Comprehensive aesthetic corrections of gynecomastia using the reproducible safe and minimally invasive surgical strategy.

BACKGROUND: Minimally invasive access and fast recovery are trends of gynecomastia surgery. We placed great importance on liposuction and modified original pull-through technique. The purpose of this study was to present a refined surgical strategy for gynecomastia in grade I and II. METHODS: The refined strategy embraced enhanced liposuction to remove the intraglandular fat sufficiently, followed by open resection of gland using the pull-through and bottom-up technique with adjuvant liposuction in the end. Surgical data were recorded and satisfactory questionnaires with 5-point scales were administered during follow-up. RESULTS: Between January 2017 and May 2022, 165 patients underwent enhanced liposuction combined with the pull-through and bottom-up technique for gland excision. Age ranged from 12 to 56 years. The median length of surgery was 100 min. A median of 300 ml of fat was aspirated and a median of 20.8 g of gland was excised. Seventy-seven patients (46.7%) responded the questionnaires at least 6 months postoperatively, and the average overall satisfaction was 4.68 ± 0.52 points. Thirteen sides of breasts developed complications with a rate of 4.0%. CONCLUSION: Enhanced liposuction combined with pull-through and bottom-up technique proved effective to treat grade I and II gynecomastia with minimal scarring and high satisfaction. The refined strategy was simple and safe, and would obtain optimal outcomes even for inexperienced surgeons.

The biomarkers associated with epithelial-mesenchymal transition in human keloids.

INTRODUCTION: A keloid is a type of benign fibrotic disease with similar features to malignancies, including anti-apoptosis, over-proliferation, and invasion. Epithelial-mesenchymal transition (EMT) is a crucial mechanism that regulates the metastatic behavior of tumors. Thus, identifying EMT biomarkers is paramount in comprehensively understanding keloid pathogenesis. METHODS: To identify the differentially expressed genes (DEGs) GSE92566 dataset, with 3 normal skin and 4 keloid tissues, was downloaded from GEO databases to identify the differentially expressed genes (DEGs). Further, EMT-related genes were downloaded from dbEMT 2.0 databases and intersected with GSE92566 DEGs to identify EMT-related-DEGs (ERDEGs). Subsequently, the ERDEGs were used for GO, KEGG, gene set enrichment analysis (GSEA), protein-protein interaction (PPI), and miRNAs-mRNAs network analysis. To predict small molecules for EMT inhibition, the ERDEGs were imported to cMAP databases, whereas hub genes were imported to DGidb databases. Finally, we carried out qRT-PCR and in vitro experiments to validate our findings. RESULTS: A total of 122 ERDEGs were identified, including 59 upregulated and 63 down-regulated genes. Moreover, enrichment analysis revealed that focal adhesion, AMPK signal pathway, Wnt signal pathway, and EMT biological process were significantly enriched. STRING databases and Cytoscape software were used to construct the PPI network and EMT-related hub genes. Further, 3 modules were explored from the PPI network using the Molecular Complex Detection (MCODE) plugin. In the Cytohubba plugin, 10 hub genes were explored, including FN1, EGF, SOX9, CDH2, PROM1, EPCAM, KRT19, ITGB1, CD24, and KRT18. These genes were then enriched for the focal adhesion pathway. We constructed a microRNA (miRNA)-mRNA network, which predicted hsa-miR-155-5p (8 edges), hsa-miR-124-3p (7 edges), hsa-miR-145-5p (5 edges), hsa-miR-20a-5p (5 edges) and hsa-let-7b-5p (4 edges) as the most connected miRNAs regulating EMT. Based on the ERDEGs and 10 hub genes mentioned above, ribavirin demonstrated high drug-targeting relevance. Subsequently, qRT-PCR confirmed that the expression of FN1, ITGB1, CDH2, and EPCAM corroborated with previous findings. qRT-PCR also showed that the expression levels of hsa-miR-124-3p and hsa-miR-145-5p were significantly lower in keloids and hsa-miR-155-5p was upregulated in keloids. Finally, by treating human keloid fibroblasts (HKFs) with ribavirin in vitro, we confirmed that ribavirin could inhibit HKFs proliferation and EMT. CONCLUSION: In summary, this work provides novel EMT biomarkers in keloids and predicts new small target molecules for keloid therapy. Our findings improve the understanding of keloid pathogenesis, providing new treatment options.

