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Carotid endarterectomy (CEA) is a surgical procedure that treats the narrowed carotid arteries, which may be narrowed by atherosclerosis. Stenting is the insertion of a wire mesh scaffold into the narrowed portion of the carotid artery to keep it open by preventing blood from clotting. Using the study done over 10 years back as a point of reference, this study will seek an update on an assessment comparing CEA and stenting in studies carried out between 2015 and to date. The PICOS (population, intervention, control, outcome, and study designs) criteria were used to construct a set of inclusion and exclusion guidelines. This meta-analysis and systematic review used two forms of investigative analysis; both quantitative and qualitative assessments. From the studies, stroke (95% CI: 0.51-0.71, P < 0.001), myocardial infarction (95% CI: 1.49-3.42, P = 0.001), and stroke or death analysis (95% CI: 0.53-0.77, P < 0.001) were noted to be significant. From the analysis, CEA was observed as having better treatment results in terms of stroke events and stroke or death incidences when compared to stenting. Carotid stenting was observed as having lower cases of myocardial infarctions when compared to endarterectomy., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2023, Vasavada et al.)

Objective  The disequilibrium between oxidant and antioxidant systems causes oxidative stress. Further, it disrupts the cell and releases reactive oxygen species (ROS), which in turn damages the vascular functions. Cyclophilin A (CypA), an immunophilin, is released in a highly regulated manner from vascular smooth muscle cells and multiplies the deleterious effects of ROS, associated with cardiovascular diseases. Thus, the aim of the present study is to correlate serum CypA levels with the severity of coronary artery disease (CAD). Materials and Methods  Study participants composed of 103 adult subjects, among whom 73 subjects were cases who were diagnosed as CAD angiographically. Thirty years of age and gender-matched subjects were taken as controls. The cases were further divided into single, double, and triple vessel disease subgroups. Blood samples were collected for the estimation of serum CypA, malondialdehyde (MDA), high-sensitive C-reactive protein (hsCRP), lipid profile, and plasma-glycated hemoglobin (HbA1C) by relevant biochemical methods. Statistical Analysis  The analysis was done using SPSS version 25. The data were expressed as median/mean and interquartile range/standard error. The groups were compared using the Mann-Whitney U-test and the Kruskal-Wallis test. p -Value less than 0.05 was considered statistically significant. Comparison of area under the curve (AUC) in receiver operating characteristic (ROC) curves was performed. A correlation was done by Spearman rank correlation. Results  The mean levels of serum CypA, hsCRP, and MDA in cases were significantly higher than those of controls (38 vs. 27 ng/mL, 18 vs. 5.1 mg/L, and 26 vs. 14 nmol/mL, p  < 0.001). A positive correlation was observed between serum levels of CypA versus hsCRP and CypA versus MDA ( r  = 0.36 p  = 0.00, r  = 0.52, p  = 0.00). At cut-off values greater than 33 ng/mL and 2.1 mg/L, serum CypA and hsCRP have 71% sensitivity, 93% specificity (AUC = 0.83), 84% sensitivity, and 70% specificity (AUC = 0.78) respectively. The number of occluded vessels was positively correlated with both CypA and hsCRP. Also, Serum CypA showed a significant positive correlation with HbA1C. Conclusion  Serum CypA can be used as a valuable biomarker for CAD., Competing Interests: Conflict of Interest The authors declare that they have no conflicts of interest., (The Indian Association of Laboratory Physicians. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. ( https://creativecommons.org/licenses/by-nc-nd/4.0/ ).)

