Allergy & Immunology
Steroid Use, Adrenal Suppression, and Emergency Department Visits in COPD Patients: A Cross-Sectional Study
This study aims to investigate the relationship between steroid use adrenal suppression and frequent emergency department (ED) visits in patients with Chronic Obstructive Pulmonary Disease (COPD).
Systemic glucocorticoids are commonly prescribed in the management of COPD exacerbations; however prolonged or repeated steroid use may lead to adrenal suppression. Although the standard steroid regimen for COPD exacerbations is short-term frequent ED visits may result in cumulative steroid exposure raising concerns about adrenal insufficiency and its clinical consequences.
This study investigates the potential association between steroid-induced adrenal suppression and frequent ED visits among COPD patients. It further examines the impact of steroid administration on cortisol and Adrenocorticotropic hormone (ACTH) levels.
This prospective cross-sectional observational study was conducted in a university-based ED. Patients with COPD with dyspnea and who presented to the ED between 06:00-08:00 were included. Demographics previous presentations to the ED medications used hormone levels and other laboratory results were recorded.
Fifty patients (82% were male) included. Sputum symptoms along with incidences of heart failure were higher in patients who received steroids in the ED. Ronchi was higher crackles and pretibial edema were lower in the patients who received steroids in the ED. Among the patients with low cortisol levels the frequency of patients who received steroids in the ED was higher than those who did not.
Primary healthcare clinicians should monitor COPD patients for potential adrenal insufficiency. Careful regulation of steroid dosages during exacerbation treatment and minimizing polypharmacy are essential to mitigate the long-term effects of prolonged steroid use.
A Rare Case of Ischial Tubercle Pressure Sore with Secondary Periperineal Necrotizing Fasciitis
Perineal necrotizing fasciitis or Fournier's gangrene is a rare but rapidly progressing condition characterized by fascial necrosis. It is a severe potentially life-threatening infection requiring prompt diagnosis and standardized treatment to optimize patient outcomes.
A 48-year-old woman with poorly controlled type 2 diabetes developed necrotizing fasciitis of the right perineum secondary to an ischial tuberosity pressure ulcer. She had a prior spinal cord injury resulting in sensory dysfunction in the lower limbs which masked significant pain. Management included surgical debridement open wound care antimicrobial therapy and a free skin graft for wound closure.
Effective treatment of necrotizing fasciitis relies on aggressive debridement and appropriate antimicrobial therapy. This case highlights the importance of early recognition and intervention to improve clinical diagnostic and management strategies.
Prognostic Value and Immune Characterization of Genes Associated with Childhood Acute Leukemia applying Single-Cell RNA Sequencing
Childhood acute lymphoblastic leukemia (cALL) the most common pediatric hematologic malignancy arises primarily from B-cell origin and is strongly associated with immune dysfunction. This article integrated single-cell and bulk transcriptomic data to identify key B-cell subsets and cALL-related molecules as biomarkers.
Single-cell RNA sequencing (scRNA-seq) Data from 2 pre-B high hyperdiploid (HHD) ALL patients and 3 healthy pediatric bone marrow samples (GSE132509) were utilized for cell clustering using the Seurat package. Functional enrichment pseudo-time trajectory and cell-cell communication analyses were performed using clusterProfiler Monocle2 and CellChat R packages respectively. Bulk RNA-seq data of 511 cALL samples in the TARGET-ALL-P2 cohort were used to construct a prognostic model via Cox and LASSO regression. Immune infiltration differences between different risk groups were analyzed using ESTIMATE MCP-counter and CIBERSORT algorithms.
The scRNA-seq analysis identified five cell subpopulations with B cells demonstrating significant enrichment in cALL samples. Notably the C2 subset was associated with cell proliferation. Ligand-receptor analysis revealed key interactions involving B cell C2. Four marker genes (CENPF IGLL1 ANP32E and PSMA2) were identified to build a risk model. Low-risk patients showed better survival while high-risk patients had higher ESTIMATE scores.
