Biomedical subjects

Mitsuo Iida

Publications and source records attributed to Mitsuo Iida.

At least 37 records · Page 2Linked to original sources

PubMed2006

Venous infarction secondary to septic cavernous sinus thrombosis.

A 65-year-old woman with poorly controlled diabetes presented bilateral miosis, bilateral abducens nerve palsy, and left hemiparesis. On MRI, cavernous sinus thrombosis, subdural empyema and hemorrhagic infarction in the frontotemporal lobe were detected. Cerebral angiogram revealed filling defect in the cavernous sinus with venous congestion but no involvement of internal carotid artery. Postmortem examination demonstrated hemorrhagic infarction in the right frontotemporal lobe as well as hemorrhagic necrosis of the pituitary gland. It should be noted that venous congestion due to cavernous sinus thrombosis may cause these complications.

Aged↗

PubMed2006

The serum pepsinogen test as a predictor of gastric cancer: the Hisayama study.

The authors examined whether a serum pepsinogen test (SPT) based on the combination of the serum pepsinogen I level and pepsinogen I/II ratio is a good predictor of gastric cancer occurrence in a general Japanese population. A total of 2,446 subjects aged > or =40 years were classified into negative, positive, and strong-positive SPT groups and were followed prospectively for 14 years (1988-2002). Compared with that for the negative SPT group (26 men, 10 women), gastric cancer incidence increased significantly for both men (n = 17; age-adjusted hazard ratio = 4.56, 95% confidence interval: 2.42, 8.60) and women (n = 6; age-adjusted hazard ratio = 5.84, 95% confidence interval: 2.00, 17.11) in the strong-positive SPT group. It was also significantly higher in the positive SPT group for men (n = 23; age-adjusted hazard ratio = 3.91, 95% confidence interval: 2.23, 6.86). These associations did not attenuate even after adjustment for other comprehensive risk factors. Stratified analysis revealed significant associations between the SPT and development of intestinal-type gastric cancer as well as of cancer in both Helicobacter pylori-negative and -positive subjects. These findings suggest that the SPT can serve as a predictor of intestinal-type gastric cancer, irrespective of H. pylori infection.

Adult↗

PubMed2006

Factors affecting recurrence in patients with Crohn's disease under nutritional therapy.

PURPOSE: This retrospective study was designed to determine risk factors for recurrence of Crohn's disease under enteral nutrition. METHODS: The clinical course of 145 patients with Crohn's disease, who were primarily induced into remission by total parenteral nutrition, was reviewed. The patients were classified into two groups: enteral nutrition group (n = 98; >/=1,200 kcal/day of enteral nutrition), or nonenteral nutrition group (n = 47;<1,200 kcal/day of enteral nutrition) according to the amount of their daily elemental or polymeric diet. Contributions of enteral nutrition and other clinical variables to the recurrence were analyzed retrospectively. A Crohn's disease activity index of >150 plus an increase in Crohn's disease activity index of >70 from the baseline value was defined as recurrence. RESULTS: Forty-two patients in the enteral nutrition group and 29 patients in the nonenteral nutrition group recurred during periods ranging from 3 to 159 months. The cumulative rate of recurrence was significantly higher in the nonenteral nutrition group than in the enteral nutrition group (P = 0.047). Among the Crohn's disease patients in the enteral nutrition group, penetrating type (relative risk, 3.89; 95 percent confidence interval, 1.58-9.62), colonic involvement (relative risk, 3.10; 95 percent confidence interval, 1.39-6.9), and previous history of surgery (relative risk, 2.48; 95 percent confidence interval, 1.16-5.33) were factors that significantly affected recurrence. In contrast, penetrating type was the only possible factor associated with recurrence in the nonenteral nutrition group (relative risk, 2.75; 95 percent confidence interval, 0.96-7.81). CONCLUSIONS: Among patients with Crohn's disease under maintenance enteral nutrition, the risk of recurrence differs according to the disease type and the site of involvement. The maintenance treatment by enteral nutrition alone seems insufficient for patients with penetrating type or with colonic involvement.

