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Κυριακή 7 Νοεμβρίου 2021

An analysis of publication trajectory in plastic surgery across the decades

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J Plast Reconstr Aesthet Surg. 2021 Oct 22:S1748-6815(21)00478-2. doi: 10.1016/j.bjps.2021.09.039. Online ahead of print.

ABSTRACT

The classic canonical publication trajectory for academicians has been well-described by a rapid increase followed by a slower decrease in productivity, leading to a plateau. This trajectory has not been investigated in plastic surgery. In this communication, we aimed to: (1) visualize the publication trajectory per decade for plastic surgeons certified from 1980 to 2010, and (2) characterize and quantify the changes in publishing trends across decades. A list of plastic and reconstructive surgeons board certified between 1980 and 2010 was obtained. Number of publications per year was recorded for each plastic surgeon. The median cumulative publication trajectory was graphed for each decade. Kruskal-Wallis analysis was performed to determine whether there were differences in number of publications across ge nerations. The trajectory for a surgeon from the 1980s follows the established canonical trajectory. Surgeons from the 1990s and 2000s had significantly more publications by board certification than those from the 1980s (7 and 8 vs. 5, respectively, p < 0.01). Surgeons from the 2010s on average achieved 8 publications by board certification. It is clear that the publication arc for plastic surgeons from successive generations has greatly changed. Over the last 40 years, there has been a trend for increasing productivity and involvement in research at a much earlier stage in career, potentially due to increasing demands for matching into residency programs.

PMID:34736850 | DOI:10.1016/j.bjps.2021.09.039

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Technique for the prevention of hernia after pedicled transverse rectus abdominis musculocutaneous flap for breast reconstruction

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J Plast Reconstr Aesthet Surg. 2021 Oct 23:S1748-6815(21)00480-0. doi: 10.1016/j.bjps.2021.09.041. Online ahead of print.

NO ABSTRACT

PMID:34736851 | DOI:10.1016/j.bjps.2021.09.041

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Patient-Reported Long-Term Outcomes After Free Vascularized Fibula Graft in Spinal Reconstruction: a 24-year Cohort

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J Plast Reconstr Aesthet Surg. 2021 Sep 20:S1748-6815(21)00425-3. doi: 10.1016/j.bjps.2021.08.036. Online ahead of print.

ABSTRACT

PURPOSE: The use of free vascularized fibula grafts (FVFG) in complex spinal deformity surgery intends to allow for life-long stability of the spine with good long-term clinical outcome. However, these long-term outcomes of this technique are still lacking. The objective of this study is to report the long-term postoperative outcomes and establish the long-term viability of this method for spinal reconstruction.

METHODS: A retrospective cohort study was conducted in all patients who underwent spinal reconstructive surgery utilizing a FVFG at a tertiary medical centre. Questionnaires taken from the participants were the Numeric Pain Rating Scale (NPRS), Oswestry Low Back Pain Disability (also known as Oswestry Disability Index (ODI)), Scoliosis Research Society 22r (SRS-22), the EQ-5D-5L and a self-ass embled questionnaire regarding donor site comorbidities and patient satisfaction.

RESULTS: Over a period of 24 years (1995-2019), we used FVFG for spinal reconstruction in 31 patients. A total of 25 patients were included in this study, 8 patients were deceased at the time of this study, and sixteen patients responded to the questionnaires. Patient satisfaction was rated 6.8 out of 10, the average SRS-22r score was 3.6, EQ-5D-5L score was 0.725, and the ODI score showed a minimal disability (0-20%) postoperatively. Overall complication-free survival was 8.9 years. Nine patients underwent a re-operation in the spinal area; five for the removal of the spinal instrumentation.

CONCLUSION: Patients reported satisfied and good long-term outcomes following FVFG surgical procedure for complex spinal deformities. Therefore, considering the alternatives, this procedure provides a good long-term solution for complex spinal deformity surgery.

PMID:34736853 | DOI:10.1016/j.bjps.2021.08.036

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Predictive Factors of Recurrence of Papillary Thyroid Microcarcinomas: Analysis of 2,538 Patients

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Int Arch Otorhinolaryngol. 2021 Feb 19;25(4):e585-e593. doi: 10.1055/s-0040-1722253. eCollection 2021 Oct.