This study examined the key role of B cells in cALL constructed a risk model with strong prognostic predictive ability applying multi-omics analysis and primarily explored its potential mechanism in immune regulation.
This study revealed the critical role of B cells in cALL and the prognostic model showed a high prediction accuracy providing a potential target for individualized treatment of cALL.
Esketamine Reduces Lung Injury Caused by Limb Ischemia-Reperfusion by Regulating Oxidative Stress via the TLR4/NF-κB/NLRP3 Pathway
Esketamine has shown promise in mitigating tissue damage caused by ischemia-reperfusion injury making it a potential therapeutic candidate for acute lung injury (ALI) induced by limb ischemia-reperfusion (LIR-ALI).
This study sought to explore the role and mechanism of esketamine in the LIR-ALI rat model.
The effects of esketamine on the LIR-ALI rats model were evaluated through histopathological examination assessment of pulmonary edema measurement of MDA and SOD levels and analysis of inflammatory cytokine levels (IL-1β etc.) in the bronchoalveolar fluid (BALF) and serum. Western blot analysis was used to assess the expressions of TLR4 NF-κB and NLRP3. TLR4 agonist LPS was used to validate the role of NF-κB/NLRP3 pathway in LIR-ALI.
Esketamine significantly alleviated LIR-induced ALI by reducing pulmonary edema inflammatory cell infiltration and oxidative stress. Elevated MDA content and suppressed SOD activity were significantly reversed by esketamine along with inactivity of the TLR4/NF-κB/NLRP3 pathway. Esketamine treatment reduced inflammatory response in BALF and serum. TLR4 activation by LPS reversed the ameliorative effects of esketamine on LIR-ALI.
Esketamine protected against LIR-induced ALI by mitigating oxidative stress and suppressing the TLR4/NF-κB/NLRP3 axis. These findings highlight the potential therapeutic value of esketamine for ALI.
Single-cell RNA Sequencing Analysis Reveals the Regulatory Functions of Copines Family Genes in Testicular Cancer Progression
The aim of this study is to investigate the expression patterns and regulatory functions of Copines family genes in different cellular subpopulations in testicular cancer based on single-cell data and to analyze the regulatory mechanism of Copines family genes in cancer.
Testicular cancer is a frequently diagnosed male tumor. Emerging evidence suggests that Copines family genes are implicated in a variety of cancer phenotypes and cancer progression. Analyzing the expression pattern of Copines family genes in testicular cancer may help improve the treatment efficacy of the cancer.
This study sought to characterize the expression profiles of Copines family genes in the cellular subpopulations of testicular cancer and to identify key signaling pathways through which they regulate cancer progression.
Based on single-cell transcriptomic data of testicular cancer we classified testicular cancer cell subpopulations and analyzed the expressions of Copines family genes in each subpopulation. Cell subpopulations were grouped according to the expression levels of Copines family genes and differentially expressed Copines family genes between the groups were screened by differential expression analysis. Functional enrichment analysis on the differentially expressed genes (DEGs) was performed with a clusterprofiler package. Functional pathways enriched by the Copines family genes were calculated by AUCell enrichment score. Copy number variation (CNV) analysis was performed using inferCNV to analyze gene mutation patterns across cellular subpopulations and pseudotime analysis was conducted using Monocle to infer cellular differentiation pathways of cellular subpopulations.
Single-cell clustering identified four major cell subpopulations namely NK/T cells tumor cells B cells and macrophages. Notably the control samples had a relatively small proportion of tumor cells. Further clustering of the tumor cells identified six cell subpopulations among which multiple Copines genes especially CPNE1 and CPNE3 showed a high expression. The testicular cancer samples were grouped by the expression patterns of Copines genes and the DEGs between groups included GNLY MGP1 CFD2 CCL21 SPARCL13 as well as some other genes involved in the malignant progression of cancer. Pseudotime analysis showed that the upregulated genes were enriched in cell migration and PI3K-Akt pathway while the downregulated genes were related to immunity. This indicated that the Copines genes regulated the cellular heterogeneity and malignant transformation in testicular cancer.