2-Methoxyestradiol inhibits the proliferation level in keloid fibroblasts through p38 in the MAPK/Erk signaling pathway.

BACKGROUND: The MAPK/Erk signaling pathway is a classic pathway in cell proliferation. Our former study showed that keloid tissue revealed a higher proliferation level than physiological scars and normal skin. As a natural metabolite of estradiol, 2-methoxyestradiol (2ME2) showed an inhibition proliferation effect on tumor cells. AIM: In this study, the treatment effect of 2ME2 and its potential mechanisms are explored. METHODS: Six keloid patients and six non-keloid patients were randomly selected from the Department of Plastic Surgery at our hospital during June 2021 to December 2021. Six groups were established: normal skin fibroblasts (N); keloid fibroblasts (K); keloid fibroblasts treated with 2ME2 (K + 2ME2); keloid fibroblasts treated with dimethyl sulfoxide (DMSO) (K + DMSO); keloid fibroblasts treated with doramapimod (K + IN); keloid fibroblasts treated with doramapimod (p38 inhibitor) and 2ME2 (K + IN+2ME2). The fibroblast activity and key factor expression of the MAPK/Erk signaling pathway were measured. RESULTS: In the results, 2ME2 significantly inhibited keloid fibroblast activity and key factor expression (except STAT1). CONCLUSION: The proliferation levels were reduced by both the p38 inhibitor and 2ME2, indicating 2ME2 may achieve an antiproliferation effect by targeting p38 in keloid fibroblasts.

Role of HIF-1α in pathogenic mechanisms of keloids.

BACKGROUDS AND OBJECTIVE: Keloids are defined as overrepairing products that develop after skin lesions. Keloids are characterized by the proliferation of fibroblasts and the overaccumulation of extracellular matrix components (mainly collagen), leading to a locally hypoxic microenvironment. Hence, this article was aimed to review hypoxia in pathogenesis of keloids. METHODS: We reviewed and summarized the relevant published studies. RESULTS: Hypoxia results in the accumulation of hypoxia-inducible factor 1α (HIF-1α) in keloids, contributing to overactivation of the fibrotic signaling pathway, epithelial-mesenchymal transition, and changes in metabolism, eventually leading to aggravated fibrosis, infiltrative growth, and radiotherapy resistance. CONCLUSION: It is, therefore, essential to understand the role of HIF-1α in the pathogenic mechanisms of keloids in order to develop new therapeutic approaches.

A comparison of proliferation levels in normal skin, physiological scar and keloid tissue.

Proliferation is an important characteristic of life, and many signaling pathways participate in this complicated process. The MAPK/Erk pathway is a classic pathway in cell proliferation. In this study, expression levels of key factors in the MAPK/Erk pathway were measured to assess the proliferation level among normal skin, physiological scar, and keloid tissue. Thirty patients were selected randomly from the Department of Plastic Surgery at Peking Union Medical College Hospital from January 2019 to December 2020. Histological appearance and fiber tissue content were observed by Hematoxylin and eosin staining and Masson staining. Expression levels of key factors in the MAPK/Erk pathway (ATF2, c-Jun, c-Myc, p38 and STAT1) and relative proteins (HIF-1α and PCNA) in tissues were detected by immunohistochemistry and analyzed as the percentage of positively stained cells in both the tissue epidermis and dermis. Western blot was used for quantitative analysis of the above factors. In results, keloid tissue showed a significantly higher fiber and less cell content. In the immunohistochemical result, higher expression of key factors was observed in the epidermis than in the dermal layer, and the expression of all factors was increased remarkably in keloid tissue. In western blot analysis, all factors (except STAT1) showed higher expression in keloid tissue. In our former research, keloid showed similar apoptosis level as physiological scar and normal skin. On combining our former conclusion and results in this study, an imbalance condition between the high proliferation level and normal apoptosis level may lead to the growth characteristics of keloid.

