Fingerprinting at the Bar. Criminal Identification in Liberal and Fascist Italy

Between the end of the nineteenth and the first half of the twentieth century, criminal anthropology was a very influential theory for criminologists throughout the western world. Proposed by the Italian alienist Cesare Lombroso, its theoretical core centred on the figure of the “criminal man,” a character atavistic instinct forced to live a life of crime. By filling a gap in the literature, this work deals with the historical and sociological circumstances in which criminal anthropology emerged and prospered, and concentrates on the impact Lombroso’s theory had on the development of scientific policing in Italy since the beginning of the twentieth century. A detailed account of the causes that favoured the rise of Lombroso’s scientific police provides an explanation for the appeal criminal anthropology exerted on western political elites. In Italy, the Lombrosian approach left his mark on the development of highly specific forensic tools like fingerprinting, and this had a strong impact on their utilisation by fascist authorities as the account of a famous case of identity fraud occurred in Italy in 1927 revealed. As a result, it is argued that the production of Lombrosian scientific policing was shaped by the wider cultural and social goals of the actors involved, as it is of any other form of knowledge. By choosing to sideline Lombrosian techniques, fascist authorities favoured the exploitation of un-scientific methods of crime prevention that, it is argued, were not perceived as inferior, anachronistic, or unreliable. Such a choice was dictated by specific social goals that favoured the implementation of constitutional anthropology on Lombrosian science of the deviance. Finally, it is suggested that this socio-historical reading of the Italian case could cast more light on the complex relationship between totalitarianism, technology, and forms public surveillance

ULTRASONOGRAPHIC FEATURES OF ADRENAL GLAND LESIONS IN DOGS CAN AID IN DIAGNOSIS

BACKGROUND: Ultrasonography to visualize adrenal gland lesions and evaluate incidentally discovered adrenal masses in dogs has become more reliable with advances in imaging techniques. However, correlations between sonographic and histopathological changes have been elusive. The goal of our study was to investigate which ultrasound features of adrenal gland abnormalities could aid in discriminating between benign and malignant lesions. To this end, we compared diagnosis based on ultrasound appearance and histological findings and evaluated ultrasound criteria for predicting malignancy. RESULTS: Clinical records of 119 dogs that had undergone ultrasound adrenal gland and histological examination were reviewed. Of these, 50 dogs had normal adrenal glands whereas 69 showed pathological ones. Lesions based on histology were classified as cortical adrenal hyperplasia (n = 67), adenocarcinoma (n = 17), pheochromocytoma (n = 10), metastases (n = 7), adrenal adenoma (n = 4), and adrenalitis (n = 4). Ultrasonographic examination showed high specificity (100%) but low sensitivity (63.7%) for identifying the adrenal lesions, which improved with increasing lesion size. Analysis of ultrasonographic predictive parameters showed a significant association between lesion size and malignant tumors. All adrenal gland lesions >20 mm in diameter were histologically confirmed as malignant neoplasms (pheochromocytoma and adenocarcinoma). Vascular invasion was a specific but not sensitive predictor of malignancy. As nodular shape was associated with benign lesions and irregular enlargement with malignant ones, this parameter could be used as diagnostic tool. Bilaterality of adrenal lesions was a useful ultrasonographic criterion for predicting benign lesions, as cortical hyperplasia. CONCLUSIONS: Abnormal appearance of structural features on ultrasound images (e.g., adrenal gland lesion size, shape, laterality, and echotexture) may aid in diagnosis, but these features alone were not pathognomic. Lesion size was the most direct ultrasound predictive criterion. Large and irregular masses seemed to be better predictors of malignant neoplasia and lesions <20 mm in diameter and nodular in shape were often identified as cortical hyperplastic nodules or adenomas

Targeting EZH2 Reprograms Intratumoral Regulatory T Cells to Enhance Cancer Immunity.

Regulatory T cells (Tregs) are critical for maintaining immune homeostasis, but their presence in tumor tissues impairs anti-tumor immunity and portends poor prognoses in cancer patients. Here, we reveal a mechanism to selectively target and reprogram the function of tumor-infiltrating Tregs (TI-Tregs) by exploiting their dependency on the histone H3K27 methyltransferase enhancer of zeste homolog 2 (EZH2) in tumors. Disruption of EZH2 activity in Tregs, either pharmacologically or genetically, drove the acquisition of pro-inflammatory functions in TI-Tregs, remodeling the tumor microenvironment and enhancing the recruitment and function of CD8+ and CD4+ effector T cells that eliminate tumors. Moreover, abolishing EZH2 function in Tregs was mechanistically distinct from, more potent than, and less toxic than a generalized Treg depletion approach. This study reveals a strategy to target Tregs in cancer that mitigates autoimmunity by reprogramming their function in tumors to enhance anti-cancer immunity

The C-terminal domain of yeast Ero1p mediates membrane localization and is essential for function

AbstractIn eukaryotes, members of the Ero1 family control oxidative protein folding in the endoplasmic reticulum (ER). Yeast Ero1p is tightly associated with the ER membrane, despite cleavage of the leader peptide, the only hydrophobic sequence that could mediate lipid insertion. In contrast, human Ero1-Lα and a yeast mutant (Ero1pΔC) lacking the 127 C-terminal amino acids are soluble when expressed in yeast. Neither Ero1-Lα nor Ero1pΔC complements an ERO1 disrupted strain. Appending the yeast C-terminal tail to human Ero1-Lα restores membrane association and allows growth of ERO1 disrupted cells. Therefore, the tail of Ero1p mediates membrane association and is crucial for function

