In vitro fermentation characteristics of blueberry anthocyanins and their impacts on gut microbiota from obese human.

It has been demonstrated that the gut microbiota may play an important intermediary role in anthocyanins' beneficial impacts on obesity. However, the microbe-related anti-obesity mechanism of blueberry anthocyanins remains unclear. In this study, the interactions between blueberry anthocyanin extracts (BAE) and gut microbiota from obese humans were explored using an in vitro fermentation model. Due to hydrolysis and metabolism by the microbiota, the contents of blueberry anthocyanins are reduced during fermentation. It was demonstrated that both aglycones and glycosides affected the degradation rate. The microbial composition evaluation revealed that BAE could alleviate obesity by promoting the colonization of probiotics such as Lachnospiraceae_UCG-004 and Bacteroides, as well as inhibiting the proliferation of harmful bacteria including Escherichia-Shigella, Clostridium_sensu_stricto_1, and Klebsiella. Blueberry anthocyanin extracts facilitate the production of short-chain fatty acids (SCFAs), which is beneficial for obesity control. The relationship between blueberry anthocyanins, gut microbiota, and SCFAs was further investigated. Overall, this data provides new insights into the positive interaction between blueberry anthocyanins and gut microbiota in obese humans.

In vitro digestion under simulated saliva, gastric and small intestinal conditions and fermentation of nicotinamide mononucleotide, and its effects on the gut microbiota.

Nicotinamide Mononucleotide (NMN) is a derivative of vitamin B3, which plays a significant role in a plethora of metabolic reactions in the human body and is intricately associated with both immunity and metabolism. Nonetheless, in the intestine metabolic pathway of NMN and the relationship between NMN, gut microbiota, and SCFAs remain hitherto obscure. This study examined the digestion of NMN in simulated saliva, gastric, and small intestine environments, as well as exploring the interaction between NMN and human gut microbiota utilizing an in vitro fermentation model. NMN was progressively degraded into nicotinamide ribose (NR), nicotinamide (NAM), and ribose, with niacinate (NA) constituting the ultimate degradation product due to hydrolysis and metabolism by microbiota. NMN was ingested by human intestinal microbiota with a slower fermentation rate. As a result of NMN ingestion by human gut bacteria，the concentrations of propionate and butyrate increased by 88% and 23%, respectively, compared to the blank control group, the proliferation of beneficial gut bacteria (Bifidobacterium, Phascolarctobacterium, Faecalibacteriun, and Alistipes) significantly increased, while the proliferation of some harmful bacteria (Sutterella, Desulfovibrio and Pseudomonas) drastically declined. These findings illustrated the metabolic processes of NMN in the intestine, elaborating the relationship between NMN, SCFAs and gut microbiota. NMN might be a potential prebiotic to improve intestinal health.

Multimedia Mercury Recovery from Coal-Fired Power Plants Utilizing N-Containing Conjugated Polymer Functionalized Fly Ash.

To recover multimedia mercury from coal-fired power plants, a novel N-containing conjugated polymer (polyaniline and polypyrrole) functionalized fly ash was prepared, which could continuously adsorb 99.2% of gaseous Hg0 at a high space velocity of 368,500 h-1 and nearly 100% of aqueous Hg2+ in the solution pH range of 2-12. The adsorption capacities of Hg0 and Hg2+ reach 1.62 and 101.36 mg/g, respectively. Such a kind of adsorbent has good environmental applicability, i.e. good resistance to coexisting O2/NO/SO2 and coexisting Na+/K+/Ca2+/Mg2+/SO42-. This adsorbent has very low specific resistances (6 × 106-5 × 109 Ω·cm) and thus can be easily collected by an electrostatic precipitator under low-voltage (0.1-0.8 kV). The Hg-saturated adsorbent can desorb almost 100% Hg under relatively low temperature (<250 °C). Characterization and theoretical calculations reveal that conjugated-N is the critical site for adsorbing both Hg0 and Hg2+ as well as activating chlorine. Gaseous Hg0 is oxidized and adsorbed in the form of HgXClX(ad), while aqueous Hg2+ is adsorbed to form a complex with conjugated-N, and parts of Hg2+ are reduced to Hg+ by conjugated-N. This adsorbent can be easily large-scale manufactured; thus, this novel solid waste functionalization method is promising to be applied in coal-fired power plants and other Hg-involving industrial scenes.