Adolescent↗

PubMed2006

Role of aldosterone in left ventricular hypertrophy in hypertension.

BACKGROUND: Aldosterone induces cardiac fibrosis in experimental animal models, but only limited information is available on the association between aldosterone and left ventricular (LV) hypertrophy in human beings. The aim of the present study was to determine the role of aldosterone in LV geometry and to investigate other types of target organ damage in hypertensive patients. METHODS: A total of 25 patients with primary aldosteronism caused by Conn's adenoma, 29 patients with renovascular hypertension, and 29 patients with essential hypertension (EHT) were included in the present study. Echocardiographic examinations and 24-h ambulatory blood pressure (BP) monitoring were conducted in all subjects. RESULTS: The mean 24-h systolic and diastolic BP in primary aldosteronism and renovascular hypertension were found to be comparable to those in EHT. However, LV mass index adjusted by age, sex, mean 24-h systolic BP, mean 24-h pulse rate, body mass index, and duration of hypertension was significantly increased in the patients with primary aldosteronism and renovascular hypertension compared with values in patients with EHT (150.2 +/- 7.7, 142.3 +/- 7.2, and 115.2 +/- 7.2 g/m(2), respectively). Hypertensive organ damages, such as proteinuria and hypertensive retinopathy, were more pronounced in the patients with renovascular hypertension; however, LV hypertrophy was especially exaggerated in patients with primary aldosteronism. CONCLUSIONS: These results indicate that aldosterone may induce LV hypertrophy in human beings as well as in experimental animals, and that angiotensin II and aldosterone may differentially participate in causing hypertensive target organ damage.

Adrenergic beta-Antagonists↗

PubMed2006

Probe EUS for the diagnosis of invasion depth in superficial esophageal cancer: a comparison between a jelly-filled method and a water-filled balloon method.

BACKGROUND AND OBJECTIVE: Diagnostic accuracy of probe EUS depends on the constant maintenance of luminal medium for acoustic coupling. This study compared the accuracy of probe EUS by a jelly-filled method (EUS-J) and by a water-filled balloon method (EUS-W) for the assessment of invasion depth in superficial esophageal cancer. DESIGN AND SETTING: A prospective, single-center study. PATIENTS: Forty superficial esophageal cancers in 38 patients. INTERVENTIONS: Patients were alternately assigned to EUS-J or EUS-W. The depth of invasion was classified into epithelium or lamina propria mucosae (D1), muscularis mucosae or superficial layer of the submucosa (D2), and deep portion of the submucosa (D3). Depiction rate, interobserver variation between 2 observers, and accuracy for the determination of invasion depth were compared between EUS-J and EUS-W. MAIN OUTCOME MEASUREMENTS AND RESULTS: Eighteen cancers were examined by EUS-J, and 22 cancers were examined by EUS-W. The actual depth of invasion was D1 in 21 cancers, D2 in 9 cancers, and D3 in 10 cancers. Depiction rate (94.4% vs 77.2%, P = .14) and interobserver agreement of EUS determination (82.3% vs 58.8%, P = .13) was higher in EUS-J than in EUS-W. The overall accuracy for the diagnosis of invasion depth was 77.8% in EUS-J and 59.1% in EUS-W (P = .18). The sensitivity for the diagnosis of D1 cancer was significantly higher in EUS-J than in EUS-W (100% vs 50%, P = .03), while the specificity was not different between the 2 procedures (81.8% vs 87.5%). CONCLUSIONS: EUS-J is superior to EUS-W for the assessment of invasion depth in superficial esophageal cancer, especially for intramucosal cancer.

Aged↗

PubMed2006

Metabolic syndrome and CKD in a general Japanese population: the Hisayama Study.

