E proteins control the development of NKγδT cells through their invariant T cell receptor.

T cell receptor (TCR) signaling regulates important developmental transitions, partly through induction of the E protein antagonist, Id3. Although normal γδ T cell development depends on Id3, Id3 deficiency produces different phenotypes in distinct γδ T cell subsets. Here, we show that Id3 deficiency impairs development of the Vγ3+ subset, while markedly enhancing development of NKγδT cells expressing the invariant Vγ1Vδ6.3 TCR. These effects result from Id3 regulating both the generation of the Vγ1Vδ6.3 TCR and its capacity to support development. Indeed, the Trav15 segment, which encodes the Vδ6.3 TCR subunit, is directly bound by E proteins that control its expression. Once expressed, the Vγ1Vδ6.3 TCR specifies the innate-like NKγδT cell fate, even in progenitors beyond the normally permissive perinatal window, and this is enhanced by Id3-deficiency. These data indicate that the paradoxical behavior of NKγδT cells in Id3-deficient mice is determined by its stereotypic Vγ1Vδ6.3 TCR complex.

Artificial Intelligence: Can It Save Lives, Hospitals, and Lung Screening?

BACKGROUND: Early detection is essential in lung cancer survival. Lung screening or incidental detection on unrelated imaging holds the most promise for early detection. With the large volume of imaging performed today, management of incidental pulmonary nodules can be difficult. We hypothesized an artificial intelligence (AI) tool could reliably read all imaging reports, detect, and effectively triage indeterminate pulmonary nodules without adding additional personnel, helping save lives. METHODS: An incidental lung nodule clinic (ILNC) was created using AI and an existing nurse practitioner. Over 26 months, the software read all radiology reports, visualizing any lung tissue. Patients with nodules >3 mm and considered indeterminate by the nurse practitioner were referred to the ILNC. High-risk patients with benign nodules were offered entry into the lung screening program. RESULTS: Of 502,632 imaging reports analyzed, 22,136 (4.4%) had positive findings. Follow-up data were lacking in 11,797 (2.3%), 911 (7.7%) were verified lost, and 518 (4.4%) were referred to the ILNC. There were 393 patients with benign nodules and accepted enrollment in the lung screening program. Mean age of enrolled patients was 61 years, and 53% were men. Workup included 499 diagnostic computed tomographic scans, 39 positron emission tomographic scans, and 27 biopsy samples that identified 15 malignancies (2.9%), with 14 lung cancers (8 stage I, 4 stage III, and 2 stage IV). Treatment included 5 lobectomies, and 4 underwent stereotactic body radiation therapy. Financials were favorable. CONCLUSIONS: AI software can supplement practitioners, help diagnose lung cancer earlier, save lives, and generate value-based revenue for the hospital.

Survivorship and Etiologies of Failure in Single-stage Revision Arthroplasty for Periprosthetic Joint Infection: A Meta-analysis.

INTRODUCTION: Single-stage revision arthroplasty for periprosthetic joint infection (PJI) may yield comparable infection-free survivorship with two-stage revision arthroplasty. It is unclear if the most common mode of failure of single-stage revision arthroplasty is infection or aseptic loosening. In this meta-analysis, we sought to (1) determine survivorship and (2) compare rates of different etiologies of failure of single-stage revision total hip arthroplasty (THA) and total knee arthroplasty (TKA). METHODS: Preferred Reporting Items for Systematic Review and Meta-analyses guidelines search was done using search terms for "single stage revision," "exchange arthroplasty," "periprosthetic infection," "PJI," and "single stage." Patient demographics such as age, body mass index, and mean follow-up time were recorded. Overall survivorship and rates of revision surgery were aggregated using a random-effects model. Comparison of septic and aseptic loosening rates was done by risk difference and associated 95% confidence interval (CI) calculation. RESULTS: Twenty-four studies were identified with 2,062 and 147 single-stage revision THA and TKA procedures performed between 1984 and 2019, respectively. The weighted mean follow-up and age were 69.8 months and 66.3 years, respectively, with 55% men overall. The all-cause revision surgery rate was 11.1% and 11.8% for THA and TKA, respectively. The revision surgery rate secondary to infection and aseptic loosening and associated 95% CI for the risk difference for THA and TKA was 5.5% and 3.3% (-1.7% to 5.0%), and 3% and 8.8% (-11.4% to 2.3%), respectively. Revision surgeries due to instability and fracture combined and mortality rate were both less than 3%. DISCUSSION: Single-stage revision THA and TKA for PJI demonstrated overall high rates of survivorship, low mortality, and revision surgeries secondary to infection and aseptic loosening to be equivalent. Aseptic loosening after single-stage revision TKA might be higher than in primary TKA. As implant survivorship from infection improves in PJI, surgeons should be aware of aseptic loosening as an equally common mode of failure.

