![ral in time and pearson correlation with spss 16.0 software ral in time and pearson correlation with spss 16.0 software](https://www.researchgate.net/profile/Amalio-Blanco/publication/280967728/figure/tbl2/AS:601618793889792@1520448506036/Means-standard-deviations-Cronbachs-alpha-and-Pearsons-correlations.png)
After oral clinical examination in accordance with the World Health Organization criteria, the patients were subjected to esophagogastroduodenoscopy (EGD), which was performed using an upper GI video endoscope (Olympus EVIS EXERA III, CV-190). 23 – 25 After baseline recording of clinical parameters, saliva was collected into a polypropylene tube, via the passive drool technique, until 2 mL of saliva was collected per patient this saliva (2 mL) was mixed with DNAgard saliva stabilizer (1.5 mL Biomatrica, San Diego, CA, USA), in accordance with the manufacturers’ instructions. Probing depth (PD) and relative attachment level (RAL) were measured at six locations per tooth (mesial, distal, lingual/palatal, and buccal/labial) using a periodontal probe. The gingival index (GI) score was recorded as follows: 0 = normal gingiva 1 = mild inflammation, slight change in color, slight edema, and no bleeding on probing (BOP) 2 = moderate inflammation, edema, redness and glazing, and BOP present and 3 = severe inflammation, marked redness and ulceration, spontaneous bleeding, and edema. The plaque index (PI) score was classified as follows: 0 = no plaque 1 = a film of plaque adheres to the gingival margin, assessed by passing a probe across the tooth surface 2 = moderate accumulation of plaque visible to the naked eye within the gingival pocket, and/or at the gingival margin and tooth surface and 3 = abundant accumulation (1- to 2-mm thick) of plaque visible to the naked eye within the gingival pocket, and/or at the gingival margin and tooth surface.
![ral in time and pearson correlation with spss 16.0 software ral in time and pearson correlation with spss 16.0 software](https://www.mdpi.com/medicina/medicina-57-00934/article_deploy/html/images/medicina-57-00934-g003-550.jpg)
Full-mouth periodontal examination was performed in all cases. pylori-associated gastric diseases who underwent esophagogastroduodenoscopy (EGD) at Suranaree University of Technology Hospital in the northeast region of Thailand from March 2017 to December 2017.
![ral in time and pearson correlation with spss 16.0 software ral in time and pearson correlation with spss 16.0 software](https://img.informer.com/p5/spss-v21-job-satisfaction.png)
Samples were obtained from patients diagnosed with H. The findings of this study may improve treatment efficacy and reduce the risk of H. pylori in saliva and its presence in the stomach, and investigated possible H. This study evaluated the association between the presence of H.
#RAL IN TIME AND PEARSON CORRELATION WITH SPSS 16.0 SOFTWARE PLUS#
To determine whether eradication therapy alone or eradication therapy plus periodontal therapy contribute to reduced recurrence, it is necessary to identify factors involved in the recurrence of H. pylori eradication may be linked to the presence of oral H. pylori DNA in dental plaque and saliva notably, the oral cavity may constitute a reservoir for gastric infection and transmission.
![ral in time and pearson correlation with spss 16.0 software ral in time and pearson correlation with spss 16.0 software](https://els-jbs-prod-cdn.jbs.elsevierhealth.com/cms/attachment/a2ac64da-d147-43af-be70-0736ae886af8/gr6_lrg.jpg)
pylori recurrence-associated gastrointestinal diseases are not clear. pylori-positive gastritis patients, the recurrence rate is relatively high (13%). 12 – 14Īlthough standard triple therapy regimens achieve successful eradication in H. pylori strains harboring cagA and vacA are more frequent among patients with peptic ulcers, gastric mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric cancers. 9 This cluster encodes a bacterial type IV secretion system that translocates cagA into host gastric epithelial cells, and has been associated with the production of vacA, which causes cytoplasmic vacuolization in gastric epithelial cells 9, 10 moreover, it has been associated with delayed healing of gastric ulcers, inhibition of re-epithelialization, and worsening of the quality of mucosal scarring. 9 The cag pathogenicity island ( cag PAI) is a cluster of genes found in strains exhibiting enhanced interactions with gastric tissue. pylori, 8 and are most closely associated with clinical outcomes of H. 7Ĭytotoxin-associated antigen ( cagA) and vacuolating cytotoxin ( vacA) are the major virulence factors of H. 6 The progression of disease depends on multiple factors, which contribute to the onset of associated gastric diseases. 1 – 4 In Thailand, the infection rate ranges from 54.1% to 76.1% 5 however, the age-standardized incidence rate of gastric cancer is relatively low in Asian countries. pylori infection has been found in approximately 50% of the global population and is etiologically linked to gastric cancers, comprising 25% of cancers related to this etiology of infection therefore, it constitutes a primary public health problem. Helicobacter pylori infection is an important gastrointestinal disease associated with the onset of gastritis, as well as gastric or duodenal ulcer disease and gastric cancer.