Acellular allogenic dermis combined with VSD for repair of abdominal wall defect: a case series.

OBJECTIVE: To explore the clinical application of acellular allogenic dermis combined with VSD in repairing abdominal wall defect combined with abdominal infection. METHODS: Clinical data of 5 cases of abdominal cavity infection with abdominal wall defect admitted in the Burn Department of Quanzhou First Hospital from January 2019 to January 2022 were collected for this study. The abdominal cavity was closed temporarily after debridement and VSD in the early stage, and the abdominal wall defect was repaired by acellular allogeneic dermis combined with autologous split-thickness skin graft in the second stage. The changes of infection indexes (WBC, CRP, PCT, Lac) before and after treatment and the clinical therapeutic effect were observed. RESULTS: In the 5 observed cases, the infection index decreased significantly, the intra-abdominal pressure was normal, and there was no abdominal wall hernia, intestinal adhesion, intestinal obstruction or any other complications. The wound of abdominal wall defect achieved stage 1 healing, the local scar tissue only has slight proliferation, and the appearance was satisfying. There was no recurrence in 6 months follow-up. CONCLUSION: Early use of VSD can effectively control abdominal infection and reduce the occurrence of intestinal fistula or other complications. In the later stage of treatment, acellular allogenic dermis combined with autologous split-thickness skin graft can effectively repair abdominal wall defect.

Tocilizumab attenuates acute lung injury in rats with sepsis by regulating S100A12/NLRP3.

OBJECTIVE: To investigate the mechanism of Tocilizumab (TCZ) in attenuating acute lung injury in rats with sepsis by regulating the S100A12/NLRP3 axis. METHODS: A rat model of sepsis was constructed using cecal ligation and puncture (CLP). Rats were treated with TCZ, and their lung tissue was collected. H&E staining was used to detect pathologic damage to lung tissue, and lung wet/dry (W/D) weight ratio was measured to assess pulmonary edema. Lipid oxidation assay and superoxide dismutase (SOD) activity assay kits were used to measure malondialdehyde (MDA) and SOD levels. Primary rat pulmonary microvascular endothelial cells (MPVECs) were treated with lipopolysaccharide (LPS) to construct a rat model of sepsis, which was then treated with TCZ. The mRNA and protein expressions of S100A12/NLRP3 were detected by qRT-PCR and western blot, respectively. S100A12 knockdown and overexpression plasmids, and NLRP3 knockdown plasmids were constructed and transfected into sepsis cells to intervene in the levels of S100A12/NLRP3. The apoptosis rate was detected by apoptosis assay. The levels of IL-6, TNF-α, and IL-10 in cells and tissues were analyzed by ELISA. RESULTS: Compared to the Sham group, the CLP group had increased W/D weight ratio of lung tissue, IL-6, TNF-α, and MDA levels, lowered IL-10 and SOD levels, and more severe tissue damage (all P<0.05). After TCZ treatment, the above indicators were improved. The expressions of S100A12/NLRP3 cells were increased in LPS-induced MPVECs, but decreased after TCZ treatment. LPS induced apoptosis, but TCZ reduced the apoptosis, weakened the secretion levels of IL-6 and TNF-α, and enhanced IL-10 secretion levels. Transfection to cause the overexpression of S100A12 or NLRP3 plasmid partially counteracted the effect of TCZ. Knockdown of S100A12 was transfected on the basis of overexpression of NLRP3, which weakened the countervailing effect of overexpressed NLRP3 on TCZ. CONCLUSION: TCZ has a therapeutic effect on lung injury in rats with sepsis by reducing the expressions of S100A12/NLRP3.

Application of Autogenous Dermis Combined With Local Flap Transplantation in Repair of Titanium Mesh Exposure After Cranioplasty.

OBJECTIVES: To investigate the clinical outcome of autogenous dermis combined with local flap transplantation in the treatment of titanium mesh exposure after cranioplasty. METHODS: We studied a total of 8 patients with titanium mesh exposure after cranioplasty. After debridement of the head wound, the autogenous dermal tissue from the lateral thigh was transplanted to the surface of titanium mesh, and the local skin flap was then applied after suturing and fixation to repair the wound on the surface of the dermis. To repair the lateral thigh dermal tissue area, a local skin flap was obtained, and a blade thick skin graft was used. RESULTS: Both dermal tissue and local skin flap survived. In the meanwhile, the donor skin area of the lateral thigh healed well, with only slight scar hyperplasia, and the titanium mesh was preserved. There was no recurrence after 6 months of follow-up. CONCLUSIONS: The application of autogenous dermis combined with local skin flap to repair titanium mesh exposure can effectively avoid skin flap necrosis, potential re-exposure of titanium mesh, sub-flap effusion, infection, and other problems. This method has an ideal effect, has easy access to materials, and reduces patients' economic burden. It is worth popularizing.

