Hypertensive State Research Articles

Assessment of Plasma Levels of Calcium, Creatinine and Glucose among Hypertensive Patients in Edo State, Nigeria

The present study needs to assess the plasma levels of calcium, creatinine and blood glucose among hypertensive patients in Edo State, Nigeria in order to ascertain whether plasma levels of these parameters are associated with hypertension in this population which will provide improved insight on proper management of hypertensive conditions. Several hereditary and lifestyle factors, including nutrition, influence blood pressure. In this regard, sodium is an important mineral that, in addition to its functions in fluid balance, action potential generation, digestive secretions, and nutrient absorption, also plays a key role in blood pressure regulation, with lower sodium intake linked to lower systolic and diastolic blood pressure. patients compared with their non-hypertensive counterparts. This could be as a result of an overactive parathyroid gland leading to excessive secretion of parathyroid hormone and the attendant increase in plasma calcium level. Regular screening for the plasma level of calcium, creatinine and blood glucose should be considered as routine tests for hypertensive patients. Adequate awareness of the risk of ignoring these parameters in hypertensive patients should be ensured.

AGE-RAGE Axis and Cardiovascular Diseases: Pathophysiologic Mechanisms and Prospects for Clinical Applications.

Advanced glycation end products (AGE), a diverse array of molecules generated through non-enzymatic glycosylation, in conjunction with the receptor of advanced glycation end products (RAGE), play a crucial role in the pathogenesis of diabetes and its associated complications. Recent studies have revealed that the AGE-RAGE axis potentially accelerated the progression of cardiovascular diseases, including heart failure, atherosclerosis, myocarditis, pulmonary hypertension, hypertension, arrhythmia, and other related conditions. The AGE-RAGE axis is intricately involved in the initiation and progression of cardiovascular diseases, independently of its engagement in diabetes. The mechanisms include oxidative stress, inflammation, alterations in autophagy flux, and mitochondrial dysfunction. Conversely, inhibition of AGE production, disruption of the binding between RAGE and its ligands, or silencing of RAGE expression could effectively impair the function of AGE-RAGE axis, thereby delaying or ameliorating the aforementioned diseases. AGE and the soluble receptor for advanced glycation end products (sRAGE) have the potential to be novel predictors of cardiovascular diseases. In this review, we provide an in-depth overview towards the biosynthetic pathway of AGE and elucidate the pathophysiological implications in various cardiovascular diseases. Furthermore, we delve into the profound role of RAGE in cardiovascular diseases, offering novel insights for further exploration of the AGE-RAGE axis and potential strategies for the prevention and management of cardiovascular disorders.

Fetal growth ultrasound in obese patients for the detection of growth abnormalities.

To examine the impact of maternal obesity on fetal growth abnormalities including fetal growth restriction (FGR) and large for gestational age (LGA) fetuses. Secondary analysis from the Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-be (nuMoM2b). The study excluded individuals with pregestational or gestational diabetes, chronic hypertension, and other major maternal medical conditions. Ultrasound assessments were performed at 16 - 21 and 22 - 29 weeks of gestation. Our exposure was the presence of pre-pregnancy obesity. Our primary outcome was rates of fetal growth abnormalities identified by ultrasound, defined as FGR (estimated fetal weight [EFW] or abdominal circumference < 10th percentile) or LGA (EFW > 90 th percentile) among obese compared to non-obese women. A secondary analysis was performed after limiting ultrasound performed from 28-29 weeks. To estimate adjusted relative risks (aRR) with 95% confidence intervals (95%CIs), we used generalized linear models with Poisson distribution and log link using robust error variance, adjusting for the predefined covariates. Of 7,354 participants, 1,443 (19.6%) had pre-pregnancy obesity while 5,911 (80.4%) did not. Pre-pregnancy obesity compared with normal weight was associated with an increased risk of fetal growth abnormalities both at 16-21 weeks (16.0% vs. 13.2%; aRR 1.23; 95%CI 1.06-1.42) and 22-29 weeks (16.0% vs. 12.1%; aRR 1.33; 95%CI 1.14-1.54). Furthermore, pre-pregnancy obesity compared with normal weight was associated with an increased risk of LGA both at 16-21 weeks (12.5% vs. 10.3%; aRR 1.24; 95%CI 1.05-1.47) and 22-29 weeks (10.6% vs. 6.9%; aRR 1.66; 95%CI 1.38-2.01). In a secondary analysis limited to the ultrasound 28-29 weeks, both fetal growth abnormalities and LGA were associated with the presence of obesity. In any of the analyses, pre-pregnancy obesity was not associated with FGR compared to normal weight. Maternal obesity is associated with an increased risk of fetal growth abnormalities and LGA fetuses.