This study revealed the potential molecular mechanism through which Copines family genes drove the progression of testicular cancer through regulating PI3K-Akt signaling pathway and cell cycle providing a new target for the development of precision treatment targeting Copines family genes and prognostic assessment of the cancer.
Sterile Inflammation and Cell Death Pathways in Liver Ischemia-Reperfusion Injury: A Review and Perspective
Hepatic Ischemia-Reperfusion Injury (IRI) is a critical complication in liver transplantation and resection driven by oxidative stress and sterile inflammation mediated by damage-associated molecular patterns (DAMPs). Current therapeutic challenges arise from interconnected cell death pathways and redundant inflammatory mechanisms.
This review synthesizes mechanistic insights into DAMP signaling and regulated cell death modalities in IRI aiming to identify translational gaps and propose precision-targeted therapies.
A literature search in PubMed using keywords “IRI” “DAMPs” and cell death modes was conducted without date restrictions. Peer-reviewed studies on human/animal models were included with qualitative synthesis of DAMP-cell death interactions.
During ischemia mitochondrial dysfunction releases HMGB1 ATP and mtDNA activating Kupffer cell TLR4/RAGE and cGAS-STING pathways triggering NLRP3 inflammasome- driven cytokine storms. Reperfusion amplifies ROS bursts lipid peroxidation and iron overload creating a self-sustaining cycle of damage. Cell death modalities exhibit spatiotemporal specificity: hepatocyte ferroptosis dominates early injury while macrophage pyroptosis and necroptosis predominate in steatotic livers during late phases. HMGB1 lactylation and mtDNA-cGAS signaling emerge as key regulators. Machine perfusion (e.g. hypothermic oxygenated perfusion) reduces biliary complications via mitochondrial resuscitation outperforming conventional drug-based therapies.
Current single-pathway targeting shows limited efficacy due to IRI’s complexity. Future strategies should integrate temporal targeting (ferroptosis inhibitors pre-reperfusion; pyroptosis blockers post-reperfusion) DAMP-neutralizing agents (anti-HMGB1 antibodies) and precision preservation combining multi-omics biomarkers with ex vivo pharmacological preconditioning. Addressing metabolic vulnerabilities in fatty livers and refining cell death-specific interventions are critical for bridging translational gaps.
Yipishen Xiezhuo Jiedu Decoction in Ameliorating Kidney Damage Through miR-223/NLRP3/Caspase-1 Pathway
Hyperuricemia Nephropathy (HN) is an emerging metabolic disorder that predisposes individuals to Chronic Kidney Disease (CKD) yet effective treatments remain limited. Inflammation plays a pivotal role in HN-induced kidney injury with the NLRP3 inflammasome serving as a central mediator of this process. This study investigates the therapeutic effects of Yipishen Xiezhuo Jiedu Decoction (YPSXZJDD) a traditional Chinese medicine on HN-induced kidney injury through the miR-223/NLRP3/Caspase-1 pathway.
The key active components of YPSXZJDD were screened using UHPLC-Q Exactive Orbitrap-MS and a Protein-Protein Interaction (PPI) network diagram was constructed to explore potential mechanisms of action. The identified components were then utilized to intervene in both cellular and animal models of hyperuricemic nephropathy evaluating their therapeutic effects and underlying mechanisms.
Catalpol and Tanshinone IIA were identified as the key active components of YPSXZJDD. These compounds significantly mitigated renal epithelial cell apoptosis and inflammation by upregulating miR-223 which in turn inhibited the NLRP3/Caspase-1 pathway. The upregulation of miR-223 led to a marked reduction in NLRP3 activity and inflammatory responses thereby alleviating HN-induced kidney damage.
