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The antimicrobial activity, surface features, wettability, and adhesion of photocatalytic xerogel AquaSun deposited on shipbuilding steel in comparison to those of a commercial antifouling paint are investigated. The antimicrobial activity of AquaSun deposited on a steel substrate pretreated with primer and tiecoat paint exposed to a microbial consortium composed of Bacillus aquimaris and Pseudomonas poae is significant and of broad scope. Taking into account the low cost, high stability, and lack of ecotoxicity of this hybrid sol–gel coating, these results are promising en route to developing novel antibacterial coatings of broad applicability. [ABSTRACT FROM AUTHOR]

Climate change, desertification, salinisation of soils and the changing hydrology of the Earth are creating or modifying microbial habitats at all scales including the oceans, saline groundwaters and brine lakes. In environments that are saline or hypersaline, the biodegradation of recalcitrant plant and animal polysaccharides can be inhibited by salt‐induced microbial stress and/or by limitation of the metabolic capabilities of halophilic microbes. We recently demonstrated that the chitinolytic haloarchaeon Halomicrobium can serve as the host for an ectosymbiont, nanohaloarchaeon 'Candidatus Nanohalobium constans'. Here, we consider whether nanohaloarchaea can benefit from the haloarchaea‐mediated degradation of xylan, a major hemicellulose component of wood. Using samples of natural evaporitic brines and anthropogenic solar salterns, we describe genome‐inferred trophic relations in two extremely halophilic xylan‐degrading three‐member consortia. We succeeded in genome assembly and closure for all members of both xylan‐degrading cultures and elucidated the respective food chains within these consortia. We provide evidence that ectosymbiontic nanohaloarchaea is an active ecophysiological component of extremely halophilic xylan‐degrading communities (although by proxy) in hypersaline environments. In each consortium, nanohaloarchaea occur as ectosymbionts of Haloferax, which in turn act as scavenger of oligosaccharides produced by xylan‐hydrolysing Halorhabdus. We further obtained and characterised the nanohaloarchaea–host associations using microscopy, multi‐omics and cultivation approaches. The current study also doubled culturable nanohaloarchaeal symbionts and demonstrated that these enigmatic nano‐sized archaea can be readily isolated in binary co‐cultures using an appropriate enrichment strategy. We discuss the implications of xylan degradation by halophiles in biotechnology and for the United Nation's Sustainable Development Goals. [ABSTRACT FROM AUTHOR]

Background: Senataxin (SETX) is a DNA/RNA helicase critical for neuron survival. SETX mutations underlie two inherited neurodegenerative diseases: Ataxia with Oculomotor Apraxia type 2 (AOA2) and Amyotrophic Lateral Sclerosis type 4 (ALS4). Methods: This review examines SETX key cellular processes and we hypothesize that SETX requires SUMO posttranslational modification to function properly. Results: SETX is localized to distinct foci during S‐phase of the cell cycle, and these foci represent sites of DNA polymerase/RNA polymerase II (RNAP) collision, as they co‐localize with DNA damage markers 53BP1 and H2AX. At such sites, SETX directs incomplete RNA transcripts to the nuclear exosome for degradation via interaction with exosome component 9 (Exosc9), a key component of the nuclear exosome. These processes require SETX SUMOylation. SETX was also recently localized within stress granules (SGs), and found to regulate SG disassembly, a process that similarly requires SUMOylation. Conclusion: SETX undergoes SUMO modification to function at S‐phase foci in cycling cells to facilitate RNA degradation. SETX may regulate similar processes in non‐dividing neurons at sites of RNAP II bidirectional self‐collision. Finally, SUMOylation of SETX appears to be required for SG disassembly. This SETX function may be crucial for neuron survival, as altered SG dynamics are linked to ALS disease pathogenesis. In addition, AOA2 point mutations have been shown to block SETX SUMOylation. Such mutations induce an ataxia phenotype indistinguishable from those with SETX null mutation, underscoring the importance of this modification. [ABSTRACT FROM AUTHOR]

