Vacuum sealing drainage to treat Fournier's gangrene.

BACKGROUND: Vacuum sealing drainage (VSD) is widely applied in complex wound repair. We aimed to compare traditional debridement and drainage and VSD in treating Fournier's gangrene (FG). METHODS: Data of patients surgically treated for FG were retrospectively analyzed. RESULTS: Of the 36 patients (men: 31, women: 5; mean age: 53.5 ± 11.3 [range: 28-74] years) included in the study, no patients died. Between-group differences regarding sex, age, BMI, time from first debridement to wound healing, number of debridements, FGSI, and shock were not statistically significant (P > 0.05). However, lesion diameter, colostomy, VAS score, dressing changes, analgesic use, length of hospital stay, and wound reconstruction method (χ2 = 5.43, P = 0.04) exhibited statistically significant differences. Tension-relieving sutures (6 vs. 21) and flap transfer (4 vs. 2) were applied in Groups I and II, respectively. CONCLUSION: VSD can reduce postoperative dressing changes and analgesic use, and shrunk the wound area, thereby reducing flap transfer in wound reconstruction.

Pgc-1α Promotes Phosphorylation, Inflammation, and Apoptosis in H9c2 Cells During the Early Stage of Lipopolysaccharide Induction.

Cardiac dysfunction in severe sepsis is associated with increased mortality. However, the molecular mechanisms underlying septic heart dysfunction remain unclear. Expression of peroxisome proliferator-activated receptor-γ coactivator 1α (Pgc-1α), concentrations of inflammatory factors, and activation of the nuclear factor kappa-B (NF-κB) signaling pathway were examined in H9c2 cells after a 24-h lipopolysaccharide (LPS) stimulation period using qPCR, enzyme-linked immunosorbent assays (ELISAs), and western blots (WBs), respectively. Pgc-1α was overexpressed and suppressed in cells using a lentivirus vector and siRNA, respectively. The effects of Pgc-1α dysfunction on the release of inflammatory factors and apoptosis were analyzed. Pgc-1α expression was increased after LPS induction for 0.5 h and returned to the pre-induction level at 2 h. Levels of IL-1ß, IL-6, and TNF-α increase after LPS induction for 0.5 h and accumulated in the culture supernatants over time. The WBs revealed the highest Pgc-1α and phospho (p)-p65 protein levels after LPS induction for 0.5 h, followed by a decrease; moreover, the cleaved-caspase-3 level increased after LPS induction for 0.5 h and increased gradually thereafter. A functional analysis of Pgc-1α revealed that overexpression of this protein enhanced LPS-induced inflammatory factors and p-p65 levels and inhibited apoptosis during the early stage after LPS induction (0.5 and 4 h). In contrast, the inhibition of Pgc-1α expression inhibited the LPS expression-associated increases in inflammatory factors and p-p65 and promoted apoptosis. Pgc-1α promoted LPS-induced p65 phosphorylation and inflammatory factor release while inhibiting apoptosis.

Assessment of inflammatory markers and mitochondrial factors in a rat model of sepsis-induced myocardial dysfunction.

The present study aimed to investigate the expression of inflammatory markers and mitochondrial function-related genes, as well as their temporal relationship with cardiac myocyte injury in a rat model of sepsis. The sepsis model was constructed using cecal ligation and puncture (CLP). Two hours after CLP, the levels of inflammatory cytokines (interleukin [IL]-1ß, IL-6, and TNFα) and myocardial function markers (serum brain natriuretic peptide [BNP], cardiac troponin-I [cTNI], and procalcitonin [PCT]) were increased significantly, falling from around 9 hours postoperatively. The concentration of nitric oxide (NO) in the heart tissue was increased 6 hours after CLP. The heart rate (HR) of rats that underwent CLP decreased 2 hours after surgery and then increased to above-normal values. The left ventricular short axis shortening (FS) and left ventricular ejection fraction (LVEF) were decreased at 2 hours postoperatively and reached a minima at 6 hours. Stroke volume (SV), cardiac output (CO), and changes and heart index (CI) results indicated myocardial dysfunction. Western blot analysis demonstrated the increased expression of mitochondrial function-related proteins and activation of mitochondrial apoptotic pathways. Hematoxylin and eosin staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays revealed that the proportion of proapoptotic cells was significantly higher in rats that underwent CLP than sham surgery at 2 to 24 hours postoperatively. Taken together, our results indicate that-in the rat model-CLP-induced sepsis leads to impaired cardiac function. Furthermore, induction of the expression of mitochondrial function-related genes indicated that myocardial cell mitochondrial function was disrupted, further aggravating cardiomyocyte apoptosis. These results provide a theoretical basis for the treatment of sepsis-induced myocardial dysfunction.

Senescent leaves of Artemisia annua are one of the most active organs for overexpression of artemisinin biosynthesis responsible genes upon burst of singlet oxygen.

To dissect and penetrate complexicity regarding the tissue-specific and environment-induced expression modes of cytosolic and plastidial terpene biosynthetic genes in A. annua, corresponding mRNAs relevant to terpene biosynthesis were quantitatively compared among distinctive organs and during different growth stages. Although all examined mRNAs gradually elevate from June to August in tested organs, a putative artemisinin biosynthesis responsible DBR2 mRNA represents the most abundant transcript anyplace and anytime. Apart from others, senescent leaves endow global activation of artemisinin biosynthetic genes and ultimately lead to enhanced artemisinin production. Direct measurement of (1)O (2) burst from senescent leaves strongly supports an involvement of (1)O (2) in conversion from precursor(s) to artemisinin. In the context of environmental stresses, physical and chemical stress signals that include those invoking (1)O (2) burst were evaluated as if inducing artemisinin biosynthetic genes. The quantitative data have reiterated a common pattern of modulating artemisinin production in A. annua by triggering (1)O (2) burst during senescence and under chilling acclimatization. In conclusion, a missing link concatenating senescence-coupled (1)O (2) generation to (1)O (2)-induced upregulation of artemisinin biosynthetic genes has been re-established, which would provide a fertile base for future endeavors pursuing further enhancements of artemisinin production.

[Photoautotrophic growth and photosynthetic characteristics of carrot callus].

Photoautotrophic carrot callus was induced by gradually lowering the sucrose concentration in culture medium. In the course of induction, the net photosynthetic rate on chlorophyll basis of callus increased gradually with the decreasing of sucrose concentration in culture medium, and the net photosynthetic rate of photoautotrophic callus could even be higher than that of leaf. In the course of changing into photoautotrophic callus, its chlorophyll content increased gradually, and the dark respiratory rate and the ratio of Chl a/Chl b decreased gradually. Parallel with these was the development of the microstructure of thylakoid of callus.