Development Of Disease Research Articles

Thromboelastogram and coagulation function index: relevance for female breast cancer

IntroductionScreening and postoperative intervention of breast tumors are critical for the effective diagnosis and treatment of disease development, and reliable diagnostic/screening methods become a key link. ObjectiveThromboelastogram (TEG), routine platelet (PLT) count, and the coagulation function indicators in patients with different breast diseases were determined and analyzed to explore their predictive value in secondary bleeding disorders.MethodsA total of 131 patients with breast diseases, admitted to Jiangsu University Affiliated Hospital from January 2019 to December 2022, were selected as the research subjects. The detection items were analyzed using the receiver operating curve (ROC) after grouping for secondary bleeding disorders of patients with breast cancer.ResultsThe reaction (R) and the coagulation (K) times were lower in the malignant breast disease group, while the coagulation angle (α), maximum amplitude (MA), coagulation index (CI), fibrinogen (FIB), and D-dimer (D-D) were higher than those in the benign breast disease group. The t-tests proved that the MA and FIB values were statistically significant (p < 0.05) in the benign and malignant breast disease groups. The R and K in patients with breast diseases were positively correlated with the activated partial thromboplastin time (aPTT) and D-D, but were negatively correlated with PLT. The α angle was negatively correlated with aPTT and D-D, but was positively correlated with PLT. The MA for PLT function was positively correlated with FIB and PLT. CI was negatively correlated with aPTT, thrombin time (TT), and D-D, but was positively correlated with PLT. ROC curve analysis showed that the CI and α angle had a significant predictive value, whereas the correlation of the other indicators was relatively low.ConclusionCoagulation tests showed significant differences in patients with breast cancer, differing from those with benign breast diseases. TEG combined with conventional coagulation indicators is potentially valuable for the prediction of secondary bleeding disorders in patients with breast cancer.

A Promising Biocontrol Agent of Bacillus velezensis VC3 against Magnaporthe oryzae and Colletotrichum gloeosporioides in Plants

Fungal diseases of plants are one of the key factors causing global crop losses. In this study, we isolated a Bacillus velezensis strain VC3, which was found to have a broad-spectrum inhibitory effect on a variety of phytopathogenic fungi through in vitro and in planta experiments, especially on Magnaporthe oryzae and Colletotrichum gloeosporioides. Further genomic and transcriptomic analyses revealed that the B. velezensis VC3 has multiple functional gene clusters encoding for the synthesis of a variety of antifungal secondary metabolites, including antimicrobial peptides (AMPs) and lipopeptides (LPs). In addition, AMPs and LPs were isolated and purified from B. velezensis VC3 fermentation broth and their antifungal activities were verified in this study. AMPs and LPs significantly inhibited spore germination, appressorium formation, and disease development, and AMPs have a better potential for controlling M. oryzae and C. gloeosporioides than LPs. These findings open new avenues for utilizing B. velezensis VC3 as biocontrol agents, providing potential sustainable solutions for agricultural production.

Integrative Analysis of Lactylome and Proteome of Hypertrophic Scar To Identify Pathways or Proteins Associated with Disease Development.

Lactylation (Kla), a recently discovered post-translational modification derived from lactate, plays crucial roles in various cellular processes. However, the specific influence of lactylation on the biological processes underlying hypertrophic scar formation remains unclear. In this study, we present a comprehensive profiling of the lactylome and proteome in both hypertrophic scars and adjacent normal skin tissues. A total of 1023 Kla sites originating from 338 nonhistone proteins were identified based on lactylome analysis. Proteome analysis in hypertrophic scar and adjacent skin samples revealed the identification of 2008 proteins. It is worth noting that Kla exhibits a preference for genes associated with ribosome function as well as glycolysis/gluconeogenesis in both normal skin and hypertrophic scar tissues. Furthermore, the functional enrichment analysis demonstrated that differentially lactyled proteins are primarily involved in proteoglycans, HIF-1, and AMPK signaling pathways. The combined analysis of the lactylome and proteome data highlighted a significant upregulation of 14 lactylation sites in hypertrophic scar tissues. Overall, our investigation unveiled the significant involvement of protein lactylation in the regulation of ribosome function as well as glycolysis/gluconeogenesis, potentially contributing to the formation of hypertrophic scars.

Association of subclinical carotid artery atherosclerosis assessed by carotid ultrasound with nonalcoholic fatty liver disease fibrosis score in young and middle-aged men.

