Sequence Analysis of Epstein‐Barr virus RPMS1 Gene in malignant hematopathy

alexandrossfakianakis shared this article with you from Inoreader Sequence Analysis of Epstein‐Barr virus RPMS1 Gene in malignant hematopathy of Northern China via Journal of Medical Virology Abstract The RPMS1 gene is the only member of the BamHI-A rightward transcripts (BARTs) family for which a full-length cDNA has been identified, and RPMS1 transcript has been confirmed in many EBV-positive malignancies. However, the effects of sequence variations of RPMS1 in hematological malignancies and their biological significance are unclear. To explore the association between RPMS1 gene variations and hematological malignancy, the RPMS1 gene of 391 EBV-positive samples from patients with EBV-positive leukemia, myelodysplastic syndromes (MDS) and lymphoma in northern China were sequenced. On the basis of phylogenetic tree and mutation characteristics of RPMS1, all the sequences were divided into five major types: RPMS1-A, RPMS1-B, RPMS1-C, RPMS1-E, and RPMS1-F. RPMS1-A type, similar to the prototype B95-8, was identified in 71.87% (281/391) of samples and was the major typ e in all subpopulations. The frequency of RPMS1-F type was significantly higher in all malignant hematopathy groups than in healthy donors. The Hodgkin lymphoma (HL) group contained more RPMS1-F than other malignant hematopathy groups, and acute myeloid leukemia (AML) contained more RPMS1-C type than other malignant hematopathy groups. Therefore, RPMS1-A is the main type of RPMS1 gene in northern China, and RPMS1-F may be associated with hematologic malignancies. This article is protected by copyright. All rights reserved. View on Web

Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Development and validation of a potential biomarker to improve the assessment of liver fibrosis progression in patients with chronic hepatitis B

alexandrossfakianakis shared this article with you from Inoreader Development and validation of a potential biomarker to improve the assessment of liver fibrosis progression in patients with chronic hepatitis B via Journal of Medical Virology Abstract Objectives We aimed to develop and validate a novel combined score to improve the assessment of liver fibrosis progression in patients with chronic hepatitis B (CHB). Methods The serum levels of hub genes were examined by qRT-PCR in three cohorts of CHB patients. Results For significant liver fibrosis (≥S2), the areas under the receiver operating characteristics curves (AUROCs) of the combined score were 0.838, 0.842 and 0.881 in the three cohorts, respectively. And for advanced liver fibrosis (≥S3), the AUROCs were 0.794, 0.801 and 0.901, respectively. Compared with the results of AUROCs for aspartate aminotransferase-to-platelet ratio (APRI) and fibrosis index based on four factors (FIB-4) in the validation cohorts, better clinical diagnostic value for assessing the progression of liver fibrosis was found in the combined score. Additionally, univariate ordered logistic regression analysis indicated that the combined score could serve as a more superior and stable risk factor than APRI and FIB-4 in the assessment of liver fibrosis. For CHB patients with normal alanine aminotransferase (ALT), our results further emphasized the diagnostic value of the combined score for significant fibrosis (≥S2) and advanced fibrosis (≥S3). Moreover, it was found that patients with the high combined score, who were associated with the advanced fibrosis stage, had higher levels of drug sensitivity and immune checkpoint expression. Conclusion The novel combined score could serve as a potential biomarker and contribute to improving the assessment of fibrosis stage in CHB patients. This article is protected by copyright. All rights reserved. View on Web

Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Cholesterol granuloma of the maxillary sinus in association with a dental implant—A case report

alexandrossfakianakis shared this article with you from Inoreader Cholesterol granuloma of the maxillary sinus in association with a dental implant—A case report via Clinical Implant Dentistry and Related Research Abstract Background Cholesterol granuloma is typically a benign granulomatous growth seen mostly in the mastoid process and the petrous temporal bone. Although cholesterol granuloma in maxillary sinus was first reported in the scientific literature in 1978, the occurrence is very rare and it is usually clinically and radiographically manifested ambiguously as maxillary sinusitis. Purpose The presence of cholesterol granuloma in the maxillary sinus in association with a dental pathology or prosthesis has been scarcely known. In this case report, we present a case of cholesterol granuloma in the maxillary sinus of a middle-aged male who had previously undergone dental implant placement in relation to that anatomical location. Materials and Methods A 64-year-old man reported to the Dental OP with a chief complaint of oral malodor, swelling, and tenderness over the right middle third of the face for the past 3 months. A cone beam computed tomography scan showed a well-defined radio-opaque lesion along with sclerosis and thinning of bone within the right maxillary antrum in relation to the dental implant placed in the 16 regions. The left maxillary sinus appeared normal. The Caldwell-Luc procedure was performed and a solitary soft lesion with yellowish-gray contents was evident within the right maxillary sinus. Histopathological examination revealed cholesterol clefts surrounded by foreign body giant cell reaction and granulation tissue formation, along with the presence of old and recent hemorrhage. A final diagnosis of cholesterol granuloma was made based on the histopathological examination report. Conclusion Based on the evidence available in the present case, we hypothesize that the localized trauma and hemorrhage initiated by implant placement in this particular anatomical location could have plausibly resulted in the occurrence of cholesterol granuloma in our patient. View on Web

Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.