Clinical application of liver stiffness measurement in patients with cavernous transformation of portal vein

xlomafota13 shared this article with you from Inoreader Clinical application of liver stiffness measurement in patients with cavernous transformation of portal vein Via Experimental and therapeutic medicine Exp Ther Med. 2021 May;21(5):442. doi: 10.3892/etm.2021.9881. Epub 2021 Feb 28. ABSTRACT The clinical outcomes differ between patients with cavernous transformation of the portal vein (CTPV) with and without cirrhosis. Therefore, invasive liver biopsy may be needed for the differential diagnosis of patients with CTPV with or without cirrhosis. The present study aimed to investigate the diagnostic efficacy of liver stiffness measurements (LSM) for the prediction of cirrhosis in patients with CTPV. A total of 20 patients with CTPV, 34 with chronic hepatitis B (CHB)-related cirrhosis and 20 healthy volunteers, were retrospectively recruited in the study. CTPV was diagnosed with contrast-enhanced computed tomography (CT) and ultrasound for the abdomen. LSM values were detected for each patient, while liver biopsy was performed in each patient in the CTPV and cirrhosis groups. The results demonstrated that LSM values were significantly lowe r in the CTPV group (12.5 kPa; range, 6.8-21.5 kPa) compared with the CHB-related cirrhosis group (21.0 kPa; range, 15.5-27.2 kPa; P=0.017). However, this was still higher compared with healthy volunteers (4.9 kPa; range 4.0-5.8 kPa; P<0.001). In addition, CTPV patients with cirrhosis (17.7 kPa; range, 13.9-30.8 kPa) exhibited significantly increased LSM values compared with those without cirrhosis (6.4 kPa; range, 5.7-7.8 kPa; P<0.001). Furthermore, LSM values in CTPV patients without cirrhosis were slightly higher compared with those of healthy volunteers (P=0.003), while no statistically significant difference was observed in LSM between CTPV patients with cirrhosis and CHB-related cirrhosis group. These findings indicated that LSM values could be used for the differential diagnosis of CTPV patients with or without cirrhosis. However, further validation studies are needed. PMID:33777190 | PMC:PMC7967803 | DOI:10.3892/etm.2021.9881 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Congenital dyserythropoietic anemia and drug-induced liver injury present as bland cholestasis: A case report

xlomafota13 shared this article with you from Inoreader Congenital dyserythropoietic anemia and drug-induced liver injury present as bland cholestasis: A case report Via Experimental and therapeutic medicine Exp Ther Med. 2021 May;21(5):456. doi: 10.3892/etm.2021.9887. Epub 2021 Mar 2. ABSTRACT Anemias and drug-induced liver injury(DILI) are separate disorders, which are difficult to diagnose. The clinical effects of DILI vary among individuals. However, the outcome determinants remain to be fully established. To the best of our knowledge, the role of anemia in DILI has yet to be reported. The present study reported on the case of one Chinese patient (male; age, 21 years) who experienced obvious drug-induced cholestasis. Of note, the hepatocyte injury was minimal compared with that in previously reported cases treated with the same drug. In addition, the patient suffered from mild hemolytic anemia with no obvious cause. A genetic pedigree analysis revealed compound heterozygous mutations in the congenital anemia-associated gene codanin 1, including the novel rare p.R1067H mutation. Treatment with ursodeoxycholic acid alone sufficed and the outcome was good. Therefore, whilst chronic hemolysis predisposed the liver to cholestasis, it could have shielded the liver from further injuries, since bilirubin, a by-product of hemolysis, is a known antioxidant. The results of the present study indicated that genetic screening may be used for the diagnosis of liver injury concurring with undiagnosed anemia. PMID:33777192 | PMC:PMC7967802 | DOI:10.3892/etm.2021.9887 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

miR-23a-3p regulates the proliferation and apoptosis of human lens epithelial cells by targeting Bcl-2 in an in vitro model of cataracts