Population Health Management effectiveness in the primary healthcare setting: a systematic review

Abstract Background Population Health Management (PHM) has shown promise as a tool in the improvement of health at scale. It works by; harnessing health-related datasets, allowing for population segmentation and risk stratification, and targeting interventions to yield positive health impact. Prior reviews on PHM, have sought to define PHM and assess feasibility. To date, there have been no systematic reviews that assess the effectiveness of PHM in achieving some or all of the quintuple aims of PHM (WHO 2023). The aim of this study is to determine the value and impact of a PHM approach in managing ambulatory care sensitive conditions (ACSCs) in the primary healthcare setting. Methods This systematic review is underpinned by a Population-Intervention-Comparator-Outcome (PICO) framework. The PROSPERO-registered study commenced in February 2024 for papers published since January 2000. Pubmed, Cinahl and Web of Science databases were used. Titles and abstracts of studies were reviewed using agreed eligibility criteria to select studies for inclusion and risk of bias assessment. Data abstraction and synthesis determined the effectiveness of PHM against agreed outcome measures. Results The search yielded 427 articles of which 19 were included. Studies addressed diabetes, hypertension, atrial fibrillation, asthma and comorbid conditions. Nearly all studies were based in the U.S.A. Almost 50% of studies showed a significant improvement in health outcomes following PHM. Study features that corresponded with positive health outcomes included; the use of population management tools, the employment of disease/population health managers and the mobilisation of medication reviews/education. Conclusions The challenges facing communities and health services require an alternative innovative approach to health such as a PHM approach. The results of this study will inform a larger body of work which seeks to establish a PHM approach to the delivery of services in the Mid-West region of Ireland. Key messages • Population health management (PHM) could be a viable mechanism for health services to serve increasing need and multi-morbid populations. • This is the first systematic review of PHM against the quintuple aims of PHM, specifically in the management of ambulatory care sensitive conditions in primary healthcare.

Effect of Short-Term Restraint Stress on the Expression of Genes Associated with the Response to Oxidative Stress in the Hypothalamus of Hypertensive ISIAH and Normotensive WAG Rats

Normotensive and hypertensive organisms respond differently to stress factors; however, the features of the central molecular genetic mechanisms underlying the reaction of the hypertensive organism to stress have not been fully established. In this study, we examined the transcriptome profiles of the hypothalamus of hypertensive ISIAH rats, modeling a stress-sensitive form of arterial hypertension, and normotensive WAG rats at rest and after exposure to a single short-term restraint stress. It was shown that oxidative phosphorylation is the most significantly enriched process among metabolic changes in the hypothalamus of rats of both strains when exposed to a single short-term restraint stress. The analysis revealed DEGs representing both a common response to oxidative stress for both rat strains and a strain-specific response to oxidative stress for hypertensive ISIAH rats. Among the genes of the common response to oxidative stress, the most significant changes in the transcription level were observed in Nos1, Ppargc1a, Abcc1, Srxn1, Cryab, Hspb1, and Fosl1, among which Abcc1 and Nos1 are associated with hypertension, and Fosl1 and Ppargc1a encode transcription factors. The response to oxidative stress specific to hypertensive rats is associated with the activation of the Fos gene. The DEG’s promoter region enrichment analysis allowed us to hypothesize that the response to oxidative stress may be mediated by the participation of the transcription factor CREB1 (Cyclic AMP-responsive element-binding protein 1) and the glucocorticoid receptor (NR3C1) under restraint stress in the hypothalamus of both rat strains. The results of the study revealed common and strain-specific features in the molecular mechanisms associated with oxidative phosphorylation and oxidative stress response in the hypothalamus of hypertensive ISIAH and normotensive WAG rats following a single short-term restraint stress. The obtained results expand the understanding of the most significant molecular targets for further research aimed at developing new therapeutic strategies for the prevention of the consequences of acute emotional stress, taking into account the hypertensive state of the patient.

