Pseudogap phase of cuprate superconductors confined by Fermi surface topology

The properties of cuprate high-temperature superconductors are largely shaped by competing phases whose nature is often a mystery. Chiefly among them is the pseudogap phase, which sets in at a doping $p^*$ that is material-dependent. What determines $p^*$ is currently an open question. Here we show that the pseudogap cannot open on an electron-like Fermi surface, and can only exist below the doping $p_{FS}$ at which the large Fermi surface goes from hole-like to electron-like, so that $p^*$ $\leq$ $p_{FS}$. We derive this result from high-magnetic-field transport measurements in La$_{1.6-x}$Nd$_{0.4}$Sr$_x$CuO$_4$ under pressure, which reveal a large and unexpected shift of $p^*$ with pressure, driven by a corresponding shift in $p_{FS}$. This necessary condition for pseudogap formation, imposed by details of the Fermi surface, is a strong constraint for theories of the pseudogap phase. Our finding that $p^*$ can be tuned with a modest pressure opens a new route for experimental studies of the pseudogap.Comment: 15 pages, 5 figures, 7 supplemental figure

Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-Naïve chronic HBV patients

Background: Immunomodulators and Nucleotide analogues have been used globally for the dealing of chronic hepatitis B virus (HBV) infection. However, the development of drug resistance is a major limitation to their long-term effectiveness. Objectives: The aim of this study was to characterize the hepatitis B virus reverse transcriptase (RT) protein variations among Iranian chronic HBV carriers who did not receive any antiviral treatments. Materials and Methods: Hepatitis B virus partial RT genes from 325 chronic in active carrier patients were amplified and directly sequenced. Nucleotide/amino acid substitutions were identified compared to the sequences obtained from the database. Results: All strains belonging to genotype D.365 amino-acid substitutions were found. Mutations related to lamivudine, adefovir, telbivudine, and entecavir occurred in (YMDD) 4% (n = 13), (SVQ) 17.23% (n = 56), (M204I/V + L180M) 2.45% (n = 8) and (M204I) 2.76% (n = 9) of patients, respectively. Conclusions: RT mutants do occur naturally and could be found in HBV carriers who have never received antiviral therapy. However, mutations related to drug resistance in Iranian treatment-naïve chronic HBV patients were found to be higher than other studies published formerly. Chronic HBV patients should be monitored closely prior the commencement of therapy to achieve the best regimen option. © 2013, KOWSAR Corp

Wiedemann-Franz law and abrupt change in conductivity across the pseudogap critical point of a cuprate superconductor

The thermal conductivity $\kappa$ of the cuprate superconductor La$_{1.6-x}$Nd$_{0.4}$Sr$_x$CuO$_4$ was measured down to 50 mK in seven crystals with doping from $p=0.12$ to $p=0.24$, both in the superconducting state and in the magnetic field-induced normal state. We obtain the electronic residual linear term $\kappa_0/T$ as $T \to 0$ across the pseudogap critical point $p^{\star}= 0.23$. In the normal state, we observe an abrupt drop in $\kappa_0/T$ upon crossing below $p^{\star}$, consistent with a drop in carrier density $n$ from $1 + p$ to $p$, the signature of the pseudogap phase inferred from the Hall coefficient. A similar drop in $\kappa_0/T$ is observed at $H=0$, showing that the pseudogap critical point and its signatures are unaffected by the magnetic field. In the normal state, the Wiedemann-Franz law, $\kappa_0/T=L_0/\rho(0)$, is obeyed at all dopings, including at the critical point where the electrical resistivity $\rho(T)$ is $T$-linear down to $T \to 0$. We conclude that the non-superconducting ground state of the pseudogap phase at $T=0$ is a metal whose fermionic excitations carry heat and charge as conventional electrons do.Comment: 10 pages, including Supplementary Materia

Molecular epidemiology of epstein-barr virus (ebv) in patients with hematologic malignancies

