bluuebunny/crossref_metadata_2025_split huggingface dataset:
PS-P06-9: PREVALENCE OF DEPRESSIVE SYMPTOMS AMONG ADOLESCENTS WITH RHEUMATIC FEVER OR RHEUMATIC HEART DISEASE ON ANTIBIOTIC PROPHYLAXIS IN A TERTIARY HOSPITAL
Authors: Yeo Al Raymond Chiong Ramos , Mangubat Michelle Noblejas 
Published: January 2023

Objective:
To determine the prevalence of depressive symptoms among adolescents diagnosed with Rheumatic Fever or Rheumatic Heart Disease on antibiotic prophylaxis at the National Childrens Hospital

Design:
A descriptive cross-sectional design that looked at the prevalence of depressive symptoms among the participants was utilized among 34 adolescents who met the inclusion criteria for the study.

Method:
This study utilized a descriptive cross-sectional design that looked at the prevalence of depressive symptoms among the adolescents ages 13–17 years old diagnosed with Rheumatic Fever or Rheumatic Heart Disease on antibiotic prophylaxis and registered at the National Childrens Hospital Cardiology Outpatient Clinic from December 1 to 31, 2021. Age, sex, duration of treatment, missed doses and presence of absence of cardiac involvement were obtained.

Results:
Thirty-four were included in this study. Majority of them were female (64.7%) with a mean age of 15.1 (SD +/-1.54). There were 29 (85.3%) who received secondary prophylaxis for more than six months at the time of interview. 28 (82.4%) were diagnosed as having Rheumatic Heart. Thirteen (38.2%) have had missed dose/s since start the of their prophylaxis. Among the 34 adolescents, 27 (79.4%) had depressive symptoms on screening with majority identified as having mild and minimal symptoms. All adolescents were followed up and advised accordingly based on the recommendations per screening results.

Conclusion:
Depression and other mental health concerns are common among adolescents, especially those with chronic health conditions such as rheumatic fever and rheumatic heart disease. Screening and initial evaluation for depressive symptoms should be done in order to identify those at risk. Prompt referrals to specialists should be facilitated when needed to prevent the unwanted consequences of depression and to improve treatment outcomes.
PS-P06-13: THE IMPACT OF BODY COMPOSITION AND ADIPOSE DISTRIBUTION ON BLOOD PRESSURE IN YOUNG AND MIDDLE-AGED ADULTS
Authors: Yu Shikai , Zhao Song , Zhang Yi , Xu Yawei 
Published: January 2023

Background and Aims:
Both body size and composition are related to BP elevation. Body adipose mass and lean/muscle mass are closely related, and thus the mutual adjustment is important when investigating the impact of one of them on BP. Besides, the proportionate contributions of various components of body composition on BP remains unknown. Thus, in the present study, by constructing models including body fat mass in various depots and body muscle mass simultaneously, we aimed to comprehensively investigate the impact of body composition and adiposity distribution on BP in young and middle-aged adults.

Methods:
14412 participants with available data on whole-body DXA measurement derived from the National Health and Nutrition Examination Survey were included. Multiple stepwise linear regression models of BP on various components of body composition were built to evaluate the true determinants of BP in terms of body composition. Then, relative importance analysis was performed to quantify the contributions of various components of body composition and adipose distribution.

Results:
The mean age of the participants was 36 years and there were 50.7% women. Linear regression with mutual adjustment showed that total fat mass, total muscle mass, and trunk fat mass were significantly and positively associated with BP, respectively; however, arm and leg fat mass were significantly and negatively associated with BP. After adjusted for potential covariates, SBP were significantly determined by trunk fat mass (β; = 0.33, P < 0.001), leg fat mass (β; = -0.12, P < 0.001), and total muscle mass (β; = 0.10, P < 0.001); DBP were significantly determined by trunk fat mass (β; = 0.52, P < 0.001), leg fat mass (β; = -0.15, P < 0.001), arm fat mass (β; = -0.23, P < 0.001), and total muscle mass (β; = 0.06, P < 0.001) in men. Similar results were observed in women. Relative importance analysis indicated that trunk fat mass was the major contribution to SBP and DBP in both men and women; meanwhile, total muscle mass also made relatively great contribution to SBP for men and women.