Impairment of neuronal tyrosine phosphatase STEP worsens post-ischemic inflammation and brain injury under hypertensive condition

Hypertension is associated with poor outcome and higher mortality in patients with ischemic stroke. The impairment of adaptive vascular mechanisms under hypertensive condition compromises collateral blood flow after arterial occlusion in patients with acute ischemic stroke resulting in hypoperfusion. The increased oxidative stress caused by hypoperfusion is thought to be a trigger for the rapid evolution of ischemic infarct volume under hypertensive condition. However, the cellular factors and pathways that contribute to the exacerbation of ischemic brain injury under hypertensive condition is not yet understood. The current study reveals that predisposition to hypertension leads to basal loss of function of the neuron-specific tyrosine phosphatase STEP, which plays a crucial role in neuroprotection against excitotoxic insult. The findings further show that a mild ischemic insult in hypertensive rats triggers an early onset and sustained activation of the neuronal extracellular signal regulated kinase (ERK MAPK), a member of the mitogen activated protein kinase family and a substrate of STEP. This leads to rapid increase in the activation of neuronal NF-κB, expression of neuronal cyclooxygenase-2 and subsequent biosynthesis of the pro-inflammatory mediator prostaglandin E2, resulting in rapid morphological transformation of microglia to the pro-inflammatory state and subsequent exacerbation of ischemic brain injury. Restoration of STEP signaling with intravenous administration of a STEP-derived peptide mimetic reduces the pro-inflammatory response in neurons, activation of microglia, and ischemic brain injury. The findings suggest that the basal loss of STEP function under hypertensive condition contributes to the exacerbation of ischemic brain injury by enhancing post-ischemic inflammatory response. The study not only presents a novel role of STEP in regulating neuroimmune communication but also highlights the therapeutic potential of a STEP-mimetic in mitigating ischemic brain damage under hypertensive condition.

Impact of Hypertension and Physical Exercise on Hemolysis Risk in the Left Coronary Artery: A Computational Fluid Dynamics Analysis.

Background and Objectives: Hypertension increases the risk of developing atherosclerosis and arterial stiffness, with secondarily enhanced wall stress pressure that damages the artery wall. The coexistence of atherosclerosis and hypertension leads to artery stenosis and microvascular angiopathies, during which the intravascular mechanical hemolysis of red blood cells (RBCs) occurs, leading to increased platelet activation, dysfunction of the endothelium and smooth muscle cells due to a decrease in nitric oxide, and the direct harmful effects of hemoglobin and iron released from the red blood cells. This study analyzed the impact of hypertension and physical exercise on the risk of hemolysis in the left coronary artery. Methods: To analyze many different cases and consider the decrease in flow through narrowed arteries, a flow model was adopted that considered hydraulic resistance in the distal section, which depended on the conditions of hypertension and exercise. The commercial ANSYS Fluent 2023R2 software supplemented with user-defined functions was used for the simulation. CFD simulations were performed and compared with the FSI simulation results. Results: The differences obtained between the FSI and CFD simulations were negligible, which allowed the continuation of analyses based only on CFD simulations. The drops in pressure and the risk of hemolysis increased dramatically with increased flow associated with increased exercise. A relationship was observed between the increase in blood pressure and hypertension, but in this case, the increase in blood pressure dropped, and the risk of hemolysis was not so substantial. However, by far, the case of increased physical activity with hypertension had the highest risk of hemolysis, which is associated with an increased risk of clot formation that can block distal arteries and lead to myocardial hypoxia. Conclusions: The influence of hypertension and increased physical exercise on the increased risk of hemolysis has been demonstrated.

Renal microRNA-144-3p is associated with transforming growth factor-β1-induced oxidative stress and fibrosis by suppressing the NRF2 pathway in hypertensive diabetic kidney disease

