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Introduction: The relative citation ratio (RCR) is a bibliometric index utilized to assess research productivity. Mean relative citation ratio (m-RCR) and weighted relative citation ratio (w-RCR) can be utilized to assess individual research quality as well as career-long productivity, respectively. We sought to determine differences in academic productivity between genders and identify demographic variables associated with increased academic productivity., Methods: A list of Plastic and Reconstructive Surgery residency programs was compiled utilizing the American Council of Academic Plastic Surgeons website. Each program department's website was utilized to generate a list of practicing surgeons and respective demographic information. Both mean and weighted RCR were obtained using the iCite, a National Institutes of Health bibliometric tool. Surgeons were excluded if any demographic or RCR data was not accessible. Chi-squared test, Mann-Whitney U test, Kruskal-Wallis test, and multivariable linear regressions were performed., Results: A total of 785 academic plastic surgeons met the criteria and were included in the analysis, 186 of whom were women and 599 men. Both academic rank and model of residency training were significantly associated with gender in chi-squared analysis (P < 0.05). Mean relative citation ratio was higher among men in departments. Mean w-RCR was higher among men of assistant professor status, chief/chairperson status, integrated model of residency training, faculty size ≥six and in departments and divisions. Academic rank and faculty size were associated with higher w-RCR upon multivariable linear regression., Conclusions: Although differences exist in mean w-RCR between men and women in plastic surgery, gender is not a predictor of increased academic productivity. RCR is an accurate means of assessing gender differences in academic productivity as it comprehensively considers both quality and quantity of research and may be superior to other, older bibliometric indices., (Copyright © 2024. Published by Elsevier Inc.)

Introduction: Twenty three years after the first successful upper extremity transplantation, the role of vascularized composite allotransplantation (VCA) in the world of transplantation remains controversial. Face and upper extremity reconstruction via transplantation have become successful options for highly selected patients with severe tissue and functional deficit when conventional reconstructive options are no longer available. Despite clear benefit in these situations, VCA has a significant potential for complications that are more frequent when compared to visceral organ transplantation. This study intended to perform an updated systematic review on such complications., Materials and Methods: MEDLINE database via PubMed, Embase and Cochrane Library were searched. Face and upper extremity VCA performed between 1998 and 2021 were included in the study. Relevant media and press conferences reports were also included. Complications related to face and upper extremity VCA were recorded and reviewed including their clinical characteristics and complications., Results: One hundred fifteen patients underwent facial (43%) or upper extremity (57%) transplantation. Overall, the surgical complication rate was 23%. Acute and chronic rejection was identified in 89% and 11% of patients, respectively. Fifty eight percent of patients experienced opportunistic infection. Impaired glucose metabolism was the most common immunosuppression-related complication other than infection. Nineteen percent of patients ultimately experienced partial or complete allograft loss., Conclusions: Complications related to VCA are a significant source of morbidity and potential mortality. Incidence of such complications is higher than previously reported and should be strongly emphasized in patient consent process. Strict patient selection criteria, complex preoperative evaluation, consideration of alternatives, and thorough disclosure to patients should be routinely performed prior to VCA indication., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: Abdominal wall allotransplantation following intestinal and multivisceral transplant procedures has proven to be successful in achieving adequate closure in patients in whom other techniques have proven inadequate. Thus far, the focus of these abdominal wall allotransplants has been on graft and overall patient survival following surgery and the implementation of immunosuppression. The purpose of this study was to review the outcomes of abdominal wall allotransplantation reported in the literature., Methods: The PubMed database was queried, and 2595 articles were found. Search criteria used were "abdominal wall transplant" and "abdominal wall allotransplant." Of these, eight met inclusion/exclusion criteria., Results: In the present study, eight publications were identified reporting abdominal wall allotransplants, for a total of 38 full-thickness abdominal wall allotransplantations performed worldwide. All studies reported abdominal wall allotransplantation in combination with visceral organ allotransplantation. Abdominal wall allotransplantations reported thus far have been nonneurotized. Abdominal wall allotransplantations have proven to be beneficial both in terms of abdominal wall closure and acting as a sentinel marker for rejection for underlying visceral organ allotransplantation. The success of abdominal wall allotransplants and their long-term survival has introduced the question of functionality and long-term durability. Cadaveric studies have shown that it is possible to neurotize abdominal wall allotransplants, and future direction toward neurotized abdominal wall allotransplantation requires tools to assess functional outcomes of these transplants., Conclusions: Abdominal wall allotransplantation is an important reconstructive option when abdominal wall closure is challenging and should be considered in combination with visceral organ allotransplantations. There may be potential benefit in neurotizing the abdominal wall allotransplant for functional use, and future studies should aim to include functional outcomes., Competing Interests: Disclosure:The authors have no financial interest or conflicts of interest to declare ., (Copyright © 2022 by the American Society of Plastic Surgeons.)

