Inflammatory Illness Research Articles

Value of ischemia-modified albumin in ankylosing spondylitis

Background/Aim: Ankylosing spondylitis (AS) is a chronic inflammatory illness with a poorly known pathogenesis. Current biomarkers that are used to estimate inflammation are normal in some patients despite having active disease. Recent studies have revealed that oxidative stress may have a role in AS and that there is a close relationship between oxidative stress and inflammation. Ischemia-modified albumin (IMA) is a promising new biomarker for oxidative stress. Thus, the aim of this study was to assess IMA levels and their relationship with disease activity and other inflammatory markers in patients with AS. Methods: This prospective case-control study included 48 patients with AS and 25 healthy controls (HCs). The measured serum levels of IMA, interleukin (IL)-17, and IL-23 were compared between patients with AS and the HC group. We also analyzed the correlation between IMA and disease activity, acute phase reactants, and HLA-B27 positivity. The Ankylosing Spondylitis Disease Activity Score with C-Reactive Protein (ASDAS-CRP) and the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) were used to determine disease activity. Results: There was no difference in serum IMA levels between the AS and HC groups (25.08 [20.49-46.83] vs. 29.89 [29.89-42.0], P=0.146). Only IL-23 was significantly higher in patients with AS (10.81 [7.25-14.06] vs. 7.95 [6.85-10.46], P=0.039). Furthermore, there was no correlation between IMA and IL-23, IL-17, CRP, ESR, BASDAI, or ASDAS-CRP (r=-0.079, P=0.593; r=-0.043, P=0.771; r=-0.018, P=0.906; r=0.047, P=0.751; r=0.281, P=0.053; r=0.162, P=0.271). There was no significant difference between IMA, IL-17, and IL-23 levels in patients with low disease activity (BASDAI <4, ASDAS-CRP <2.1) and high disease activity (BASDAI ≥4, ASDAS-CRP ≥2.1) (BASDAI: P=0.146, P=0.303, P=0.071, and ASDAS-CRP: P=0.451, P=0.410, P=0.324, respectively). There was no difference in IMA levels between HLA-B27-positive patients and HLA-B27-negative patients (P=0.070). Conclusion: Although oxidative stress has been suggested to play a role in AS pathogenesis, we did not find an increase in serum levels of IMA, an oxidative stress biomarker, in patients with AS. Our results suggest that IMA may not be a reliable indicator of inflammation. Further research is needed to determine whether IMA may have a role as a biomarker in AS.

Identification of potential drug targets for rheumatoid arthritis from genetic insights: a Mendelian randomization study

IntroductionRheumatoid arthritis (RA) is a chronic inflammatory illness that mostly affects the joints of the hands and feet and can reduce life expectancy by an average of 3 to 10 years. Although tremendous progress has been achieved in the treatment of RA, a large minority of patients continue to respond poorly to existing medications, owing in part to a lack of appropriate therapeutic targets.MethodsTo find therapeutic targets for RA, a Mendelian randomization (MR) was performed. Cis-expression quantitative trait loci (cis-eQTL, exposure) data were obtained from the eQTLGen Consortium (sample size 31,684). Summary statistics for RA (outcome) were obtained from two largest independent cohorts: sample sizes of 97,173 (22,350 cases and 74,823 controls) and 269,377 (8279 cases and 261,098), respectively. Colocalisation analysis was used to test whether RA risk and gene expression were driven by common SNPs. Drug prediction and molecular docking was further used to validate the medicinal value of drug targets.ResultsSeven drug targets were significant in both cohorts in MR analysis and supported by localization. PheWAS at the gene level showed only ATP2A1 associated with other traits. These genes are strongly associated with immune function in terms of biological significance. Molecular docking showed excellent binding for drugs and proteins with available structural data.ConclusionThis study identifies seven potential drug targets for RA. Drugs designed to target these genes have a higher chance of success in clinical trials and is expected to help prioritise RA drug development and save on drug development costs.