BACKGROUND: Metabolic syndrome has been linked with various atherosclerotic diseases, but has not been evaluated sufficiently as a risk factor for the development of chronic kidney disease (CKD) in the general population. METHODS: We followed up 1,440 community-dwelling individuals without CKD aged 40 years or older for 5 years and examined the effects of metabolic syndrome, defined by the modified National Cholesterol Education Program Adult Treatment Panel III criteria, on the development of CKD. RESULTS: During follow-up, 88 subjects experienced CKD. The age- and sex-adjusted 5-year cumulative incidence of CKD was significantly greater in subjects with than without metabolic syndrome (10.6% versus 4.8%; P < 0.01). In multivariate analysis, even after adjustment for other confounding factors, including insulinemia, metabolic syndrome remained an independent risk factor for the occurrence of CKD (odds ratio, 2.08; 95% confidence interval [CI], 1.23 to 3.52). Compared with subjects with 1 or fewer metabolic syndrome component, multivariate-adjusted odd ratios for CKD in subjects with 2, 3, and 4 or more metabolic syndrome components were 1.13 (95% CI, 0.60 to 2.12), 1.90 (95% CI, 0.98 to 3.69), and 2.79 (95% CI, 1.32 to 5.90), respectively. The rate of change in kidney function during 5 years decreased significantly in subjects with 4 or more metabolic syndrome components compared with those with 1 or fewer component in the age group of 40 to 59 years, whereas it also was significantly low in subjects with 3 metabolic syndrome components in the group aged 60 years or older. CONCLUSION: Our findings suggest that metabolic syndrome is a significant risk factor for the development of CKD in the general population.

Adult↗

PubMed2006

Deletion of the SOCS3 gene in liver parenchymal cells promotes hepatitis-induced hepatocarcinogenesis.

BACKGROUND & AIMS: A recent study has suggested that the methylation silencing of the suppressor of cytokine signaling-3 (SOCS3), a negative regulator of interleukin-6-related cytokines, could be involved in hepatocellular carcinoma (HCC). However, the roles of SOCS3 in hepatocellular carcinogenesis and hepatitis have not been established. We investigated the effect of deleting the SOCS3 gene on the development of hepatitis and HCC in hepatitis C virus-infected patients and mouse models. METHODS: The expression of SOCS genes in HCC and non-HCC regions of patient samples was determined by real-time reverse-transcription polymerase chain reaction and immunoblotting. The conditional knockout approach in mice was used to determine the hepatocyte-specific roles of SOCS3. To generate a liver-specific deletion, floxed SOCS3 (SOCS3(fl/fl)) mice were crossed with albumin-Cre transgenic mice. Hepatitis and HCC were induced by administering concanavalin A and diethylnitrosamine, respectively. RESULTS: SOCS3 expression was reduced in the HCC regions compared with the non-HCC regions. Carcinogen-induced hepatic tumor development was enhanced by deletion of the SOCS3 gene, which was associated with higher levels of the targets of signal transducers and activators of transcription (ie, B-cell lymphoma-XL, B-cell lymphoma-2, C-myelocytomatosis, cyclin D1, and vascular endothelial growth factor). In the concanavalin A-mediated hepatitis model, deletion of the SOCS3 gene in the hepatocytes protected against liver injury through suppression of interferon-gamma signaling and induction of the antiapoptotic protein Bcl-XL. CONCLUSIONS: Deletion of the SOCS3 gene in hepatocytes promotes the activation of STAT3, resistance to apoptosis, and an acceleration of proliferation, resulting in enhanced hepatitis-induced hepatocarcinogenesis.

Adult↗

PubMed2006

Blockade of tumor necrosis factor-alpha-converting enzyme improves experimental small intestinal damage by decreasing matrix metalloproteinase-3 production in rats.