Efficient and accurate compound scaling for convolutional neural networks.

Designing efficient and accurate network architectures to support various workloads, from servers to edge devices, is a fundamental problem as the use of Convolutional Neural Networks (ConvNets) becomes increasingly widespread. One simple yet effective method is to scale ConvNets by systematically adjusting the dimensions of the baseline network, including width, depth, and resolution, enabling it to adapt to diverse workloads by varying its computational complexity and representation ability. However, current state-of-the-art (SOTA) scaling methods for neural network architectures overlook the inter-dimensional relationships within the network and the impact of scaling on inference speed, resulting in suboptimal trade-offs between accuracy and inference speed. To overcome those limitations, we propose a scaling method for ConvNets that utilizes dimension relationship and runtime proxy constraints to improve accuracy and inference speed. Specifically, our research notes that higher input resolutions in convolutional layers lead to redundant filters (convolutional width) due to increased similarity between information in different positions, suggesting a potential benefit in reducing filters while increasing input resolution. Based on this observation, the relationship between the width and resolution is empirically quantified in our work, enabling models with higher parametric efficiency to be prioritized through our scaling strategy. Furthermore, we introduce a novel runtime prediction model that focuses on fine-grained layer tasks with different computational properties for more accurate identification of efficient network configurations. Comprehensive experiments show that our method outperforms prior works in creating a set of models with a trade-off between accuracy and inference speed on the ImageNet datasets for various ConvNets.

Phytochrome B mediates dim-light-reduced insect resistance by promoting the ethylene pathway in rice.

Increasing planting density is one of the most effective ways to improve crop yield. However, one major factor that limits crop planting density is the weakened immunity of plants to pathogens and insects caused by dim light (DL) under shade conditions. The molecular mechanism underlying how DL compromises plant immunity remains unclear. Here, we report that DL reduces rice (Oryza sativa) resistance against brown planthopper (BPH; Nilaparvata lugens) by elevating ethylene (ET) biosynthesis and signaling in a Phytochrome B (OsPHYB)-dependent manner. The DL-reduced BPH resistance is relieved in osphyB mutants, but aggravated in OsPHYB overexpressing plants. Further, we found that DL reduces the nuclear accumulation of OsphyB, thus alleviating Phytochrome Interacting Factor Like14 (OsPIL14) degradation, consequently leading to the up-regulation of 1-Aminocyclopropane-1-Carboxylate Oxidase1 (OsACO1) and an increase in ET levels. In addition, we found that nuclear OsphyB stabilizes Ethylene Insensitive Like2 (OsEIL2) by competitively interacting with EIN3 Binding F-Box Protein (OsEBF1) to enhance ET signaling in rice, which contrasts with previous findings that phyB blocks ET signaling by facilitating Ethylene Insensitive3 (EIN3) degradation in other plant species. Thus, enhanced ET biosynthesis and signaling reduces BPH resistance under DL conditions. Our findings provide insights into the molecular mechanism of the light-regulated ET pathway and host-insect interactions and potential strategies for sustainable insect management.

Simulated Digestion and Fermentation In Vitro by Obese Human Gut Microbiota of Sulforaphane from Broccoli Seeds.

BACKGROUND: sulforaphane is a kind of isothiocyanate, which is obtained by hydrolysis of glucosinolate by the unique myrosinase in plants. It has been proved to prevent the occurrence of many chronic diseases, such as obesity, diabetes and cancer. OBJECTIVE: The impact of SFN on obese human gut flora, however, has not been established. METHODS: In this research, SFN was isolated from broccoli seeds and then refined to achieve 95% purity. Next, an investigation was conducted into the digestion and fermentation processes of SFN. RESULTS: The stability of the SFN in simulated saliva, gastric fluid, and intestinal juice provides evidence that it can reach the gut and be available for utilization by gut microflora. In vitro fermentation of SFN by gut microbes in obese patients results in alteration in constitution of microbiota and production of short chain fatty acids. As the result of SFN ingestion by human gut bacteria, the content of butyric and valeric acids increased 1.21- and 1.46-fold, respectively. In obese human guts, the relative abundances of the beneficial genera including Lactobacillus, Weissella, Leuconosto, Algiphilus and Faecalibacterium significantly increased, whilst the detrimental genera, such as Escherichia-Shigella, Klebsiella, Clostridium_sensu_stricto_1, Sutterella, Megamonas and Proteus drastically declined. CONCLUSION: Taken together, these findings demonstrate that SFN can be used as a nutraceutical ingredient for obese patients and for improving human health.

