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One crucial problem that plants faced during their evolution, particularly during the transition to growth on land, was how to transport water, nutrients, metabolites, and small signaling molecules within a large, multicellular body. As a solution to this problem, land plants developed specific tissues for conducting molecules, called water-conducting cells (WCCs) and food-conducting cells (FCCs). The well-developed WCCs and FCCs in extant plants are the tracheary elements and sieve elements, respectively, which are found in vascular plants. Recent molecular genetic studies revealed that transcriptional networks regulate the differentiation of tracheary and sieve elements, and that the networks governing WCC differentiation are largely conserved among land plant species. In this review, we discuss the molecular evolution of plant conducting cells. By focusing on the evolution of the key transcription factors that regulate vascular cell differentiation, the NAC transcription factor VASCULAR-RELATED NAC-DOMAIN for WCCs and the MYB-coiled-coil (CC)-type transcription factor ALTERED PHLOEM DEVELOPMENT for sieve elements, we describe how land plants evolved molecular systems to produce the specialized cells that function as WCCs and FCCs.

Rhamnogalacturonan I (RG-I) comprises approximately one quarter of the pectin molecules in land plants, and the backbone of RG-I consists of a repeating sequence of [2)-α-L-Rha(1-4)-α-D-GalUA(1-] disaccharide. Four Arabidopsis thaliana genes encoding RG-I rhamnosyltransferases (AtRRT1 to AtRRT4), which synthesize the disaccharide repeats, have been identified in the glycosyltransferase family (GT106). However, the functional role of RG-I in plant cell walls and the evolutional history of RRTs remains to be clarified. Here, we characterized the sole ortholog of AtRRT1–AtRRT4 in liverwort, Marchantia polymorpha , namely, MpRRT1. MpRRT1 had RRT activity and genetically complemented the At RRT1 -deficient mutant phenotype in A. thaliana . However, the Mp RRT1 -deficient M. polymorpha mutants showed no prominent morphological changes and only an approximate 20% reduction in rhamnose content in the cell wall fraction compared to that in wild-type plants, suggesting the existence of other RRT gene(s) in the M. polymorpha genome. As expected, we detected RRT activities in other GT106 family proteins such as those encoded by Mp RRT3 in M. polymorpha and FRB1/ At RRT8 in A. thaliana , the deficient mutant of which affects cell adhesion. Our results show that RRT genes are more redundant and diverse in GT106 than previously thought.

Pectin is one of the three key cell wall polysaccharides in land plants and consists of three major structural domains: homogalacturonan, rhamnogalacturonan I (RG-I) and RG-II. Although the glycosyltransferase required for the synthesis of the homogalacturonan and RG-II backbone was identified a decade ago, those for the synthesis of the RG-I backbone, which consists of the repeating disaccharide unit [→2)-α- l -Rha-(1 → 4)-α- d -GalUA-(1→], have remained unknown. Here, we report the identification and characterization of Arabidopsis RG-I:rhamnosyltransferases (RRTs), which transfer the rhamnose residue from UDP-β- l -rhamnose to RG-I oligosaccharides. RRT1, which is one of the four Arabidopsis RRTs, is a single-spanning transmembrane protein, localized to the Golgi apparatus. RRT1 was highly expressed during formation of the seed coat mucilage, which is a specialized cell wall with abundant RG-I. Loss-of-function mutation in RRT1 caused a reduction in the level of RG-I in the seed coat mucilage. The RRTs belong to a novel glycosyltransferase family, now designated GT106. This is a large plant-specific family, and glycosyltransferases in this family seem to have plant-specific roles, such as biosynthesis of plant cell wall polysaccharides. Pectin, the major gelling component of the plant cell wall, is rich in galacturonic acids that compose the backbones of pectic polysaccharides. Now, researchers have identified a new family of enzymes responsible for synthesizing the backbone of pectin, RG-I.

