Analytic Formulae for T Violation in Neutrino Oscillations.

Recently, a concept known as µTRISTAN, which involves the acceleration of µ+, has been proposed. This initiative has led to considerations of a new design for a neutrino factory. Additionally, leveraging the polarization of µ+, measurements of T violation in neutrino oscillations are also being explored. In this paper, we present analytical expressions for T violation in neutrino oscillations within the framework of standard three-flavor neutrino oscillations, a scenario involving nonstandard interactions, and a case of unitarity violation. We point out that examining the energy spectrum of T violation may be useful for probing new physics effects.

Changes in diaphragm thickness and 6-min walking distance improvement after inspiratory muscle training in patients with chronic obstructive pulmonary disease: Clinical trial.

Aim: Inspiratory muscle training (IMT) improves respiratory muscle function and exercise tolerance in patients with chronic obstructive pulmonary disease (COPD), but the detailed mechanism is unclear. The purpose of this study is to elucidate the mechanism of functional improvement by IMT from P0.1, an index of respiratory central output, and thickness of diaphragm (Tdi), a noninvasive and reliable ultrasound examination. Methods: This clinical trial study enrolled 13 elderly patients with COPD. IMT was performed using the POWER breathe® Medic Plus breathing trainer in combination with each participant's outpatient rehabilitation regimen. Starting at 20% of the maximal inspiratory pressure (PImax) and increasing to 50%, the participants performed 30 IMT repetitions twice a day for 2 months. P0.1 is the value of airway-occlusion pressure at 0.1 s after the start of inspiratory flow, and Tdi was measured at rest and maximal breathing. Results: PImax and 6-min walking distance(6MWD) significantly increased after training. Tdi at resting inspiration and expiration, and maximal inspiration also significantly increased after training. In addition, the Borg Scale scores for dyspnea and leg fatigue and the respiratory rate of the 1-min recovery period after the 6MWD significantly decreased. There was no significant difference in P0.1. Conclusions: These results suggest that the effects of IMT may be attributed to the improved peripheral factors rather than to the central factors in elderly COPD patients.

Light-controlled pKa value of chiral Brønsted acid catalysts in enantioselective aza-Friedel-Crafts reaction.

Bis(dithienylethene)-based BINOL-derived phosphoric acid (DTE-BPA) has been developed as a light-controlled chiral organocatalyst for the first time. The photoinduced modulation of the reactivity and selectivity via the open/close isomerization of the DTE scaffold led to superior light-controlled ability in the enantioselective aza-Friedel-Crafts reaction of aldimines with indoles. DFT studies showed that photoisomerization is accompanied by a shift of 1.1 pKa units between the open and closed isomers.

TIMP3 promotes the maintenance of neural stem-progenitor cells in the mouse subventricular zone.

Adult neural stem cells (NSCs) in the mouse subventricular zone (SVZ) serve as a lifelong reservoir for newborn olfactory bulb neurons. Recent studies have identified a slowly dividing subpopulation of embryonic neural stem-progenitor cells (NPCs) as the embryonic origin of adult NSCs. Yet, little is known about how these slowly dividing embryonic NPCs are maintained until adulthood while other NPCs are extinguished by the completion of brain development. The extracellular matrix (ECM) is an essential component of stem cell niches and thus a key determinant of stem cell fate. Here we investigated tissue inhibitors of metalloproteinases (TIMPs)-regulators of ECM remodeling-for their potential roles in the establishment of adult NSCs. We found that Timp2, Timp3, and Timp4 were expressed at high levels in slowly dividing NPCs compared to rapidly dividing NPCs. Deletion of TIMP3 reduced the number of adult NSCs and neuroblasts in the lateral SVZ. In addition, overexpression of TIMP3 in the embryonic NPCs suppressed neuronal differentiation and upregulated the expression levels of Notch signaling relating genes. These results thus suggest that TIMP3 keeps the undifferentiated state of embryonic NPCs, leading to the establishment and maintenance of adult NSCs.

Reduction in hsCRP levels is associated with decreased incidence of cardiovascular events in Japanese hypertensive women but not in men.

