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JDR Clinical and Translational Research Jan 2024Describe associations between dental caries and dental plaque microbiome, by dentition and family membership.
OBJECTIVE
Describe associations between dental caries and dental plaque microbiome, by dentition and family membership.
METHODS
This cross-sectional analysis included 584 participants in the Center for Oral Health Research in Appalachia Cohort 1 (COHRA1). We sequenced the 16S ribosomal RNA gene (V4 region) of frozen supragingival plaque, collected 10 y prior, from 185 caries-active (enamel and dentinal) and 565 caries-free (no lesions) teeth using the Illumina MiSeq platform. Sequences were filtered using the R DADA2 package and assigned taxonomy using the Human Oral Microbiome Database.
RESULTS
Microbiomes of caries-active and caries-free teeth were most similar in primary dentition and least similar in permanent dentition, but caries-active teeth were significantly less diverse than caries-free teeth in all dentition types. Streptococcus mutans had greater relative abundance in caries-active than caries-free teeth in all dentition types ( < 0.01), as did in primary and mixed dentition ( < 0.01). sp. HMT 203 had significantly higher relative abundance in caries-free than caries-active teeth in all dentition types ( < 0.01). In a linear mixed model adjusted for confounders, the relative abundance of was significantly greater in plaque from caries-active than caries-free teeth ( < 0.001), and the relative abundance of sp. HMT 203 was significantly lower in plaque from caries-active than caries-free teeth ( < 0.001). Adding an effect for family improved model fit for sp. HMT 203 but not.
CONCLUSIONS
The diversity of supragingival plaque composition from caries-active and caries-free teeth changed with dentition, but was positively and sp. HMT 203 was negatively associated with caries regardless of dentition. There was a strong effect of family on the associations of sp. HMT 203 with the caries-free state, but this was not true for and the caries-active state.
KNOWLEDGE TRANSFER STATEMENT
Patients' and dentists' concerns about transmission of bacteria within families causing caries should be tempered by the evidence that some shared bacteria may contribute to good oral health.
Topics: Humans; Dental Caries; Dentition; Adenosine Deaminase; Cross-Sectional Studies; Dental Caries Susceptibility; Intercellular Signaling Peptides and Proteins; Microbiota; Streptococcus mutans
PubMed: 36154330
DOI: 10.1177/23800844221121260 -
Aging Jul 2023ADAR is an enzyme involved in adenosine-inosine RNA editing. However, the role of ADAR in tumorigenesis, progression, and immunotherapy has not been fully elucidated.
BACKGROUND
ADAR is an enzyme involved in adenosine-inosine RNA editing. However, the role of ADAR in tumorigenesis, progression, and immunotherapy has not been fully elucidated.
METHODS
The TCGA, GTEx and GEO databases were extensively utilized to explore the expression level of ADAR across cancers. Combined with the clinical information of patients, the risk profile of ADAR in various cancers was delineated. We identified pathways enriched in ADAR and their related genes and explored the association between ADAR expression and the cancer immune microenvironment score and response to immunotherapy. Finally, we specifically explored the potential value of ADAR in the treatment of the bladder cancer immune response and verified the critical role of ADAR in the development and progression of bladder cancer through experiments.
RESULTS
ADAR is highly expressed in most cancers at both the RNA and protein level. ADAR is associated with the aggressiveness of some cancers, especially bladder cancer. In addition, ADAR is associated with immune-related genes, especially immune checkpoint genes, in the tumor immune microenvironment. Moreover, ADAR expression is positively correlated with tumor mutation burden and microsatellite instability in a variety of cancers, indicating that ADAR could be used as a biomarker of immunotherapy. Finally, we demonstrated that ADAR is a key pathogenic factor in bladder cancer. ADAR promoted proliferation and metastasis of bladder cancer cells.
CONCLUSION
ADAR regulates the tumor immune microenvironment and can be used as a biomarker of the tumor immunotherapy response, providing a novel strategy for the treatment of tumors, especially bladder cancer.
