Autumn grass treated with a hydrolysable tannin extract versus lactic acid bacteria inoculant: Effects on silage fermentation characteristics and nutritional value and on performance of lactating dairy cows

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Abstract

Hydrolysable tannins (HT) show potential as silage additive for autumn herbage silages, high in (rumen degradable) protein, as they may reduce proteolysis. Additionally, they have abilities to form pH-reversible tannin–protein complexes, non-degradable in the rumen but degradable in the abomasum and intestines of ruminants. Therefore they can improve milk N efficiency and shift N excretions from urine to faeces, possibly mitigating the environmental impact of ruminants. In this study, two small bunker silos were filled with autumn grass. One was treated with 20 g/kg DM HT extract (TAN) (TannoSan-L), the other with 8 mg/kg DM inoculant containing lactic acid bacteria (INO) (Bonsilage Fit G). Secondly, micro-silos (2.75 L) were filled with four treatments; (1) grass without additive (CON) (n = 5); (2) TAN (n = 5); (3) INO (n = 5); and (4) TAN + INO (n = 5). The bunker silos were used in a cross-over feeding experiment with periods of 4 weeks involving 22 lactating Holstein cows (average ± SD: 183 ± 36.3 days in milk, 665 ± 71.0 kg body weight, and 33.8 ± 3.91 kg/day milk yield). The HT dose was insufficient to reduce proteolysis or alter chemical composition and nutritional value in the micro- and bunker silages. Including grass silage added with TAN (3.2 g HT/kg DM) in the diet, did not affect feed intake nor fat and protein corrected milk yield in comparison to feeding the grass silage added with INO in a similar diet. The TAN-fed cows had an increased faecal N excretion and decreased apparent total-tract N and organic matter digestibility, but no improvement in the cows’ N utilization could be confirmed in milk and blood urea levels. Overall, feeding an autumn grass silage treated with 20 g/kg chestnut HT extract did not affect the performance of dairy cows in comparison to feeding an autumn grass silage treated with a lactic acid bacteria inoculant.

The role of the HORMA domain proteins ATG13 and ATG101 in initiating autophagosome biogenesis

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The role of the HORMA domain proteins ATG13 and ATG101 in initiating autophagosome biogenesis

Autophagy research in the past three decades has provided a detailed parts list of the initiation machinery. However, the regulation of its assembly and disassembly remains enigmatic. We summarize the role of HORMA domain proteins ATG13 and ATG101 in autophagosome biogenesis and explore how their hypothetical catalysed metamorphosis could be a responsive switch to conditionally activate autophagy initiation.


Autophagy is a process of regulated degradation. It eliminates damaged and unnecessary cellular components by engulfing them with a de novo-generated organelle: the double-membrane autophagosome. The past three decades have provided us with a detailed parts list of the autophagy initiation machinery, have developed important insights into how these processes function and have identified regulatory proteins. It is now clear that autophagosome biogenesis requires the timely assembly of a complex machinery. However, it is unclear how a putative stable machine is assembled and disassembled and how the different parts cooperate to perform its overall function. Although they have long been somewhat enigmatic in their precise role, HORMA domain proteins (first identified in Hop1p, Rev7p and MAD2 proteins) autophagy-related protein 13 (ATG13) and ATG101 of the ULK-kinase complex have emerged as important coordinators of the autophagy-initiating subcomplexes. Here, we will particularly focus on ATG13 and ATG101 and the role of their unusual metamorphosis in initiating autophagosome biogenesis. We will also explore how this metamorphosis could potentially be purposefully rate-limiting and speculate on how it could regulate the spontaneous self-assembly of the autophagy-initiating machinery.

Autophagy as a caretaker of nuclear integrity

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Autophagy as a caretaker of nuclear integrity

Dysregulation of nuclear function has been implicated in many human diseases. Thus, identifying and characterizing quality control mechanisms that regulate nuclear structure and function is essential. Herein, we discuss autophagy pathways responsible for the degradation of diverse nuclear cargoes across eukaryotic species and highlight the need for a better understanding of nuclear cargo composition and packaging mechanisms, which remain largely uncharacterized.


Due to their essential functions, dysregulation of nuclear pore complexes (NPCs) is strongly associated with numerous human diseases, including neurodegeneration and cancer. On a cellular level, longevity of scaffold nucleoporins in postmitotic cells of both C. elegans and mammals renders them vulnerable to age-related damage, which is associated with an increase in pore leakiness and accumulation of intranuclear aggregates in rat brain cells. Thus, understanding the mechanisms which underpin the homeostasis of this complex, as well as other nuclear proteins, is essential. In this review, autophagy-mediated degradation pathways governing nuclear components in yeast will be discussed, with a particular focus on NPCs. Furthermore, the various nuclear degradation mechanisms identified thus far in diverse eukaryotes will also be highlighted.

