Increased serum IgE in alcohol abusers

Background: It has been reported that total serum IgE is increased in patients with alcoholic cirrhosis, but it is not clear if this fact is related to alcoholic liver disease or to alcohol intake. Objective: To measure serum IgE in a group of chronic alcoholics with different stages of liver injury in order to elucidate if IgE increase is related to alcoholic liver damage. Patients and methods: Total serum IgE was determined by enzyme immunoassay in 186 chronic alcoholic patients (137 male/49 female) and 101 healthy controls. Patients and controls with known reasons for IgE elevation were excluded. Among alcoholic patients, 24 had fatty liver, 28 hepatic fibrosis, 29 alcoholic hepatitis, and 67 liver cirrhosis (38 patients were not evaluable concerning liver injury). Results: Total serum IgE was found to be increased in alcoholics (median 154.5IU/mL, range 1–7329IU/mL) with respect to healthy controls (median 20IU/mL, range < 1–1417 IU/mL) (P < 0.001). IgE increase was moderate (180–1000 IU/mL) in 60 alcoholics (32.3%) and marked (> 1000 IU/mL) in 27 (14.5%). Male alcoholics had higher IgE levels than females (median 191 IU/mL and range 1–7329 IU/mL vs 105IU/mL and range 2–2189IU/mL) (P= 0.009). On logistic regression analysis, alcoholism, male sex and younger age (but not smoking) were independently associated with higher IgE levels. No clear relationship was noted between serum IgE and severity of alcoholic liver disease. Thus, no correlation was observed between IgE and parameters of liver function (serum bilirubin, albumin or prothrombin index). Likewise, IgE concentrations were not significantly different in patients with liver cirrhosis with respect to patients with less severe liver disease. Serum IgE was increased (> 180 IU/mL) in 47.8 % of cirrhotics and in 44% of patients without liver cirrhosis. In contrast, other immunoglobulins (IgG, IgA and IgM) were significantly correlated with liver dysfunction. Conclusion: Chronic alcoholism should be considered as a cause of increased total serum IgE, regardless of the severity of the underlying liver disease.     

Fine structure of the developing epidermis in the embryo of the American alligator (Alligator mississippiensis,Crocodilia, Reptilia)

The morphological transition from the simple epidermis that contacts the amniotic fluid of embryonic crocodilians to the adult epidermis required in a terrestrial environment has never been described. We used light and electron microscopy to study the development, differentiation and keratinisation of the epidermis of the American alligator, Alligator mississippiensis, between early and late stages of embryonic skin formation. In early embryonic development, the epidermis consists of a flat bilayer. As it develops, the bilayered epidermis comes to lie beneath the peridermis. Glycogen is almost absent from the bilayered epidermis but increases in basal and suprabasal cells when scales form. Glycogen disappears from suprabasal cells that accumulate keratin. The peridermis and 1 or 2 subperidermal layers form an embryonic epidermis that is partially or totally lost before hatching. These cells accumulate coarse filaments and form reticulate bodies. Mucous and lamellate granules are produced in the Golgi apparatus and are partly secreted extracellularly. The embryonic cells darken with the formation of larger reticulate bodies that aggregate with intermediate filaments and other cell organelles, as their nuclear chromatin condenses. Thin β‐cells resembling those of scutate scales of birds develop beneath the embryonic epidermis and form a stratified β‐layer that varies in thickness in different body regions. The epidermis differentiates first in the back, tail and belly. At the beginning of β‐cell differentiation, the cytoplasm contains sparse bundles of α‐keratin filaments, glycogen and lipid droplets or vacuoles apparently derived from the endoplasmic reticulum and Golgi apparatus. These organelles disappear rapidly as irregular bundles of electron‐dense β‐keratin filaments accumulate and form larger bundles. The larger bundles consist of 3 nm thick electron‐pale keratin microfibrils and are derived from the assemblage of β‐keratin molecules produced by ribosomes. While in mammals the epidermal barrier is formed by α‐keratinocytes, in the alligator the barrier is formed by β‐keratin cells. The β‐layer is reduced or absent from the small hinge region between scales. In the latter areas the barrier is made of a or a mixture of α/β keratinocytes. Thus alligators resemble birds where the β‐keratin molecules are deposited directly over an α‐keratin scaffold, rather than an initial production of β‐keratin packets which then merge with α‐keratin, as occurs in the Chelonia and Lepidosauria. The pigmentation of the epidermis of embryos is mostly derived from epidermal melanocytes.     

Biobanking in the digital pathology era

Digital Pathology is becoming more and more important to achieve the goal of precision medicine. Advances in whole-slide imaging, software integration, and the accessibility of storage solutions have changed the pathologists’ clinical practice, not only in terms of laboratory workflow but also for diagnosis and biomarkers analysis. In parallel with the pathology setting advancement, translational medicine is approaching the unprecedented opportunities unrevealed by artificial intelligence (AI). Indeed, the increased usage of biobanks’ datasets in research provided new challenges for AI applications, such as advanced algorithms, and computer-aided techniques. In this scenario, machine learning-based approaches are being propose in order to improve biobanks from biospecimens collection repositories to computational datasets. To date, evidence on how to implement digital biobanks in translational medicine is still lacking. This viewpoint article summarizes the currently available literature that supports the biobanks’ role in the digital pathology era, and to provide possible practical applications of digital biobanks.     

Longitudinal neuropsychological evaluation of HIV-infected intravenous drug users

The present study aimed to describe the cognitive status of a group of HIV-positive asymptomatic intravenous drug users (IVDU) and changes which occurred over a 12-month follow-up period. Forty-two HIV positive IVDU were selected and matched for age, sex, educational level and pattern of drug abuse with 39 seronegative IVDU controls. Baseline and follow-up evaluation included neuropsychological tests exploring attention, language, memory, logic and visuomotor abilities, biological markers and clinical parameters. About one-third of both seropositive and seronegative subjects showed at baseline slight cognitive deficits, ‘which did not change during the follow-up period.