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Background: The application of nasolabial perforator flap for nasal reconstruction has been reported previously with satisfactory outcomes, but the outcomes and risk factors of postoperative adverse events have been unclear to plastic surgeons. Aims: To statistically analyze the effectiveness of the nasolabial perforator flap in nasal reconstruction and the risk factor of postoperative complications and re‐operation. Patients/Methods: This retrospective study evaluated 58 Chinese patients who underwent nasal reconstruction with the nasolabial perforator flap from 2009 to 2021. The esthetic and blood supply outcomes were measured by plastic surgeons on a 5‐point Likert scale. Binary logistic regression was used to determine the risk factors associated with postoperative complications and re‐operation. Results: The mean age of the cohort was 66.4 ± 2.0 years. The defect size ranged from 6.5 × 5.5 mm2 to 40 × 70 mm2, and 48.3% of defects covered more than one nasal subunit. Venous congestion occurred in 4.9% of flaps, and the immediate overall postoperative score was 7.72/10. More than one nasal subunit of involvement was the risk factor associated with re‐operation (p = 0.004), but no risk factor was associated with complications. Conclusions: The nasolabial perforator flap is reliable for nasal reconstruction with good esthetic outcomes and fewer complications. However, a large number of involved subunits may lead to multiple surgeries for flap trimming in easterners. [ABSTRACT FROM AUTHOR]

Bioremediation of sediment organic pollution has been intensely investigated, but the degradation of complex organic compounds, pesticide residues, and polychlorinated biphenyls (PCBs) remains poorly studied. In this study, sediments were collected from Zhanjiang Mangrove Reserve and inoculated in an inorganic salt medium using only biphenyl (BP) and PCBs as the carbon sources to obtain a PCB-degrading strain. A gram-negative bacterium that metabolized PCBs was isolated and identified as Klebsiella Lw3 by 16S rDNA phylogenetic analysis. Genomic sequencing showed that this bacterium possessed genes related to BP/PCB degradation, and its GC content was 58.2%; we identified 3326 cellular pathways. Gas chromatography–mass spectrometry was employed to test the PCB degrading ability; the results showed that the strain had a good degradation effect on PCB3 at concentrations of 5, 10, 20, 40, and 60 mg/L and that the final degradation rate was higher than 97% after 96 h. Interestingly, this strain showed good biodegradability of PCBs despite having no classical PCB degradation pathway, providing a new direction for Klebsiella research with practical significance for in situ bioremediation of PCB contamination. Overall, this study provides valuable insights into the genetic structure of PCB-degrading strains as well as eco-friendly and low-cost PCB degradation and lays a foundation for the discovery of new degradation pathways. [ABSTRACT FROM AUTHOR]

Background: Chromolaena odorata Linn. (CO) is a perennial herb that is enriched with flavonoids and exhibits immune regulatory activities. For these characteristics, CO can be used as a potential immunoregulator based on the immunosuppression state. Objectives: The aim of this study was to assess the effects of flavonoids extracted from CO (FCO) on immune regulation and evaluate their mechanism of action by network pharmacology (NP), followed by in vivo confirmation. Materials and Methods: FCO were ultrasonically extracted through immersion in alcohol. The potential targets were predicted using a "FCO–immunosuppression–target" network. When the functional enrichment analyses were conducted, a mice model was employed to demonstrate the effects. The hematological indexes and serum levels of immunoglobulin G (IgG), immunoglobulin M (IgM), interferon-γ (INF-γ), interleukin 2 (IL-2), and tumor necrosis factor-α (TNF-α) were measured. The variations observed in immune organs and the changes in expressions of INF-γ, T-box transcription factor 21 (Tbx-21), and GATA Binding Protein 3 (GATA3) were reported. Results: NP results showed that a total of 198 targets of FCO were involved in immunosuppression. As indicated by the functional analysis results, FCO impacted T helper (Th) cell differentiation, which might be a vital functional pathway underlying its immune regulatory effects. During animal experiments, the values of hematological indexes, serum levels of IgG, IgM, and TNF-α, and the immune organ indexes increased in FCO groups, and the relative mRNA expressions of INF-γ and Tbx-21 and less damage of the spleen and thymus were reported. Conclusion: FCO impacts Th1 and Th2 differentiation pathways and assists in immunosuppression by regulating the secretion of various cytokines and the expression of associated genes, which demonstrates FCO as a promising natural immunoregulator. [ABSTRACT FROM AUTHOR]

To the Editor: Sparganosis is a worldwide parasitic zoonosis caused by infection with spargana, the plerocercoid larvae of various diphyllobothroid tapeworms belonging to the genus Spirometra (1-3). Sparganosis poses a [...]

