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Robotic-assisted thoracoscopic surgery (RATS), an evolution of minimally-invasive video-assisted thoracoscopic surgery (VATS), has recently emerged as the standard of care approach for pulmonary lobectomy for lung cancer. Despite increased upfront costs, RATS provides high-resolution, three-dimensional visualization of the operative field and enhanced instrument maneuverability with greater degrees of freedom. Several studies have demonstrated that RATS is non-inferior to VATS and may be associated with more complete mediastinal lymph node dissection and reduced risk of open conversion, length of stay, and intraoperative blood loss. In this chapter, we discuss the fundamental principles of robotic-assisted pulmonary lobectomy, indications and advantages of a robotic approach, and our operative technique.

Coronary artery disease requiring surgical revascularization is prevalent in United States Veterans. We aimed to investigate preoperative predictors of 30-day mortality following coronary artery bypass grafting (CABG) in the Veteran population. The Veterans Affairs Surgical Quality Improvement (VASQIP) national database was queried for isolated CABG cases between 2008 and 2018. The primary outcome was 30-day mortality. A multivariable logistic regression was performed to assess for independent predictors of the primary outcome. A P-value of0.05 was considered statistically significant. A total of 32,711 patients were included. The 30-day mortality rate was 1.37%. Multivariable analysis identified the following predictors of 30-day mortality: African-American race (OR 1.46, 95% CI 1.09-1.96); homelessness (OR 6.49, 95% CI 3.39-12.45); female sex (OR 2.15, 95% CI 1.08-4.30); preoperative myocardial infarction within 7 days (OR 1.49, 95% CI 1.06-2.10) or more than 7 days before CABG (OR 1.34, 95% CI 1.04-1.72); partially/fully dependent functional status (OR 1.44, 95% CI 1.07-1.93); chronic obstructive pulmonary disease (OR 1.54, 95% CI 1.24-1.92); mild (OR 1.48, 95% CI 1.04-2.11) and severe aortic stenosis (OR 2.06, 95% CI 1.37-3.09); moderate (OR 1.88, 95% CI 1.31-2.72), or severe (OR 2.99, 95% CI 1.71-5.22) mitral regurgitation; cardiomegaly (OR 1.73, 95% CI 1.35-2.22); NYHA Class III/IV heart failure (OR 2.05, 95% CI 1.10-3.83); and urgent/emergent operation (OR 1.42, 95% CI 1.08-1.87). The 30-day mortality rate in US Veterans undergoing isolated CABG between 2008 and 2018 was 1.37%. In addition to established clinical factors, African-American race and homelessness were independent demographic predictors of 30-day mortality.

Macrophage phenotype in the tumor microenvironment correlates with prognosis in NSCLC. Immunosuppressive macrophages promote tumor progression, whereas proinflammatory macrophages may drive an antitumor immune response. How individual NSCLCs affect macrophage phenotype is a major knowledge gap.To systematically study the impact of lung cancer cells on macrophage phenotypes, we developed an in vitro co-culture model that consisted of molecularly and clinically annotated patient-derived NSCLC lines, human cancer-associated fibroblasts, and murine macrophages. Induced macrophage phenotype was studied through quantitative real-time polymerase chain reaction and validated in vivo using NSCLC xenografts through quantitative immunohistochemistry and clinically with The Cancer Genome Atlas (TCGA)-"matched" patient tumors.A total of 72 NSCLC cell lines were studied. The most frequent highly induced macrophage-related gene was Arginase-1, reflecting an immunosuppressive M2-like phenotype. This was independent of multiple clinicopathologic factors, which also did not affect M2:M1 ratios in matched TCGA samples. In vivo, xenograft tumors established from high Arginase-1-inducing lines (ArgIn our in vitro co-culture model, a large panel of patient-derived NSCLC lines most frequently induced high-expression Arginase-1 in co-cultured mouse macrophages, independent of major clinicopathologic and oncogenotype-related factors. Arg

Gastric cancer is an aggressive solid-tumor malignancy with poor prognosis. The epidemiologic face of gastric cancer is changing and further insight into its heterogenous immunohistopathologic nature is needed to develop personalized therapies for specific patient populations. In this review, we highlight changes in gastric cancer epidemiology with a special emphasis on racial and ethnic variations and discuss the implications of current clinical and preclinical treatment advances.