Reduced iron and cobalt levels in response to curcumin supplementation are not responsible for the prolonged larval development and do not affect the oxidative stress tolerance and polyamine status of D. melanogaster

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Reduced iron and cobalt levels in response to curcumin supplementation are not responsible for the prolonged larval development and do not affect the oxidative stress tolerance and polyamine status of D. melanogaster

Curcumin supplementation, similar to the iron chelator bathophenanthroline, lowered the iron but also the cobalt content, and to a lesser extent affected the manganese and zinc status of D. melanogaster. However, these alterations in trace metal balance did not affect catalase activity, oxidative stress tolerance, and polyamine status in fruit flies. In contrast, in curcumin-supplemented mice, the spleen exhibits an elevated spermidine production, which is most probably related to a compensatory growth due to curcumin-induced iron deficiency.


Abstract

Recent reports indicated that the phytochemical curcumin possesses iron-chelating activity. Here, by employing the fruit fly Drosophila melanogaster, we conducted feeding studies supplementing curcumin or, as a control, the iron chelator bathophenanthroline (BPA). First, the absorption and further metabolization of dietary curcuminoids were proved by metabolomics analyses. Next, we found that 0.2% dietary curcumin, similar to BPA, lowered the iron but also the cobalt content, and to a lesser extent affected the manganese and zinc status. Supplementation during larval stages was required and sufficient for both compounds to elicit these alterations in adult animals. However, curcumin-induced retarded larval development was not attributable to the changed trace metal status. In addition, a reduction in the iron content of up to 70% by curcumin or BPA supplementation did not reduce heme-dependent catalase activity and tolerance toward H2O2 in D. melanogaster. Moreover, polyamines were not influenced by curcumin treatment and decreased iron levels. This was confirmed for selected organs from 0.2% curcumin-treated mice, except for the spleen. Here, elevated spermidine level and concomitant upregulation of genes involved in polyamine production were associated with a putatively anemia-derived increased spleen mass. Our data underline that the metal-chelating property of curcumin needs to be considered in feeding studies.

Impact of fibrosis on liver‐related event incidence in nonalcoholic fatty liver disease: A multicenter observational study

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Abstract

Aim

There are few reports on the prognosis of liver-related events in Japanese patients with nonalcoholic fatty liver disease (NAFLD). We undertook an observational study to compare the prognosis between fibrotic and nonfibrotic groups in Japanese NAFLD patients.

Methods

Prognosis in 393 NAFLD patients who underwent liver biopsy between April 2013 and April 2015 at multiple centers were investigated. The time to onset of liver-related events, cardiovascular events, development of extrahepatic cancers, and death were compared between the pathologically fibrotic nonalcoholic steatohepatitis (NASH) group and nonalcoholic fatty liver (NAFL) + nonfibrotic NASH group. A similar analysis was carried out based on the fibrotic classification diagnosed using four noninvasive fibrosis prediction models.

Results

The mean age and body mass index at the time of liver biopsy was 55.7 years old and 28.04 kg/m2, respectively The cumulative incidence of liver-related events at 1080 days after liver biopsy was 5.79% in the pathologically fibrotic NASH group and 0% in the NAFL + nonfibrotic NASH group, with a significant difference (p = 0.0334). The cumulative incidence of liver-related events was significantly higher in the positive group for the prediction model than in the negative group in all four models (all p values were <0.0001). There was no significant difference between the pathologically fibrotic NASH group and NAFL + nonfibrotic NASH group in terms of cumulative incidence of cardiovascular events, development of extrahepatic cancers, and death.

Conclusions

The incidence of liver-related events was significantly higher in the fibrotic NASH group than that of the NAFL + nonfibrotic NASH group in Japanese NAFLD patients.

Dapagliflozin improves diabetic cognitive impairment via indirectly modulating the mitochondria homeostasis of hippocampus in diabetic mice

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Dapagliflozin improves diabetic cognitive impairment via indirectly modulating the mitochondria homeostasis of hippocampus in diabetic mice

The goal of this study is to determine the underlying mechanism and look into dapagliflozin's impact on diabetic cognitive impairment. Diabetes-induced cognitive dysfunction was attenuated by dapagliflozin and the effect was indirect rather than direct.


