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Purpose: To analyze complications and potential risk factors associated with immediate prepectoral direct-to-implant breast reconstruction (DTIBR)., Methods: 295 patients (326 operated breasts) with DTIBR between March 2021 and December 2023 were included in this prospective study. Postoperative complications (postoperative bleeding, seroma, infection, necrosis, wound dehiscence, implant exchange/loss) were analyzed for potential risk factors by descriptive and logistic regression analyses., Results: The implant was covered by TiLOOP® Bra Pocket in 227 breasts (69.6%), by "dual-plane" technique in 20 breasts (6.1%), by acellular dermal matrix (ADM) in 1 breast (0.3%). No additional support was used for 78 breasts (23.9%). The use of mesh did not increase the risk for complications. Major complications requiring surgical revision occurred due to postoperative bleeding in 22 (6.7%), seroma in 2 (0.6%), infection in 13 (4.0%), necrosis in 10 (3.1%), and wound dehiscence in 10 (3.1%) breasts. Thirteen (4.0%) implants were exchanged, and 5 (1.5%) were explanted without substitution. One patient had to switch to autologous reconstruction due to skin necrosis. The main reasons for the removal/exchange of implants were infections (11 breasts, 3.4%) and necrosis (4 breasts, 1.2%). The risk for necrosis, infection, and wound dehiscence was mainly associated with the type of incision, especially skin-reducing incisions, and body mass index (BMI) ≥ 30 kg/m 2 ., Conclusion: Severe complications occurred primarily in patients with a BMI ≥ 30 kg/m 2 and when skin-reducing surgical techniques were performed., Trial Registry: This study was retrospectively registered at the German Clinical Trials Register (DRKS) on 20.06.2024., Drks-Id: DRKS00034493. https://drks.de/search/de/trial/DRKS00034493 ., Competing Interests: Declarations. Conflict of interest: E Bensmann received support from pfm medical GmbH, Applied Medical Germany GmbH, and Polytech Health & Aesthetics GmbH for a surgical workshop at the Department of Gynecology, Breast Center, Red Cross Hospital, Munich, Germany. A Andrulat was principal investigator of the PRO-Pocket study (Sponsor pfm medical GmbH). All other authors have no relevant financial or non-financial interests to disclose. Consent to participate: Informed consent was obtained from all individual participants included in the study. Ethics approval: This study was performed in line with the principles of the Declaration of Helsinki. Approval was granted by the Ethics Committee of Technical University Munich (25.11.2020; 660/20 S-EB)., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Objectives: The purpose of this study is to determine if there is a difference in outcomes for patients with blunt and penetrating vascular injuries of the pelvis., Methods: Data were abstracted from the Trauma Quality Improvement Program database from 2011 to 2015. Patients >18 years with hypogastric, iliac, uterine, or ovarian arterial or venous injuries were included. Individuals with an AIS head or chest score >3 were excluded., Results: Of the 2559 patients included, the mean age was 43 years (±19), 75.25% were male, and 32.6% had a comorbidity. 64.9% presented with blunt injury (mean ISS of 23 (±12)). 74.9% experienced a complication. The median hospital length of stay (LOS) and ICU LOS were 10 days and 4 days, respectively. 6.7% had an adverse discharge. Mortality occurred in 8.3%. On bivariate analysis, patients who sustained blunt trauma were older (51 vs 31 years), female (32.7% vs 10.1%), had a higher ISS (25.71 vs 17.65), and had a longer hospital LOS (16.65 vs 13.88). Patients with penetrating trauma had an increased chance of complications (78.4% vs 73.0%) and mortality (10.7% vs 7.0%). Multivariate analysis revealed in patients with blunt injuries have more complications (OR: 1.950 CI: 0.886-4.291 P = .097), a lower ISS (OR: 0.919, CI: 0.908-0.930, P < .001, were more likely to have an adverse discharge (OR: 2.05, CI: 1.62-2.60, P = .000), and had a higher risk of mortality (OR: 4.08 CI: 2.78-6.41 P < .000)., Conclusion: Patients with blunt pelvic vessel injuries are at risk for an increased number of complications and have a higher risk of mortality. Those who survive are more likely to have an adverse discharge.

