Single-cell transcriptome reveals a novel mechanism of C-Kit+-liver sinusoidal endothelial cells in NASH.

AIM: To understand how liver sinusoidal endothelial cells (LSECs) respond to nonalcoholic steatohepatitis (NASH). METHODS: We profiled single-LSEC from livers of control and MCD-fed mice. The functions of C-Kit+-LSECs were determined using coculture and bone marrow transplantation (BMT) methods. RESULTS: Three special clusters of single-LSEC were differentiated. C-Kit+-LSECs of cluster 0, Msr1+-LSECs of cluster 1 and Bmp4+Selp+-VECs of cluster 2 were revealed, and these cells with diverse ectopic expressions of genes participated in regulation of endothelial, fibrosis and lipid metabolism in NASH. The number of C-Kit+-primary LSECs isolated from MCD mice was lower than control mice. Immunofluorescence co-staining of CD31 and C-KIT showed C-Kit+-LSECs located in hepatic sinusoid were also reduced in NASH patients and MCD mice, compared to AIH patients and control mice respectively. Interestingly, lipotoxic hepatocytes/HSCs cocultured with C-Kit+-LSECs or the livers of MCD mice receipting of C-Kit+-BMCs (bone marrow cells) showed less steatosis, inflammation and fibrosis, higher expression of prolipolytic FXR and PPAR-α, lower expression of TNF-α and α-SMA. Furthermore, coculturing or BMT of C-Kit+-endothelial derived cells could increase the levels of hepatic mitochondrial LC3B, decrease the degree of mitochondrial damage and ROS production through activating Pink1-mediated mitophagy pathway in NASH. CONCLUSIONS: Hence, a novel transcriptomic view of LSECs was revealed to have heterogeneity and complexity in NASH. Importantly, a cluster of C-Kit+-LSECs was confirmed to recovery Pink1-related mitophagy and NASH progression.

Examining the exposure-reception-retention link in realistic communication environments via VR and eye-tracking: The VR billboard paradigm.

Exposure is key to message effects. No effects can ensue if a health, political, or commercial message is not noticed. Yet, existing research in communication, advertising, and related disciplines often measures 'opportunities for exposure' at an aggregate level, whereas knowing whether recipients were 'actually exposed' to a message requires a micro-level approach. Micro-level research, on the other hand, focuses on message processing and retention, takes place under highly controlled laboratory conditions with forced message exposure, and largely ignores how recipients attend selectively to messages under more natural conditions. Eye-tracking enables us to assess actual exposure, but its previous applications were restricted to screen-based reading paradigms lacking ecological validity or field studies that suffer from limited experimental control. Our solution is to measure eye-tracking within an immersive VR environment that creates the message delivery and reception context. Specifically, we simulate a car ride down a highway alongside which billboards are placed. The VR headset (HP Omnicept Pro) provides an interactive 3D view of the environment and holds a seamlessly integrated binocular eye tracker that records the drivers' gaze and detects all fixations on the billboards. This allows us to quantify the nexus between exposure and reception rigorously, and to link our measures to subsequent memory, i.e., whether messages were remembered, forgotten, or not even encoded. An empirical study shows that incidental memory for messages differs based on participants' gaze behavior while passing the billboards. The study further shows how an experimental manipulation of attentional demands directly impacts drivers' gaze behavior and memory. We discuss the large potential of this paradigm to quantify exposure and message reception in realistic communication environments and the equally promising applications in new media contexts (e.g., the Metaverse).

Amorphous carbon nanosheets suitable for deep eutectic solvent electrolyte toward cryogenic energy storage.

The emerging deep eutectic solvent (DES) electrolyte has great potential in realizing commercial-scale application of electric double-layer capacitors (EDLCs) served in low temperature environment. That goal, however, rests with how to design the interface structure of electrode materials for well-matching with DES electrolyte. Herein, porous carbon nanosheets (PCNs) were obtained from coal tar pitch through Friedel-Crafts acylation reaction and melting salt intercalation process. The morphology, specific surface area and porosity of porous carbon nanosheets were regulated by tailoring the abundance of the dangling-bonds grafted on the CTP molecules. Profiting from the large specific surface area, suitable pore structure and good two-dimensional structure to provide more active sites and enhance ion transport capacity, the PCNs-0.10 delivers a maximal specific capacitance of 504F g-1 at 0.1 A g-1, which is overmatch than most of previously reported for other carbon materials. As-assembled symmetrical EDLCs using K+ DES electrolyte, can be assembled to work at -40 °C to 75 °C and exhibit satisfactory energy density. The strategy proposed here has opened a new way for exploring the large-scale preparation of electrode materials suitable for ultra-low temperature capacitors.

