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CNS small vessel disease (CSVD) causes 25% of strokes and contributes to 45% of dementia cases. Prevalence increases with age, affecting about 5% of people aged 50 years to almost 100% of people older than 90 years. Known causes and risk factors include age, hypertension, branch atheromatous disease, cerebral amyloid angiopathy, radiation exposure, immune-mediated vasculitides, certain infections, and several genetic diseases. CSVD can be asymptomatic; however, depending on location, lesions can cause mild cognitive dysfunction, dementia, mood disorders, motor and gait dysfunction, and urinary incontinence. CSVD is diagnosed on the basis of brain imaging biomarkers, including recent small subcortical infarcts, white matter hyperintensities, lacunes, cerebral microbleeds, enlarged perivascular spaces, and cerebral atrophy. Advanced imaging modalities can detect signs of disease even earlier than current standard imaging techniques. Diffusion tensor imaging can identify altered white matter connectivity, and blood oxygenation level-dependent imaging can identify decreased vascular reactivity. Pathogenesis is thought to begin with an etiologically specific insult, with or without genetic predisposition, which results in dysfunction of the neurovascular unit. Uncertainties regarding pathogenesis have delayed development of effective treatment. The most widely accepted approach to treatment is to intensively control well-established vascular risk factors, of which hypertension is the most important. With better understanding of pathogenesis, specific therapies may emerge. Early identification of pathologic characteristics with advanced imaging provides an opportunity to forestall progression before emergence of symptoms.

Synesthesia literally means a "union of the senses" whereby two or more of the five senses that are normally experienced separately are involuntarily and automatically joined together in experience (1, 2, 3). For example, some synesthetes experience a color when they hear a sound, although many instances of synesthesia also occur entirely within the visual sense. In this paper, I first mainly engage critically with Sollberger's view that there is reason to think that at least some synesthetic experiences can be viewed as truly veridical perceptions, and not as illusions or hallucinations (4). Among other things, I explore the possibility that many forms of synesthesia can be understood as experiencing what I will call "second-order secondary properties," that is, experiences of properties of objects induced by the secondary qualities of those objects. In doing so, I shed some light on why synesthesia is typically one-directional and its relation to some psychopathologies such as autism.

The cholinergic heat-labile neurotoxin produced by Clostridium species is primarily responsible for the clinical manifestations of botulism. The classic phenotypic presentation of botulism consists of subacute descending flaccid paralysis with intact sensory function. Traditionally, it is classified into 3 main forms (foodborne, wound-related, and infantile) on the basis of primary site of toxin entry into the human nervous system. Toxemia is the common pathophysiology in all forms of botulism. Adult intestinal toxemia botulism is an extremely rare form of the disease with pathogenesis similar to that of infant-type botulism. Symptomatic adults usually have an anatomic abnormality in the gastrointestinal tract leading to changes in normal gut flora. The current case is an addition to the growing literature on this unusual clinical variant of botulism.

Partial ornithine transcarbamylase deficiency (pOTCD), an enzymatic defect within the urea cycle, is an increasingly recognized etiology for hyperammonemia of unclear source following a stressor within female adults. Here we present a case of newly diagnosed pOTCD following a systemic stressor and prolonged hospitalization course. From a neurological perspective, prompt recognition provided the patient with a swift and near complete recovery. We briefly review the pertinent literature pertaining to this genetically based condition including historical context and current therapeutic approaches. Given the potential morbidity of prolonged hyperammonemia, neurohospitalists need to be aware of partial ornithine transcarbamylase as an entity.