Non-alcoholic Fatty Liver Disease (NAFLD) is a widespread liver disorder caused by excess fat accumulation in the liver with no significant alcohol consumption. This condition has been linked to the development of cardiovascular diseases (CVD) and atherosclerosis. Carotid intima-media thickness (CIMT) and carotid plaques, which are established markers of subclinical atherosclerosis, were used to assess CVD risk. However, few studies have explored the correlation between NAFLD and subclinical atherosclerosis, especially in young and middle-aged men. A study on 200 male patients aged 18-55 years aimed to investigate the association between NAFLD fibrosis score (NFS) and CIMT, as well as carotid plaque presence. The study, conducted between July 2023 and January 2024, included CIMT measurements and plaque assessments performed using B-mode ultrasound. Participants were divided into two groups based on CIMT values and plaque presence, and NFS was analyzed for its association with CIMT and plaque. Participants with higher CIMT values had a significantly higher NFS (-2.9 ± 1.13 vs. -1.9 ± 1.4, P < 0.001) than those with lower CIMT values. Similarly, participants with carotid plaque also exhibited a higher NFS (-2.5 ± 1.3 vs. -1.7 ± 1.4, P = 0.002). Multivariate logistic regression analysis showed that NFS was a strong predictor of both increased CIMT (odds ratio [OR]: 1.564%95 CI 1.035-2.363; P = 0.034) and carotid plaque presence (OR: 1.605%95 CI 1.118-2.290; P = 0.010). These results emphasize the potential role of NFS as a marker of subclinical atherosclerosis in young and middle-aged men.

The Biomolecular Basis of Gut Microbiome on Neurological Diseases

The human gastrointestinal (GI) tract harbors many microorganisms, including viruses, protozoa, archaea, fungi, and bacteria. Altogether, these microbes constitute what we know as the gut microbiome (GM). These commensal communities have important implications for human health. They influence physiological processes through different mechanisms, including synthesizing neurotransmitters, regulating enzymatic pathways, and releasing molecules responsible for different signal pathways. The interaction between GM and brain function has been associated with the development and pathogenesis of neuropsychiatric diseases. This review discusses current studies targeting the regulation and modulation of GM in nerve, neuroendocrine, and immune pathways. Thus, we analyze current evidence on transcription, changes in composition, and specific interactions between the gut and brain from a biomolecular perspective. Special attention is paid to mood disorders and neurodegenerative diseases.

Discovery of Novel Antioomycete Metabolites from the Marine-Derived Fungus Paraconiothyrium sporulosum.

In our screening program for natural products that are effective in controlling plant diseases, we found that the culture filtrate of Paraconiothyrium sporulosum SFC20160907-M11 effectively suppressed the development of tomato late blight disease caused by Phytophthora infestans. Using a bioassay-guided fractionation of antioomycete activity, 12 active compounds (1-12) were obtained from an ethyl acetate extract of the culture filtrate. Chemical structures of five new compounds 1-5 were determined by the extensive analyses of nuclear magnetic resonance (NMR), high resolution mass spectrometry (HRMS), and circular dichroism (CD) data. Interestingly, mycosporulonol (1) and botrallin (8) completely inhibited the growth of P. infestans at concentrations of 8 and 16 μg/mL, respectively. Furthermore, the spray treatment of 1 and 8 (500 μg/mL) successfully protected tomato seedlings against P. infestans with disease control values of 92%. Taken together, these results suggest that the culture filtrates of P. sporulosum SFC20160907-M11 and their bioactive metabolites can be used as new antioomycete agents for Phytophthora late blight control.

High salt intake and HIV infection on endothelial glycocalyx shedding in salt-sensitive hypertension

The endothelial glycocalyx is closely associated with various physiological and pathophysiological events. Significant modification of the endothelial glycocalyx is an early process in the pathogenesis of cardiovascular disease. High dietary salt and HIV infection damages the endothelial glycocalyx causing endothelial dysfunction and increasing the risk for salt-sensitive hypertension and cardiovascular disease. The two factors, HIV infection and dietary salt are critical independent predictors of hypertension and cardiovascular disease and often synergize to exacerbate and accelerate disease pathogenesis. Salt-sensitive hypertension is more common among people living with HIV and is associated with risk for cardiovascular disease, stroke, heart attack and even death. However, the underlying mechanisms linking endothelial glycocalyx damage to dietary salt and HIV infection are lacking. Yet, both HIV infection/treatment and dietary salt are closely linked to endothelial glycocalyx damage and development of salt-sensitive hypertension. Moreover, the majority of individuals globally, consume more salt than is recommended and the burden of HIV especially in sub-Sahara Africa is disproportionately high. In this review, we have discussed the missing link between high salt and endothelial glycocalyx shedding in the pathogenesis of salt-sensitive hypertension. We have further elaborated the role played by HIV infection and treatment in modifying endothelial glycocalyx integrity to contribute to the development of hypertension and cardiovascular disease.

