Antibiotic susceptibility and biofilm forming ability of Staphylococcus aureus isolated from Jordanian patients with diabetic foot ulcer.

Background and Objectives: Microbial biofilm is characterized by the irreversible attachment of planktonic cells to a surface and is usually associated with high antimicrobial resistance with worsening the wound healing. The objective of the study was to determine the prevalence of Staphylococcus aureus in diabetic foot ulcers (DFUs) of diabetic patients and to investigate antibiotic susceptibility patterns of these isolates. In addition to screen biofilm forming ability of isolated S. aureus. Materials and Methods: A total of 112 non-healing wound swabs of diabetic foot patients were collected and cultured on different culture media to identify and characterize 98 isolates. The S. aureus isolates were examined for their antibiotic susceptibility to different antimicrobial agents. Furthermore, S. aureus isolates were evaluated for their biofilm production capability using the Tissue Culture Plate Method (TPC). The level of icaA gene expression was determined by RT-PCR. Results: The results of this study showed that these non-healing wounds yield positive cultures, with an average of 1.67 organisms per sample. The isolates showed highest resistance against oxacillin (95.2%) and lowest resistance against linezolid (3.7%). All isolates were biofilm producers and a significant association with the icaA gene expression level was recorded. Conclusion: This study showed that S. aureus isolates have a great ability to produce biofilms that are associated with the chronicity of wounds in diabetic patients. Routine screening for biofilm formers in chronic wounds and their antibiotic susceptibility testing will help in early treatment and prevent any other complications.

Determination of Toxic Elements in Cannabinoid and Opioid Drugs and Their Impact on Addicts' Health: A Comparative Study.

Drug addiction is associated with significant health risks, including cardiovascular complications, cancer, and mental disorders. Illicit drugs, such as cannabinoids and opioids, including prescription medications, are widely consumed and have profound health consequences. Understanding the health effects of the toxic elements in these substances is critical for overdose prevention and effective recovery strategies. This study aimed to determine toxic elements, including arsenic (As), cadmium (Cd), mercury (Hg), and nickel (Ni), in cannabinoid and opioid drugs and in biological samples (whole blood, scalp hair, and serum) from 311 male drug abuse patients aged 15-60 years with a history of drug abuse. The participants were categorized into three age groups. The comparative analysis involved 113 reference subjects of the same age groups. The sample preparation employed microwave-assisted acid digestion, and the toxic elements were quantified using atomic absorption spectrophotometry. Accuracy was ensured using certified reference materials for hair, whole blood, and serum samples. Drug-addicted subjects had significantly higher concentrations of toxic elements (arsenic, cadmium, mercury, and nickel) in biological samples than referent subjects (p > 0.001). Elevated levels of these toxic elements may increase susceptibility to infections, possibly due to malnutrition, drug-related effects, and additional contaminants. These findings necessitate further studies to explore the long-term health outcomes, potential treatment options, and broader socioeconomic impacts of substance abuse. This study serves as a baseline for future research in this critical public health field.

Bioremediation of Neonicotinoid Pesticide, Imidacloprid, Mediated by Bacillus cereus.

Imidacloprid, a toxic pesticide of the chloronicotinyl category, is employed extensively in agricultural fields, and its exposure causes serious health issues. Biodegradation is considered to be a green and economical approach to remediate pesticides. Herein, imidacloprid degradation efficiency of Bacillus sp. is highlighted, among which Bacillus cereus exhibited the greatest degradation; optimization of experimental variables (pH, imidacloprid and agitation time) via Box-Behnken factorial design and analysis of variance (ANOVA) revealed 92% biodegradation at the initial substrate concentration of 0.03 mM, aerobically in 11 days under favorable pH 7. The subsequent metabolites, identified through liquid chromatography-mass spectrometry, were 5-hydroxy imidacloprid, imidacloprid-guanidine and 6-chloronicotinic acid.

Enzalutamide Overcomes Dihydrotestosterone-Induced Chemoresistance in Triple- Negative Breast Cancer Cells via Apoptosis.

BACKGROUND: Triple-negative breast cancer is challenging to treat due to its heterogeneity and lack of therapeutic targets. Hence, systemic chemotherapy is still the mainstay in TNBC treatment. Unfortunately, patients commonly develop chemoresistance. Androgen signalling through its receptor is an essential player in breast cancer, where it has been shown to confer chemoresistance to TNBC cells. OBJECTIVE: The objective of the study was to elucidate the mechanistic effects of enzalutamide in the chemoresponse of TNBC cells to doxorubicin through the apoptosis pathway. METHODS: MDA-MB-231 and MDA-MB-453 cells were used as model systems of TNBC. Cell viability and apoptosis were investigated upon treatment of cells with doxorubicin in the presence of dihydrotestosterone (DHT) and/or enzalutamide. Caspase 3/7 activity and TUNEL assays were performed to assess the induction of apoptosis. The expression of apoptosis-regulatory genes was assayed by qPCR for the detection of expression changes. RESULTS: Enzalutamide decreased the viability of MDA-MB-231 and MDA-MB- 453 cells and reduced DHT-induced chemoresistance of both cell lines. It also increased the chemosensitivity towards doxorubicin in MDA-MB-231 cells. Increasing DNA degradation and caspase 3/7 activity were concomitant with these outcomes. Moreover, enzalutamide downregulated the expression of the anti-apoptosis genes, mcl1 and bcl2, in MDA-MB-231 cells, while increasing the expression of the pro-apoptotic gene bid. On the other hand, DHT upregulated the expression of the anti-apoptosis genes, mcl1 and bcl2, in both cell lines. CONCLUSION: DHT increased the expression of the anti-apoptosis genes mcl1 and bcl2 in the TNBC cells, presumably leading to cell survival via the prevention of doxorubicin-induced apoptosis. On the other hand, enzalutamide may sensitize the cells to doxorubicin through downregulation of the bid/bcl2/mcl1 axis that normally activates the executive caspases, caspase 3/7. The activities of the latter enzymes were apparent in DNA degradation at the late stages of apoptosis.