The lapatinib–taxane combination led to shorter PFS than trastuzumab–taxane in HER2+ metastatic breast cancer. We investigated the prognostic and predictive effects of pretreatment serum HER2, CAIX, and TIMP-1. MA.31 accrued 652 patients; 537 (82%) were centrally confirmed HER2+. Biomarkers were categorized for univariate and multivariable predictive investigations with a median cut-point, ULN cut-points (15 ng/ml for HER2; 506 pg/ml for CAIX; 454 pg/ml for TIMP-1), and custom cut-points (30 and 100 ng/ml for HER2). Stratified step-wise forward Cox multivariable analysis examined continuous and categorical effects of biomarkers on PFS in the ITT and central HER2+ populations; central HER2+ biomarker results are shown. Serum was banked for 472 (72%) of 652 patients. Higher serum HER2 (>median; >15; >30; or >100 ng/ml; p = 0.05–0.002); higher CAIX (>median; >506 pg/ml; p = 0.02; p = 0.001); and higher TIMP-1 (> median; > 454 pg/ml; p = 0.001; p = 0.02) had shorter univariate PFS. In multivariable analysis, higher continuous TIMP-1 was associated with significantly shorter PFS: HR = 1.001 (95% CI = 1.00–01.002; p = 0.004). Continuous serum HER2 and CAIX were not significantly associated with PFS. HER2 of 15 ng/ml or higher had shorter PFS (p = 0.02); higher categorical CAIX had shorter PFS (p = 0.01–0.08). Interaction terms of HER2, CAIX, and TIMP-1 with treatment were not significant; the predictive test power was low. Higher levels of serum TIMP-1, CAIX, and HER2 were significant prognostic biomarkers of shorter PFS. We found no significant interaction between serum biomarkers and response to lapatinib versus trastuzumab. Evaluation of TIMP-1 and CAIX-targeted therapy in addition to HER2-targeted therapy appears warranted in patients with elevated serum levels of these biomarkers.

Introduction: Left atrial enlargement (LAE) is associated with atrial fibrillation, a frequent cause of large vessel occlusion (LVO) leading to ischemic stroke. Leptomeningeal collaterals protect tissue from ischemia, but the association between collaterals and structural heart disease is not well described. We aim to investigate the association between LAE and cerebral collaterals during acute LVO when microvasculature, vasodilation, and chronotropic competence are critically important. Hypothesis: Left atrial enlargement is associated with poor collaterals. Methods: We reviewed consecutive patients presenting with middle cerebral and internal carotid LVO who underwent thrombectomy from 2012 to 2017. Patients with CT angiogram of the head and echocardiogram were included. Poor collaterals were defined as ≤ 50% filling on CT angiogram. LAE was defined as left atrial volume index ≥ 35 mL/m 2 . Multivariate logistic regression analysis was performed to evaluate the relationship between LAE and poor collaterals with adjustment for age and hypertension. Results: There were 128 eligible patients. The mean age was 68± 15 years, median NIHSS was 17, and 51 (39.8%) had LAE. Baseline characteristics are described in the table. Poor collaterals were observed in 50 (39%) patients. Patients with LAE were more likely to have poor collaterals compared to those with normal left atrial size (52.9% vs. 29.9%, p=0.009). After adjusting for age and hypertension, a trend towards association remained (OR 2.00, p=0.089). Conclusion: Our results indicate that patients with LVO and LAE were more likely to have poor collaterals. Further research is warranted to determine the cause of the association. One possibility is shared pathophysiology affecting both cardiac and cerebral vasculature such as microvascular disease or endothelial dysfunction. Alternatively, structural heart disease causing chronotropic incompetence may lead to poor collateral filling.

Background: In the phase 3 BFORE trial (NCT02130557), treatment with bosutinib resulted in a significantly higher major molecular response rate at 12months versus imatinib in the modified intent-to-treat (mITT) population of patients with newly diagnosed chronic phase chronic myeloid leukemia (CP CML). Assessment of patient-reported outcomes (PROs) was an exploratory objective. Methods: Patients with newly diagnosed CP CML were randomized 1:1 to receive once-daily bosutinib 400mg or imatinib 400mg as first-line therapy. Patients completed the Functional Assessment of Cancer Therapy-Leukemia (FACT-Leu) and EuroQoL-5 Dimensions (EQ-5D) questionnaires at baseline, every 3 months for the first 24 months of treatment, every 6 months thereafter, and at treatment completion. We report PRO results at month 12 in the mITT population (bosutinib: n = 246; imatinib: n = 241). Results: Mean FACT-Leu combined and subscale scores were similar at baseline in the bosutinib and imatinib arms; at month 12, all scores demonstrated improvement or maintenance of health-related quality of life (HRQoL) in both treatment arms. Repeated-measures mixed-effects models showed no significant difference between bosutinib and imatinib for any FACT-Leu score. Functional health status, as measured by EQ-5D, also demonstrated improvement or maintenance with bosutinib and imatinib at month 12. Conclusions: Similar improvements in PROs compared with baseline were seen after 12 months of treatment with first-line bosutinib or imatinib in the BFORE trial. Newly diagnosed patients with CP CML receiving bosutinib or imatinib can preserve or improve HRQoL during treatment, although clinical efficacy was superior with bosutinib