Background Intradialytic hypotension (IDH) has traditionally been associated with cardiovascular diseases (CVD). Recent demographic shifts in hemodialysis (HD) patients, including an aging population, have altered mortality patterns and led to a decline in CVD mortality. Considering these changes, we aimed to re-evaluate the prognostic impact of intradialytic hypotension in a contemporary aging HD cohort. Methods This is a single-center retrospective cohort study, including 228 HD patients. In each patient, 12 consecutive HD records were examined to count numbers of IDH episodes. The patients were then divided into two groups: an IDH group for patients with at least one episode of IDH ( n  = 111) and a non-IDH group ( n  = 117) for those without an episode of IDH. We analyzed all-cause mortality and causes of death, including a comparison of CVD and non-CVD mortality between the two groups over a median follow-up period of 5.7 (2.3–7.8) years. Results The age of the study population was 65.4 ± 12.7 years, and the median dialysis vintage was 7.2 (2.8–12.7) years. The IDH group experienced an average of 3.9 episodes of IDH during the 12 HD sessions. During the follow-up period, 91 patients (39.9%) died. Multivariate analysis identified IDH and ischemic heart disease as independent risk factors for all-cause mortality. All-cause mortality was higher in the IDH group than in the non-IDH group (51.4% versus 29.1%, p  < 0.01). While CVD mortality was similar between the groups (16.2% versus 15.4%, p  = 1.00), non-CVD mortality significantly increased in the IDH group (35.1% versus 13.7%, p  < 0.01), predominantly owing to infections. Patients with IDH exhibited significantly lower serum albumin levels (3.4 versus 3.6 g/dL, p  < 0.01) and higher C-reactive protein levels (median 0.2 versus 0.1 mg/dL, p  = 0.04), which may reflect malnutrition and chronic inflammation. Conclusions IDH is associated with an increased risk of all-cause mortality, particularly of non-CVD, including deaths from infection and malnutrition.

Supplementation with rare earth elements (REEs) such as lanthanum and cerium has been shown to promote plant elongation and/or increase crop yields. On the other hand, there are reports that REE supplementation of plants has no such effect. The appropriate modes for REE utilization and the underlying mechanism are not fully understood. In this study, we investigated how REE supplementation of plants under low light stress affects plant growth and gene expression. Under low light stress conditions, tomato root elongation was observed to be reduced by about half. This suppression of root elongation was found to be considerably alleviated by 20 mM lanthanum ion supplementation. This effect was plant-species-dependent and nutrient-condition-dependent. Under low light stress, the expression of the genes for phytochrome-interacting factor, which induces auxin synthesis, and several auxin-synthesis-related proteins were markedly upregulated by lanthanum ion supplementation. Thus, we speculate that REE supplementation of plants results in auxin-induced cell elongation and alleviates growth suppression under stress conditions.

Organelle stress exacerbates podocyte injury, contributing to perturbed lipid metabolism. Simultaneous organelle stresses can occur in the kidney in the diseased state; therefore, a thorough analysis of organelle communication is crucial for understanding the progression of kidney diseases. Although organelles closely interact with one another at membrane contact sites, limited studies have explored their involvement in kidney homeostasis. The endoplasmic reticulum (ER) protein, PDZ domain–containing 8 (PDZD8), is implicated in multiple-organelle-tethering processes and cellular lipid homeostasis. In this study, we aimed to elucidate the role of organelle communication in podocyte injury using podocyte-specific Pdzd8 -knockout mice. Our findings demonstrated that Pdzd8 deletion exacerbated podocyte injury in an accelerated obesity–related kidney disease model. Proteomic analysis of isolated glomeruli revealed that Pdzd8 deletion exacerbated mitochondrial and endosomal dysfunction during podocyte lipotoxicity. Additionally, electron microscopy revealed the accumulation of abnormal, fatty endosomes in Pdzd8 -deficient podocytes during obesity-related kidney diseases. Lipidomic analysis indicated that glucosylceramide accumulated in Pdzd8 -deficient podocytes, owing to accelerated production and decelerated degradation. Thus, the organelle-tethering factor, PDZD8, plays a crucial role in maintaining mitochondrial and endosomal homeostasis during podocyte lipotoxicity. Collectively, our findings highlight the importance of organelle communication at the 3-way junction among the ER, mitochondria, and endosomes in preserving podocyte homeostasis.

BackgroundTranscatheter arterial chemoembolization (TACE) is widely used for unresectable hepatocellular carcinoma (HCC). The purpose of this study was to investigate incidence and risk factors of contrast-induced nephropathy (CIN) after TACE in patients with HCC.MethodsIn this single-center retrospective study, we examined 461 consecutive TACE sessions in 260 patients between January 2003 and October 2015. CIN was defined as an increase in serum creatinine levels by ≥ 0.5 mg/dl or ≥ 25% from baseline within 72 h after TACE. We calculated incidence rate of CIN and tried to identify its risk factors by logistic regression analysis.ResultsTwenty-one cases of CIN (5%) were observed in 461 TACE sessions. One patient required subsequent hemodialysis transiently. In univariate analysis, tumor size > 5 cm [odds ratio (OR) 5.76, 95% confidence interval (CI) 2.34–14.14, p < 0.001], chronic kidney disease (OR 2.54, 95% CI 1.05–6.14, p = 0.04), serum hemoglobin level [OR 0.79 (per 1 g/dl increase), 95% CI 0.64–0.98, p = 0.03] and serum albumin level [OR 0.44 (per 1 g/dl increase), 95% CI 0.19–1.02, p = 0.05] were associated with the development of CIN. Stepwise logistic regression methods showed that tumor size > 5 cm (OR 7.81, 95% CI 2.99–20.46, p < 0.001) and serum albumin [OR 0.29 (per 1 g/dl increase), 95% CI 0.11–0.75, p = 0.01] were risk factors of CIN.ConclusionsIn this study, HCC tumor size and lower serum albumin level were independent predictors of CIN after TACE.