Delayed Cholecystectomy Management for Mirizzi Syndrome.

Mirizzi syndrome is defined as a common hepatic duct obstruction from a cystic duct stone, which results in a severe inflammatory reaction that distorts biliary anatomy and makes surgical intervention challenging. Most case reports describe an open subtotal cholecystectomy as the most common surgical technique with few reports detailing successful laparoscopic interventions. This case involves an 11-year-old African American female who presented with right upper quadrant abdominal pain and imaging consistent with Mirizzi syndrome. She was taken for a laparoscopic cholecystectomy that was quickly aborted due to extensive inflammation. She subsequently underwent endoscopic decompression of her biliary tree by gastroenterology. She returned to the operating room six weeks later for a successful interval cholecystectomy. This case illustrates a unique report of delayed cholecystectomy for management of Mirizzi syndrome, which highlights a potential management strategy that avoids technically difficult laparoscopic cholecystectomy in the acute inflammatory period.

Hypofibrinogenemic Massive Transfusion Trauma Patients Experience Worse Outcomes.

INTRODUCTION: Uncontrolled hemorrhage accounts for up to 40% of trauma-related mortality. Previous reports demonstrate that decreased fibrinogen levels during traumatic hemorrhage are associated with worse outcomes. Cryoprecipitate is used to replace fibrinogen for patients in hemorrhagic shock undergoing massive transfusion (MT), though the optimal ratio of cryoprecipitate to fresh frozen plasma (FFP), packed red blood cells (PRBCs), and platelets remains undefined. The purpose of this study is to investigate the effect of admission fibrinogen level and the use of cryoprecipitate on outcomes in trauma patients undergoing MT. METHODS: A prospective practice management guideline was established to obtain fibrinogen levels on adult trauma patients undergoing MT at a level I trauma center from December 2019 to December 2021. Ten units of cryoprecipitate were administered every other round of MT. Thromboelastography (TEG) was also obtained at the initiation and completion of MT. Patient demographic, injury, transfusion, and outcome data were collected. Hypofibrinogenemic (<200 mg/dL) patients at initiation of MT were compared to patients with a level of 200 mg/dL or greater. RESULTS: A total of 96 out of 130 patients met criteria and underwent MT with a median admission fibrinogen of 170.5 mg/dL. Hypofibrinogenemia was associated with elevated INR (1.26 vs 1.13, P < .001) and abnormal TEG including decreased alpha angle (68.1 vs 73.3, P < .001), increased K time (1.7 vs 1.1, P < .001), and decreased max amplitude (58 vs 66, P < .001). Patients with hypofibrinogenemia received more PRBC (10 vs 7 U, P = .002), FFP (9 vs 6 U, P = .003), and platelets (2 vs 1 U, P = .004) during MT. Hypofibrinogenemic patients demonstrated greater mortality than patients with normal levels (50% vs 23.5%, P = .021). Older age, decreased GCS, and elevated injury severity score (ISS) were risk factors for mortality. Increased fibrinogen was associated with lower odds of mortality (P = .001). Age, ISS, and fibrinogen level remained significantly associated with mortality in a multivariable analysis. Overall, fibrinogen in post-MT survivors showed an increase in median level compared to admission (231 vs 177.5 mg/dL, P < .001). CONCLUSION: Trauma patients undergoing MT with decreased admission fibrinogen demonstrate increased mortality. Other mortality risk factors include older age, decreased GCS, and higher ISS. Patients with increased fibrinogen levels had lower odds of mortality in a multivariable model. Post-MT survivors demonstrated significantly higher fibrinogen levels than pre-MT patients. Hypofibrinogenemic patients also had worse TEG parameters and required more PRBCs, FFP, and platelets during MT. Further studies are needed to assess the optimal volume of fibrinogen replacement with cryoprecipitate during MT to improve trauma patient mortality.

Harvest of All-Soft Tissue Quadriceps Tendon Autograft for Anterior Cruciate Ligament Reconstruction With or Without Closure of Resulting Defect Has No Effect on Patellar Height.

