Mesoscopic ring element growth and deformation induced biofilm streamer evolution in microfluidic channels.

In a fluid environment, biofilms usually form and grow into streamers attached to solid surfaces. Existing research on single streamers studied their formation and failure modes. In the experiment on biofilm growth in a microfluidic channel, we found that rings composed of bacteria and an extracellular matrix are important elements on a mesoscopic scale. In the fluid environment, the failure of these ring elements causes damage to streamers. We simulated the growth and deformation of the ring structure in the micro-channel using multi-agent simulation and fluid-structure coupling of a porous elastic body. Based on this, we simulated the biofilm evolution involving multi-ring deformation, which provides a new length scale to study the biofilm streamer dynamics in fluid environments.

Association of STAT3 gene polymorphisms with systemic lupus erythematosus in a Chinese Han population.

OBJECTIVE: Evidence supports the important role of STAT3 in SLE; however, association between STAT3 gene polymorphisms and SLE risk needs discussion. METHODS: Three hundred SLE patients and 380 healthy controls from Chinese Han population were included. DNA is extracted from peripheral blood mononuclear cells and the clinical characteristics of patients are collected. STAT3 gene polymorphisms (rs6503695, rs744166, rs9912773, and rs12601982) were genotyped by the Kompetitive Allele-Specific PCR (KASP) method. SPSS 26.0 was utilized to analyze the genetic susceptibility of SLE and STAT3 gene polymorphisms. RESULTS: Frequencies of genotypes CT, TT, and TT+CT were significantly lower in SLE patients compared with those in healthy controls with respect to rs6503695 (p = .007, p < .001, p = .001). Frequencies of rs744166 genotypes AG, AA, and AA+AG were decreased in SLE patients as compared to those in healthy controls (p = .034, p = .006, p = .009). The recessive models (CC vs GG+GC) for rs9912773 and (AA vs GG+GA) for rs12601982 were significantly related to SLE patients (p = .014, p = .035). Moreover, allele C of rs6503695 was related to optic nerve damage in SLE patients (p = .036). rs744166 allele G was correlated with positive rash and albuminuria in SLE patients (p = .006, p = .014). For rs9912773, SLE patients carrying genotype GG had higher serum C3 and C4 levels compared to genotype GC+CC (p = .029, p = .028). The rs12601982 allele G was strongly associated with positive hypocomplementemia in SLE patients (p = .034). SLE patients carrying genotypes GG, GC, and CC had different SLEDAI score for rs12601982 (GG vs GC vs CC, p = .003). CONCLUSION: STAT3 gene polymorphisms associated with SLE susceptibility.

Continuous compression with asynchronous ventilation improves CPR prognosis? A meta-analysis from human and animal studies.

BACKGROUND: The cardiopulmonary resuscitation (CPR) compression to ventilation strategy remains controversial. We conducted a meta-analysis to compare the outcomes between continuous chest compressions CPR with asynchronous ventilation (CCC-CPR) and interrupted chest compressions CPR with synchronous ventilation (ICC-CPR) in cardiac arrest. METHODS: PubMed, Web of Science, Embase, MEDLINE (Ovid/LWW) and the Cochrane Libraries were searched up from inception to July 31, 2022. Human and animal studies comparing CCC-CPR versus ICC-CPR were included. Outcome variables were return of spontaneous circulation (ROSC), time to ROSC, survival to discharge, 1-month survival, survival at 4 h, good neurological function, mean arterial pressure (MAP) and other clinical parameters. Jadad Scale and Newcastle-Ottawa Scale were used to assess the study quality and risk of bias. RESULTS: The systematic search identified eight studies on humans and twelve studies on animal trials. There were no significant differences in ROSC (odd ratios [OR] 1.07; 95% confidence interval [CI]: 0.86-1.32; P = 0.55), survival to hospital discharge (OR 1.04; 95%CI 0.77-1.42; P = 0.79), 1-month survival (OR 1.07; 95%CI 0.84-1.36; P = 0.57), and good neurological outcome (OR 0.92; 95%CI 0.84-1.01, P = 0.09) between CCC-CPR and ICC-CPR in human studies. In animal trials, CCC-CPR had significantly higher rate of ROSC (OR = 1.81; 95% CI: 0.94-3.49; P = 0.07), survival at 4 h (OR 2.57; 95% CI: 1.16-5.72; P = 0.02) and MAP (mean difference [MD] 0.79, 95% CI: 0.04-1.53; P = 0.04), even though no significant differences in ROSC time, arterial potential of hydrogen (pH) and partial tension of carbon dioxide (PaCO2). CONCLUSION: CCC-CPR did not show superiority in human outcomes compared with ICC-CPR, but its effect value was significantly increased in animal experiments. We should take the positive outcomes from animals and apply them to human models, and more physiological mechanisms need to be confirmed in CPR patients with different compression-ventilation strategies to improve the prognosis of cardiac arrest.

