Archives

  • 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04
  • Our analysis demonstrated that ADA is a transpicuous and

    2024-03-11

    Our analysis demonstrated that ADA is a transpicuous and rapid test with high sensitivity and specificity for diagnosis of TBM decidedly. The summary sensitivity and specificity were 0.89 and 0.91 respectively, indicating a sufficient level for overall diagnostic accuracy. The modality of SROC curve indicated a reliable summary for the diagnostic study, which revealed the trade-off between sensitivity and specificity. Our analysis showed that the AUC was 0.96 (based on the SROC curve), representing that overall accuracy was also high. Bivariate approach was used to estimate DOR in our meta-analysis; the DOR combined the data from sensitivity and specificity and demonstrated the test's accuracy as a single number. The DOR with binary classification is a measure of the efficiency of a diagnostic test. The DOR value ranged from 0 to infinity, in which higher values indicated appropriate discriminatory test performance. In this study, the analysis showed that the mean DOR was 77; in addition, it AICAR synthesis was significantly higher than two previous meta-analysis probes.17, 18 The kappa statistic for measuring agreement between two test (ADA test and gold standard) was precise and considerable [kappa = 0.75 (95% CI: 72–78%)]. Thence, representing a high level of discriminatory power, overall accuracy and was applicable in the TMB diagnosis. It is indicated that a PLR more than 10 and NLR less than 0.1 provides convincing diagnostic evidence; moreover, a PLR more than 5 and NLR less than 0.2 provides strong diagnostic evidence to rule in/rule out diagnoses respectively in most circumstances.20, 21 These data advocated that a negative ADA could not be used alone as a justification to exclude or discontinue anti-TB treatment. The choice of therapeutic strategy should be used according to the microscopic examination outcomes for a smear or a culture for M. tuberculosis, as well as other clinical prognosis, such as response to anti-TB treatment.
    Conclusions
    Conflict of interest
    Introduction We recently observed an association of colon cancer with polymorphic sites within the ADA gene [1]. In subjects with cancer there is a higher proportion of *1/*1 genotype in the ADA2 locus and of ADA6*1 allele carriers in ADA6 locus. We reasoned that genetic variability within the ADA gene could be involved in the growth of other types of solid tumors prompting us to search for a possible association with uterine leiomyomas. Leiomyoma is a benign tumor [2] common in females and usually does not give significant clinical disturbances. In some cases, however, relevant clinical signs are manifest requiring surgical intervention to remove the tumor. Adenosine Deaminase irreversibly deaminates adenosine to inosine influencing the control of adenosine concentration in body fluids: high concentration of this substances could inhibit immune response by T lymphocytes [3], [4]. The ADA gene, located on chromosome 20, is composed of 12 exons: several single nucleotide polymorphic sites have been described within the gene but their role in human diseases have not been yet fully elucidated. We have studied three polymorphic sites of ADA: ADA1, located on the exon 1 and corresponding to the biochemical ADA polymorphism described by Spencer et al. [5], ADA2 located on intron 2 and ADA6 located on exon 6. ADA1 polymorphism shows two alleles ADA1*1 and ADA1*2 that are associated with differences in ADA activity, ADA1*1 being more active than ADA1*2.
    Material and methods ADA genotypes were determined by DNA analysis as previously described [1], [6]. Sense and anti-sense primers for the three polymorphisms are reported in a previous paper [6], Chi square test and Odds ratio analysis were performed using SPSS package [7]. Demographic and clinical data of the women with leiomyomas have been reported in a previous paper [8].
    Results Table 1 shows the distribution of ADA1, ADA2 and ADA6 genotypes in women with leiomyomas and in controls. A higher proportion of ADA2*1/*1 genotype and of carriers of ADA6*1 allele is observed in women with leiomyomas as compared to controls.