Biological sex is associated with heterogeneous responses to IL-6 receptor inhibitor treatment in COVID-19—A retrospective cohort study

COVID-19 is associated with higher inflammatory markers, illness severity and mortality in males compared to females. Differences in immune responses to COVID-19 may underpin sex- specific outcome differences. We hypothesised that anti-IL-6 receptor monoclonal antibodies are associated with heterogenous treatment effects between male and female patients. We conducted a retrospective cohort study assessing the interaction between biological sex and anti-IL-6 receptor antibody treatment with respect to hospital mortality or progression of respiratory failure. We used a Cox proportional hazards regression model to adjust for age, ethnicity, steroid use, baseline C-reactive protein, and COVID-19 variant. We included 1274 patients, of which 58% were male and 15% received anti-IL-6 receptor antibodies. There was a significant interaction between sex and anti-IL-6 receptor antibody use on progression to respiratory failure or death (p = 0.05). For patients who did not receive anti-IL-6 receptor antibodies, the risk of death was slightly higher in males (HR = 1.13 (0.72–1.79)), whereas in patients who did receive anti-IL-6 receptor antibodies, the risk was lower in males (HR = 0.65 (0.32–1.33)). There was a heterogenous treatment effect with anti-IL-6 receptor antibodies between males and females; with anti-IL-6 receptor antibody use having a greater benefit in preventing progression to respiratory failure or death in males (p = 0.05).

The Role of CX3CL1-CX3CR1 Axis, C3, C4 & ESR Abs in pathogenicity of Iraqi patients with SLE

Background: Systematic Lupus erythematosus (SLE) has been described as a chronic inflammatory illness where chemokines play an essential role in its pathogenesis CX3CL1and CX3CR1 are chemokines that described their crucial role in immune response in SLE patients. Aim of the study: To evaluate the serum level of CX3CL1- CX3CR1, C3, C4 & ESR Abs in SLE patients without treatment and compare their level with those under treatment (hydroxychloroquine,predeslone 5-20mg, D3). Patients collecting and Methods: 120 females with SLE and healthy, with ages ranging between 20-40 years, were involved in this investigation from Medical City (Consultant of Arthritis, Consultant of Dermatology, Lobby of Hematology and Arthritis)/ Baghdad Teaching Hospital and from Al-Imameen Al-Kazimeen Teaching Hospital from August 26 to October 18, 2021. The samples included 80females with SLE (40 females as early diagnosed patients (G2) without treatment, 40 females as patients that received treatment subjects (hydroxychloroquine, predeslone 5-20mg, D3) (G3), while the control group included 40 healthy females (G1). Five mL of venous blood were obtained from patients and healthy females for measuring C3, C4, ESR and serum levels of CX3CL1 and CX3CR1, which were measured using the ELISA method. Results: Our findings demonstrated a significant increase in the serum levels of CX3CL1, CX3CR1, and ESR. Also, there were significant decreases in serum levels of C3 and C4 in SLE patients (with and without treatment) compared to the control group, and a significant difference was detected between SLE patients without treatment and patients receiving treatment. Conclusion: Based on our results, CX3CL1 and CX3CR1 chemokines may have a role in the pathogenesis of SLE as they are increased in SLE patients. In addition, serum CX3CL1 levels can be used as an independent biomarker of SLE activity. Furthermore, low levels of c3 and c4 and high levels of ESR are considered diagnostic indicators of SLE disease in people. Keywords: Systemic lupus erythematosus, CX3CL1; CX3CR1. C3,C4

Scope of Homoeopathy in Pelvic Inflammatory Disease

Pelvic inflammatory disease (PID) is an infectious and inflammatory ailment of the upper female genital tract, which includes the uterus, fallopian tubes, and associated pelvic tissues. In India, the prevalence of pelvic inflammatory disease ranges between 1 and 2%. N gonorrhoeae and C trachomatis are the organisms most usually isolated in instances of acute PID. Homoeopathic treatments are beneficial in the treatment of both acute and chronic pelvic inflammatory illness, as well as in preventing additional complications. Keywords: Pelvic inflammatory disease, PID, Homoeopathy

Anandamide reduces the migration of lymphocytes to the intestine by CB2 activation and reduces TNF-α in the target organs, protecting mice from graft-versus-host disease