Baicalein ameliorates oxidative stress and brain injury after intracerebral hemorrhage by activating the Nrf2/ARE pathway via miR-106a-5p/PHLPP2 axis.

Intracerebral hemorrhage (ICH) is a devastating stroke subtype. Baicalein (BAI) has been reported to be effective in ischemic stroke. The aim of the present study was to investigate the mechanism of BAI on brain injury after ICH. Firstly, ICH mouse models were established by injecting collagenase into the right of basal ganglia, followed by detection of neurobehavioral scores, brain edema, oxidative stress (OS) level, neuronal apoptosis and pathological changes. Average neurologic scores, brain water content, and blood-brain barrier permeability and MDA level in ICH mice were reduced after BAI treatment, while serum SOD and GSH-Px levels were increased and neuronal apoptosis and pathological injury of the brain tissues were mitigated. miR-106a-5p downregulation averted the effect of BAI on ICH mice. miR-106a-5p targeted PHLPP2 and PHLPP2 overexpression reversed the effect of BAI on ICH mice. BAI activated the Nrf2/ARE pathway by inhibiting PHLPP2 expression. In conclusion, BAI inhibited OS and protected against brain injury after ICH by activating the Nrf2/ARE pathway through the miR-106a-5p/PHLPP2 axis.

PGGait: Gait Recognition Based on Millimeter-Wave Radar Spatio-Temporal Sensing of Multidimensional Point Clouds.

Gait recognition, crucial in biometrics and behavioral analytics, has applications in human-computer interaction, identity verification, and health monitoring. Traditional sensors face limitations in complex or poorly lit settings. RF-based approaches, particularly millimeter-wave technology, are gaining traction for their privacy, insensitivity to light conditions, and high resolution in wireless sensing applications. In this paper, we propose a gait recognition system called Multidimensional Point Cloud Gait Recognition (PGGait). The system uses commercial millimeter-wave radar to extract high-quality point clouds through a specially designed preprocessing pipeline. This is followed by spatial clustering algorithms to separate users and perform target tracking. Simultaneously, we enhance the original point cloud data by increasing velocity and signal-to-noise ratio, forming the input of multidimensional point clouds. Finally, the system inputs the point cloud data into a neural network to extract spatial and temporal features for user identification. We implemented the PGGait system using a commercially available 77 GHz millimeter-wave radar and conducted comprehensive testing to validate its performance. Experimental results demonstrate that PGGait achieves up to 96.75% accuracy in recognizing single-user radial paths and exceeds 94.30% recognition accuracy in the two-person case. This research provides an efficient and feasible solution for user gait recognition with various applications.

The porous structure induced heterogeneous and localized failure of the biofilm in microfluidic channels.

Understanding the mechanism of biofilm distribution and detachment is very important to effectively improve water treatment and prevent blockage in porous media. The existing research is more related to the local biofilm evolving around one or few microposts and the lack of the integral biofilm evolution in a micropost array for a longer growth period. This study combines microfluidic experiments and mathematical simulations to study the distribution and detachment of biofilm in porous media. Microfluidic chips with an array of microposts with different sizes are designed to simulate the physical pore structure of soil. The research shows that the initial formation and distribution of biofilm are influenced by bacterial transport velocity gradients within the pore space. Bacteria prefer to aggregate areas with smaller microposts, leading to the development of biofilm in those regions. Consequently, impermeable blockage structures form in this area. By analyzing experimental images of biofilm structures at the later stages, as well as coupling fluid flow and porous medium, and the finite element simulation, we find that the biofilm detachment is correlated with the morphology and permeability (kb) (from 10-15 to 10-9 m2) of the biofilm. The simulations show that there are two modes of biofilm detachment, such as internal detachment and external erosion.