Research and design of an intelligent fish tank system.

In order to improve the hardware configuration and interaction mode of the fish tank system and realize the diversification of client functions, the purpose of real-time remote monitoring and management is achieved. A set of IoT intelligent fish tank system composed of sensor unit, signal processing unit and wireless transmission unit was designed. The system improves the algorithm of the data collected by the sensor, and proposes an improved first-order lag average filtering algorithm. The system uses composite collection information, intelligent processing, chart data analysis and other methods to transmit the processed data to the cloud server through the WIFI communication module. An APP is designed on the remote monitoring and control end, and a visual data interface of the smart fish tank is made, and the user can modify the environmental parameters conducive to the biological survival inside the fish tank through the APP, it brings great convenience to the family fish tank, and the test shows that the system network is stable and fast in response, and the overall purpose of the intelligent fish tank system is achieved.

[Port-owned Mobile Source Air Pollutant Emission Inventory].

Based on the comprehensive development of the emission inventory of air pollution sources, the emission inventory of self-owned mobile sources of Tianjin coastal ports was researched and formulated. In this study, a gridded emission inventory with a resolution of 3 km×3 km was established for six types of air pollutants from road and non-road mobile sources. The spatial and temporal distribution characteristics of pollutant emissions were analyzed, and the uncertainty of the inventory was analyzed using the Monte Carlo method. The results showed that in 2020, the self-owned mobile sources of coastal ports emitted 148.22 t PM10, 135.34 t PM2.5, 1061.04 t SO2, 4027.16 t NOx, 756.60 t CO, and 237.07 t VOCs, of which the total emissions of road and non-road mobile sources accounted for 6.66% and 93.34% of the mobile source emissions, respectively. The main contributors to motor vehicle pollutant emissions from road mobile sources in the whole port area were small, medium, and large passenger vehicles (gasoline) and heavy trucks (diesel). The main contributors to the pollutants emitted by non-road mobile sources were ships and construction machinery. Uncertainty analysis results showed that the overall uncertainty of mobile sources ranged from -13.3% to 16.53%.

Vsig4+ resident single-Kupffer cells improve hepatic inflammation and fibrosis in NASH.

BACKGROUND: The role of macrophages in the pathogenesis of nonalcoholic steatohepatitis (NASH) is complex and unclear. METHODS: Single-cell RNA sequencing was performed on nonparenchymal cells isolated from NASH and control mice. The expression of Vsig4+ macrophages was verified by qPCR, flow cytometry and immunohistochemistry. Primary hepatic macrophages were cocultured with primary hepatocytes or hepatic stellate cells (LX2) cells by Transwell to detect immunofluorescence and oil red O staining. RESULTS: Two main single macrophage subsets were identified that exhibited a significant change in cell percentage when NASH occurred: resident Kupffer cells (KCs; Cluster 2) and lipid-associated macrophages (LAMs; Cluster 13). Nearly 82% of resident single KCs in Cluster 2 specifically expressed Cd163, and an inhibited subgroup of Cd163+ resident single-KCs was suggested to be protective against NASH. Similar to Cd163, Vsig4 was both enriched in and specific to Cluster 2. The percentage of Vsig4+-KCs was significantly decreased in NASH in vivo and in vitro. Hepatocytes and hepatic stellate cells produced less lipid droplet accumulation, proinflammatory protein (TNF-α) and profibrotic protein (α-SMA) in response to coculture with Vsig4+-KCs than in those cocultured with lipotoxic KCs. CONCLUSIONS: A subgroup of Vsig4+ resident single-KCs was shown to improve hepatic inflammation and fibrosis in NASH.

Microphase Separation Engineering toward 3D Porous Carbon Assembled from Nanosheets for Flexible All-Solid-State Supercapacitors.

