions in noninfarcted septum as well as in peri-infarct area decreased with captopril or losartan treatment, compared to those of the untreated rats. In noninfarcted septum of untreated rats, TGF-beta1 mRNA expression increased more than two fold (P < 0.05 vs. pre-MI) 5 and 10 days after MI. Captopril or losartan treatment suppressed the acute induction of TGF-beta1 mRNA expressions. These results indicate that ACE inhibitor or AT1 receptor antagonist treatment after nontransmural infarction 1) attenuates LV remodeling as in transmural infarction and 2) decreases interstitial fibrosis at least partly by blocking the acute induction of TGF-beta1 mRNA expression.

Heart failure in Korean elderly patients - clinical features, prognosis and prognostic factors.

Heart failure (HF) is very common in the elderly but there are not sufficient data about the clinical characteristics and prognostic factors of HF among the Asian elderly patients. The aim of the study was to find out the clinical characteristics, survival, and prognostic factors of HF in Korean elderly patients. Among elderly patients admitted from February 1995 to February 1998, the patients with a discharge diagnosis of HF were enrolled. Through the medical record review, the diagnosis was confirmed and clinical parameters to affect survival were identified. Total number of the subjects was 104 [age: 77+/-7 years (65-96), male:female=36:68, follow-up duration: 20+/-14 months, LVEF: 46+/-16%]. Ischemic heart disease (IHD) was the most common cause of HF (42%) followed by valvular heart disease (28%), and hypertension (20%). The 1-year survival rate was 71.3%. Advanced age [risk ratio (RR): 1.41 per 5 years of age; 95% CI: 1.11-1.80] and reduced left ventricular ejection fraction (0.69 per 10%, 0.52-0.93), poor initial functional class (2.40, 1.15-5.00), diabetes (2.79, 1.30-5.97) and past history of HF (2.37, 1.10-5.10) badly affected the survival rates. When the Cox proportional hazard model was applied for multivariate analysis, only aging (1.64 per 5 years of age, 1.19-2.28) and diabetes (4.92, 1.83-13.23) predicted poor prognosis. Twenty-seven percent of the patients had diastolic HF (LVEF>45%, LVEDD<55 mm) who had higher survival rates with marginal significance (0.35, 0.10-1.17, P=0.09).

Length-dependent modulation of smooth muscle activation: effects of agonist, cytochalasin, and temperature.

We tested the hypothesis that mechanical strain modulates agonist sensitivity of smooth muscle by measuring myosin phosphorylation and contractile force in bovine tracheal smooth muscle activated by various concentrations of the muscarinic receptor agonist carbachol and at various muscle lengths. Increasing carbachol concentration by 10,000-fold did not restore myosin phosphorylation levels at shorter muscle lengths to the level at optimal length (Lo). Maximum levels of myosin phosphorylation induced by carbachol at 0.6, 0.8, and 1.0 Lo were similar but became lower at <0.6 Lo. Cytochalasin D significantly attenuated carbachol-induced contraction by 54%. In addition, cytochalasin D treatment induced a parallel downward shift in the length-myosin phosphorylation relation. Lowering temperature from 37 to 23 degrees C did not significantly change the length dependencies of carbachol-induced active force and myosin phosphorylation. These results have led us to conclude that 1) agonist sensitivity and maximum level of activation (as measured by myosin phosphorylation) are targets of length-dependent modulation, 2) actin filaments involved in contraction and length-dependent modulation are distinct in sensitivity to cytochalasin D, and 3) length-dependent modulation is relatively temperature insensitive.

Reciprocal change in angiotensinogen mRNA expression in rat myocardium and liver after myocardial infarction.

The aim of this study was to analyze sequential change of angiotensinogen (Ao) mRNA expression in rat liver and noninfarcted myocardium after myocardial infarction (MI). Female sprague-Dawley rats were subjected either to left coronary artery occlusion or sham operation. Three weeks after MI, coronary artery ligation resulted in comparable infarct sizes. A hypokinetic thin anterior wall and remarkable dilatation of the left ventricle, as well as decreased contractility (left ventricular end-systolic dimension = 6.0+/-0.4, 3.3+/-0.2, LV end-diastolic dimension = 7.9+/-0.3, 5.9+/-0.2 mm, and fractional shortening = 25.3+/-3.1%, 45.1+/-3.3%) were shown in the MI and sham group, respectively, by echocardiography (P < 0.01). Experimental MI caused a significant fall in systolic blood pressure (MI 90+/-5.0, vs sham 130+/-7.5 mmHg; P< 0.01) and significantly higher left ventricular end-diastolic pressure (MI 21+/-1.5, vs sham 11+/-1.0 mmHg: P < 0.01). At 4, 18, and 24h after MI, liver Ao mRNA levels, as shown by Northern blot analysis, had increased by up to four times (Ao/glyceraldehyde-3-phosphate dehydrogenase (GAPDH) = 1.4+/-0.1 and 6.0+/-0.2 at baseline and 4h after MI, respectively (P < 0.01). After sham surgery, however, the corresponding increase was slight (maximal 1.5-fold). Three days after MI, liver mRNA had returned to the baseline level. In contrast, ATG mRNA expression in noninfarcted myocardium, as shown by reverse transcription-polymerase chain reaction and Southern blotting, decreased transiently during the acute phase. It returned to its baseline level within 3 days, and then increased further (Ao/ GAPDH = 2.9+/-0.6, 0.3+/-0.1, 3.2+/-0.8, and 3.7+/-0.8 at baseline, 24h, 3 days, and 3 weeks after MI, respectively). In conclusion, it can be stated that after MI, the Ao gene contributes, acutely in the liver and chronically in the myocardium, to the maintenance of hemodynamic homeostasis during the acute phase and ventricular remodeling during the chronic phase.

Right hemisphere abnormalities in major depression: quantitative electroencephalographic findings before and after treatment.

The quantitative EEGs of drug-free depressed patients were analyzed and compared to age and sex-matched controls, using spectral analysis. In addition, QEEGs of depressed patients after clinical improvement resulting from 6 weeks of antidepressant treatment were also analyzed. The subjects were 20 patients suffering from major depression (DSM-III-R). Scores on the Hamilton Rating Scale for Depression (HRSD) of all patients showed a reduction of more than 50% at the end of the 6th week. The results show: (1) delta and theta bipolar absolute powers of the right hemisphere increased in drug-free depressed patients, compared to controls. (2) No changes in all bands of QEEG were found after clinical improvement resulting from 6 weeks of treatment. These results suggest that the right hemisphere plays an important role in major depression, and that a reduction in symptoms is not necessarily indicative of an improvement in underlying major depression.