Recent studies have identified a unique cancer-associated fibroblast (CAF) population termed antigen-presenting CAFs (apCAFs), characterized by the expression of major histocompatibility complex class II molecules, suggesting a function in regulating tumor immunity. Here, by integrating multiple single-cell RNA-sequencing studies and performing robust lineage-tracing assays, we find that apCAFs are derived from mesothelial cells. During pancreatic cancer progression, mesothelial cells form apCAFs by downregulating mesothelial features and gaining fibroblastic features, a process induced by interleukin-1 and transforming growth factor β. apCAFs directly ligate and induce naive CD4+ T cells into regulatory T cells (Tregs) in an antigen-specific manner. Moreover, treatment with an antibody targeting the mesothelial cell marker mesothelin can effectively inhibit mesothelial cell to apCAF transition and Treg formation induced by apCAFs. Taken together, our study elucidates how mesothelial cells may contribute to immune evasion in pancreatic cancer and provides insight on strategies to enhance cancer immune therapy. Citation Format: Huocong Huang, Zhaoning Wang, Yuqing Zhang, Rachana N. Pradhan, Debolina Ganguly, Raghav Chandra, Gilbert Murimwa, Steven Wright, Xiaowu Gu, Ravikanth Maddipati, Sören Müller, Shannon J. Turley, Rolf A. Brekken. Mesothelial cell-derived antigen-presenting cancer-associated fibroblasts induce expansion of regulatory T cells in pancreatic cancer [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer; 2022 Sep 13-16; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2022;82(22 Suppl):Abstract nr C078.

This chapter explores the pathogenesis, diagnosis, and treatment of infections of the gallbladder and bile ducts. Bacterial infections of the biliary tract range from simple biliary colonization to fulminant, life-threatening infections requiring prompt diagnosis and treatment. Acute cholecystitis is a common disorder that manifests as acute inflammation of the gallbladder. The pathogenesis of this disease involves obstruction of the cystic duct by an impacted gallstone at the gallbladder neck with resulting inflammation. Acute ascending cholangitis refers to inflammation and infection of the intra- and extrahepatic biliary tree. While bacterial infection secondary to an obstructed gallstone or stricture is the most common etiology, cholangitis can result from parasitic infections, autoimmune diseases, and chemical irritants. The pathogenesis of acute cholangitis involves a combination of factors including ductal obstruction, injury to the biliary epithelium, and the presence of bacteria in bile.

BACKGROUND Adult congenital heart disease (CHD) transplant recipients historically experienced worse survival early after transplantation. We aim to review updated trends in adult CHD transplantation. METHODS We performed a single center case series of adult cardiac transplants from January 2013 through July 2020. Outcomes of patients with CHD were compared to non-CHD. The primary outcome was overall survival. Secondary outcomes included a variety of post-operative complications. RESULTS 18/262 (7%) transplants were CHD recipients. CHD patients were younger with median age 41 (32-47) versus 58 (48-65) (P

Cardiac tumors are uncommon, and the vast majority of them are metastases from extracardiac sources. Metastatic spread to the heart causes symptoms by mechanical obstruction of circulation, direct myocardial invasion, or distal embolization. We herein report a case of a 58-year-old male who presented to the hospital with multilobar intracranial embolic infarcts who was found to have small cell lung cancer (SCLC) with invasion of the left atrium and pulmonary artery resulting in malignant embolic stroke. Cerebral tumor thromboembolism from SCLC is extremely rare. This case demonstrates the thromboembolic risk associated with metastatic endoluminal cardiac tumors. Cardiol Res. 2019;10(3):188-192 doi: https://doi.org/10.14740/cr752w