PARK7/DJ-1 deficiency impairs microglial activation in response to LPS-induced inflammation

BackgroundSpecific microglia responses are thought to contribute to the development and progression of neurodegenerative diseases, including Parkinson’s disease (PD). However, the phenotypic acquisition of microglial cells and their role during the underlying neuroinflammatory processes remain largely elusive. Here, according to the multiple-hit hypothesis, which stipulates that PD etiology is determined by a combination of genetics and various environmental risk factors, we investigate microglial transcriptional programs and morphological adaptations under PARK7/DJ-1 deficiency, a genetic cause of PD, during lipopolysaccharide (LPS)-induced inflammation.MethodsUsing a combination of single-cell RNA-sequencing, bulk RNA-sequencing, multicolor flow cytometry and immunofluorescence analyses, we comprehensively compared microglial cell phenotypic characteristics in PARK7/DJ-1 knock-out (KO) with wildtype littermate mice following 6- or 24-h intraperitoneal injection with LPS. For translational perspectives, we conducted corresponding analyses in human PARK7/DJ-1 mutant induced pluripotent stem cell (iPSC)-derived microglia and murine bone marrow-derived macrophages (BMDMs).ResultsBy excluding the contribution of other immune brain resident and peripheral cells, we show that microglia acutely isolated from PARK7/DJ-1 KO mice display a distinct phenotype, specially related to type II interferon and DNA damage response signaling, when compared with wildtype microglia, in response to LPS. We also detected discrete signatures in human PARK7/DJ-1 mutant iPSC-derived microglia and BMDMs from PARK7/DJ-1 KO mice. These specific transcriptional signatures were reflected at the morphological level, with microglia in LPS-treated PARK7/DJ-1 KO mice showing a less amoeboid cell shape compared to wildtype mice, both at 6 and 24 h after acute inflammation, as also observed in BMDMs.ConclusionsTaken together, our results show that, under inflammatory conditions, PARK7/DJ-1 deficiency skews microglia towards a distinct phenotype characterized by downregulation of genes involved in type II interferon signaling and a less prominent amoeboid morphology compared to wildtype microglia. These findings suggest that the underlying oxidative stress associated with the lack of PARK7/DJ-1 affects microglia neuroinflammatory responses, which may play a causative role in PD onset and progression.

RNF213 promotes Treg cell differentiation by facilitating K63-linked ubiquitination and nuclear translocation of FOXO1

Autoreactive CD4+ T helper cells are critical players that orchestrate the immune response both in multiple sclerosis (MS) and in other neuroinflammatory autoimmune diseases. Ubiquitination is a posttranslational protein modification involved in regulating a variety of cellular processes, including CD4+ T cell differentiation and function. However, only a limited number of E3 ubiquitin ligases have been characterized in terms of their biological functions, particularly in CD4+ T cell differentiation and function. In this study, we found that the RING finger protein 213 (RNF213) specifically promoted regulatory T (Treg) cell differentiation in CD4+ T cells and attenuated autoimmune disease development in an FOXO1-dependent manner. Mechanistically, RNF213 interacts with Forkhead Box Protein O1 (FOXO1) and promotes nuclear translocation of FOXO1 by K63-linked ubiquitination. Notably, RNF213 expression in CD4+ T cells was induced by IFN-β and exerts a crucial role in the therapeutic efficacy of IFN-β for MS. Together, our study findings collectively emphasize the pivotal role of RNF213 in modulating adaptive immune responses. RNF213 holds potential as a promising therapeutic target for addressing disorders associated with Treg cells.

Systemic inflammatory markers in ageing, Alzheimer's disease and other dementias.