Chronic kidney disease (CKD) is a global health problem characterized by progressive renal fibrosis and excessive extracellular matrix deposition. Oxidative stress and epigenetic regulation, particularly through microRNAs (miRNAs), play crucial roles in the pathogenesis of CKD. In this study, we investigated the role of urinary miR-144-3p, which is upregulated in rats with CKD induced by diabetes and hypertension, in renal fibrosis progression, particularly its regulation of the nuclear factor erythroid-2-related factor 2 (NRF2) pathway. Our findings revealed elevated miR-144-3p levels and reduced NRF2 and target gene levels in kidney tissues of streptozotocin-treated spontaneously hypertensive rats. In vitro experiments demonstrated that miR-144-3p directly binds to the 3'-untranslated region of nrf2, suppressing the NRF2 pathway in renal tubular epithelial cells. Additionally, the profibrogenic factor transforming growth factor (TGF)-β1 increased miR-144-3p expression. TGF-β1-induced NRF2 suppression and reactive oxygen species elevation were found to be mediated through miR-144-3p upregulation. In vivo, cilostazol, an antiplatelet drug with an NRF2-activating effect, ameliorated renal injury in diabetic hypertensive rats by decreasing TGF-β1 and miR-144-3p levels while increasing NRF2 and its target gene levels in the kidneys. These findings highlight the potential therapeutic value of targeting the miR-144-3p/NRF2 pathway to attenuate CKD progression in hypertensive diabetic conditions.

Multifactorial analysis of risk factors for foot ulcers in patients with neurovascular complications of diabetes.

Diabetic foot ulcers (DFU) are a major complication associated with significant morbidity and mortality. While numerous studies have investigated risk factors for these ulcers in general, few have focused specifically on patients with Neurovascular Complications of Diabetes. This study aimed to evaluate the prevalence and risk factors for DFU in this specific population. We analyzed data from the National Institutes of Health (NIS) database for the years 2017-2019, involving a cohort of 161,834 patients aged over 18 who were diagnosed with neurovascular complications of diabetes. Demographic characteristics (age, gender, ethnicity), hospital characteristics, comorbidities, and other relevant data were included for analysis. A binary logistic regression model was generated to identify independent risk factors for DFU. The prevalence of DFU among patients with neurovascular complications of diabetes was 29.4% during the period from 2017 to 2019. Compared to patients without DFU, those with DFU had longer hospitalization times and higher costs. The multiple regression analysis revealed that Iron-deficiency anemia (OR, 1.10; 95% CI, 1.01-1.11; P=0.019), Hypertension (OR, 1.07; 95% CI, 1.03-1.11; P=0.001), Obesity (OR, 1.08; 95% CI, 1.06-1.11; P<0.001), Peripheral vascular disorders (PVD) (OR, 1.69; 95% CI, 1.65-1.74; P<0.001), Osteomyelitis (OR, 7.10; 95% CI, 6.89-7.31; P<0.001), Tinea pedis (OR, 1.89; 95% CI, 1.59-2.26; P<0.001), Sepsis (OR, 1.24; 95% CI, 1.20-1.28; P<0.001), and onychomycosis (OR, 1.26; 95% CI, 1.13-1.42; P<0.001) were independent predictors for DFU in this population. The study found a high prevalence of DFU in patients with neurovascular complications of diabetes. Identifying and addressing risk factors such as deficiency anemia, hypertension, obesity, PVD, infections, and foot conditions may contribute to reducing the prevalence of DFU in this vulnerable population.

Hypertension-Induced Biomechanical Modifications in the Aortic Wall and Their Role in Stanford Type B Aortic Dissection.

Hypertension is a major risk factor for the type B aortic dissection (TBAD), while many patients do not manage or regulate their hypertension consistently, leading to stable or unstable hypertension. Currently, the effects of stable and unstable hypertension on the biomechanical properties of the aorta remain unclear. The objective was to identify a blood pressure state that represents a greater risk for TBAD development. A total of 183 samples (108 axial and 75 circumferential) were divided into three groups. Fatigue tensile tests were carried out to simulate normotension, stable hypertension, and unstable hypertension conditions, respectively. Uniaxial tensile tests were performed; thus, the elastic modulus, energy loss, and the peeling force were assessed to evaluate the biomechanical properties. Compared with normal blood pressure, the modulus of elastic fibers decreased under stable hypertension (0.05 ± 0.02 MPa vs. 0.11 ± 0.03 MPa, p < 0.001) and unstable hypertension (0.08 ± 0.02 MPa, p = 0.008), while collagen fibers increased under stable hypertension (2.14 ± 0.51 MPa vs. 1.10 ± 0.24 MPa, p < 0.001) but decreased under unstable hypertension (0.52 ± 0.14 MPa, p < 0.001) in the axial direction. Similar trends were observed circumferentially. Energy loss was highest under unstable hypertension (0.16 ± 0.03 vs. 0.08 ± 0.03, p < 0.001). Peeling force was significantly reduced under stable hypertension (81.69 ± 12.72 N/m vs. 111.10 ± 27.65 N/m, p < 0.001) and further under unstable hypertension (71.37 ± 16.13 N/m, p < 0.001). Stable and unstable hypertension significantly impair the biomechanical properties of the aortic wall, with unstable hypertension leading to greater damage. Hypertensive patients are recommended to strictly follow medical advice to control blood pressure to avoid a higher risk of TBAD due to improper blood pressure management.

