Processed herbs have been widely used in eastern and western medicine; however, the mechanism of the medicinal effects has not been revealed yet. It is commonly believed that the central...

A combination therapy of RhizomaPolygonati (RP) with goji (Lycium chinense) has earned a long history in the prescriptions to promote male health. However, the mechanisms at both molecular and nanoscale quantum levels are unclear. Here, we found that processed RP extract induces apoptosis and cell cycle arrest in cancer cells, thereby inhibiting prostate cancer cell proliferation enhanced by processed goji extract associated with an augment of the nanoscale herbzyme of phosphatase. For network pharmacology analysis, RP-induced PI3K-AKT pathways are essential for both benign prostatic hyperplasia and prostate cancer, and the RP/goji combination induces potent pathways which include androgen and estrogen response, kinase regulation, apoptosis, and prostate cancer singling. In addition, the experimental investigation showed that the prostate cancer cells are sensitive to RP extract for inhibiting colony formation. Finally, the natural compound baicalein found in RP ingredients showed a linked activity of top-ranked signaling targets of kinases including MAPK, AKT, and EGFR by the database of cMAP and HERB. Thus, both the nanozyme and ingredients might contribute to the RP in anti-prostate cancer which can be enhanced by goji extract. The proposed nanoscale RP extract might be of significance in developing novel anti-prostate cancer agents by combining goji compositions and targeted therapy compounds.

Background Quantum nanodots especially carbon nanoparticles (CNPs) have been widely studied in biomedicine in imaging, and drug delivery, but anti-cancer mechanisms remain elusive. Methods Here, we investigated a type of cell death induced by food (beet, soybean) derived CNPs in cancer cells and tested whether CNPs induced DNA damage and resistant to anti-cancer agent PARP inhibitor (PARPi) could be overcome by quantum calculations, TEM, AFM, FT-IR, soft agar assay, and cytotoxicity assay. Results At high doses, CNPs derived from beet lead to a pop-like apoptosis (Carbopoptosis) in cancer cells. Quantum mechanical calculations confirmed CNPs binding with phosphate groups as well as DNA bases. At low doses, CNPs develop PARPi drug resistance through interactions between CNPs and PARPi. A synergistic drug effect was achieved with the combination of phosphatase inhibitor (PPi), PARPi, and CNPs. This is corroborated by the fact that sulfur modulated CNPs which exhibit super high phosphatase nanozyme activity abrogated the CNPs induced colony formation in anchorage-independent cancer cell growth. Conclusion Thus, our data suggest the CNPs intrinsic nanozyme activity of phosphatase may crosstalk with drug resistance, which can be reversed upon modulations.

Background and objectives: Patients admitted to the intensive care unit (ICU) have an increased risk of hospital-acquired infection (HAI). A diagnosis of cancer alone increases the risk of sepsis three–five-fold, which further increases the risk of nosocomial infection, subsequently deteriorates results, and leads to high mortality. In this study, we aimed to assess the mortality rate among hematologic oncologic patients with suspected infection who were subsequently admitted to the ICU and the predictive factors that are associated with high ICU mortality. Materials and Methods: This retrospective cohort study was conducted in the hematological oncology critical care unit of a tertiary care hospital between November 2017 and February 2021. We analyzed anonymized medical records of hospitalized hematologic oncologic patients who were suspected or proven to have infection in the hematology-oncology department and were subsequently transferred to the ICU. Results: Both shorter hospitalization and shorter ICU stay length were observed in survivors [9.2 (7.7–10.4)] vs. non-survivors [10 (9.1–12.9), p = 0.004]. Sepsis had the highest hazard ratio (7.38) among all other factors, as patients with sepsis had higher mortality rates (98% among ICU non-survivors and 57% among ICU survivors) than those who had febrile neutropenia. Conclusions: The overall ICU mortality in patients with hematologic malignancies was 66%. Sepsis had the highest hazard ratio among all other predictive factors, as patients with sepsis had higher mortality rates than those who had febrile neutropenia. Chronic hepatitis (HBV and HCV) was significantly associated with higher ICU mortality.

ObjectivesThere is limited published literature on the genetic risks of chronic inflammatory related disease (eg, obesity and cardiovascular disease) among the Central Asia population. The aim is to determine potential genetic loci as risk factors for obesity for the Kazakhstani population.SettingKazakhstan.ParticipantsOne hundred and sixty-three Kazakhstani nationals (ethnic groups: both Russians and Kazakhs) were recruited for the cross-sectional study. Linear regression models, adjusted for confounding factors, were used to examine the genetic associations of single nucleotide polymorphisms (SNPs) in 19 genetic loci with obesity (73 obese/overweight individuals and 90 controls).ResultsOverall, logistic regression analyses revealed genotypes C/T in CRP (rs1205), A/C in AGTR1 (rs5186), A/G in CBS (rs234706), G/G in FUT2 (rs602662), A/G in PAI-1 (rs1799889), G/T (rs1801131) and A/G (rs1801133) in MTHFR genes significantly decrease risk of overweight/obesity. After stratification for ethnicity, rs234706 was significantly associated with overweight/obesity in both Russians and Kazakhs, while rs1800871 was significant in Kazakhs only.ConclusionsThis study revealed that variations in SNPs known to be associated with cardiovascular health can also contribute to the risks of developing obesity in the population of Kazakhstan.