Late blight caused by the oomycete Phytophthora infestans is a disease of potato and tomato of worldwide relevance and is widespread throughout Europe and the Mediterranean region. While pathogen populations in northern Europe have been sampled and characterized for many years, the genetic structure of populations from southern Europe, including Italy, has been less studied. Between 2018 and 2019, we collected 91 samples of P. infestans from potato and tomato crops in Italy, Algeria, and Tunisia on FTA cards and genotyped them using 12‐plex microsatellites. These samples were compared to genotypes of P. infestans previously collected within the framework of the EuroBlight network and from published sources. Four clonal lineages were identified: 13_A2 (Blue 13), 2_A1, 23_A1, and 36_A2. Two other isolates collected could not be matched to any currently known clonal lineage. The 13_A2 and 36_A2 lineages were found exclusively in southern Italy and Algeria, while 2_A1 was only found in Algeria. This is the first report of the 36_A2 lineage in Italy. Two isolates from Solanum nigrum were 13_A2, suggesting this weed host could be a reservoir of inoculum. The 23_A1 lineage was found widely on infected tomato crops in Italy and is the same as the lineage US‐23 that is widespread in North America. Differences in genotypes across the country suggests that there may be different sources of introduction into Italy, possibly via infected seed tubers from other countries in Europe, tubers for consumption from North Africa, or tomatoes. [ABSTRACT FROM AUTHOR]

Background: Although Huntington's disease (HD) is caused by a single dominant gene, it is clear that there are genetic modifiers that may influence the age of onset and disease progression.Objectives: We sought to investigate whether new inflammation-related genetic variants may contribute to the onset and progression of HD.Methods: We first used postmortem brain material from patients at different stages of HD to look at the protein expression of toll-like receptor 4 (TLR4) and triggering receptor expressed on myeloid cells 2 (TREM2). We then genotyped the TREM2 R47H gene variant and 3 TLR4 single nucleotide polymorphisms in a large cohort of HD patients from the European Huntington's Disease Network REGISTRY.Results: We found an increase in the number of cells expressing TREM2 and TLR4 in postmortem brain samples from patients dying with HD. We also found that the TREM2 R47H gene variant was associated with changes in cognitive decline in the large cohort of HD patients, whereas 2 of 3 TLR4 single nucleotide polymorphisms assessed were associated with changes in motor progression in this same group.Conclusions: These findings identify TREM2 and TLR4 as potential genetic modifiers for HD and suggest that inflammation influences disease progression in this condition. © 2019 International Parkinson and Movement Disorder Society. [ABSTRACT FROM AUTHOR]

Huntington disease (HD) is a progressive autosomal dominant neurodegenerative disorder in which patients typically present with uncontrolled involuntary movements and subsequent cognitive decline. In 1993, a CAG trinucleotide repeat expansion in the coding region of the huntingtin (HTT) gene was identified as the cause of this disorder. This extended CAG repeat results in production of HTT protein with an expanded polyglutamine tract, leading to pathogenic HTT protein conformers that are resistant to protein turnover, culminating in cellular toxicity and neurodegeneration. Research into the mechanistic basis of HD has highlighted a role for bioenergetics abnormalities stemming from mitochondrial dysfunction, and for synaptic defects, including impaired neurotransmission and excitotoxicity. Interference with transcription regulation may underlie the mitochondrial dysfunction. Current therapies for HD are directed at treating symptoms, as there are no disease‐modifying therapies. Commonly prescribed drugs for involuntary movement control include tetrabenazine, a potent and selective inhibitor of vesicular monoamine transporter 2 that depletes synaptic monoamines, and olanzapine, an atypical neuroleptic that blocks the dopamine D2 receptor. Various drugs are used to treat non‐motor features. The HD therapeutic pipeline is robust, as numerous efforts are underway to identify disease‐modifying treatments, with some small compounds and biological agents moving into clinical trials. Especially encouraging are dosage reduction strategies, including antisense oligonucleotides, and molecules directed at transcription dysregulation. Given the depth and breadth of current HD drug development efforts, there is reason to believe that disease‐modifying therapies for HD will emerge, and this achievement will have profound implications for the entire neurotherapeutics field. [ABSTRACT FROM AUTHOR]