Purpose: To evaluate the radiographic effect of quadriceps tendon harvest on patellar height and to determine whether closure of a quadriceps graft harvest defect resulted in a significant change in patellar height compared to nonclosure. Methods: We conducted a retrospective review of prospectively enrolled patients. The institutional database was queried and all patients who underwent quadriceps autograft anterior cruciate ligament reconstruction between 2015 and March 2020 were included. Graft harvest length in millimeters and final graft diameter after preparation for implantation were obtained from the operative record and demographic data were obtained from the medical record. Radiographic analysis was performed of eligible patients using standard ratios of patellar height: Insall-Salvati (IS), Blackburn-Peele (BP), and Caton-Deschamps (CD). Measurements were performed using digital calipers on a digital imaging system by 2 postgraduate fellow surgeons. Preoperative and postoperative radiographs were performed at 0° according to a standard protocol. Postoperative radiographs were performed 6 weeks postoperatively in all cases. Preoperative patellar height ratios were compared with postoperative patellar height ratios for all patients using t-tests. Subanalysis was then performed to compare the effect of closure of with nonclosure on patellar height ratios using repeated-measures analysis of variance. Interrater reliability between the 2 reviewers was assessed using an intraclass correlation coefficient calculation. Results: In total, 70 patients met final inclusion criteria. There were no statistically significant changes from pre- to postoperative values for either reviewer for IS (reviewer 1, P = .47; reviewer 2, P = .353), BP (reviewer 1, P = .98; reviewer 2, P = .907), or CD (reviewer 1, P = .107; reviewer, 2 P = .188). The closure and nonclosure groups were adequately powered and no statistically significant demographic differences between the closure and nonclosure groups was identified for sex (P = .066), age (P = .343), weight (P = .881), height (P = .42), laterality (P = 1), meniscal repair (P = .332), graft diameter (P = .068), or graft length (P = .183). According to the repeated measures analysis of variance, closure of the quadriceps defect had no significant impact on any of the knee ratios. However, reviewer identity had a significant influence on the CD ratio. Intraclass correlation coefficient analysis revealed excellent agreement between reviewers for the IS (0.982) and BP (0.954) ratios, but only moderate-to-good agreement for the CD (0.751) ratio. Conclusions: Harvest of quadriceps tendon graft does not result in radiographic changes in patellar height. Furthermore, closure of the quadriceps defect does not appear to result in radiographic changes in patellar height. Level of Evidence: III, retrospective comparative trial.

Multiplexed screens identify RAS paralogues HRAS and NRAS as suppressors of KRAS-driven lung cancer growth.

Oncogenic KRAS mutations occur in approximately 30% of lung adenocarcinoma. Despite several decades of effort, oncogenic KRAS-driven lung cancer remains difficult to treat, and our understanding of the regulators of RAS signalling is incomplete. Here to uncover the impact of diverse KRAS-interacting proteins on lung cancer growth, we combined multiplexed somatic CRISPR/Cas9-based genome editing in genetically engineered mouse models with tumour barcoding and high-throughput barcode sequencing. Through a series of CRISPR/Cas9 screens in autochthonous lung cancer models, we show that HRAS and NRAS are suppressors of KRASG12D-driven tumour growth in vivo and confirm these effects in oncogenic KRAS-driven human lung cancer cell lines. Mechanistically, RAS paralogues interact with oncogenic KRAS, suppress KRAS-KRAS interactions, and reduce downstream ERK signalling. Furthermore, HRAS and NRAS mutations identified in oncogenic KRAS-driven human tumours partially abolished this effect. By comparing the tumour-suppressive effects of HRAS and NRAS in oncogenic KRAS- and oncogenic BRAF-driven lung cancer models, we confirm that RAS paralogues are specific suppressors of KRAS-driven lung cancer in vivo. Our study outlines a technological avenue to uncover positive and negative regulators of oncogenic KRAS-driven cancer in a multiplexed manner in vivo and highlights the role RAS paralogue imbalance in oncogenic KRAS-driven lung cancer.

Stmol: A component for building interactive molecular visualizations within streamlit web-applications.