ABSTRACT 3,3′,4,4′,5-Pentachlorobiphenyl (PCB126) cause multiple adverse effects in organisms including animals and humans. Although PCB toxicities are linked to oxidative damage in rodents, the mechanism in early life stages of zebrafish is not clear. To explore the developmental toxicity mechanism of PCB126, three paradigms (toxicological phenotypes, biochemical changes, and molecular changes) were studied in 3-h postfertilization (hpf) zebrafish ( Danio rerio) embryos exposed to different PCB126 concentrations (0, 16, 32, 64, and 128 μg/L) until 168 hpf. Developmental malformations, including pericardial and yolk sac edema, impaired lower jaw growth, spinal curvature, head edema and failure to inflate the swim bladder were observed, some as early as 72 hpf. Mortality was not apparent in early stages but significantly increased in a dose-dependent manner from 144 hpf onward. A dose-dependent significant increase in malformation rate was observed from 72 hpf onward with up to 100% at 132 hpf in embryos exposed to 128 μg/L of PCB126. Higher doses of PCB126 significantly decreased the copper-zinc superoxide dismutase (CuZn-Sod), catalase (Cat), and glutathione peroxidase (Gpx) enzyme activities at 96, 132 hpf, but markedly declined from thereafter. PCB126 at 128 μg/L significantly increased the malondialdehyde content at 72, 96, and 132 hpf. The transcriptional gene expression of antioxidant enzymes Cat and Gpx was upregulated in embryos exposed to 64 μg/L of PCB126 at 24 and 96 hpf. Sod1 messenger RNA (mRNA) was low in embryos exposed to 32 μg/L at 72 and 96 hpf but was induced in embryos exposed to 64 and 128 μg/L doses at 132 hpf. Collectively, the results suggest oxidative stress as a major factor in the induction of multiple developmental abnormalities in early life stages of zebrafish exposed to PCB126. However, the relationship between the antioxidant enzyme activity and the mRNA expression was not clear and the potential reasons for this are discussed. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 295-303, 2016. [ABSTRACT FROM AUTHOR]

ABSTRACT Dioxin-like PCB126 is a persistent organic pollutant that causes a range of syndromes including developmental toxicity. Dioxins have a high affinity for aryl hydrocarbon receptor (AhR) and induce cytochrome P4501A (CYP1A). However, the role of CYP1A activity in developmental toxicity is less clear. To better understand dioxin induced developmental toxicity, we exposed zebrafish ( Danio rerio) embryos to PCB126 at concentrations of 0, 16, 32, 64, and 128 μg L−1 from 3-h post-fertilization (hpf) to 168 hpf. The embryonic survival rate decreased at 144 and 168 hpf. The fry at 96 hpf displayed gross developmental malformations, including pericardial and yolk sac edema, spinal curvature, abnormal lower jaw growth, and non-inflated swim bladder. The pericardial and yolk sac edema rate significantly increased and the heart rate declined from 96 hpf compared with the controls. PCB126 did not alter the hatching rate. To elucidate the mechanism of PCB126-induced developmental toxicity, we conducted ethoxyresorufin- O-deethylase (EROD) in vivo assay to determine CYP1A enzyme activity, and real-time PCR to study the induction of CYP1A mRNA gene expression in embryo/larval zebrafish at 24, 72, 96, and 132 hpf. In vivo EROD activity was induced by PCB126 at 16 μg L−1 concentration as early as 72 hpf but significant increases were observed only in zebrafish exposed to 64 and 128 μg L−1 doses ( p < 0.005) at 72, 96, and 132 hpf. Induction of CYP1A mRNA expression was significantly upregulated in zebrafish exposed to 32 and 64 μg L−1 at 24, 72, 96, and 132 hpf. Overall, the severe pericardial and yolk sac edema and reduced heart rate suggest that heart defects are a sensitive endpoint, and the general trend of dose-dependent increase in EROD activity and induction of CYP1A mRNA gene expression provide evidence that the developmental toxicity of PCB126 to zebrafish embryos is mediated by activation of AhR. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 201-210, 2016. [ABSTRACT FROM AUTHOR]

Several reports indicate that some Gαq-coupled receptors antagonize the activation of phosphatidylinositol (PI) 3-kinase by receptor tyrosine kinases. We used Rat-1 fibroblasts expressing the α1A adrenergic receptor to study how this Gαq-coupled receptor inhibits platelet-derived growth factor (PDGF) activation of PI 3-kinase. Phenylephrine (PE) stimulation of the α1A adrenergic receptor inhibited PDGF-induced binding of PI 3-kinase to the PDGF receptor (PDGFR) and phosphorylation of the PDGFR at Tyr751, which forms a docking site for PI 3-kinase. By contrast, activation of phospholipase Cγ by PDGF and phosphorylation of the PDGFR at Tyr716 and Tyr771 were not inhibited by PE. The protein tyrosine phosphatase SHP-2, which dephosphorylates Tyr751 on the PDGFR, was more active in cells treated with PDGF plus PE than in cells treated with either agent alone. PDGF-induced PI 3-kinase signaling was also inhibited by treatment of cells with Pasteurella multocida toxin to activate Gαq. These results suggest that the α1A adrenergic receptor, and perhaps other Gαq-coupled receptors, uses tyrosine dephosphorylation to block PI 3-kinase activation by PDGF. [Copyright &y& Elsevier]