Systemic inflammation with alterations in inflammatory markers is involved in aging and Alzheimer's disease. However, few studies have investigated the longitudinal trajectories of systemic inflammatory markers during aging and Alzheimer's disease, and specific markers contributing to Alzheimer's disease remain undetermined. In this study, a longitudinal cohort (cohort 1: n = 290; controls, 136; preclinical Alzheimer's disease, 154) and a cross-sectional cohort (cohort 2: n = 351; controls, 62; Alzheimer's disease, 63; vascular dementia, 58; Parkinson's disease dementia, 56; behavioural variant frontotemporal dementia, 57; dementia with Lewy bodies, 55) were included. Plasma levels of inflammatory markers were measured every 2 years during a 10-year follow-up in the longitudinal cohort and once in the cross-sectional cohort. The study demonstrated that the inflammatory markers significantly altered during both aging and the development of Alzheimer's disease. However, only complement C3, interleukin-1β, and interleukin-6 exhibited significant changes in participants with preclinical Alzheimer's disease, and their longitudinal changes were significantly associated with the development of Alzheimer's disease compared to controls over the 10-year follow-up. In the cross-sectional cohort, complement C3 demonstrates specificity to Alzheimer's disease, while interleukin-1β and interleukin-6 were also altered in other dementias. The study provides a new perspective on the involvement of inflammatory markers in the aging process and the development of Alzheimer's disease, implying that regulating inflammation may have a pivotal role in promoting successful aging and in the prevention and treatment of Alzheimer's disease.

The effect of vitamin D on the development of Hashimoto's disease and the reduction of the inflammatory process in its course - review

Introduction Hashimoto's disease is an autoimmune chronic lymphocytic thyroiditis. It is a common condition, more frequent in women. Its diagnosis is based on the presence of specific antithyroid antibodies in the patient's blood which lead to the destruction of the thyroid gland. This can result in the development of hypothyroidism, requiring levothyroxine replacement therapy. Aim of the review A summary of the information gathered so far on the involvement of vitamin D in the development and course of Hashimoto's disease. Results The articles analyzed have mixed results. Most of them show a positive correlation between vitamin D and Hashimoto's disease, paying particular attention to the contribution of vitamin D in moderating the inflammatory process in HT. Other studies show significant differences in vitamin D levels between groups with different HT severity. Others show a negative correlation between vitamin D levels and the development of Hashimoto's disease. Conclusions Large well-controlled randomized double blind trials are needed in order to determine the exact role of vitamin D in Hashimoto’s disease.

Perindopril and losartan affect ACE-2 and IL-6 expression in obese rat model

Obesity has emerged as a worldwide health concern due to its increasing prevalence. Adipocytes have the ability to express angiotensin-converting enzyme 2 receptors (ACE2) and several adipocytokines. These expressions could lead to the activation of a cytokine storm, which in turn promotes the development of cardiovascular diseases. The aim of this study was to investigate the impact of perindopril and losartan exposure on the ACE2 and interleukin 6 (IL-6) levels in adipocyte cells. This study used an in vivo true experimental design utilizing a post-test-only control group. A total of 24 adult male albino rats were divided into four groups, one group served as the non-obese (negative control), while the other three groups were obese: (1) the positive control (untreated obese rats); (2) perindopril group (2 mg/kg BW/day orally for 4 weeks); and (3) losartan group (20 mg/kg BW/day for 4 weeks). Afterwards, the rats were euthanized, and the visceral fat tissue were obtained during dissection. The levels of ACE2 and IL-6 were measured using the enzyme-linked immunosorbent assay (ELISA). Losartan administration in obese rats resulted in a notable elevation in ACE2 levels compared to both the perindopril group (losartan vs perindopril, p=0.011) and the positive control (p=0.004). In addition, the treatment of perindopril and losartan in obese rats resulted in a significant reduction in IL-6 levels when compared to the positive control (perindopril vs positive control, p=0.020; losartan vs positive control, p=0.002, respectively). This study provides insight into the administration of perindopril and losartan, which could suppress the pro-inflammatory (IL-6) but increase the ACE2 levels in adipose tissue.

Assessment of the impact of physical and chemical factors of the production environment on the morphological state of target organs in an animal experiment