Exacerbating orthodontic tooth movement in mice with salt-sensitive hypertension

Background/purposeOrthodontic tooth movement (OTM) is a critical aspect of dental treatment that requires the precise control of bone remodeling processes. Hypertension (HTN) can affect the effectiveness of OTM. Salt-sensitive hypertension (SSHTN) is of particular concern due to its detrimental effects on bone health, potentially altering orthodontic outcomes. This study aimed to investigate the effects of SSHTN on OTM using a mouse model. Materials and methodsMale mice were divided into a normal and an SSHTN group. The SSHTN model was generated by administering N(ω)-nitro-l-arginine methyl ester (l-NAME) followed by a high-salt diet. The OTM was performed using a nickel-titanium (Ni-Ti) closed-coil spring, and the tooth movement was measured after 12 days. Silicone imprinting was used to estimate the OTM distance. Osteoclast activity was assessed using tartrate-resistant acid phosphatase (TRAP) staining of decalcified maxillary sections. ResultsSSHTN mice exhibited significantly increased tooth movement compared to normal mice. This enhanced movement was associated with more osteoclasts in the SSHTN group than in the control group. These findings suggest that SSHTN increases OTM levels by promoting bone resorption. ConclusionSSHTN significantly affected OTM by enhancing osteoclast activity and increasing tooth movement. These results underscore the importance of considering hypertensive conditions in orthodontic treatment planning as they may require adjustments in force application to prevent potential adverse effects.

WITHDRAWN: Non-Contact Blood Pressure Monitoring from Radar Signals by a Temporal-Spatial Feature Fusion Network

Non-contact blood pressure (BP) monitoring offers a comfortable and uninterrupted means of BP assessment, free from the constraints of physical contact. This capability is particularly better for the routine surveillance of BP for individuals with hypertension, burn injuries, skin sensitivities, and other pertinent conditions. In this study, we proposed a Temporal-Spatial Feature Fusion Network (TSFN), a radar-based, non-contact approach for BP monitoring. The TSFN architecture combines Residual Networks (ResNet) for the meticulous extraction of spatial features from radar signals, Gated Recurrent Unit (GRU) for the discernment of temporal dynamics, and Multiple Head Attention (MHA) to selectively emphasize crucial information. These components collectively ensure precise BP detection from radar signals. To enhance the model's robustness, a Pseudo-Huber loss function was employed to refine the optimization process, providing a smoother gradient transition and improved stability. Evaluations demonstrated impressive accuracies, with mean errors of 0.24±6.78 mmHg for systolic blood pressure (SBP) and 0.25±5.13 mmHg for diastolic blood pressure (DBP). These outcomes meet the standards set by the British Hypertension Society (BHS) for grade ‘A’ benchmarks for SBP and DBP measurements. Notably, the TSFN model avoids the need for complex feature engineering, demonstrating its effectiveness in monitoring BP fluctuations across diverse physiological states at 2s intervals. This feature highlights its potential applicability in real-time monitoring systems, offering a promising solution for continuous, non-contact BP monitoring.

