Aesthetic Removal of Foreign Body Granulomas of Forehead Via Pretrichial Approach.

ABSTRACT: In the field of plastic surgery, various filler types have been developed, which are widely used for cosmetic or reconstruction purposes. However, unregulated substances often injected by unlicensed practitioners may cause difficult-to-treat side effects, such as foreign body granulomas. Since the forehead is an exposed area and the lesions are likely extensive, complete surgical removal with inconspicuous scar can be difficult. In addition, pharmacological treatments, such as steroids, have only a temporary effect. The authors report successful cases of foreign body removal combined with subcutaneous forehead lift via a pretrichial approach for cosmetic satisfaction.Ten patients who had received illegal filler injections that resulted in chronic granulomas on the forehead were studied. The granulomas were confirmed using sonography, and simultaneous foreign body removal and subcutaneous forehead lifts using pretrichial incisions were planned. For the surgical method, the forehead flap was carefully elevated to a uniform thickness in the subcutaneous plane via a pretrichial incision, and the foreign body was removed, paying attention to the forehead contour and nerve damage; excess skin was excised from the top of the flap to tighten the remaining skin on the forehead.None of the patients developed complications, such as skin necrosis, infection, hematoma, or wound dehiscence, during the follow-up period. The functional and aesthetic outcomes were satisfactory in all the patients.The subcutaneous forehead lift via a pretrichial incision seems to facilitate foreign body removal and improve the forehead deformity by tightening the remaining skin.

Surgical Management of Total Sternal Cleft in a Pentalogy of Cantrell Neonate.

Sternal cleft is a rare malformation with significant morbidity and mortality. It has been associated with other midline fusion defects, most significantly Cantrell's pentalogy, involving the sternum, pericardium, heart, diaphragm, and abdominal wall. This study reported a successfully managed case of a newborn with a total sternal cleft and Cantrell's pentalogy. A review of literature and pertinent management principles was also conducted.

Implant Delivery Technique for Prepectoral Reconstruction after Endoscopic-assisted Nipple-sparing Mastectomy.

Prepectoral breast reconstruction through a small axillary incision during endoscopic-assisted nipple-sparing mastectomy or robotic nipple-sparing mastectomy is difficult. Cases involving implants covered with an acellular dermal matrix (ADM) are particularly difficult. Therefore, a new delivery technique for ADM-covered implants is needed. The ADM pocket for complete coverage of the implant is made with double-crossed ADMs. The pocket end is open and sutured at the funnel entry. After insetting the ADM pocket at the mastectomy site through an axillary incision, the implant is delivered from a funnel to the ADM pocket by squeezing. Prepectoral breast reconstruction with the new delivery technique for implants covered with ADM pockets proved easy and safe. Our new implant delivery technique could be a good option for prepectoral breast reconstruction after minimal breast surgery.

Reconstruction of Sacral Pressure Ulcer Using a Modified Parasacral Perforator-Based Flap (Maple Leaf Design): An Easier Method for Beginners.

Background. Many different operative options have been used to cover sacral defects. Perforator flap enables wide defect reconstruction with long pedicle and a large arc of rotation while preserving gluteus maximus muscle, but the risk of vessel injury can jeopardize flap survival. Perforator-based flap, the flap transposed without skeletonization of the perforator, requires much experience to be perfect in flap design to achieve tension-free closure. Methods. Fourteen modified parasacral perforator-based flap procedures were carried out on 14 patients. The records of patients at Chungnam National University Hospital from February 2017 to January 2020 were retrospectively reviewed. Results. All 14 flaps survived completely. One patient developed localized hematoma, and another presented with latent seroma. No donor or recipient site dehiscence or recurrence occurred during follow-up. Conclusion. We present our experience of a parasacral perforator-based flap with modified design of bilobed flaps. It could be performed easily and safely with less wound dehiscence and serve as a good practice model for young surgeons to cover small to moderately sized defects.

KB-34, a newly synthesized chalcone derivative, inhibits lipopolysaccharide-stimulated nitric oxide production in RAW 264.7 macrophages via heme oxygenase-1 induction and blockade of activator protein-1.

