Extrinsic Conditions for the Occurrence and Characterizations of Self-Healing Polyurea Coatings for Improved Medical Device Reliability: A Mini Review

The development of self-healing materials has gained significance in the medical field to enhance the longevity and reliability of medical devices and implants. Material degradation caused by mechanical stress, environmental factors, and damage during use can lead to failure and necessitate manual inspection and maintenance. Self-healing materials, including polymers and elastomers, offer a promising solution by activating microdamage repair mechanisms. Polyurea coatings, known for their durability, flexibility, and versatility, have found widespread applications in various industries to prevent corrosion and abrasion and impact damage. This review focuses on the self-healing capability of polyurethane coatings and the efficacy of fabricated microcapsules. Experimental results elucidate the necessary conditions for achieving self-healing in polyurethane coatings encapsulated with suitable healing agents. These factors directly impact the self-healing potential of polyurea coatings and provide insights for medical device manufacturers seeking optimal coatings. The report also discusses challenges in fabrication and sample preparation, along with limitations of the project and recommendations for future research

Table_3_Oxygen enrichment protects against intestinal damage and gut microbiota disturbance in rats exposed to acute high-altitude hypoxia.XLS

Acute high-altitude hypoxia can lead to intestinal damage and changes in gut microbiota. Sustained and reliable oxygen enrichment can resist hypoxic damage at high altitude to a certain extent. However, it remains unclear whether oxygen enrichment can protect against gut damage and changes in intestinal flora caused by acute altitude hypoxia. For this study, eighteen male Sprague–Dawley rats were divided into three groups, control (NN), hypobaric hypoxic (HH), and oxygen-enriched (HO). The NN group was raised under normobaric normoxia, whereas the HH group was placed in a hypobaric hypoxic chamber simulating 7,000 m for 3 days. The HO group was exposed to oxygen-enriched air in the same hypobaric hypoxic chamber as the HH group for 12 h daily. Our findings indicate that an acute HH environment caused a fracture of the crypt structure, loss of epithelial cells, and reduction in goblet cells. Additionally, the structure and diversity of bacteria decreased in richness and evenness. The species composition at Phylum and Genus level was characterized by a higher ratio of Firmicutes and Bacteroides and an increased abundance of Lactobacillus with the abundance of Prevotellaceae_NK3B31_group decreased in the HH group. Interestingly, after oxygen enrichment intervention, the intestinal injury was significantly restrained. This was confirmed by an increase in the crypt depth, intact epithelial cell morphology, increased relative density of goblet cells, and higher evenness and richness of the gut microbiota, Bacteroidetes and Prevotellaceae as the main microbiota in the HO group. Finally, functional analysis showed significant differences between the different groups with respect to different metabolic pathways, including Amino acid metabolism, energy metabolism, and metabolism. In conclusion, this study verifies, for the first time, the positive effects of oxygen enrichment on gut structure and microbiota in animals experiencing acute hypobaric hypoxia.</p

Table_1_Oxygen enrichment protects against intestinal damage and gut microbiota disturbance in rats exposed to acute high-altitude hypoxia.XLS