xlomafota13 shared this article with you from Inoreader miR-23a-3p regulates the proliferation and apoptosis of human lens epithelial cells by targeting Bcl-2 in an <em>in vitro</em> model of cataracts Via Experimental and therapeutic medicine Exp Ther Med. 2021 May;21(5):436. doi: 10.3892/etm.2021.9853. Epub 2021 Feb 26. ABSTRACT Cataracts account for ~50% of the cases of blindness in individuals worldwide. The apoptosis of lens epithelial cells (LECs) occurs during the formation of cataracts, which is a non-congenital condition. Numerous microRNAs (miRs) have been reported to regulate apoptosis in LECs. For instance, miR-23a expression levels were shown to be upregulated in cataractous lenses; however, the function of miR-23a in cataracts remains undetermined. To establish an in vitro model of cataracts, human LECs, HLE-B3 cells, were induced with 200 µmol/l H2O2 for 24 h. HLE-B3 cells were transfected with the miR-negative control (NC) mimic, miR-23a-3p mimic, miR-NC inhibitor, miR-23a-3p inhibitor, small interfering RNA (siRNA) targeting BCL2 (siRNA-BCL2) and siRNA-NC. The expression levels of miR-23a-3p were detected using reverse transcrip tion-quantitative PCR. The interaction between miR-23a-3p and the 3'-untranslated region (UTR) of the target mRNA BCL2 was predicted by TargetScan 7.1, and further validated using a dual luciferase reporter assay. The BCL2 protein expression levels were analyzed using western blotting, cell proliferation was determined using a CCK-8 assay and the levels of cell apoptosis were analyzed using flow cytometric analysis. The results of the present study revealed that the expression levels of miR-23a-3p were significantly upregulated, while the expression levels of BCL2 were significantly downregulated in H2O2-induced HLE-B3 cells compared to untreated control cells. BCL2 was shown to be a target of miR-23a-3p. The miR-23a-3p inhibitor subsequently attenuated H2O2-induced apoptosis and increased the proliferation of HLE-B3 cells, which was partially reversed by siRNA-BCL2. In conclusion, the findings of the current study suggested that the inhib ition of miR-23a-3p may attenuate H2O2-induced cataract formation by targeting BCL2, thus providing a novel therapeutic target for the treatment of patients with cataracts in the clinic. PMID:33777189 | PMC:PMC7967796 | DOI:10.3892/etm.2021.9853 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Dysregulation of lncRNA SNHG1/miR-145 axis affects the biological function of human carotid artery smooth muscle cells as a mechanism of carotid artery restenosis

xlomafota13 shared this article with you from Inoreader Dysregulation of lncRNA SNHG1/miR-145 axis affects the biological function of human carotid artery smooth muscle cells as a mechanism of carotid artery restenosis Via Experimental and therapeutic medicine Exp Ther Med. 2021 May;21(5):423. doi: 10.3892/etm.2021.9867. Epub 2021 Feb 25. ABSTRACT Carotid angioplasty and stenting have developed into reliable options for patients with carotid stenosis. However, postoperative restenosis remains a serious and unresolved problem. Restenosis is partly caused by the proliferation of vascular smooth muscle cells. As certain long non-coding RNAs (lncRNAs) affect cell proliferation and migration, the present study aimed to investigate them as novel biomarkers for restenosis development and to further reveal the potential underlying mechanisms. The expression of lncRNA small nucleolar RNA host gene 1 (SNHG1) and microRNA145 (miR-145) in human carotid artery smooth muscle cells (hHCtASMCs) was analyzed using reverse transcription-quantitative PCR. In addition, a luciferase reporter assay was performed to investigate the interaction between SNHG1 and miR-145. The effects of the SNHG1/miR-145 axis on the proliferation and migration of hHCtASMCs were evaluated by Cell Counting Kit-8 and Transwell assays. Serum SNHG1 and miR-145 expression levels were increased and decreased, respectively, in patients with restenosis (all P<0.001). High SNHG1 and low miR-145 were identified as risk factors for restenosis onset (all P<0.01). Furthermore, decreasing SNHG1 expression levels in hHCtASMCs inhibited cell proliferation and migration. The luciferase reporter assay and expression results demonstrated that miR-145 may be a target of SNHG1 and mediated the effects of SNHG1 on hHCtASMC proliferation and migration. The results obtained suggested that abnormal expression of SNHG1 and miR-145 may be risk factors for restenosis. The present study revealed that the SNHG1/miR-145 axis regulates hHCtASMC proliferation and migration, indicating its potential for restenosis prevention and treatment. PMID:33777187 | PMC:PMC7967805 | DOI:10.3892/etm.2021.9867 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