A new photodynamic therapy photosensitizer (p1) promotes apoptosis of keloid fibroblasts by targeting caspase-8.

Photodynamic therapy (PDT) is a new therapy for treating cancer with less toxicity, high selectivity, good cooperativity, and repetitive usability. However, keloid treatment by PDT is mainly focused on clinical appearance, and few studies have been conducted on the mechanisms of PDT. In this study, key factors of the classical mitochondrial apoptosis signaling pathway were measured to assess the effect of a new PDT photosensitizer (p1). A specific inhibitor of caspase-8 (Z-IETD-FMK) was also used to verify the possible mechanisms. Twelve samples were obtained from 12 patients (six with keloids and six without) selected randomly from the Department of Plastic Surgery at Peking Union Medical College Hospital from January to December 2020. After cell culture, fibroblasts were divided into 13 groups. The morphology of fibroblasts in each group was observed by microscopy. Cell activity was measured by cell counting kit-8, and cell apoptotic morphology was observed by TUNEL staining. The reactive oxygen species (ROS) relative value was measured by a ROS test kit. The expression levels of key mitochondrial factors (caspase-3, caspase-8, cytochrome-c, Bax, and Bcl-2) were assessed by western blot, and mRNA expression of caspase-3 and caspase-8 was measured by RT-qPCR. We showed that p1 had a satisfactory proapoptotic effect on keloid fibroblasts by increasing the expression of ROS, caspase-3, caspase-8, and cytochrome-c, and decreasing the Bcl-2/Bax ratio; however, this effect was partially inhibited by Z-IETD-FMK, indicating that caspase-8 may be one of the p1's targets to achieve the proapoptotic effect.

Effect of hydrogen intervention on refractory wounds after radiotherapy: A case report.

BACKGROUND: Patients with keloids who receive radiotherapy (RT) after surgery can develop refractory wounds that cannot be healed by the patient's own repair system. Such chronic wounds are uneven and complex due to persistent abscess and ulceration. Without external intervention, they can easily result in local tissue necrosis or, in severe cases, large area tissue resection, amputation, and even death. CASE SUMMARY: This article describes the use of hydrogen to treat a 42-year-old female patient with a chronic wound on her left shoulder. The patient had a skin graft that involved implanting a dilator under the skin of her left shoulder, and then transferring excess skin from her shoulder onto scar tissue on her chest. The skin grafting was followed by two rounds of RT, after which the shoulder wound had difficulty healing. For six months, the patient was treated with 2 h of hydrogen inhalation (HI) therapy per day, in addition to application of sterile gauze on the wound and periodic debridement. We also performed one deep, large, sharp debridement to enlarge the wound area. The wound healed completely within 6 mo of beginning the HI treatment. CONCLUSION: After HI therapy, the patient showed superior progress in reepithelialization and wound repair, with eventual wound closure in 6 mo, in comparison with the previous failures of hyperbaric oxygen and recombinant bovine basic fibroblast growth factor therapies. Our work showed that HI therapy could be a new strategy for wound healing that is cleaner, more convenient, and less expensive than other therapies, as well as easily accessible for further application in clinical wound care.

Corrigendum to "Adipose-Derived Stromal Cells Attenuate Adipose Inflammation in Obesity through Adipocyte Browning and Polarization of M2 Macrophages".

[This corrects the article DOI: 10.1155/2019/1731540.].

Dura cells in the etiopathogenesis of Crouzon syndrome: the effects of FGFR2 mutations in the dura cells on the proliferation of osteoblasts through the hippo/YAP mediated transcriptional regulation pathway.