Preconditioning (PC) is a cell adaptive response to oxidative stress and, with regard to neurons, can be considered as a neuroprotective strategy. The aim of the present study was to verify how neuronal‐like differentiated SH‐SY5Y cells adapt to a mild and transient H2O2‐induced oxidative stress and, hence, whether may be considered as more sensitive cell model to study PC pathways. A first screening allowed to define H2O2 concentrations for PC (10μM‐50μM), applied before damage(100μM H2O2). Cell viability measured 24 hours after 100μM H2O2–induced damage was ameliorated by 24‐hour pre‐exposure to low‐concentration H2O2 (10μM‐30μM) with cell size as well restored. Markers for apoptosis (Bcl‐2 and Bad), inflammation (iNOS), and redox system (MnSOD) were also determined, showing that, in cells pre‐exposed to 10μM H2O2 and then submitted to 100μM H2O2, Bcl‐2 levels were higher, Bad and iNOS levels were lower than those observed in damaged cells, and MnSOD levels were unchanged. Such findings show that (1) neuronal‐like differentiated SH‐SY5Y cells are a suitable model to investigate PC response and more sensitive to the effect of a mild and transient H2O2‐induced oxidative stress with respect to other neuronal cells; (2) 10μM H2O2–induced PC is mediated by apoptotic and inflammatory pathways, unlike antioxidant system; (3) such neuroprotective strategy and underlying signals proven in neuronal‐like differentiated SH‐SY5Y cells may contribute to understand in vivo PC mechanisms and to define a window for pharmacological intervention, namely, related to ischemic brain damage. Significance of the study: Neuronal‐like differentiated SH‐SY5Y cells are a suitable model to investigate PC, an endogenous neuroprotective response to a mild and transient H2O2‐induced oxidative stress, elicited by 24‐hour exposure to very low H2O2 concentrations and mediated by both apoptotic and inflammatory pathways. This model reflects in vivo PC mechanisms occurring after brain trauma and provides novel information about pathways and time of protection useful for an appropriate pharmacological intervention. [ABSTRACT FROM AUTHOR]

Ammonium- and Fe( II)-rich fluid flows, known from deep-sea hydrothermal systems, have been extensively studied in the last decades and are considered as sites with high microbial diversity and activity. Their shallow-submarine counterparts, despite their easier accessibility, have so far been under-investigated, and as a consequence, much less is known about microbial communities inhabiting these ecosystems. A field of shallow expulsion of hydrothermal fluids has been discovered at depths of 170-400 meters off the base of the Basiluzzo Islet (Aeolian Volcanic Archipelago, Southern Tyrrhenian Sea). This area consists predominantly of both actively diffusing and inactive 1-3 meters-high structures in the form of vertical pinnacles, steeples and mounds covered by a thick orange to brown crust deposits hosting rich benthic fauna. Integrated morphological, mineralogical, and geochemical analyses revealed that, above all, these crusts are formed by ferrihydrite-type Fe3+ oxyhydroxides. Two cruises in 2013 allowed us to monitor and sampled this novel ecosystem, certainly interesting in terms of shallow-water iron-rich site. The main objective of this work was to characterize the composition of extant communities of iron microbial mats in relation to the environmental setting and the observed patterns of macrofaunal colonization. We demonstrated that iron-rich deposits contain complex and stratified microbial communities with a high proportion of prokaryotes akin to ammonium- and iron-oxidizing chemoautotrophs, belonging to Thaumarchaeota, Nitrospira, and Zetaproteobacteria. Colonizers of iron-rich mounds, while composed of the common macrobenthic grazers, predators, filter-feeders, and tube-dwellers with no representatives of vent endemic fauna, differed from the surrounding populations. Thus, it is very likely that reduced electron donors (Fe2+ and NH4+) are important energy sources in supporting primary production in microbial mats, which form a habitat-specific trophic base of the whole Basiluzzo hydrothermal ecosystem, including macrobenthic fauna. [ABSTRACT FROM AUTHOR]