Conclusions:
Both fat mass and muscle mass were independently associated with and substantially contributed to SBP in both men and women. After adjustment for other measurements of body composition and potential covariates, trunk fat mass was positively associated with BP and was the most dominant contributor to BP; however, leg fat mass was negatively associated with BP.
PS-R01-1: BLOOD PRESSURE FLUCTUATIONS AND THE INDOOR ENVIRONMENT WITH A HIGHLY INSULATED AND AIRTIGHT MODEL HOUSE DURING THE COLD WINTER SEASON
Authors: Nakagami Hironori , Katsuya Tomohiro , Rakugi Hiromi 
Published: January 2023

At cold temperatures, blood vessels constrict to suppress heat dissipation to maintain a constant core body temperature, leading to increased blood pressure (BP). Increased BP affects the increased mortality from cardiovascular disease in cold seasons. We examined the effect of the indoor environment on BP fluctuations with an automatic BP monitor during the cold winter season (Mar 3rd to 10th in 2019), both at home and in a highly insulated and airtight model house (Model House). The indoor environments were recorded by installing data loggers equipped with temperature sensors in various rooms. BP was measured once per hour in the daytime (from 3 or 4 pm to 12 pm and from 6 am to 1 pm) and once every two hours in the nighttime (from 12 pm to 6 am). This study protocol was approved by the Nara Hospital, Kindai University Ethics Committee	(No. 527). Four subjects (two couples) (Subject 1–4: 60, 59, 59, 56 years old, respectively) were enrolled, who took no medication for high BP. The room temperature at the home of Subjects 1 and 2 was low. In contrast, the room temperature of the Model House was high and stable throughout the day, even if the outside temperature at nighttime was very low on that day. The 24-hour BP of Subject 1 tended to be higher in their home than in the Model House [average ± SD (standard deviation) of the systolic BP (mmHg):131 ± 21.7 vs. 120 ± 16.6, diastolic BP (mmHg): 87 ± 14.6 vs. 82 ± 16.4]. Surprisingly, the 24-hour BP of Subject 2 was high throughout the day and was extremely higher in their home than in the Model House [systolic BP (mmHg): 171 ± 33.8 vs. 148 ± 22.7, diastolic BP (mmHg): 102 ± 20.4 vs. 88 ± 11.4]. The same trend was observed for Subject 2 in the blood pressure variation (CV) which was defined as SD divided mean BP [CV of the systolic BP (%):19.4 vs. 15.3, diastolic BP (%): 20.0 vs. 13.0]. Compared with that of Subjects 1 and 2, the room temperature at the home of Subjects 3 and 4 was relatively high in the living room, and the BPs of Subjects 3 and 4 tended to be similar in both their home and the Model House. To prevent cardiovascular events at home, a suitable indoor thermal environment for BP management should be proposed, especially in the winter season.
PS-BPB01-1: SPARC IS INDUCED AT THE EARLY STAGE OF VASCULAR ENDOTHELIAL DYSFUNCTION TO COMPENSATE INFLAMMATION IN DOCA-SALT HYPERTENSIVE RATS
Authors: Toba Hiroe , Kobara Miyuki , Nakata Tetsuo 
Published: January 2023

Objective:
Extracellular matrix (ECM) regulates various cellular functions as well as provides structural support. SPARC (secreted protein acidic and rich in cysteine) is one of the ECM components, which participates in various cellular functions, especially during morphogenesis and tissue remodeling. We have reported that 1) SPARC, which increases in accordance with renal injury, causes collagen deposition through ADAMTS1 (a disintegrin and metalloproteinase with thrombospondin type 1 motif) production, and 2) renin-angiotensin system is placed in the upstream of SPARC overexpression in the hypertensive rat kidney. The present study investigated the roles for SPARC in vascular endothelial cell dysfunction and inflammation in the setting of hypertension.

