N6-methyladenosine (m6A) methylation modification is one of the most prevalent epigenetic modifications of eukaryotic RNA. m6A methylation is widely associated with many biological processes through ...the modification of RNA metabolism and is associated with multiple disease states. As a newly discovered regulatory cell death in recent years, ferroptosis is an iron-dependent cell death characterized by excessive lipid peroxidation. Emerging evidence supports that ferroptosis has a significant role in the progression of diverse diseases. Besides, the key regulators of ferroptosis exhibit aberrant m6A levels under different pathological conditions. However, the correlation between m6A-modified ferroptosis and multiple diseases has not been well elucidated. In this review, we summarized the functions of m6A in ferroptosis, which are associated with the initiation and progression of multiple diseases. Investigating the role of m6A in ferroptosis might both facilitate a better understanding of the pathogenesis of these diseases and provide new opportunities for targeted treatment.
Display omitted
The traditional pattern-making process is very time-consuming and requires professional fashion design knowledge. In order to develop a form-fitting garment to meet customer’s individual needs, ...pattern makers must rely on a “trial and error” procedure until the customer is satisfied. In this paper, we proposed a “what you see is what you get” (WYSIWYG) way to efficiently develop garment patterns. First, a three-dimensional (3D) garment, using an extracted outline from a garment flat or figure, is modeled in a gravitational virtual environment. The modeled garment is then adjusted until it meets design requirements. Next, the adjusted 3D garment model is expanded by smoothing out the folds and wrinkles. Construction curves are drawn on the surface of the expanded 3D garment model according to design requirements. These curves divide the 3D garment model’s surface into many small 3D surfaces. Then, 2D garment patterns are obtained by unfolding these subdivided 3D surfaces. Finally, the flattened 2D patterns are stretched and shrank according to the fabric elasticity. The final patterns can be used for making real garments.
Compared to the current 3D garment pattern-making methods, our proposed method is more robust and well-rounded; not only is the proposed approach versatile towards both tight-fitting and loose-fitting clothing, but also requires no prior knowledge of pattern-making from the user. It also involves garment ease allowance, fabric elasticity, and draping, three factors that had not been previously considered all at once during smart pattern-making procedures, in the designing process.
Display omitted
•A novel interactive pattern-making technology is proposed in this research.•Our method doesn’t require prior pattern-making knowledge from the user.•Garment ease allowance and fabric elasticity are both involved.•Our method is suitable for both tight and loose garments.
PI3K and STAT3 are frequently activated in cancer progression. However, little is known about the underlying mechanisms by which PI3K and STAT3 regulate head and neck squamous cell cancer (HNSCC) ...growth. The lncRNA HOX transcript antisense RNA (
) was found to modulate the progression of HNSCC. In this study, we attempted to establish the correlation of PI3K/STAT3/HOTAIR signaling with the progression of HNSCC and its sensitivity toward platinum-based and targeted anti-EGFR combination therapy.
We first analyzed the STAT3/HOTAIR and PI3K/AKT level in human HNSCC samples. We then activated or suppressed STAT3/HOTAIR and determined the effects on HNSCC cell proliferation
and the growth of UM1 xenograft tumor, an orthotopic model of HNSCC. The sensitivity of HNSCC cells toward cisplatin and cetuximab was determined by
assays.
HNSCC samples showed significantly robust expression/activation of STAT3, HOTAIR, PI3K, and AKT, compared with normal squamous epithelium. STAT3 inhibition with WP1066 decreased HOTAIR level and sensitized HNSCC to cisplatin or cetuximab. STAT3 promoted HOTAIR transcription and its interaction with pEZH2-S21, resulting in enhanced growth of HNSCC cells. In addition, overexpression of HOTAIR promoted the growth of UM1 xenograft tumors
Our results suggest that STAT3 signaling promotes HNSCC progression via regulating HOTAIR and pEZH2-S21 in HNSCC with PI3K overexpression/activation. These findings provide a rationale to target the STAT3/HOTAIR/pEZH2-S21 regulatory axis for treating patients with HNSCC.
.
Intercellular transfer of mitochondria and mitochondrial components through extracellular vesicles (EVs), including microvesicles and exosomes, is an area of intense interest. The cargos that are ...carried by EVs define their biological activities. Mitochondria are in charge of bioenergetics and maintenance of cell viability. Increasing evidences indicate the presence of intact mitochondria or mitochondrial components in EVs, which raises many questions, how they are engulfed into EVs and what do they do? Here, we present what is currently known about the presence and function of various mitochondrial constituent in EVs. We also review current understanding about how and why mitochondrial components are encapsulated into EVs.