The study of the morphological state of target organs of outbred (nonlinear) laboratory mice ICR (CD-1), which were under prolonged dynamic influence of physical and chemical factors of the production environment under model conditions, is of wide research interest, as it allows to assess the impact of these factors at the tissue and cellular level and to identify the presence of pathological changes in relation to the group control that was not exposed to the studied factors of the production environment during the 90-day experiment, which has clinical and practical significance. When assessing the 90-day dynamics (from 0 days – 6 months (background) to 30–60–90 days – 7–8–9 months) of the impact of environmental factors on the morphological state of tissues and organs of outbred (nonlinear) laboratory mice ICR (CD-1), generally accepted and unified methods were used. Animals (weighing 45–50 gr., sexually mature age – 6 months) were divided into 3 experimental groups (vibration exposure, noise exposure, chemical exposure) of 30 individuals each (15 females and 15 males) and 1 control group (15 females and 15 males), kept in standard comfortable conditions, and not exposed to the factors of the production environment. The experiment was conducted in accordance with the rules adopted by the European Convention for the Protection of Animals Used for Experimental Scientific Purposes (Strasbourg, 1986), after approval by the Ethical commission of the Novosibirsk Research Institute of Hygiene of Rospotrebnadzor. Statistical processing of the research materials was carried out using standard Statistica 10.0 application programs. The morphological analysis of the target organs of experimental animals revealed the presence of a complex of pathological changes in the 90-day dynamics of the impact of factors of the production environment, compared with the morphological state of the organs in the control group. The results obtained have clinical and practical significance, as they allow us to justify preventive measures aimed at preventing the negative impact of long-term production factors on the labor contingent. Further study of the morphological state of target organs of ICR laboratory mice exposed to prolonged dynamic exposure to physical and chemical factors of the production environment under model conditions will contribute to the establishment of mechanisms for the development of occupational diseases and the development of scientifically based medical and hygienic measures aimed at preserving the health of the labor contingent in the management of labor longevity.

CISD2 regulates oxidative stress and mitophagy to maintain the balance of the follicular microenvironment in PCOS

ABSTRACT Objectives To observe the CISD2 expression among PCOS patients and to explore its profound impact on the follicular microenvironment. Moreover, we want to elucidate the intricate mechanistic contribution of CISD2 to the onset and progression of PCOS. Methods Oxidase NOX2, mitophagy-related proteins, and CISD2 were detected by WB. The changes in mitochondrial structure and quantity were observed by transmission electron microscopy. Mitochondrial and lysosome colocalization was used to detect the changes of mitophagy. MDA kit, GSH and GSSG Assay kit and ROS probe were used to detect oxidative stress damage. Results We found that CISD2, mitophagy and oxidase in the GCs of PCOS patients were significantly increased. Testosterone stimulation leads to the increase of oxidase, mitophagy, and CISD2 in KGN cells. CISD2 inhibition promoted the increase of mitophagy, and the activation of mitochondria-lysosome binding, while alleviating the oxidative stress. Conclusions Inhibition of CISD2 can improve the occurrence of oxidative stress by increasing the level of mitophagy, thus affecting the occurrence and development of PCOS diseases.

Interrelationship between thyroid hormones and reduced renal function, a review article

BackgroundUnderstanding the relationship of thyroid hormones with the development of chronic kidney disease (CKD) has important clinical implications for managing patients with both thyroid and kidney dysfunction. In this review, our purpose was to provide a thorough comprehension of the interplay between thyroid hormones, thyroid dysfunctions, and CKD.SummaryWhile there is evidence linking thyroid hormone levels to renal diseases, the association between thyroid hormones, specifically within the normal range, and the risk of CKD incidence is still a subject of debate. The Google Scholar, PubMed, Scopus, and Web of Science, were searched using the medical subject heading (MeSH) terms for the relevant keywords up to December 2023.ConclusionBased on the review, the development of CKD is more consistently associated with higher serum TSH and thereafter lower serum free T3 levels; however, its association with free T4 is more controversial. Furthermore, subclinical and overt hypothyroidisms were considerably associated with incident CKD. Hyperthyroidism and Hashimoto thyroiditis might increase the risk of CKD.

The concentration of P-selectin in the blood serum of patients with chronic kidney disease

BACKGROUND. Endothelial dysfunction (ED) plays an important role in the development and progression of chronic kidney disease (CKD). However, there is insufficient information in the literature on changes in the expression of vascular wall endothelial adhesive molecules in patients with kidney disease.THE AIM: to study the content of P-selectin in the blood of patients with CKD and to evaluate its effect on the development of ED and atherosclerotic changes.PATIENTS AND METHODS. 128 patients with CKD (41% of men and 59% of women) were monitored, with an average age of 63.5±1.7 years. The diagnosis of CKD was made in accordance with the recommendations of KDIGO (2012). The concentration in serum of P-selectin was determined by solid-phase enzyme immunoassay using a set of reagents "Cloud-Clone Corp. P-selectin ELISA" (China).RESULTS. All patients were divided into 6 groups depending on the stage of CKD. In CKD C1 - C3a stage, an increase in the concentration of P-selectin in blood serum was revealed. Starting from the C3b stage of CKD, the values of P-selectin begin to decrease significantly, especially sharply at the C5d stage.CONCLUSION. An increase in the concentration of P-selectin in blood serum can serve as an indication for in-depth dynamic monitoring of coagulogram and lipidogram parameters, a decrease in the concentration of P-selectin in blood serum is highly likely to indicate adverse changes in the geometry of the arterial bed. In this regard, it is advisable to determine the pulse wave velocity and the Agatston index.