Recent studies have identified a unique cancer-associated fibroblast (CAF) population termed antigen-presenting CAFs (apCAFs), characterized by the expression of major histocompatibility complex class II molecules, suggesting a function in regulating tumor immunity. Here, by integrating multiple single-cell RNA-sequencing studies and performing robust lineage-tracing assays, we find that apCAFs are derived from mesothelial cells. During pancreatic cancer progression, mesothelial cells form apCAFs by downregulating mesothelial features and gaining fibroblastic features, a process induced by interleukin-1 and transforming growth factor β. apCAFs directly ligate and induce naive CD4

Background The plasticity of macrophage phenotype within the tumor microenvironment (TME) correlates with prognosis in non-small cell lung cancer (NSCLC).1 M2-like macrophages promote immunosuppression and facilitate tumor progression, while M1-like macrophages may drive an inflammatory antitumor immune response.2 Through a novel co-culture model comprised of cancer cells, cancer-associated fibroblasts (CAFs), and macrophages, we investigated whether NSCLC oncogenotype impacts macrophage phenotype and postulated that the immunosuppressive activity of macrophages is mediated through tumor-secreted soluble molecules. If identified and inhibited, these may re-sensitize cancer cells to immune surveillance and enhance antitumor immunity. Methods We developed an in vitro co-culture system (patient-derived NSCLC cells, human CAFs, and mouse macrophages) to interrogate impact of NSCLC cells and CAFs on macrophage phenotype. Expression of salient macrophage genes (i.e. ARG1, NOS2, IL-1β, IL-6, CHIL-3, SOCS3) was investigated through species-specific qPCR. Whole-genome RNA sequencing (RNAseq) in select cases was conducted and cytokine arrays measuring expression of 40 inflammatory cytokines were performed. Positive controls included stimulation of macrophages with LPS and IL-4. Results More than 70 NSCLC cell lines were characterized in the co-culture assay. Three highly reproducible clusters of macrophage phenotypes were identified: high Arginase (immunosuppressive), high IL-1β (inflammatory) and high SOCS3 (inflammatory, involved in JAK-STAT3 pathway) (figure 1).3 4 Major oncogenotypes (i.e. KRAS, TP53, STK11, EGFR, BRAF mutation) did not correlate with macrophage phenotype (figure 2). Analyses of differences between the 3 clusters is ongoing. 10 exemplar NSCLC lines representing each of these 3 clusters were selected for RNA sequencing (mouse genes) and cytokine array protein (human) profiling. Across all clusters, we found suppression of macrophage endocytosis pathways and activation of scavenger receptor A (SRA) signaling, reflecting an M2-like phenotype.5 We also observed increased expression of human IL-6, IL-8, and MCP1, which are implicated in suppression of innate immune sensing of tumor cells (figure 3). RNAseq of CAF lines demonstrated mixed inflammatory and myofibroblastic phenotypes (figure 4), with increased expression of genes associated with macrophage recruitment and activation including: IL-6, CSF-1, CXCL6, CCL2, and CCL7.6 Conclusions Through this novel co-culture model (figure 5), we demonstrate that patient-derived NSCLC cells reproducibly induce three major macrophage phenotypes in an oncotype-independent manner. Furthermore, cytokine release from NSCLC cells and CAFs is implicated in this process. This co-culture model provides a physiologically consistent experimental platform to identify tumor cell and CAF features that drive macrophage phenotype which may be suitable for targeted therapy. Acknowledgements We thank the McDermott Center Next-Generation Sequencing Core at UT Southwestern. Figure 5 was created with Biorender.com References Sumitomo R, Hirai T, Fujita M, et al. M2 tumor associated macrophages promote tumor progression in non small cell lung cancer. Exp Ther Med 2019 Dec 1;18(6):4490–8. Chen Y, Song Y, Du W, et al. Tumor-associated macrophages: an accomplice in solid tumor progression. J. Biomed. Sci 2019 Dec;26(1):1–3. Orecchioni M, Ghosheh Y, Pramod A, et al. Macrophage polarization: different gene signatures in M1 (LPS+) vs. classically and M2 (LPS–) vs. alternatively activated macrophages. Front. Immunol 2019 May 24;10:1084. Wilson HM. SOCS proteins in macrophage polarization and function. Front. Immunol 2014 Jul 28;5:357. Sun Y, Xu S. Tumor-associated CD204-positive macrophage is a prognostic marker in clinical stage I lung adenocarcinoma. Biomed Res. Int 2018 Jan 1;2018. O’Hayre M, Salanga C, Handel T, et al. Chemokines and cancer: migration, intracellular signalling and intercellular communication in the microenvironment. Biochem. J 2008 Feb 1;409(3):635–49