OBJECTIVE: Tumor necrosis factor (TNF)-alpha-converting enzyme (TACE), which has been purified, regulates maturity of TNF-alpha. Matrix metalloproteinases (MMPs) play a key role in various inflammatory conditions. The incidence of intestinal damage has increased, but the mechanism and treatment have not been well understood. The purpose of this study was to investigate the roles of TACE and MMP in indomethacin (Indo)-induced intestinal damage as well as the therapeutic effects of TACE inhibitor and selective MMP inhibitor (sMMPi) on this intestinal damage in rats. MATERIAL AND METHODS: In the first experiment, serial changes in intestinal ulcers and the production of MMP were investigated. In the second experiment, we assessed the effect of three TACE and/or MMP inhibitors and the production of TNF-alpha, TACE, MMP-3, -9 and tissue inhibitor of MMP (TIMP)-1. The rats were divided into five groups: a control group, and four groups that received Indo alone, Indo plus TACE inhibitor (GM6001), Indo plus a selective MMP-3 inhibitor and Indo plus an MMP-9/13 inhibitor, respectively. RESULTS: MMP-3 was overexpressed at 24 h after Indo administration, when intestinal injury was most prominent macroscopically and microscopically. GM6001 significantly decreased ulcer severity and suppressed MMP-3 in a dose-dependent fashion. The selective MMP-3 inhibitor dose-dependently ameliorated intestinal damage to the same degree as GM6001, but the MMP-9 inhibitor had no effect on the injury. CONCLUSIONS: MMP-3 inhibition ameliorates intestinal damage without apparently affecting either TNF-alpha or TACE production and the dose-response curve suggests that the beneficial effect of the so-called TACE inhibitor is actually mainly mediated via MMP-3 inhibition rather than TNF-alpha inhibition.

ADAM Proteins↗

PubMed2006

Successful treatment of six patients with neuroleptic malignant syndrome associated with myoglobulinemic acute renal failure.

Neuroleptic malignant syndrome is a rare but potentially lethal, rare reaction to neuroleptics which is characterized by altered levels of consciousness, extrapyramidal effects, autonomic instability, hyperthermia, and elevated serum creatine phosphokinase levels. The most serious complication of neuroleptic malignant syndrome is acute renal failure. We investigated six cases of neuroleptic malignant syndrome associated with myoglobulinemic acute renal failure due to rhabdomyolysis and effect of hemodialysis or hemodiafiltration. The patients were five males and one female with a mean age of 43.5 yr. All of the patients, who developed acute renal failure induced from rhabdomyolysis, had previously received butyrophenone (haloperidol), phenothiazine, benzamide, iminomide, benzisoxazole, antidepressants, and hypnotics (benzodiazepine and barbiturate) for the treatment of schizophrenia. The clinical manifestations of neuroleptic malignant syndrome were characterized by altered consciousness, muscle rigidity and weakness, fever, and excessive perspiration. The peak laboratory data were blood urea nitrogen 102 +/- 26 (mean +/- SD) mg/dL, serum creatinine 9.1 +/- 2.1 mg/dL, serum creatine phosphokinase 229,720 +/- 289,940 IU/L, and all of them developed oliguric acute renal failure. Dantrolene sodium administration was given to five cases and hemodialysis or hemodiafiltration was performed in all of them. The serum creatinine level after hemodialysis or hemodiafiltration was 1.4 +/- 1.0 mg/dL. All patients were successfully cured of acute renal failure by hemodialysis or hemodiafiltration. As a result, myoglobulinemic acute renal failure associated with neuroleptic malignant syndrome was successfully treated by hemodialysis or hemodiafiltration.

Acute Kidney Injury↗

PubMed2006

Angiotensin I-converting enzyme gene polymorphism modifies the smoking-cancer association: the Hisayama Study.

We examined the long-term contribution of smoking and angiotensin I-converting enzyme (ACE) gene I/D polymorphism to total cancer deaths in a prospective study of a general Japanese population. A total of 937 subjects aged 40 years or older were selected from an original cohort of 1621 subjects and were followed up for 32 years. During the follow-up period, 176 subjects died of cancer. Cancer mortality increased significantly with increasing current smoking levels. Although no clear relationship was observed between ACE genotypes and fatal cancer, the interaction term between current smoking and ACE genotype DD was found to be significant. In stratified analysis by ACE genotype after controlling for age, sex, alcohol intake, body mass index, glucose intolerance, serum total cholesterol and systolic blood pressure, the risk of fatal cancer in currently smoking subjects with genotype DD was twofold greater than that in subjects with genotypes II and ID. Among current smokers, subjects with genotype DD also showed a significantly greater risk of death due to cancer compared with those with genotypes II and ID combined (hazard ratio 1.77; 95% confidence interval 1.04-3.00; P=0.03). In conclusion, our findings suggest that ACE genotype DD enhances the association between smoking and cancer death in the general population.