The Endonasal Endoscopic Management of Cerebrospinal Fluid Rhinorrhea

xlomafota13 shared this article with you from Inoreader The Endonasal Endoscopic Management of Cerebrospinal Fluid Rhinorrhea Via leak of cerebrospinal fluid Cureus. 2021 Feb 20;13(2):e13457. doi: 10.7759/cureus.13457. ABSTRACT Introduction Cerebrospinal fluid (CSF) rhinorrhea is the result of a bony defect at the skull base with disruption of the arachnoid, dura mater, and sinonasal mucosa that leads to an active CSF leak and flow of clear fluid from the nose. The endoscopic repair of CSF leaks and skull defects have been used by an increasing number of surgeons and is the standard of care for repairing CSF leaks. Materials and methods We conducted a retrospective study of all cases of CSF leaks managed via the endonasal endoscopic approach from 2010 to 2020 at a tertiary referral hospital of King Fahad Specialist Hospital, Dammam (KFSH-D). Results Over 10 years, 61 procedures were performed on a total of 56 patients (average age, 39.9 years) with 26 spontaneous CSF leaks and 30 traumatic CSF leaks. The leak sites were frontal bone in 14% of the cases, the roof of the ethmoid in 25%, the cribrifo rm plate of ethmoid in 39%, and the walls of sphenoid sinus in 21%; multiple site defects were found in eight patients. The defect was localized by high-resolution computed tomography (CT) of the paranasal sinuses and skull base and magnetic resonance imaging (MRI) in all patients. CT cisternography, intrathecal fluorescein injection, and topical application of fluorescein dye were used in patients as required. A combination of free grafts and flaps materials were used in most patients. A middle and inferior turbinate graft was used in 12 patients, a septal cartilage graft in 18 patients, and a pedicled nasoseptal flap in 12 patients. The success rate was 92% after the first closure attempt. A recurrence of CSF leaks was observed in four patients. The mean hospitalization time was 6.5 days. The postoperative follow-up period ranged from one year to 10 years with a mean postoperative follow-up time of three years. Conclusions The endonasal endoscopic approach is the current standard of care for repairing most CSF leaks and skull base defects. We have had an excellent experience with endonasal endoscopic CSF leak repair, with high success rates and low morbidity. Our results support the effectiveness and safety of this technique and should encourage otolaryngologists to apply the procedure in cases of CSF leak. PMID:33777546 | PMC:PMC7984942 | DOI:10.7759/cureus.13457 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Compartmentalization: An Open Technique for Frontal Sinus Repair and Preservation-Description of Technique and Early Case Series

xlomafota13 shared this article with you from Inoreader Compartmentalization: An Open Technique for Frontal Sinus Repair and Preservation-Description of Technique and Early Case Series Via leak of cerebrospinal fluid J Neurol Surg B Skull Base. 2021 Apr;82(2):189-195. doi: 10.1055/s-0039-1696683. Epub 2019 Sep 12. ABSTRACT Background Cranialization or obliteration is widely accepted intervention for traumatic or intentional breach of the frontal sinus. These techniques, however, result in the loss of frontal sinus function and have a persistent risk of cerebrospinal fluid (CSF) leak and mucocele. Compartmentalization is an open technique for repair of the frontal sinus using allograft onlay and a vascularized periosteal flap that allows for preservation of frontal sinus function. Objective The main objective of this article is to describe the technique for compartmentalization of the frontal sinus and demonstrate its efficacy and complication rate with an early patient series. Methods Our technique includes the following key components: harvesting of a pedicled periosteal flap, frontal sinus repair through a bifrontal craniotomy with minimal mucosa removal, ensuring the patency of the nasal frontal outflow tract, and separation of the brain from the frontal sinus with a dual layer of periosteum and allograft. All cases of frontal sinus repair using the compartmentalization technique at our institution were reviewed. Charts were reviewed for CSF leak, mucocele, and other complications. Results Twenty-three patients underwent the described frontal sinus repair technique 17 for tumor and 6 for trauma. There were no CSF leaks and no mucoceles. One patient experienced postoperative anemia and a "parameningeal reaction" that were managed with a short course of antibiotics. Conclusions Compartmentalization, due to its sinus preservation and low complication rate, represents a meaningful step forward in neurosurgical technique for open frontal sinus repair. However, long-term outcomes are necessary to fully evaluate risk of mucocele. PMID:33777633 | PMC:PMC7987381 | DOI:10.1055/s-0039-1696683 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Reconstruct the anterior commissure with intralaryngeal mucosal flap

xlomafota13 shared this article with you from Inoreader Reconstruct the anterior commissure with intralaryngeal mucosal flap Via Clinical Otolaryngology Abstract An anterior glottic web formation occurs from either congenital or acquired causes.1 Acquired anterior glottic web is the most common type of glottic web, and can be caused by surgical, iatrogenic, or external trauma. The severity of clinical symptoms, which include dysphonia or dyspnea, varies significantly according to the extent of the web.2,3 The prevention of glottic web formation is extremely important for surgical intervention on the anterior commissure. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.