These effects required β1 integrin on ECs, except for arteriole formation in the ischemic part of the myocardium. Furthermore, this integrin subunit was also relevant for basal and mechanically induced proliferation of human coronary artery ECs. Notably, β1 integrin was needed for cardioprotection induced by transient LAD occlusions, and the absence of endothelial β1 integrin resulted in impaired growth of blood vessels into the infarcted myocardium and reduced cardiac function after permanent LAD occlusion.  We showed that endothelial β1 integrin is required for adaptation of the heart to cardiac ischemia and protection from myocardial infarction. We showed that endothelial β1 integrin is required for adaptation of the heart to cardiac ischemia and protection from myocardial infarction.Primary immune thrombocytopenia (ITP) is an acquired autoimmune bleeding disorder. Monocytes and macrophages are the major cells involved in autoantibody-mediated platelet clearance in ITP. In the present study, we found increased percentages of peripheral blood proinflammatory CD16+ monocytes and elevated frequencies of splenic tumor necrosis factor-α (TNF-α)-expressing macrophages in ITP patients compared with healthy controls. Concurrently, we observed elevated TNF-α secretion in plasma as well as higher TNF-α mRNA expression in total peripheral blood mononuclear cells and CD14+ monocytes of ITP patients. Of note, in vitro TNF-α blockade with neutralizing antibody remarkably reduced polarization to M1 macrophages by inhibiting the nuclear factor kappa B (NF-κB) signaling pathway. Moreover, TNF-α blockade dampened macrophage phagocytosis and T cell stimulatory capacity. read more Finally, in passive and active murine models of ITP, anti-TNF-α therapy reduced the number of nonclassical monocytes and M1 macrophages, ameliorated the retention of platelets in spleen and liver, and increased the platelet count of ITP mice. Taken together, TNF-α blockade decreased the number and function of proinflammatory subsets of monocytes and macrophages by inhibiting the NF-κB signaling pathway, leading to remarkable attenuation of antibody-mediated platelet destruction. Thus, TNF-α blockade may be a promising therapeutic strategy for the management of ITP.  Monocyte-platelet aggregates (MPAs) are a sensitive marker of in vivo platelet activation in acute coronary syndrome (ACS) and associated with clinical outcomes. MicroRNAs (miRs) play an important role in the regulation of platelet activation, and may influence MPA formation. Both, miRs and MPA, could be influenced by the type of P2Y12 inhibitor.  To study the association of platelet-related miRs with MPA formation in ACS patients on dual antiplatelet therapy (DAPT), and to compare miRs and MPA levels between prasugrel- and ticagrelor-treated patients.  We analyzed 10 circulating platelet-related miRs in 160 consecutive ACS patients on DAPT with low-dose aspirin and either prasugrel (  = 80) or ticagrelor (  = 80). MPA formation was measured by flow cytometry without addition of platelet agonists and after simulation with the toll-like receptor (TLR)-1/2 agonist Pam3CSK4, adenosine diphosphate (ADP), or arachidonic acid (AA). In multivariate regression analyses, we identified miR-21 (β = 9.50, 95% confidence interval [CI] 1.60-17.40,  = 0.019) and miR-126 (β = 7.50, 95% CI 0.55-14.44,  = 0.035) as independent predictors of increased MPA formation in vivo and after TLR-1/2 stimulation. In contrast, none of the investigated miRs was independently associated with MPA formation after stimulation with ADP or AA. Platelet-related miR expression and MPA formation did not differ significantly between prasugrel- and ticagrelor-treated patients.  Platelet-related miR-21 and miR-126 are associated with MPA formation in ACS patients on DAPT. miRs and MPA levels were similar in prasugrel- and ticagrelor-treated patients. Platelet-related miR-21 and miR-126 are associated with MPA formation in ACS patients on DAPT. miRs and MPA levels were similar in prasugrel- and ticagrelor-treated patients.  The accuracy of smartphone sound level meter applications (SLMAs) has been investigated with varied results, based on differences in platform, device, app, available features, test stimuli, and methodology.  This article determines the accuracy of smartphone SLMAs with and without calibration of external and internal microphones for measuring sound levels in clinical rooms.  Quasi-experimental research design comparing the accuracy of two smartphone SLMAs with and without calibration of external and internal microphones.  Two iOS-based smartphone SLMAs (NIOSH SLM and SPL Meter) on an iPhone 6S were used with and without calibrated external and internal microphones. Measures included (1) white noise (WN) stimuli from 20 to 100 dB sound pressure level in a sound-treated test booth and (2) sound levels in quiet in four nonsound-treated clinical rooms and in simulated background sound conditions using music at 45, 55, and 80 dBA. Chi-square analysis was used to determine a significant difference (  ≤ 0.measure room sound levels and to monitor background noise levels throughout the provision of clinical services. The SLMAs studied with calibrated external or internal microphones are able to verify the room environment for audiologic screening at 1,000, 2,000, and 4,000 Hz at 20 dB hearing level (American Academy of Audiology and American Speech-Language-Hearing Association) using supra-aural earphones (American National Standards Institute S3.1-1999 [R2018]). However, the tested SLMAs overestimated low-level sound  less then  40 dBA, even when the external or internal microphones were calibrated. Clinicians are advised to calibrate the microphones prior to using measurement systems involving smartphones and SLMAs to measure room sound levels and to monitor background noise levels throughout the provision of clinical services.Pain is common but often underrecognized after stroke. Poststroke pain (PSP) hinders recovery, impairs quality of life, and is associated with the psychological state of patients with stroke. The most common subtypes of PSP include central PSP, complex regional pain syndrome, shoulder pain, spasticity-related pain, and headache. The pathophysiologies of these PSP subtypes are not yet clearly understood, and PSP is refractory to conventional treatment in many patients. However, recent studies have proposed potential pathophysiologies of PSP subtypes, which may help prioritize therapies that target specific mechanisms.