A Voice Cloning Method Based on the Improved HiFi-GAN Model.

With the aim of adapting a source Text to Speech (TTS) model to synthesize a personal voice by using a few speech samples from the target speaker, voice cloning provides a specific TTS service. Although the Tacotron 2-based multi-speaker TTS system can implement voice cloning by introducing a d-vector into the speaker encoder, the speaker characteristics described by the d-vector cannot allow for the voice information of the entire utterance. This affects the similarity of voice cloning. As a vocoder, WaveNet sacrifices speech generation speed. To balance the relationship between model parameters, inference speed, and voice quality, a voice cloning method based on improved HiFi-GAN has been proposed in this paper. (1) To improve the feature representation ability of the speaker encoder, the x-vector is used as the embedding vector that can characterize the target speaker. (2) To improve the performance of the HiFi-GAN vocoder, the input Mel spectrum is processed by a competitive multiscale convolution strategy. (3) The one-dimensional depth-wise separable convolution is used to replace all standard one-dimensional convolutions, significantly reducing the model parameters and increasing the inference speed. The improved HiFi-GAN model remarkably reduces the number of vocoder model parameters by about 68.58% and boosts the model's inference speed. The inference speed on the GPU and CPU has increased by 11.84% and 30.99%, respectively. Voice quality has also been marginally improved as MOS increased by 0.13 and PESQ increased by 0.11. The improved HiFi-GAN model exhibits outstanding performance and remarkable compatibility in the voice cloning task. Combined with the x-vector embedding, the proposed model achieves the highest score of all the models and test sets.

mTORC2 Facilitates Liver Regeneration Through Sphingolipid-Induced PPAR-α-Fatty Acid Oxidation.

BACKGROUND & AIMS: During liver regeneration after partial hepatectomy, the function and metabolic pathways governing transient lipid droplet accumulation in hepatocytes remain obscure. Mammalian target of rapamycin 2 (mTORC2) facilitates de novo synthesis of hepatic lipids. Under normal conditions and in tumorigenesis, decreased levels of triglyceride (TG) and fatty acids (FAs) are observed in the mTORC2-deficient liver. However, during liver regeneration, their levels increase in the absence of mTORC2. METHODS: Rictor liver-specific knockout and control mice underwent partial hepatectomy, followed by measurement of TG and FA contents during liver regeneration. FA metabolism was evaluated by analyzing the expression of FA metabolism-related genes and proteins. Intraperitoneal injection of the peroxisome proliferator-activated receptor α (PPAR-α) agonist, p53 inhibitor, and protein kinase B (AKT) activator was performed to verify the regulatory pathways involved. Lipid mass spectrometry was performed to identify the potential PPAR-α activators. RESULTS: The expression of FA metabolism-related genes and proteins suggested that FAs are mainly transported into hepatocytes during liver regeneration. The PPAR-α pathway is down-regulated significantly in the mTORC2-deficient liver, resulting in the accumulation of TGs. The PPAR-α agonist WY-14643 rescued deficient liver regeneration and survival in mTORC2-deficient mice. Furthermore, lipidomic analysis suggested that mTORC2 deficiency substantially reduced glucosylceramide (GluCer) content. GluCer activated PPAR-α. GluCer treatment in vivo restored the regenerative ability and survival rates in the mTORC2-deficient group. CONCLUSIONS: Our data suggest that FAs are mainly transported into hepatocytes during liver regeneration, and their metabolism is facilitated by mTORC2 through the GluCer-PPAR-α pathway, thereby establishing a novel role for mTORC2 in lipid metabolism.

Cytokinin Confers Brown Planthopper Resistance by Elevating Jasmonic Acid Pathway in Rice.