Acute high-altitude hypoxia can lead to intestinal damage and changes in gut microbiota. Sustained and reliable oxygen enrichment can resist hypoxic damage at high altitude to a certain extent. However, it remains unclear whether oxygen enrichment can protect against gut damage and changes in intestinal flora caused by acute altitude hypoxia. For this study, eighteen male Sprague–Dawley rats were divided into three groups, control (NN), hypobaric hypoxic (HH), and oxygen-enriched (HO). The NN group was raised under normobaric normoxia, whereas the HH group was placed in a hypobaric hypoxic chamber simulating 7,000 m for 3 days. The HO group was exposed to oxygen-enriched air in the same hypobaric hypoxic chamber as the HH group for 12 h daily. Our findings indicate that an acute HH environment caused a fracture of the crypt structure, loss of epithelial cells, and reduction in goblet cells. Additionally, the structure and diversity of bacteria decreased in richness and evenness. The species composition at Phylum and Genus level was characterized by a higher ratio of Firmicutes and Bacteroides and an increased abundance of Lactobacillus with the abundance of Prevotellaceae_NK3B31_group decreased in the HH group. Interestingly, after oxygen enrichment intervention, the intestinal injury was significantly restrained. This was confirmed by an increase in the crypt depth, intact epithelial cell morphology, increased relative density of goblet cells, and higher evenness and richness of the gut microbiota, Bacteroidetes and Prevotellaceae as the main microbiota in the HO group. Finally, functional analysis showed significant differences between the different groups with respect to different metabolic pathways, including Amino acid metabolism, energy metabolism, and metabolism. In conclusion, this study verifies, for the first time, the positive effects of oxygen enrichment on gut structure and microbiota in animals experiencing acute hypobaric hypoxia.</p

Table_4_Oxygen enrichment protects against intestinal damage and gut microbiota disturbance in rats exposed to acute high-altitude hypoxia.XLSX

Acute high-altitude hypoxia can lead to intestinal damage and changes in gut microbiota. Sustained and reliable oxygen enrichment can resist hypoxic damage at high altitude to a certain extent. However, it remains unclear whether oxygen enrichment can protect against gut damage and changes in intestinal flora caused by acute altitude hypoxia. For this study, eighteen male Sprague–Dawley rats were divided into three groups, control (NN), hypobaric hypoxic (HH), and oxygen-enriched (HO). The NN group was raised under normobaric normoxia, whereas the HH group was placed in a hypobaric hypoxic chamber simulating 7,000 m for 3 days. The HO group was exposed to oxygen-enriched air in the same hypobaric hypoxic chamber as the HH group for 12 h daily. Our findings indicate that an acute HH environment caused a fracture of the crypt structure, loss of epithelial cells, and reduction in goblet cells. Additionally, the structure and diversity of bacteria decreased in richness and evenness. The species composition at Phylum and Genus level was characterized by a higher ratio of Firmicutes and Bacteroides and an increased abundance of Lactobacillus with the abundance of Prevotellaceae_NK3B31_group decreased in the HH group. Interestingly, after oxygen enrichment intervention, the intestinal injury was significantly restrained. This was confirmed by an increase in the crypt depth, intact epithelial cell morphology, increased relative density of goblet cells, and higher evenness and richness of the gut microbiota, Bacteroidetes and Prevotellaceae as the main microbiota in the HO group. Finally, functional analysis showed significant differences between the different groups with respect to different metabolic pathways, including Amino acid metabolism, energy metabolism, and metabolism. In conclusion, this study verifies, for the first time, the positive effects of oxygen enrichment on gut structure and microbiota in animals experiencing acute hypobaric hypoxia.</p

Table_2_Oxygen enrichment protects against intestinal damage and gut microbiota disturbance in rats exposed to acute high-altitude hypoxia.XLS

Acute high-altitude hypoxia can lead to intestinal damage and changes in gut microbiota. Sustained and reliable oxygen enrichment can resist hypoxic damage at high altitude to a certain extent. However, it remains unclear whether oxygen enrichment can protect against gut damage and changes in intestinal flora caused by acute altitude hypoxia. For this study, eighteen male Sprague–Dawley rats were divided into three groups, control (NN), hypobaric hypoxic (HH), and oxygen-enriched (HO). The NN group was raised under normobaric normoxia, whereas the HH group was placed in a hypobaric hypoxic chamber simulating 7,000 m for 3 days. The HO group was exposed to oxygen-enriched air in the same hypobaric hypoxic chamber as the HH group for 12 h daily. Our findings indicate that an acute HH environment caused a fracture of the crypt structure, loss of epithelial cells, and reduction in goblet cells. Additionally, the structure and diversity of bacteria decreased in richness and evenness. The species composition at Phylum and Genus level was characterized by a higher ratio of Firmicutes and Bacteroides and an increased abundance of Lactobacillus with the abundance of Prevotellaceae_NK3B31_group decreased in the HH group. Interestingly, after oxygen enrichment intervention, the intestinal injury was significantly restrained. This was confirmed by an increase in the crypt depth, intact epithelial cell morphology, increased relative density of goblet cells, and higher evenness and richness of the gut microbiota, Bacteroidetes and Prevotellaceae as the main microbiota in the HO group. Finally, functional analysis showed significant differences between the different groups with respect to different metabolic pathways, including Amino acid metabolism, energy metabolism, and metabolism. In conclusion, this study verifies, for the first time, the positive effects of oxygen enrichment on gut structure and microbiota in animals experiencing acute hypobaric hypoxia.</p