Hypoxic Preconditioned Tibetan Mesenchymal Stem Cell-derived Exosomes Ameliorate Pulmonary Vascular Remodeling in Hypoxic Pulmonary Hypertension Rats

BackgroundPulmonary hypertension associated with hypoxia frequently manifests in a range of long-standing lung disorders. A strategy to augment the therapeutic efficacy of mesenchymal stem cells (MSCs) involves subjecting them to hypoxic preconditioning, which bolsters the emission of exosomes exhibiting enhanced bioactivities through paracrine mechanisms. The objective of this research is to explore the healing impact of preconditioning with hypoxia on MSC-extracted exosomes in relation to vascular structural changes within the lungs of rodents afflicted by hypoxia-induced pulmonary arterial hypertension. Methods and ResultsThis research entailed the successful isolation, cultivation of mesenchymal stem cells from Tibetan umbilical cords, alongside the extraction of their exosomes. Our results highlight that exosomes derived from hypoxia-conditioned Tibetan cord mesenchymal stem cells (H-Tibetan-exo) demonstrated superior efficacy in suppressing pulmonary vascular structural changes compared to those from normoxic conditions (N-Tibetan-exo) in a rat model of hypoxia-induced pulmonary hypertension (HPH).In an effort to replicate pulmonary hypertension conditions within a laboratory setting, we subjected rat pulmonary arterial smooth muscle cells (rPASMCs) to a low oxygen environment. Our findings revealed that exosomes derived from high-altitude Tibetans (H-Tibetan-exo) showed a superior capacity in suppressing the growth of rPASMCs compared to those obtained from normoxic Tibetans (N-Tibetan-exo). Additionally, the Transwell assay revealed a more significant inhibition of rPASMCs migration by H-Tibetan-exo. The investigation of PI3K-AKT-mTOR pathway protein expression through western blot analysis revealed that under hypoxic conditions, there was an elevation in the phosphorylation status of these proteins in both cellular and tissue settings. Furthermore, the H-Tibetan-exo exhibited more effective inhibition of rPASMCs proliferation and a more significant downregulation of PI3K-AKT-mTOR pathway protein phosphorylation levels compared to the N-Tibetan-exo. ConclusionsH-Tibetan-exo significantly ameliorates pulmonary vascular remodeling in hypoxic pulmonary hypertension more effectively than N-Tibetan-exo. The enhancement observed could be linked to reduced activity of the PI3K-AKT-mTOR pathway. This discovery sheds fresh light on managing hypoxic pulmonary hypertension, highlighting the potential therapeutic benefits of H-Tibetan-exo in mitigating its development.

Placental Tissue Calcification and Its Molecular Pathways in Female Patients with Late-Onset Preeclampsia.

Preeclampsia (PE) is a complex multisystem disease characterized by hypertension of sudden onset (>20 weeks' gestation) coupled with the presence of at least one additional complication, such as proteinuria, maternal organ dysfunction, or uteroplacental dysfunction. Hypertensive states during pregnancy carry life-threatening risks for both mother and baby. The pathogenesis of PE develops due to a dysfunctional placenta with aberrant architecture that releases factors contributing to endothelial dysfunction, an antiangiogenic state, increased oxidative stress, and maternal inflammatory responses. Previous studies have shown a correlation between grade 3 placental calcifications and an elevated risk of developing PE at term. However, little is known about the molecular pathways leading to placental calcification. In this work, we studied the gene and protein expression of c-Jun N-terminal kinase (JNK), Runt-related transcription factor 2 (RUNX2), osteocalcin (OSC), osteopontin (OSP), pigment epithelium-derived factor (PEDF), MSX-2/HOX8, SOX-9, WNT-1, and β-catenin in placental tissue from women with late-onset PE (LO-PE). In addition, we employed von Kossa staining to detect mineral deposits in placental tissues. Our results show a significant increase of all these components in placentas from women with LO-PE. Therefore, our study suggests that LO-PE may be associated with the activation of molecular pathways of placental calcification. These results could be the starting point for future research to describe the molecular mechanisms that promote placental calcification in PE and the development of therapeutic strategies directed against it.

Investigating the pathophysiology and evolution of internal carotid dissection: a fluid-structure interaction simulation study.