Plants have evolved a sophisticated defense system that employs various hormone pathways to defend against attacks by insect pests. Cytokinin (CK) plays an important role in plant growth and stress tolerance, but the role of CKs in plant-insect interaction remains largely unclear. Here, we report that CKs act as a positive regulator in rice resistance against brown planthopper (BPH), a devastating insect pest of rice. We found that BPH feeding promotes CK biosynthesis and signaling in rice. Exogenous application of CKs significantly increased the rice resistance to BPH. Increasing endogenous CKs by knocking out cytokinin oxidase/dehydrogenase (OsCKXs) led to enhanced resistance to BPH. Moreover, the levels of the plant hormone jasmonic acid (JA) and the expression of JA-responsive genes were elevated by CK treatment and in OsCKXs knockout plants. Furthermore, JA-deficient mutant og1 was more susceptible to BPH, and CK-induced BPH resistance was suppressed in og1. These results indicate that CK-mediated BPH resistance is JA-dependent. Our findings provide the direct evidence for the novel role of CK in promoting insect resistance, and demonstrate that CK-induced insect resistance is JA-dependent. These results provide important guidance for effective pest management strategies in the future.

Growth-Promoting Mechanism of Bismuth-Doped Cu(In,Ga)Se2 Solar Cells Fabricated at 400 °C.

The classical high-temperature synthesis process of Cu(In,Ga)Se2 (CIGS) solar cells limits their applications on high-temperature intolerant substrates. In this study, a novel low-temperature (400 °C) fabrication strategy of CIGS solar cells is reported using the bismuth (Bi)-doping method, and its growth-promoting mechanism is systematically studied. Different concentrations of Bi are incorporated into pure chalcopyrite quaternary target sputtered-CIGS films by controlling the thickness of the Bi layer. Bi induces considerable grain growth improvement, and an average of approximately 3% absolute efficiency enhancement is achieved for Bi-doped solar cells in comparison with the Bi-free samples. Solar cells doped with a 50 nm Bi layer yield the highest efficiency of 13.04% (without any antireflective coating) using the low-temperature technology. The copper-bismuth-selenium compounds (Cu-Bi-Se, mainly Cu1.6Bi4.8Se8) are crucial in improving the crystallinity of absorbers during the annealing process. These Bi-containing compounds are conclusively observed at the grain boundaries and top and bottom interfaces of CIGS films. The growth promotion is found to be associated with the superior diffusion capacity of Cu-Bi-Se compounds in CIGS films, and these liquid compounds function as carriers to facilitate crystallization. Bi atoms do not enter the CIGS lattices, and the band gaps (Eg) of absorbers remain unchanged. Bi doping reduces the number of CIGS grain boundaries and increases the copper vacancy content in CIGS films, thereby boosting the carrier concentrations. Cu-Bi-Se compounds in grain boundaries significantly enhance the conductivity of grain boundaries and serve as channels for carrier transport. The valence band, Fermi energy level (EF), and conduction band of Bi-doped CIGS films all move downward. This band shift strengthens the band bending of the CdS/CIGS heterojunction and eventually improves the open circuit voltage (Voc) of solar cells. An effective doping method and a novel mechanism can facilitate the low-temperature preparation of CIGS solar cells.

An R2R3 MYB transcription factor confers brown planthopper resistance by regulating the phenylalanine ammonia-lyase pathway in rice.

Brown planthopper (BPH) is one of the most destructive insects affecting rice (Oryza sativa L.) production. Phenylalanine ammonia-lyase (PAL) is a key enzyme involved in plant defense against pathogens, but the role of PAL in insect resistance is still poorly understood. Here we show that expression of the majority of PALs in rice is significantly induced by BPH feeding. Knockdown of OsPALs significantly reduces BPH resistance, whereas overexpression of OsPAL8 in a susceptible rice cultivar significantly enhances its BPH resistance. We found that OsPALs mediate resistance to BPH by regulating the biosynthesis and accumulation of salicylic acid and lignin. Furthermore, we show that expression of OsPAL6 and OsPAL8 in response to BPH attack is directly up-regulated by OsMYB30, an R2R3 MYB transcription factor. Taken together, our results demonstrate that the phenylpropanoid pathway plays an important role in BPH resistance response, and provide valuable targets for genetic improvement of BPH resistance in rice.