The findings of this study underscore the critical role of miR-223 in regulating the NLRP3 inflammasome and highlight its potential as a therapeutic target for HN. The inhibition of the NLRP3/Caspase-1 pathway by miR-223 significantly reduces inflammation and renal injury demonstrating the therapeutic efficacy of YPSXZJDD. These results offer a novel perspective on the application of traditional Chinese medicine in treating HN highlighting the importance of miR-223 in regulating inflammation.
This study demonstrates that YPSXZJDD alleviates HN-induced kidney injury by upregulating miR-223 and inhibiting the NLRP3/Caspase-1 pathway. The therapeutic potential of YPSXZJDD is supported by its ability to mitigate inflammation and renal damage offering a promising approach for HN treatment. Further research into the broader role of miR-223 in kidney disease and related conditions is warranted to expand the understanding of its therapeutic applications.
Immunocytes Play a Crucial Role as Mediators in the Protective Effects of D-β-Hydroxybutyrate Dehydrogenase 1 against Type 2 Diabetes Mellitus: A Mendelian Randomization Study
Observational studies suggest an association between the immune system and type 2 diabetes. The present study sought to ascertain the causal relationship between BDH1 and type 2 diabetes and investigate whether immunocytes mediate this relationship.
Appropriate single nucleotide polymorphisms (SNPs) were carefully selected from publicly available GWAS databases based on rigorous criteria to ensure the validity of the Mendelian randomization (MR) analysis. Inverse variance weighting (IVW) was employed as the primary approach for assessing effect sizes supplemented by four sensitivity analysis techniques: weighted median simple mode weighted mode and MR-Egger regression tests all aimed at ensuring the robustness and reliability of the IVW results. Reverse MR was conducted to confirm the feasibility of the mediation analysis. Lastly Cochran’s Q test MR Egger intercept regression and MR-PRESSO analysis were utilized to examine heterogeneity and horizontal pleiotropy.
The expression of BDH1 is inversely associated with the risk of type 2 diabetes with an odds ratio of 0.97 (95% CI: 0.95-0.99). IgD+ CD38+ B cell absolute count (20.7%) HLA DR on dendritic cell (18.7%) BAFF-R on CD20- CD38- B cell (9.5%) CD25 on IgD+ CD24+ B cell (4.1%) and BAFF-R on IgD+ B cell (3.4%) all exhibit certain mediating effects whereas IgD+ CD38+ B cell absolute count activated and resting CD4 regulatory T cell % CD4+ T cell transitional B cell absolute count CD28- CD8 dim T cell absolute count CD45 on HLA DR+ CD8+ T cell FSC-A on HLA DR+ natural killer and SSC-A on plasmacytoid dendritic cell exert masking effects.
The findings indicate that immunocytes could serve as a crucial mediating mechanism through which BDH1 exerts its protective effect against type 2 diabetes offering novel insights for the prevention and therapeutic management of the disease.
Diagnostic Biomarkers and Targeted Drug Prediction for Acute Kidney Injury: A Computational Approach
Acute Kidney Injury (AKI) is a clinical syndrome with rapid onset and poor prognosis and existing diagnostic methods suffer from low sensitivity and delay. To achieve early identification and precise intervention there is an urgent need to discover new precise biomarkers.
AKI samples were acquired from Gene Expression Omnibus (GEO) database. AKI-related module genes were identified using the “WGCNA” package. The “Limma” package was used to filter Differentially Expressed Genes (DEGs). Protein interaction networks were constructed by intersecting key modular genes with DEGs and six algorithms (MCC MNC Degree EPC Closeness and Radiality) in the cytoHubba plug-in were combined to screen candidate genes. Diagnostic biomarkers were cross-screened using LASSO regression with Support Vector Machine–Recursive Feature Elimination (SVM-RFE) machine learning algorithm and their predictive performance was verified by Receiver Operating Characteristic (ROC) analysis. Transcription Factors (TFs) regulatory network was constructed applying Cytoscape 3.8.0. Finally the prediction and molecular docking analysis of potential target drugs were performed using the DSigDB database and AutoDockTools.