Abstract

Cognitive impairment is increasingly recognized as an important comorbidity of diabetes progression; however, the underlying molecular mechanism is unclear. Dapagliflozin, an inhibitor of sodium-glucose co-transporter 2 (SGLT2), has shown promising effects against diabetes in rodent experiments and human clinical assays. This study aimed to determine the underlying mechanism and examine the effect of dapagliflozin on diabetic cognitive impairment. To create an in vivo model of diabetic cognitive impairment, streptozotocin (STZ)-induced diabetic mice were used. Dapagliflozin was administered to mice for 8 weeks. The context fear condition and Morris water maze test was used to evaluate mice's behavioral change. Western blotting was used to evaluate protein expression. Hematoxylin and eosin (HE) and Nissl staining were applied to monitor morphological and structural changes. Congo red staining was performed to identify the formation of senile plaques. Mitochondria morphology was examined using a transmission electron microscope, and blood flow in the mouse cerebral cortex was measured using a laser Doppler imaging assay. Comparison to the diabetes mellitus (DM) group, the dapagliflozin group had lower glucose levels. Behavioral studies have shown that dapagliflozin can restore memory deficits in diabetic mice. The murky cell membrane edges and Nissl bodies more difficult to identify in the DM group were revealed by HE and Nissl staining, which were both improved by dapagliflozin treatment. Dapagliflozin inhibited the progression of Aβ generation and the reduced cerebral blood flow in the DM group was rescued. After dapagliflozin treatment, damaged mitochondria and lack of SGLT2 in the hippocampus and cortex of diabetic mice were repaired. Diabetes-induced cognitive dysfunction was attenuated by dapagliflozin and the effect was indirect rather than direct.

Neutrophil extracellular traps formation in the lesional skin of various types of pyoderma gangrenosum

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Abstract

Pyoderma gangrenosum (PG) is a chronic neutrophilic disorder characterized by recurrent painful ulcers. Aseptic inflammation by neutrophils plays an essential role, and neutrophil extracellular traps (NETs) formation can contribute to the pathogenesis of PG. Seventy-five patients were diagnosed as having PG in our department, among which 58 ulcerative, 4 bullous, 3 pustular and 10 vegetative type. We examined the 20 skin biopsy specimens (11 ulcerative, 3 bullous, 2 pustular and 4 vegetative type), and local NETs formation in various types of PG was compared among each type. The biopsied specimens were double labelled for myeloperoxidase, citrullinated histone H3. Immunofluorescent images indicated that the histopathologic location and depth of NETs formation in PG varied by the clinical subtypes. In ulcerative PG, NETs formation was observed in the upper to deep dermis. In bullous PG, NETs formation was mainly observed in the epidermis. Pustular type showed NETs formation in the epidermis near the pustules, and in vegetative type, showed NETs formation mainly in the upper dermis. These results indicate that NETting neutrophils play an important role in the pathogenesis of various forms of PG, although the location and depth of NETs formation in the skin lesion of PG differ depending on each type. Further studies are necessary to examine what factors identify different clinical features of PG.

Is there a relationship between enchytraeids diversity and community with soybean (Glycine max L.) productivity in no‐till system in subtropical soils of Brazil?

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Is there a relationship between enchytraeids diversity and community with soybean (Glycine max L.) productivity in no-till system in subtropical soils of Brazil?

All genera were more abundant in high productivity than low productivity. The points with high productivity presented highest average richness. Enchytraeids demonstrating potential bioindicators of soil quality and consequently of soybean productivity in the no-tillage system for subtropical soils in Brazil.


Abstract

The relationship between the productivity of crops of agricultural interest and their interactions with physicochemical soil properties is widely explored. However, there is still a gap concerning the contribution of biological soil attributes and especially the relationship between crop productivity and the structures of organism communities within the soil, such as the enchytraeids. This paper aimed to evaluate the diversity and structures of enchytraeids communities in subtropical soils and their relationship with soybean productivity and soil properties within a no-tillage system. This study was conducted in soybean growing grounds working under no-till farming systems in southern Brazil. Samples were collected according to ISO 23611-3 and extracted with the hot–wet methodology. The organisms were identified up to their genus level. Enchytraeids density increased with the increase of soybean productivity for both evaluated crops. Enchytraeus, Fridericia, and Hemienchytraeus were more abundant in high productivity and genus Achaeta was only found in the second crop and was not a sensitive indicator toward changes in soybean productivity. Regarding the relationship between the enchytraeid community and soil attributes, the variables clay, phosphorus, moisture contents, pH, Ca/Mg as well as carbon and nitrogen from soil and litter, affected Enchytraeidae distribution. Enchytreids showed significant correlations with soybean productivity in the no-tillage system for subtropical soils in Brazil, demonstrating potential bioindicators of soil quality and consequently of soybean productivity.