This review highlights current management of patients with concomitant cerebral amyloid angiopathy (CAA) and atrial fibrillation (AF). We review quantifying risk of ischemic and hemorrhagic stroke as well as treatments to minimize future risk. Ischemic stroke risk in AF can be quantified by CHA2DS2-VASc and assessing left atrial echocardiographic characteristics. Patients deemed not low risk by CHA2DS2-VASC should be anticoagulated. CAA increases intracranial hemorrhage risk. CAA biomarkers include cortical microbleeds (CMBs), cortical superficial siderosis (cSS), convexal subarachnoid hemorrhage (cSAH), and lobar intracerebral hemorrhage (ICH). CAA with prior lobar ICH has an annual recurrence rate of 8.9%. CAA with cSAH carries an even higher annual lobar ICH risk of 19%. CMBs are associated with a dose-dependent risk of ICH, which rises with OACs. In patients with AF, antithrombotics should be avoided in CAA with predominant ICH, cSS, or cSAH features. Those with ≥ 2 CMB require in-depth risk-benefit analysis using a multidisciplinary approach.

This chapter reviews the interdisciplinary field sometimes called "philosophical ­psychopathology", which is also related to "philosophy of psychiatry". It focuses on various psychopathologies with special attention to how they negatively impact and distort conscious experience, such as amnesia, somatoparaphrenia, schizophrenia, visual agnosia, autism, and Dissociative Identity Disorder (DID). The chapter discusses "philosophy of psychiatry", covering the overlapping topics of psychopathy, mental illness, and moral responsibility. It summarizes a number of disorders that challenge our notion of personal identity and self. Many of these disorders forced authors to discuss the importantly related philosophical problems of personal identity, the unity of consciousness, and free will and moral responsibility. It is worth mentioning one important launching point for some related work in abnormal psychology and psychopathology, namely, the discovery of "blindsight", which is very frequently discussed in the philosophical literature regarding its implications for consciousness and unconscious visual processing.

Salmonella infection commonly occurs in the gastrointestinal tract secondary to fecal-oral transmission of the bacterium. Extraintestinal Salmonella is typically seen in the biliary system and is very rarely observed in the thoracic cavity. Salmonella infection in the thymus is an even more unusual presentation of extraintestinal Salmonella, with only one previous case reported in the literature. Thymic abscesses are already a rare clinical entity and have been reported to result from infection with Staphylococcus aureus. We report a case of a 59-year-old man with a non-typhoidal Salmonella infection of a large symptomatic thymoma that was treated with surgical drainage and antibiotic therapy.

Bosutinib is a Src/Abl tyrosine kinase inhibitor indicated for adults with newly-diagnosed Philadelphia positive chronic myeloid leukemia or with resistant/intolerant disease. We report the final results of a phase I/II study of second-line bosutinib in chronic phase chronic myeloid leukemia patients after imatinib failure (n=284). Median follow up and treatment durations were 54.8 (range 0.6-96.3) and 25.6 (0.2-96.3) months, respectively. At years 2 and 5, 54% and 40% of patients, respectively, remained on bosutinib. Cumulative major cytogenetic response and complete cytogenetic response rates (newly-attained or maintained from baseline) were 58% and 46%, respectively, by year 2 and 60% and 50% by year 5. Kaplan-Meier probability of maintaining major and complete cytogenetic response was 76% and 78%, respectively, at year 2 and 71% and 69% at year 5. Cumulative incidence of on-treatment disease progression/death was similar at years 5 (19%) and 2 (15%); Kaplan-Meier overall survival was 91% at year 2 and 84% at year 5. Of 169 patients who had discontinued bosutinib by year 5, 38 did so after year 2, most commonly for disease progression (n=11). Most adverse events initially occurred within two years. Overall, gastrointestinal events were the most common (diarrhea 86%, nausea 46%, vomiting 37%); the most common grade 3/4 toxicity was thrombocytopenia (25%). None of the 4 on-treatment deaths in years 3-5 were related to bosutinib. Bosutinib demonstrated durable efficacy and manageable toxicity through year 5 confirming its importance in the treatment of chronic phase chronic myeloid leukemia patients resistant/intolerant to prior imatinib. This trial was registered at clinicaltrials.gov identifier: 00261846.

