Early bruising detection of ‘Korla’ pears by low-cost visible-LED structured-illumination reflectance imaging and feature-based classification models

IntroductionNondestructive detection of thin-skinned fruit bruising is one of the main challenges in the automated grading of post-harvest fruit. The structured-illumination reflectance imaging (SIRI) is an emerging optical technique with the potential for detection of bruises.MethodsThis study presented the pioneering application of low-cost visible-LED SIRI for detecting early subcutaneous bruises in ‘Korla’ pears. Three types of bruising degrees (mild, moderate and severe) and ten sets of spatial frequencies (50, 100, 150, 200, 250, 300, 350, 400, 450 and 500 cycles m-1) were analyzed. By evaluation of contrast index (CI) values, 150 cycles m-1 was determined as the optimal spatial frequency. The sinusoidal pattern images were demodulated to get the DC, AC, and RT images without any stripe information. Based on AC and RT images, texture features were extracted and the LS-SVM, PLS-DA and KNN classification models combined the optimized features were developed for the detection of ‘Korla’ pears with varying degrees of bruising.Results and discussionIt was found that RT images consistently outperformed AC images regardless of type of model, and LS-SVM model exhibited the highest detection accuracy and stability. Across mild, moderate, severe and mixed bruises, the LS-SVM model with RT images achieved classification accuracies of 98.6%, 98.9%, 98.5%, and 98.8%, respectively. This study showed that visible-LED SIRI technique could effectively detect early bruising of ‘Korla’ pears, providing a valuable reference for using low-cost visible LED SIRI to detect fruit damage

Cerebral collateral flow defines topography and evolution of molecular penumbra in experimental ischemic stroke

International audienceIntracranial collaterals are dynamically recruited after arterial occlusion and are emerging as a strong determinant of tissue outcome in both human and experimental ischemic stroke. The relationship between collateral flow and ischemic penumbra remains largely unexplored in pre-clinical studies. The aim of the present study was to investigate the pattern of collateral flow with regard to penumbral tissue after transient middle cerebral artery (MCA) occlusion in rats. MCA was transiently occluded (90min) by intraluminal filament in adult male Wistar rats (n=25). Intracranial collateral flow was studied in terms of perfusion deficit and biosignal fluctuation analyses using multi-site laser Doppler monitoring. Molecular penumbra was defined by topographical mapping and quantitative signal analysis of Heat Shock Protein 70kDa (HSP70) immunohistochemistry. Functional deficit and infarct volume were assessed 24h after ischemia induction. The results show that functional performance of intracranial collaterals during MCA occlusion inversely correlated with HSP70 immunoreactive areas in both the cortex and the striatum, as well as with infarct size and functional deficit. Intracranial collateral flow was associated with reduced areas of both molecular penumbra and ischemic core and increased areas of intact tissue in rats subjected to MCA occlusion followed by reperfusion. Our findings prompt the development of collateral therapeutics to provide tissue-saving strategies in the hyper-acute phase of ischemic stroke prior to recanalization therapy

The choroid plexus is a key cerebral invasion route for T cells after stroke.

Neuroinflammation contributes substantially to stroke pathophysiology. Cerebral invasion of peripheral leukocytes-particularly T cells-has been shown to be a key event promoting inflammatory tissue damage after stroke. While previous research has focused on the vascular invasion of T cells into the ischemic brain, the choroid plexus (ChP) as an alternative cerebral T-cell invasion route after stroke has not been investigated. We here report specific accumulation of T cells in the peri-infarct cortex and detection of T cells as the predominant population in the ipsilateral ChP in mice as well as in human post-stroke autopsy samples. T-cell migration from the ChP to the peri-infarct cortex was confirmed by in vivo cell tracking of photoactivated T cells. In turn, significantly less T cells invaded the ischemic brain after photothrombotic lesion of the ipsilateral ChP and in a stroke model encompassing ChP ischemia. We detected a gradient of CCR2 ligands as the potential driving force and characterized the neuroanatomical pathway for the intracerebral migration. In summary, our study demonstrates that the ChP is a key invasion route for post-stroke cerebral T-cell invasion and describes a CCR2-ligand gradient between cortex and ChP as the potential driving mechanism for this invasion route

Differential plasticity and fate of brain-resident and recruited macrophages during the onset and resolution of neuroinflammation

Microglia and border-associated macrophages (BAMs) are brain-resident self-renewing cells. Here, we examined the fate of microglia, BAMs, and recruited macrophages upon neuroinflammation and through resolution. Upon infection, Trypanosoma brucei parasites invaded the brain via its border regions, triggering brain barrier disruption and monocyte infiltration. Fate mapping combined with single-cell sequencing revealed microglia accumulation around the ventricles and expansion of epiplexus cells. Depletion experiments using genetic targeting revealed that resident macrophages promoted initial parasite defense and subsequently facilitated monocyte infiltration across brain barriers. These recruited monocyte-derived macrophages outnumbered resident macrophages and exhibited more transcriptional plasticity, adopting antimicrobial gene expression profiles. Recruited macrophages were rapidly removed upon disease resolution, leaving no engrafted monocyte-derived cells in the parenchyma, while resident macrophages progressively reverted toward a homeostatic state. Long-term transcriptional alterations were limited for microglia but more pronounced in BAMs. Thus, brain-resident and recruited macrophages exhibit diverging responses and dynamics during infection and resolution