Aged↗

PubMed2006

Effects of angiotensin II receptor antagonist on impaired endothelium-dependent and endothelium-independent relaxations in type II diabetic rats.

BACKGROUND: Diabetes mellitus is an important risk factor for cardiovascular diseases, and vasodilator dysfunction may contribute to vascular complications in diabetes. We previously demonstrated that the angiotensin II receptor blocker (ARB) corrected the impaired endothelium-derived hyperpolarizing factor (EDHF)-mediated arterial hyperpolarization and relaxation associated with hypertension or aging, partially independently of blood pressure. OBJECTIVE: To test whether EDHF-mediated, as well as endothelium-independent, relaxations would be altered in arteries from type II diabetic Goto-Kakizaki rats, and whether ARB would correct these alterations. METHODS: Goto-Kakizaki rats were treated with either the ARB candesartan or a combination of hydralazine and hydrochlorothiazide for 8 weeks, beginning at 10 weeks of age. Membrane potentials and contractile responses were recorded from the isolated mesenteric arteries. RESULTS: The two treatments lowered blood pressure comparably. Acetylcholine-induced, EDHF-mediated hyperpolarization and relaxation in mesenteric arteries were markedly impaired in untreated Goto-Kakizaki rats compared with age-matched Wistar rats, and neither ARB nor the combination therapy improved these responses. On the other hand, relaxations to endothelium-derived nitric oxide, assessed in rings precontracted with high potassium solution, were similar among the four groups. Relaxation to the nitric oxide donor sodium nitroprusside and that to levcromakalim, an ATP-sensitive K-channel opener, were also impaired in untreated Goto-Kakizaki rats, and the response to sodium nitroprusside was partially improved in treated Goto-Kakizaki rats. CONCLUSIONS: These findings suggest that EDHF-mediated hyperpolarization and relaxation and endothelium-independent relaxations are both impaired in arteries of type II diabetic rats, and antihypertensive treatment with or without ARB partially corrects endothelium-independent relaxations to the nitric oxide donor but not EDHF-mediated responses.

Angiotensin II Type 1 Receptor Blockers↗

PubMed2006

Chronic fluvastatin treatment alters vascular contraction by inhibiting the Rho/Rho-kinase pathway.

1. In the present study, we investigated the effects of chronic treatment of stroke-prone spontaneously hypertensive rats (SHRSP) with the statin fluvastatin on vascular Rho/Rho-kinase pathway mediated contraction, which has been shown to be upregulated in hypertension. 2. Contribution of the Rho/Rho-kinase pathway to noradrenaline-induced contraction of arteries from SHRSP was assessed by the inhibitory effect of Y-27632, a Rho/Rho-kinase inhibitor. Stroke-prone spontaneously hypertensive rats were treated with fluvastatin (10 mg/kg per day) for 1 month. 3. Treatment with fluvastatin tended to attenuate the contraction to noradrenaline and significantly decreased the Y-27632-sensitive component of the contraction in controls compared with fluvastatin-treated rats. 4. RhoA, as assessed by western blotting, was also reduced by fluvastatin treatment. 5. These findings suggest that chronic treatment with fluvastatin reduces the contractile response associated with Rho/Rho-kinase in arteries of hypertensive rats.

Amides↗

PubMed2006

Effect of the non-steroidal anti-inflammatory drug sulindac on colorectal adenomas of uncolectomized familial adenomatous polyposis.