Streamlit is an open-source Python coding framework for building web-applications or "web-apps" and is now being used by researchers to share large data sets from published studies and other resources. Here we present Stmol, an easy-to-use component for rendering interactive 3D molecular visualizations of protein and ligand structures within Streamlit web-apps. Stmol can render protein and ligand structures with just a few lines of Python code by utilizing popular visualization libraries, currently Py3DMol and Speck. On the user-end, Stmol does not require expertise to interactively navigate. On the developer-end, Stmol can be easily integrated within structural bioinformatic and cheminformatic pipelines to provide a simple means for user-end researchers to advance biological studies and drug discovery efforts. In this paper, we highlight a few examples of how Stmol has already been utilized by scientific communities to share interactive molecular visualizations of protein and ligand structures from known open databases. We hope Stmol will be used by researchers to build additional open-sourced web-apps to benefit current and future generations of scientists.

Mitochondrial calcium uniporter stabilization preserves energetic homeostasis during Complex I impairment.

Calcium entering mitochondria potently stimulates ATP synthesis. Increases in calcium preserve energy synthesis in cardiomyopathies caused by mitochondrial dysfunction, and occur due to enhanced activity of the mitochondrial calcium uniporter channel. The signaling mechanism that mediates this compensatory increase remains unknown. Here, we find that increases in the uniporter are due to impairment in Complex I of the electron transport chain. In normal physiology, Complex I promotes uniporter degradation via an interaction with the uniporter pore-forming subunit, a process we term Complex I-induced protein turnover. When Complex I dysfunction ensues, contact with the uniporter is inhibited, preventing degradation, and leading to a build-up in functional channels. Preventing uniporter activity leads to early demise in Complex I-deficient animals. Conversely, enhancing uniporter stability rescues survival and function in Complex I deficiency. Taken together, our data identify a fundamental pathway producing compensatory increases in calcium influx during Complex I impairment.

Delineating the RAS Conformational Landscape.

Mutations in RAS isoforms (KRAS, NRAS, and HRAS) are among the most frequent oncogenic alterations in many cancers, making these proteins high priority therapeutic targets. Effectively targeting RAS isoforms requires an exact understanding of their active, inactive, and druggable conformations. However, there is no structural catalog of RAS conformations to guide therapeutic targeting or examining the structural impact of RAS mutations. Here we present an expanded classification of RAS conformations based on analyses of the catalytic switch 1 (SW1) and switch 2 (SW2) loops. From 721 human KRAS, NRAS, and HRAS structures available in the Protein Data Bank (206 RAS-protein cocomplexes, 190 inhibitor-bound, and 325 unbound, including 204 WT and 517 mutated structures), we created a broad conformational classification based on the spatial positions of Y32 in SW1 and Y71 in SW2. Clustering all well-modeled SW1 and SW2 loops using a density-based machine learning algorithm defined additional conformational subsets, some previously undescribed. Three SW1 conformations and nine SW2 conformations were identified, each associated with different nucleotide states (GTP-bound, nucleotide-free, and GDP-bound) and specific bound proteins or inhibitor sites. The GTP-bound SW1 conformation could be further subdivided on the basis of the hydrogen bond type made between Y32 and the GTP γ-phosphate. Further analysis clarified the catalytic impact of G12D and G12V mutations and the inhibitor chemistries that bind to each druggable RAS conformation. Overall, this study has expanded our understanding of RAS structural biology, which could facilitate future RAS drug discovery. SIGNIFICANCE: Analysis of >700 RAS structures helps define an expanded landscape of active, inactive, and druggable RAS conformations, the structural impact of common RAS mutations, and previously uncharacterized RAS inhibitor-binding modes.

Association of TP53 and CDKN2A Mutation Profile with Tumor Mutation Burden in Head and Neck Cancer.

PURPOSE: Head and neck squamous cell carcinoma (HNSCC) is a frequently devastating cancer that affects more than a half million people annually worldwide. Although some cases arise from infection with human papillomavirus (HPV), HPV-negative HNSCC is more common, and associated with worse outcome. Advanced HPV-negative HNSCC may be treated with surgery, chemoradiation, targeted therapy, or immune checkpoint inhibition (ICI). There is considerable need for predictive biomarkers for these treatments. Defects in DNA repair capacity and loss of cell-cycle checkpoints sensitize tumors to cytotoxic therapies, and can contribute to phenotypes such as elevated tumor mutation burden (TMB), associated with response to ICI. Mutation of the tumor suppressors and checkpoint mediators TP53 and CDKN2A is common in HPV-negative HNSCC. EXPERIMENTAL DESIGN: To gain insight into the relation of the interaction of TP53 and CDKN2A mutations with TMB in HNSCC, we have analyzed genomic data from 1,669 HPV-negative HNSCC tumors with multiple criteria proposed for assessing the damaging effect of TP53 mutations. RESULTS: Data analysis established the TP53 and CDKN2A mutation profiles in specific anatomic subsites and suggested that specific categories of TP53 mutations are more likely to associate with CDKN2A mutation or high TMB based on tumor subsite. Intriguingly, the pattern of hotspot mutations in TP53 differed depending on the presence or absence of a cooccurring CDKN2A mutation. CONCLUSIONS: These data emphasize the role of tumor subsite in evaluation of mutational profiles in HNSCC, and link defects in TP53 and CDKN2A to elevated TMB levels in some tumor subgroups.