A great deal of interest has reemerged recently in the study of surface waves. The possibility to control and manipulate electromagnetic wave propagations at will opens many new research areas and leads to lots of novel applications in engineering. In this paper, we will present a comprehensive modeling and design approach for surface wave cloaks, based on graded-refractive-index materials and the theory of transformation optics. It can be also applied to any other forms of surface wave manipulation, in terms of amplitude and phase. In this paper, we will present a general method to illustrate how this can be achieved from modeling to the final design. The proposed approach is validated to be versatile and allows ease in manufacturing, thereby demonstrating great potential for practical applications. [ABSTRACT FROM AUTHOR]

Sgf73, a core component of SAGA, is the yeast orthologue of ataxin-7, which undergoes CAG-polyglutamine repeat expansion leading to the human neurodegenerative disease spinocerebellar ataxia type 7 (SCA7). Deletion of SGF73 dramatically extends replicative lifespan (RLS) in yeast. To further define the basis for Sgf73-mediated RLS extension, we performed ChIP-Seq, identified 388 unique genomic regions occupied by Sgf73, and noted enrichment in promoters of ribosomal protein (RP)-encoding genes. Of 388 Sgf73 binding sites, 33 correspond to 5′ regions of genes implicated in RLS extension, including 20 genes encoding RPs. Furthermore, half of Sgf73-occupied, RLS-linked RP genes displayed significantly reduced expression in sgf73Δ mutants, and double null strains lacking SGF73 and a Sgf73-regulated, RLS-linked RP gene exhibited no further increase in replicative lifespan. We also found that sgf73Δ mutants display altered acetylation of Ifh1, an important regulator of RP gene transcription. These findings implicate altered ribosomal protein expression in sgf73Δ yeast RLS and highlight altered acetylation as a pathway of relevance for SCA7 neurodegeneration. [ABSTRACT FROM AUTHOR]

Critical lower limb ischaemia is a diffuse pathology that could cause claudication, severe ischaemic pain and tissue loss. The common treatment includes modification of risk factors, pharmacological therapy and endovascular or surgical revascularisation of the lower limb to restore a pulsatile flow distally. Spinal cord stimulator is seen as a valid alternative in patients unsuitable for revascularisation after endovascular or surgical revascularisation failure and as adjuvant therapy in the presence of a functioning bypass in patients with extensive tissue loss and gangrene presenting a slow and difficult wound healing. We report our experience on spinal cord stimulation ( SCS) indication and implantation in patients with critical lower limb ischaemia, at a high-volume centre for the treatment of peripheral arterial disease. [ABSTRACT FROM AUTHOR]