BACKGROUND: The aim of the present study was to elucidate the effect of sulindac on uncolectomized familial adenomatous polyposis (FAP). METHODS: Seven FAP patients (SU group) without proctocolectomy were given sulindac 300 mg/day orally for 12 months. Six FAP patients without sulindac (non-SU group) served as controls. Colorectal lesions were assessed by protrusion index (no. radiolucent areas/cm(2); PI) under barium enema examination and non-polypoid lesion were assessed under chromoscopy prior to and at the end of the observation period. In the SU group, germline adenomatous polyposis coli (APC) mutation was determined by protein truncation test. RESULTS: In the SU group, PI decreased significantly in the distal colon (from 3.0 +/- 1.1 to 1.1 +/- 0.8/cm(2), P < 0.02) and in the proximal colon (from 3.4 +/- 2.4 to 0.9 +/- 1.3/cm(2), P < 0.02). The PI in the non-SU group slightly but significantly increased in the distal colon (from 1.0 +/- 0.8 to 1.2 +/- 0.9/cm(2); P < 0.05) and it remained unchanged in the proximal colon (from 0.6 +/- 0.3 to 0.7 +/- 0.3/cm(2); P > 0.05). Chromoscopy at the end of observation identified non-polypoid lesions in five patients in the SU group, whereas such lesions were not found in the non-SU group (71% vs 0%, P = 0.016). Decrease in PI was not different among distal APC mutation (exons 1-9), proximal APC mutation (exons 10-15) and negative mutation. CONCLUSION: Sulindac reduces colorectal adenomas of protruding type in uncolectomized FAP. The effect of sulindac may be unrelated to genotype of FAP.

Adenomatous Polyposis Coli↗

PubMed2006

Increased asymmetric pulvinar magnetic resonance imaging signals in Creutzfeldt-Jakob disease with florid plaques following a cadaveric dura mater graft.

A 9-year-old Japanese girl received a cadaveric dura mater graft during surgery following a head injury with brain contusion. She continued to do well, but when she became 19-years-old, she gradually showed a violent character and was treated in a psychiatric hospital. Another 6 years later, 200 months after the procedure, she developed a progressive gait ataxia, which subsequently led to her death within 10 months of onset. An autopsy showed she had CJD. This patient represents an atypical case of dura-associated CJD (dCJD) with unusual clinicopathological features including the late occurrence of myoclonus, an absence of periodic synchronous discharges in the electroencephalogram, and the presence of widespread florid plaques. However, our detection of an asymmetrical increase in the MRI-derived images of pulvinar nuclei has not been previously observed in other atypical cases of dCJD. Because atypical dCJD cases share several clinicopathological features with those of vCJD, and because asymmetrical hyperintense signals in the pulvinar have been observed in some neuropathologically confirmed vCJD cases, we had some difficulty in a differential diagnosis between atypical dCJD and vCJD. This is the first atypical dCJD case showing a pulvinar high signal compared with all other basal ganglia on MRI.

Brain Injuries↗

PubMed2006

Quantitative analysis of neurofibrillary pathology in a general population to reappraise neuropathological criteria for senile dementia of the neurofibrillary tangle type (tangle-only dementia): the Hisayama Study.

Senile dementia of the neurofibrillary tangle type (SD-NFT) is characterized by numerous neurofibrillary tangles (NFT) in the hippocampal region and the absence or minimal presence of senile plaques throughout the brain. We analyzed 207 demented subjects and 68 non-demented subjects autopsied in the Hisayama study to investigate the clinicopathological aspects of SD-NFF in the general Japanese population. The prevalence of SD-NFT in the consecutive autopsy cases was 8/207 (3.9%), comprising three men and five women. The average age at onset and death was 83.8 +/- 6.8 (mean +/- SD; standard deviation) and 88.1 +/- 7.6 years, respectively. A mild memory disturbance preceded a decrease in the ability to undertake the activities of daily living and the diagnosis of dementia. Focal cerebral symptoms, such as aphasia and paralysis, did not appear during the disease course of any subject. Gross examination of the brains showed moderate to severe diffuse cerebral atrophy with brain weight loss (mean +/- SD; standard deviation: 1118.1 +/- 124.0 g). Histologically, there were abundant NFT and neuropil threads predominantly in or limited to the limbic cortex. The density of NFT in the CA1/subiculum in SD-NFT was much higher than the densities in the other hippocampal regions. The average density of NFT in CA1 in SD-NFT subjects was 115.4 per 100 x field (range 23-247), that in Alzheimer disease (AD) subjects was 80.1 (range 1-227), and that in non-demented elderly subjects was 37.2 (range 0-203). Although many previous papers have reported that the densities of NFT in the limbic system in SD-NFT were significantly higher than those in AD, there was considerable overlap of NFT densities in CA1 among the non-demented elderly, AD subjects and SD-NFT subjects.