Background: Epstein-Barr virus (EBV) is associated with different malignant diseases, such as Hodgkin lymphoma (HL) and lymphoproliferative disorders. Patients with hematologic malignancies by variable severity could be suspected for the infection with different types of this virus. This preliminary study reported the genotyping and related viral load of Epstein-Barr virus in Iranian patients with hematologic malignancies for estimation of possible factors affecting malignancy. Methods: Peripheral blood mononuclear cells (PBMC) of HL (n=20), NHL (n=29), acute lymphocytic leukemia (ALL) (n=18) and chronic lymphocytic leukemia (CLL) (n=12) were obtained. After DNA extraction, a nested-PCR and a conventional-PCR targeting EBNA-2 and EBNA-3C genes were performed. A real-time PCR assay for viral load quantitation carried out. Standard curve analysis used for evaluation of amplification specificity. Results: Of 79 included patients, 34 (43) were EBV positive. There were 23.5 (8/34), 38.2 (13/34), 23.5 (8/34), 14.8 (5/34) in HL, NHL, ALL and CLL groups, respectively. Also, the main genotype was genotype I (91.2) which it follows by 8.8 (3/34) genotype II. The real-time PCR assay showed the mean viral load ± std. deviation was 2.75�105 ± 1.202�106 copies/μg DNA and the higher viral load was seen in NHL patients. Conclusion: This preliminary investigation in Iran shows that the main EBV genotype into our region probably is genotype I (91.2) which it is similar to others. We could not find any statistically significant association between the virus infection and viral load with any specific disease and patients' demographic data. © 2020, Asian Pacific Organization for Cancer Prevention

Novel and emerging mutations of SARS-CoV-2: Biomedical implications

Coronavirus disease-19 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The SARS-CoV-2 virus strains has geographical diversity associated with diverse severity, mortality rate, and response to treatment that were characterized using phylogenetic network analysis of SARS-CoV-2 genomes. Although, there is no explicit and integrative explanation for these variations, the genetic arrangement, and stability of SARS-CoV-2 are basic contributing factors to its virulence and pathogenesis. Hence, understanding these features can be used to predict the future transmission dynamics of SARS-CoV-2 infection, drug development, and vaccine. In this review, we discuss the most recent findings on the mutations in the SARS-CoV-2, which provide valuable information on the genetic diversity of SARS-CoV-2, especially for DNA-based diagnosis, antivirals, and vaccine development for COVID-19. © 202

Corrigendum to: �Novel and emerging mutations of SARS-CoV-2: Biomedical implications� Biomed. Pharmacother. 139 (2021) 111599 (Biomedicine & Pharmacotherapy (2021) 139, (S075333222100384X), (10.1016/j.biopha.2021.111599))

The authors regret the incorrect publication of affiliations of some of the authors in the original article. The correct affiliation of the authors are presented below: Elmira Mohammadia,b Fatemeh Shafieec Kiana Shahzamanid Mohammad Mehdi Ranjbare Abbas Alibakhshif Shahrzad Ahangarzadehg Leila Beikmohammadih,i Laleh Shariatij,k Soodeh Hooshmandil Behrooz Ataeim Shaghayegh HaghjooyJavanmarda a Applied Physiology Research Center, Cardiovascular Research Institute, Department of Physiology, Isfahan University of Medical Sciences, Isfahan, Iran b Core Research Facilities, Isfahan University of Medical Sciences, Isfahan, Iran c Department of Pharmaceutical Biotechnology, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran d Isfahan Gastroenterology and Hepatology Research Center (lGHRC), Isfahan University of medical sciences, Isfahan, Iran e Razi Vaccine and Serum Research Institute, Agricultural Research, Education, and Extension Organization (AREEO), Karaj, Iran f Molecular Medicine Research Center, Hamadan University of Medical Sciences, Hamadan, Iran g Infectious Diseases and Tropical Medicine Research Center, Isfahan University of Medical Sciences, Isfahan, Iran h Department of Biochemistry, Erasmus University Medical Center, Rotterdam, The Netherlands i Stem Cell and Regenerative Medicine Center of Excellence, Tehran University of Medical Sciences, 14155-6559 Tehran, Iran j Biosensor Research Center, School of Advanced Technologies in Medicine, Isfahan University of Medical Sciences, Isfahan, Iran k Department of Biomaterials, Nanotechnology and Tissue Engineering, School of Advanced Technologies in Medicine, Isfahan University of Medical Sciences, Isfahan, Iran l Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran m Nosocomial Infection Research Center, Isfahan University of Medical Sciences, Isfahan, Iran The authors would like to apologise for any inconvenience caused. © 202