Topics: Humans; Carcinogenesis; Cell Proliferation; Clinical Relevance; Immunotherapy; Prognosis; Tumor Microenvironment; Urinary Bladder Neoplasms; Adenosine Deaminase
PubMed: 37414093
DOI: 10.18632/aging.204853 -
Clinical Chemistry and Laboratory... Jun 2024Ascites is the pathological accumulation of fluid within the peritoneal cavity. It often occurs as results of liver cirrhosis, malignant neoplasia, tuberculous... (Review)
Review
Ascites is the pathological accumulation of fluid within the peritoneal cavity. It often occurs as results of liver cirrhosis, malignant neoplasia, tuberculous infection, cardiac insufficiency, renal diseases, etc. Determining the etiology is an essential step in the management of patients with new-onset ascites. Abdominal paracentesis with appropriate ascitic fluid analysis is probably the most cost-effective method of determining the cause of ascites. We performed a literature search of PubMed and identified articles published in the field of ascites, to evaluate diagnostic values of various parameters in defining the etiologies of ascites and then provides diagnostic algorithm for patients with new-onset ascites. In patients with ascites, the constituent ratio of underlying etiology varies between developed and developing countries. It is a challenge to define the etiologies of ascites in developing countries. Routine ascitic fluid analysis should include the serum ascites albumin gradient (SAAG), total protein concentration, cell count and differential. Optional ascitic fluid analysis includes cholesterol, fluid culture, cytology, tumor markers, lactate dehydrogenase, adenosine deaminase (ADA), triglyceride, amylase, glucose, brain natriuretic peptide (BNP), etc. Our review evaluated diagnostic values of the above parameters in defining the etiologies of ascites. Diagnostic algorithm established in this review would provide a practical and convenient diagnostic strategy for clinicians in diagnosing patients with new-onset ascites.
Topics: Humans; Ascites; Ascitic Fluid; Algorithms; Diagnosis, Differential
PubMed: 38112289
DOI: 10.1515/cclm-2023-1112 -
Korean Journal of Family Medicine Jul 2023Elevated pulmonary serum adenosine deaminase (ADA) levels signify lung tissue damage and severe tuberculosis (TB). Serum ADA assays can be used as an additional...
BACKGROUND
Elevated pulmonary serum adenosine deaminase (ADA) levels signify lung tissue damage and severe tuberculosis (TB). Serum ADA assays can be used as an additional criterion for assessing TB treatment response and as a prognostic marker in patients with pulmonary TB. The Bandim TB and Karnofsky Performance Scale (KPS) scores were developed based on available clinical data and investigations to allow physicians to evaluate disease treatment and response. This study examined the use of a clinical scoring system (Bandim TB and KPS scores) in the context of serum ADA activity.
METHODS
Forty adults (aged >18 years) diagnosed with pulmonary TB by Ziehl-Neelsen staining for acid-fast bacilli and/or cartridge-based nucleic acid amplification test were recruited. Standardized questionnaires were used to record Bandim TB and KPS scores. Serum ADA levels were estimated using a commercial kit.
RESULTS
The Bandim TB score was positively associated (ρ=0.74, P≤0.001) and the KPS score was negatively associated (ρ=-0.69, P≤0.001) with serum ADA levels.
CONCLUSION
Subjective and objective clinical scores of pulmonary TB were strongly correlated with serum ADA levels. Knowledge of clinical scores corresponding to serum ADA levels could help physicians understand stage and progression of the disease which may aid in early detection and better management, and reduce disease transmission in a TB-endemic country.
PubMed: 37491987
DOI: 10.4082/kjfm.22.0191 -
PloS One 2023We report here the first occurrence of an adenosine deaminase-related growth factor (ADGF) that deaminates adenosine 5' monophosphate (AMP) in preference to adenosine....
We report here the first occurrence of an adenosine deaminase-related growth factor (ADGF) that deaminates adenosine 5' monophosphate (AMP) in preference to adenosine. The ADGFs are a group of secreted deaminases found throughout the animal kingdom that affect the extracellular concentration of adenosine by converting it to inosine. The AMP deaminase studied here was first isolated and biochemically characterized from the roman snail Helix pomatia in 1983. Determination of the amino acid sequence of the AMP deaminase enabled sequence comparisons to protein databases and revealed it as a member of the ADGF family. Cloning and expression of its cDNA in Pichia pastoris allowed the comparison of the biochemical characteristics of the native and recombinant forms of the enzyme and confirmed they correspond to the previously reported activity. Uncharacteristically, the H. pomatia AMP deaminase was determined to be dissimilar to the AMP deaminase family by sequence comparison while demonstrating similarity to the ADGFs despite having AMP as its preferred substrate rather than adenosine.