Graft-versus-host disease (GVHD) is a serious inflammatory illness that often occurs as a secondary complication of bone marrow transplantation. Current therapies have limited effectiveness and fail to achieve a balance between inflammation and the graft-versus-tumor effect. In this study, we investigate the effects of the endocannabinoid anandamide on the complex pathology of GVHD. We assess the effects of an irreversible inhibitor of fatty acid amine hydrolase or exogenous anandamide and find that they increase survival and reduce clinical signs in GVHD mice. In the intestine of GVHD mice, treatment with exogenous anandamide also leads to a reduction in the number of CD3+, CD3+CD4+, and CD3+CD8+ cells, which reduces the activation of CD3+CD4+ and CD3+CD8+ cells, as assessed by enhanced CD28 expression, a T cell co-stimulatory molecule. Exogenous AEA was also able to reduce TNF-α and increase IL-10 in the intestine of GVHD mice. In the liver, exogenous AEA reduces injury, TNF-α levels, and the number of CD3+CD8+ cells. Interestingly, anandamide reduces Mac-1α, which lowers the adhesion of transplanted cells in mesenteric veins. These effects are mimicked by JWH133—a CB2 selective agonist—and abolished by treatment with a CB2 antagonist. Furthermore, the effects caused by anandamide treatment on survival were related to the CB2 receptor, as the CB2 antagonist abolished it. This study shows the critical role of the CB2 receptor in the modulation of the inflammatory response of GVHD by treatment with anandamide, the most prominent endocannabinoid.

Serum Cytokine Profiles in Patients with Rheumatoid Arthritis Before and After Treatment with Methotrexate.

Rheumatoid arthritis (RA) is an inflammatory autoimmune illness affecting around 1% of the population globally. Cytokines have a crucial role in the pathogenesis of RA. The objectives of the present study were to compare the serum cytokine profiles between methotrexate (MTX)-treated and MTX-naive RA patient groups, MTX-treated RA patient group and healthy controls, and MTX-naive RA patient group and healthy controls. Enzyme linked immunosorbent assay (ELISA) kits were used to quantify the serum concentrations of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-17, IL-6, interferon-gamma (IFN-γ), and IL-10 in 80 RA patients (48 MTX treated and 32 MTX naive) and 80 healthy controls. For all cytokine assays, absorbance was measured at 450 nm using a microplate reader (Bio-Rad). Independent sample t-test was used to compare the serum cytokine concentrations between the study groups using SPSS version 25. MTX-treated RA patient group had significantly reduced serum levels of TNF-α (36.13 ± 17.64 versus 45.82 ± 23.07, *P = 0.037), IL-17 (307.85 ± 151.74 versus 435.42 ± 241.19, **P = 0.006), and IFN-γ (414.93 ± 212.13 versus 527.15 ± 269.61, *P = 0.041) compared to MTX-naive RA patients. Both MTX-treated and MTX-naive RA patient groups had significantly high serum levels of TNF-α, IL-1β, IL-17, IL-6, IFN-γ, and IL-10 when compared to healthy controls (***P < 0.001). Downregulation of the serum concentrations of certain key cytokines, viz. TNF-α, IL-17, and IFN-γ, demonstrates the anti-inflammatory effect of MTX in RA patients.

Computational Design of Potent and Selective d-Peptide Agonists of the Glucagon-like Peptide-2 Receptor.

Here, we designed three d-GLP-2 agonists that activated the glucagon-like peptide-2 receptor (GLP-2R) cyclic adenosine monophosphate (cAMP) accumulation without stimulating the glucagon-like peptide-1 receptor (GLP-1R). All the d-GLP-2 agonists increased the protein kinase B phosphorylated (p-AKT) expression levels in a time- and concentration-dependent manner in vitro. The most effective d-GLP-2 analogue boosted the AKT phosphorylation 2.28 times more effectively compared to the native l-GLP-2. The enhancement in the p-AKT levels induced by the d-GLP-2 analogues could be explained by GLP-2R's more prolonged activation, given that the d-GLP-2 analogues induce a lower β-arrestin recruitment. The higher stability to protease degradation of our d-GLP-2 agonists helps us envision their potential applications in enhancing intestinal absorption and treating inflammatory bowel illness while lowering the high dosage required by the current treatments.