Arterial dissection, a condition marked by the tearing of the carotid artery's inner layers, can result in varied clinical outcomes, including progression, stability, or spontaneous regression. Understanding these outcomes' underlying mechanisms is crucial for enhancing patient care, particularly with the increasing use of computer simulations in medical diagnostics and treatment planning. The aim of this study is to utilize computational analysis of blood flow and vascular wall to: (1) understand the pathophysiology of stroke-like episodes in patients with carotid artery dissection; and (2) assess the effectiveness of this method in predicting the evolution of carotid dissection. Utilizing contrast-enhanced magnetic resonance angiography (MRA), we segmented images of the patient's right internal carotid artery. These images were transformed into 3D solids for simulation in Ansys multifisic software, employing a two-way fluid structure interaction (FSI) analysis. Simulations were conducted across two wall conditions (atherosclerotic and normal) and three pressure states (hypotension, normotension, hypertension). The simulations indicated a significant pressure discrepancy between the true and false lumens of the artery. This suggests that flap motion and functional occlusion under hypertensive conditions could be the cause of the clinical episodes. Thrombotic risk and potential for dissection extension were not found to be critical concerns. However, a non-negligible risk of vessel dilation was assessed, aligning with the patient's clinical follow-up data. This study highlights specific hemodynamic parameters that could elucidate carotid artery dissection's mechanisms, offering a potential predictive tool for assessing dissection progression and informing personalized patient care strategies.

The Role of social care in health organizations for managing chronic Medical Conditions: A Comprehensive Review

This review examines the role of social care in managing chronic medical conditions within health organizations. Chronic diseases such as diabetes, hypertension, and cardiovascular conditions require comprehensive management strategies that extend beyond medical treatment to address the broader social determinants of health, including socioeconomic factors, social support systems, and community resources. The integration of social care into healthcare settings has emerged as a critical approach to improving patient outcomes and reducing healthcare costs. This review highlights the impact of social care models, such as Accountable Care Organizations (ACOs) and Health Homes, on chronic disease management. By analyzing current literature and case studies, the review explores how health organizations have successfully integrated social services to support patients with chronic conditions. Challenges such as funding, workforce development, and institutional barriers are also discussed. The findings suggest that a multidisciplinary approach combining medical care with social support can enhance care continuity, patient engagement, and long-term disease management. This review emphasizes the need for policy changes and innovative models to facilitate the effective integration of social care into chronic disease management frameworks.

Adaptive integration of history variables in constrained mixture models for organ-scale growth and remodeling.

In the last decades, many computational models have been developed to predict soft tissue growth and remodeling (G&R). The constrained mixture theory describes fundamental mechanobiological processes in soft tissue G&R and has been widely adopted in cardiovascular models of G&R. However, even after two decades of work, large organ-scale models are rare, mainly due to high computational costs (model evaluation and memory consumption), especially in long-range simulations. We propose two strategies to adaptively integrate history variables in constrained mixture models to enable large organ-scale simulations of G&R. Both strategies exploit that the influence of deposited tissue on the current mixture decreases over time through degradation. One strategy is independent of external loading, allowing the estimation of the computational resources ahead of the simulation. The other adapts the history snapshots based on the local mechanobiological environment so that the additional integration errors can be controlled and kept negligibly small, even in G&R scenarios with severe perturbations. We analyze the adaptively integrated constrained mixture model on a tissue patch for a parameter study and show the performance under different G&R scenarios. To confirm that adaptive strategies enable large organ-scale examples, we show simulations of different hypertension conditions with a real-world example of a biventricular heart discretized with a finite element mesh. In our example, adaptive integrations sped up simulations by a factor of three and reduced memory requirements to one-sixth. The reduction of the computational costs gets even more pronounced for simulations over longer periods. Adaptive integration of the history variables allows studying more finely resolved models and longer G&R periods while computational costs are drastically reduced and largely constant in time.

Posterior reversible encephalopathy syndrome and parkinsonism as the first manifestation of primary hyperparathyroidism - a report of two cases.

Primary hyperparathyroidism (PHPT) may be asymptomatic or present with renal calculi, secondary osteoporosis, fractures and neuropsychiatric manifestations. Posterior reversible encephalopathy syndrome (PRES) and parkinsonism are atypical manifestations that may be rarely associated with PHPT. We report two patients who presented with the conditions mentioned above. The first patient involved a 38-year-old woman who presented with diminution of vision, seizures, altered behavior and hypertension over eight months. An MRI of the brain done had shown vasogenic edema involving the parieto-occipital regions, suggestive of PRES. A metabolic screen revealed PTH-dependent hypercalcemia that was localized to the left inferior parathyroid gland. Following focused parathyroidectomy, there was improvement in sensorium, vision and normalization of blood pressure. The second patient was of a 74-year-old man who presented with progressive extrapyramidal symptoms of gait abnormalities and rigidity since the past eight months. He was initiated on Selegeline and Levodopa for the same purpose, and subsequently reported minimal improvement in symptoms. Investigations revealed PHPT associated with a right inferior parathyroid adenoma. Within two weeks following surgery, there was an improvement in rigidity and gait and he was able to ambulate without support. PRES has been reported to occur in the context of preeclampsia, hypertension, infection, sepsis and autoimmune conditions. PRES associated with hypercalcemia is rarely reported. While extra-pyramidally related manifestations are described in hypoparathyroidism, PHPT related parkinsonism is not commonly encountered. Identifying the underlying aetiology and initiation of corrective measures may lead to amelioration of patient symptomatology. The occurrence of PRES and parkinsonism is rare in primary hyperparathyroidism; the two patients described above highlight the importance of screening for hypercalcemia in the setting of neurological manifestations.