BACKGROUND: FGFR2 (fibroblast growth factor receptor 2) mutations are implicated in the etiopathogenesis of syndromic craniosynostosis, and C278F- or C342Y-FGFR2 mutations can lead to Crouzon syndrome. The dura mater exerts crucial effects in the regulation of cranial suture development. However, the underlying mechanisms of these biological processes are rarely studied. This research explored and analyzed the biological function of FGFR2 overexpressed by dura cells on cranial osteoblasts. METHODS: Dura cells and cranial osteoblasts from C57BL/6 mice aged 6 days were obtained and cultured respectively. Lentivirus-FGFR2 constructs were engineered with C278F- and C342Y-FGFR2 mutations. The dura cells were infected with the constructs and co-cultured with osteoblasts in a trans-well system. Four experimental groups were established, namely the Oste group, the Oste+Dura-vector group, the Oste+Dura-C278F group, and the Oste+Dura-C342Y group. FACS, CCK8, and EdU assays were used to evaluate the osteoblast proliferation levels. Western blot and RT-qPCR were used to measure the expressions of the factors related to proliferation, differentiation, and apoptosis. Furthermore, the expression levels of the key factors in the Hippo/YAP-PI3K-AKT proliferation pathway were measured and analyzed. Finally, rescue experiments were performed with an RNA interfering assay. RESULTS: The proliferation and differentiation levels of the osteoblasts in the Oste+Dura-C278F and Oste+Dura-C342Y groups were significantly up-regulated, but the apoptosis levels in the four groups were not significantly different. The YAP, TEADs1-4, p-PI3K, and p-AKT1 expressions in the mutant FGFR2 groups were higher than the corresponding expressions in the control groups, and the results of the rescue experiments showed a reverse expression tendency, which further confirmed the effects of the FGFR2 mutations in the dura cells on the proliferation of the osteoblasts and the underlying possible mechanisms. CONCLUSION: Our studies suggest that the Crouzon mutations (C278F- and C342Y-) of FGFR2 in dura cells can enhance osteoblast proliferation and differentiation and might influence the pathogenesis of craniosynostosis by affecting the Hippo/YAP-PI3K-AKT proliferation signaling pathway.

Facial microcystic adnexal carcinoma - treatment with a "jigsaw puzzle" advancement flap and immediate esthetic reconstruction: A case report.

BACKGROUND: Microcystic adnexal carcinoma (MAC) is a rare malignant tumor of the skin that is commonly found on the face. It grows slowly and has a low mortality rate. However, for various reasons, including strong histological invasiveness, clinical inexperience and inadequate procedure design, immediate or permanent facial deformity may occur after surgical operations. CASE SUMMARY: This article describes a middle-aged female artist who was diagnosed with MAC on the left upper lip. She declined the recommended treatment plan, which included two-stage reconstruction, skin grafting, or surgery that could have resulted in obvious facial dysfunction or esthetic deformity. We accurately designed a personalized procedure involving a "jigsaw puzzle advancement flap" for the patient based on the lesion location and the estimated area of skin loss. The procedure was successful; both pathological R0 resection and immediate and long-term esthetic reconstruction effects were achieved. CONCLUSION: This study suggests that when treating facial MAC or other skin malignancies, a surgical team should have sufficient plastic surgery-related knowledge and skills. An optimal surgical plan for an individual is needed to achieve good facial esthetics and functional recovery and shorten the treatment course.

Chinese medical students' interest in COVID-19 pandemic.

BACKGROUND: The outbreak of coronavirus disease 2019 (COVID-19) happened in early December and it has affected China in more ways than one. The societal response to the pandemic restricted medical students to their homes. Although students cannot learn about COVID-19 through clinical practice, they can still pay attention to news of COVID-19 through various channels. Although, as suggested by previous studies, some medical students have already volunteered to serve during the COVID-19 pandemic, the overall willingness of Chinese medical students to volunteer for such has not been systematically examined. AIM: To study Chinese medical students' interest in the relevant knowledge on COVID-19 and what roles they want to play in the pandemic. METHODS: Medical students at Peking Union Medical College were surveyed via a web-based questionnaire to obtain data on the extent of interest in the relevant knowledge on COVID-19, attitude towards volunteerism in the pandemic, and career preference. Logistic regression modeling was used to investigate possible factors that could encourage volunteerism among this group in a pandemic. RESULTS: A total of 552 medical students responded. Most medical students showed a huge interest in COVID-19. The extent of students' interest in COVID-19 varied among different student-classes (P < 0.05). Senior students had higher scores than the other two classes. The number of people who were 'glad to volunteer' in COVID-19 represented 85.6% of the respondents. What these students expressed willingness to undertake involved direct, indirect, and administrative job activities. Logistic regression analysis identified two factors that negatively influenced volunteering in the pandemic: Student-class and hazards of the voluntary job. Factors that positively influenced volunteering were time to watch COVID-19 news, predictable impact on China, and moral responsibility. CONCLUSION: More innovative methods can be explored to increase Chinese medical students' interest in reading about the relevant knowledge on COVID-19 and doing voluntary jobs during the pandemic.