ABSTRACT

Introduction The incidence of papillary thyroid microcarcinoma (PTMC) has increased, and its treatment remains controversial. Objective To identify the clinical and pathological factors predictive of tumor recurrence. Methods We retrospectively analyzed 2,538 consecutive patients treated for PTMC, most submitted to total thyroidectomy (98%) follow ed by radioactive iodine (RAI) ablation (51.7%) at a cancer center from 1996 to 2015. The patients were stratified according to the American Thyroid Association (ATA) risk categories (low, intermediate, or high), and the clinicopathological features were evaluated by multivariate Cox regression analysis to identify independent prognostic factors for recurrence. Results After a mean follow-up of 58 months (range: 3 to 236.5 months), tumor recurrence was diagnosed in 63 (2.5%) patients, mostly in the lymph nodes. Distant metastasis occurred in 2 (0.1%) patients. There were no cancer-related deaths. The multivariate analysis showed that age < 55 years ( p = 0.049; hazard ratio [HR]: 2.54; 95% confidence interval [95%CI]: 0.95 to 0.99), multifocality ( p = 0.032; HR: 1.76; 95%CI: 1.05 to 2.96), and the presence of lymph-node metastasis ( p < 0.001; HR: 3.69; 95%CI: 2.07-6.57) were independent risk factors for recurrence. Recurrence was observed in 29 (1 .5%) out of 1,940 low-risk patients, 32 (5.4%) out of 590 intermediate-risk patients, and in 2 (25%) out of 8 high-risk patients. Conclusions The prognosis of PTMC is excellent, favoring a conservative treatment for most patients. Age < 55 years, multifocality, and node metastasis at diagnosis, as well the ATA staging system effectively predict the risk of recurrence. The presence of these risk factors can help identify patients who should be considered for more aggressive management and more frequent follow-up.

PMID:34737832 | PMC:PMC8558954 | DOI:10.1055/s-0040-1722253

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Study of Binaural Auditory Cortical Response in Children with History of Recurrent Otitis

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Int Arch Otorhinolaryngol. 2020 Nov 30;25(4):e490-e495. doi: 10.1055/s-0040-1718527. eCollection 2021 Oct.

ABSTRACT

Introduction Any type of sensory deprivation in childhood resulting from conductive hearing loss may impair the development of peripheral and central auditory pathway structures with negative consequences for binaural processing. Objective To characterize and compare monoaural and binaural auditory responses in neonates and children without and with a history of recurrent otitis. Methods The study included participants from 0 to 8 years and 11 months old, in good general health conditions, of both genders, divided into a control group, with no history of otitis, and a study group, with history of recurrent otitis. Cortical potential with speech stimulus /ba/-/da/ was used as collection procedure. The arithmetic calculation of the 512 points of the wave was performed to obtain the grand average of the waves o f the subjects in both groups. The Shapiro-Wilk and mixed repeated measures analysis of covariance (ANCOVA) statistical tests were performed to analyze the group effect, the condition, and the interaction (group versus condition) controlling the effect of the age-sex covariable. Results There was a statistically significant difference between the groups for all latency values; and for the P1, N1, P2, and N2 latencies, the differences between the groups occurred in the three analyzed conditions (right and left ears and binaural), revealing the influence of sensory deprivation. There were no significant differences in relation to wave amplitudes. Conclusion There are differences in the cortical potential with speech stimuli and in the binaural interaction component of children with and without history of recurrent otitis.

PMID:34737818 | PMC:PMC8558962 | DOI:10.1055/s-0040-1718527

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The role of TNFTNFα/p53 pathway in endometrial cancer mouse model administered with apple seed extract

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Histol Histopathol. 2021 Nov 5:18393. doi: 10.14670/HH-18-393. Online ahead of print.

ABSTRACT

Recent studies regarding the ability to relieve and reconstitute the endometrium in the treatment of endometrial cancer are limited. In this study, to analyze endometrial cancer, early endometrial cancer was induced by injecting a colon cancer cell line into the lower abdominal cavity of mice. Subsequently, the apple seed extract was administered orally to determine if the extract could affect the endometrial cancer. Administration of apple seed extract to the endometrial cancer model confirmed that the apoptosis suppressing mechanism was downregulated concurrently with the reduced expression of NF-κB. In contrast, the TNFα/p53 pathway upregulated the apoptosis. A number of clinical inferences could be derived from the results of this study; moreover, the administration of apple seed extract in a cancer metastasis model has not been reporte d in earlier toxicity induction studies. The results of this study indicated that the apple seed extract partially enhances apoptosis and the immune function related factors in endometrial cells. By improving tissue remodeling, the extract may help to restore the endometrium.

PMID:34738229 | DOI:10.14670/HH-18-393

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LPS-induced inflammatory response and apoptosis are mediated by Fra-1 upregulation and binding to YKL-40 in A549 cells

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Exp Ther Med. 2021 Dec;22(6):1474. doi: 10.3892/etm.2021.10909. Epub 2021 Oct 22.

