High energy density storage, antifungal activity and enhanced bioimaging by green self-doped heteroatom carbon dots.

Self-heteroatom-doped N-carbon dots (N-CDs) with a 2.35 eV energy gap and a 65.5% fluorescence quantum yield were created using a one-step, efficient, inexpensive, and environmentally friendly microwave irradiation method. FE-SEM, EDX, FT-IR, XRD, UV-VIS spectroscopy, FL spectroscopy, and CV electrochemical analysis were used to characterise the produced heteroatom-doped N-CDs. The graphitic carbon dot surface is doped with heteroatom functional groups such (S, P, K, Mg, Zn) = 1%, in addition to the additional passivating agent (N), according to the EDX surface morphology and the spontaneous heteroatom doping was caused by the heterogeneous chemical composition of pumpkin seeds. These spontaneous heteroatom-doped N-CDs possess quasispherical amorphous graphitic structure with an average size of less than 10 nm and the interplaner distance of 0.334 nm. Calculations utilising cyclic voltammetry showed that the heteroatom-doped N-CDs placed on nickel electrodes had a high specific capacitance value of 1044 F/g at a scan rate of 10 mV/s in 3 M of KOH electrolyte solution. Furthermore, it demonstrated a high energy and power density of 28.50 Wh/kg and 3350 W/kg, respectively. The higher value of specific capacitance and energy density were attributed to the fact that the Ni/CDs electrode material possesses both EDLC and PC properties due to the sufficient surface area and the multiple active sites of the prepared N-CDs. Furthermore, the heteroatom N-CDs revealed the antifungal action and bioimaging of the "Cladosporium cladosporioides" mould, which is mostly accountable for economic losses in agricultural products. The functional groups of nitrogen, sulphur, phosphorus, and zinc on the surface of the CDs have strong antibacterial and antifungal properties as well as fluorescence enhanced bioimaging.

Effect of insulin-like growth factor I on HIV type 1 long terminal repeat-driven chloramphenicol acetyltransferase expression.

In this study, we have investigated the ability of insulin-like growth factor I (IGF-I) to inhibit HIV long terminal repeat (LTR)-driven gene expression. Using COS 7 cells cotransfected with tat and an HIV LTR linked to a chloramphenicol acetyltransferase (CAT) reporter, we observed that physiological levels of IGF-I (10(-9) M) significantly inhibited CAT expression in a concentration- and time-dependent manner. IGF-I did not inhibit CAT expression in COS 7 cells transfected with pSVCAT, and did not affect CAT expression in the absence of cotransfection with tat. Transfection of HIV-1 proviral DNA into COS 7 cells +/- IGF-I resulted in a significant decrease (p < 0.05) in infectious virion production. Both IGF-I and Ro24-7429 inhibited LTR-driven CAT expression, while TNF-alpha-enhanced CAT expression was not affected by IGF-I. On the other hand, a plasmid encoding parathyroid hormone-related peptide exhibited dramatic additivity of inhibition of CAT expression in COS 7 cells. Finally, we show that in Jurkat or U937 cells cotransfected with HIVLTRCAT/tat, IGF-I significantly inhibited CAT expression. Further, interleukin 4 showed in U937 cells inhibition of CAT expression that was not additive to IGF-I induced inhibition. Our data demonstrate that IGF-I can specifically inhibit HIVLTRCAT expression. This inhibition may occur at the level of the tat/TAR interaction. Finally, this IGF-I effect is seen in target cell lines and similar paths of inhibition may be involved in the various cell types employed.

Identification of sequences downstream of the primer binding site that are important for efficient replication of human immunodeficiency virus type 1.

Reverse transcription of retroviruses is initiated from an 18-nucleotide (nt) primer binding site (PBS), located within the 5' region of viral genomic RNA, to which the host cell-derived tRNA primer is annealed and also involves viral genomic sequences outside the PBS. We constructed proviral DNA clones of human immunodeficiency virus (HIV) that had selective deletions of either a 7-nt segment found immediately downstream of the PBS or an extended nontranslated 54-nt stretch located immediately downstream of the PBS and containing the aforementioned 7-nt segment. Synthesis of minus-strand strong-stop DNA was assessed with MT-4 cells infected with viruses derived from COS-7 cells that had been transfected with these various constructs. We found that similar levels of minus-strand strong-stop DNA as well as DNA produced after template switching were expressed in MT-4 cells infected with COS-7-derived wild-type viruses or with viruses that had the 7-nt segment deleted. In contrast, significantly lower levels of viral DNA were detected in MT-4 cells after infection with viruses that had deletions of the 54-nt stretch. Furthermore, the molecular clone containing the 7-nt deletion was able to replicate with wild-type kinetics, while that containing the 54-nt deletion displayed a significantly diminished capacity in this regard. Further deletion analysis showed that a 16-nt segment at the 3' end of this 54-nt segment was largely responsible for these effects. We also conducted studies to determine levels of viral mRNA in COS-7 cells that had been transfected with equivalent amounts of DNA derived from either a wild-type HIV construct or our various deletion mutants. In the case of transfections performed with the 7-nt deletion mutant and wild-type HIV DNA, high levels of viral mRNA transcripts were detected, which was not the case for the 54 nt-deletion mutant. However, these various mRNAs possessed similar stabilities, as shown through studies in which transcript formation was arrested by treatment of cells with actinomycin D. Thus, the 54-nt segment of 5' nontranslated RNA, located downstream of the PBS, is involved in efficient expression of each of viral DNA, mRNA, and infectious virus.