Comprehensive characterization of PTEN mutational profile in a series of 34,129 colorectal cancers.

Loss of expression or activity of the tumor suppressor PTEN acts similarly to an activating mutation in the oncogene PIK3CA in elevating intracellular levels of phosphatidylinositol (3,4,5)-trisphosphate (PIP3), inducing signaling by AKT and other pro-tumorigenic signaling proteins. Here, we analyze sequence data for 34,129 colorectal cancer (CRC) patients, capturing 3,434 PTEN mutations. We identify specific patterns of PTEN mutation associated with microsatellite stability/instability (MSS/MSI), tumor mutational burden (TMB), patient age, and tumor location. Within groups separated by MSS/MSI status, this identifies distinct profiles of nucleotide hotspots, and suggests differing profiles of protein-damaging effects of mutations. Moreover, discrete categories of PTEN mutations display non-identical patterns of co-occurrence with mutations in other genes important in CRC pathogenesis, including KRAS, APC, TP53, and PIK3CA. These data provide context for clinical targeting of proteins upstream and downstream of PTEN in distinct CRC cohorts.

Structure of TFIIK for phosphorylation of CTD of RNA polymerase II.

During transcription initiation, the general transcription factor TFIIH marks RNA polymerase II by phosphorylating Ser5 of the carboxyl-terminal domain (CTD) of Rpb1, which is followed by extensive modifications coupled to transcription elongation, mRNA processing, and histone dynamics. We have determined a 3.5-Å resolution cryo-electron microscopy (cryo-EM) structure of the TFIIH kinase module (TFIIK in yeast), which is composed of Kin28, Ccl1, and Tfb3, yeast homologs of CDK7, cyclin H, and MAT1, respectively. The carboxyl-terminal region of Tfb3 was lying at the edge of catalytic cleft of Kin28, where a conserved Tfb3 helix served to stabilize the activation loop in its active conformation. By combining the structure of TFIIK with the previous cryo-EM structure of the preinitiation complex, we extend the previously proposed model of the CTD path to the active site of TFIIK.

A novel biosynthetic scaffold mesh reinforcement affords the lowest hernia recurrence in the highest-risk patients.

INTRODUCTION: Patients with higher postoperative infection risk undergoing ventral hernia repair (VHR) have limited options for mesh use. Biosynthetic mesh is intended to utilize the durability of synthetic mesh combined with the biocompatibility of biologic mesh. We sought to assess the outcomes of a novel biosynthetic scaffold mesh for VHR in higher risk patients over a 12-month postoperative period. METHODS: Two cohorts of 50 consecutive patients who underwent VHR with TELA Bio OviTex biosynthetic or synthetic mesh were retrospectively compared. Endpoints included surgical site occurrence (SSO), readmission rate, and hernia recurrence following VHR at 12 months postoperatively. RESULTS: OviTex mesh placement was associated with higher risk Ventral Hernia Working Group (VHWG) distribution and more contaminated CDC wound class distribution compared to synthetic mesh placement (VHWG grade 3: 68% vs. 6%, p < 0.001; CDC class > I: 70% vs. 6%, p < 0.001). Additionally, concomitant procedures were performed more often with OviTex mesh placement than synthetic mesh placement (70% vs 10%, p < 0.001). The OviTex mesh performed comparably to synthetic mesh in terms of incidences of SSO (36% vs 22%, p = 0.19), readmission rates (24% vs 14%, p = 0.31), and hernia recurrence (6% vs 12%, p = 0.74). On further evaluation, patients who developed SSO with OviTex mesh (n = 18) had a 17% hernia recurrence whereas those with synthetic mesh (n = 11) had an associated 55% hernia recurrence (p = 0.048). CONCLUSIONS: The OviTex biosynthetic mesh was used in higher risk patients and performed similarly to synthetic mesh in regards to rate of SSO, readmissions, and hernia recurrence. Furthermore, patients who developed SSO with Ovitex mesh were significantly less likely to have hernia recurrence than those with synthetic mesh. Overall, the data suggest that biosynthetic mesh is a more desirable option for definitive hernia repair in higher risk patients.

