Neurocysticercosis is a neurologic parasitic disease caused by the encysted larva of the tapeworm Taenia solium and is the most important parasitic disease of the human central nervous system. It is the most common cause of acquired epilepsy in endemic settings and constitutes a public health challenge for most of the developing world. Nowadays, however, as a result of globalization, neurocysticercosis is being seen more frequently in developed countries as well. Neurocysticercosis is acquired through fecal-oral contamination, and the disease course is complex, with two intermediate hosts (ie, pigs and humans) and a definitive host (humans). Traditionally, it has been classified into active and nonactive forms according to disease location. Radiologists must be aware of its imaging appearance, which is quite variable, as is the differential diagnosis. Imaging findings depend on several factors, including the stage of the life cycle of T solium at presentation; the number and location (ie, subarachnoid, cisternal, or intraventricular) of parasites; and associated complications such as vascular involvement (ie, arteritis with or without infarction), inflammatory response (ie, edema, gliosis, or arachnoiditis), and, in ventricular forms, degree of obstruction. Thus, the diagnostic approach, management, and prognosis for neurocysticercosis differ widely depending on the type of infection.

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In recent years, we have used a variety of tau immunological markers combined with the dye thiazin red (TR), an accurate marker to differentiate the fibrillar from the nonfibrillar state of both amyloid-beta and tau in Alzheimer's disease (AD). In this study, we used TR as a potential diagnostic marker of AD in frozen-thawed (F-T) brain tissue and imprint cytology. Control experiments included the use of Thioflavin-S staining, fixed tissue, and some double-labeled material with TR and selected tau markers, including AT100, MC1, Alz-50, TG-3, Tau-C3, and S396. Our results indicate that TR retains its strong affinity for both tangles and plaques in unfixed F-T tissue and imprint cytology. This information provides a potential use of TR as an accurate diagnostic tool for the rapid postmortem diagnosis of AD neuropathology. This study shows the advantages of TR on cytology mainly because tools for the fast postmortem diagnosis of AD are practically nonexistent. In addition, we observed Tau-C3 immunoreactivity in extracellular tangles, suggesting that the Tau-C3 epitope is characteristically stable. Moreover, this study demonstrates that chemical fixation is not necessarily required for tau immunoreactivity on histological sections.

Pituitary adenomas (PA) are the second most common intracranial tumors. These neoplasms are classified according to the hormone they produce. The majority of PA occur sporadically, and their molecular pathogenesis is incompletely understood. The present transcriptomic and methylomic analysis of PA revealed that they segregate into three molecular clusters according to the transcription factor driving their terminal differentiation. First cluster, driven by NR5A1, consists of clinically non-functioning PA (CNFPA), comprising gonadotrophinomas and null cell; the second cluster consists of clinically evident ACTH adenomas and silent corticotroph adenomas, driven by TBX19; and the third, POU1F1-driven TSH-, PRL- and GH-adenomas, segregated together. Genes such as CACNA2D4, EPHA4 and SLIT1, were upregulated in each of these three clusters, respectively. Pathway enrichment analysis revealed specific alterations of these clusters: calcium signaling pathway in CNFPA; renin-angiotensin system for ACTH-adenomas and fatty acid metabolism for the TSH-, PRL-, GH-cluster. Non-tumoral pituitary scRNAseq data confirmed that this clustering also occurs in normal cytodifferentiation. Deconvolution analysis identify potential mononuclear cell infiltrate in PA consists of dendritic, NK and mast cells. Our results are consistent with a divergent origin of PA, which segregate into three clusters that depend on the specific transcription factors driving late pituitary cytodifferentiation.

Ample animal studies demonstrate that neuropeptides NPY and α-MSH expressed in Arcuate Nucleus and Nucleus of the Tractus Solitarius, modulate glucose homeostasis and food intake. In contrast is the absence of data validating these observations for human disease. Here we compare the post mortem immunoreactivity of the metabolic neuropeptides NPY, αMSH and VGF in the infundibular nucleus, and brainstem of 11 type-2 diabetic and 11 non-diabetic individuals. α-MSH, NPY and tyrosine hydroxylase in human brain are localized in the same areas as in rodent brain. The similar distribution of NPY, α-MSH and VGF indicated that these neurons in the human brain may share similar functionality as in the rodent brain. The number of NPY and VGF immuno positive cells was increased in the infundibular nucleus of diabetic subjects in comparison to non-diabetic controls. In contrast, NPY and VGF were down regulated in the Nucleus of the Tractus Solitarius of diabetic patients. These results suggest an activation of NPY producing neurons in the arcuate nucleus, which, according to animal experimental studies, is related to a catabolic state and might be the basis for increased hepatic glucose production in type-2 diabetes.

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Corticotroph cells give rise to aggressive and rare pituitary neoplasms comprising ACTH-producing adenomas resulting in Cushing disease (CD), clinically silent ACTH adenomas (SCA), Crooke cell adenomas (CCA) and ACTH-producing carcinomas (CA). The molecular pathogenesis of these tumors is still poorly understood. To better understand the genomic landscape of all the lesions of the corticotroph lineage, we sequenced the whole exome of three SCA, one CCA, four ACTH-secreting PA causing CD, one corticotrophinoma occurring in a CD patient who developed Nelson syndrome after adrenalectomy and one patient with an ACTH-producing CA. The ACTH-producing CA was the lesion with the highest number of single nucleotide variants (SNV) in genes such as USP8, TP53, AURKA, EGFR, HSD3B1 and CDKN1A. The USP8 variant was found only in the ACTH-CA and in the corticotrophinoma occurring in a patient with Nelson syndrome. In CCA, SNV in TP53, EGFR, HSD3B1 and CDKN1A SNV were present. HSD3B1 and CDKN1A SNVs were present in all three SCA, whereas in two of these tumors SNV in TP53, AURKA and EGFR were found. None of the analyzed tumors showed SNV in USP48, BRAF, BRG1 or CABLES1. The amplification of 17q12 was found in all tumors, except for the ACTH-producing carcinoma. The four clinically functioning ACTH adenomas and the ACTH-CA shared the amplification of 10q11.22 and showed more copy-number variation (CNV) gains and single-nucleotide variations than the nonfunctioning tumors.