The sediment budget is a key concept and tool for characterizing the mobilization, transfer and storage of fine sediment within a catchment. Caesium-137 measurements can provide valuable information on gross and net erosion rates associated with sheet and rill erosion that can be used to establish the slope component of a catchment sediment budget. However, there is a need to validate the use of 137Cs measurements for this purpose, because their reliability has sometimes been questioned. The study reported focuses on a small (3·04 ha) steepland (mean slope 37%) catchment in Southern Italy. It exploits the availability of information on the medium-term sediment output from the catchment provided by the construction of a reservoir at its outlet in 1978 and the existence of estimates of soil redistribution rates derived from 137Cs measurements made on 68 replicate soil cores collected from the slopes of a substantial proportion of the catchment in 2001, to validate the use of 137Cs measurements to construct the slope component of the catchment sediment budget. An additional 50 replicate soil cores were collected from the catchment slopes for 137Cs analysis, to complement the data already available. Nine cores collected from the area occupied by the reservoir were used to estimate the mean annual sediment input to the reservoir. In the absence of evidence that the poorly developed channel system in the catchment was either a significant sediment source or sink, it was possible to directly compare the estimate of net soil loss from the catchment slopes (7·33 Mg ha−1 y−1) with the estimate of sediment output from the catchment provided by the reservoir deposits (7·52 Mg ha−1 y−1). Taking account of the uncertainties involved, the close agreement of the two values is seen as providing a convincing validation of the use of 137Cs measurements to both estimate soil redistribution rates and as a basis for constructing the slope component of the sediment budget of a small catchment. Copyright © 2015 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Dark ocean microbial communities are actively involved in chemoautotrophic and anaplerotic fixation of bicarbonate. Thus, aphotic pelagic realm of the ocean might represent a significant sink of CO2 and source of primary production. However, the estimated metabolic activities in the dark ocean are fraught with uncertainties. Typically, deep-sea samples are recovered to the sea surface for downstream processing on deck. Shifts in ambient settings, associated with such treatments, can likely change the metabolic activity and community structure of deep-sea adapted autochthonous microbial populations. To estimate influence of recovery and short-term handling of deep-sea samples, we monitored the succession of bathypelagic microbial community during its 3 days long on deck incubation. We demonstrated that at the end of exposition, the deep-sea archaeal population decreased threefold, whereas the bacterial fraction doubled in size. As revealed by phylogenetic analyses of amoA gene transcripts, dominance of the active ammonium-oxidizing bathypelagic T haumarchaeota groups shifted over time very fast. These findings demonstrated the simultaneous existence of various 'deep-sea ecotypes', differentially reacting to the sampling and downstream handling. Our study supports the hypothesis that metabolically active members of meso- and bathypelagic T haumarchaeota possess the habitat-specific distribution, metabolic complexity and genetic divergence at subpopulation level. [ABSTRACT FROM AUTHOR]

Objective Growing evidence suggests that neurodegenerative diseases are associated with metabolic disorders, but the mechanisms are still unclear. Better comprehension of this issue might provide a new strategy for treatment of neurodegenerative diseases. We investigated possible roles of adiponectin ( APN), the antidiabetes protein, in the pathogenesis of α-synucleinopathies. Methods Using biochemical and histological methods, we investigated autopsy brain of α-synucleinopathies including Parkinson's disease ( PD) and dementia with Lewy bodies ( DLB), and analyzed the effects of APN in cellular and in mouse models of α-synucleinopathies. Results We observed that APN is localized in Lewy bodies derived from α-synucleinopathies, such as Parkinson's disease and dementia with Lewy bodies. In neuronal cells expressing α-synuclein ( αS), aggregation of αS was suppressed by treatment with recombinant APN in an Adipo RI- AMP kinase pathway-dependent manner. Concomitantly, phosphorylation and release of αS were significantly decreased by APN, suggesting that APN may be antineurodegenerative. In transgenic mice expressing αS, both histopathology and movement disorder were significantly improved by intranasal treatment with globular APN when the treatment was initiated in the early stage of the disease. In a mouse model, reduced levels of guanosine and inosine monophosphates, both of which are potential stimulators of aggregation of αS, might partly contribute to suppression of aggregation of αS by APN. Interpretation Taken together, APN may suppress neurodegeneration through modification of the metabolic pathway, and could possess a therapeutic potential against α-synucleinopathies. [ABSTRACT FROM AUTHOR]