Gut microbial factors predict disease severity in a mouse model of multiple sclerosis.

Gut bacteria are linked to neurodegenerative diseases but the risk factors beyond microbiota composition are limited. Here we used a pre-clinical model of multiple sclerosis (MS), experimental autoimmune encephalomyelitis (EAE), to identify microbial risk factors. Mice with different genotypes and complex microbiotas or six combinations of a synthetic human microbiota were analysed, resulting in varying probabilities of severe neuroinflammation. However, the presence or relative abundances of suspected microbial risk factors failed to predict disease severity. Akkermansia muciniphila, often associated with MS, exhibited variable associations with EAE severity depending on the background microbiota. Significant inter-individual disease course variations were observed among mice harbouring the same microbiota. Evaluation of microbial functional characteristics and host immune responses demonstrated that the immunoglobulin A coating index of certain bacteria before disease onset is a robust individualized predictor of disease development. Our study highlights the need to consider microbial community networks and host-specific bidirectional interactions when aiming to predict severity of neuroinflammation.

Reactivation of hepatitis B virus infection – an important aspect of multifaceted problem

In this editorial we comment on the article published in the recent issue of the World Journal of Gastroenterology . We focus specifically on the problem of occult hepatitis B virus (HBV) infection, that is a result of previous hepatitis B (PHB) and a source for reactivation of HBV. The prevalence of PHB is underestimated due to the lack of population testing programs. However, this condition not only complicate anticancer treatment, but may be responsible for the development of other diseases, like cancer or autoimmune disorders. Here we unveil possible mechanisms responsible for realization of these processes and suggest practical approaches for diagnosis and treatment.

Characterization of obesity-related diseases and inflammation using single cell immunophenotyping in two different diet-induced obesity models.

Obesity is a growing problem worldwide and a major risk factor for many chronic diseases. The accumulation of adipose tissue leads to the release of significant amounts of pro-inflammatory cytokines and adipokines, resulting in a low-grade systemic inflammation. However, the mechanisms behind the development of obesity-related diseases are not fully understood. Therefore, our study aimed to investigate the pathological changes and inflammatory processes at systemic level and in individual organs in two different diet-induced mouse obesity models. Male C57BL6/J mice were fed by high-fat diet (HFD), high-fat/high-fructose diet (HFD + FR) or normal chow for 21 weeks starting at 3 months of age (n = 15 animals/group). Insulin resistance was tested by oral glucose tolerance test. Pathological changes were investigated on hematoxylin-eosin-stained liver and brown adipose tissue sections. The gene expression levels of adipokines and cytokines were analyzed by qPCR in adipose tissues, whereas serum protein concentrations were determined by multiplex immunoassays. Immunophenotyping of isolated blood, bone marrow and spleen cells was performed by single-cell mass cytometry. Weight gain, glucose intolerance and hepatic steatosis were more severe in the HFD + FR group than in the control and HFD groups. This was accompanied by a higher level of systemic inflammation, as indicated by increased expression of pro-inflammatory genes in visceral white adipose tissue and by a higher serum TNFα level. In addition, immunophenotyping revealed the increase of the surface expressions of CD44 and CD69 on various cell types, such as CD8+ and CD4 + T-cells, B-cells and macrophages, in animals with obesity. The combination of HFD with fructose supplementation promotes more properly the symptoms of metabolic syndrome. Therefore, the combined high-fat/high-fructose nutrition can be a more suitable model of the Western diet. However, despite these differences, both models showed immunophenotypic changes that may be associated with increased risk of obesity-related cancer.

Reactivation of hepatitis B virus infection – an important aspect of multifaceted problem

In this editorial we comment on the article published in the recent issue of the World Journal of Gastroenterology . We focus specifically on the problem of occult hepatitis B virus (HBV) infection, that is a result of previous hepatitis B (PHB) and a source for reactivation of HBV. The prevalence of PHB is underestimated due to the lack of population testing programs. However, this condition not only complicate anticancer treatment, but may be responsible for the development of other diseases, like cancer or autoimmune disorders. Here we unveil possible mechanisms responsible for realization of these processes and suggest practical approaches for diagnosis and treatment.