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Background: CKD has a high global prevalence with a consistent estimated global CKD prevalence of between 11 to 13% with the majority stage 3. Patients with CKD undergoing hemodialysis have low immunity and are prone to sepsis. Presepsin is a highly specific biomarker for the early diagnosis of sepsis because presepsin is increased in the blood in the early phase of infection and may be a helpful and valuable biomarker in early diagnosis of sepsis. Therefore, presepsin may have application for the early diagnosis of sepsis in patients with CKD.Purpose This prospective study evaluated the diagnostic value of serum presepsin (soluble CD14-ST) levels for sepsis in chronic kidney disease (CKD) and the influence of undergoing hemodialysis on serum presepsin Methods: This study included 291 patients with CKD and 101 patients with normal renal function and sepsis. Presepsin levels were increased in patients with CKD with or without sepsis or hemodialysis compared to controls, and were highest in patients with CKD and sepsis undergoing hemodialysis. Results: Presepsin levels were similar in patients with CKD with sepsis and no hemodialysis and patients with normal renal function and sepsis, but these levels were lower than in patients with CKD without sepsis undergoing hemodialysis. Presepsin, procalcitonin (PCT) and C-reactive protein (CRP) levels had diagnostic value for sepsis; however, presepsin was a better predictor of sepsis than PCT or CRP in patients with CKD not undergoing hemodialysis. Presepsin level had limited diagnostic value for sepsis in patients with CKD undergoing hemodialysis. In CKD complicated with sepsis, presepsin level was significantly correlated with CRP level, Sequential Organ Failure Assessment score, partial pressure of oxygen and body temperature; there was no correlation between presepsin level and these indicators in CKD without sepsis. Conclusion: These findings suggest physicians should incorporate information on biomarkers with medical history, clinical symptoms, physical signs, and other tests related to sepsis for its diagnosis in patients with CKD undergoing hemodialysis. Presepsin was a better predictor of sepsis in patients with CKD not undergoing hemodialysis.

Vascular smooth muscle cells (VSMCs) are associated with differentiated, organized, and contractile phenotype under the effect of various types of physiological conditions those are associated with migratory, proliferative, and synthetic phenotype under the effect of various types of stimuli, which dysfunction drives many cardiovascular diseases. Abnormal cell proliferation and invasion of VSMCs are among the primary causes of hypertension. Apatinib is a small-molecule tyrosine kinase inhibitor (TKI) that highly selectively binds to and strongly inhibits VEGFR-2. Previous studies have confirmed that the TKIs can raise blood pressure through RhoA/ROCK pathway. LARG is a key gene in the RhoA/ROCK pathway and plays a critical role in the continuous vasoconstriction function because it regulates part of signal transduction in VSMCs. In this study, an in vitro experiment was conducted to observe that apatinib caused dysfunction of MOVAS cells through the RhoA/ROCK signalling pathway and Y27632, a nonspecific ROCK inhibitor, and knockout of LARG gene can improve the proliferation, antiapoptosis, oxidative stress, and mitochondrial autophagy of apatinib-induced MOVAS cells. These findings suggest that activation of the RhoA/ROCK signalling pathway could be the underlying mechanism of apatinib-induced dysfunction of MOVAS cells, while ROCK inhibitor and knockout of LARG gene have potential therapeutic value.

