Search

In the face of severe internal economic challenges and rising hostile geopolitical landscape, Xi Jinping's unprecedented third term has garnered much attention as the way in which these challenges are addressed will not only impact China's internal governance on development issues but also its foreign policy and strategy. The paper attempts to examine the implications of Xi's strategy and policy—from its stated goals to actions and outcomes—for Malaysia with respect to opportunities and challenges and its strategic response. The analysis benefits from the insights from the international political economy, which explores how the apparent weak unity government under Anwar Ibrahim's administration amid tough domestic challenges and rising hostile geopolitical environment strives to reconcile the imperative of its domestic legitimation to prioritize immediate economic benefits over potential security concerns. Despite the reinvigorating Malaysia-China relations has brought tangible results, paving the way for more mutually beneficial trade and investment opportunities and partnerships, the external pressure caused Malaysia under Anwar's administration to maintain Malaysia's hedging under uncertainties in structural conditions rather than balancing or bandwagoning. Malaysia's inclination to hedge is against the various risks associated with the uncertainty inherent in US-China rivalry—e.g. uncertainty in the future of Sino-American relations, uncertainty in Xi Jinping's long-term strategic goals, uncertainty surrounding China's slowing economy, diffuse threats, and uncertain reliable and sustainable allied supports. The recent rapid expansion of China's investment in the country to avoid tariffs imposed by the US on certain products of China could be a double-edged sword. While smaller power like Malaysia with heavy economic dependence on China and the US will confront greater external constraints to maintain strategic ambiguity and keep its strategic options open, managing tradeoffs in foreign policy choices continues to be driven and constrained by the imperative of elite's domestic legitimation embedded in the state-market-society interactions. [ABSTRACT FROM AUTHOR]

Introduction: Albumin plays a vital role in improving osmotic pressure and hemodynamics. A lower serum albumin level may cause pulmonary congestion and edema and contribute to myocardial dysfunction, diuresis resistance, and fluid retention in acute heart failure. Hypothesis: We hypothesized that AHF patients with normal serum albumin have shorter hospital stays. Methods: Using Electronic Medical Records, patients admitted from May 2020 through May 2021 aged >18, ICD-10, and positive Framingham Heart Failure Diagnostic Criteria were included. We excluded patients without albumin records and eGFRs less than 30 mL/min/1.73 m2. Prolonged hospitalization was defined as >8 days of hospitalization. Results: During index emergency department visits, patients were symptomatic (New York Heart Association), aged median of 70 years (Interquartile range (IQR) 18), 59% (n = 103) were male, predominantly White (73%, n = 128), and had a high Charleston Comorbidity index score [5, IQR (4–7)]. Nearly one-fourth (23%, n = 41) of the patients had <3.5 g/dL albumin levels. The median length of hospital stay was eight days (IQR of 11). Comparing differences between lengths of hospital stays (< 8 vs. >8 days), there was different serum albumin (3.9 + 0.48 vs. 3.6 + 0.53, p <.001) and left ventricular ejection fraction (45% (range 26–63) versus 30% (range 24–48), p =.004). An increased serum albumin decreased prolonged hospitalization (odds ratio (OR), 0.28; 95% confidence interval (CI), 0.14–0.55, p = <0.001). Patients in the lower albumin group had higher NT-proBNP (median: 8521 (range 2025–9134) versus 5147 (range 2966–14,795) pg/ml, p =.007) and delay in administering intravenous diuretics (391 (167–964) minutes versus 271 (range 157–533) minutes, p =.02). Conclusion: Hypoalbuminemia is strongly associated with prolonged hospitalization. Timely and effective diuretic therapy may reduce hospital stay durations, particularly with albumin supplementation. [ABSTRACT FROM AUTHOR]

Diuretic drugs act on electrolyte transporters in the kidney to induce diuresis and are often used in chronic kidney disease (CKD), given that nephron loss creates a deficit in the ability to excrete dietary sodium, which promotes an increase in plasma volume. This rise in plasma volume is exacerbated by CKD-induced systemic and intra-renal activation of the renin-angiotensin-aldosterone-system, which further limits urinary sodium excretion. In the absence of a compensatory decrease in systemic vascular resistance, increases in plasma volume induced by sodium retention can manifest as a rise in systemic arterial blood pressure. Management of sodium and volume overload in patients with CKD is therefore typically based on restriction of dietary sodium intake and the use of diuretic agents to enhance urinary sodium excretion. Thiazide and thiazide-type diuretics are foundational therapies for the management of hypertension, whereas loop diuretics are often needed for volume overload, which might also require combination therapies. Mineralocorticoid receptor antagonists have an important role in the management of diuretic-resistant volume overload or treatment-resistant hypertension. Additionally, diuretics can be used for the diagnosis of kidney diseases and in the management of hyperkalaemia or hypokalaemia, hyponatraemia, hypercalcaemia and hypomagnesaemia., Competing Interests: Competing interests: R.A. served as a member of the executive steering committees of the FIDELIO and FIGARO trials, continues to serve on the steering committee of the FIND-CKD and CONFIDENCE trials and as the principal investigator for CONFIDENCE; all of these trials are funded by Bayer. R.A. serves as a consultant for Bayer, Covance, and Boehringer Ingelheim; served on the executive steering committees for Akebia for their HIF-PHI trials and as a consultant; chairs adjudication committees for Alnylam and Intercept Pharma and Data safety monitoring boards for Chinook, Vertex, and Eloxx. R.A. receives royalties from UpToDate and serves as Associate Editor of the American Journal of Nephrology and Nephrology Dialysis and Transplantation. The other authors declare no competing interests., (© 2025. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.)

Contraction of the heart is driven by cyclical interactions between myosin and actin filaments powered by ATP hydrolysis. The modular structure of heart muscle and the organ-level synchrony of the heartbeat ensure tight reciprocal coupling between this myosin ATPase cycle and the macroscopic cardiac cycle. The myosin motors respond to the cyclical activation of the actin and myosin filaments to drive the pressure changes that control the inflow and outflow valves of the heart chambers. Opening and closing of the valves in turn switches the myosin motors between roughly isometric and roughly isotonic contraction modes. Peak filament stress in the heart is much smaller than in fully activated skeletal muscle, although the myosin filaments in the two muscle types have the same number of myosin motors. Calculations indicate that only ~5% of the myosin motors in the heart are needed to generate peak systolic pressure, although many more motors are needed to drive ejection. Tight regulation of the number of active motors is essential for the efficient functioning of the healthy heart - this control is commonly disrupted by gene variants associated with inherited heart disease, and its restoration might be a useful end point in the development of novel therapies., Competing Interests: Competing interests: The author declares no competing interests., (© 2024. Springer Nature Limited.)