Although hierarchitectures could energize carbon materials to address the challenges encountered in emerging flexible energy storage, how to make the trade-offs among specific surface area, pore configuration, and conductivity is still a lingering issue. Herein, 3D porous carbon assembled by nanosheets (HCAs) with tunable hierarchical porous structure is acquired from amphiphilic coal tar pitch and chitosan by means of a facile microphase separation strategy without any templates. The polar molecular chains of chitosan and the surrounding pitch molecules with strong π-π* bonds self-assemble respectively to form hierarchical pores and a network of nanosheets in a stepped pyrolysis process. Due to the combined effects of the meso-dominant porous structure, high specific surface area, and nitrogen-rich nature, the as-assembled symmetric all-solid-state supercapacitor with a wide voltage range of 0-1.8 V delivers a specific capacitance of 296 F g-1 at 0.2 A g-1 and an energy density of 27 Wh kg-1 at a power density of 450 W kg-1. The strategy of microphase separation is proposed originally to design and to fabricate carbon materials with multilevel nanoarchitectural trade-offs for high-performance supercapacitors.

Hepatocyte-derived exosomal miR-27a activateshepatic stellate cells through the inhibitionof PINK1-mediated mitophagy in MAFLD.

The role of exosome-mediated mitophagy in the crosstalk between hepatocytes (HCs) and hepatic stellate cells (HSCs) in metabolic-associated fatty liver disease (MAFLD) remains unknown. Serum exosomal miR-27a levels were markedly increased and positively correlated with liver fibrosis in MAFLD patients and mice. Exosomal miR-27a was released from lipotoxic HCs and specifically transmitted to recipient-activated HSCs. PINK1, the key target of miR-27a, primarily mediates mitophagy. Overexpression of miR-27a or knockdown of PINK1 or lipotoxic HC-exosomal miR-27a impaired mitochondria (inhibiting mitophagy, respiration, membrane potential, and transcription while promoting reactive oxygen species production) in activated HSCs and stimulated HSC-derived fibroblasts (promoting activation and proliferation while inhibiting autophagy). High exosomal miR-27a serum levels and a lack of hepatic PINK1-mediated mitophagy were directly related to liver fibrosis in MAFLD mice. Lipotoxic HC exosome transplantation aggravated the degree of PINK1-mediated mitophagy suppression, steatohepatitis, lipidosis, and fibrosis in the livers of MAFLD mice with cirrhosis. Both in vitro and in vivo, exosomes derived from miR-27a-knockdown HCs could not facilitate the abovementioned deteriorating effects. In conclusion, lipotoxic HC-exosomal miR-27a plays a pivotal role in inhibiting mitophagy and in promoting MAFLD-related liver fibrosis by negatively regulating PINK1 expression.

Zinc-α2-glycoprotein 1 attenuates non-alcoholic fatty liver disease by negatively regulating tumour necrosis factor-α.

BACKGROUND: Zinc-α2-glycoprotein 1 (AZGP1) plays important roles in metabolism-related diseases. The underlying molecular mechanisms and therapeutic effects of AZGP1 remain unknown in non-alcoholic fatty liver disease (NAFLD). AIM: To explore the effects and potential mechanism of AZGP1 on NAFLD in vivo and in vitro. METHODS: The expression of AZGP1 and its effects on hepatocytes were examined in NAFLD patients, CCl4-treated mice fed a high fat diet (HFD), and human LO2 cells. RESULTS: AZGP1 levels were significantly decreased in liver tissues of NAFLD patients and mice. AZGP1 knockdown was found to activate inflammation; enhance steatogenesis, including promoting lipogenesis [sterol regulatory element-binding protein (SREBP)-1c, liver X receptor (LXR), fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and stearoyl CoA desaturase 1 (SCD)-1], increasing lipid transport and accumulation [fatty acid transport protein (FATP), carnitine palmitoyl transferase (CPT)-1A, and adiponectin], and reducing fatty acid ß-oxidation [farnesoid X receptor (FXR) and peroxisome proliferator-activated receptor (PPAR)-α]; accelerate proliferation; and reverse apoptosis in LO2 cells. AZGP1 overexpression (OV-AZGP1) had the opposite effects. Furthermore, AZGP1 alleviated NAFLD by blocking TNF-α-mediated inflammation and intracellular lipid deposition, promoting proliferation, and inhibiting apoptosis in LO2 cells. Finally, treatment with OV-AZGP1 plasmid dramatically improved liver injury and eliminated liver fat in NAFLD mice. CONCLUSION: AZGP1 attenuates NAFLD with regard to ameliorating inflammation, accelerating lipolysis, promoting proliferation, and reducing apoptosis by negatively regulating TNF-α. AZGP1 is suggested to be a novel promising therapeutic target for NAFLD.