ABSTRACT

Acute respiratory distress syndrome (ARDS) is a multifactorial syndrome that leads to increased morbidity and mortality in infants and children. The identification of novel biomarkers is critical for the treatment of ARDS. The present study aimed to investigate the effects of chitinase-3-like-1 protein (CHI3L1 or YKL-40) in an in vitro model of ARDS and to explore the potential underlying mechanisms. The in vitro model of ARDS was established in A549 alveolar epithelial type II cells, which were treated by lipopolysaccharide (LPS) to induce inflammation. Transfection was performed to alter YKL-40 expression. The mRNA and protein expression of YKL-40 was determined using reverse transcription-quantitative PCR and western blotting, respectively. Cell Counting Kit-8 and TUNEL assays were used to evaluate the cell viability and apoptosi s, respectively. The production of cytokines was evaluated using specific ELISA kits. The relationship between YKL-40 and Fos-related antigen 1 (Fra-1) was verified using luciferase reporter and chromatin immunoprecipitation assays. The expression of the apoptotic proteins was detected using western blotting. The expression levels of YKL-40 and Fra-1 were increased in LPS-treated A549 cells. Higher levels of pro-inflammatory cytokines and induction of cell apoptosis were observed in LPS-treated A549 cells compared with the control. YKL-40 knockdown in LPS-treated A549 cells significantly decreased the production of pro-inflammatory cytokines and reduced cell apoptosis, whereas it concomitantly caused upregulation of Bax and downregulation of Bcl-2, cleaved caspase-3 and cleaved caspase-9. In addition, Fra-1 could directly bind to YKL-40 promoter and regulate its expression level. Overexpression of YKL-40 partly decreased the inhibitory effects of Fra-1 knockdown on the inflammatory response and induction of apoptosis. In summary, the findings from the present study indicated that Fra-1 could bind to YKL-40 and regulate its expression, whereas YKL-40 knockdown could further suppress LPS-induced inflammatory response and apoptosis in A549 cells. These data may provide novel evidence on the diagnosis and therapy of ARDS.

PMID:34737814 | PMC:PMC8561753 | DOI:10.3892/etm.2021.10909

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5-Aminolevulinic acid combined with ferrous iron improves glucose tolerance in high-fat diet-fed mice via upregulation of glucose transporter 1

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Exp Ther Med. 2021 Dec;22(6):1454. doi: 10.3892/etm.2021.10889. Epub 2021 Oct 15.

ABSTRACT

Decreased mitochondrial metabolism suppresses glucose metabolism, resulting in obesity and diabetes. The present study aimed to investigate mechanisms underlying the 5-aminolevulinic acid (5-ALA) hydrochloride-mediated increase in glucose uptake in high-fat diet (HFD)-fed mice in vivo and C2C12 myotube cells in vitro. C57BL/6N male mice (20 weeks old) were fed either HFD or normal diet (ND) for 4 weeks. A total of five HFD-fed mice were orally administered with 300 mg/kg 5-ALA hydrochloride and 47.1 mg/kg sodium ferrous citrate (SFC; HFD + 5-ALA/SFC), whereas ND and other HFD-fed mice were orally administered with saline. After 4 weeks, these mice were intraperitoneally administered with 2 g/kg glucose and 3.2 mg/kg 2-deoxyglucose (2DG) for intraperitoneal glucose tolerance test (IPGTT) and glucose uptake test. Body weights, plasma glucose levels and the area under the curve of IPGTT were lower in mice treated with HFD + 5-ALA/SFC compared with in those treated with HFD alone. 2DG uptake in the gastrocnemius muscle and heart were more significantly improved in the HFD + 5-ALA/SFC mice compared with the HFD-fed mice. Furthermore, 5-ALA/SFC increased 2DG uptake in C2C12 cells to a similar level to the insulin-treated group. Moreover, it increased glucose transport (GLUT)1 translocation in the plasma membrane by 2.5-fold relative to the controls without affecting GLUT1 expression; however, it had no effect on GLUT4 translocation. Therefore, 5-ALA/SFC enhanced gastrocnemius and cardiac glucose uptake in HFD-fed mice, and upregulated GLUT1 translocation to the plasma membrane, but not GLUT4 in C2C12 myotube cells. Therefore, it could potentially be used as a novel drug for the treatment of diabetes.

PMID:34737794 | PMC:PMC8561763 | DOI:10.3892/etm.2021.10889

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Ursolic acid ameliorates adipose tissue insulin resistance in aged rats via activating the Akt-glucose transporter 4 signaling pathway and inhibiting inflammation

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Exp Ther Med. 2021 Dec;22(6):1466. doi: 10.3892/etm.2021.10901. Epub 2021 Oct 20.