Network pharmacology and molecular docking reveal the mechanism of Qinghua Xiaoyong Formula in Crohn's disease.

Crohn's disease (CD) is a chronic inflammatory illness of the digestive system with unknown etiology, and its incidence is increasing worldwide. However, there are currently no effective treatments or medications available for individuals with CD. Therefore, novel therapeutic strategies are urgently needed. The bioactive compounds and targets associated with compounds of Qinghua Xiaoyong Formula (QHXYF) were examined using The Traditional Chinese Medicine Systems Pharmacology database, and 5 disease target databases were also used to identify CD-related disease targets. A total of 166 overlapping targets were identified from QHXYF-related and CD-related disease targets and they were found to be enriched in oxidative stress-related pathways and the PI3K/AKT signaling pathway. Molecular docking was then used to predict how the bioactive compounds would bind to the hub targets. It was found that quercetin could be the core bioactive compound and had good binding affinity to the top 5 hub targets. Finally, animal experiments were performed to further validate the findings, and the results revealed that QHXYF or quercetin inhibited 2,4,6-trinitrobenzenesulfonic acid-induced inflammation and oxidative stress processes by inhibiting the PI3K/AKT pathway, thereby improving CD symptoms. These findings suggest that QHXYF and quercetin may be potential novel treatments for CD.

Novel gonorrhea strain in the United States of America leading to increase of sexually transmitted diseases load: is it an outcome of inexorable process of developing antibiotic resistance?

Novel gonorrhea strain in the United States of America leading to increase of sexually transmitted diseases load: is it an outcome of inexorable process of developing antibiotic resistance?

Effect of Calcitriol Treated Mesenchymal Stem Cells as an Immunomodulation Micro-environment on Allergic Asthma in a Mouse Model.

Allergic asthma is a chronic inflammatory illness of the respiratory system characterized by an increase in the number of inflammatory cells in the airways and trouble breathing. Mesenchymal stem cells (MSCs) have the potential to be used in inflammatory diseases as a cellular immunosuppressive treatment. They express calcitriol receptors and communicate with other immunocytes, which increases their anti-inflammatory activity. This study aimed to determine the effects of calcitriol-treated MSC treatment on allergic asthma pathways in a mouse model. To generate a mouse model of asthma, the mice were sensitized intraperitoneally with ovalbumin (OVA) and aluminum hydroxide emulsion and then challenged intra-nasally with OVA. On day 14, experimental mice received tail vein injections of calcitriol-treated MSCs in PBS prior to allergen exposure. The cytokines assays including IL-4, 10, 12, 17, TGF-β and IFN-γ, splenocytes proliferation, and histological examination of lungs samples were performed. The mice were sensitized with OVA and the response to dexamethasone treatment was compared. Calcitriol-treated MSCs significantly increased the levels of IL-12, TGF-β, and IFN-γ compared to non-treated MSCs groups. Moreover, calcitriol-treated and non-treated MSCs significantly decreased IL-4 and IL-17 compared to asthmatic groups. The results of the histopathological examination showed that calcitriol-treated MSCs reduced the accumulation of inflammatory cells and bronchial wall thickening in comparison with the asthma group. Using the allergic asthma model, we were able to show that calcitriol-treated MSCs had an inhibitory impact on airway inflammation. Our findings suggest that the injection of calcitrioltreated MSCs may be a viable treatment option for allergic asthma.