Hypertension is one of the main adverse effects of antiangiogenic tumor drugs and thus limits their application. The mechanism of hypertension caused by tyrosine kinase inhibitors (TKIs) targeting vascular endothelial growth factors is mainly related to inhibition of the nitric oxide (NO) pathway and activation of the endothelin pathway, as well as vascular rarefaction and increased salt sensitivity; consequently, prevention and treatment differ for this type of hypertension compared with primary hypertension. Apatinib is a highly selective TKI approved in China for the treatment of advanced or metastatic gastric cancer. The RhoA/ROCK pathway is involved in the pathogenesis of hypertension and mediates smooth muscle contraction, eNOS inhibition, endothelial dysfunction and vascular remodeling. In this study, in vivo experiments were performed to explore whether the RhoA/ROCK signaling pathway is part of a possible mechanism of apatinib in the treatment of gastric cancer-induced hypertension and the impairment of vascular remodeling and left ventricular function. Y27632, a selective small inhibitor of both ROCK1 and ROCK2, was combined with apatinib, and its efficacy was evaluated, wherein it can reduce hypertension induced by apatinib treatment in gastric cancer mice and weaken the activation of the RhoA/ROCK pathway by apatinib and a high-salt diet (HSD). Furthermore, Y-27632 improved aortic remodeling, fibrosis, endothelial dysfunction, superior mesenteric artery endothelial injury, left ventricular dysfunction and cardiac fibrosis in mice by weakening the activation of the RhoA/ROCK pathway. The expression of RhoA/ROCK pathway-related proteins and relative mRNA levels in mice after apatinib intervention were analyzed by various methods, and blood pressure and cardiac function indexes were compared. Endothelial and cardiac function and collagen levels in the aorta were also measured to assess vascular and cardiac fibrosis and to provide a basis for the prevention and treatment of this type of hypertension.

Objective The aim to discuss the close relationship between the common biological mechanisms of breast cancer and hypertension, inflammation and oxidative stress, breast cancer gene mutations breast cancer susceptibility gene (BRCA), G protein-coupled receptor kinase (GRK4), etc. and breast cancer treatment includes chemotherapy, Endocrine therapy, Targeted therapy and anti-angiogenesis drugs. In anti-angiogenesis drugs focusing on the mechanism of tyrosine kinase inhibitors (TKI) that may activate the rhoa/rock pathway to cause hypertension, as well as the relationship between breast cancer and antihypertensive drugs includes angiotensin-converting enzyme inhibitors (ACEIs), Calcium channel blockers (CCBs) and β-blockers (BBs)will be explored. Background Cardiovascular diseases (CVD) and tumors are the two major types of diseases with the highest mortality rates, while hypertension accounts for the largest proportion of CVDs. A large number of the same or similar risk factors are shared between hypertension and tumors, and they influence each other. Many patients, particularly elderly patients, often present with the coexistence of the two diseases. As medical advances have enabled clinicians to cure tumors, many patients with cancer live longer, leading to a gradual increase in the incidence of CVDs, including hypertension. With the second highest incidence among tumors, breast cancer has gradually attracted widespread attention and has been the topic of numerous studies. Studies have confirmed that CVD is one of the causes of death in elderly patients with breast cancer. Methods Publications from 1985 to 2020 were retrieved from the Web Of Science, Cochrane Library, PubMed, EMBASE and MEDLINE database. We used a mix of MeSH and keywords. Conclusions Hypertension and cancer may share a common mechanism. The screening and risk assessment of breast cancer in patients with hypertension must be strengthened. Breast cancer cardiology is the interdisciplinary study of oncology and cardiology, and in-depth research in this field may result in long-term improvements in the survival and prognosis of patients with both clinical hypertension and breast cancer.

The storage device based on Nonvolatile Memory (NVM devices) has high read/write speed and embedded processor. It is a useful way to improve the efficiency of Key-Value (KV) application. However it still has some limitations such as limited capacity, poorer computing power compared with CPU, and complex I/O system software. Thus it is not an effective way to construct KV storage system with NVM devices directly. We analyze the characteristics of NVM devices and demands of KV application to design the matrix KV storage system based on NVM Devices. The group collaboration management based on Bloomfilter, intragroup optimization based on competition, embedded KV management based on B+-tree, and the new interface of KV storage system are presented. Then, the embedded processor in the NVM device and CPU can be comprehensively utilized to construct a matrix KV pair management system. It can improve the storage and management efficiency of massive KV pairs, and it can also support the efficient execution of KV applications. A prototype is implemented named MKVS (the matrix KV storage system based on NVM devices) to test with YCSB (Yahoo! Cloud System Benchmark) and to compare with the current in-memory KV store. The results show that MKVS can improve the throughput by 5.98 times, and reduce the 99.7% read latency and 77.2% write latency.