To test our hypothesis that the magnitude of reduction in hsCRP achieved by antihypertensive medications may predict the benefit for cardiovascular outcomes in hypertensive individuals, we performed subanalysis of the ATTEMPT-CVD study. The hypertensive participants enrolled in the ATTMEPT-CVD study were categorized into two groups according to whether achieved reduction in hsCRP levels at 6 months after initiation of antihypertensive medications from baseline was equal to or greater than 40% (responder group) or less than 40% (non-responder group). Baseline characteristics and blood pressure during follow-up period were similar between the groups. For women, the incidence of cardiovascular events was significantly less in responder group than non-responder group (P < 0.0221). However, for men, there was no significant difference between the groups regarding incident cardiovascular events (P = 0.2434). There was a significant interaction (P = 0.0187) between sexes for incident cardiovascular events. Our results provide the evidence suggesting that substantial reduction (40% or greater reduction) in hsCRP on antihypertensive medication predicts the benefit for cardiovascular outcomes in hypertensive women but it does not in hypertensive men. The magnitude of achieved reduction in hsCRP by antihypertensive medications seems to be a useful indicator of successful treatment in Japanese hypertensive women.This trial was registered with ClinicalTrials.gov, number NCT01075698.

Total adiponectin is associated with incident cardiovascular and renal events in treated hypertensive patients: subanalysis of the ATTEMPT-CVD randomized trial.

The predictive value of serum adiponectin for hypertensive cardiovascular outcomes is unknown. This study was performed to investigate the association of adiponectin with incident cardiovascular and renal events (CV events) in hypertensive patients. We performed post-hoc analysis on 1,228 hypertensive patients enrolled in the ATTEMPT-CVD study, a prospective randomized study comparing the effects of two antihypertensive therapies. The participants were divided into quartiles of baseline serum total adiponectin or high molecular weight (HMW) adiponectin. Multivariable Cox proportional hazards analysis was performed to determine the prognostic factors associated with CV events. Kaplan-Meier analysis for CV events by quartiles of baseline total adiponectin showed that patients in the highest total adiponectin quartile (Q4) had more CV events (P = 0.0135). On the other hand, no significant difference was noted regarding the incidence of CV events among patients stratified by HMW adiponectin quartile (P = 0.2551). Even after adjustment for potential confounders, the highest total adiponectin quartile (Q4) remained independently associated with incident CV events in hypertensive patients (HR = 1.949: 95%CI 1.051-3.612; P = 0.0341). These results showed that total adiponectin, but not HMW adiponectin, was independently associated with the incidence of CV events in treated hypertensive patients, thereby highlighting total adiponectin as a valuable predictor for hypertensive cardiovascular outcomes.

Anemia is an independent risk factor for cardiovascular and renal events in hypertensive outpatients with well-controlled blood pressure: a subgroup analysis of the ATTEMPT-CVD randomized trial.

To investigate whether anemia is an independent risk factor for cardiovascular and renal events in hypertensive outpatients, we performed a subgroup analysis of the ATTEMPT-CVD study based on baseline hemoglobin. The ATTEMPT-CVD study was a multicenter, prospective, randomized study of hypertensive outpatients that compared the efficacy of angiotensin receptor blocker (ARB)-based antihypertensive treatment with non-ARB antihypertensive treatment over 3 years. In the present subanalysis, ATTEMPT-CVD study participants (n = 1213) were categorized into the anemic group and nonanemic group according to their baseline hemoglobin. We compared the anemic and nonanemic groups mainly in regard to the incidence of cardiovascular and renal events and blood pressure. We also performed a multivariable Cox proportional hazards analysis to determine the prognostic factors that were independently associated with cardiovascular and renal events. Of the 1213 patients enrolled in the ATTEMPT-CVD, 194 patients had anemia (mostly mild anemia) and 1019 patients did not. Blood pressure was well-controlled during the 3 years of antihypertensive therapy in both the anemic and nonanemic groups. However, the incidence of cardiovascular and renal events was significantly greater in the anemic group than in the nonanemic group (HR = 1.945: 95%CI 1.208-3.130; P = 0.0062). Even after adjustment, anemia was independently associated with cardiovascular and renal events (HR = 1.816: 95%CI 1.116-2.955; P = 0.0163) in overall hypertensive patients with well-controlled blood pressure. Anemia, even mild anemia, is an independent risk factor for cardiovascular and renal events in hypertensive outpatients whose blood pressure is well-controlled. Thus, anemia may be a novel therapeutic target for cardiovascular and renal diseases in hypertensive outpatients with anemia.