Gastrodin Alleviates Angiotensin II-Induced Hypertension and Myocardial Apoptosis via Inhibition of the PRDX2/p53 Pathway In Vivo and In Vitro.

Gastrodin, a highly potent compound found in the traditional Chinese medicine Gastrodia elata Blume, exhibits significant antihypertensive properties. However, its role and the mechanism behind its protective effects on hypertensive cardiac conditions are not well understood. This study aims to investigate the cardiac protective effects and underlying mechanisms of gastrodin in angiotensin II (Ang II)-induced hypertensive models, both in vivo and in vitro. Treatment with gastrodin significantly decreased blood pressure and the heart weight/tibial length (HW/TL) ratio and attenuated cardiac dysfunction and pathological damage in Ang II-infused C57BL/6 mice. RNA sequencing analysis (RNA-seq) revealed 697 up-regulated and 714 down-regulated transcripts, along with 1105 signaling pathways, in Ang II-infused C57BL/6 mice following gastrodin treatment, compared to Ang II-induced hypertensive mice. Furthermore, the analyses of the top 30 Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway indicated significant enrichment in apoptosis and the peroxiredoxin 2 (PRDX2)/p53 pathway. Consistently, gastrodin treatment significantly reduced myocardial apoptosis in both the cardiac tissues of Ang II-induced hypertensive mice and Ang II-stimulated H9c2 cells. Additionally, gastrodin treatment significantly decreased the protein levels of PRDX2, p53, cleaved caspase-3, cleaved caspase-9, and Bax/Bcl-2 ratio in the cardiac tissues of Ang II-infused mice and H9c2 cells stimulated with Ang II. In conclusion, gastrodin treatment can mitigate hypertension-induced myocardial apoptosis in hypertensive mice by inhibiting the PRDX2/p53 pathway.

The Pattern of Practice in the Management of Early Diabetic Kidney Disease.

Background and objectives Diabetes is a leading cause of kidney failure in various regions worldwide. To detect renal disease in individuals with diabetes, screening typically involves evaluating the glomerular filtration rate and measuring albuminuria. Although there are established guidelines for these screenings, adherence to them varies. This study aims to examine the prevalence of albuminuria screening among adults with diabetes mellitus (DM) and to assess the different practices in managing these patients across primary and tertiary care settings. Methods This cross-sectional observational study involved adult patients with DM attending outpatient clinics in both primary and tertiary care settings. Patient data were gathered using a standardized form, excluding those with established chronic kidney disease (CKD) who were under nephrology care. Results The study included 1,010 patients, with 303 (30%) from primary care clinics and 707 (70%) from tertiary care clinics. The cohort comprised 582 (58%) females, with a median age of 62 years (IQR: 55-70), and approximately 990 (98%) had type 2 DM (T2DM). Annual albumin-to-creatinine ratio (ACR) screening was conducted for 498 out of 1,010 patients (49%) (95% confidence interval {CI}: 46%-52%). Screening compliance was notably higher in primary care settings compared to tertiary care clinics. Older patients (over 60 years) and those with hypertension or cardiac conditions were less likely to undergo screening. Among those screened, 185 of 498 patients (37%) (95% CI: 33%-41%) had abnormal albuminuria (ACR > 3). Conclusion Albuminuria is a significant indicator of progressing renal disease and cardiovascular risk. The annual screening rate for albuminuria in diabetic patients is inadequate. Primary care physicians show better adherence to screening guidelines compared to their tertiary care counterparts. Increasing physician awareness about the importance of screening could improve guideline compliance and mitigate the adverse effects of albuminuria.