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Conventional photography can only provide a two-dimensional image of the scene, whereas emerging imaging modalities such as light field enable the representation of higher dimensional visual information by capturing light rays from different directions. Light fields provide immersive experiences, a sense of presence in the scene, and can enhance different vision tasks. Hence, research into light field processing methods has become increasingly popular. It does, however, come at the cost of higher data volume and computational complexity. With the growing deployment of machine-learning and deep architectures in image processing applications, a paradigm shift toward learning-based approaches has also been observed in the design of light field processing methods. Various learning-based approaches are developed to process the high volume of light field data efficiently for different vision tasks while improving performance. Taking into account the diversity of light field vision tasks and the deployed learning-based frameworks, it is necessary to survey the scattered learning-based works in the domain to gain insight into the current trends and challenges. This paper aims to review the existing learning-based solutions for light field imaging and to summarize the most promising frameworks. Moreover, evaluation methods and available light field datasets are highlighted. Lastly, the review concludes with a brief outlook for future research directions.

Dengue virus causes dengue hemorrhagic fever (DHF) and has been associated to fatal cases worldwide. The liver is one of the most important target tissues in severe cases, due to its intense viral replication and metabolic role. microRNAs role during infection is crucial to understand the regulatory mechanisms of DENV infection and can help in diagnostic and anti-viral therapies development. We sequenced the miRNome of six fatal cases and compared to five controls, to characterize the human microRNAs expression profile in the liver tissue during DHF. Eight microRNAs were differentially expressed, including miR-126-5p, a regulatory molecule of endothelial cells, miR-122-5p, a liver specific homeostasis regulator, and miR-146a-5p, an interferon-regulator. Enrichment analysis with predicted target genes of microRNAs revealed regulatory pathways of apoptosis, involving MAPK, RAS, CDK and FAS. Immune response pathways were related to NF- kB, CC and CX families, IL and TLR. This is the first description of the human microRNA and isomicroRNA profile in liver tissues from DHF cases. The results demonstrated the association of miR-126-5p, miR-122-5p and miR-146a-5p with DHF liver pathogenesis, involving endothelial repair and vascular permeability regulation, control of homeostasis and expression of inflammatory cytokines.

The spleen plays a pivotal role in the pathogenesis of visceral leishmaniasis. In severe forms of the disease, the spleen undergoes changes that can compromise its function in surveilling blood-circulating pathogens. In this study, we present an integrated analysis of the structural and gene expression alterations in the spleens of three patients with relapsing visceral leishmaniasis, two of whom were coinfected with HIV. Our findings reveal that the IL6 signaling pathway plays a significant role in the disorganization of the white pulp, while BCL10 and ICOSLG are associated with spleen organization. Patients coinfected with HIV and visceral leishmaniasis exhibited lower splenic CD4+ cell density and reduced expression of genes such as IL15 . These effects may contribute to a compromised immune response against L . infantum in coinfected individuals, further impacting the structural organization of the spleen.

Cutaneous leishmaniasis (CL) is caused by the bite of the infected sand fly, which inoculates parasites of spp and triggers an immune response. An exacerbated cutaneous inflammatory response is crucial for controlling parasite burden but can also promote tissue damage. This study aimed to characterize the populations of natural killer (NK), CD57 , CD4 , and CD8 T cells, CD20 B cells, as well as CD68 macrophages, in biopsies of ulcerated CL lesions, and quantify the production of perforin , grazyme B , interleukin 1 beta (IL-1β ) and Tumor Necrosis Factor (TNF-α cells). We then correlated these parameters with necrosis, inflammation and the number of amastigotes. CD4 T cells were positively correlated to the extent of inflammation, B cells and IL-1β were associated with the extent of necrosis, CD68 macrophages and perforin were correlated with the number of amastigotes, and CD57 NK cells was correlated to CD68 macrophages and amastigotes. In sum, the finding suggests that the production of cytotoxic granules and cytokines by inflammatory cells contributes to tissue damage in CL lesions.

This study evaluated hepatic pathological and phenotypic alterations, along with the inflammatory response, following sequential dengue virus (DENV) infection in Callithrix penicillata, a relevant model for human endemic scenarios. Twenty-six animals were initially infected subcutaneously with DENV-3. Thirteen were euthanized between 1 and 7 days post-infection (dpi) to assess the acute phase, and up to 60 dpi for the convalescent phase. The remaining animals received a secondary DENV-2 infection two months later. Liver samples underwent histopathological and immunohistochemical analysis. Viral antigens were identified in hepatocytes, Kupffer cells, and Councilman bodies. Observed liver changes included apoptosis, lytic necrosis, midzonal inflammation, Kupffer cell hyperplasia and hypertrophy, sinusoidal dilation, and hemosiderin deposition. Both primary and secondary infections increased activated macrophages, NK cells, S-100 protein, and B lymphocytes. Primary infection was associated with elevated CD4+ T cells, IFN-γ, TGF-β, IL-10, and Fas expression, whereas secondary infection induced higher IFN-γ, TNF-α, IL-8, Fas, and VCAM levels. These findings mirror hepatic alterations in severe human dengue cases and underscore the role of direct viral effects and immune dysregulation in liver injury. The results support C. penicillata as a suitable non-human primate model for studying DENV pathogenesis.