Brassinosteroids mediate susceptibility to brown planthopper by integrating with the salicylic acid and jasmonic acid pathways in rice.

Improved knowledge of the interactions between plants and insects will facilitate better insect control in crops. Brassinosteroids (BRs) play a vital role in plant growth, developmental processes, and responses to pathogen infection, but the role of BRs in interactions between plants and insects remain largely unknown. In this study, we characterized a negative role of BRs in rice defense against brown planthopper (BPH, Nilaparvata lugens) and examined its underlying mechanisms. We found that BPH infestation suppressed the BR pathway while successively activating the salicylic acid (SA) and jasmonic acid (JA) pathways. In addition, BR-overproducing mutants and plants treated with 24-epibrassinolide (BL) showed increased susceptibility to BPH, whereas BR-deficient mutants were more resistant than the wild-type. BRs down-regulated the expression of genes related to the SA pathway and reduced SA content while genes related to the JA pathway were up-regulated and JA content increased after BPH infestation. Furthermore, BR-mediated suppression of the SA pathway was impaired both in JA-deficient and JA-insensitive mutants. Our results demonstrate that BRs promote the susceptibility of rice plants to BPH by modulating the SA and JA pathways.

Marker assisted pyramiding of two brown planthopper resistance genes, Bph3 and Bph27 (t), into elite rice Cultivars.

BACKGROUND: Brown planthopper (BPH) is the most destructive insect in rice production. Breeding of resistant cultivars is the most cost-effective and environment-friendly strategy for BPH management; however, resistant cultivars are currently hampered by the rapid breakdown of BPH resistance. Thus, there is an urgent need to use more effective BPH resistance genes or pyramiding different resistance genes to develop more durable resistant rice cultivars. RESULTS: Here a dominant BPH resistance gene Bph27(t) were introgressed into a susceptible commercial japonica variety Ningjing3 (NJ3) and indica variety 93-11 using marker-assisted selection (MAS), respectively. Further, Bph27(t) and a durable BPH resistance gene Bph3 was pyramided by intercrossing single-gene introgressed lines through MAS. The introgression of BPH resistance genes significantly improved the BPH resistance and reduced the yield loss caused by BPH. CONCLUSION: The development of single and two genes pyramided lines in this study provides innovative resources for molecular breeding of durable BPH-resistant rice cultivars and BPH management through resistant cultivars.

Effects of medicinal mushroom (Sparassis crispa) on wound healing in streptozotocin-induced diabetic rats.

BACKGROUND: The impaired wound healing in diabetes mellitus is a major clinical problem. Sparassis crispa (SC) is a medicinal mushroom and its beta-glucan content is more than 40%. This study investigated whether oral administration of SC could improve the impaired wound healing in diabetic rats. METHODS: Full-thickness skin wounds were created on the backs of streptozotocin (STZ)-induced diabetic rats. Diabetic rats were then divided into 2 groups: SC-treated group that was orally administered doses of 1,000 mg/kg body weight per day of SC for 4 weeks and a control group without SC administration. Moreover, collagen synthesis of purified beta-glucan from SC was estimated in vitro. RESULTS: Wound closure was significantly accelerated by oral administration of SC. Furthermore, in SC-treated wounds there were significant increases in macrophage and fibroblast migration, collagen regeneration, and epithelialization compared with the control group. The levels of type I collagen synthesized by cultured human dermal fibroblasts for the SC group were significantly higher than those for the control group. CONCLUSIONS: SC can improve the impaired healing of diabetic wounds. This effect might involve an increase in the migration of macrophages and fibroblasts, and beta-glucan from SC directly increases the synthesis of type I collagen. Therefore, the use of SC may be extended to the clinical setting and prove an effective promoter of wound healing in patients with diabetes.

Edaravone prevents Fas-induced fulminant hepatic failure in mice by regulating mitochondrial Bcl-xL and Bax.