MicroRNA-194 inactivates hepatic stellate cells and alleviates liver fibrosis by inhibiting AKT2.

BACKGROUND: Activation of hepatic stellate cells (HSCs) is a pivotal event in the onset and progression of liver fibrosis. Loss of microRNA-194 (miR-194) has been reported in activated HSCs, but the actual role of miR-194 in liver fibrosis remains uncertain. AIM: To explore the role and potential mechanism of miR-194-mediated regulation of liver fibrosis in vitro and in vivo. METHODS: The expression of miR-194 was examined in human fibrotic liver tissues, activated HSCs, and a carbon tetrachloride (CCl4) mouse model by qPCR. The effects of AKT2 regulation by miR-194 on the activation and proliferation of HSCs were assessed in vitro. For in vivo experiments, we reintroduced miR-194 in mice using a miR-194 agomir to investigate the functions of miR-194 in liver fibrosis. RESULTS: MiR-194 expression was notably lacking in activated HSCs from both humans and mice. Overexpression of miR-194 (OV-miR-194) inhibited α-smooth muscle actin (α-SMA) and type I collagen (Col I) expression and suppressed cell proliferation in HSCs by causing cell cycle arrest in G0/G1 phase. AKT2 was predicted to be a target of miR-194. Notably, the effects of miR-194 knockdown in HSCs were almost blocked by AKT2 deletion, indicating that miR-194 plays a role in HSCs via regulation of AKT2. Finally, miR-194 agomir treatment dramatically ameliorated liver fibrosis in CCl4-treated mice. CONCLUSION: We revealed that miR-194 plays a protective role by inhibiting the activation and proliferation of HSCs via AKT2 suppression. Our results further propose miR-194 as a potential therapeutic target for liver fibrosis.

linc-SCRG1 accelerates liver fibrosis by decreasing RNA-binding protein tristetraprolin.

The biologic roles of long noncoding RNAs (lncRNAs) in liver fibrosis remained unknown. Through microarray analysis, linc-SCRG1 (a lncRNA with transcript length 3118 bp) was found up-regulated 13.62-fold in human cirrhotic tissues. Quantitative PCR verified that linc-SCRG1 increased along with liver fibrosis progression in human tissues and in activated LX2 cells induced by TGF-ß1. Knockdown of linc-SCRG1 significantly reversed the effects of TGF-ß1 on LX2, including inhibiting activation, promoting apoptosis, reducing proliferation, lessening invasion, and down-regulating genes [fibrosis-related mRNA: α-smooth muscle actin ( α-SMA), type I collagen, and B-cell lymphoma-2; invasion-related mRNA: matrix metallopeptidase-2 ( MMP-2), MMP-9, and MMP-13; inflammation-related mRNA: TNF-α, IL-6, and IL-10]. linc-SCRG1 had binding sites with tristetraprolin (TTP), a kind of RNA-binding protein, and specifically combined to TTP proteins. Overexpression of linc-SCRG1 would cause TTP mRNA unstably and proteins decreasing. TTP mRNA was proved having negative relevance with linc-SCRG1 and was gradually reduced during human liver fibrosis progression. Overexpressing TTP resulted in knockdown of lincSCRG1 and degraded downstream target genes ( MMP-2 and TNF-α) in activated LX2. Overexpressing TTP had the same effects as small interfering RNA-lincSCRG1 (si- lincSCRG1), whereas knockdown of TTP had reversal effects on si- lincSCRG1 in activated LX2. In summary, linc-SCRG1 reduced TTP and restricted its degradation of target genes TNF-α and MMP-2. Therefore, linc-SCRG1 had a repressing TTP-elicited inactivation effect on hepatic stellate cell (HSC) phenotypes. Inhibition of linc-SCRG1 may be a novel therapeutic approach to inactivate HSCs and extenuate human liver fibrosis.-Wu, J.-C., Luo, S.-Z., Liu, T., Lu, L.-G., Xu, M.-Y. linc-SCRG1 accelerates liver fibrosis by decreasing RNA-binding protein tristetraprolin.

[Role of noninvasive mechanical ventilation in patients with severe avian influenza A (H7N9) complicated with acute respiratory distress syndrome].