A total of 498 key modular genes significantly associated with AKI were screened and 88 AKI-related DEGs and 18 candidate genes were further identified. Importantly four biomarkers with high diagnostic value (DDX17 FUBP1 PABPN1 and SF3B1) were screened and validated using dual machine learning algorithms including LASSO regression and SVM-RFE. The area under the ROC curve (AUC) values for these biomarkers were greater than 0.8 indicating good predictive performance. Moreover 19 TFs and 17 miRNA of SF3B1 10 TFs and 58 miRNA of PABPN1 15 TFs and 60 miRNA of FUBP1 together with 13 TFs and 109 miRNA of DDX17 were screened. Drug prediction and molecular docking analysis revealed that Demecolcine and Testosterone Enanthate stably bind to certain markers.
Four potential biomarkers closely related to AKI were identified which may be involved in the occurrence and progression of AKI by regulating key processes such as transcription. The predicted Demecolcine and Testosterone Enanthate may also be involved in the repair of renal injury by regulating key target genes. Although further experimental validation is still needed these may still provide new intervention strategies for the treatment of AKI.
To conclude four AKI biomarkers with high diagnostic value were screened by integrating multiple computational methods revealing a new perspective on the molecular mechanism of AKI. The results provided a new theoretical basis for achieving early precision diagnosis and individualized treatment of AKI.
Association of Anti-TPO Antibody and Inflammatory Markers with Thyroid Ultrasound Findings
The objective of this study was to evaluate the demographic clinical laboratory and ultrasonographic characteristics of patients diagnosed with subclinical hypothyroidism with a particular emphasis on the anti-thyroid peroxidase (anti-TPO) antibody and inflammatory biomarkers.
The study included 157 patients diagnosed with subclinical hypothyroidism categorised into anti-TPO-positive and anti-TPO-negative groups. A retrospective comprehensive evaluation comprising demographic data thyroid medication status ultrasonographic characteristics and laboratory parameters was conducted and statistically analysed between the groups.
Of 157 patients 48.4% were anti-TPO positive. This group was significantly associated with increased levothyroxine (LT4) use and sonographic parenchymal heterogeneity. However there were no significant differences in nodule presence number size or structure. A positive correlation was found between anti-TPO and ferritin levels. In addition a positive correlation was observed between the thyroid-stimulating hormone (TSH)/free T4 ratio and the solidity of nodules as well as between TSH and the neutrophil-to-lymphocyte ratio (NLR). Surprisingly a negative correlation was found between anti-TPO levels and the number of nodules as well as the cystic characterisation of the nodules.
In our study higher levels of anti-TPO and TSH were associated with inflammatory markers such as ferritin and NLR suggesting a possible link with systemic inflammation. Furthermore anti-TPO and the TSH/T4 ratio also showed associations with specific sonographic features of the thyroid gland.
TSH and anti-TPO levels might be associated with systemic inflammation and thyroid sonographic findings in patients with subclinical hypothyroidism. More studies on larger patient populations should confirm the same results to suggest their clinical significance.
Network Pharmacology Unveils Multi-Systemic Intervention of Panax notoginseng in Osteoporosis via Key Genes and Signaling Pathways
Panax notoginseng (Burk.) F. H. Chen (PN) is a traditional Chinese medicine that has been applied to prevent and treat osteoporosis. The mechanism of PN for osteoporosis remained a mystery.
The objective of this study was to reveal the therapeutic effect and illuminate the possible mechanism of PN for osteoporosis.