Associations of passive muscle stiffness, muscle stretch tolerance, and muscle slack angle with range of motion: individual and sex differences.

Joint range of motion (ROM) is an important parameter for athletic performance and muscular injury risk. Nonetheless, a complete description of muscular factors influencing ROM among individuals and between men and women is lacking. We examined whether passive muscle stiffness (evaluated by angle-specific muscle shear modulus), tolerance to muscle stretch (evaluated by muscle shear modulus at end-ROM), and muscle slack angle of the triceps surae are associated with the individual variability and sex difference in dorsiflexion ROM, using ultrasound shear wave elastography. For men, ROM was negatively correlated to passive muscle stiffness of the medial and lateral gastrocnemius in a tensioned state and positively to tolerance to muscle stretch in the medial gastrocnemius. For women, ROM was only positively correlated to tolerance to muscle stretch in all muscles but not correlated to passive muscle stiffness. Muscle slack angle was not correlated to ROM in men and women. Significant sex differences were observed only for dorsiflexion ROM and passive muscle stiffness in a tensioned state. These findings suggest that muscular factors associated with ROM are different between men and women. Furthermore, the sex difference in dorsiflexion ROM might be attributed partly to that in passive muscle stiffness of plantar flexors.

Cardiovascular and renal protective role of angiotensin blockade in hypertension with advanced CKD: a subgroup analysis of ATTEMPT-CVD randomized trial.

The ATTEMPT-CVD study was prospective randomized active-controlled trial and the main findings had been reported. According to baseline GFR and albuminuria categories, we divided the patients of the ATTEMPT-CVD study into 2 subgroups: (Group 1) the patients with at least one of eGFR of <45 ml/min per 1.73 m2 and UACR of ≥300 mg/g creatinine, defined as G3b and/or A3; (Group 2) the patients except for Group 1, defined as the other patients. In patients with G3b and/or A3, the incidence of cardiovascular events was significantly less in ARB group than in non-ARB group (11 vs 22, respectively) (HR = 0.465: 95%CI = 0.224-0.965; P = 0.040). UACR was significantly less in ARB group than in non-ARB group during follow-up period in patients with G3b and/or A3 (P = 0.0003), while eGFR, plasma BNP levels, and blood pressure were comparable between ARB and non-ARB groups. Allocation to ARB therapy was a significant independent prognostic factor for cardiovascular events in patients with G3b and/or A3 (P = 0.0268). On the other hand, in the other patients, the occurrence of cardiovascular events was comparable between ARB and non-ARB groups. In patients with advanced CKD, ARB-based therapy may confer greater benefit in prevention of cardiovascular events than non-ARB therapy.

A trial of telmisartan prevention of cardiovascular diseases (ATTEMPT-CVD): Biomarker study.

AIMS: A trial of telmisartan prevention of cardiovascular disease (ATTEMPT-CVD) was performed to compare the effects of angiotensin II receptor blocker (ARB) therapy and those of non-ARB standard therapy on biomarker level changes and the incidence of cardiovascular events in hypertensive patients. METHODS AND RESULTS: In this multicenter, open-label, randomized, parallel-group, comparative study, the effects of ARB therapy and those of non-ARB standard therapy on urinary albumin creatinine ratio (UACR) and plasma brain natriuretic peptide (BNP) level changes were investigated for three years from the start of antihypertensive treatment as the primary endpoints. The incidences of cardiovascular composite events were compared between the two groups, and the relationship between the incidence of the events and biomarker changes were investigated as secondary endpoints. The study started with 615 patients in the ARB group and 613 patients in the non-ARB group. The ARB group had a significant effect on UACR and plasma BNP level changes compared with the non-ARB group. Fewer cardiovascular events occurred in the ARB group, but the difference was not statistically significant. UACR and plasma BNP levels at baseline were associated with cardiovascular events. CONCLUSION: This study provided the first evidence that ARB treatment caused a smaller increase in plasma BNP and a greater decrease in UACR than non-ARB treatment, independently of blood pressure control, and gives a novel insight into the significance of BNP and UACR as predictors of cardiovascular and renal risk on antihypertensive treatment.

Sirt7 Contributes to Myocardial Tissue Repair by Maintaining Transforming Growth Factor-ß Signaling Pathway.

