ABSTRACT
Highly specific detection of tumor-associated biomarkers remains a challenge in the diagnosis of prostate cancer. In this research, Maackia amurensis (MAA) was used as a recognition element in the functionalization of an electrochemical impedance-spectroscopy biosensor without a label to identify cancer-associated aberrant glycosylation prostate-specific antigen (PSA). The lectin was immobilized on gold-interdigitated microelectrodes. Furthermore, the biosensor's impedance response was used to assess the establishment of a complex binding between MAA and PSA-containing glycans. With a small sample volume, the functionalized interdigitated impedimetric-based (IIB) biosensor exhibited high sensitivity, rapid response, and repeatability. PSA glycoprotein detection was performed by measuring electron transfer resistance values within a concentration range 0.01-100 ng/mL, with a detection limit of 3.574 pg/mL. In this study, the ability of MAA to preferentially recognize α2,3-linked sialic acid in serum PSA was proven, suggesting a potential platform for the development of lectin-based, miniaturized, and cost effective IIB biosensors for future disease detection.
Subject(s)
Biosensing Techniques , Prostatic Neoplasms , Male , Humans , Lectins/chemistry , Biomarkers, Tumor , Prostate-Specific Antigen , Maackia/metabolism , Prostate/metabolism , Prostatic Neoplasms/diagnosis , Biosensing Techniques/methodsABSTRACT
Prostate cancer is currently diagnosed using the conventional gold standard methods using prostate-specific antigen (PSA) as the selective biomarker. However, lack of precision in PSA screening has resulted in needless biopsies and delays the treatment of potentially fatal prostate cancer. Thus, identification of glycans as novel biomarkers for the early detection of prostate cancer has attracted considerable attention due to their reliable diagnostic platform compared with the current PSA systems. Therefore, biosensing technologies that provide point-of-care diagnostics have demonstrated the ability to detect various analytes, including glycosylated micro- and macro-molecules, thereby enabling versatile detection methodologies. This highlight article discusses recent advances in the biosensor-based detection of prostate cancer glycan biomarkers and the innovative strategies for the conjugation of nanomaterials adapted to biosensing platforms. Finally, the article is concluded with prospects and challenges of prostate cancer biosensors and recommendations to overcome the issues associated with prostate cancer diagnosis.
Subject(s)
Biomarkers, Tumor/analysis , Biosensing Techniques , Prostate-Specific Antigen/analysis , Prostatic Neoplasms/diagnosis , Glycosylation , Humans , MaleABSTRACT
BACKGROUND: Renal denervation (RDN) may lower blood pressure (BP); however, it is unclear whether medication changes may be confounding results. Furthermore, limited data exist on pattern of ambulatory blood pressure (ABP) response-particularly in those prescribed aldosterone antagonists at the time of RDN. METHODS: We examined all patients treated with RDN for treatment-resistant hypertension in 18 UK centres. RESULTS: Results from 253 patients treated with five technologies are shown. Pre-procedural mean office BP (OBP) was 185/102 mmHg (SD 26/19; n = 253) and mean daytime ABP was 170/98 mmHg (SD 22/16; n = 186). Median number of antihypertensive drugs was 5.0: 96 % ACEi/ARB; 86 % thiazide/loop diuretic and 55 % aldosterone antagonist. OBP, available in 90 % at 11 months follow-up, was 163/93 mmHg (reduction of 22/9 mmHg). ABP, available in 70 % at 8.5 months follow-up, was 158/91 mmHg (fall of 12/7 mmHg). Mean drug changes post RDN were: 0.36 drugs added, 0.91 withdrawn. Dose changes appeared neutral. Quartile analysis by starting ABP showed mean reductions in systolic ABP after RDN of: 0.4; 6.5; 14.5 and 22.1 mmHg, respectively (p < 0.001 for trend). Use of aldosterone antagonist did not predict response (p > 0.2). CONCLUSION: In 253 patients treated with RDN, office BP fell by 22/9 mmHg. Ambulatory BP fell by 12/7 mmHg, though little response was seen in the lowermost quartile of starting blood pressure. Fall in BP was not explained by medication changes and aldosterone antagonist use did not affect response.