Hospitals often have limited ability to obtain primary clinical data from electronic health records to use in assessing quality and safety. We outline a new model that uses administrative data to gauge the safety of care at the hospital level. The model is based on a set of highly undesirable events (HUEs) defined using administrative data and can be customized to address the priorities and needs of different users. Patients with HUEs were identified using discharge abstracts from July 1, 2008 through June 30, 2010. Diagnoses were classified as HUEs based on the associated present-on-admission status. The 2-year study population comprised more than 6.5 million discharges from 161 hospitals. The proportion of hospitalizations including at least one HUE during the 24-month study period varied greatly among hospitals, with a mean of 7.74% (SD 2.3%) and a range of 13.32% (max, 15.31%; min, 1.99%). The whole-patient measure of safety provides a global measure to use in assessing hospitals with the patient's entire care experience in mind. As administrative and clinical datasets become more consistent, it becomes possible to use administrative data to compare the rates of HUEs across organizations and to identify opportunities for improvement.

An extracardiac Fontan operation through a right thoracotomy incision is an alternative approach in children who have an ascending aorta that is in close proximity to the sternum, as in aortic atresia or transposed great vessels, and in those who have had prior mediastinitis.

Limb-shaking transient ischemic attacks (LSTIAs) are a phenomenon that occurs due to transient hypoperfusion to a cerebral motor territory with a chronically outstripped autoregulatory vascular reserve. First described in 1962 by Miller Fisher, the pathogenesis and the global understanding of this presentation have undergone a significant advancement throughout the years. Typically, patients will present with this syndrome of transient hypoperfusion in the context of extracranial carotid intrinsic vessel stenosis or by intracranial vascular stenosis to select motor pathways. We present within this case report a novel mechanism by which LSTIAs may emerge. Through this knowledge, clinicians may need to consider expansion of their diagnostic breadth to include proximal vasculature luminal integrity.

Summary Background: Myxomas arising from the eustachian valve are exceedingly rare. Case Report: A 72-year-old Jamaican- Chinese woman was evaluated for worsening dyspnea. The 2-dimensional and real time 3-dimensional transesophageal echocardiogram showed a 75 mm length × 44 mm width, multilobulated, mobile mass arising from the eustachian valve occupying the entire right atri -al and right ventricular cavities extending into the coronary sinus, right ventricular outflow tract, and proximal inferior vena cava. The patient underwent successful resection of the mass and re-placement of the tricuspid valve. Histopathologic examination confirmed the diagnosis of atrial myxoma. Conclusions: This is the largest myxoma found on a Eustachian valve. key words: myxoma • eustachian valve • right atrial myxoma Full-text PDF: http://www.amjcaserep.com/fulltxt.php?ICID=882593 Word count: 830 Tables: — Figures: 4 References: 15 Author’s address: Wilbert S. Aronow, Cardiology Division, New York Medical College, Macy Pavilion, Room 138, Valhalla, NY 10595, U.S.A., e-mail: wsaronow@aol.com

A 46-year-old previously healthy man presented with 1 week of headache, nausea, vomiting and dizziness. He was found to have cranial nerve deficits, his cerebrospinal fluid (CSF) demonstrated a lymphocytic pleocytosis and brain MRI suggested rhombencephalitis. Although Gram stains and cultures of his CSF did not identify a pathogen, Listeria monocytogenes DNA was detected by the FilmArray Meningitis/Encephalitis panel within 2 hours of performing a lumbar puncture. He was treated with ampicillin and gentamicin and had a near-complete recovery. This case highlights the importance of recognising L. monocytogenes infection as a cause of acute cranial nerve impairment with MRI findings suggestive of brainstem encephalitis. It also highlights the frequently atypical CSF profile and low yield of culture in L. monocytogenes rhombencephalitis and the value of multiplex PCR testing of CSF to rapidly identify this pathogen and permit targeted therapy.