BACKGROUND: Sirt7, 1 of the 7 members of the mammalian sirtuin family, promotes oncogenic transformation. Tumor growth and metastasis require fibrotic and angiogenic responses. Here, we investigated the role of Sirt7 in cardiovascular tissue repair process. METHODS AND RESULTS: In wild-type mice, Sirt7 expression increased in response to acute cardiovascular injury, including myocardial infarction and hind-limb ischemia, particularly at the active wound healing site. Compared with wild-type mice, homozygous Sirt7-deficient (Sirt7(-/-)) mice showed susceptibility to cardiac rupture after myocardial infarction, delayed blood flow recovery after hind-limb ischemia, and impaired wound healing after skin injury. Histological analysis showed reduced fibrosis, fibroblast differentiation, and inflammatory cell infiltration in the border zone of infarction in Sirt7(-/-) mice. In vitro, Sirt7(-/-) mouse-derived or Sirt7 siRNA-treated cardiac fibroblasts showed reduced transforming growth factor-ß signal activation and low expression levels of fibrosis-related genes compared with wild-type mice-derived or control siRNA-treated cells. These changes were accompanied by reduction in transforming growth factor receptor I protein. Loss of Sirt7 activated autophagy in cardiac fibroblasts. Transforming growth factor-ß receptor I downregulation induced by loss of Sirt7 was blocked by autophagy inhibitor, and interaction of Sirt7 with protein interacting with protein kinase-Cα was involved in this process. CONCLUSION: Sirt7 maintains transforming growth factor receptor I by modulating autophagy and is involved in the tissue repair process.

ASK1 is involved in cognitive impairment caused by long-term high-fat diet feeding in mice.

Although high-fat diet intake is known to cause obesity and diabetes, the effect of high-fat diet itself on cognitive function remains to be clarified. We have previously shown that apoptosis signal-regulating kinase 1 (ASK1) is responsible for cognitive impairment caused by chronic cerebral hypoperfusion. The present work, by using ASK1 deficient mice, was undertaken to explore the influence of chronic high-fat diet intake on cognitive function and the role of ASK1. Cognitive function in wild-type mice fed high-fat diet from 2 to 24 months of age was significantly impaired compared to those fed control diet, which was associated with the significant white matter lesions, reduction of hippocampal capillary density, and decrement of hippocampal neuronal cell. However, ASK1 deficiency abolished the development of cognitive impairment and cerebral injury caused by high-fat diet. Our results provided the evidence that high-fat diet itself causes cognitive impairment and ASK1 participates in such cognitive impairment.

Telmisartan enhances mitochondrial activity and alters cellular functions in human coronary artery endothelial cells via AMP-activated protein kinase pathway.

OBJECTIVE: Mitochondrial dysfunction plays an important role in cellular senescence and impaired function of vascular endothelium, resulted in cardiovascular diseases. Telmisartan is a unique angiotensin II type I receptor blocker that has been shown to prevent cardiovascular events in high risk patients. AMP-activated protein kinase (AMPK) plays a critical role in mitochondrial biogenesis and endothelial function. This study assessed whether telmisartan enhances mitochondrial function and alters cellular functions via AMPK in human coronary artery endothelial cells (HCAECs). METHODS AND RESULTS: In cultured HCAECs, telmisartan significantly enhanced mitochondrial activity assessed by mitochondrial reductase activity and intracellular ATP production and increased the expression of mitochondria related genes. Telmisartan prevented cellular senescence and exhibited the anti-apoptotic and pro-angiogenic properties. The expression of genes related anti-oxidant and pro-angiogenic properties were increased by telmisartan. Telmisartan increased endothelial NO synthase and AMPK phosphorylation. Peroxisome proliferator-activated receptor gamma signaling was not involved in telmisartan-induced improvement of mitochondrial function. All of these effects were abolished by inhibition of AMPK. CONCLUSIONS: Telmisartan enhanced mitochondrial activity and exhibited anti-senescence effects and improving endothelial function through AMPK in HCAECs. Telmisartan could provide beneficial effects on vascular diseases via enhancement of mitochondrial activity and modulating endothelial function through AMPK activation.

A case of Werner's syndrome with cardiac syndrome X and heart failure with preserved ejection fraction.