Proliferative signaling by ERBB proteins and RAF/MEK/ERK effectors in polycystic kidney disease.

A primary pathological feature of polycystic kidney disease (PKD) is the hyperproliferation of epithelial cells in renal tubules, resulting in formation of fluid-filled cysts. The proliferative aspects of the two major forms of PKD-autosomal dominant PKD (ADPKD), which arises from mutations in the polycystins PKD1 and PKD2, and autosomal recessive PKD (ARPKD), which arises from mutations in PKHD1-has encouraged investigation into protein components of the core cell proliferative machinery as potential drivers of PKD pathogenesis. In this review, we examine the role of signaling by ERBB proteins and their effectors, with a primary focus on ADPKD. The ERBB family of receptor tyrosine kinases (EGFR/ERBB1, HER2/ERBB2, ERBB3, and ERBB4) are activated by extracellular ligands, inducing multiple pro-growth signaling cascades; among these, activation of signaling through the RAS GTPase, and the RAF, MEK1/2, and ERK1/2 kinases enhance cell proliferation and restrict apoptosis during renal tubuloepithelial cyst formation. Characteristics of PKD include overexpression and mislocalization of the ERBB receptors and ligands, leading to enhanced activation and increased activity of downstream signaling proteins. The altered regulation of ERBBs and their effectors in PKD is influenced by enhanced activity of SRC kinase, which is promoted by the loss of cytoplasmic Ca2+ and an increase in cAMP-dependent PKA kinase activity that stimulates CFTR, driving the secretory phenotype of ADPKD. We discuss the interplay between ERBB/SRC signaling, and polycystins and their depending signaling, with emphasis on thes changes that affect cell proliferation in cyst expansion, as well as the inflammation-associated fibrogenesis, which characterizes progressive disease. We summarize the current progress of preclinical and clinical trials directed at inhibiting this signaling axis, and discuss potential future strategies that may be productive for controlling PKD.

MicroRNAs downregulated following immune activation of rat testis.

PROBLEM: Little is known about how infection and the response to inflammation affect the microRNA (miRNA) profile of the male reproductive tract. We hypothesized that expression of inflammatory-related miRNAs would be altered following immune activation of rat testis. METHOD OF STUDY: Testis total RNA was purified from Sprague-Dawley rats 3 or 6 hours after receiving a 5 mg/kg intraperitoneal injection of bacterial lipopolysaccharide (LPS) and examined by qPCR using an 84-panel miRNA array. RESULTS: Five inflammatory-related miRNAs showed a greater than twofold downregulation (P<.05) in the 3-hour group (rno-let-7f-5p, rno-miR-200c-3p, rno-miR-23a-3p, rno-miR-23b-3p, rno-miR-98-5p) and five from the 6-hour group (rno-miR-17-5p, rno-miR-19a-3p, rno-miR-34a-5p, rno-miR-34c-5p, rno-miR-449a-5p). CONCLUSION: Review of the literature has revealed that these miRNAs also play important roles in the maintenance of fertility, formation and elimination of cancer, and development of the male reproductive tract. Further study will lead to a greater understanding of male reproductive immunology and related health issues.

H. Pylori in a gastric schwannoma: a case report.

Schwannomas are benign, often asymptomatic, slow-growing tumors that originate from Schwann cells of the neural sheath. Although H. Pylori has been associated with gastric adenocarcinoma, there has never been a recorded association with schwannoma formation. We present a 64-year-old woman who underwent a laparoscopic partial wedge gastrectomy for an incidentally discovered gastric mass. Histologic examination was consistent with schwannoma; however, chronic inflammation with microorganisms morphologically consistent with H. Pylori was also present. This case suggests the first recorded case of H. Pylori in an immunohistochemically confirmed gastric schwannoma.

The Impact of Radiation on an Unusual Case of Omental Epithelioid Angiosarcoma.

Epithelioid angiosarcoma is a rare high-grade tumor with irregular vascular morphology. We report an unusual case of intra-abdominal epithelioid angiosarcoma affecting the omentum and peritoneal surfaces resulting in significant hemorrhagic and inflammatory changes. As in other cases of this tumor this patient had previously undergone radiation treatment for a history of cervical cancer.