Mycobacterium tuberculosis protease Rv3090 is associated with late cell apoptosis and participates in organ injuries and mycobacterial dissemination in mice.

Tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis (Mtb). Mtb can overcome macrophage intracellular killing and lead to persistent infections. The proteases of Mtb are critical virulence factors that participate in immune responses. We determined that Rv3090 is a cell wall-associated protease and a potential pathogenic factor. To characterize the role of Rv3090 in Mtb, recombinant Msg_Rv3090 and Msg_pAIN strains were constructed to infect macrophages and mice. Lactate dehydrogenase assays and flow cytometry results showed that Rv3090 induces late macrophage apoptosis. In vivo infection experiments indicated that Rv3090 could induce hepatocyte and lung cell apoptosis and cause pathological damage to the spleen, livers and lungs. Msg_Rv3090 specifically stimulated the secretion of inflammatory cytokines including TNF-α, IL-6 and IL-1ß. Overexpression of Rv3090 significantly promoted the survival of Msg in livers and lungs. Thus, Rv3090 protease triggered late cell apoptosis and contributed to the pathogenicity and dissemination of Mtb.

Outcome of cardiopulmonary resuscitation with different ventilation modes in adults: A meta-analysis.

BACKGROUND: The optimal airway management strategy for cardiac arrest remains unclear. This study aimed to compare the effects of different initial airway interventions on improving clinical outcomes based on the 2010 cardiopulmonary resuscitation (CPR) guidelines and later. METHODS: We searched PubMed, EMBASE, and the Cochrane Library for CPR articles tailored to each database from October 19, 2010, to July 31, 2021, to compare endotracheal intubation (ETI), supraglottic airway (SGA), or bag-valve-mask ventilation (BMV). The initial results and long-term results were investigated by meta-analysis. RESULTS: Twenty-five articles (n = 196,486) were included. The ROSC rate in the ETI group (ES = 0.49, 95% CI: 0.38-0.59) was significantly higher than that in the SGA group (ES = 0.27, 95% CI: 0.20-0.34) and BMV group (ES = 0.24, 95% CI: 0.17-0.31). The rate of ROSC upon admission to the hospital in the ETI group (ES = 0.27, 95% CI: 0.13-0.42) was significantly higher than that in the SGA group (ES = 0.18, 95% CI: 0.13-0.23) and BMV group (ES = 0.16, 95% CI: 0.10-0.22). Compared with the BMV group (ES = 0.09, 95% CI: 0.04-0.14) and the SGA group (ES = 0.08, 95% CI: 0.05-0.10), the ETI group (ES = 0.14, 95% CI: 0.10-0.17) had a higher discharge rate, but all of the groups had the same neurological outcome (ETI group [ES = 0.06, 95% CI: 0.04-0.08], BMV group [ES = 0.05, 95% CI: 0.03-0.08] and SGA group [ES = 0.04, 95% CI: 0.03-0.05]). CONCLUSIONS: Opening the airway is significantly associated with improved clinical outcomes, and the findings suggest that effective ETI based on mask ventilation should be implemented as early as possible once the patient has experienced cardiac arrest.

Interleukin 2 regulates the activation of human basophils.

Basophils are important effector cells in allergic disorders and anti-parasitic immune response. A number of activators including interleukin 3 (IL-3) and IgE have been identified in the regulation of human basophils expressing mediators such as histamine and leukotriene C4 (LTC4) and cytokines, including IL-4 and IL-13. Human basophils express high levels of IL-2 receptors. However, the function of the IL-2 pathway in basophils remains unknown. Here, we identified that IL-2 induced the activation of human basophils in vitro to express a variety of inflammatory cytokines and chemokines including IL-5, IL-13, GM-CSF and CCL-17. This effect by IL-2 is confirmed by an upstream regulator analysis using Ingenuity pathway analysis. Of note, one of the top regulated cytokines, IL-5, was for the first time identified to be induced by IL-2 in human basophils rather than IL-3 or anti-IgE. Immunofluorescence analysis of skin specimens from bullous pemphigoid and eczema revealed that infiltrating basophils in skin lesions widely expressed IL-5 and GM-CSF. Together, our findings reveal IL-2 as a novel regulator of human basophils. This adds a new layer to support the importance of basophils in allergic disorders.