We herein report a case of Werner's syndrome (WS) with cardiac syndrome X (CSX) and heart failure with preserved ejection fraction (HFpEF), receiving nicorandil treatment. A 58-year-old woman with chest discomfort on exercise was suspected of having effort-angina pectoris because of broad ST-depression in electrocardiogram of exercise test and reversible defect in the posterior-wall portion of left ventricle in exercise thallium201 myocardial scintigraphy. This patient also exhibited HFpEF, diagnosed by increased ratio of early-transmitral-flow-velocity to tissue-Doppler early-diastolic mitral annular velocity (E/e') in echocardiography and plasma B-type natriuretic peptide (BNP) levels. However, coronary angiography revealed no organic stenosis in epicardial coronary arteries, and coronary physiological measurements by PressureWire™ (St. Jude Medical, St Paul, MN, USA) demonstrated that coronary flow reserve (CFR) was greatly decreased. Because impaired CFR represents coronary microvascular dysfunction in the absence of obstructive coronary narrowing, we diagnosed CSX, and initiated the administration of nicorandil to improve coronary microcirculation. After three-month-treatment of nicorandil, the patient's symptoms were diminished, and reversible defect in exercise myocardial scintigraphy was improved. Furthermore, both E/e' and BNP were decreased, indicating the improvement of HFpEF via the restoration of microvascular dysfunction. Thus, nicorandil administration could bring beneficial effects in WS with CSX and HFpEF, accompanied by coronary microcirculation dysfunction. .

Tissue inhibitor of metalloproteinase-3 knockout mice exhibit enhanced energy expenditure through thermogenesis.

Tissue inhibitors of metalloproteinases (TIMPs) regulate matrix metalloproteinase activity and maintain extracellular matrix homeostasis. Although TIMP-3 has multiple functions (e.g., apoptosis, inhibition of VEGF binding to VEGF receptor, and inhibition of TNFα converting enzyme), its roles in thermogenesis and metabolism, which influence energy expenditure and can lead to the development of metabolic disorders when dysregulated, are poorly understood. This study aimed to determine whether TIMP-3 is implicated in metabolism by analyzing TIMP-3 knockout (KO) mice. TIMP-3 KO mice had higher body temperature, oxygen consumption, and carbon dioxide production than wild-type (WT) mice, although there were no differences in food intake and locomotor activity. These results suggest that metabolism is enhanced in TIMP-3 KO mice. Real-time PCR analysis showed that the expression of PPAR-δ, UCP-2, NRF-1 and NRF-2 in soleus muscle, and PGC-1α and UCP-2 in gastrocnemius muscle, was higher in TIMP-3 KO mice than in WT mice, suggesting that TIMP-3 deficiency may increase mitochondrial activity. When exposed to cold for 8 hours to induce thermogenesis, TIMP-3 KO mice had a higher body temperature than WT mice. In the treadmill test, oxygen consumption and carbon dioxide production were higher in TIMP-3 KO mice both before and after starting exercise, and the difference was more pronounced after starting exercise. Our findings suggest that TIMP-3 KO mice exhibit enhanced metabolism, as reflected by a higher body temperature than WT mice, possibly due to increased mitochondrial activity. Given that TIMP-3 deficiency increases energy expenditure, TIMP-3 may present a novel therapeutic target for preventing metabolic disorders.

Correlation between extent of myocardial fibrosis assessed by cardiac magnetic resonance and cardiac troponin T release in patients with nonischemic heart failure.

Persistently high cardiac troponin T (cTnT) levels reflect myocardial damage in heart failure (HF). The presence and extent of myocardial fibrosis assessed by cardiac magnetic resonance (CMR) and high levels of cTnT predict poor prognosis in various cardiomyopathies. However, the association between myocardial fibrosis and transcardiac cTnT release has not been evaluated. This study investigated the correlation between myocardial fibrosis and transcardiac cTnT release from nonischemic failing myocardium. Serum cTnT levels were measured in aortic root (Ao) and coronary sinus (CS) using highly sensitive assay (detection limit >5 ng/L) in 74 nonischemic patients with HF who underwent CMR. Transcardiac cTnT release (ΔcTnT [CS-Ao]) represented the difference between CS and Ao-cTnT levels. Myocardial fibrosis was quantified by late gadolinium enhancement (LGE) volume and %LGE on CMR. cTnT was detectable in 65 patients (88%), and ΔcTnT (CS-Ao) levels were available (ΔcTnT [CS-Ao] >0 ng/L) in 60 patients (81%). LGE was observed in 42 patients (57%), and ΔcTnT (CS-Ao) levels were available in 41 LGE-positive patients (98%). In patients with available cTnT release, ΔcTnT (CS-Ao) levels were significantly higher in LGE-positive patients than those in LGE-negative patients (4.3 [2.2-5.5] vs 1.5 [0.9-2.6] ng/L; p = 0.001). Log (ΔcTnT [CS-Ao]) levels were correlated with LGE volume (r = 0.460, p = 0.003) and %LGE (r = 0.356, p = 0.03). In conclusion, the amount of transcardiac cTnT release was higher in LGE-positive patients than LGE-negative patients and correlated with the extent of LGE in nonischemic patients with HF. These results suggested that ongoing myocardial damage correlates with the presence and extent of myocardial fibrosis.