Difenoconazole disrupts carp intestinal physical barrier and causes inflammatory response via triggering oxidative stress and apoptosis

As a common fungicide, difenoconazole (DFZ) is widespread in the natural environment and poses many potential threats. Carp makes up a significant proportion of China's freshwater aquaculture population and are vulnerable to the DFZ. Therefore, this study investigated the effects of DFZ (0.488 mg/L and 1.953 mg/L) exposure for 4 d on the intestinal tissues of carp and explored the mechanisms. Specifically, DFZ exposure caused pathological damage to the intestinal tissues of carp, reducing the expression levels of intestinal tight junction proteins, and leading to damage to the intestinal barrier. In addition, DFZ exposure activated the NF-κB signaling pathway, increasing the levels of pro-inflammatory factors (TNF-α, IL-1β, IL-6) and decreasing the levels of anti-inflammatory factors (IL-10, TGF-β1). As disruption of the intestinal barrier is closely linked to oxidative stress and apoptosis, we have conducted research in both areas for this reason. The results showed that DFZ exposure elevated reactive oxygen species in carp intestines, decreased antioxidant enzyme activity, and suppressed the expression of oxidative stress-related genes. TUNEL results showed that DFZ induced the onset of apoptosis. In addition, the expression levels of apoptosis-related genes and proteins were examined. Western blotting results showed that DFZ could upregulate the protein expression levels of Bax, Cytochrome C and downregulate the protein levels of Bcl-2. qPCR results showed that DFZ could upregulate the transcript levels of Bax, Caspase-3, Caspase-8 and Caspase-9 and downregulate the transcript levels of Bcl-2 transcript levels. This suggests that DFZ can induce apoptosis of mitochondrial pathway in carp intestine. In conclusion, DFZ can induce oxidative stress and apoptosis in carp intestine, leading to the destruction of intestinal physical barrier and the occurrence of inflammation. Our data support the idea that oxidative stress and apoptosis are important triggers of pesticide-induced inflammatory bowel illness.

"Medicine food homology" plants promote periodontal health: antimicrobial, anti-inflammatory, and inhibition of bone resorption.

"Medicine food homology" (MFH) is a term with a lengthy history. It refers to the fact that a lot of traditional natural products have both culinary and therapeutic benefits. The antibacterial, anti-inflammatory and anticancer effects of MFH plants and their secondary metabolites have been confirmed by numerous research. A bacterially generated inflammatory illness with a complicated pathophysiology, periodontitis causes the loss of the teeth's supporting tissues. Several MFH plants have recently been shown to have the ability to prevent and treat periodontitis, which is exhibited by blocking the disease's pathogens and the virulence factors that go along with them, lowering the host's inflammatory reactions and halting the loss of alveolar bone. To give a theoretical foundation for the creation of functional foods, oral care products and adjuvant therapies, this review has especially explored the potential medicinal benefit of MFH plants and their secondary metabolites in the prevention and treatment of periodontitis.

Role of the SARS‑COV2 infection in the evolution of acute pancreatitis (Review).

Acute pancreatitis is characterized as an inflammatory illness that is life-threatening and causes necrosis as well as simple edema when pancreatic enzymes are activated intraglandularly. It is not known whether severe acute respiratory syndrome coronavirus 2 causes acute pancreatitis. Patients with acute pancreatitis who test positive for coronavirus disease 2019 (COVID-19) frequently have biliary or alcoholic causes. It is unclear how common acute pancreatitis is in patients with COVID-19. By contrast with patients without COVID-19, however, COVID-19-positive patients with acute pancreatitis have a higher mortality as well as a higher risk of necrosis and admission to an intensive care unit. The most common cause of mortality in COVID-19-positive individuals with concurrent severe pancreatitis is acute respiratory distress syndrome. The present study discussed research on the link between COVID-19 infection and acute pancreatitis.

TLR5 Signaling in the Regulation of Intestinal Mucosal Immunity.

Toll-like receptor 5 (TLR5) is a pattern recognition receptor that specifically recognizes flagellin and consequently plays a crucial role in the control of intestinal homeostasis by activating innate and adaptive immune responses. TLR5 overexpression, on the other hand, might disrupt the intestinal mucosal barrier, which serves as the first line of defense against harmful microbes. The intestine symbiotic bacteria, mucous layer, intestinal epithelial cells (IECs), adherens junctions (such as tight junctions and peripheral membrane proteins), the intestinal mucosal immune system, and cytokines make up the intestinal mucosal barrier. Impaired barrier function has been linked to intestinal illnesses such as inflammatory bowel disease (IBD). IBD is a persistent non-specific inflammatory illness of the digestive system with an unknown cause. It is now thought to be linked to infection, environment, genes, immune system, and the gut microbiota. The significance of immunological dysfunction in IBD has received more attention in recent years. The purpose of this paper is to explore TLR5's position in the intestinal mucosal barrier and its relevance to IBD.