Chalcones, a subclass of the flavonoid family, are widely known for their anti-inflammatory and anti-oxidative properties. In the present study, we synthesized the chalcone derivative, KB-34 (3-Phenyl-1-(2,4,6-tris (methoxymethoxy)phenyl)prop-2-yn-1-one), and examined its effect on nitric oxide (NO) production. KB-34 potently inhibited nitrite production in RAW 264.7 macrophages stimulated by lipopolysaccharide (LPS). KB-34 treatment also markedly inhibited inducible nitric oxide synthase (iNOS) expression, as assessed by Western blot and quantitative RT-PCR analyses. Treatment of cells with KB-34 significantly inhibited LPS-induced transcriptional activation by activator protein-1 (AP-1) as determined by luciferase reporter gene assay, whereas nuclear factor-kappaB (NF-kappaB) activity was not affected by KB-34, indicating that down-regulation of iNOS gene expression by KB-34 is mainly attributed by blockade of AP-1 activation. We also demonstrated that KB-34 treatment led to an increase in heme oxygenase-1 (HO-1) mRNA and protein expression, mediated by stimulating the expression of nuclear factor-erythroid 2-related factor 2 (Nrf2). Treatment with SnPP, a selective inhibitor of HO-1, reversed the KB-34-mediated inhibition of nitrite production, suggesting that HO-1 plays an important role in the suppression of NO production by KB-34. In contrast, SnPP treatment did not counteract the KB-34-mediated suppression of AP-1 activity, suggesting that inhibition of AP-1 activation by KB-34 is independent of HO-1 induction. Taken together, these results indicate that KB-34 suppresses NO production in LPS-stimulated RAW 264.7 macrophages via simultaneous induction of HO-1 expression and blockade of AP-1 activation. This study reveals that KB-34 would be a promising agent for the treatment of inflammation-associated disease.

Isoliquiritigenin inhibits cell proliferation by a heme oxygenase-dependent pathway in rat hepatic stellate cells.

We evaluated whether the antiproliferative effects of isoliquiritigenin (ISL) on rat hepatic stellate cells (HSCs) are related to the induction of heme oxygenase 1 (HO-1) expression. ISL significantly inhibited serum- or growth factor-induced HSC proliferation. The inhibition of platelet-derived growth factor (PDGF)-induced proliferation by ISL was associated with the mitogen-activated protein kinase and phosphatidylinositol 3-kinase-Akt-p70 (S6K) pathways. ISL induced the expression of HO-1 in HSCs. Using the chemical inhibitor tin protoporphyrin, we also found that the inhibitory action of ISL on PDGF-induced proliferation is mediated by HO-1. These data suggest that HO-1 expression is responsible for the antiproliferative effect of ISL on HSCs.

Butein blocks tumor necrosis factor alpha-induced interleukin 8 and matrix metalloproteinase 7 production by inhibiting p38 kinase and osteopontin mediated signaling events in HT-29 cells.

In this study, we evaluated whether butein can inhibit the effects of tumor necrosis factor alpha (TNF-alpha), an inflammatory mediator, in intestinal epithelial HT-29 cells. Butein significantly inhibited TNF-alpha-induced interleukin 8 (IL-8) secretion and mRNA expression. Moreover, butein suppressed the expression of matrix metalloproteinase 7 (MMP-7) mRNA and extracellular pro-MMP-7 secretion. The signal transduction study revealed that butein significantly attenuates p38 phosphorylation and inhibits osteopontin (OPN) mediated inhibitory factor kappaBalpha (I-kappaBalpha) phosphorylation in TNF-alpha-stimulated HT-29 cells. Using specific kinase inhibitors, we also found that blocking the p38 pathway is critical for, and blocking of OPN-mediated I-kappaBalpha phosphorylation pathway is at least for, the inhibitory effect by butein on TNF-alpha-induced IL-8 and MMP-7 expression. Furthermore, using an MMP inhibitor, we showed that IL-8 lies upstream of MMP-7 in the TNF-alpha-induced signaling process in HT-29 cells. Collectively, these results suggest that butein may be an effective agent for the treatment of intestinal inflammation.

2',4',6'-Tris(methoxymethoxy) chalcone attenuates hepatic stellate cell proliferation by a heme oxygenase-dependent pathway.

Proliferation of hepatic stellate cells (HSCs) is central for the development of fibrosis during liver injury. We have shown previously that butein (3,4,2',4'-tetrahydroxychalcone) suppresses myofibroblastic differentiation of rat HSCs. Our aim in this study was to determine whether a new synthetic chalcone derivative, 2',4',6'-tris(methoxymethoxy) chalcone (TMMC) inhibits HSC proliferation induced by serum- or platelet-derived growth factor (PDGF). TMMC significantly inhibited growth factor-induced HSC proliferation. The inhibition of PDGF-induced proliferation by TMMC was associated with the phosphatidylinositol 3-kinase-Akt-p70(S6K) pathways. TMMC induced the expression of heme oxygenase 1 (HO-1) in HSCs. Using the chemical inhibitor tin protoporphyrin, we also found that the inhibitory action of TMMC on PDGF-induced proliferation is mediated by HO-1. Glutathione (GSH) depletion produced by TMMC activated extracellular signal-regulated kinase (ERK), which led to c-Fos expression and transactivation of activator protein 1 (AP-1) and HO-1 gene expression in the HSCs. These results demonstrate that TMMC preferentially activates ERK and that this activation leads to the transcriptional activation of AP-1 and consequently to HO-1 expression. HO-1 expression might be responsible for the antiproliferative effect of TMMC on HSCs.

Polyozellin inhibits nitric oxide production by down-regulating LPS-induced activity of NF-kappaB and SAPK/JNK in RAW 264.7 cells.