Background: Frailty results in increased vulnerability to adverse outcomes following trauma. We investigated the association between the 5-item modified frailty index (mFI-5) and outcomes in geriatric trauma patients., Methods: The 2011-2016 Trauma Quality Improvement Program database was used to study outcomes in patients ≥ 65 years old. The mFI-5 was measured and categorized into no frailty (mFI-5 = 0), moderate frailty (mFI-5 = 0.2), and severe frailty (mFI-5 ≥ 0.4). Multivariable logistic regression analyses were performed to identify independent factors of mortality and complications., Results: 26,963 cases met the inclusion criteria, of whom 25.5% were not frail, 38% were moderately frail, and 36.6% were severely frail. Mean age (± SD) was 76 ± 7 years, 61.5% were male, and 97.8% sustained blunt injuries. Median Injury Severity Score (ISS) was 17 (IQR = 10-26), and the median Glasgow Coma Scale was 15 (IQR = 12-15). Overall mortality was 30.6%. Factors independently associated with mortality were age (OR = 1.07 per year, 95%CI 1.06-1.07), blunt trauma (OR = 1.44, 95%CI 1.19 -1.75), ISS (OR = 1.04 per unit increase in ISS, 95%CI 1.03-1.04), and severe frailty (OR = 1.23, 95%CI 1.15-1.32). Interestingly, male sex and GCS appeared to be protective factors with OR of 0.88 (95%CI 0.83 - 0.93) and 0.89 per point change in GCS (95%CI 0.88-0.9), respectively. Moderate (OR = 1.27, 95%CI 1.19-1.25) and severe frailty (OR = 1.49, 95%CI 1.-1.59) were significantly associated with in-hospital complications., Conclusion: Moderate and severe frailty were significant predictors of complications. Only severe frailty was associated with short-term mortality. The mFI-5 can be used as an objective measure to stratify risks in geriatric trauma., (© 2022. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.)

Genomic imprinting is a form of gene dosage regulation in which a gene is expressed from only one of the alleles, in a manner dependent on the parent of origin. The mechanisms governing imprinted gene expression have been investigated in detail and have greatly contributed to our understanding of genome regulation in general. Both DNA sequence features, such as CpG islands, and epigenetic features, such as DNA methylation and non-coding RNAs, play important roles in achieving imprinted expression. However, the relative importance of these factors varies depending on the locus in question. Defining the minimal features that are absolutely required for imprinting would help us to understand how imprinting has evolved mechanistically. Imprinted retrogenes are a subset of imprinted loci that are relatively simple in their genomic organisation, being distinct from large imprinting clusters, and have the potential to be used as tools to address this question. Here, we compare the repeat element content of imprinted retrogene loci with non-imprinted controls that have a similar locus organisation. We observe no significant differences that are conserved between mouse and human, suggesting that the paucity of SINEs and relative abundance of LINEs at imprinted loci reported by others is not a sequence feature universally required for imprinting.

Human umbilical vein endothelial cells (HUVEC) exposed to the female sex hormone estradiol show different kinds of effects including increased elasticity, activation of plasma membrane Na+/H+ exchange, prostacyclin production, prevention of apoptosis and many others. The aim of this study was the systematic analysis of the immunolabelling of estrogen receptors (ERs), ERalpha and ERbeta, in HUVEC after stimulation with different commercially available ER modulators and ER agonists or antagonists. HUVEC response to these substances was shown to be regulated via ERbeta. ERalpha immunolabelling or up-regulation was abrogated after application of estrogen derivatives, selective estrogen receptor modulators (SERM) and ER agonists or antagonists. Immunolabelling of ERbeta was significantly increased by estradiol, estrone, ethinylestradiol and tumour necrosis factor alpha (TNFalpha). SERM, such as Tamoxifen, and pure antagonists, such as ICI 182.780, stimulated ERbeta in HUVEC at low concentrations, whereas higher concentrations inhibited ERbeta immunolabelling. The pure estrogen receptor agonist 2,3-bis (4-hydroxyphenyl) proprionitrile (DPN) exhibited its activating potential at low concentrations. In contrast, higher concentrations resulted in a down-regulation of ERbeta. Estrogenic effects in HUVEC, independent of stimulation or inhibition, are mediated via the ERbeta. SERM such as Tamoxifen and ER antagonists such as ICI 182.780 act as ER activators in low concentrations, whereas higher concentrations lead to inhibitory effects.

Several reports deal with possible effects of female sex hormones on human umbilical vein endothelial cells (HUVEC) including elasticity, activation of plasma membrane Na+/H+ exchange, VEGF receptor Flk-1/KDR and many others. In contrast to those findings, some publications pointed out that HUVEC lack expression of both the estrogen receptor (ER) and/or the progesterone receptor (PR). Because the majority of these investigations were carried out at a time period, when only one ER and one PR was known, the aim of this study was the systematic analysis of ERalpha and ERbeta as well as PR-A and PR-B expression in HUVEC with specific monoclonal antibodies by immunocytochemistry and quantitative RT-PCR (TaqMan). As a result, we could show that HUVEC lack ERalpha but express ERbeta. The expression of ERbeta could be significantly upregulated with 17beta-estradiol on mRNA and protein level. In addition, HUVEC express PR-A but not PR-B. PR-A expression could be significantly upregulated with progesterone, again on mRNA and protein level. We conclude that estrogenic effects on HUVEC are mediated via the ERbeta and gestagens act via the PR-A pathway.