Apoptosis signal-regulating kinase 1 is a novel target molecule for cognitive impairment induced by chronic cerebral hypoperfusion.

OBJECTIVE: There are currently no specific strategies for the treatment or prevention of vascular dementia. White matter lesions, a common pathology in cerebral small vessel disease, are a major cause of vascular dementia. We investigated whether apoptosis signal-regulating kinase 1 (ASK1) might be a key molecule in cerebral hypoperfusion, associated with blood-brain barrier breakdown and white matter lesions. APPROACH AND RESULTS: A mouse model of cognitive impairment was developed by inducing chronic cerebral hypoperfusion in white matter including the corpus callosum via bilateral common carotid artery stenosis (BCAS) surgery. BCAS-induced white matter lesions caused cognitive decline in C57BL/6J (wild-type) mice but not in ASK1-deficient (ASK1(-/-)) mice. Phosphorylated ASK1 increased in wild-type mouse brains, and phosphorylated p38 and tumor necrosis factor-α expression increased in corpus callosum cerebral endothelial cells after BCAS in wild-type mice but not in ASK1(-/-) mice. BCAS decreased claudin-5 expression and disrupted blood-brain barrier in the corpus callosum of wild-type but not ASK1(-/-) mice. Cerebral nitrotyrosine was increased in wild-type and ASK1(-/-) BCAS mice. Cerebral phosphorylated ASK1 did not increase in wild-type mice treated with NADPH-oxidase inhibitor. A p38 inhibitor and NADPH-oxidase inhibitor mimicked the protective effect of ASK1 deficiency against cognitive impairment. Specific ASK1 inhibitor prevented cognitive decline in BCAS mice. In vitro oxygen-glucose deprivation and tumor necrosis factor-α stimulation caused the disruption of endothelial tight junctions from wild-type mice but not ASK1(-/-) mice. CONCLUSIONS: Oxidative stress-ASK1-p38 cascade plays a role in the pathogenesis of cognitive impairment, through blood-brain barrier breakdown via the disruption of endothelial tight junctions. ASK1 might be a promising therapeutic target for chronic cerebral hypoperfusion-induced cognitive impairment.

Level of serum antibody against a periodontal pathogen is associated with atherosclerosis and hypertension.

Inflammation has a role in the pathogenesis of atherosclerosis, which causes hypertension. Results from some studies have suggested links between periodontal disease and atherosclerosis, but links between periodontal disease and hypertension have been seldom studied. We investigated whether periodontal disease and serum antibody level were associated with hypertension. We studied 127 patients (93 men and 34 women, mean age 68±9 years) who were admitted with ischemic heart disease to our institution. A composite periodontal risk score was calculated from five periodontal vector scores. The levels of serum antibody against Porphyromonas gingivalis (Pg) were measured. Pulse pressure, mean blood pressure (BP) and pulse wave velocity were used as indices of atherosclerosis. We divided patients into two groups according to the levels of serum antibody against Pg: higher or equal to the median (high Pg antibody group) and lower than the median (low Pg antibody group).There was no difference in the use of antihypertensive agents between the two groups. The composite periodontal risk score (P=0.0003), systolic BP (P=0.030), diastolic BP (P=0.038), pulse pressure (P=0.050) and mean BP (P=0.055) were higher in the high Pg antibody group than in the low Pg antibody group. The composite periodontal risk score (r=0.320, P=0.0003), systolic BP (r=0.212, P=0.017), diastolic BP (r=0.188, P=0.035) and mean BP (r=0.225, P=0.011) correlated with the level of serum antibody against Pg, even after adjustment for age. An elevated antibody level against Pg indicates advanced periodontal disease and suggests advancement of atherosclerosis and hypertension.