The Traditional Chinese Medicine Database and Analysis Platform was searched to screen the potent ingredients of the PN and to analyze the potential therapeutic targets for osteoporosis. We excavated four disease databases to collect osteoporosis-related genes. After integrating the gene expression profile of osteoporosis and the chemical-protein data of PN a protein-protein interaction network was constructed to demonstrate the interactions among the gene products. GO function KEGG pathway and docking analyses were executed.
Network pharmacology obtained 31 active ingredients and 134 targets for the treatment of osteoporosis. The key components were beta-elemene quercetin methyl palmitate oleic acid and hexanal. The results of GO and KEGG analyses showed that Panax notoginseng was beneficial for osteoporosis by influencing the main pathways including AGE-RAGE signaling pathway in diabetic complications TNF signaling pathway IL-17 signaling pathway p53 signaling pathway NF-kappa B signaling pathway PI3K-Akt signaling pathway MAPK signaling pathway FoxO signaling pathway and Wnt signaling pathway modulating inflammation metabolism cell proliferation cell survival growth and angiogenesis. Panax notoginseng intervened in osteoporosis through multi-components multi-targets and multi-pathways.
This study illustrates the mechanism of Panax notoginseng for osteoporosis providing broader insights for novel research and developments of the Panax species for osteoporosis.
Bioinformatics Analysis Reveals Microrchidia Family Genes as the Prognostic and Therapeutic Markers for Colorectal Cancer
The aim of this study is to examine the role of the microrchidia (MORC) family a group of chromatin remodeling proteins as the therapeutic and prognostic markers for colorectal cancer (CRC).
MORC protein family genes are a highly conserved nucleoprotein superfamily whose members share a common domain but have distinct biological functions. Previous studies have analyzed the roles of MORCs as epigenetic regulators and chromatin remodulators; however the involvement of MORCs in the development and pathogenesis of CRC was less examined.
The current work examined the role of the MORCs as the therapeutic and prognostic markers for CRC.
The expressions and prognostic significance of MORC family genes in CRC were explored. The role of these genes in tumor immunity was comprehensively analyzed in terms of their functions in immune cell infiltration tumor microenvironment (TME) and their interaction with immune regulatory genes such as immunosuppressive genes immune checkpoints and immunostimulatory genes. The relations between MORC family genes tumor mutation burden (TMB) DNA mismatch repair (MMR) RNA methylation microsatellite instability (MSI) and drug sensitivity were investigated using the R statistical software. The expressions of MORC4 in 150 CRC tissues and 60 paracancer tissues were detected by immunohistochemical method. CRC cell proliferation migration and invasion were measured by cell counting kit-8 (CCK-8) scratch assay and transwell cell invasion assay.
The expressions of MORC2 and MORC4 were significantly upregulated whereas those of MORC1 and MORC3 were noticeably downregulated in CRC in comparison to their expressions in normal colorectal mucosal tissues. Patients with high-expressed MORC2 showed a more unfavorable prognosis than those with a low MORC2 level. Functional annotation analysis identified 100 MORC family genes with the most significant negative or positive correlations to diabetic cardiomyopathy amyotrophic lateral sclerosis oxidative phosphorylation Huntington’s disease thermogenesis Parkinson’s disease olfactory transduction Alzheimer’s disease prion disease. MORC3 expression was positively correlated with Stromal score Immune score and ESTIMATE score while MORC2 expression was negatively related to the three scores in CRC these correlations were not statistically significant. Additionally the MORC family genes were significantly positively correlated with tumor-infiltrating immune cells such as T helper cells and exhibited close relations to some immunosuppressive genes such as CXCR4 and PVR immunostimulatory genes such as TGFBR1 KDR and CD160 as well as some immune checkpoint genes. It was found that the expressions of some members of MORC family genes were positively correlated with DNA methylation MSI TMB MMRs and drug sensitivity in CRC and that the mRNA and protein levels of MORC4 were remarkably upregulated in CRC tissues than in adjacent normal tissues (P<0.05). In the MORC4 knockdown group DLD-1 cell proliferation was more inhibited than in the negative control (NC) and siRNA groups (P<0.05). Furthermore the migratory capacity of DLD-1 cells and the number of cells crossing the basement membrane in the MORC4 knockdown group were reduced compared to the NC and siRNA groups (all P<0.05).