The spleen undergoes changes during acute and chronic infections, which may contribute to immune dysregulation and disease aggravation. In fatal cases of COVID-19, pronounced splenic changes are noted. However, the role played by these alterations in patient mortality remains poorly understood. Objectives: We aim to characterize structural alterations and changes in splenic cell populations in fatal COVID-19 cases, as a potential substrate for immune dysfunction associated with bacterial coinfection and mortality in severe infectious diseases. In this study, we characterized the histological and cellular changes observed in the spleens of nine patients who died from COVID-19. Spleens from five healthy individuals were used as a reference. Histopathological analysis and immunolabeling techniques were employed to evaluate tissue architecture, cell composition, cytokine production, and cell death. COVID-19-associated changes included atrophy of the white pulp (WP), reduced cellular density in the red pulp (RP), and reticular fiber fragmentation. Leukocyte phenotyping revealed substantial lymphocyte depletion across all splenic compartments, accompanied by plasma cell accumulation. These alterations correlated with increased numbers of IL-6- and TNF-producing cells. Additionally, a high density of TUNEL-positive cells indicated widespread cell death in the spleens of COVID-19 patients. These findings suggest that the spleen contributes to the inflammatory response in infection, acting both as a source of inflammatory cytokines as well as a site of leukocyte, particularly lymphocyte, death both in association with the exacerbated release of IL-6 and TNF.

In general, the fusion of visible-light and infrared images produces a composite representation where both data are pictured in a single image. The successful development of image/video fusion algorithms relies on realistic infrared/visible-light datasets. To the best of our knowledge, there is a particular shortage of databases with registered and synchronized videos from the infrared and visible-light spectra suitable for image/video fusion research. To address this need we recorded an image/video fusion database using infrared and visible-light cameras under varying illumination conditions. Moreover, different scenarios have been defined to better challenge the fusion methods, with various contexts and contents providing a wide variety of meaningful data for fusion purposes, including non-planar scenes, where objects appear on different depth planes. However, there are several difficulties in creating datasets for research in infrared/visible-light image fusion. Camera calibration, registration, and synchronization can be listed as important steps of this task. In particular, image registration between imagery from sensors of different spectral bands imposes additional difficulties, as it is very challenging to solve the correspondence problem between such images. Motivated by these challenges, this work introduces a novel spatiotemporal video registration method capable of generating registered and temporally aligned infrared/visible-light video sequences. The proposed workflow improves the registration accuracy when compared to the state-of-the art. By applying the proposed methodology to the recorded database we have generated the visible-light and infrared video database for image fusion, a publicly available database to be used by the research community to test and benchmark fusion schemes.

To compare microscopic and immunologic features in the spleens of patients who died of pulmonary hemorrhage and shock caused by leptospirosis (11 cases) or Gram-positive/-negative bacterial septic shock (10 cases) to those from control spleens (12 cases from splenectomy). Histological features in the red pulp and white pulp were analyzed using archived samples by a semi quantitative score. Immunohistochemistry was used for the recognition of immune cell markers, cytokines, caspase-3 and antigens. The control group differed significantly from the leptospirosis and septic shock patients which demonstrate strong similarities: diffuse congestion in the red pulp with a moderate to intense infiltration of plasma cells and polymorphonuclear cells; follicles with marked atrophy; high density of CD20 cells; low density of NK, TCD4 and active caspase-3 positive cells and strong expression of IL-10; leptospirosis patients had higher S100 and TNF-α positive cells in the spleen than the other groups. The results suggest that an immunosuppressive state develops at the terminal stage of severe leptospirosis with pulmonary hemorrhage and shock similar to that of patients with septic shock, with diffuse endothelial activation in the spleen, splenitis, and signs of disturbance in the innate and adaptive immunity in the spleen. The presence of leptospiral antigens in 73% of the spleens of the leptospirosis patients suggests the etiological agent contributes directly to the pathogenesis of the lesions. Our results support therapeutic approaches involving antibiotic and immunomodulatory treatments for leptospirosis patients and suggest that leptospirosis patients, which are usually young men with no co-morbidities, form a good group for studying sepsis and septic shock.

Dermatophytosis is a cutaneous mycosis caused by a plethora of keratinophilic fungi, but Trichophyton rubrum is the most common etiological agent. Despite its high prevalence worldwide, little is known about the host defense mechanisms in this infection, particularly the in situ immune response. Using an immunohistochemistry approach, we investigated the density of CD1a+, factor XIIIa+ and CD68+ cells in the skin of dermatophytosis patients. Langerhans cells (CD1a+ cells) were significantly decreased in the epidermis of patients, both in affected and unaffected areas. In the dermis, however, no differences in the density of macrophages (CD68+ cells) and dermal dendrocytes (factor XIIIa+ cells) were observed. These results suggest that the decreased number of Langerhans cells may be a risk factor for development of dermatophytosis.

Psoriasis is a chronic, inflammatory disease affecting the skin and joints. The pathogenesis of this disease is associated with genetic, environmental and immunological factors, especially unbalanced T cell activation and improper keratinocyte differentiation. Psoriatic lesion infiltrate is composed of monocytes and T cells, and most studies have focused on the participation of T cells in the pathogenesis of this disease. Here we investigated the contribution of mononuclear phagocytes in the immunopathology observed in psoriatic patients. Significant increases in the levels of TNF, IL-1β, CXCL9, as well as the soluble forms of CD14 and CD163, were observed within the lesions of psoriatic patients compared to skin biopsies obtained from healthy individuals. Moreover, we found an association between the levels of CCL2, a monocyte attractant chemokine, and disease severity. In conclusion, our findings suggest a potential role for mononuclear phagocytes in the pathogenesis of psoriasis.