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36. Marine Aluminum Phosphate–Sulfate Authigenesis as a Phosphorus Sink During Mid‐Proterozoic Oxygenation

Author

Baozeng Xie, Maxwell Lechte, Xiaoying Shi, Xi Wang, Limin Zhou, Xiqiang Zhou, Kang‐Jun Huang, Zhenfei Wang, Xinqiang Wang, and Dongjie Tang

Subjects
svanbergite, ironstone, oxygenation, phosphorus cycling, mid‐Proterozoic, Geophysics. Cosmic physics, QC801-809
Abstract

Abstract Enhanced continental phosphorus input into the ocean has been suggested as a potential trigger for the transient oxygenation events during the mid‐Proterozoic; however, the response of phosphorus cycling to these marine oxygenations remains unclear. Here, we report the changes in phosphorus cycling associated with a ∼1.7 Ga transient oxygenation. Abundant authigenic aluminum phosphate–sulfate mineral svanbergite (SrAl3(PO4) (SO4) (OH)6; 8.02 ± 4.92 wt%) is identified within the ∼1.7 Ga Yunmengshan ironstones from the Xiong'er Basin, North China and other contemporaneous basins. This observation provides new evidence to support the suggestion that early diagenetic aluminum phosphate‐sulfate minerals could have represented a critical sink of marine phosphorus during the Proterozoic. We suggest that atmospheric oxygenation and concomitant changes in porewater redox chemistry may have enhanced the formation of early diagenetic phosphates, leading to a negative feedback on the oceanic phosphorus reservoir and atmospheric oxygen levels.

Published
2024
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37. Pathophysiology of Overactive Bladder and Pharmacologic Treatments Including β3-Adrenoceptor Agonists -Basic Research Perspectives

Author

Joonbeom Kwon, Duk Yoon Kim, Kang Jun Cho, Mamoru Hashimoto, Kanako Matsuoka, Tadanobu Kamijo, Zhou Wang, Sergei Karnup, Anne M. Robertson, Pradeep Tyagi, and Naoki Yoshimura

Subjects
overactive bladder, pathophysiology, β3-adrenergic receptors, β3-agonists, Diseases of the genitourinary system. Urology, RC870-923
Abstract

Overactive bladder (OAB) is a symptom-based syndrome defined by urinary urgency, frequency, and nocturia with or without urge incontinence. The causative pathology is diverse; including bladder outlet obstruction (BOO), bladder ischemia, aging, metabolic syndrome, psychological stress, affective disorder, urinary microbiome, localized and systemic inflammatory responses, etc. Several hypotheses have been suggested as mechanisms of OAB generation; among them, neurogenic, myogenic, and urothelial mechanisms are well-known hypotheses. Also, a series of local signals called autonomous myogenic contraction, micromotion, or afferent noises, which can occur during bladder filling, may be induced by the leak of acetylcholine (ACh) or urothelial release of adenosine triphosphate (ATP). They can be transmitted to the central nervous system through afferent fibers to trigger coordinated urgency-related detrusor contractions. Antimuscarinics, commonly known to induce smooth muscle relaxation by competitive blockage of muscarinic receptors in the parasympathetic postganglionic nerve, have a minimal effect on detrusor contraction within therapeutic doses. In fact, they have a predominant role in preventing signals in the afferent nerve transmission process. β3-adrenergic receptor (AR) agonists inhibit afferent signals by predominant inhibition of mechanosensitive Aδ-fibers in the normal bladder. However, in pathologic conditions such as spinal cord injury, it seems to inhibit capsaicin-sensitive C-fibers. Particularly, mirabegron, a β3-agonist, prevents ACh release in the BOO-induced detrusor overactivity model by parasympathetic prejunctional mechanisms. A recent study also revealed that vibegron may have 2 mechanisms of action: inhibition of ACh from cholinergic efferent nerves in the detrusor and afferent inhibition via urothelial β3-AR.

Published
2024
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