A woman with a history of congenital heart disease status post multiple valve operations including mitral valve repair presented with 2 months of low back pain and general malaise. Blood cultures returned positive for Gram-positive cocci. While transthoracic echocardiography did not identify vegetations, transoesophageal echocardiography visualised vegetations on the patient’s mitral valve, which had previously undergone repair with annuloplasty. The patient was found to have infectious endocarditis (IE), caused byGemella morbillorum. The patient was treated with over 6 weeks of intravenous antibiotics. Cases ofGemella-associated IE are rare and largely relegated to case reports. This report aims to contribute to the literature regarding this subject, and to further characterise the presentation and treatment ofGemella-associated IE. Additionally, this report emphasises the importance of maintaining a high suspicion of IE in a patient with non-specific malaise in the setting of prior cardiac valve operation.

Simple Summary Cancer-associated fibroblasts (CAFs) are key players in the tumor microenvironment. They are responsible for potentiating growth and metastasis through versatile functions, including maintenance of the extracellular matrix, blood vessel formation, modulation of tumor metabolism, suppression of antitumor immunity, and promotion of chemotherapy resistance. As such, CAFs are associated with poor prognosis and have emerged as a focus of anticancer research. In this review, we discuss the origins of CAFs, their heterogenous subtypes and their properties. We then detail the current state of preclinical and clinical research targeting CAF activities. We believe the limited efficacy of current cancer therapeutic approaches is driven by an incomplete understanding of CAF functions and by a nonstandardized CAF classification system. Therefore, we suggest a unified CAF classification based on specific functions to develop a new class of therapies that will focus on targeting the pro-tumorigenic properties of CAFs during tumor progression. Abstract Cancer-associated fibroblasts (CAFs) are indispensable architects of the tumor microenvironment. They perform the essential functions of extracellular matrix deposition, stromal remodeling, tumor vasculature modulation, modification of tumor metabolism, and participation in crosstalk between cancer and immune cells. In this review, we discuss our current understanding of the principal differences between normal fibroblasts and CAFs, the origin of CAFs, their functions, and ultimately, highlight the intimate connection of CAFs to virtually all of the hallmarks of cancer. We address the remarkable degree of functional diversity and phenotypic plasticity displayed by CAFs and strive to stratify CAF biology among different tumor types into practical functional groups. Finally, we summarize the status of recent and ongoing trials of CAF-directed therapies and contend that the paucity of trials resulting in Food and Drug Administration (FDA) approvals thus far is a consequence of the failure to identify targets exclusive of pro-tumorigenic CAF phenotypes that are mechanistically linked to specific CAF functions. We believe that the development of a unified CAF nomenclature, the standardization of functional assays to assess the loss-of-function of CAF properties, and the establishment of rigorous definitions of CAF subpopulations and their mechanistic functions in cancer progression will be crucial to fully realize the promise of CAF-targeted therapies.

Lung cancer (LC) is an aggressive malignancy with early metastatic spread and poor prognosis. Gastrointestinal metastases from primary LC are extremely rare with highly variable presentations. In this report, we review the case of a patient who presented with peritonitis secondary to perforated sigmoid mass as the first manifestation of metastatic squamous cell LC.

