Insights into Land Plant Evolution Garnered from the Marchantia polymorpha Genome.

The evolution of land flora transformed the terrestrial environment. Land plants evolved from an ancestral charophycean alga from which they inherited developmental, biochemical, and cell biological attributes. Additional biochemical and physiological adaptations to land, and a life cycle with an alternation between multicellular haploid and diploid generations that facilitated efficient dispersal of desiccation tolerant spores, evolved in the ancestral land plant. We analyzed the genome of the liverwort Marchantia polymorpha, a member of a basal land plant lineage. Relative to charophycean algae, land plant genomes are characterized by genes encoding novel biochemical pathways, new phytohormone signaling pathways (notably auxin), expanded repertoires of signaling pathways, and increased diversity in some transcription factor families. Compared with other sequenced land plants, M. polymorpha exhibits low genetic redundancy in most regulatory pathways, with this portion of its genome resembling that predicted for the ancestral land plant. PAPERCLIP

Middle-preserving pancreatectomy for multifocal intraductal papillary mucinous neoplasms of the pancreas: report of a case

Multifocal or continuous pancreatic lesion is identified frequently but finding an appropriate surgical approach is quite challenging. Total pancreatectomy is a useful procedure. However, postoperative endocrine and exocrine disturbance is inevitable. Recently, the safety and feasibility of parenchyma preserving pancreatectomy, including middle-preserving pancreatectomy (MPP), have been reported. MPP is a combined procedure of pancreaticoduodenectomy and distal pancreatectomy, while preserving the body of the pancreas, for cases of multifocal pancreatic lesions. So far, there have only been a few reports that have described MPP. We report a case of MPP for multifocal intraductal papillary mucinous neoplasms of the pancreas, describe the surgical procedure, and discuss the feasibility of MPP as parenchyma-preserving pancreatectomy with reference to the literature

Long-term treatment of evocalcet in hemodialysis patients with secondary hyperparathyroidism: a five-year prospective cohort study in 147 Japanese patients

Abstract Background Cinacalcet hydrochloride (cinacalcet), an oral calcimimetics for secondary hyperparathyroidism (SHPT), has been widely used worldwide. In contrast, evocalcet, an improved derivative of cinacalcet, was approved only in Japan in 2018 and has not received approval overseas. Consequently, the available information on the long-term use of evocalcet relies solely on data from a 1-year dosing phase III clinical trial. Methods The cohort of 147 chronic hemodialysis patients on cinacalcet to manage SHPT was simultaneously switched to the lowest dose of evocalcet (1 mg/day) and prospectively followed for 5 years in real-world clinical settings. Results The median evocalcet dose was 1 mg/day at 0.5 years, and it remained stable at 2 mg/day from 1 to 5 years after the prescription initiation. Additionally, serum parathyroid hormone, corrected calcium, phosphorus, and total alkaline phosphatase levels showed no significant changes compared with their levels at the time of the switch and remained stable over the 5-year period. Furthermore, no adverse events related to vital signs, serum biochemistries, or upper gastrointestinal symptoms were observed in patients during treatment with evocalcet. Conclusions These results suggest that only a small number of patients require higher evocalcet doses, and that SHPT can be effectively managed with low-dose evocalcet for 5 years. Additionally, the drug’s long-term safety has been confirmed. Trial registration: name of the registry: Prescription change from cinacalcet hydrochloride to evocalcet in hemodialysis patients. Trial registration number R000041815. Trial registration UMIN000036702. Registered 10 May 2019—retrospectively registered. https://center6.umin.ac.jp/cgi-open-bin/ctr/ctr_his_list.cgi?recptno=R000041815

Follistatin, an Activin Antagonist, Ameliorates Renal Interstitial Fibrosis in a Rat Model of Unilateral Ureteral Obstruction

Activin, a member of the TGF-β superfamily, regulates cell growth and differentiation in various cell types. Activin A acts as a negative regulator of renal development as well as tubular regeneration after renal injury. However, it remains unknown whether activin A is involved in renal fibrosis. To clarify this issue, we utilized a rat model of unilateral ureteral obstruction (UUO). The expression of activin A was significantly increased in the UUO kidneys compared to that in contralateral kidneys. Activin A was detected in glomerular mesangial cells and interstitial fibroblasts in normal kidneys. In UUO kidneys, activin A was abundantly expressed by interstitial α-SMA-positive myofibroblasts. Administration of recombinant follistatin, an activin antagonist, reduced the fibrotic area in the UUO kidneys. The number of proliferating cells in the interstitium, but not in the tubules, was significantly lower in the follistatin-treated kidneys. Expression of α-SMA, deposition of type I collagen and fibronectin, and CD68-positive macrophage infiltration were significantly suppressed in the follistatin-treated kidneys. These data suggest that activin A produced by interstitial fibroblasts acts as a potent profibrotic factor during renal fibrosis. Blockade of activin A action may be a novel approach for the prevention of renal fibrosis progression