Design and method:
Rats were treated with deoxycorticosterone acetate (DOCA) and 1% salt water for 0, 1, 2 or 3 weeks. Blood pressure was measured by tail-cuff methods, and thoracic aorta was isolated to examine acetylcholine-induced vasodilatory response, macrophage infiltration by immunohistochemistry, and protein expression of SPARC and ADAMTS1 by Western blotting. In the separate experiment, angiotensin II (10–7mol/L, 6hr) or SPARC recombinant protein (100nmol/L, 24hr) was treated to cultured rat aortic endothelial cells (RAECs) with/without siRNA targeting SPARC and ADAMTS1. MCP-1 and LOX-1 mRNA levels were measured by real-time RT-PCR.

Result:
DOCA-salt caused time-dependent increases in systolic blood pressure, impairment of endothelium-dependent vasodilation, and macrophage infiltration into the adventitial area of the aorta. The expression of SPARC in the DOCA-salt rat aorta was enhanced at week1 and week2 compared to week0. ADAMTS1 expression tended to increase from week1 and showed significant increases at week3. In RAECs, SPARC and ADAMTS1 gene knockdown aggravated angiotensin II-induced overexpression of LOX-1 and MCP-1 mRNA, indicating anti-inflammatory effects of SPARC. On the other hand, SPARC recombinant protein treatment induced the upregulation of LOX-1 and MCP-1.

Conclusions:
SPARC may be induced at the early stage of vascular injury to compensate inflammation under the existence of angiotensin II. We need further investigation into the diverse effects of SPARC and the relationship between SPARC and ADAMTS1.
PS-BPB02-1: POSSIBLE DIFFERENTIAL EFFECTS OF SACUBITRIL/VALSARTAN AND VALSARTAN AGAINST HYPERTENSION AND CARDIORENAL INJURY IN A MOUSE MODEL OF CARDIORENAL SYNDROME
Authors: Tsukamoto Shunichiro , Wakui Hiromichi , Uehara Tatsuki , Azushima Kengo , Shiba Yuka , Tamura Kouichi 
Published: January 2023

Objective:
Angiotensin receptor-neprilysin inhibitors (ARNI) are potential therapeutic candidates for the treatment of cardiorenal syndrome. Although evidence is accumulating on the therapeutic effects of ARNI for heart failure and hypertension, the effects of ARNI on kidney disease or cardiorenal syndrome are controversial. To address this issue, we investigated the organ-protective effect of ARNI on cardiorenal syndrome using the ANS [Ang II (A) + nephrectomy (N) + saline (S)] mice, which is the cardiorenal syndrome model.

Design and method:
C57BL/6 mice were divided into 5 groups: Control (sham operation) group, ANS (ANS + vehicle treatment) group, Val M [ANS + moderate dose of valsartan treatment (30 mg/kg/day)] group, ARNI [ANS + sacubitril/valsartan treatment (60 mg/kg/day)] group, and Val H [ANS + high dose of valsartan treatment (60 mg/kg/day)] group. Sacrifice was performed after 4 weeks, and various analyses were conducted.

Results:
ARNI, Val M, and Val H treatment groups attenuated the elevation of blood pressure in ANS mice; valsartan exerted its antihypertensive effect in a dose-dependent manner, and the antihypertensive effect of the ARNI group was intermediate between Val M and Val H groups. Regardless of the strength of the antihypertensive effect, the ARNI group was most effective in preventing the decrease in cardiac contraction and cardiac fibrosis in ANS mice. However, the ARNI group was insufficient to suppress urinary albumin excretion and renal fibrosis in ANS mice. Both valsartan groups suppressed urinary albumin excretion in ANS mice, as well as renal fibrosis and glomerular swelling. In addition, RNA sequencing analysis suggested that ARNI and valsartan may involve different molecular mechanisms in the kidney.

