Comparison of the effects of synthesis methods of B,N, S,and P-doped carbon dots with high photoluminescence properties on HeLa tumor cells

Although heteroatom doping is widely used to promote the optical properties of carbon dots for biological applications, the synthesis process still has problems such as multi-step process, complicating the setting of instrument along with uncontrolled products. In the present study, some elements such as boron, nitrogen, sulfur, and phosphor were intentionally doped into citric acid-based carbon dots by furnace- and microwave-assisted direct and simple carbonization processes. The process produced nanoparticles with an average diameter of 5–9 nm with heteroatoms (B, N, S, and P) placed on the core and surface of carbon dots. Among the doped carbon dots prepared, boron-doped carbon dots obtained by the microwave-assisted (B-CDs2) process showed the highest photoluminescence intensity with a quantum yield (QY) of about 32.96%. All obtained carbon dots exhibit good stability (at pH 6–12 and high ionic strength concentrations up to 0.5 M), whereas cytotoxicity analysis showed that all doped carbon dots are low-toxic with an average cell viability percentage above 80% up to 500 μg mL⁻¹. It can be observed from the CLSM image of all doped carbon dots that the doping process not only increases the QY percentage, but also might accelerate the HeLa uptake on it and produce strong carbon dot emission at the cytoplasm of the cell. Thus, the proposed synthesis process is promising for high-potency bioimaging of HeLa cancer cells.

Investigation of the effect of nitrogen, boron, sulphur, and phosphor as doping elements on carbon dots, where boron-carbon dots performed good potential for bioimaging application with best optical properties and specific targeting features.     

Polymorphisms in IL10 may alter CD4 T-cell counts in Indonesian HIV patients beginning antiretroviral therapy

Interleukin 10 (IL-10) is a potent anti-inflammatory cytokine influenced by single nucleotide polymorphisms (SNP) located in upstream regulatory regions. Here we address the effects of five SNP (rs1518111, rs3021094, rs3024491, rs1800872 and rs1800871) on CD4 T-cell counts in Indonesian HIV patients assessed before ART and over 12 months on treatment. Heterozygosity at rs1518111 or rs1800872 associated with low CD4 T-cell counts at all time points. Both alleles were carried in two haplotypes. Haplotype 21122 (present in 30% of participants) associated with low CD4 T-cell counts, whereas 21222 (in 6% of participants) did not. Hence untyped SNP(s) tagged by 21122 may depress CD4 T-cell counts. The association with heterozygosity suggests synergy with an allele from a haplotype lacking rs1518111 and/or rs1800872.     

Synthesis of N-(phenylcarbamothioyl)-benzamide derivatives and their cytotoxic activity against MCF-7 cells

Cancer is one of the leading causes of death both in developing countries and across the globe. In Indonesia, cancer ranks as the fifth primary cause of death following heart disease, stroke, respiratory tract and diarrhea. Therefore, studies on thiourea derivative compounds as anticancer agents have been profoundly conducted but still require further continuous development. In the present study, we aimed tosynthesize new anticancer compounds of N-(phenylcarbamothioyl)-benzamide derivatives, namely N-(phenylcarbamothioyl)-4-bromobenzamide and N-(phenylcarbamothioyl)-4-fluorobenzamide compounds and assess their activities against MCF-7 breast cancer cells. The initial step was to predict the drug-receptor activity through docking between the tested compounds using epidermal growth factor receptor (EGFR) (PDB code: 1M17). The compounds were futher synthesized from the reactions between benzoyl chloride derivatives and N-phenylthiourea. The structures of the new compounds were identifiedusing FTIR, ¹H NMR, ¹³C NMR and mass spectra. The cytotoxic activities (IC₅₀) to breast cancer cells of MCF-7 N-(phenylcarbamothioyl)-4-bromobenzamide compound and N-(phenylcarbamothioyl)-4-fluorobenzamide were 0.27 mM and 0.31 mM, respectively. These two new compounds had better cytotoxic activities than those of the currenthydroxyurea-based anticancer drugs (the reference compound) with an IC₅₀ value of 9.76 mM. Furthermore, these two newcompounds were not toxic to Vero normal cells. Therefore, they possessedtremendous potentials as the candidates for new drugs against breastcancer.     

Characterization of Natural Killer Cells in HIV Patients Beginning Therapy with a High Burden of Cytomegalovirus

Background: Active infections with cytomegalovirus (CMV) increase NK cell expression of the inhibitory receptor LIR-1 and the activating receptor NKG2C in transplant recipients. However, the effects of CMV on NK cells are different in HIV patients stable on antiretroviral therapy (ART) and have not been analyzed in young HIV patients beginning ART.

Methodology: We followed a cohort of 78 Indonesian HIV patients beginning ART. CMV antibodies were measured in plasma before ART (baseline), and after 1, 3, 6, and 12 months. CMV DNA was sought in blood granulocytes at baseline by quantitative PCR assay and a deletion in the NKG2C gene was identified by PCR. NK cell profiles were monitored by flow cytometry in 19 patients stratified by the presence of CMV DNA. Healthy controls (n = 17) were assessed once.

Results: All 78 patients were CMV seropositive and 41 had detectable CMV DNA. CMV DNA+ patients had higher proportions of total NK cells and CD16⁺ NK cells at baseline, but similar expression of LIR-1 and NKp30 on NK cells on ART. However, levels of CMV antibody were inversely related to median LIR-1 expression on NK cells. A dramatic elevation in cells expressing NKG2C was restricted to CMV DNA+ patients heterozygous for the NKG2C deletion. Patients with High NKG2C expression had lower levels of CMV antibodies.

Conclusion: A subpopulation of NK cells expressing NKG2C was induced by CMV replication in HIV patients heterozygous for a deletion in this gene. Individuals with an abundant NKG2C⁺ and LIR-1⁺ NK cells displayed lower levels of CMV reactive antibody.