Data_Sheet_1_Oxygen enrichment protects against intestinal damage and gut microbiota disturbance in rats exposed to acute high-altitude hypoxia.docx

Acute high-altitude hypoxia can lead to intestinal damage and changes in gut microbiota. Sustained and reliable oxygen enrichment can resist hypoxic damage at high altitude to a certain extent. However, it remains unclear whether oxygen enrichment can protect against gut damage and changes in intestinal flora caused by acute altitude hypoxia. For this study, eighteen male Sprague–Dawley rats were divided into three groups, control (NN), hypobaric hypoxic (HH), and oxygen-enriched (HO). The NN group was raised under normobaric normoxia, whereas the HH group was placed in a hypobaric hypoxic chamber simulating 7,000 m for 3 days. The HO group was exposed to oxygen-enriched air in the same hypobaric hypoxic chamber as the HH group for 12 h daily. Our findings indicate that an acute HH environment caused a fracture of the crypt structure, loss of epithelial cells, and reduction in goblet cells. Additionally, the structure and diversity of bacteria decreased in richness and evenness. The species composition at Phylum and Genus level was characterized by a higher ratio of Firmicutes and Bacteroides and an increased abundance of Lactobacillus with the abundance of Prevotellaceae_NK3B31_group decreased in the HH group. Interestingly, after oxygen enrichment intervention, the intestinal injury was significantly restrained. This was confirmed by an increase in the crypt depth, intact epithelial cell morphology, increased relative density of goblet cells, and higher evenness and richness of the gut microbiota, Bacteroidetes and Prevotellaceae as the main microbiota in the HO group. Finally, functional analysis showed significant differences between the different groups with respect to different metabolic pathways, including Amino acid metabolism, energy metabolism, and metabolism. In conclusion, this study verifies, for the first time, the positive effects of oxygen enrichment on gut structure and microbiota in animals experiencing acute hypobaric hypoxia.</p

p150^glued-Associated Disorders Are Caused by Activation of Intrinsic Apoptotic Pathway

<div><p>Mutations in p150^glued cause hereditary motor neuropathy with vocal cord paralysis (HMN7B) and Perry syndrome (PS). Here we show that both overexpression of p150^glued mutants and knockdown of endogenous p150^glued induce apoptosis. Overexpression of a p150^glued plasmid containing either a HMN7B or PS mutation resulted in cytoplasmic p150^glued-positive aggregates and was associated with cell death. Cells containing mutant p150^glued aggregates underwent apoptosis that was characterized by an increase in cleaved caspase-3- or Annexin V-positive cells and was attenuated by both zVAD-fmk (a pan-caspase inhibitor) application and caspase-3 siRNA knockdown. In addition, overexpression of mutant p150^glued decreased mitochondrial membrane potentials and increased levels of translocase of the mitochondrial outer membrane (Tom20) protein, indicating accumulation of damaged mitochondria. Importantly, siRNA knockdown of endogenous p150^glued independently induced apoptosis via caspase-8 activation and was not associated with mitochondrial morphological changes. Simultaneous knockdown of endogenous p150^glued and overexpression of mutant p150^glued had additive apoptosis induction effects. These findings suggest that both p150^glued gain-of-toxic-function and loss-of-physiological-function can cause apoptosis and may underlie the pathogenesis of p150^glued-associated disorders.</p></div

Depletion of p150^glued does not induce damaged mitochondria accumulation.