Comparison of Serum Levels of SIL-2R, IL-6, IL-10, TNF-α, CRP, ESR and Fibrinogen in Patients with Active and Inactive Behçet’s Disease

Behçet's disease (BD) is a chronic inflammatory illness that affects the entire body and is characterized by recurring episodes of oral aphthae, ocular and cutaneous lesions, and scrotal or vaginal ulcerations. The involvement of other organs and systems increases mortality in addition to the significant morbidity. This study involved a total of 40 participants, 20 of whom were healthy controls and 20 of whom were patients (of the 20 Behçet's patients, 12 (60%) were in the active phase and 8 (40%) were in the inactive phase). There was no therapy being given to any of the 20 patients that would have affected their cytokine levels. Only young men made up the patient and control groups because both early onset and male sex are signs of poor prognosis. The ELISA method was used to measure the levels of serum cytokines. The statistical analysis of the derived numerical values employed the Mann-Whitney U Test. We found a significant correlation between serum cytokine levels and classical acute phase markers in active Behçet’s patients. ESR (P &lt; 0,001), CRP (P &lt; 0,001), fibrinogen (P &lt; 0,001), IL-10 (P &lt; 0,001), IL-6 (P &lt; 0,001), SIL-2R (P &lt; 0,001) and TNFα (P &lt; 0,001). There was no statistically significant difference in serum levels of classical acute phase markers ESR (P = 0,746), CRP (P = 0,476) and fibrinogen (P = 0,940) when inactive Behçet’s patients and healthy controls were compared. However, serum levels of IL-10 (P &lt; 0,001), IL-6 (P = 0,001), SIL-2R (P &lt; 0,001) and TNFα (P = 0,001) were statistically different between inactive Behcet's patients and the control group. Our research shows that even in the inactive phase, serum cytokine levels of Behçet’s patients are much higher than the healthy control group. However, the levels of ESR, CRP and fibrinogen, which are classical acute phase markers, were found at normal levels in Behçet’s patients in the inactive phase. These findings show that measurement of serum interleukin levels will enable us to take preventive measures for morbidity and mortality follow-up of Behçet's patients.

Menopausal Transition and the Development of Rheumatoid Arthritis An Overview

Rheumatoid arthritis (RA) is a chronic immune-mediated inflammatory illness caused by an accumulation of inflammatory infiltration in the synovial membrane, which leads to the progressive deterioration of joint architecture. Women are three times more likely than men to have RA, with more severe functional loss and disability. The purpose of this review is to study the shifts in the hormonal system brought on by menopause and their potential links with RA. Females are more likely to develop RA as a result of hereditary and environmental interactions of sex hormones and their effects on the immune system. Rapid declines in ovarian function and systemic estrogen have been linked to postmenopausal increases in proinflammatory cytokines such as IL-6, TNF-α, and IL-1β. The majority of the data from the literature review imply that female hormone characteristics that can be influenced by hereditary and environmental variables impact the development of autoimmune illnesses, including RA.

Cross talk between bacterial and human gene networks enriched using ncRNAs in IBD disease