Hyperbaric oxygen therapy relieved pruritus and pain of keloid patients.

Objective: Keloid patients usually have local pruritus and pain. In our clinical work, we have found keloid patients after receiving hyperbaric oxygen (HBO) therapy reflect less pruritus and pain. The hypothesis was that patients with keloid and a history of HBO therapy would have less pruritus and pain than patients without HBO therapy, and the pruritus or pain-related factors were detected in keloid with/without HBO therapy and normal skin. Methods: Three groups of samples were established: keloid samples from patients with HBO therapy for two weeks before and after surgery (H group); keloid samples from patients without HBO therapy (G group); normal skin samples from patients without obvious scar (N group). Hematoxylin and eosin (H&E) staining was used to observe morphological changes. Pruritus/pain related factors: Tryptophan Hydroxylase1 (TPH1), connexin-43 (Cx43) and transient receptor potential vanilloid type 1 (TRPV1) were detected by immunofluorescence and western blot technology. The expression of these factors' mRNA was also measured by the real-time quantitative polymerase chain reaction (RT-qPCR). Results: Among three groups, G group presented significantly highest expression levels of TPH1, Cx43 and TRPV1, conversely, N group presented significantly lowest expression levels of TPH1, Cx43 and TRPV1. Conclusion: TPH1, Cx43 and TRPV1 were overexpressed in the samples of keloid patients, indicating that the pruritus and pain of keloid might be related to these factors. Furthermore, TPH1, Cx43 and TRPV1 were expressed highest in keloid patients without HBO therapy, indicating that HBO therapy might relief pruritus of keloid patients by regulating these factors.

Adipose-Derived Stromal Cells Attenuate Adipose Inflammation in Obesity through Adipocyte Browning and Polarization of M2 Macrophages.

Obesity is a metabolic condition associated with multiple health problems such as endocrine and metabolic dysfunction and chronic inflammation in adipose tissues. In this study, the ADSCs could be stimulated to differentiate into brown adipocyte with rosiglitazone treatment based on the Oil-Red-O staining trial. Furthermore, the multilocular lipid droplets located in the center was increased in differentiated brown adipocytes, and brown fat-associated proteins, UCP1, PPAR-γ, and LPL were highly expressed in brown adipocytes differentiated from ADSCs. Additionally, the results of animal experiments showed that both weight and amount of VLDL and LDL were decreased in the serum of obese mice after transplantation of rosiglitazone-induced brown adipocytes, while the level of HDL increased. Moreover, the proteins associated with lipid metabolism, LPA and UCP1, were downregulated, and the inflammatory response was suppressed through inhibition of the ITGAM/NF-κB-mediated proinflammatory responses and polarization of M2 macrophages. Similarly, the amounts of proinflammatory cytokines, TNF-α, IL-6, and IL-1ß were decreased after rosiglitazone-induced brown adipocyte transplantation. On the contrary, anti-inflammatory cytokine IL-10 was significantly increased in both groups of obese mice, with or without brown adipocyte transplantation. Therefore, the adipose-derived stromal cells with induced browning could promote lipid consumption and alternative polarization of M2 macrophages to attenuate adipose inflammation in obesity mouse models, which thus provides a potential therapy for obesity.

Postconditioning with inhaled hydrogen attenuates skin ischemia/reperfusion injury through the RIP-MLKL-PGAM5/Drp1 necrotic pathway.