Aged↗

PubMed2006

Prediction of cognitive function by arterial stiffness in the very elderly.

BACKGROUND: Cognitive function is impaired in elderly subjects, so the aim of the present study was to determine the role of arterial stiffness on cognitive function. METHODS AND RESULTS: Cognitive function and arterial stiffness were assessed by the Mini-Mental State Examination (MMSE) and measurement of the brachial-ankle pulse wave velocity (PWV), respectively. The cross-sectional association of the MMSE score and PWV was studied in 203 subjects (87 men, 116 women), all of whom were 85 years old. Sex distribution, systolic and diastolic blood pressures did not differ between the normal (MMSE score >or=24, n=128) and impaired MMSE groups (MMSE score <24, n=75). In contrast, the PWV was significantly increased in the impaired MMSE group than in the normal MMSE group (25.0+/-0.8 vs 22.9+/-0.5 m/s, p<0.05). In multiple regression analysis, the PWV was also independently and significantly associated with the MMSE score. CONCLUSIONS: These results suggest that cognitive function could be predicted by arterial stiffness, as assessed by the PWV, in the very old. Preventing atherosclerosis may play an important role in preserving normal cognitive function until very old age.

Aged, 80 and over↗

PubMed2006

Gender-related association of serum uric acid and left ventricular hypertrophy in hypertension.

BACKGROUND: The aim of the present study was to determine whether sex differences contribute to the association of serum uric acid and left ventricular hypertrophy in individuals with hypertension. METHODS AND RESULTS: Seventy participants with essential hypertension (34 men, 36 women; 54.4 +/- 1.6 years old) were enrolled to undergo echocardiography to calculate the left ventricular mass index (LVMI). Twenty-four-hour ambulatory blood pressure monitoring was done to assess blood pressure level precisely. The LVMI was significantly correlated with serum uric acid (r = 0.295, p = 0.013) in all participants. After controlling for factors such as age, sex, mean 24-h systolic blood pressure, creatinine clearance, and duration of hypertension, serum uric acid was still found to be significantly and independently associated with LVMI. Because serum uric acid was significantly higher in men than in women (6.8 +/- 0.3 and 5.1 +/- 0.2 mg/dl, respectively), subsequent analysis was performed by gender. Multiple regression analysis revealed that the LVMI was significantly and independently associated with serum uric acid in women, but not in men. CONCLUSIONS: The potential effect of uric acid on LV hypertrophy is more pronounced in female than in males with essential hypertension.

Age Factors↗

PubMed2006

Valsartan improves the lower limit of cerebral autoregulation in rats.

The effects of angiotensin II type 1 receptor blockers (ARBs) on cerebral blood flow (CBF) autoregulation have not been fully clarified. Thus, we examined the acute effect of valsartan, the most selective ARB, on CBF autoregulation in spontaneously hypertensive rats. Intravenous administration of valsartan (0.3 mg/kg) reduced the mean arterial pressure (MAP) from 184+/-5 (mean+/-SEM) to 174+/-5 mmHg (p<0.001) without affecting CBF as measured by laser-Doppler flowmetry. The lower limit of CBF autoregulation (the MAP at which the CBF was 80% of the baseline value) in the valsartan-treated group (122+/-3 mmHg) was significantly lower than that in the control group (135+/-4 mmHg, p<0.05). Reverse transcribed-polymerase chain reaction and immunohistochemical staining demonstrated that both angiotensin II type 2 receptors and angiotensin II type 1 receptors (AT1Rs) were expressed in endothelial and smooth muscle cells of the rat cerebral arteries. These results suggest that specific inhibition of AT1Rs in the cerebral circulation causes the leftward shift of the lower limit of autoregulation.

Angiotensin II Type 1 Receptor Blockers↗