Interleukin 3-induced GITR promotes the activation of human basophils.

Human basophils regulate allergic reactions by secreting histamine, interleukin 4 (IL-4) and IL-13 through key surface receptors FcεRI as well as IL-3R, which are constitutively expressed on basophils. IL-3/IL-3R signaling axis plays key roles in regulating the development and activation of basophils. We and others have shown that IL-3-induced surface receptors e.g. ST2, IL-17RB and IL-2 receptors regulate the biology of basophils. However, the expression and function of IL-3-induced surface proteins on human basophils remain to be elucidated. We in this study aimed to identify new basophil activation regulators by transcriptomic analysis of IL-3-stimulated basophils. Gene expression microarray analysis of IL-3-treated basophils revealed 2050 differentially expressed genes, of which 323 genes encoded surface proteins including GITR. We identified that GITR was preferentially induced by IL-3 rather than anti-IgE, IL-33, fMLP and C5a. IL-3-induced GITR was suppressed by inhibitors targeting JAK2, PI3K and MEK1/2. Stimulation of IL-3-treated basophils by GITR enhanced the expression of IL-4 and IL-13. Moreover, IgE-mediated degranulation was enhanced by GITRL in the presence of IL-3. This transcriptomic analysis of IL-3-activated basophils helps to identify novel activation regulator. IL-3-induced GITR promoted the activation of basophils, adding new evidence supporting GITR as an important player in Th2-associated immune responses.

MicroRNA-92a-1-5p influences osteogenic differentiation of MC3T3-E1 cells by regulating ß-catenin.

Osteoblastic differentiation is a complex process that is critical for proper bone formation. An increasing number of studies have suggested that microRNAs (miRNAs) are pivotal regulators in various physiological and pathological processes, including osteogenesis. Here, we discuss the influence of miRNA-92a-1-5p on osteogenic differentiation. We found that miR-92a-1-5p was obviously downregulated during osteogenic differentiation of MC3T3-E1 cells. Gain-of-function and loss-of-function experiments revealed that miR-92a-1-5p was a negative regulator of osteogenic differentiation. Experimental validation demonstrated that ß-catenin, which acts as a positive regulator of osteogenic differentiation, was negatively regulated by miR-92a1-5p. The findings of this study provide new insights into the possibility of miR-92a1-5p being a potential therapeutic target in the management of bone regeneration-related diseases.

Patellofemoral kinematic characteristics in anterior cruciate ligament deficiency and reconstruction.

BACKGROUND: It is very important to dynamically evaluate the functional outcome in the knee after anterior cruciate ligament (ACL) reconstruction under physiological weight bearing. The objective of the current study is that we would like to compare the patellofemoral joint kinematics in three ACL status: ACL intact, ACL deficiency, ACL reconstruction. METHODS: Twenty patients with unilateral ACL deficient knees were recruited as preoperative group. Six months after ACL reconstruction, these ten subjects were included as postoperative subjects. Ten normal subjects with healthy knees as the control group. Each subject was asked to walk up a custom set of stairs and a single-plane fluoroscopic imaging system was used to determine the 6DOF kinematics of the injured knees, ACL reconstructed knees, and intact knees. RESULTS: ACL deficient knees showed reduced patellar flexion angle and reduced distal patellar translation during knee flexion. ACL reconstructed knees showed abnormal patellofemoral joint kinematics compared to ACL intact and ACL deficient knees, exhibiting increased patellar external rotation, lateral tilt, lateral translation during knee flexion. CONCLUSION: These findings imply that some alterations persist after ACL deficiency and ACL reconstruction. These abnormal changes will be the onset of degeneration in patellofemoral joint even if the ACL is reconstructed in a way that restores the clinical anteroposterior stability of the knee. Some biomechanical changes should be made to improve the outcome of intervention especially in surgical treatment like ACL reconstruction.