Topics: Animals; AMP Deaminase; Adenosine Deaminase; Adenosine; Mollusca; Intercellular Signaling Peptides and Proteins; Adenosine Monophosphate
PubMed: 37471401
DOI: 10.1371/journal.pone.0286435 -
SAGE Open Medical Case Reports 2024Deficiency of adenosine deaminase 2 is a rare monogenic multi-organ disease of children and less often adults resulting from mutations in the adenosine deaminase 2 gene....
Deficiency of adenosine deaminase 2 is a rare monogenic multi-organ disease of children and less often adults resulting from mutations in the adenosine deaminase 2 gene. We present a case of a 35-year-old Palestinian male with adenosine deaminase 2 deficiency and maturity-onset diabetes of the young type 2. The patient initially presented with complaints of swelling in his neck and night sweats, leading to a diagnosis of Hodgkin lymphoma. Subsequent evaluation revealed a recurrence of Hodgkin lymphoma, along with symptoms of otitis media, upper respiratory tract infection, and a rash around the mouth. Genetic testing confirmed mutations in the adenosine deaminase 2 gene and glucokinase genes, confirming the diagnosis of deficiency of adenosine deaminase 2 and maturity-onset diabetes of the young type 2, respectively. The patient was treated with Intravenous immunoglobulin, antiviral drugs, and oral hypoglycemic drugs, showing improvement in symptoms and laboratory tests. This case highlights the importance of considering rare genetic disorders in patients with unusual or refractory clinical manifestations, and the need for a multidisciplinary approach in such cases.
PubMed: 38881977
DOI: 10.1177/2050313X241260148 -
Cellular & Molecular Biology Letters Jan 2024Rheumatoid arthritis (RA) is an autoimmune disease involving T and B lymphocytes. Autoantibodies contribute to joint deterioration and worsening symptoms. Adenosine...
Rheumatoid arthritis (RA) is an autoimmune disease involving T and B lymphocytes. Autoantibodies contribute to joint deterioration and worsening symptoms. Adenosine deaminase (ADA), an enzyme in purine metabolism, influences adenosine levels and joint inflammation. Inhibiting ADA could impact RA progression. Intracellular ATP breakdown generates adenosine, which increases in hypoxic and inflammatory conditions. Lymphocytes with ADA play a role in RA. Inhibiting lymphocytic ADA activity has an immune-regulatory effect. Synovial fluid levels of ADA are closely associated with the disease's systemic activity, making it a useful parameter for evaluating joint inflammation. Flavonoids, such as quercetin (QUE), are natural substances that can inhibit ADA activity. QUE demonstrates immune-regulatory effects and restores T-cell homeostasis, making it a promising candidate for RA therapy. In this review, we will explore the impact of QUE in suppressing ADA and reducing produced the inflammation in RA, including preclinical investigations and clinical trials.
Topics: Humans; Adenosine; Adenosine Deaminase; Arthritis, Rheumatoid; Inflammation; Quercetin; Adenosine Deaminase Inhibitors
PubMed: 38225555
DOI: 10.1186/s11658-024-00531-7 -
Journal of Medical Biochemistry Oct 2023Tuberculous pleuritis (TP) is one of the most common extra-pulmonary tuberculosis form. Because of tuberculous pleurisy is hard to diagnose due to slow course of disease...
Tuberculous pleuritis (TP) is one of the most common extra-pulmonary tuberculosis form. Because of tuberculous pleurisy is hard to diagnose due to slow course of disease and lack of specificity in symptoms and diagnostic methods. In that reason, we need multidisciplinary approach and efficient biomarkers. Acid-fast bacilli (AFB) staining, cultures and pathophysiological biopsy finding from the majority of patients are positive only in less than 10%. Löwenstein culture results need time about 6-8 weeks what delays diagnosis. Adenosine deaminase (ADA) is biomarker with high sensitivity and specificity (more than 90%) and considered as gold standard of biomarkers in the diagnosis of TP. It is very hard to distinguish malignant from TP with lymphocyte predomination, but in patient with malignant pleural effusion the level of ADA is decreased, opposite from TP. ADA in pleural punctate is a fast, simple, efficient and economical way for clarification the etiology of the pleural effusion as tuberculous pleurisy. Also, many studies have proved the role of ADA in the response to treatment for tuberculosis at follow up period.
PubMed: 38084235
DOI: 10.5937/jomb0-44018 -
Emerging Microbes & Infections Dec 2023Cytokine dynamics in patients with coronavirus disease 2019 (COVID-19) have been studied in blood but seldomly in respiratory specimens. We studied different cell...