Inflammatory bowel disease (IBD) is a long-term inflammatory immune-mediated gut illness with several extra-intestinal complications. The aims of this study were to identify a novel network-based meta-analysis approach on the basis of the combinations of the differentially expressed genes (DEGs) from microarray data, to enrich the functional modules from human protein–protein interaction (PPI) and gene ontology (GO) data, and to profile the ncRNAs on the genes involved in IBD. The gene expression profiles of GSE126124, GSE87473, GSE75214, and GSE95095 are obtained from the Gene Expression Omnibus (GEO) database based on the study criteria between 2017 and 2022. The DEGs were screened by the R software. DEGs were then used to examine gene ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. The ncRNAs including the miRNAs and ceRNAs were predicted on the PPIs visualized using Cytoscape. Enrichment analysis of genes with differential expression (n = 342) using KEGG and GO showed that the signaling pathways related with staphylococcus aureus and pertussis bacterial infections may stimulate the immune system and exacerbate IBD via the interaction with human proteins including Fibrinogen gamma chain (FGG), Keratin 10 (KRT10), and Toll like receptor 4 (TLR4). By building a ceRNA network, lncRNA XIST and NEAT1 were determined by affecting common miRNAs, hsa-miR-6875-5p, hsa-miR-1908-5p, hsa-miR-186-5p, hsa-miR-6763-5p, hsa-miR-4436a, and hsa-miR-520a-5p. Additionally, the chromosome regions including NM_001039703 and NM_006267, which produce the most potent circRNAs play a significant role in the ceRNA network of IBD. Also, we predicted the siRNAs that would be most effective against the bacterial genes in staphylococcus aureus and pertussis infections. These findings suggested that three genes (FGG, KRT10, and TLR4), six miRNAs (hsa-miR-6875-5p, hsa-miR-1908-5p, hsa-miR-186-5p, hsa-miR-4436a, hsa-miR-520a-5p, and hsa-miR-6763-5p), two lncRNAs (XIST and NEAT1), and chromosomal regions including NM_001039703 and NM_006267 with the production of the most effective circRNAs are involved in the ncRNA-associated ceRNA network of IBD. These ncRNA profiles are related to the described gene functions and may play therapeutic targets in controlling inflammatory bowel disease.

Granuloma annulare with alopecia areata in a 6-year-old girl: a case report

BackgroundDermatologic signs and symptoms can be the manifestations of a single disease or different diseases, and it is proven that some are associated with one another. These connections are not fully understood, but the answer lies in the pathophysiology of each disease.Case presentationWe report the case of a 6-year-old Middle-Eastern girl who presented with two skin lesions on the dorsum of her foot, along with scaling of her soles and palms, face skin discoloration, and areas of patchy alopecia on her scalp. She was diagnosed as a case of acute onset of granuloma annulare with alopecia areata and dermatitis. The treatment regimen for the patient’s scalp consisted of topical minoxidil and betamethasone and three sessions with 1-month intervals of triamcinolone acetonide intralesional injections, which demonstrated modest effectiveness in treating alopecia areata.ConclusionGranuloma annulare is a benign inflammatory illness with no known cause that might be difficult to cure. The clinical course and prognosis might vary greatly depending on the disease subtype, and associating symptoms and diseases, such as alopecia areata, should be considered.

Does depression in mid-life predispose to greater cognitive decline in later life in the Whitehall II cohort?

BackgroundLater-life depression appears to have different symptomatology and possibly underlying pathology to younger adults. Depression is linked to dementia but whether it is a risk factor or an early sign of dementia remains unclear. Neuroinflammation is increasingly recognised in both conditions. AimsTo investigate the link between depression, inflammation and dementia. We hypothesised that recurrent depression increases the rate of cognitive decline in older adults and that this effect is modified by anti-inflammatory medication. MethodsWe used data from Whitehall II including cognitive test results and reliable measures to assess depression. Depression was defined as a self-reported diagnosis or a score of ≥20 on the CESD. The presence/absence of inflammatory illness was assessed using a standardised list of inflammatory conditions. Individuals with dementia, chronic neurological and psychotic conditions were excluded.Logistic and linear regression was used to examine the effect of depression on cognitive test performance and the effect of chronic inflammation. LimitationsLack of clinical diagnoses of depression. ResultsThere were 1063 individuals with and 2572 without depression. Depression did not affect deterioration in episodic memory, verbal fluency or the AH4 test at 15-year follow up. We found no evidence of an effect of anti-inflammatory medication. Depressed individuals had worse cross-sectional performance on the Mill Hill test and tests of abstract reasoning and verbal fluency at both baseline and 15-year follow-up. ConclusionsUsing a UK based study with a long follow-up interval we have shown that depression in individuals aged >50 is not associated with increased cognitive decline.