This study explored the flap-protective effects of high concentrations of hydrogen (HCH) inhalation in a rat flap ischemia/reperfusion (I/R) injury model and the potential mechanism of necroptosis. Forty-five male Sprague-Dawley rats were randomly divided into three groups: SH, IR and HCH groups. After undergoing 3 h of I/R management, the surgery groups were treated with ambient air (SH and IR) and high concentrations of hydrogen (HCH). On the third postoperative day, blood perfusion in the flap was measured using Laser Doppler flowmeters. RIP1, RIP3, MLKL, PGAM5 and Drp1 were examined by immunological detection and RT-qPCR. Compared to the IR group, larger areas of the skin flaps from the SH and HCH groups survived and displayed more blood perfusion. RIP1, RIP3, MLKL, PGAM5 and Drp1 were expressed at high levels in the IR group, and their expression was significantly decreased in the HCH group. In the SH and HCH groups, the necrotic factors measured here showed similar expression levels, which were significantly lower than the levels in the IR group, indicating that HCH-mediated protective effects on rat skin I/R necrosis may be associated with the necrotic pathway.

Necroptosis was found in a rat ischemia/reperfusion injury flap model.

BACKGROUND: Necroptosis is a new form of cell death that has been identified as a third pathway causing cell death. In this study, necrostatin-1 (Nec-1) was used to determine whether necroptosis exists in a rat ischaemia/reperfusion injury flap model. METHODS: In this study, twenty male Sprague-Dawley rats were divided randomly into two groups: a control group (CTL group) and a Nec-1 group. Each abdominal skin flap underwent 3 h of ischaemia and then reperfusion. Fifteen minutes before and after reperfusion, phosphate buffer saline (PBS) was administered intraperitoneally to the CTL group, while Nec-1 was administered intraperitoneally to the Nec-1 group. Twenty-four hours after reperfusion, the whole flap was divided equally into 54 sections. Flap blood perfusion was measured. One sample was taken randomly from each row. Morphological changes, apoptosis, receptor-interacting protein-1 (RIP-1) expression and caspase-3 activity were observed and detected. The measurements between the two groups were compared with the independent t-test, and a P value of <0.05 was considered statistically significant. RESULTS: Compared to flaps in the CTL group, flaps in the Nec-1 group showed longer survival rates, better blood perfusion and less inflammatory infiltration. The total flap area considered to have survived was 70.88 ±â€Š10.28% in the CTL group, whereas 80.56 ±â€Š5.40% of the area was found to be living in the Nec-1 group (Nec-1 vs. CTL, t = -2.624, P < 0.05). For some rows, there were significant differences in cell apoptosis between the two groups, the apoptosis index (AI) in rows "9 cm", "7 cm", "6 cm" and "5 cm" was significantly lower in the Nec-1 group than that in the CTL group (Nec-1 vs. CTL, P < 0.05). RIP-1 expression was much lower in the Nec-1 group than that in the CTL group in rows "5 cm" to "9 cm" (Nec-1 vs. CTL, P < 0.05). No significant differences in caspase-3 activity were found. CONCLUSION: According to the results, necroptosis was present in a rat abdominal ischaemia/reperfusion injury flap model.

A parasternal intercostal perforator flap for esthetic reconstruction after complete chest keloid resection: A retrospective observational cohort study.

OBJECTIVE: To report on the outcome of 35 patients with chest keloids who were treated with intercostal perforator flap surgery plus local radiotherapy at our hospital. METHODS: We retrospectively analyzed the data of patients with chest keloid who under surgical resection at the Department of Plastic Surgery, Peking Union Medical College Hospital, Beijing, China between March 2014 and July 2017. We retrieved patient demographic data, donor site position, the perforator pedicle, flap size, angle of flap rotation, complications, and recurrences from the medical records. All patients underwent perforator flap surgery for complete keloid resection followed by radiation at postoperative day 1 and 8 for a total dose 16-18 Gy. RESULTS: Thirty-five patients were included in the retrospective analysis. Their mean age was 45.3 years (range 24-67 years). The mean keloid area was 5-7 cm × 6-10 cm. Surgeries were successful in all cases. There were no perioperative complications. Good outcome with no apparent scar growth was achieved in 88.6% of the cases, and 11.4% of the cases achieved satisfactory outcome with partial scar growth in the incision, but no keloid was observed. Twenty-four months after surgery, none of the resected keloids recurred and none of the donor sites developed new keloids. CONCLUSION: Intercostal perforator flap surgery is an effective and safe approach for repair of wound formed as a result of excision of relatively large chest keloids which cannot be directly appositioned.