<p>(A) Control siRNA or DCTN1 siRNA transfected cells were fixed and co-stained with antibodies against LAMP2 (green) and TOM20 (red), and analyzed using confocal microscopy. Bars, 10 μm. (B) Control siRNA or DCTN1 siRNA transfected HeLa cells were analyzed by immunoblotting with antibodies against complex I, TOM20, and actin. (C, D) Densitometry analysis of complex I (C) and TOM20 (D) levels relative to actin was performed. (E, F) DCTN1 siRNA transfected HeLa cells were incubated with Mitotracker-Red CMXRos and intracellular fluorescence intensity was measured by flow cytometry. The histograms of MitoTracker-Red CMXRos fluorescence (E) and the percentages of cells with reduced mitochondrial potentials (F) are shown. The error bar indicates each standard deviation. Statistics are from three independent experiments: N.S., not significant.</p

Mutant p150^glued proteins activate intrinsic apoptotic pathways.

<p>(A) HeLa cells transfected with GFP-empty, GFP-tagged wild-type or mutant (G59S or G71R) p150^glued were fixed and stained with DAPI after 24 and 48 h. GFP-positive cells were counted from three independent experiments. The percentage of GFP-positive cells with nuclear abnormalities is shown. (B) Ratio of transfected HeLa cells with nuclear abnormalities after treatment with or without z-VAD (100 μM) for 24 hours. Values are relative to the GFP-empty value, which is set at 1. (C, D) Transfected SH-SY5Y cells after treatment with or without z-VAD (100 μM) for 48 h were stained with Annexin V and PI, and GFP-positive cells were analyzed by flow cytometry. (E) HeLa cells transfected with GFP-tagged wild-type or mutant p150^glued were fixed and stained with an antibody against cleaved caspase-3. Bars, 10 μm. (F) Twenty-four hours after transfection, SH-SY5Y cells were fixed and stained with a cleaved caspase-3 antibody. GFP-positive cells were analyzed by flow cytometry and the mean fluorescent intensity was calculated. (G) HeLa cells were transfected with control scrambled siRNA or caspase-3 siRNA for 72 h and immunoblotting analysis was performed to monitor the knockdown efficiency of the caspase-3 siRNA. (H) Twenty-four hours after transfection with control siRNA or caspase-3 siRNA, HeLa cells were transfected with GFP-empty, GFP-tagged wild-type or mutant p150^glued. Forty-eight hours after transfection, cells were fixed and stained with DAPI, and ratios of GFP-positive cells with nuclear abnormalities were analyzed. Values are relative to the GFP-empty value, which is set at 1. The error bar indicates each standard deviation. Statistics are from three independent experiments: N.S., not significant; *, p<0.05; **, p<0.01; ***, p<0.001.</p

Disease-associated p150^glued mutant proteins form aggregates.

<p>(A) Schematic of the p150^glued subunit of dynactin. (B) HeLa cells transfected with GFP-tagged wild-type or mutant p150^glued were fixed and stained with an antibody against α-tubulin (red) after 24 h and analyzed using confocal microscopy. Insets show higher magnification of the boxed areas. Bars, 10 μm. (C) The percentages of GFP-positive cells that contained aggregates are shown. The error bar indicates each standard deviation. Statistics are from three independent experiments. (D, E) Electron micrographic examination of HeLa cells transfected with GFP-tagged G59S p150^glued and immunolabeled with an antibody against GFP. (E) High magnification of the boxed area shown in (D). Intracytoplasmic aggregates (a) are labeled.</p