This experiment was conducted to investigate the antibacterial effects of essential oils (EO) in vitro and the influence of EO on growth performance, intestinal morphology and oxidation resistance ...and cecal microflora of yellow-feathered broilers. A total of 720 one-day-old male yellow feather broilers were randomly assigned into 4 treatments with 6 replicate cages of 30 broilers each. The groups were as follows: CON group (basal diet), EO200 group (basal diet + 200 mg/kg EO), EO400 group (basal diet + 400 mg/kg EO), and EO600 group (basal diet + 600 mg/kg EO). The experiment lasted for 48 d. Results showed that the growth and biofilm formation of avian pathogenic E. coli O78 and Salmonella pullorum were limited by adding EO to the diet (P < 0.05). Besides, birds fed with EO had greater (P < 0.05) average daily feed intake (ADFI), average daily gain (ADG), and body weight (BW) during d 1 to 21, 22 to 42, and 1 to 48 and lower (P < 0.05) feed: gain (F:G) than those fed with basal diet during d 22 to 42 and 1 to 48. Moreover, the activity of antioxidant enzyme and the intestinal permeability were improved in the EO400 and EO600 groups rather than the CON group on d 21 (P < 0.05). There were significant differences in cecal microbial composition and enrichment of metabolic pathways of birds among all groups by 16S-based sequencing. In summary, some dose of EO improved bacteriostatic ability, antioxidant ability, and intestinal health of broilers which contributed to the growth performance improvement of yellow-feathered broilers, which can be a promising antibiotic alternative for improving poultry production.
This study was conducted to investigate the effects of feeding fermented mulberry leaf powder (FMLP) on growth performance, slaughter performance, and meat quality of broilers. A total of 360 ...1-day-old chickens were randomly divided into 5 groups. The control group was fed basal diet (CON), 3% FMLP, 6% FMLP, 9% FMLP, and 3% unfermented mulberry leaf powder. The (MLP) group was fed basal diet supplemented with 3%, 6%, 9% fermented mulberry leaf powder, and 3% MLP, respectively. The experiment lasted for 56 days, with 1–28 days as the starter phase and 29–56 days as the grower phase. The results on the growth performance showed that diets supplemented with 3% FMLP significantly increased the ratio of villus height to crypt depth in the duodenum, jejunum, and ileum of broilers, enhanced the activity of intestinal amylase and digestibility of dry matter and crude protein, improved the average daily gain (ADG), and decreased the feed to gain ratio (F/G) (p < 0.05). Compared with the control group diet, the 3% FMLP group diet significantly increased the breast muscle yield (p < 0.05), reduced the abdominal fat ratio (0.1 < p < 0.05), and improved the slaughter performance of broilers. The 3% MLP group diet increased the shear force of breast muscle (p < 0.05) and thigh muscle of broilers compared to the control group, and adding FMLP could reverse the above results. Additionally, relative to the control group, FMLP supplementation improved the contents of inosine monophosphate (IMP), total amino acids (TAA), essential amino acids (EAA), and delicious amino acids (DAA) in breast and thigh muscle, and improved polyunsaturated fatty acids (PUFA) and essential fatty acids (EFA) in breast muscle; the 6% and 9% FMLP groups showed preferably such effects (p < 0.05). In conclusion, dietary supplementation of FMLP can improve the digestion and absorption of nutrients, and then improve the growth performance of broilers; it also has a positive effect on improving slaughter performance and meat quality.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, UILJ, UKNU, UL, UM, UPUK
Perfluorooctane sulfonate (PFOS), one kind of persistent organic pollutants, is associated with insulin resistance (IR) in general population. However, the exact mechanism is still obscure. In this ...study, we found that 50 μM PFOS caused IR in L-02 hepatocytes after 1 h, and induced autophagy and mitochondrial calcium (Ca2+) accumulation as early as 0.5 h. Inhibiting autophagy relieved mitochondrial Ca2+ overload and then reversed IR. Mitochondria were aggregated at cell periphery, and extracellular Ca2+ from IP3R2 on the plasma membrane, rather than endoplasmic reticulum Ca2+, was the priority source of mitochondrial Ca2+ uptake at early stages of PFOS exposure. Furthermore, we discovered that the linkage connecting autophagy and mitochondrial Ca2+ response was detyrosinated α-tubulin, which autophagy-dependently ascended, interacted with VDAC1 and enhanced the formation of IP3R2-VDAC1-MICU1 complex. Consistently, PFOS caused IR, activated autophagy, induced mitochondrial Ca2+ overload, increased the level of detyrosinated α-tubulin, and promoted the formation of IP3R2-VDAC1-MICU1 complex in the liver of C57BL/6J mice exposed to 2.5 mg/kg/day PFOS for 6 weeks. This study clarified that autophagy and mitochondrial Ca2+ accumulation were the early and triggering event that caused PFOS-related IR, also unveiled a novel mechanism regulating mitochondrial Ca2+ homeostasis.