Correlations of Myeloperoxidase (MPO), Adenosine deaminase (ADA), C-C motif chemokine 22 (CCL22), Tumour necrosis factor alpha (TNFα) and Interleukin-6 (IL-6) mRNA expression in the nasopharyngeal specimens with the diagnosis and severity of SARS-CoV-2 infections.
Cytokine dynamics in patients with coronavirus disease 2019 (COVID-19) have been studied in blood but seldomly in respiratory specimens. We studied different cell markers and cytokines in fresh nasopharyngeal swab specimens for the diagnosis and for stratifying the severity of COVID-19. This was a retrospective case-control study comparing Myeloperoxidase (MPO), Adenosine deaminase (ADA), C-C motif chemokine ligand 22 (CCL22), Tumour necrosis factor alpha (TNFα) and Interleukin-6 (IL-6) mRNA expression in 490 (327 patients and 163 control) nasopharyngeal specimens from 317 (154 COVID-19 and 163 control) hospitalized patients. Of the 154 COVID-19 cases, 46 died. Both total and normalized MPO, ADA, CCL22, TNFα, and IL-6 mRNA expression levels were significantly higher in the nasopharyngeal specimens of infected patients when compared with controls, with ADA showing better performance (OR 5.703, 95% CI 3.424-9.500, < 0.001). Receiver operating characteristics (ROC) curve showed that the cut-off value of normalized ADA mRNA level at 2.37 × 10 had a sensitivity of 81.8% and specificity of 83.4%. While patients with severe COVID-19 had more respiratory symptoms, and elevated lactate dehydrogenase, multivariate analysis showed that severe COVID-19 patients had lower CCL22 mRNA (OR 0.211, 95% CI 0.060-0.746, = 0.016) in nasopharyngeal specimens, while lymphocyte count, C-reactive protein, and viral load in nasopharyngeal specimens did not correlate with disease severity. In summary, ADA appears to be a better biomarker to differentiate between infected and uninfected patients, while CCL22 has the potential in stratifying the severity of COVID-19.
Topics: Humans; COVID-19; Interleukin-6; Tumor Necrosis Factor-alpha; Retrospective Studies; Adenosine Deaminase; Case-Control Studies; Peroxidase; Ligands; SARS-CoV-2; Cytokines; Chemokines; Nasopharynx; Chemokine CCL22
PubMed: 36482706
DOI: 10.1080/22221751.2022.2157338 -
Journal of Clinical Immunology Oct 2023We present the case of a 24-year-old male with CNS granulomatosis due to an immunodeficiency syndrome which was identified as deficiency of adenosine deaminase 2 (DADA2)...
PURPOSE
We present the case of a 24-year-old male with CNS granulomatosis due to an immunodeficiency syndrome which was identified as deficiency of adenosine deaminase 2 (DADA2) as a cause of brainstem infarction.
METHODS
Case report and detailed description of the clinical course of diagnosis and treatment.
CASE
The patient's medical history consisted of an unknown immunodeficiency syndrome. Based on former findings, common variable immunodeficiency (CVID) was diagnosed. The patient suffered from three consecutive brainstem strokes of unknown etiology within 3 years. An MRI scan detected gadolinium-enhancing, granulomatous-suspect lesions in the interpeduncular cistern, temporal lobe, and tegmentum. Laboratory analysis was compatible with CVID, with leukopenia and immunoglobulin deficiency. Because granulomatous CNS inflammation was suspected, the patient received methylprednisolone immunosuppressive therapy, which led to partially regressive MRI lesions. However, in contrast to imaging, the patient showed a progressive cerebellar syndrome, indicating plasma exchange therapy and immunoglobulin treatment, which led to rapid symptom amelioration. After a relapse and a further stroke, expanded analysis confirmed DADA2 (and not CVID) as the inflammatory cause for recurrent stroke. After starting the therapy with immunoglobulins and adalimumab, no further strokes occurred.
CONCLUSION
We present the case of a young adult with diagnosis of DADA2 as a cause for recurrent strokes due to vasculitis. This stroke etiology is rare but should be considered as a cause of recurrent stroke of unknown origin in young patients to avoid a disabling disease course by disease-specific treatment options.
Topics: Male; Young Adult; Humans; Adult; Adenosine Deaminase; Intercellular Signaling Peptides and Proteins; Immunologic Deficiency Syndromes; Stroke; Common Variable Immunodeficiency; Immunoglobulins; Brain Stem Infarctions
PubMed: 37306896
DOI: 10.1007/s10875-023-01526-3