Background: Primary sclerosing cholangitis (PSC) is a progressive cholestatic disorder with liver transplantation (LT) being the only definitive treatment in end-stage disease. Recurrence of PSC after LT is a significant concern which can lead to graft loss. The aim of this study is to find out the disease recurrence and long-term outcome after living donor liver transplantation (LDLT) in PSC., Methods: We conducted a retrospective review of all patients undergoing LDLT for PSC at our centre. Of 2268 adult LTs from August 2004 to July 2018, 32 (1.4%) patients underwent LDLT for PSC including 6 with PSC and autoimmune hepatitis overlap. The data were reviewed to look for PSC recurrence, complications, and overall survival. All patients received tacrolimus-based immunosuppression. Data are shown as number, percentage, median, and interquartile range (IQR)., Result: The mean age of 32 LDLT recipients was 44 ± 12 years (males 22, females 10). At the time of transplantation, the mean child's score was 9 ± 1.6 and model for end-stage liver disease score was 18.9 ± 6.4. Ulcerative colitis was seen in 7 patients and none had cholangiocarcinoma. Majority of patients (n = 29) received right lobe graft and all but 3 underwent hepaticojejunostomy for biliary reconstruction. PSC recurrence was seen in 6 (20%) patients during a median follow-up of 59 (29-101) months, after exclusion of 2 patients with early mortality. A total of five patients died during follow-up, and one of these deaths was due to PSC recurrence. There were 2 perioperative deaths due to sepsis and 3 deaths on follow-up (sepsis in 2 and PSC recurrence in 1)., Conclusion: LDLT can be performed in PSC with good overall long-term outcomes., (© 2020 Indian National Association for Study of the Liver. Published by Elsevier B.V.)

Melanoma patients with additional positive lymph nodes in the completion lymph node dissection (CLND) following a positive sentinel lymph node (SLN) biopsy would have a poorer prognosis than patients with no additional positive lymph nodes. We hypothesize that the progression of disease from the SLN to the non-SLN compartment is orderly and is associated with the worsening of the disease status. Thus, the SLN and non-SLN compartments are biologically different in that cancer cells, in general, arrive in the SLN compartment before spreading to the non-SLN compartment. To validate this concept, we used a large cohort of melanoma patients from our prospective SLN database in an academic tertiary medical center. Adult cutaneous melanoma patients (n = 291) undergoing CLND after a positive SLN biopsy from 1994 to 2009 were analyzed. Comparison of 5-year disease-free survival and 5-year overall survival between positive (n = 66) and negative (n = 225) CLND groups was made. The 5-year disease-free survival rates were 55% (95% CI 49-62%) for patients with no additional LN on CLND versus 14% (95% CI 8-26%) in patients with positive LN on CLND (p < 0.0001, log-rank test). The median disease-free survival time was 7.4 years with negative CLND (95% CI 4.4-15+ years) and 1.2 years with positive CLND (95% CI 1.0-1.8 years). The 5-year overall survival rates were 67% (95% CI 61-74%) for negative CLND versus 38% (95% CI 28-52%) for positive CLND (p < 0.0001, log-rank test). The median overall survival time was 12.1 years for negative CLND (95% CI 9.3-15+ years) and 2.5 years for positive CLND (95% CI 2.2-5.7 years). This study shows that CLND status is a significant prognostic factor for patients with positive SLNs undergoing CLND. Also, it suggests an orderly progression of metastasis from the SLN to the non-SLN compartment. Thus, the SLN in the regional nodal basin draining the primary melanoma may serve as an important gateway for metastasis to the non-SLN compartment and beyond to the systemic sites.

Axonal pathology is a key contributor to long-term disability in multiple sclerosis (MS), an inflammatory demyelinating disease of the central nervous system (CNS), but the mechanisms that underlie axonal pathology in MS remain elusive. Evidence suggests that axonal pathology is a direct consequence of demyelination, as we and others have shown that the node of Ranvier disassembles following loss of myelin. In contrast to the node of Ranvier, we now show that the axon initial segment (AIS), the axonal domain responsible for action potential initiation, remains intact following cuprizone-induced cortical demyelination. Instead, we find that the AIS is disrupted in the neocortex of mice that develop experimental autoimmune encephalomyelitis (EAE) independent of local demyelination. EAE-induced mice demonstrate profound compromise of AIS integrity with a progressive disruption that corresponds to EAE clinical disease severity and duration, in addition to cortical microglial reactivity. Furthermore, treatment with the drug didox results in attenuation of AIS pathology concomitantly with microglial reversion to a less reactive state. Together, our findings suggest that inflammation, but not demyelination, disrupts AIS integrity and that therapeutic intervention may protect and reverse this pathology. GLIA 2016;64:1190-1209., (© 2016 Wiley Periodicals, Inc.)