Long noncoding RNAs Colorectal Neoplasia Differentially Expressed and taurine-upregulated gene 1 are downregulated in sepsis and positively regulate each other to suppress the apoptosis of cardiomyocytes.

Long noncoding RNAs (lncRNAs) Colorectal Neoplasia Differentially Expressed (CRNDE) and taurine-upregulated gene 1 (TUG1) play similar roles in sepsis, indicating the existence of the crosstalk between them. Sepsis is a major cause of injuries in heart, which are related to high mortality rates. This study was therefore carried out to analyze the potential crosstalk between CRNDE and TUG1 in sepsis, with a focus on sepsis-induced cell apoptosis in heart. Expression of CRNDE and TUG1 was analyzed with RT-qPCR. Correlations between them were analyzed by Pearson's correlation coefficient. CRNDE and TUG1 were overexpressed in cardiomyocytes to determine the relationship between them. The roles of CRNDE and TUG1 in regulating the apoptosis of cardiomyocytes were explored by cell apoptosis assay. We found that both CRNDE and TUG1 were downregulated in sepsis. In cardiomyocytes, LPS treatment resulted in the downregulation of CRNDE and TUG1. Overexpression of CRNDE and TUG1 in cardiomyocytes increased the expression levels of each other. Under lipopolysaccharide (LPS) treatment, decreased apoptosis rates of cardiomyocytes were observed after CRNDE and TUG1 overexpression. CRNDE and TUG1 co-overexpression showed a stronger effect. In conclusion, CRNDE and TUG1 are downregulated in sepsis and they positively regulate each other to suppress the apoptosis of cardiomyocytes.

Application of damage control surgery in patients with sacrococcygeal deep decubitus ulcers complicated by sepsis.

OBJECTIVE: To evaluate the clinical application of damage control surgery (DCS) in patients with sacrococcygeal deep decubitus ulcers complicated by sepsis. METHODS: We conducted a 3-year retrospective clinical study of 32 patients with deep sacrococcygeal bedsores and sepsis admitted from January 2018 to January 2021. According to the concept of DCS, the wound was temporarily closed with vacuum sealing drainage after primary debridement, and a local rhomboid flap was designed to repair the wound in the second stage. Finally, the clinical therapeutic effect was observed. RESULTS: Twenty-nine patients were treated with skin flap translocation and were cured clinically. Specifically, the skin flap survived in 27 of the 29 patients after the first translocation attempt (success rate of 93.1%). One patient developed incisional dehiscence, and one patient developed a hydrocele under the skin flap. CONCLUSIONS: Application of DCS in patients with sacrococcygeal deep decubitus ulcers complicated by sepsis improves the therapeutic success rate and reduces the risks of the operation and complication rate. It has unique advantages and is worthy of clinical promotion.

microRNA-98 protects sepsis mice from cardiac dysfunction, liver and lung injury by negatively regulating HMGA2 through inhibiting NF-κB signaling pathway.

Recently, MicroRNA-98 (miR-98) works as a biomarker in some diseases, such as lung cancer, Schizophrenia, and breast cancer, but there still lack of studies on the function of miR-98 during sepsis. Thus, our study is conducted to figure out the function of miR-98 for the regulation of cardiac dysfunction, liver and lung injury in sepsis mice. Cecum ligation and puncture was used to establish the sepsis mice model. Next, miR-Con and agomiR-98 were injected into the tail vein of mice 48 h after modeling. Then, expression of miR-98, HMGA2, NF-κB, inflammatory factors, apoptosis-related proteins in myocardial, liver and lung tissues of septic mice were determined. Moreover, other indices that were associated with cardiac dysfunction, liver and lung injury in septic mice were detected. Finally, bioinformatics analysis and luciferase activity assay were utilized to validate the binding site between miR-98 and HMGA2. miR-98 was poorly expressed, while HMGA2, NF-κB pathway-related proteins were highly expressed in myocardial, liver, and lung tissues of mice with sepsis. Upregulated miR-98 inhibited HMGA2, NF-κB, TNF-α, IL-6, Bcl-2 and increased IL-10, Cleaved caspase-3 and Bax expression in myocardial, liver, and lung tissues of septic mice. Upregulation of miR-98 decreased LVEDP, CTn-I, BNP, ALT, AST, TBIL, LDH, and PaCO2 while increased +dp/dt max, -dp/dt max, pH and PaO2 in sepsis mice. miR-98 was a direct target gene of HMGA2. Our study provides evidence that miR-98 protects sepsis mice from cardiac dysfunction, liver and lung injury by negatively mediating HMGA2 via the inhibition of the NF-κB signaling pathway.