Conclusions:
The ARNI group showed better cardioprotective effects than both of valsartan treatment groups, but not sufficient kidney protection. These results of present study using a mouse model of cardiorenal syndrome suggested that the relationship between the antihypertensive effects and the organ protective effects of cardiorenal injury may be different between angiotensin II receptor blocker (ARB) and ARNI.
PS-BPB02-3: TARGETING FORMYL PEPTIDE RECEPTORS AS A NOVEL APPROACH TO TREAT HYPERTENSION-INDUCED ADVERSE CARDIOVASCULAR REMODELLING AND DYSFUNCTION
Authors: Singh Jaideep , Jackson Kristy L , Gumanti Audrey , Fang Haoyun , Woodman Owen L , Ritchie Rebecca H , Greening David , Head Geoffrey A , Qin Chengxue 
Published: January 2023

Introduction:
Chronic unresolved inflammation has been shown to contribute to the development and progression of hypertension-induced cardiovascular damage. Failure to resolve inflammation exacerbates the risk and severity of cardiovascular disease. Currently, available therapies have limited efficacy in treating hypertension and its associated complications. Formyl peptide receptors (FPR) play a critical role in the regulation of resolution of inflammation. We have previously discovered that a FPR small-molecule prototype Cmpd17b exerts cardioprotective and vasoprotective effects against acute and severe inflammatory cardiac insults, but its impact on a chronic inflammatory insult in cardiovascular diseases, such as hypertension, has not been explored.

Aim and hypothesis:
To investigate the therapeutic potential of a FPR agonist, Cmpd17b on cardiac and vascular remodelling and function, and blood pressure regulation in hypertensive mice.

Methods:
Male C57BL/6 mice (12 weeks old) were implanted with a radiotelemetry probe to measure MAP (mean arterial pressure). Hypertensive mice (AngII infused at 0.7 mg/kg/day, subcutaneously) and normotensive mice (saline infused, subcutaneously) underwent 24-hour blood pressure recordings via telemetry at baseline and during 4 weeks daily treatment with Cmpd17b (50 mg/kg/day, intraperioneally) or its vehicle. Sympathetic nervous system (SNS) activity was assessed using power spectral analysis. At week 4, cardiac and vascular function was assessed using B-mode and M-mode echocardiography. At the end of the study, heart and arteries were collected, cardiac and vascular remodelling (fibrosis and hypertrophy) and function, and cutting-edge comparative qualitative proteomics were assessed.

Results:
Cmpd17b reduced MAP, SNS activity, cardiac and vascular adverse remodelling and dysfunction in hypertensive mice (Table). Cutting-edge quantitative proteomics analysis revealed that hypertension-induced significant adverse structural remodelling (110 proteins in the heart and 60 proteins in the aorta) and mitochondrial dysregulation (38 in the heart and 91 in the aorta), consisted with function and pathology observed. Those changes were prevented by FPR agonism (53 structural cardiac proteins and 38 vascular structural proteins) and (24 cardiac mitochondrial proteins and 36 vascular mitochondrial proteins).

Conclusions:
Our study demonstrated for the first time that FPR prototype small-molecule Cmpd17b reduced hypertension-induced cardiovascular damage, supporting the development of FPR-based therapy to treat cardiovascular complications in systemic hypertension.
PS-BPB02-4: LEFT VENTRICLE HYPERTROPHY AND DYSFUNCTION WERE EXAGGERATED BY P2RX7 KNOCKOUT BUT UNAFFECTED BY P2RX7 PHARMACOLOGIC BLOCKADE IN ANGIOTENSIN II-INFUSED MICE
Authors: Berillo Olga , Shokoples Brandon , Comeau Kevin , Higaki Akinori , Caillon Antoine , Paradis Pierre , Schiffrin Ernesto L 
Published: January 2023