Polymorphisms in the transcription factor IFN regulatory factor 5 (IRF5) are strongly associated in human genetic studies with an increased risk of developing the autoimmune disease systemic lupus erythematosus. However, the biological role of IRF5 in lupus pathogenesis has not previously been tested in an animal model. In this study, we show that IRF5 is absolutely required for disease development in the FcγRIIB−/−Yaa and FcγRIIB−/− lupus models. In contrast to IRF5-sufficient FcγRIIB−/−Yaa mice, IRF5-deficient FcγRIIB−/−Yaa mice do not develop lupus manifestations and have a phenotype comparable to wild-type mice. Strikingly, full expression of IRF5 is required for the development of autoimmunity, as IRF5 heterozygotes had dramatically reduced disease. One effect of IRF5 is to induce the production of the type I IFN, IFN-α, a cytokine implicated in lupus pathogenesis. To address the mechanism by which IRF5 promotes disease, we evaluated FcγRIIB−/−Yaa mice lacking the type I IFN receptor subunit 1. Unlike the IRF5-deficient and IRF5-heterozygous FcγRIIB−/−Yaa mice, type I IFN receptor subunit 1-deficient FcγRIIB−/−Yaa mice maintained a substantial level of residual disease. Furthermore, in FcγRIIB−/− mice lacking Yaa, IRF5-deficiency also markedly reduced disease manifestations, indicating that the beneficial effects of IRF5 deficiency in FcγRIIB−/−Yaa mice are not due only to inhibition of the enhanced TLR7 signaling associated with the Yaa mutation. Overall, we demonstrate that IRF5 plays an essential role in lupus pathogenesis in murine models and that this is mediated through pathways beyond that of type I IFN production.

Purpose. A case of elevated creatine phosphokinase (CPK) levels associated with linezolid therapy in a patient on chronic antihyperlipidemic therapy is presented. Summary. A 79-year-old Caucasian man with a primary diagnosis of acute hemoptysis secondary to pneumonia was admitted to the medical–surgical intensive care unit. A chest radiograph showed a large, right, lower-lobe infiltrate with alveolar consolidation. The patient’s medical history included hyperlipidemia that was chronically treated with lovastatin and gemfibrozil. Methicillin-resistant Staphylococcus aureus (MRSA) pneumonia was suspected and confirmed. Vancomycin 1 g i.v. every 12 hours was administered for approximately 10 days into the admission and switched to linezolid 600 mg i.v. every 12 hours after a lack of response to vancomycin. On hospital day 11, the patient’s CPK concentration was 47 units/L. Seven days later, his CPK concentration was 2584 units/L and his lovastatin and gemfibrozil were discontinued on that day. The patient’s CPK concentration peaked at 5369 units/L on the following day, and linezolid was discontinued at that point. One week later, his CPK concentration was 28 units/L. Approximately two weeks after the patient’s CPK levels normalized, he developed numerous complications. The patient died as a result of respiratory failure 11 days after being extubated, which occurred about 38 days after his admission. Although concomitant use of statins and gemfibrozil is known to increase the risk for CPK elevations, the continued rise in CPK levels after discontinuation of antihyperlipidemic therapy and the rapid time course for normalization after linezolid discontinuation are more consistent with an event associated with linezolid initiation. Conclusion. A patient on chronic antihyperlipidemic therapy developed elevated CPK levels after receiving linezolid for the treatment of MRSA pneumonia.

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease that is characterized by autoantibody production and inflammatory disease involving multiple organs. Premature atherosclerosis is a common complication of SLE and results in substantial morbidity and mortality from cardiovascular disease (CVD). The reasons for the premature atherosclerosis in SLE are incompletely understood, although chronic inflammation is thought to play an important role. There is currently no known preventative treatment of premature atherosclerosis in SLE. Mycophenolate mofetil (MMF) is an immunosuppressive agent that is commonly used for treatment of patients with SLE. In order to study the impact of this drug on murine lupus disease including premature atherosclerosis development, we treated gld.apoE(-/-) mice, a model of SLE and accelerated atherosclerosis, with MMF. We maintained seven-week old gld.apoE(-/-) mice on a high cholesterol Western diet with or without MMF. After 12 weeks on diet, mice receiving MMF showed decreased atherosclerotic lesion area compared to the control group. MMF treatment also improved the lupus phenotype, indicated by a significant decrease circulating autoantibody levels and ameliorating lupus nephritis associated with this model. This data suggests that the effects of MMF on the immune system may not only be beneficial for lupus, but also for inflammation driving lupus-associated atherosclerosis.

