ISC26 After successful EVT for stroke, early MRI shows residual hypoperfusion in a substantial subset of patients. Perfusion deficits mainly reflected distal emboli and were not associated with inflammatory biomarkers.

In acute ischemic stroke (AIS) due to large-vessel occlusion (LVO), endovascular treatment (EVT) achieves over 80% recanalization rates and improves functional outcomes.¹ However, nearly half of recanalized patients fail to achieve functional independence,¹ a phenomenon termed futile recanalization.^2,3 Mechanisms of futile recanalization include early extensive infarct core—that is, tissue that is already irreversibly damaged at the time of reperfusion—as well as edema, hemorrhagic transformation, and no-reflow.³ The latter, defined as impaired capillary reperfusion despite angiographic success, has gained increasing attention.^4–15

In experimental models, no-reflow occurs early after arterial reopening and is driven by multifactorial microvascular dysfunction.^16–19 Reported mechanisms include astrocyte and endothelial swelling, pericyte contraction, leukocytes, platelets and erythrocytes aggregation, and the release of inflammatory mediators.^20–24 Regarding the latter, cytokines and adhesion molecules have been implicated in its pathogenesis in preclinical studies.²⁴ These findings have led to the hypothesis that inflammation may contribute to microvascular perfusion failure after EVT, potentially opening the door to targeted therapeutic interventions.^20–24 However, this has never been systematically investigated in humans.

In clinical practice, persistent hypoperfusion on post-EVT computed tomography (CT) perfusion or magnetic resonance perfusion imaging is frequently interpreted as a radiological correlate of no-reflow.^4–15 Yet this interpretation remains uncertain. First, no direct histological evidence of no-reflow has been demonstrated in human stroke to date. Second, most imaging-based studies on no-reflow have included patients with residual distal emboli,^10,12,25 which cause residual hypoperfusion on a macrovascular level.²⁶ Third, many studies did not exclude confounders, such as perfusion abnormalities caused by carotid stenosis, parenchymal hemorrhage, or reocclusion.¹⁴ These limitations may explain the wide variability in the reported prevalence of postthrombectomy hypoperfusion, from 0% to 80%.^14,25.

An intranasal flu antibody can protect against both influenza A and B in mice and nonhuman primates and is safe in humans, according to new preclinical experiments and two phase one clinical trials published in Science TranslationalMedicine.

Intranasal CR9114 is safe in humans, and twice-daily dosing confers protection against influenza virus challenge in macaques.

Here, Lintao Qu & team illuminate a neuroimmune mechanism in a mouse gout model involving MRGPRX2 signaling in synovial mast cells that drives pain and joint inflammation:

The figure: Mouse knee joint sections show treatment with an antibody against neuropeptide substance P (SP) decreases infiltration of neutrophils (Ly6G) and macrophages (CD68) into the synovium (S) in gout arthritis compared with control.

⁵Department of Endocrinology, Second Affiliated Hospital, University of South China, Hengyang, Hunan, China.

⁶College of Pharmacy, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada.

⁷Center of Research Excellence in Allergy and Immunology, Research Department, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.

Now online! Meningeal blood vessel blockage enhances anti-tumor immunity against GBM in preclinical models by expanding dural resident border-associated macrophages, which are equipped with an elevated antigen-presentation function and are poised for effective T cell activation, suggesting a surgical strategy for potentiating GBM immunotherapy.