Hyperbaric oxygen therapy improves the effect of keloid surgery and radiotherapy by reducing the recurrence rate.

OBJECTIVE: Keloids are exuberant cutaneous scars that form due to abnormal growth of fibrous tissue following an injury. The primary aim of this study was to assess the efficacy and mechanism of hyperbaric oxygen therapy (HBOT) to reduce the keloid recurrence rate after surgical excision and radiotherapy. METHODS: (1) A total of 240 patients were randomly divided into two groups. Patients in the HBOT group (O group) received HBOT after surgical excision and radiotherapy. Patients in the other group were treated with only surgical excision and radiotherapy (K group). (2) Scar tissue from recurrent patients was collected after a second operation. Hematoxylin and eosin (H&E) staining was used to observe keloid morphology. Certain inflammatory factors (interleukin-6 (IL-6), hypoxia-inducible factor-1α (HIF-1α), tumor necrosis factor-α (TNF-α), nuclear factor κB (NF-κB), and vascular endothelial growth factor (VEGF)) were measured using immunohistochemical staining. RESULTS: (1) The recurrence rate of the O group (5.97%) was significantly lower than that of the K group (14.15%), P<0.05. Moreover, patients in the O group reported greater satisfaction than those in the K group (P<0.05). (2) Compared with the recurrent scar tissue of the K group, the expression levels of the inflammatory factors were lower in the recurrent scar tissue of the O group. CONCLUSIONS: Adjunctive HBOT effectively reduces the keloid recurrence rate after surgical excision and radiotherapy by improving the oxygen level of the tissue and alleviating the inflammatory process.

Clinical features and treatment options for mitral regurgitation in elderly inpatients.

OBJECTIVE: To summarize clinical characteristics and treatment strategy of Chinese elderly mitral regurgitation (MR) inpatients under the current guidelines, and to identify factors related to treatment options in them. METHODS: A single center retrospective study was conducted in which patients hospitalized in Fuwai hospital from May 1st of 2014 to April 30 of 2015 with moderate to severe MR assessed by transthoracic echocardiography were enrolled consecutively (n = 1741). Patients > 60 years old were grouped as elderly group (n = 680) and patients < 60 years were grouped as control group (n = 1061). The elderly group was categorized into two subgroups based on surgical status. RESULT: s The mean age of the elderly group was 66.98 ± 5.94 years. The most common reason of MR in elderly group was degenerative MR (41.18%). Atherosclerotic risk factors such as hypertension, diabetes or hyperlipidaemia were more commonly observed in elderly group than the control group (45.44% vs. 25.17%, P < 0.001; 19.56% vs. 8.48%, P < 0.001; 35.29% vs. 19.51%, P < 0.001). Elderly group had higher EuroscoreIIscore (5.54 ± 2.42 vs. 3.15 ± 1.66), greater left ventricular end diastolic diameter (LVEDD) (57.72 ± 12.3 vs. 57.33 ± 10.19 mm) and a lower surgery rate (54.71% vs. 63.91%); P < 0.05. Age, left ventricular ejection fraction (LVEF), regurgitation grade, EuroScore-II high risk stratification and having diabetes were identified as factors associated with therapy decisions in elderly MR patients. CONCLUSIONS: Valve surgery was denied in 45.29% of elderly MR inpatients. Older age, impaired LVEF, lower regurgitation grade, EuroScore-II high risk stratification, and having diabetes were factors most significantly associated with surgery denial among elderly Chinese inpatients with MR.

IgG4 and IgE co-positive group found in idiopathic orbital inflammatory disease.