Background Intraabdominal hypertension (IAH) and abdominal compartment syndrome (ACS) are devastating complications of surgery. Patients who undergo complex ventral hernia repair (CVHR) may be at risk for IAH and ACS. Methods We performed a retrospective review of 175 patients who underwent CVHR by a single surgeon. Body mass index (BMI), prior hernia repair, operative time, bladder pressure, serum creatinine, sedation, paralytic therapy, and ventilator support were reviewed. Results IAH was identified in 33 patients; 11 patients developed ACS. Paralytic therapy was employed in 29 patients for an average of 1.4 days. Elevated BMI was independently associated with an increased risk of IAH (p = 0.006) and ACS (p = 0.02). Conclusion Patients who undergo CVHR are at risk of developing IAH and ACS in the postoperative period. Elevated BMI and longer operative time are independent risk factors for the development of IAH. IAH and ACS can be successfully managed with surgical critical care.

Simple Summary Colorectal cancer (CRC) is the third most common cancer worldwide. Metastasis to secondary organs, such as the liver and lungs, is a key driver of CRC-related mortality. The tumor microenvironment, which consists of the primary cancer cells, as well as associated support and immune cells, significantly affects the behavior of CRC cells at the primary tumor site, as well as in metastatic lesions. In this paper, we review the role of the individual components of the tumor microenvironment on tumor progression, immune evasion, and metastasis, and we discuss the implications of these components on antitumor therapies. Abstract Colorectal cancer (CRC) is the third most common malignancy and the second most common cause of cancer-related mortality worldwide. A total of 20% of CRC patients present with distant metastases, most frequently to the liver and lung. In the primary tumor, as well as at each metastatic site, the cellular components of the tumor microenvironment (TME) contribute to tumor engraftment and metastasis. These include immune cells (macrophages, neutrophils, T lymphocytes, and dendritic cells) and stromal cells (cancer-associated fibroblasts and endothelial cells). In this review, we highlight how the TME influences tumor progression and invasion at the primary site and its function in fostering metastatic niches in the liver and lungs. We also discuss emerging clinical strategies to target the CRC TME.

BackgroundActivation of the Wnt/ß-catenin pathway in non-small cell lung cancer (NSCLC) is associated with tumor growth and metastasis. Activation of this pathway in tumor cells may also modulate the immune tumor microenvironment (TME) by polarizing macrophages into an immunosuppressive M2-like phenotype. We tested whether treatment of co-cultures of human NSCLC cells, cancer-associated fibroblasts (CAFs) and macrophages with Tegavivint (Iterion Therapeutics), a novel compound that targets TBL1 to inhibit ß-catenin function that is in early-phase clinical trials, altered the phenotype of mouse macrophages in vitro.MethodsOur prior work testing a large panel of patient-derived NSCLC lines in co-cultures of CAFs and mouse bone marrow-derived macrophages (BMDMs) demonstrated that individual NSCLC lines reproducibly generated several macrophage phenotypes, one of which was immunosuppressive (high expression of Arginase-1). We prepared co-cultures of NSCLC cells (H1666 and H2009) (70%), human CAFs (25%) and mouse BMDMs (5%) and demonstrated conversion to the macrophage high Arginase-1 immunosuppressive phenotype by monitoring quantitative expression of mouse genes with qRT-PCR. Expression of ß-catenin protein relative to GAPDH by Western blot was determined before and after treatment with Tegavivint (10 and 20 nM). Co-cultures were treated with Tegavivint (10 nM) for 48 and 72 hours and qRT-PCR for mouse macrophage-specific genes reflecting an immunosuppressive M2-like or an inflammatory, immunostimulatory M1-like phenotype (Arginase-1 and iNos, respectively) was performed. Positive controls consisted of stimulation of macrophages with IL-4 and LPS (to generate M2-like and M1-like phenotypes, respectively). Cytotoxicity assays (MTS and crystal violet) to determine the IC50 of Tegavivint were performed on NSCLC and macrophage cells.ResultsTegavivint IC50 values for NSCLCs were 17–40 nM. At 10 nM, Tegavivint had no cytotoxic effect on macrophages. Treatment with Tegavivint decreased NSCLC expression of ß-catenin by ~30–40%. When co-cultures of NSCLCs, human CAFs, and mouse BMDMs were treated with 10 nM Tegavivint, we found that macrophage expression of Arginase-1 was significantly inhibited at 48 and 72 hours of treatment (figure 1).Abstract 919 Figure 1Tegavivint reduces Arginase-1 mRNA expression from macrophages co-cultured with CAFs and H1666 (A) and H2009 (B) patient-derived NSCLC cell lines after 72-hour treatment. *: pConclusionsTegavivint, at pharmacologically achievable doses and concentrations that have little or no cytotoxic effect on NSCLCs or macrophages, decreases tumor cell ß-catenin expression, and reduces the immunosuppressive macrophage phenotype (reduced macrophage Arginase-1 expression) induced by co-cultures of patient-derived NSCLCs and CAFs. These preclinical data set the stage for future clinical translation of Tegavivint as a NSCLC therapeutic in combination with immunotherapy approaches.AcknowledgementsSupported by P50 CA070907 and Physician-Scientist Institutional Award from the Burroughs Wellcome Fund (TARDIS Fellowship)