This report presents a case in which oral soft tissue lesions were the first signs of multiple myeloma (MM) following a solid-organ transplantation. A 75-year-old man presented with bilateral primary oral gingival masses in the posterior mandible approximately 2 months after tooth extractions. A panoramic radiograph appeared normal and did not reveal "punched-out" lytic lesions of the bone, a classic sign of MM. A biopsy of the gingival masses was performed, and the resulting diagnosis was a plasma cell neoplasm. After a hematologic screening, positron emission tomography/computed tomography, and bone marrow biopsy, the diagnosis of MM with extensive disease was confirmed. Oral manifestations of MM are common, making the patient's oral health history an integral part of diagnosis. Although the isolated gingival hypertrophy observed in the present case is an atypical oral presentation, an understanding of the maxillofacial manifestations of MM is important to ensure diagnosis in the early stages of disease.

Background: Breast cancer frequently metastasizes to the brain, colonizing a neuro-inflammatory microenvironment. The molecular pathways facilitating this colonization remain poorly understood., Methods: Expression profiling of 23 matched sets of human resected brain metastases and primary breast tumors by two-sided paired t test was performed to identify brain metastasis-specific genes. The implicated DNA repair genes BARD1 and RAD51 were modulated in human (MDA-MB-231-BR) and murine (4T1-BR) brain-tropic breast cancer cell lines by lentiviral transduction of cDNA or short hairpin RNA (shRNA) coding sequences. Their functional contribution to brain metastasis development was evaluated in mouse xenograft models (n = 10 mice per group)., Results: Human brain metastases overexpressed BARD1 and RAD51 compared with either matched primary tumors (1.74-fold, P < .001; 1.46-fold, P < .001, respectively) or unlinked systemic metastases (1.49-fold, P = .01; 1.44-fold, P = .008, respectively). Overexpression of either gene in MDA-MB-231-BR cells increased brain metastases by threefold to fourfold after intracardiac injections, but not lung metastases upon tail-vein injections. In 4T1-BR cells, shRNA-mediated RAD51 knockdown reduced brain metastases by 2.5-fold without affecting lung metastasis development. In vitro, BARD1- and RAD51-overexpressing cells showed reduced genomic instability but only exhibited growth and colonization phenotypes upon DNA damage induction. Reactive oxygen species were present in tumor cells and elevated in the metastatic neuro-inflammatory microenvironment and could provide an endogenous source of genotoxic stress. Tempol, a brain-permeable oxygen radical scavenger suppressed brain metastasis promotion induced by BARD1 and RAD51 overexpression., Conclusions: BARD1 and RAD51 are frequently overexpressed in brain metastases from breast cancer and may constitute a mechanism to overcome reactive oxygen species-mediated genotoxic stress in the metastatic brain., (Published by Oxford University Press 2014.)