The expressions of MORC family genes were significantly different in CRC samples which was related to the immune cell infiltration and prognosis of CRC. Thus the MORC family genes were considered as markers for indicating the clinical immunotherapy and prognostic outcome of CRC.
Protective Effect of Vitamin D Supplementation Against Atherosclerotic Cardiovascular Disease in Type 1 Diabetes Mellitus Model
Cardiovascular disease (CVD) is a leading cause of mortality on a global scale with a higher prevalence observed among men. This study investigated the protective effect of vitamin D supplementation on CVD.
A cohort of thirty mice was divided into three groups: control T1 diabetic and T1 diabetic groups that received vitamin D treatment. For each mouse in the three groups measurements were taken of body weight blood glucose levels glycated hemoglobin (HbA1c) lipid profile cardiac enzymes troponin I adropin nitric oxide (NO) endothelin-1 and Vascular endothelial growth factor (VEGF). In addition measurements were taken for the overall lymphocyte count as well as the CD3+ CD4+ CD8+ CD4+ CD25+ and CD8+ CD25+ cell counts in all mice.
The diabetic mice that received vitamin D treatment exhibited significant reductions in blood glucose levels HbA1c levels lipid profile cardiac enzymes troponin I endothelin-1 and VEGF levels as compared to the untreated diabetic group (p < 0.01). Furthermore there was an observed rise in adropin and NO levels in diabetic mice that received vitamin D treatment compared to the untreated diabetic group (p < 0.05). The diabetic mice treated with vitamin D exhibited a substantial decrease in total lymphocyte counts compared to the untreated diabetic and control animals (p < 0.0001). Regarding the CD3+ subset it was shown that diabetic mice subjected to vitamin D treatment had notably elevated levels of these cells compared to both the untreated diabetic and control groups (p < 0.0001). In addition the administration of vitamin D resulted in a substantial decrease in the numbers of CD4+ and CD8+ cells in the group of individuals with diabetes (p < 0.0001). The diabetes group that received vitamin D treatment had significantly reduced populations of CD4+ CD25+ and CD8+ CD25+ compared to the untreated diabetic group (p < 0.0001).
Vitamin D maintains the integrity of the cardiovascular system through the reduction of blood glucose levels and lipid profile. Moreover its supplementation prevents atherosclerotic CVD by suppressing inflammatory reactions.
Oral Microbiota Associated with Clinical Efficacy of Ustekinumab in Crohn’s Disease
Crohn’s Disease (CD) is a chronic inflammatory gastrointestinal disease. Ustekinumab (UST) has been utilized as a therapeutic option for CD patients. However approximately 40-60% of patients exhibit an inadequate response to UST. Accumulating evidence has confirmed the involvement of oral bacteria in the development of CD. Nevertheless the relationship between oral microbiota and the efficacy of UST therapy in CD patients has remained unexplored.
We recruited 28 healthy individuals and 53 CD patients 47 of whom completed the entire UST therapy. Oral samples and clinical data were collected. The clinical response and clinical remission were defined based on the CDAI score. Oral samples were analyzed by 16S rRNA gene sequencing. The analysis of sequence data was performed by QIIME and R.
We revealed the oral microbial difference between the Healthy Control (HC) group and the CD group. The enrichment of Fusobacteria Leptotrichia Capnocytophaga and Campylobacter and the diminution of Haemophilus and Rothia were observed in the CD group. Differences in oral microbiota were also identified among patients with different efficacy of UST. Compared to the response and remission groups both the non-response and non-remission groups showed significantly higher levels of Fusobacteria and Leptotrichia. Predictive models for clinical response and clinical remission in UST were developed based on oral microbiota with the Area Under the Curve (AUC) value of 0.944 and 0.930 respectively.