Introduction: Macrophages are key architects of the immune landscape in the tumor microenvironment (TME), and the plasticity of macrophage phenotype correlates with prognosis in non-small cell lung cancer (NSCLC). M2-like macrophages promote immunosuppression and facilitate tumor progression, while M1-like macrophages may drive an inflammatory antitumor immune response. We investigated if NSCLC oncogenotype impacts macrophage phenotype in a novel tumor cell, cancer-associated fibroblast (CAF) and macrophage co-culture model. We hypothesize that macrophage-mediated immunosuppression is driven in part through tumor-secreted signaling molecules that, if identified and blocked, may re-sensitize cancer cells to immune surveillance and enhance antitumor immunity. Methods: We developed an in vitro co-culture system (patient-derived NSCLC cells, human CAFs, and mouse macrophages) to interrogate impact of NSCLC cells and CAFs on macrophage phenotype. Through species specific qPCR we measured the expression salient macrophage genes (i.e. Arginase, NOS2, IL-1β, IL-6, CHIL-3, SOCS3) in the co-cultures. We also performed whole genome RNA sequencing (RNAseq) in select cases and evaluated protein expression using cytokine arrays measuring expression of 40 inflammatory cytokines. Positive controls included stimulation of macrophages with LPS and IL-4. Results: We characterized the effect of over 70 NSCLC cell lines in the co-culture assay. Three highly reproducible clusters of macrophage phenotypes were identified: high Arginase (immunosuppressive), high IL-1β (inflammatory) or high SOCS3 (inflammatory, involved in JAK-STAT3 pathway). Major NSCLC oncogenotypes (i.e. KRAS, TP53, STK11, EGFR, BRAF mutation) did not correlate with macrophage phenotype. Analyses of differences between the 3 clusters is ongoing. We selected 10 exemplar NSCLC lines representing each of these 3 clusters for RNA sequencing (mouse genes) and cytokine array protein (human) profiling. Across all clusters, we found suppression of macrophage endocytosis pathways and activation of scavenger receptor A (SRA) signaling (M2-like phenotype) and increased expression of human IL-6, IL-8, and MCP1, which are implicated in suppression of innate immune sensing of tumor cells. RNAseq of CAF lines demonstrated mixed inflammatory and fibroblastic phenotype, with increased expression of genes associated with macrophage recruitment and activation including: IL-6, CSF-1, CXCL6, CCL2, and CCL7. Conclusions: We demonstrate in a novel co-culture model that patient-derived NSCLC cells reproducibly induce three major macrophage phenotypes. Cytokine release from NSCLC cells and CAFs are implicated in this process. This co-culture model provides a robust, physiologically consistent experimental platform to identify tumor cell and CAF features that drive macrophage phenotype. Citation Format: Josiah Flaming, Raghav Chandra, Luc Girard, Debolina Ganguly, Jason Toombs, John D. Minna, Rolf A. Brekken. Lung cancer cells and cancer-associated fibroblasts drive macrophage polarization in a co-culture model [abstract]. In: Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; 2020 Oct 19-20. Philadelphia (PA): AACR; Cancer Immunol Res 2021;9(2 Suppl):Abstract nr PO021.