Fulminant hepatic failure is a serious disease that has a poor cure rate unless liver transplantation is performed. Edaravone, a free radical scavenger, has been approved for the treatment of acute cerebral infarction, and its mechanism of action involves scavenging free radicals generated in ischemic tissues. We assessed the ability of 3-methyl-1-phenyl-2-pyrazolim-5-one (edaravone) to prevent Fas-induced acute liver failure in mice and examined the mechanisms underlying the observed effects. BALB/c mice were administered 0.25 microg/g (i.v.) body weight of a purified hamster agonist anti-Fas monoclonal antibody (clone Jo2). The mice also received either edaravone or isotonic sodium chloride solution before or after Jo2 treatment. Edaravone improved the survival rate of the mice markedly. Histopathological findings and serum aspartate aminotransferase levels showed that edaravone reduced the degree of liver injury caused by Jo2. Terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick end labeling staining showed that edaravone reduced the number of apoptotic hepatocytes. Edaravone also prevented cytochrome c release and caspase 3 activity, recognized as markers of apoptosis after mitochondrial disruption. Therefore, we considered that the antiapoptotic activity of edaravone involved blocking signals in the mitochondria-dependent pathway of Fas-induced apoptosis. Mitochondrial Bcl-xL and Bax, which form a channel in the mitochondrial membrane and, by their balance, regulate its permeability, are involved in mitochondrial disruption. Western blotting showed that the Bcl-xL-Bax ratio of the edaravone group was much higher than that of the control group. In conclusion, edaravone might protect hepatocytes from Fas-induced mitochondria-dependent apoptosis by regulating mitochondrial Bcl-xL and Bax.

Fibronectin prevents endotoxin shock after partial hepatectomy in rats via inhibition of nuclear factor-kappaB and apoptosis.

Fibronectins (Fns) are involved in a number of biologic processes, such as cellular adhesion, motility, differentiation, apoptosis, hemostasis, wound healing, and ischemic injury. We investigated the possible mechanism underlying the protective action of plasma Fn (pFn) on endotoxin shock following partial hepatectomy in rats. Lipopolysaccharide (LPS) was administered intravenously to male Sprague-Dawley rats within 48 hrs of 70% hepatectomy. Prior to LPS administration, pFn or human serum albumin was given intravenously. The survival rate of the pFn-treated group was improved markedly compared with that of the controls. The levels of inflammatory cytokines and nitric oxide (NO) in serum were significantly lower in the pFn-treated group than in the control group. Expression of inducible nitric oxide synthase (iNOS) in hepatocytes also was reduced following pFn treatment. The degree of apoptosis and necrosis in the remnant liver was significantly lower in the pFn-treated rats than the controls. Furthermore, pFn pretreatment greatly inhibited the activation of nuclear factor-kappaB (NF-kappaB), caspase 3 and 8 activities, and cytochrome c release, and caused a decrease in mitochondrial Bcl-x(L). Plasma Fn prevents endotoxin-induced liver injury at least in part through inhibition of NF-kappaB activation, which causes the reduction of iNOS expression and NO production by hepatocytes, and through the downregulation of inflammatory cytokines and promotion of Bcl-x(L) expression.

Topical application of plasma fibronectin in full-thickness skin wound healing in rats.

Fibronectin (Fn) has been shown to play an important role in wound healing because it appears to be the stimulus for migration of fibroblasts and epidermal cells. The purpose of this study was to investigate whether topical application of plasma Fn (pFn) improves healing of full-thickness skin wounds in rats. A round section of full-thickness skin (diameter of approximately 15 mm) was resected in rats. Animals were then divided into two groups, and wounds were treated topically with a single application of human plasma albumin (control group) or human pFn (FN group). Wound closure rate, hydroxyproline concentration, and histologic features (immunohistochemical staining) were evaluated. The FN group had a significantly higher wound closure rate and hydroxyproline level in the skin than the control group. Histologic analysis of macrophage and fibroblast migration, collagen regeneration, and epithelialization were significantly increased in the FN group compared with the control group. A single topical application of pFn increased the migration of macrophages, myofibroblasts, and fibroblasts. Moreover, further release of transforming growth factor-beta1 from activated fibroblasts, keratinocytes, and epithelial cells may also contribute to the beneficial effect of pFn on wound healing.

Effect of plasma fibronectin on the incisional wound healing in rats.