Oral microbiota was relevant to the UST efficacy in patients with CD based on the predictive model. These findings suggest that oral microbiota could serve as a non-invasive prognostic biomarker for UST treatment in CD patients.
Evaluation and Association of Hematological and Biochemical Parameters of Untreated COVID-19 Patients on the basis of Differences in Ethnicity and Curcumin as a Possible Treatment
CBC (complete blood count) tests along with RPM (Renal parameters) and LFT (Liver function tests) are clinically important for coronavirus patients; curcumin can serve as a possible treatment for SARS- CoV.
The objective of the study was to determine the relationship of CBC parameters with renal parameters and liver function tests and to develop the hypothesis that curcumin may be the best and non-invasive drug for coronavirus.
The differences between the results of 91 confirmed cases of COVID-19 (symptomatic and asymptomatic) and 100 controls were assessed by an independent t-test and Mann-Witney U Wilcoxon test. Microscopy hematological tools and techniques were used to assess the improvements/abnormalities in blood components and parameters.
This is a case control study along with the feasibility of curcumin as COVID treatment. The association between parameters was assessed by Pearson & Spearman correlation analysis. The level of significance was p < 0.05. Changes were observed in urea (p = 0.000) creatinine (p = 0.02) total bilirubin (p = 0.000) SGPT (ALT) (p = 0.000) RBC (p = 0.001) HGB (p = 0.001) MCV (p = 0.002) MCH (p = 0.03) MPV PDW NE% LY% and MO% EO% (p = 0.00) in comparison to normal controls. Differences in the correlation of electrolytes RPM and LFT tests along with CBC parameters in Pakistani and Chinese individuals provided a new idea for using various diagnostic and therapeutic tools in different ethnic groups. The COVID-19 infected blood components and parameters showed rapid improvement/recovery especially the total count of platelets and WBCs (lymphocytes and basophils) HGB HCT MCV and MCH.
Curcumin drugs can be used as an immediate remedy/treatment to cure COVID-19 patients.
Associative Learning in Subclinical Hypothyroidism at Different Ranges of Thyroid Stimulating Hormone: A Cambridge Neuropsychological Test Automated Battery (CANTAB) Study of Visual Paired Association Learning Task
Associative learning deficits are constantly found in subclinical hypothyroidism (SCH). Despite achieving normal thyroid stimulating hormone (TSH) levels a considerable number of patients undergoing levothyroxine (LT-4) treatment frequently complain about memory retrieval. The Paired Association Learning (PAL) task involves computerised testing on the CANTAB- Cambridge Neuropsychological Test Automated Battery also considered a screening tool for Alzheimer’s disease (AD).
This study aimed to investigate the impact of different levels of TSH on visual associative learning in SCH and determine if these impairments were reversed with LT-4.
A total of 134 participants were included in this cross-sectional study. Group 1: 35 healthy controls; patients with SCH (Group 2: 33 newly identified cases; Group 3: 32 patients on LT-4 with elevated TSH; Group 4: 34 euthyroid but on LT-4). A thyroid profile and a neuropsychological clinical assessment were done. The visual PAL task was performed on CANTAB.
PAL was significantly impaired (p = <0.05) in all 3 patient groups as compared to Group 1. The PAL total errors (adjusted) scores were significantly higher in Groups 2 and 3 indicating that associative learning is definitely impaired in SCH reaching levels previously seen in patients with AD.
Our findings encourage screening for visual associative learning or memory retrieval in patients with SCH. The study present has established a more reasonable threshold of TSH 2.5mIU/L to encourage examination of associative learning and the initiation of LT-4 in SCH. Poor PAL task performance in patients with SCH may have significant implications in clinical settings for suspecting AD.