AIM: To reveal the cytokines involved in idiopathic orbital inflammatory disease (IOID) and the relationship between Th17 cells, IgE and IOID pathogenesis. METHODS: Whole blood samples were processed immediately after collection and serological IgG4, IgG, and IgE antibodies were tested using ELISA. IOID and orbital cavernous hemangioma (CH) tissue samples underwent Bio-Plex multiplex cytokine detection. Hematoxylin-Eosin (HE) staining of all paraffin samples suggested the histological features of IOIDs, and expressions of IgG4 and IL-17A in affected tissues were detected by immunohistochemistry. RESULTS: Among 40 IOID plasma samples, 52.5% (21/40) were positive for IgG4 and 25% (10/40) were positive for IgE. Overlapped IgG4 or IgE positive samples accounted for 22.5% (9/40). Therefore, IOID samples were separated into three groups. The IgE+/IgG4+ group had a relevantly lower level of pro-inflammatory cytokine expression. IL-4 (Th2 cell related), IL-10 and TGF-ß1 (Treg cell immunity related) were elevated in all three groups. Some of the Th17 cell related cytokines (i.e. IL-17A/F, IL-25, IL-23, and IL-33) displayed higher expression levels in the IgE-/IgG4- group compared to the other two groups. CONCLUSION: We discovered an IgG4-IgE co-positive group as well as Th17 cell immune involvement in IgG4-IgE co-negative subgtroup in IOID for the first time. The pathogenesis of IOID could differ from different subgroups according to the IgG4 and IgE detection. Therefore, we recommend that, Treatment stratagy should be made according to the clinical assessment of IgG4-IgE and Th17 profile detection.

2-Methoxyestradiol improves the apoptosis level in keloid fibroblasts through caspase-dependent mechanisms in vitro.

Apoptosis is a form of programmed cell death that occurs in multicellular organisms. Fibroblasts are the main cellular ingredients in keloid tissue, which has a relatively low apoptosis level. A natural metabolite of estradiol, 2-Methoxyestradiol (2ME2) exerts a pro-apoptotic effect on tumor cells. In this study, the expression levels of key factors in the apoptosis pathway and the expression level of the proliferating cell nuclear antigen (PCNA) were measured to assess the levels of apoptosis and proliferation in both normal skin fibroblasts and keloid fibroblasts. Twelve samples were obtained from 12 patients: 6 keloid patients and 6 non-keloid patients. All 12 of the patients were randomly selected from the Department of Plastic Surgery at Peking Union Medical College Hospital from June 2016 to December 2016. After cell culture, fibroblasts were divided into the following 6 groups: normal skin fibroblasts (S); keloid fibroblasts (K); keloid fibroblasts treated with 2ME2 (2ME2); keloid fibroblasts treated with DMSO (DMSO); keloid fibroblasts treated with the caspase inhibitor Ac-DEVD-CHO (IN); and keloid fibroblasts treated with both Ac-DEVD-CHO and 2ME2 (IN+2ME2). Fibroblasts at up to passage 3 were used for analysis. Cell activity was measured by the cell counting kit-8. TUNEL staining was used to observe the cell apoptotic morphology. The key apoptosis factors (caspase-3, caspase-8, caspase-9, Bcl-2, Bax, and cytochrome-c) and PCNA expression levels were detected by immunofluorescence analysis and Western blotting. A certain concentration of 2ME2 was also used in group S to evaluate the toxicity. Compared with that in the other groups, 2ME2 significantly inhibited cell activity and led to apoptotic appearance of fibroblasts. In protein analysis, 2ME2 remarkably increased the expression of apoptosis factors and decreased the PCNA expression. Apoptosis levels were reduced by both the caspase inhibitor and 2ME2; thus indicating that the pro-apoptosis effect of 2ME2 was achieved through a caspase-dependent mechanism in keloid fibroblasts. Toxicity assessment showed that 2ME2 had a very low influence on normal skin fibroblasts. 2ME2, considered to be a new promising type of chemotherapy drug, exerts a pro-apoptosis effect by regulating the caspase family and an anti-proliferation effect towards keloid fibroblasts, and it presents low toxicity towards normal fibroblasts in vitro.