Objective:
Extracellular adenosine triphosphate released from damaged cells binds to the P2X7 receptor (P2RX7) to activate of immune cells. Our preliminary data demonstrated that P2RX7 plays a role in vascular injury of hypertensive mice. Angiotensin (Ang) II-induced hypertension, vascular injury and aortic perivascular infiltration of activated T cell were attenuated by P2rx7 knockout or P2RX7 pharmacologic blockade. However, whether P2RX7 is involved in Ang II-induced cardiac dysfunction and hypertrophy is unknown. We hypothesized that Ang II-induced left ventricular (LV) dysfunction and hypertrophy would be blunted by P2rx7 knockout or P2RX7 antagonism.

Design and method:
Ten-to-12-week-old male C57BL/6J wild-type (WT) and P2rx7-/-
mice were infused or not with Ang II (1000 ng/kg/min) for 14 days. A second set of Ang II-infused WT mice was infused with the P2RX7 antagonist AZ10606120 (694 ng/kg/min) or vehicle for 14 days. Cardiac LV function and remodeling were determined by ultrasound. Total RNA was isolated from the heart using the mirVana miRNA isolation kit. Relative expression was calculated using the Pfaffl method with 40S ribosomal protein S16 (Rps16) as a reference gene. Hypertrophic and fibrotic markers were studied by reverse transcription-quantitative PCR (RT-qPCR) in cardiac ventricles.

Results:
Ang II-induced 1.5-fold increase in LV mass/body weight (P < 0.001) and ∽25% decrease in fractional shortening in WT mice and mice receiving AZ10606120 (P < 0.05). These changes were exaggerated in P2rx7-/-
mice (LV mass/body weight: 1.7-fold increase, fractional shortening: 54% decrease, P < 0.05), but not in mice receiving AZ10606120. Ang II-induced atrial natriuretic peptide (Nppa/Rps16: 7-fold, P < 0.001) and α-skeletal actin 1 expression (Acta1/Rps16: 6-fold, P < 0.001) tended to be further increased in P2rx7-/-
mice (Nppa/Rps16: 14-fold and Acta1/Rps16: 12-fold), but not in AZ10606120-treated mice. Ang II-induced myosin heavy chain 7B (14-fold, P < 0.05) was unaffected by P2rx7 knockout or P2RX7 antagonism. Ang II caused a 1.5-fold increase in transforming growth factor β; 1 only in P2rx7-/-
mice (P < 0.05).

Conclusion:
Ang II-induced LV hypertrophy and dysfunction were exaggerated by P2rx7 knockout but were not affected by P2RX7 pharmacologic blockade.
PS-BPB02-8: CURCUMIN, AN INHIBITOR OF P300-HAT ACTIVITY, PREVENTS HYPERTENSION-INDUCED CARDIAC HYPERTROPHY WITH PRESERVED SYSTOLIC FUNCTION IN DAHL RATS
Authors: Sunagawa Yoichi , Hamabe-Horiike Toshihide , Funamoto Masafumi , Katanasaka Yasufumi , Hasegawa Koji , Morimoto Tatsuya 
Published: January 2023

Background:
Hypertension causes left ventricular hypertrophy (LVH) with a preserved systolic function. While LVH might be a compensatory process, its presence of LVH is associated with an increased incidence of cardiovascular events and heart failure. Recently, we found that curcumin, a major curcuminoid isolated from Curcuma longa, inhibits the histone acetyltransferase (HAT) activity of p300 as well as the p300-induced acetylation of histones and a hypertrophy-responsive transcription factor, GATA-4, in cultured cardiomyocytes. Furthermore, curcumin prevents deterioration of the systolic function in rat heart failure models in vivo. However, whether curcumin prevents the development of hypertension-induced LVH at an early stage of hypertension is unclear.