ABSTRACT

Ageing often results in insulin resistance (IR) and chronic inflammation, and adipose is one of the tissues in which inflammation and IR occur earliest during this process. The present study investigated the effect and underlying mechanisms of ursolic acid (UA) on adipose IR and inflammation in ageing rats. Specific pathogen-free male Sprague-Dawley rats were randomly divided into 4 groups: i) Young normal (young); ii) untreated ageing (aged); and groups supplemented with UA either iii) low-UA 10 mg/kg (UA-L) or iv) high-50 mg/kg (UA-H). Animals in the UA-treated groups received 10 or 50 mg/kg UA (suspended in 5% Gum Arabic solution). The rats in the corresponding aged group and young groups received vehicle (5% Gum Arabic) alone. All rats were intragastrically treated once daily by oral gavage for 7 weeks. The day before the experiment terminate d, overnight fasting blood (~700 µl) was collected and plasma was prepared to measure biochemical indicators; western blotting was performed to analyze the expression of insulin signaling proteins [(insulin receptor substrate 1 (IRS-1), phosphorylated (p)-IRS-1, PI3K, glucose transporter 4 (GLUT4), Akt and p-Akt)] and inflammatory factors (NF-κB, IL-6 and IL-1β) in the epididymis white adipose tissue (eWAT). The results revealed that treatment with UA-H decreased eWAT weight, the ratio of eWAT weight/body weight, fasted insulin and triglyceride levels, the homeostasis model assessment of insulin resistance and adipose tissue insulin resistance index in ageing rats, indicating the amelioration of systemic and adipose tissue IR, compared with the aged group. Mechanistically, UA-H administration upregulated p-protein kinase B, the ratio of p-Akt to protein kinase B and total and cellular membrane GLUT4 protein levels in eWAT of ageing rats. Conversely, UA inhibited the increase in N F-κB expression and proinflammatory cytokines IL-6 and IL-1β. However, these alterations were not observed in the rats of the aged group. Taken together, the findings of the present study indicated that UA may ameliorate adipose IR, which is associated with activation of the Akt-GLUT4 signaling pathway and inhibition of inflammation in ageing rats. These data provide a basis for the development of effective and safe drugs or functional substances, such as UA, for the prevention and treatment of metabolic diseases.

PMID:34737806 | PMC:PMC8561770 | DOI:10.3892/etm.2021.10901

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Specificity protein 1-activated bone marrow stromal cell antigen 2 accelerates pancreatic cancer cell proliferation and migration

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Exp Ther Med. 2021 Dec;22(6):1459. doi: 10.3892/etm.2021.10894. Epub 2021 Oct 20.

ABSTRACT

Bone marrow stromal cell antigen 2 (BST2) has been reported to act as an oncogene in the tumorigenesis of numerous types of cancer. Bioinformatics analysis has predicted the binding interaction between BST2 and specificity protein 1 (SP1) and the involvement of SP1 in pancreatic cancer. Therefore, the present study set out to verify this interaction and determine how it may affect pancreatic cancer progression. Normal human pancreatic duct epithelial cells (HPDE6-C7) and pancreatic cancer cell lines (SW1990, BxPC3, PANC1 and PSN-1) were selected for western blotting and reverse transcription-quantitative PCR detection of BST2 expression. Colony formation, Cell Counting Kit-8 and wound healing assays were performed to detect the proliferative and migratory abilities of PANC1 cells following transfection with small interfering RNA against BST2. The expression of proliferation and migration markers were assayed using western blotting. Chromatin immunoprecipitation and luciferase reporter assays were employed to verify the bioinformatics prediction of BST2-SP1 binding. PANC1 cell proliferation and migration were analyzed following BST2 knockdown and SP1 overexpression. In comparison with HPDE6-C7 cells, all four pancreatic cancer cell lines were found to exhibit increased BST2 expression levels to varying degrees, with the highest levels observed in PANC1 cells. BST2 knockdown inhibited PANC1 cell colony formation, proliferation and migration. Additionally, SP1 was shown to bind to the BST2 promoter and could promote PANC1 cell proliferation and migration when overexpressed. However, BST2 knockdown rescued SP1 overexpression-induced PANC1 cell colony formation, proliferation and migration. In conclusion, activation of BST2 by the transcription factor SP1 was shown to accelerate pancreatic cancer cell proliferation and migration , suggesting that BST2 and SP1 may be plausible therapeutic targets in targeted therapy for pancreatic cancer.

PMID:34737799 | PMC:PMC8561758 | DOI:10.3892/etm.2021.10894

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