Display omitted
•Autophagy and mitochondrial Ca2+ overload precede and trigger PFOS-related IR.•PFOS-activated autophagy induces mitochondrial Ca2+ accumulation.•The interaction between VDAC1 and plasma membrane IP3R2 is investigated.•The interaction between VDAC1 and MICU1 is investigated.•Detyrosinated α-tubulin connects autophagy and mitochondrial Ca2+ response.
Maternal antibody IgG, the main antibody in colostrum, plays an important role in neonates protection. Commensal microbiota is closely related to host antibody repertoire. However, there are few ...reports on how maternal gut microbiota affects maternal antibody IgG transfer. In the present study, we investigated the effects of altering the gut microbiota (treated with antibiotics during pregnancy) on maternal IgG transportation and offspring absorption and explored its underlying mechanisms. Results showed that antibiotic treatment during pregnancy significantly decreased maternal cecal microbial richness (Chao1 and Obesrved species) and diversity (Shannon and Simpson). Plasma metabolome enriched significant changes in the process of bile acid secretion pathway, and the concentration of deoxycholic acid, a secondary metabolite of microorganisms was lowered. Flow cytometry analysis indicated that antibiotic treatment promoted the number of B cells and abated the number of T, DC and M1 cells in intestinal lamina propria of dams. Surprisingly, the serum IgG level in antibiotic treated dams was significantly increased, while IgG contents in colostrum was decreased. Moreover, pregnancy antibiotic treatment in dams was reduced the expression of FcRn, TLR4 and TLR2 in breast of dams and in duodenum and jejunum of neonates. Furthermore, TLR4
and TLR2
knock-out mice showed a lower FcRn expression in breast of dams and in duodenum and jejunum of neonates. These findings suggest that maternal intestine bacteria may affect the maternal IgG transfer through regulating the breast TLR4 and TLR2 of dams.
Perfluorooctane sulfonate (PFOS) is known as a persistent organic pollutant. A significant correlation between PFOS and liver ferroptosis has been unveiled, but the precise mechanism needs to be ...elucidated. In prior research, we found that PFOS treatment provoked mitochondrial iron overload. In this study, we observed a gradual increase in lysosomal iron in L-O2 cells after exposure to PFOS for 0.5–24 h. In PFOS-exposed L-O2 cells, suppressing autophagy relieved the lysosomal iron overload. Inhibiting transient receptor potential mucolipin 1 (TRPML1), a calcium efflux channel on the lysosomal membrane, led to a further rise in lysosomal iron levels and decreased mitochondrial iron overload during PFOS treatment. Suppressing VDAC1, a subtype of voltage-dependent anion-selective channels (VDACs) on the outer mitochondrial membrane, had no impact on PFOS-triggered mitochondrial iron overload, whereas restraining VDAC2/3 relieved this condition. Although silencing VDAC2 relieved PFOS-induced mitochondrial iron overload, it had no effect on PFOS-triggered lysosomal iron overload. Silencing VDAC3 alleviated PFOS-mediated mitochondrial iron overload and led to an additional increase in lysosomal iron. Therefore, we regarded VDAC3 as the specific VDACs subtype that mediated the lysosomes-mitochondria iron transfer. Additionally, in the presence of PFOS, an enhanced association between TRPML1 and VDAC3 was found in mice liver tissue and L-O2 cells. Our research unveils a novel regulatory mechanism of autophagy on the iron homeostasis and the effect of TRPML1-VDAC3 interaction on lysosomes-mitochondria iron transfer, giving an explanation of PFOS-induced ferroptosis and shedding some light on the role of classic calcium channels in iron transmission.
Display omitted
•Autophagy induces lysosomal iron overload under PFOS exposure.•TRPML1 mediates PFOS-provoked iron transfer between lysosomes and mitochondria.•VDAC3, not VDAC1/2, mediates PFOS-induced lysosomes-mitochondria iron transfer.•TRPML1 interacts with VDAC3 under PFOS exposure.•Lysosomes-mitochondria iron transmission mediates the ferroptosis elicited by PFOS.
PDF