Tumor necrosis factor-α induced protein 6 attenuates acute lung injury following paraquat exposure.

CONTEXT: Paraquat exposure commonly occurs in the developing countries and the mortality rate is high. However, there is currently no consensus on the efficacy of treatment for paraquat exposure. OBJECTIVE: The study was aimed to explore the effects of tumor necrosis factor-α (TNF-α) induced protein 6 (TSG-6) on acute lung injury (ALI) following paraquat exposure in rats. MATERIALS AND METHODS: Male Sprague-Dawley (SD) rats were randomly divided into the sham group (n = 8), the paraquat group (n = 8), and the paraquat TSG-6-treated group (n = 8). Rats were administered with 50 mg/kg of paraquat intraperitoneally. At 1 h after exposure, rats were treated with 30 µg of recombinant human TSG-6 (rhTSG-6) intraperitoneally. After 6 h of exposure, ALI scores were evaluated by histology and the expression of pro-inflammatory cytokines in lung was assayed using real-time RT-PCR. RESULTS: ALI scores were significantly lower in the paraquat TSG-6-treated group, compared with the paraquat group (p < 0.05). The expression of interleukin (IL)-1ß, IL-6, and TNF-α mRNA was significantly lower in the paraquat TSG-6-treated group, compared with the paraquat group (p < 0.01, respectively). DISCUSSION AND CONCLUSION: Administration of rhTSG-6 attenuates ALI following paraquat exposure by suppressing inflammatory response.

[Tumor necrosis factor-α induced protein 6 attenuates acute kidney injury following paraquat poisoning in rats].

OBJECTIVE: To explore the effects of tumor necrosis factor-α induced protein 6 (TSG-6) on acute kidney injury (AKI) following paraquat poisoning in rats. METHODS: Twenty-four male Sprague-Dawley (SD) rats were randomly divided into sham group (n=8), model group (n=8) and TSG-6-treated group (n=8) using a randomized number table. Rats were given an injection of 50 mg/kg of paraquat intraperitoneally (total volume was equalled to sterile normal saline) in model and TSG-6-treated groups. Rats in sham group were given 2 mg/kg of sterile saline. After 1 hour of paraquat administration, rats were treated with 30 µg of recombinant human TSG-6 intraperitoneally in TSG-6-treated group. After 6 hours of paraquat administration, serum was collected to assess renal function, then rats were sacrificed and renal tissues were immediately harvested. AKI score was evaluated by renal histopathology and gene expression of pro-inflammatory cytokines including interleukins (IL-1ß and IL-6) and tumor necrosis factor-α (TNF-α) in kidney was assayed with real-time reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Compared with sham group, blood urea nitrogen (BUN), creatinine (Cr) and AKI score were significantly increased in model group (BUN: 22.64 ± 2.36 mmol/L vs. 7.09 ± 0.65 mmol/L, t=6.986, P=0.000; Cr: 177.28 ± 18.67 µmol/L vs. 60.32 ± 3.11 µmol/L, t=7.134, P=0.000; AKI score: 9.14 ± 0.28 vs. 0.30 ± 0.23, t=9.013, P=0.000). Moreover, the mRNA expressions of IL-1ß, IL-6 and TNF-α were significantly elevated in model group (IL-1ß mRNA: 3.23±0.28 vs. 1.00 ± 0.07, t=5.874, P=0.000; IL-6 mRNA: 4.16 ± 0.37 vs. 1.00 ± 0.08, t=7.125, P=0.000; TNF-α mRNA: 3.85 ± 0.31 vs. 1.00 ± 0.10, t=6.342, P=0.000). However, serum BUN, Cr, AKI score and the mRNA expressions of IL-1ß, IL-6 and TNF-α in TSG-6-treated group were significantly lower than those in model group (BUN: 14.07 ± 5.23 mmol/L vs. 22.64 ± 2.36 mmol/L, t=2.533, P=0.026; Cr: 112.76 ± 14.81 µmol/L vs. 177.28 ± 18.67 µmol/L, t=2.778, P=0.016; AKI score: 5.35 ± 0.19 vs. 9.14 ± 0.28, t=2.885, P=0.013; IL-1ß mRNA: 2.26 ± 0.19 vs. 3.23 ± 0.28, t=2.457, P=0.023; IL-6 mRNA: 2.92±0.29 vs. 4.16 ± 0.37, t=2.975, P=0.011; TNF-α mRNA: 2.58 ± 0.23 vs. 3.85 ± 0.31, t=2.564, P=0.019). CONCLUSIONS: TSG-6 attenuates AKI following paraquat poisoning by suppressing inflammatory response.