Despite important progress in adjuvant and neoadjuvant therapies, metastatic disease often develops in breast cancer patients and remains the leading cause of their deaths. For patients with established metastatic disease, therapy is palliative, with few breaks and with mounting adverse effects. Many have hypothesized that a personalized or precision approach (the terms are used interchangeably) to cancer therapy, in which treatment is based on the individual characteristics of each patient, will provide better outcomes. Here, we discuss the molecular basis of breast cancer metastasis and the challenges in personalization of treatment. The instability of metastatic tumors remains a leading obstacle to personalization, because information from a patient's primary tumor may not accurately reflect the metastasis, and one metastasis may vary from another. Furthermore, the variable presence of tumor subpopulations, such as stem cells and dormant cells, may increase the complexity of the targeted treatments needed. Although molecular signatures and circulating biomarkers have been identified in breast cancer, there is lack of validated predictive molecular markers to optimize treatment choices for either prevention or treatment of metastatic disease. Finally, to maximize the information that can be obtained, increased attention to clinical trial design in the metastasis preventive setting is needed., (Copyright © 2013 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)

In humans, cutaneous metastasis of transitional cell carcinoma (TCC) has been attributed to direct extension, lymphatic or hematogenous dissemination, or surgical implantation. The purpose of this study was to characterize the clinical and histologic features of cutaneous TCC metastasis, confirmed by uroplakin-III immunohistochemistry, in dogs. The 12 cases were 9 spayed female and 3 neutered male dogs, 6 to 14 years old (mean, 11 years). Four dogs had a history of urinary incontinence. Three had undergone abdominal surgery for TCC diagnosis or treatment. The primary neoplasms were 7 papillary infiltrating and 5 nonpapillary infiltrating TCC. Cutaneous lesions were detected at a mean of 123 days (median, 38 days) after diagnosis of the primary TCC and appeared as plaques, papules, or nodules in, with 1 exception, perineal, inguinal, or ventral abdominal dermis or subcutis. Of 8 dogs with dermal TCC, 5 had epidermal erosion or ulceration. In 10 dogs, TCC was detected in cutaneous lymphatic vessels, identified by endothelial immunoreactivity for Prox1. Metastases were also detected in lymph nodes in all dogs and at distant noncutaneous sites, usually the lungs, in 10 dogs. Mean survival after diagnosis was 162 days (median, 90 days). Despite medical treatment of 10 dogs after the development of cutaneous metastasis, remission was not achieved; 4 dogs had stable disease. Although TCC could have spread to skin by direct extension or lymphatic or vascular dissemination, the proximity of most cutaneous metastases to the vulva or prepuce raises the additional possibility of transepidermal spread through urine-scalded skin.

A 5-month-old mongrel puppy with a history of respiratory disease presented with progressive neurologic dysfunction. Hematologic results included leukocytosis (neutrophilia with a left shift) and lymphopenia. A mass in the right forebrain, identified by magnetic resonance imaging, was biopsied during decompressive craniectomy. The histologic diagnosis was granulomatous meningoencephalitis with intralesional amoebae. The dog died within 24 hours of surgery. At necropsy, a well-demarcated granuloma was confined to the cerebrum, but granulomatous pneumonia was disseminated through all lobes of the lung. Concurrent infections included canine distemper, canine adenoviral bronchiolitis, and oral candidiasis. Canine distemper virus probably caused immunosuppression and increased susceptibility to secondary infections.

Chemical exposures are important risks for development of hepatocellular carcinoma (HCC). One such chemical, diethylnitrosamine (DENA), is present in food products as well as in industrial and research settings. Further examination of tumors induced by DENA may yield clues to human risk. HCC from seven rhesus macaques exposed to DENA was selected from a tissue archive to examine for evidence of Wnt/beta-catenin signaling events, which are frequently associated with HCC. DENA exposure durations ranged from 8 to 207 months, and total accumulated dose ranged from 0.7 to 4.08 mg. Unexposed colony breeder macaques served as controls. Previously unrecognized HCC metastases were discovered in lungs of three macaques. Overexpression of beta-catenin and glutamine synthetase was detected by immunohistochemistry in six confirmed primary HCC and all metastatic HCC, which implicated Wnt/beta-catenin activation. Concomitant beta-catenin gene mutation was detected in one primary HCC; similar findings have been reported in human and rodent HCC. Neither beta-catenin mutation nor beta-catenin overexpression appeared to influence metastatic potential. Accumulation of intracellular proteins involved in Wnt/beta-catenin signaling during HCC oncogenesis in rhesus macaques exposed to DENA appears to include other mechanisms, in addition to mutation of beta-catenin gene.