China
Africa
Explore chapters and articles related to this topic
Cellular Regulation of Kinin Receptors
Published in Sami I. Said, Proinflammatory and Antiinflammatory Peptides, 2020
Adelbert A. Roscher, Alexander Faussner
There is also compelling evidence linking BK with the pathophysiological processes that accompany a variety of inflammatory or allergic airway diseases, such as allergic rhinitis, viral rhinitis, and asthma (15,16). The local release of kinins in the airways involves activation of the kinin-forming system by tissue kallikrein from airway cells or from invaded neutrophils. In neutrophils the coexistence of tissue kallikrein and kininogens has been demonstrated, which might provide an important additional source for kinin generation during inflammatory conditions (68). This activation of the kinin-forming system can be mediated via viral or bacterial inflammation inducing local trauma, activation of coagulation pathways (Hageman factor and thrombin), or immune reactions. Excessive release of kinins can then activate specific B1 and B1 receptors that are widely distributed in the lung. High densities of B1 receptors have been identified mainly in larger airways occurring on bronchial and pulmonary blood vessels of all sizes and in the lamina propria subjacent to the basal epithelial cell layer (69). In smaller airways, B1 receptors are also detectable on airway smooth muscle, submucosal glands, and nerve fibers of intrapulmonary bronchi. B1 receptors have recently been shown to occur in pathological states of the lung within the fibrous tissues and basement membrane of alveoli and capillaries (21).
Prediction of pre-eclampsia
Published in Pankaj Desai, Pre-eclampsia, 2020
Another biochemical marker that has been studied and found some popularity is the excretion of urinary kallikrein. Renal functions have been shown to be significantly affected in pre-eclampsia. This test is believed to reflect the status of renal excretory function. It was with this rationale that urinary kallikrein levels were estimated to predict pre-eclampsia.
Prostate Cancer
Published in Manit Arya, Taimur T. Shah, Jas S. Kalsi, Herman S. Fernando, Iqbal S. Shergill, Asif Muneer, Hashim U. Ahmed, MCQs for the FRCS(Urol) and Postgraduate Urology Examinations, 2020
Which of the following information on molecular markers in prostate cancer is CORRECT?PCA3, a non-coding RNA, is under expressed in prostate cancer.Ki-67 antigen is detected by immunohistochemical staining and correlates with outcome after radical prostatectomy.Kallikrein 3 level is reduced in metastatic prostate cancer.High molecular weight cytokeratin binds to prostate cancer cells confirming the diagnosis of cancer over HGPIN.PSA doubling time is a useful tool that outperforms total PSA in the diagnosis of prostate cancer.
Inhibition of plasma kallikrein–kinin system to alleviate renal injury and arthritis symptoms in rats with adjuvant-induced arthritis
Published in Immunopharmacology and Immunotoxicology, 2018
Jie Zhu, Hui Wang, Jingyu Chen, Wei Wei
The kallikrein–kinin system (KKS) is an important endogenous enzyme system. Physiologically, KKS modulates the function of cardiovascular, kidneys and nervous system4. The KKS consists of two major cascades: ‘plasma KKS’ and ‘tissue KKS’. Plasma kallikrein is different from tissue kallikrein in molecular weight, biological functions and immunological properties5,6. Plasma KKS was involved in thrombosis, fibrinolysis and played a critical role during inflammatory processes in many diseases, such as heart disease, kidney disease and cancer5,7–9. Plasma KKS consists of four plasma proteins: prekallikrein, factor XII, factor XI and high molecular weight kininogen (HK). Upon activation, pre-kallikrein (PK) is converted to the active form kallikrein, which cleaves HK to release bradykinin (BK)10. Plasm KKS was also associated with the adaptive immune responses11. BK is a potent peptide that participates in inflammation, edema and vascular dilation and could change the transformation of antigen-specific T lymphocytes to Th1 and Th2 cell12,13.
Serine protease inhibitors to treat inflammation: a patent review (2011-2016)
Published in Expert Opinion on Therapeutic Patents, 2018
Feryel Soualmia, Chahrazade El Amri
Plasma kallikrein is a well-established target in particular in HAE attack for which several compounds have been developed. Plasma kallikrein plays an important role in a variety of physiologic processes, including, but not limited to, blood pressure regulation, the contact activation pathway of blood coagulation, fibrinolysis, inflammation, and pain. Therefore, targeting plasma kallikrein offers novel strategies not previously explored to interfere with thrombosis and vascular inflammation in a broad variety of diseases [133–135]. Table 2 gathers the most recent patents on PK inhibitors, the majority of them are from private companies. The selected chemical structures are reported in Figure 2. Kalvista Pharmaceuticals was particularly very efficient in term of diversity of chemical scaffolds, including bicyclic [118], N-(heteroarylmethyl)-heteroaryl-carboxamide derivatives [119], benzylamine derivatives [123], and heterocyclic derivatives [122].
Omalizumab is not just an anti-immunoglobulin E
Published in Journal of Dermatological Treatment, 2022
Goknur Ozaydin-Yavuz, Ibrahim Halil Yavuz, Hüseyin Serhat İnalöz, Cagdas Boyvadoglu
Kallikrein is a mediator that plays an important role in vasodilation and inflammation. In the study of Juhlin, it was reported that kallikrein causes late cutaneous reactions in patients with urticaria (18). The effectiveness of kallikrein inhibitors in angioedema shows that they can be an important mediator in urticaria (19). In our study, an increase was found in serum kallikrein levels. However, no significant improvement was found in clinical urticaria scores. This result may show that the increase in kallikrein level in patients using omalizumab has no clinical effect.