OBJECTIVE: Human infection with avian influenza A (H7N9) is an acute contagious respiratory disease. Acute respiratory distress syndrome (ARDS) is a common complication in patients with severe avian influenza A (H7N9), for whom mechanical ventilation (MV) is an important supportive method. A patient, suffered from severe avian influenza A (H7N9) and complicated with ARDS, was admitted to the Second Affiliated Hospital of Guizhou Medical University in January 2017. With very intensive care for oxygenation, respiration and consciousness, and monitoring, she was successfully cured by comprehensive managements, among which noninvasive mechanical ventilation (NIV) was the major respiratory support method. The result demonstrate that, in patients with conscious state, satisfied expectoration ability and relatively good cooperation, and with close observation of oxygenation and respiratory rate, NIV may be accepted as an effective method for patient with ARDS caused by severe avian influenza A (H7N9).

Clinical characteristics from co-infection with avian influenza A H7N9 and Mycoplasma pneumoniae: a case report.

BACKGROUND: More and more cases of human infections with avian influenza A H7N9 have been reported since it was first mentioned in 2013 in China, but concurrence of influenza A H7N9 with Mycoplasma pneumoniae, however, has never been described. Here, we reported the case of a woman co-infected by influenza A H7N9 and Mycoplasma pneumoniae, whose treatment process was a little bit longer and a little bit complicated as well. CASE PRESENTATION: Our patient was an 80-year-old Chinese woman who presented with fever, cough, chest tightness, and shortness of breath. A computed tomography scan showed obvious infiltrations at lower parts of both lungs. Arterial blood gas analysis confirmed a severe respiratory failure (type I). Her sputum and throat swabs were checked for nucleic acid of influenza A and the result was positive for influenza A H7N9. She was diagnosed as having severe influenza A H7N9 and acute respiratory distress syndrome, and was admitted to an intensive care unit. She was given comprehensive treatment, including oseltamivir, methylprednisolone, immunoglobulin, gastric protection, and noninvasive mechanical ventilation. Her condition improved 4 days later. However, some symptoms exacerbated again 2 days later with ground-glass changes appearing in upper area of right lung and the titer of antibody to Mycoplasma pneumoniae rising from 1:80 to 1:640. She was reasonably considered to be infected with Mycoplasma pneumoniae as well, and azithromycin and moxifloxacin were added to her treatment. Oseltamivir was discontinued because of three consecutive negative results of nucleic acid for influenza A H7N9, but anti-Mycoplasma treatment was continued. Although her symptoms and abnormal changes on computed tomography scan slowly went away, she finally recovered from the mixed infection after a total of 33 days of management. CONCLUSION: In patients with confirmed influenza A H7N9 infection whose condition worsens again, especially with new infiltration or lung ground-glass infiltration, one should suspect infection by other pathogens such as Mycoplasma pneumoniae.

Obesity May Provide Pro-ILC3 Development Inflammatory Environment in Asthmatic Children.

The prevalence of obesity in children has dramatically increased in the last few decades, and obesity has also emerged as an important risk factor for asthma. Innate mechanisms have been shown to be involved in both diseases, particularly through the recently described innate lymphoid cells (ILCs), in which ILC3s have been linked to obesity both in human and in murine models. The aim of this study was to explore whether being overweight in asthmatic children was associated with elevated circulating ILC3 or elevated messenger RNA (mRNA) levels of RORC, IL-17A, and IL-22. Our results showed significantly elevated ILC3 frequencies in overweight asthmatic children compared with nonoverweight controls based on the detection of Lin+CD127+IL-23R+ cells by flow cytometry. Moreover, elevated ILC3 frequencies positively correlated with the mRNA expression of RORC which has been identified as a transcription factor of ILC3s. The relative mRNA expression level of IL-17A was also upregulated in overweight compared to nonoverweight children, as was the relative mRNA level of IL-22. However, there were no correlations between ILC3 frequencies or the expressions of RORC, IL-17A, and IL-22 and asthma severity. These results suggested that childhood obesity is an independent factor that is associated with an elevated frequency of circulating ILC3s and higher expressions of RORC, IL-22, and IL-17A.

STAT3 aggravates TGF-ß1-induced hepatic epithelial-to-mesenchymal transition and migration.