We used a combination of molecular and microbiological approaches to determine the activity, abundance and diversity of archaeal populations inhabiting meromictic saline Lake Faro ( Messina, Italy). Analysis of archaeal 16 S rRNA, amoA, accA and hbd genes and transcripts revealed that sub- and anoxic layers of Lake Faro are primarily inhabited by the organisms related to the clusters of Marine Group I.1a of Thaumarchaeota frequently recovered from oxygen-depleted marine ecosystems. These organisms dominated the metabolically active archaea down to the bottom of the lake, indicating their adaptation to recurrent changes in the levels of water column hypoxia. The upper microaerobic layer of Lake Faro redoxcline has the maximal rates of dark primary production much lower than those of other previously studied pelagic redoxclines, but comparable to the values of meso- and bathypelagic areas of Mediterranean Sea. Application of bacterial inhibitors, especially azide, significantly declined the CO2 fixation rates in the low interface and monimolimnion, whereas archaea-specific inhibitor had effect only in upper part of the redoxcline. Based on these findings, we hypothesize that dark bicarbonate fixation in suboxic zone of Lake Faro results mainly from archaeal activity which is affected by the predicted lack in oxygen in lower layers. [ABSTRACT FROM AUTHOR]

In this study, we examined whether melatonin treatment would increase new cell formation in the hippocampus in ovariectomized (OVX) mice. Chronic exogenous melatonin administration increased bromodeoxyuridine (BrdU) (OVX-sham 72 ± 3.2 versus OVX-mel 122 ± 12.0; P < 0.05) and doublecortin (DCX) (OVX-sham 88 ± 3.1 versus OVX-mel 176 ± 9.9; P < 0.05) immunoreactive cells in the hippocampus of ovariectomized mice. This neuronal development was correlated with synaptic plasticity, identified using the Golgi impregnation method to quantify dendritic spines in mouse dentate gyrus (DG). Finally, the antidepressant-like state of the animals was evaluated by the tail suspension test. The results indicate that melatonin acts on birth, survival, and differentiation of new neurons in the hippocampus, stimulates maturation of spines, and exerts an antidepressant-like action under estrogen-deprived conditions, in both a strain- and gender-independent manner, suggesting that this indoleamine may be useful in improving brain functions. [ABSTRACT FROM AUTHOR]

Melatonin, involved in circadian cycle, provides protective effects on neuronal cells and acts as antidepressant by restoration of corticosterone levels. A mouse model of anxiety/depressive-like behavior, induced by chronic corticosterone treatment, has been used to evaluate behavior and adult hippocampal neurogenesis in mice and their possible modulation under melatonin. With this aim, CD1 mice were subjected to 7 wk of corticosterone administration, and then behavioral tests as novelty-suppressed feeding, open field and a forced swim test were performed. Cell proliferation in hippocampal dentate gyrus (DG) was investigated by 5-bromo-2′-deoxyuridine and doublecortin immunohistochemistry techniques, and stereological procedure was used to quantify labeled cells. Golgi-impregnated method was used to evaluate the changes of dendritic spines in DG neurons. A new therapeutic approach with antidepressant-like substances (3 wk) such as melatonin (8 mg/kg) was employed to possibly modulate neural development in the adult hippocampus and the behavioral changes. The depressive-like state caused by chronic corticosterone treatment was reversed by exogenous administration of melatonin; the proliferation of progenitor cells in mice hippocampus was significantly reduced under chronic corticosterone treatment (cort− 83.7 ± 20.3 versus cort+ 60.5 ± 18.2; P < 0.05), whereas long-term treatment with melatonin prevented the corticosterone-induced reduction in hippocampal cell proliferation (cort− 60.5 ± 18.2 versus mel 133.4 ± 26.9; P < 0.05). Corticosterone-treated mice exhibited a reduced spine density, which was ameliorated by melatonin administration. These findings suggest a strong correspondence between behavior and neurogenesis, strengthening the hypothesis that neurogenesis contributes to the effects of melatonin as an antidepressant. [ABSTRACT FROM AUTHOR]