The mechanism of biofilm detachment in porous medium under flow field.

Biofilms are communities formed by bacteria adhering to surfaces, widely present in porous medium, and their growth can lead to clogging. Our experiment finds that under certain flow conditions, biofilms detach in pores and form a dynamically changing flow path. We define detachment that occurs far from the boundary of the flow path (with a distance greater than 200 µm) as internal detachment and detachment that occurs at the boundary of the flow path as external detachment. To understand the mechanism of biofilm detachment, we study the detachment behaviors of the Bacillus subtilis biofilm in a porous medium in a microfluidic device, where Bacillus subtilis strain is triple fluorescent labeled, which can represent three main phenotypes during the biofilm formation: motile cells, matrix-producing cells, and spores. We find that slow small-scale internal detachment occurs in regions with very few motile cells and matrix-producing cells, and bacterial movement in these areas is disordered. The increase in the number of matrix-producing cells induces clogging, and after clogging, the rapid detachment of the bulk internal biofilm occurs due to the increased pressure difference at the inlet and outlet. When both internal and external detachments occur simultaneously, the number of matrix-producing cells in the internal detachment area is 2.5 times that in the external detachment area. The results indicate that biofilm detachment occurs in areas with fewer matrix-producing cells, as matrix-producing cells can help resist detachment by secreting extracellular polymeric substances (EPSs).

Construction of Bi/Bi2O3 particles embedded in carbon sheets for boosting the storage capacity of potassium-ion batteries.

Bismuth-based materials have attracted interest in potassium-ion batteries (PIBs). However, the large volume expansion prevents further use of bismuth-based materials for potassium storage. This work employs a two-step synthesis method to innovatively synthesize of Bi/Bi2O3 nanoparticles assembled on N-doped porous carbon sheets (Bi/Bi2O3@CN). The layered structures with uniformly shaped and N-doped porous carbon skeleton buffer the expansion of Bi and the Bi/Bi2O3 particles increase the capacity of potassium storage. In brief, the Bi/Bi2O3@CN served as anode in half-cell of PIBs have a good rate capacity of more than 234.7 mAh/g at 20 A/g. The specific capacity retention was 73 % compared with 322.16 mAh/g at 1 A/g, demonstrating good holding capacity for diverse current densities. The cycle also displays 163 mAh/g after 1500 cycles at 2 A/g in the KPF6 metal salt solution, showing its potential as one of the anode materials in PIBs.

Synergistic effects of BTN3A1, SHP2, CD274, and STAT3 gene polymorphisms on the risk of systemic lupus erythematosus: a multifactorial dimensional reduction analysis.

OBJECTIVE: Systemic lupus erythematosus is a complex autoimmune disorder, and evidence supports the significance of genetic polymorphisms in SLE genetic susceptibility. The aim of this study was to assess the effects of BTN3A1 (butyrophilin 3A1), SHP2 (Src homology-2 containing protein tyrosine phosphatase), CD274 (programmed cell death 1 ligand 1), and STAT3 (signal transducer-activator of transcription 3) gene interactions on SLE risk. MATERIALS AND METHODS: Two hundred and ninety patients diagnosed with SLE and 370 healthy controls were recruited. A multifactor dimensionality reduction (MDR) approach was used to determine the epistasis among single nucleotide polymorphisms (SNPs) on the BTN3A1 (rs742090), SHP2 (rs58116261), CD174 (rs702275), and STAT3 (rs8078731) genes. The best risk prediction model was identified in terms of precision and cross-validation consistency. RESULTS: Allele A and genotype AA were negatively related to genetic susceptibility of SLE for BTN3A1 rs742090 (OR = 0.788 (0.625-0.993), P = 0.044; OR = 0.604 (0.372-0.981), P = 0.040). For STAT3 rs8078731, allele A and genotype AA were positively related to the risk of SLE (OR = 1.307 (1.032-1.654), P = 0.026; OR = 1.752 (1.020-3.010), P = 0.041). MDR analysis revealed the most significant interaction between BTN3A1 rs742090 and SHP2 rs58116261. The best risk prediction model was a combination of BTN3A1 rs742090, SHP2 rs58116261, and STAT3 rs8078731 (accuracy = 0.5866, consistency = 10/10, OR = 1.9870 (1.5964-2.4731), P = 0.001). CONCLUSION: These data indicate that risk prediction models formed by gene interactions (BTN3A1, SHP2, STAT3) can identify susceptible populations of SLE. Key Points • BTN3A1 rs742090 polymorphism was a protective factor for systemic lupus erythematosus, while STAT3 rs8078731 polymorphism was a risk factor. • There was a strong synergistic effect of BTN3A1 rs742090 and SHP2 rs58116261, and interaction among BTN3A1 rs742090, SHP2 rs58116261, and STAT3 rs8078731 constructed the best model to show association with SLE risk.