BACKGROUND: Abdominal wall repair after celiotomy is important because insufficient incisional wound strength results in wound failures such as fascial dehiscence and herniation. Plasma fibronectin (pFn) has been shown to play an important role in wound healing. The purpose of this study was to investigate whether pFn improves incisional wound healing in a rat skin incision and celiotomy model. METHODS: Rats underwent a linear skin incision in the dorsal plane or a full-thickness incisional wound (celiotomy) in the abdominal wall. The same operative procedures were performed on rats whose pFn levels were reduced by antirat pFn serum. The wounds were sutured, and purified human pFn or albumin was given intravenously. RESULTS: After the celiotomy, pFn levels decreased immediately and reached a minimum at 3 h after incision. A single injection of pFn (10 mg/kg) significantly increased the breaking strength of the skin and the bursting pressure of the abdominal wall. The amount of hydroxyproline in the skin incisional wound with pFn was significantly greater than with an injection of albumin as control. In rats with pFn levels decreased by antirat pFn serum, a single administration of pFn significantly increased the breaking strength of the skin and the bursting pressure of the abdominal wall compared to a control injection of albumin. CONCLUSIONS: It is important for wound healing to maintain sufficiently high levels of pFn. A single intravenous injection of pFn after celiotomy may be useful in the prevention of fascial dehiscence and herniation.

Effects of plasma fibronectin on the healing of full-thickness skin wounds in streptozotocin-induced diabetic rats.

BACKGROUND: Fibronectin has been shown to assist in wound healing. Impaired wound healing in diabetes mellitus is characterized by a reduction in plasma fibronectin (pFn) at the wound site. This study investigated whether topical application of pFn could improve the impaired wound healing in diabetic rats. MATERIALS AND METHODS: Full-thickness skin wounds were created on the backs of streptozotocin (STZ)-induced diabetic rats. Immediately, human pFn was introduced into the wound bed, while wounds receiving human serum albumin or normal saline were used as controls. Wound closure was monitored using well-recognized wound-healing parameters: epithelialization, vascularization, collagen deposition, and migration of fibroblasts were examined histologically. Transforming growth factor (TGF)-beta1 was measured by immunochemistry. Hydroxyproline levels also were assessed in the wound skin. RESULTS: Wound closure was significantly accelerated by local application of pFn. Furthermore, pFn-treated wounds showed increased fibroblast vascularization, collagen regeneration, and epithelialization. The numbers of infiltrating fibroblasts expressing TGF-beta1 and hydroxyproline levels in pFn-treated wounds were significantly higher than those in the controls. CONCLUSIONS: pFn can improve the impaired healing of diabetic wounds and this effect might involve an increase in the activity of fibroblasts and increased release of TGF-beta1.

Fibronectin prevents D-galactosamine/lipopolysaccharide-induced lethal hepatic failure in mice.

Plasma fibronectin (FN) has a broad range of biological functions involved in cellular adhesion, motility, differentiation, apoptosis, hemostasis, wound healing, reticuloendothelial system function, and ischemic injury. In this study, we examined the effects of FN on D-galactosamine (GalN)/lipopolysaccharide (LPS)-induced fulminant liver failure in mice. Female Balb/c mice received intraperitoneal injection of 50 mug/kg of LPS and 400 mg/kg of GalN simultaneously. Thirty minutes before GalN/LPS administration, human plasma FN (FN group) or the same dose of human serum albumin (control group) was given intravenously. GalN/LPS induced a marked decrease in plasma FN, which was reversed by FN pretreatment. The survival rate of the FN group was markedly improved in a dose-dependent manner compared with that of the control group (survival rate 0%). FN prevented increases in the concentrations of serum enzymes and total bilirubin related to liver injury. FN pretreatment significantly suppressed tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and interleukin (IL)-6 levels, and enhanced IL-10 levels in serum and liver tissue compared with the control group. Moreover, TUNEL staining, caspase 3 and 8 activities, and necrosis in the remnant liver were significantly decreased in the FN-treated rats compared with the controls. Furthermore, FN pretreatment inhibited the activation of nuclear factor (NF)-kappaB and increased the expression of Bcl-xL protein in liver tissue. These results suggest that FN protected against GalN/LPS-induced liver failure by a mechanism involving inhibition of NF-kappaB activation, which caused down-regulation of TNF-alpha and involved up-regulation of IL-10, and elevation of Bcl-xL induced a blockage of apoptotic signals, by which apoptosis of hepatocytes caused by GalN/LPS was suppressed.