Pediatric short bowel syndrome (SBS) is a serious condition which occurs in children with congenital or acquired reduction in length of the small intestine. SBS results in excessive fluid loss, nutrient malabsorption, electrolyte abnormalities, increased susceptibility to infections, parenteral nutrition associated complications and affects weight gain and growth. In children, SBS is debilitating and uniformly fatal without treatment. The primary goal of treatment is to restore enteral autonomy and reduce long-term dependence on parenteral support by increasing the absorptive potential of the remnant intestine. In this review, the medical and surgical management of SBS including pharmacologic agents, parenteral nutrition, dietary strategies, surgical lengthening procedures, and small bowel transplant will be discussed.

Previous studies showed that patients (pts) with atrial fibrillation (AF) who undergo surgical left atrial appendage occlusion (LAAO) concurrently with other cardiac surgery have reduced long-term risk for mortality and stroke. We aimed to study the hospital outcomes of concurrent surgical LAAO and

Palatal tremor (previously called palatal myoclonus) is an extremely rare movement disorder characterised by involuntary, rhythmic contractions of the palatal muscles. Due to its rarity, this cryptic neurological finding is practically challenging to discover, and often missed by clinicians unless specifically looked for during physical examination. Palatal tremor was first described by Politzer in 1862. Its prevalence data are lacking in the literature, with only a few hundred cases reported. The most notable pathological change is hypertrophic degeneration of the inferior olivary nuclei, which are presumed to be the pacemaker of symptomatic palatal tremor. The rhythmic inferior olivary activity is transmitted to the brainstem reticular centres controlling bulbar and limb functions.1 Two forms of palatal tremor have been described: essential and symptomatic. The aetiology of essential palatal …

We have previously reported the association of hyperglycemia and mortality after ischemic stroke. This study attempts to answer the hypothesis, if hyperglycemia at arrival, is associated with early mortality and functional outcome in patients with acute non-traumatic intracerebral hemorrhage (ICH). The study cohort consisted of 237 patients who presented to the ED with ICH and had blood glucose measured on ED presentation. The presence of hyperglycemia on presentation was correlated with outcome measures including volume of hematoma, intraventricular extension of hematoma (IVE), stroke severity, functional outcome at discharge, and date of death. Of the cohort of 237 patients, a total of 47 patients had prior history of Diabetes Mellitus (DM). Median blood glucose at presentation was 140 mg/dl (Inter-quartile range 112–181 mg/dl). DM patients had higher glucose levels on arrival (median 202 mg/dl for DM vs. 132.5 mg/dl for non-DM, P

Cystic swellings of the neck in children have limited differential diagnoses, often either lymphatic or vascular malformations. Other cystic inflammations can be the result of tuberculous abscesses, suppurated lymph nodes and actinomycosis. Microfilaria causing lmphadenovarix of head-neck region has not yet been described in the literature. A 10-year-old Indian boy presented with an asymptomatic cystic neck mass of 8 months duration. Aspiration of the swelling demonstrated numerous Wuchereria bancrofti microfilaria and the patient responded well to 6 weeks of daily anti-filarial treatment using diethylcarbamazine citrate (6mg kg(-1) day(-1)). This appears to be the first report of microfilariae-associated lymphadenovarix of head-neck region. Though rare, filariasis should be considered as a differential diagnosis for aberrant swellings where lymphatic filarids are endemic.