Trajectory analysis of Bacillus subtilis in micro-droplets.

In order to study Bacillus subtilis biofilm formation in microdroplets, we use microfluidics technology to make the droplets and confocal microscopy to capture bacterial movement and biofilm formation in the droplets. We develop a multi-target tracking methodology, using a YOLOv5 detector to identify cells and a DeepSORT algorithm to track cell movements. We find that Bacillus subtilis bacteria with autonomous migration and biofilm-forming ability prefer to cluster and swarm near the microdroplet surface, rather than in the droplet interior. Bacterial mobility depends on phenotype and spatial location within the droplet. The motile cells move about 3.5 times faster than the matrix-producing cells. When the cells are near the wall of the droplet, the direction of the motion of motile cells is along that wall. When the cells are inside the droplet, the direction of the motion of motile cells is disordered, i.e., there is no clear directional or goal-oriented movement. This contrast increases the cell contact probability and facilitates the formation of a Bacillus subtilis biofilm in the droplet. Furthermore, we develop a mathematical model to describe the motion behavior of Bacillus subtilis in microdroplets, which is useful for exploring the influence of motility on biofilm formation.

Neuropeptide Y, a potential marker for lupus, promotes lupus development.

OBJECTIVE: Relationship between neuropeptide Y (NPY) serum levels, NPY genetic mutation with systemic lupus erythematosus (SLE) pathogenesis is yet to be clarified, and role of NPY in development of SLE needs elucidation. METHOD: This study included 460 SLE patients, 472 non-SLE cases, 500 healthy volunteers. Serum NPY, matrix metalloproteinase-1 (MMP-1) and MMP-8 levels were tested by ELISA. Genotyping 7 NPY single nucleotides polymorphisms (SNPs) (rs5573, rs5574, rs16129, rs16138, rs16140, rs16147, rs16478) was obtained by Kompetitive Allele-Specific PCR (KASP) method. Pristane-induced lupus mice were treated with NPY-Y1 receptor antagonist, and histological analysis, serological changes of the mice were evaluated. RESULTS: NPY serum concentrations were significantly increased in SLE patients when compared to that in healthy volunteers, non-SLE cases. Rs5573 G allele, rs16129 T allele, rs16147 G allele frequencies were significantly different between SLE cases and healthy controls. Rs5574 TT + TC genotypes were related to levels of IgG, C3, C4 and erythrocyte sedimentation rate, and rs16138 GG + GC genotypes correlated with SLE cases with anti-double-stranded deoxyribonucleic acid antibody (anti-dsDNA) (+). Serum MMP-1, MMP-8 concentrations were higher in SLE patients, and NPY levels were significantly related to MMP-1, MMP-8 levels. After treatment of lupus mice with NPY-Y1 receptor antagonist, damage of liver, spleen and kidney was alleviated, production of autoantibodies (anti-nuclear antibody (ANA), total IgG, anti-dsDNA) and MMP-1, MMP-8 was down-regulated, and differentiation of CD3+, CD8+ T cells, B cells, monocytes, macrophages, T helper 1 (Th1), Th2, Th17 cells was reversed. CONCLUSION: NPY may be a biomarker for lupus, which may promote occurrence and development of lupus.

Progression of oncolytic virus in liver cancer treatment.

