Kallikrein promotes the release of kinins, which have been shown in in vitro studies to improve motility, viability and metabolism in human spermatozoa. The effects of kallikrein therapy on 25 males attending an infertility clinic was assessed, regarding endogenous spermatozoal ATP content, as well as other semen parameters. Thirteen of the 25 patients showed an improvement in either count, morphology, motility, viability, or a combination of these, after 3 months Kallikrein therapy. ATP levels in responders dropped by 58.8% (p less than 0.001). In nonresponders ATP levels did not change significantly. This indicates that improvement in spermatozoal parameters corresponds with increased ATP consumption, following Kallikrein therapy.
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http://dx.doi.org/10.1111/j.1439-0272.1987.tb02345.x | DOI Listing |
Cancer Med
January 2025
Department of Urology, Queen Elizabeth University Hospital, Glasgow, UK.
Background: To assess how centralisation of cancer services via robotic surgery influenced positive surgical margin (PSM) occurrence and its associated risk of biochemical recurrence (BCR) in cases of pT2 prostate cancer (PC).
Methods: Retrospective analysis of all radical prostatectomy (RP) cases performed in the West of Scotland during the period from January 2013 to June 2022. Primary outcomes were PSM and BCR.
Sci Rep
January 2025
Department of Nuclear Medicine, TUM University Hospital rechts der Isar, TUM School of Medicine and Health, Technical University of Munich (TUM), Munich, Germany.
Prostate-specific membrane antigen (PSMA)-targeted positron emission tomography (PET) has improved localization of prostate cancer (PC) lesions in biochemical recurrence (BCR) for salvage radiotherapy (SRT). We conducted a retrospective review of patients undergoing F-rhPSMA-7 or F-flotufolastat (F-rhPSMA-7.3)-PET-guided SRT compared with conventional-SRT (C-SRT) without PET.
View Article and Find Full Text PDFJCI Insight
January 2025
Medicine, Washington University School of Medicine, St. Louis, United States of America.
Hereditary angioedema is an autosomal dominant disorder caused by defects in C1-esterase inhibitor (C1-INH), resulting in poorly controlled activation of the kallikrein-kinin system and bradykinin overproduction. C1-INH is a heavily glycosylated protein in the serine protease inhibitor (SERPIN) family, yet the role of these glycosylation sites remains unclear. To elucidate the functional impact of N-glycosylation in the SERPIN domain of C1-INH, we engineered four sets consisting of 26 variants at or near the N-linked sequon (NXS/T).
View Article and Find Full Text PDFJAMA Netw Open
January 2025
Erasmus MC Cancer Institute, University Medical Center Rotterdam, Rotterdam, the Netherlands.
Importance: Active surveillance (AS) for patients with prostate cancer (PC) often includes fixed repeat prostate biopsies that do not account for the varying risk of reclassification to significant disease. Given the invasive nature and potential complications of biopsies, a personalized approach is needed to balance the burden of biopsies with the risk of missing disease progression.
Objective: To develop and externally validate a dynamic model that predicts an individual's risk of PC reclassification during AS.
Zhongguo Zhong Yao Za Zhi
December 2024
Institute of Basic Theory on Integrated Traditional Chinese and Western Medicine, College of Integrated Traditional Chinese Medicine and Western Medicine, Hunan University of Chinese Medicine Changsha 410208, China.
Blood stasis-heat syndrome is one of the common syndromes of ischemic stroke, which is manifested as syndromes of blood stasis and heat during the pathological progression of patients with ischemic stroke, but there is a lack of systematic research on its biological essence. Thromboinflammation reaction is a newly proposed pathological mechanism highly associated with thrombosis and inflammatory reaction, and it refers to the fact that under the mediation of von Willebrand factor(vWF) and the kallikrein-kinin system, thrombosis and inflammatory reaction interact with each other. Activation of T cells and neutrophils further aggravates thrombosis and worsens the pathological progression of ischemic stroke.
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