Substantial Histone Reduction Modulates Genomewide Nucleosomal Occupancy and Global Transcriptional Output

The basic unit of genome packaging is the nucleosome, and nucleosomes have long been proposed to restrict DNA accessibility both to damage and to transcription. Nucleosome number in cells was considered fixed, but recently aging yeast and mammalian cells were shown to contain fewer nucleosomes. We show here that mammalian cells lacking High Mobility Group Box 1 protein (HMGB1) contain a reduced amount of core, linker, and variant histones, and a correspondingly reduced number of nucleosomes, possibly because HMGB1 facilitates nucleosome assembly. Yeast nhp6 mutants lacking Nhp6a and -b proteins, which are related to HMGB1, also have a reduced amount of histones and fewer nucleosomes. Nucleosome limitation in both mammalian and yeast cells increases the sensitivity of DNA to damage, increases transcription globally, and affects the relative expression of about 10% of genes. In yeast nhp6 cells the loss of more than one nucleosome in four does not affect the location of nucleosomes and their spacing, but nucleosomal occupancy. The decrease in nucleosomal occupancy is non-uniform and can be modelled assuming that different nucleosomal sites compete for available histones. Sites with a high propensity to occupation are almost always packaged into nucleosomes both in wild type and nucleosome-depleted cells; nucleosomes on sites with low propensity to occupation are disproportionately lost in nucleosome-depleted cells. We suggest that variation in nucleosome number, by affecting nucleosomal occupancy both genomewide and gene-specifically, constitutes a novel layer of epigenetic regulation

Fatty acid metabolism complements glycolysis in th selective regulatory t cell expansion during tumor growth

The tumor microenvironment restrains conventional T cell (Tconv) activation while facilitating the expansion of Tregs. Here we showed that Tregs’ advantage in the tumor milieu relies on supplemental energetic routes involving lipid metabolism. In murine models, tumor-infiltrating Tregs displayed intracellular lipid accumulation, which was attributable to an increased rate of fatty acid (FA) synthesis. Since the relative advantage in glucose uptake may fuel FA synthesis in intratumoral Tregs, we demonstrated that both glycolytic and oxidative metabolism contribute to Tregs’ expansion. We corroborated our data in human tumors showing that Tregs displayed a gene signature oriented toward glycolysis and lipid synthesis. Our data support a model in which signals from the tumor microenvironment induce a circuitry of glycolysis, FA synthesis, and oxidation that confers a preferential proliferative advantage to Tregs, whose targeting might represent a strategy for cancer treatment

The coding and long noncoding single-cell atlas of the developing human fetal striatum.

Deciphering how the human striatum develops is necessary for understanding the diseases that affect this region. To decode the transcriptional modules that regulate this structure during development, we compiled a catalog of 1116 long intergenic noncoding RNAs (lincRNAs) identified de novo and then profiled 96,789 single cells from the early human fetal striatum. We found that D1 and D2 medium spiny neurons (D1- and D2-MSNs) arise from a common progenitor and that lineage commitment is established during the postmitotic transition, across a pre-MSN phase that exhibits a continuous spectrum of fate determinants. We then uncovered cell type-specific gene regulatory networks that we validated through in silico perturbation. Finally, we identified human-specific lincRNAs that contribute to the phylogenetic divergence of this structure in humans. This work delineates the cellular hierarchies governing MSN lineage commitment

An intestinal Th17 subset is associated with inflammation in crohn's disease and activated by adherent-invasive Escherichia coli (aiec)

IFNγ-producing ex-Th17-cells ("Th1/17") were shown to play a key pathogenic role in experimental colitis and are abundant in the intestine. Here, we identified and characterized a novel, potentially colitogenic subset of Th17-cells in the intestine of patients with Crohn's Disease (CD). Human Th17-cells expressing CCR5 ("pTh17") co-expressed T-bet and RORC/γt and produced very high levels of IL-17, together with IFN-γ. They had a gene signature of Th17 effector cells and were distinct from established Th1/17-cells. pTh17-cells, but not Th1/17-cells, were associated with intestinal inflammation in CD, and decreased upon successful anti-TNF therapy with infliximab. Conventional CCR5(-)Th17-cells differentiated to pTh17 cells with IL-23 in vitro. Moreover, anti-IL-23 therapy with risankizumab strongly reduced pTh17-cells in the intestine. Importantly, intestinal pTh17-cells were selectively activated by adherent-invasive Escherichia coli (AIEC), but not by a commensal/probiotic E. coli strain. AIEC induced high levels of IL-23 and RANTES from DC. Intestinal CCR5 +Th1/17-cells responded instead to Cytomegalovirus and were reduced in UC, suggesting an unexpected protective role. In conclusion, we identified an IL-23-inducible subset of human intestinal Th17-cells. pTh17 cells produced high levels of pro-inflammatory cytokines, were selectively associated with intestinal inflammation in CD, and responded to CD-associated AIEC, suggesting a key colitogenic role