Background Aortic arch calcification (AAC) is a well-known risk factor for death in patients on hemodialysis (HD); however, the causes of death among them have not been well studied. The study aimed to investigate the distribution of causes of death and long-term prognosis among different degrees of AAC in HD patients. Methods A retrospective cohort study was conducted on patients undergoing HD at two clinics in Japan. AAC grades 0 to 3 were categorized by chest radiograph at baseline, and mortality and causes of death were collected. A subgroup analysis was performed to evaluate the relationship between causes of death and age, diabetes mellitus, and dialysis vintage in each AAC grade. Results A total of 321 patients were included in the analysis. During 5.2 ± 2.1 years, 117 patients died, and the death rates in AAC grades 0, 1, 2, and 3 were 19.3% (17/88), 35.2% (51/145), 46.3% (25/54), and 70.6% (24/34), respectively. The major causes of death were cardiovascular disease (CVD, 39.3%), infection (20.5%), and malignancy (15.4%) in the entire cohort. In AAC grade 3, CVD mortality (33.3%) remains as the most common cause of death, although death of infection (29.2%) and malnutrition (16.7%) increased markedly. A subgroup analysis showed that AAC grade 3 was mostly old, non-diabetic patients with a long dialysis vintage and was susceptible to death of infection or malnutrition. Conclusions CVD was the most common cause of death among all AAC grades, although death of infection and malnutrition markedly increased in those with severe AAC. Attention should be paid to CVD, infection, and malnutrition in HD patients with severe AAC.

Xylem vessels are important for water conduction in vascular plants. The VASCULAR-RELATED NAC-DOMAIN (VND) family proteins, master regulators of xylem vessel cell differentiation in Arabidopsis thaliana, can upregulate a set of genes required for xylem vessel cell differentiation, including those involved in secondary cell wall (SCW) formation and programmed cell death (PCD); however, it is not fully understood how VND activity levels influence these processes. Here, we examined the Arabidopsis VND7-VP16-GR line, in which VND7 activity is post-translationally activated by treatments with different concentrations of dexamethasone (DEX), a synthetic glucocorticoid. Our observations showed that 1 nM DEX induced weak SCW deposition, but not PCD, whereas 10 or 100 nM DEX induced both SCW deposition and PCD. The decreased chlorophyll contents and SCW deposition were apparent after 24 h of 100 nM DEX treatment, but became evident only after 48 h of 10 nM DEX treatment. Moreover, the lower DEX concentrations delayed the upregulation of VND7 downstream genes, and decreased their induction levels. They collectively suggest that the regulation of VND activity is important not only to initiate xylem vessel cell differentiation, but also regulate the quality of the xylem vessels through VND-activity-dependent upregulation of the PCD- and SCW-related genes.

Lactic acid bacteria (LAB) exert health-beneficial effects by regulating innate immunity in the intestinal tract. Due to growing health awareness, the demand for LAB and studies have focused on identifying beneficial LAB strains is increasing, especially those that stimulate innate immunity. In this study, the LAB strain D279 (NITE_BP-03645, Latilactobacillus sakei ) was isolated from among 741 LAB strains that were analyzed for their ability to induce interleukin 12 (IL-12) production and was subsequently characterized. D279 induced the highest expression of IL-12 among the screened LABs. Furthermore, D279 significantly activated antiviral genes and preferentially induced interferon (IFN)λ expression in vitro , which plays a critical role in the epithelial tissue, thereby conferring strong anti-influenza potency without inflammation. However, it decreased the IFNα levels. The administration of pasteurized D279 to mice resulted in strong anti-influenza potency, with higher natural killer (NK) cell activity and a lower viral load in the lung than in the control. Importantly, none of the D279-administered mice were sacrificed during the viral infection tests. These results suggest that D279 administration confers beneficial effects by regulating innate immunity and that it may be relevant for commercial use in the future.