Polyozellin, isolated from Polyozellus multiplex (Thelephoraceae), was investigated for its anti-inflammatory activity in the murine macrophage cell line RAW 264.7. Polyozellin inhibited both lipopolysaccharide (LPS)-induced nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) gene expression in a dose-dependent manner. The effects of polyozellin on the activation of nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein (MAP) kinases in these cells were studied in order to elucidate the underlying mechanism. Polyozellin suppressed the activation of both LPS-induced NF-kappaB and the stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK), but had no effect on the extracellular signal-regulated kinase (ERK) or p38. These data suggest that polyozellin suppresses iNOS expression by inhibiting the activation of NF-kappaB and SAPK/JNK, leading to the inhibition of NO production.

Anti-inflammatory activity of 20(S)-protopanaxadiol: enhanced heme oxygenase 1 expression in RAW 264.7 cells.

20( S)-Protopanaxadiol (PPD) is one of the metabolites of ginsenosides from Panax ginseng. In this study, we demonstrate that PPD inhibits the increase in lipopolysaccharide (LPS)-induced inducible nitric oxide synthase (iNOS) expression through inactivation of nuclear factor-kappaB by preventing degradation of inhibitory factor-kappaBalpha. PPD also induces heme oxygenase 1 (HO-1) expression in RAW 264.7 cells, at the mRNA and protein levels, in the presence and absence of LPS. This effect is associated with suppression of LPS-induced nitric oxide (NO) production and iNOS expression. The HO-1 inducer hemin is associated with the suppression of LPS-induced NO production in a dose-dependent manner, and the HO-1 inhibitor tin protoporphyrin attenuates the inhibitory activity of PPD on LPS-induced NO production. These results provide evidence for the role of HO-1 in the inhibition of LPS-induced NO production by PPD.

Tetrandrine induces apoptosis in hepatic stellate cells.

We have previously reported that tetrandrine reduced hepatic stellate cell activation and collagen accumulation in liver fibrosis induced by biliary obstruction. In the present study, we examined the apoptosis-inducing effect of tetrandrine on activated hepatic stellate cells, as the therapeutic goal in hepatic fibrosis is to eliminate the activated hepatic stellate cells by apoptosis. We used rat hepatic stellate cells transformed by Simian virus 40 (T-HSC/Cl-6) to overcome the limitations inherent in studying primary cultures of hepatic stellate cells. Tetrandrine treatment at doses of 25 and 50 microg/ml for 12 h induced apoptosis as confirmed by DNA fragmentation and increased sub-G1 DNA content as detected by flow cytometric analysis. Tetrandrine also induced the activation of caspase-3 protease and subsequent proteolytic cleavage of poly(ADP-ribose) polymerase. In conclusion, our results demonstrate that tetrandrine induces apoptosis of T-HSC/Cl-6 cells, and these results should contribute to the development of new agents for the treatment of hepatic fibrosis.

Protective effect of Rhodiola sachalinensis extract on carbon tetrachloride-induced liver injury in rats.

This study was carried out to investigate the protective effect of an aqueous extract from the root of Rhodiola sachalinensis (RSE) on liver injury induced by repetitive administration of carbon tetrachloride in rats. RSE was given orally to rats at doses of 50, 100 or 200 mg/kg throughout the carbon tetrachloride treatment for 28 days. In rats treated with carbon tetrachloride, the levels of hydroxyproline and malondialdehyde (MDA) in the liver, and serum enzyme activities were significantly increased. RSE treatment significantly reduced the levels of liver hydroxyproline and MDA, and serum enzyme activities, in accordance with improved histological findings. Immunohistological findings indicated RSE treatment inhibited hepatic stellate cell activation, which is a major step for collagen accumulation during liver injury. These data suggest that RSE protects the liver from repetitive injury induced by carbon tetrachloride in rats.

Scutellaria baicalensis inhibits liver fibrosis induced by bile duct ligation or carbon tetrachloride in rats.

This study was carried out to investigate the antifibrotic effects of methanol extracts from the traditional Chinese medicinal herb, the root of Scutellaria baicalensis Georgi, on liver fibrosis induced by bile duct ligation and scission (BDL) or carbon tetrachloride (CCl4) in rats. Liver fibrosis was assessed by histological observations and by measuring levels of liver hydroxyproline, lipid peroxidation based on malondialdehyde (MDA) production, and serum enzyme activities. The morphological characteristics of livertissuewere examined by Masson'strichrome staining and immunostaining against smooth muscle cell alpha-actin. In both models, the levels of hydroxyproline and MDA in liver were significantly increased. Treatment with a methanol extract of S. baicalensis significantly reduced the levels of liver hydroxyproline and MDA, with improved histological findings. In both models, the liver areas positive for smooth muscle cell alpha-actin were considerably decreased by treatment with oral methanol extract of S. baicalensis (150 mg kg(-1) daily for 28 days). A methanol extract of S. baicalensis root inhibits fibrosis and lipid peroxidation in rat liver induced by BDL or CCl4.