The liver plays a crucrial role in detoxification, metabolism, and nutrient storage. Because liver cancer ranks among the top three leading causes of death globally, there is an urgent need for developing treatment strategies for liver cancer. Although traditional approaches such as radiation, chemotherapy, surgical removal, and transplantation are widely practiced, the number of patients with liver cancer continues to increase rapidly each year. Some novel therapeutics for liver cancer have been studied for many years. In the past decade, oncolytic therapy has emerged, in which viruses selectively infect and destroy cancer cells while sparing normal cells. However, oncolytic virotherapy for liver cancer remains relatively obscure due to the aggressive nature of the disease and the limited effectiveness of treatment. To keep pace with the latest developments in oncolytic tumor therapy for liver cancer, this review summarizes basic science studies and clinical trials conducted within 5 years, focusing on the efficacy and safety profiles of the five most commonly used oncolytic viruses: herpes simplex virus, adenovirus, influenza virus, vaccinia virus, and coxsackievirus.

Association between blood pressure variability and risk of kidney function decline in hypertensive patients without chronic kidney disease: a post hoc analysis of Systolic Blood Pressure Intervention Trial study.

BACKGROUND: Blood pressure variability (BPV) is a risk factor for poor kidney function independent of blood pressure (BP) in chronic kidney disease (CKD). Little is known about the association between kidney function decline and BPV in hypertensive patients without CKD. METHODS: A post-hoc analysis of the Systolic Blood Pressure Intervention Trial (SPRINT) was performed. BPV was measured as standard deviation (SD) and average real variability (ARV). Cox proportional hazard models were employed to explore the relationship between BPV and incident CKD and albuminuria. RESULTS: A total of 5700 patients were included, with a mean age of 66.4 years old. During a median of 3.29 years follow-up, 150 (2.6%) patients developed CKD and 222 (7.2%) patients developed albuminuria. Patients were divided into four groups according to the quartiles of BPV. Compared with SBPV Q1, the incidence of CKD was higher in SBPV Q2-Q4; hazard ratios and 95% confidence interval were 1.81 (1.07-3.04), 1.85 (1.10-3.12) and 1.90 (1.13-3.19), respectively. The association between incident CKD and albuminuria with DBPV was less significant than SBPV. Similar results were found when measuring BPV as ARV and SD. No interaction was detected in BP-lowering strategy and SBPV on incident CKD and albuminuria ( P  > 0.05). CONCLUSION: This study found that BPV was a risk factor for incident CKD and albuminuria in patients without CKD, especially SBPV. Although intensive BP control increased the risk of CKD, the association between SBPV and kidney function decline did not differ between the two treatment groups. REGISTRATION: URL: https://clinicaltrials.gov/ , Unique identifier: NCT01206062.

Effect of Intensive Blood Pressure Control on Cardiovascular Outcomes in Cancer Survivors.

BACKGROUND: To evaluate whether cancer modifies the effect of intensive blood pressure control on major cardiovascular outcomes. METHODS: Using data of the SPRINT (Systolic Blood Pressure Intervention Trial), we compared the risk of the composite outcomes of myocardial infarction, other acute coronary syndromes, stroke, heart failure, and cardiovascular death in patients with and without a history of cancer. Using Cox proportional hazards regression, we tested interactions between history of cancer and intensive blood pressure control on major cardiovascular outcomes. RESULTS: The study included a total of 9336 patients, with a mean age of 67.9±9.4 years, among whom 2066 (22.2%) were cancer survivors. Over a median follow-up of 3.2 years, 561 primary cardiovascular outcomes were observed. Cancer survivors had a similar risk of experiencing the primary outcome compared with patients without cancer after multivariable adjustment (adjusted hazard ratio, 0.94 [95% CI, 0.77-1.15]). Intensive blood pressure control reduced risk of the primary cardiovascular outcome similarly for cancer survivors (hazard ratio, 0.70 [95% CI, 0.51-0.97]) and patients without cancer (HR, 0.76 [95% CI, 0.63-0.93]; P for interaction 0.74). CONCLUSIONS: In SPRINT study, intensive blood pressure treatment reduced the risk of major cardiovascular events in cancer survivors to a similar extent to that of patients without cancer. Cancer history not requiring active treatment in last 2 years should not be an obstacle to intensive treatment of hypertension. This post hoc analysis should be considered as hypothesis-generating and merit further clinical trial. REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT01206062.