Melatonin (N-acetyl-5-methoxytryptamine) is an efficient free radical scavenger and antioxidant, both in vitro and in vivo. The role of melatonin as an immunomodulator is, in some cases, contradictory. In this study we have investigated the therapeutic efficacy of melatonin in rats subjected to Pelagia noctiluca crude venom (of the familia Pelaguiidae; and genus Pelagia) induced acute paw inflammation. In particular, injection of the venom into the paw of rats elicited an acute inflammatory response characterized by accumulation of fluid containing a large number of polymorphonuclear neutrophils in the paw and subsequent lipid peroxidation. Furthermore, the venom promoted an expression of iNOS, nitrotyrosine and the activation of the nuclear enzyme poly (ADP-ribose) polymerase as determined by immunohistochemical analysis of paw tissues. Administration of melatonin 30 min, 1 and 6 hr after the challenge with the venom, caused a significant reduction in all the parameters of inflammation measured. Thus, based on these findings we propose that melatonin may be useful a treatment of local acute inflammation induced by P. noctiluca crude venom. [ABSTRACT FROM AUTHOR]

Spinocerebellar ataxia type 7 (SCA7) represents a rare and severe autosomal dominantly inherited ataxic disorder and is among the known CAG-repeat, or polyglutamine, diseases. In contrast to other currently known autosomal dominantly inherited ataxic disorders, SCA7 may manifest itself with different clinical courses. Because the degenerative changes evolving during these different clinical courses are not well known, many neurological disease symptoms still are unexplained. We performed an initial pathoanatomical study on unconventional thick tissue sections of the brain of a clinically diagnosed and genetically confirmed adult-onset SCA7 patient with progressive visual impairments. In this patient we observed loss of myelinated fibres in distinct central nervous fibre tracts, and widespread degeneration of the cerebellum, telencephalon, diencephalon and lower brainstem. These degenerative changes offer appropriate explanations for a variety of less-understood neurological symptoms in adult-onset SCA7 patients with visual impairments: gait, stance and limb ataxia, falls, dysarthria, dysphagia, pyramidal signs, Parkinsonian features, writing problems, impairments of saccades and smooth pursuits, altered pupillary functions, somatosensory deficits, auditory deficits and mental impairments. [ABSTRACT FROM AUTHOR]

The liver is morphologically and functionally modulated by sex hormones. Long-term use of oral contraceptives (OCs) and anabolic androgenic steroids (AASs) can induce both benign (hemangioma, adenoma, and focal nodular hyperplasia [FNH]) and malignant (hepatocellular carcinoma [HCC]) hepatocellular tumors. Hepatic adenomas (HAs) are rare, benign neoplasms usually occurring in young women, the development and the complications of which have been related to the strength of OCs and the duration of their use. HA incidence has fallen since the introduction of pills containing smaller amounts of estrogens. FNH is a benign lesion, most commonly seen in young women, which is thought to represent a local hyperplastic response of hepatocytes to a vascular abnormality. Because of the female predominance and the young age at onset, a role of female hormones has been suggested. Furthermore, a large proportion of women with FNH (50–75%) are OC users. Liver hemangiomas (LHs) are the most common benign liver tumors and are seen more commonly in young adult females. The female predilection and clinical observations of LH growth under conditions of estrogenic exposure suggest a possible role for estrogen in the pathogenesis of LHs. HCC has become one of the most widespread tumors in the world in recent years, representing the sixth leading cancer and the third most common cause of death from cancer. Apart from liver cirrhosis, numerous other factors responsible for its onset have been proposed: hepatitis infections from virus B (HBV) and C (HCV), alcohol, smoking, and aflatoxin. However, regardless of etiology, chronic liver diseases progress at unequal rates in the two sexes, with the major sequelae, such as cirrhosis and HCC, being more frequent in men than in women. These epidemiological data have prompted researchers to investigate the relationship between sex hormones and liver tumors. The human liver expresses estrogen and androgen receptors and experimentally both androgens and estrogens have been implicated in stimulating hepatocyte proliferation and may act as liver tumor inducers or promoters. [ABSTRACT FROM AUTHOR]

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