Objective:
To solve this problem, we have utilized a salt-sensitive Dahl rat (DS) model of hypertension.

Methods:
We randomized 6-week-old DS (n = 19) and control salt-resistant Dahl rats (DR, n = 10) to curcumin or the vehicle group. Then, these rats were given a high-salt diet and subjected to daily oral treatment with 50 mg/kg/day of curcumin or its vehicle (1% Gum arabic) for 6 weeks.

Results:
There were no differences between curcumin and vehicle in any data examined before treatment (6 weeks of age). The high-salt diet-induced a similar degree of hypertension in these two groups of DS compared with DR. At 12 weeks of age, transthoracic echocardiography in the vehicle group showed that the LV wall thickness, LV mass, and LV fractional shortening were significantly higher in DS compared with DR, and the LV systolic and diastolic dimensions were significantly smaller in DS than DR. Curcumin treatment significantly (p < 0.01) decreased the LV wall thickness in DS but not DR. Curcumin also significantly (p < 0.01) decreased the LV mass in DS, but not in DR. However, LV fractional shortening in DS was similar between the two groups. Curcumin also prevented the increases in hypertension-induced myocardial cell hypertrophy and perivascular fibrosis. Furthermore, curcumin significantly attenuated the up-regulation of hypertrophy-response gene transcriptions as well as acetylation of GATA4 but not phosphorylation of ERK1/2 and GATA4 in the heart.

Conclusions:
The natural compound, curcumin, inhibits the development of hypertension-induced concentric LVH without affecting the systolic function through inhibition of GATA4-acetylation. Thus, this compound might be applicable to patients with early-stages hypertensive heart diseases.
PS-BPB04-3: ENHANCEMENT EFFECTS OF GINSENOSIDE-RG2 ON SOME ANTIHYPERTENSIVE AGENTS-INDUCED SUPPRESSION OF ADRENAL CATECHOLAMINE RELEASE
Authors: Ki Young Jae , Koh Young Youp , Lim Dong Yoon 
Published: January 2023

Objective:
The present study was aimed to investigate the effects of ginsenoside-Rg2 (Rg2), one of panaxadiol-type saponins, which is isolated from Korean Red ginseng, in some antihypertensive agents-induced reduction on the release of catecholamines (CA) from the perfused model of the rat adrenal medullae.

Design and Methods:
The adrenal gland was isolated and perfused with Krebs-bicarbonate. The CA amoiunt in the perfusate was measured directly by using the fluorospectrophotometer.

Results:
Ginsenoside-Rg2 (3∼30 μM) during perfusion into an adrenal vein for 90 min significantly inhibited the CA secretion evoked by acetylcholine (ACh) in a dose- and time-dependent fashion. Also, olmesartan (AT1 receptor blocker, 15 μM), simvastatin (an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, 60 μM), enalapril (an inhibitor of angiotensin converting enzyme, 150 μM), and cilnidipine (a voltage-dependent L-type Ca2+ channel blocker, 3 μM) significantly reduced the CA secretion evoked by ACh and angiotensin II (Ang II), respectively. In the simultaneous presence of ginsenoside-Rg2 (10 μM) along with four antihypertensive agents (olmesartan, enalapril, simvastatin or cilnidipine), the CA secretion evoked by ACh and Ang II was more strongly inhibited compared with that of each antihypertensive agent-treatment alone.

Conclusion:
Collectively, these results demonstrate that ginsenoside-Rg2 as well as antihypertensive agents can inhibit the CA secretion evoked by activation of both cholinergic and AT1 receptors from the perfused rat adrenal medulla. When this ginsenoside-Rg2 was used in combination with different antihypertensive agents, their effects of antihypertensive agents on reduction of adrenal CA secretion were significantly enhanced, which may also be clinically beneficial for the treatment of cardiovascular diseases.