Signal transducer and activator of transcription 3 (STAT3) has been shown to affect epithelial-to-mesenchymal transition (EMT) in cancers. We investigated the underlying molecular mechanisms of STAT3 crosstalk with Snail-Smad3/transforming growth factor (TGF)-ß1 signaling pathways during the EMT in hepatocellular carcinoma (HCC). STAT3 and TGF-ß1 expressions are examined in liver tissues of HCC patients and rats. The effect of IL-6/ STAT3 crosstalk with Snail-Smad3/TGF-ß1 on EMT, carcinogenesis, migration and invasion are tested in vitro and in vivo. Phosphorylation of STAT3 and TGF-ß1 proteins are universally high and positively co-expressed in HCC tissues from human and rats. Hepatic lower p-STAT3 proteins are related to earlier tumor stages in HCC patients. AG490 (a JAK2-specific inhibitor) treatment could reduce tumor numbers and sizes depending on suppression of STAT3 signaling in HCC rats. TGF-ß1 could induce EMT along with an E-cadherin decrease, while vimentin, Snail, p-Smad2/3, and p-STAT3/STAT3 increase in HepG2. SIS3 (a specific inhibitor of Smad3) could markedly inhibit Snail, Vim and p-STAT3 along with blocking phosphorylation of Smad3, but E-cadherin could be activated in HepG2. IL-6 activates STAT3 signaling and then has cascading consequences for activating Snail-Smad3/TGF-ß1 and vimentin as well as migration and invasion in liver cancer cells. In contrast, AG490 has an effect that inhibits phosphorylation of STAT3, lowers Snail-p-Smad3 protein levels, decreases TGF-ß1-related PAI-1 promoter activation and then reduces migration or invasion of liver cancer cells. STAT3 functions as a positive regulator to activate TGF-ß1-induced EMT and metastasis of HCC. STAT3 and the Snail-Smad3/TGF-ß1 signaling pathways synergistically augment EMT and migration in HCC.

Effects of social isolation, re-socialization and age on cognitive and aggressive behaviors of Kunming mice and BALB/c mice.

Both Kunming (KM) mice and BALB/c mice have been widely used as rodent models to investigate stress-associated mental diseases. However, little is known about the different behaviors of KM mice and BALB/c mice after social isolation, particularly cognitive and aggressive behaviors. In this study, the behaviors of KM and BALB/c mice isolated for 2, 4 and 8 weeks and age-matched controls were evaluated using object recognition, object location and resident-intruder tests. The recovery of behavioral deficits by re-socialization was also examined for the isolated mice in adolescence. Our study showed that isolation for 2, 4 and 8 weeks led to cognitive deficits and increased aggressiveness for both KM and BALB/c mice. An important finding is that re-socialization could completely recover spatial/non-spatial cognitive deficits resulted from social isolation for both KM and BALB/c mice. In addition, age only impacted aggressiveness of KM mice. Moreover, isolation duration showed different impacts on cognitive and aggressive behaviors for both KM and BALB/c mice. Furthermore, BALB/c mice showed weak spatial/non-spatial memory and low aggressiveness when they were at the same age and isolation duration, compared to KM mice. In conclusion, KM mice and BALB/c mice behaved characteristically under physiology and isolation conditions.

[The clinical classification method research of keloid].

OBJECTIVE: To explore the clinical classification method of keloids and providing a thread for the treatment of keloids. METHODS: To summarize the 600 cases of keloid patients we accepted and diagnosed from November 2004 to October 2012, and filling in keloid patients information sheet, recording the keloids form by photographs, analyzing the treatment, putting forward the classification method of keloids in clinic. RESULTS: According to the position and quantity that keloids grow, the keloid patients are divided into four major categories:one in single site, one in each site, more than one in single site and more than one in each site; According to the area and thickness of keloids, the keloid single lesion is divided into four subclasses: type of small area and thin, type of small area and thick, type of large areas and thin,type of large areas and thick; According to the number of lesions, keloid multiple lesions is divided into two subgenera: isolated multiple and dispersion multiple, different kinds of keloids suit different methods of treatment. CONCLUSION: The clinical classification method of keloids can be used to provide thought for the treatment of keloids, and have a good application value.

Maggot therapy for repairing serious infective wound in a severely burned patient.

The larvae of musca domestica were put in use to discard the dead tissue of a case of severe burn. A total of 50 000 aseptic maggots were put onto the infective wound surface, and aseptic dressings overlaid the surface. Three days later, another 20 000 maggots were put onto the wound for the second therapy. After twice maggot debridement, most necrotic muscle tissues of the wound were cleaned up, and eventually fresh granulation tissue grew and later the wound was covered and healed by 3 times of skin grafting. The result demonstrates that maggot therapy is safe and effective with no adverse complications except pain.