My aim in this paper is to show that consciousness entails self‐consciousness by focusing on the relationship between consciousness and memory. More specifically, I addreess the following questions: (1) does consciousness require episodic memory?; and (2) does episodic memory require self‐consciousness? With the aid of some Kantian considerations and recent empirical data, it is argued that consciousness does require episodic memory. This is done after defining episodic memory and distinguishing it from other types of memory. An affirmative answer to (2) is also warranted especially in the light of the issues raised in answering (1). I claim that ‘consciousness entails self‐consciousness’ is thereby shown via the route through episodic memory, i.e. via affirmative answers to (1) and (2). My aim is to revive this Kantian thesis and to bring together current psychological research on amnesia with traditional philosophical perspectives on consciousness and memory.

Government-mandated reporting of health care-associated infections (HAIs) and new reimbursement regulations place a premium on accurate and reliable detection of HAIs. This commentary addresses the challenges and opportunities of having consistent, well-defined, and continuous methods in place to ensure the reliability and validity of HAI detection and reporting. In addition, such procedures could support the development and expertise of infection preventionists. A Web-based clinical vignette model is suggested for improving HAI reporting for hospitals participating in the Centers for Disease Control and Prevention's National Healthcare Safety Network.

Background: Management of malignant renal tumors involving the inferior vena cava (IVC) depends on tumor extension within the cava. Methods: Of 295 patients treated for renal cancer, propagation of tumor mass through the renal vein to IVC was seen in 22 (7%) patients. Cephalad extension of the tumor was suprarenal: infrahepatic in 12, retrohepatic in 6, and within the right atrium in 4 patients. All patients had radical nephrectomy, cavotomy, and complete resection of tumors except 1 with diffuse peritoneal metastasis. Results: Twenty-one patients had curative resections. No operative deaths and no instances of pulmonary embolism or exsanguination occurred. Seventeen patients were alive at 2 years and 12 at 5 years, resulting in 77% and 55% survival rates, respectively. Conclusions: An aggressive approach for vena cava involvement from malignant renal neoplasms resulted in prevention of tumor embolus, minimization of blood loss, and maintenance of venous return to the heart.

We argue that analyzing everyday memory failures in terms of the "unity of consciousness" can elucidate the bases of such failures. A perfect unity amongst one's mental states is rare. In extreme cases the unity of consciousness can breakdown in dramatic fashion (e.g., in Dissociative Identity Disorder), but such breakdowns also occur in less dramatic ways that affect us in everyday life. For example, disruptions in the unity of consciousness can result in everyday memory failures, such as forgetting to put on a tie for an important formal meeting. After providing some philosophical background into the notions of "unity of consciousness" and "functionalism," we offer preliminary analyses of three examples of everyday memory failure. We then introduce and develop what we call the "unity model" of memory failure and show how it explains the examples. We also describe different ways that unity can break down which, in turn, can lead to memory failure and inappropriate behavior. We then show how slips of action and other kinds of cognitive failures (e.g., memory blocks) differ from everyday memory failures. Finally, we examine alternative models (e.g., Absentmindedness and Multimodal) arguing that the unity model is preferable, and then show how our model is consistent with some experimental results.

Background Inadequate data exist regarding the management of acute major pulmonary embolism. Various modalities that are used, including thrombolytics and embolectomy, have not been shown to conclusively improve mortality when compared to heparin. In the past, open pulmonary embolectomy was reserved for patients with severe hemodynamic instability because of its high mortality rate. Our objective was to analyze our experience with early embolectomy as an alternative for the treatment of major pulmonary embolism. Methods A retrospective review of charts of all patients undergoing pulmonary embolectomy at our institution over the last two years was performed. Patients were followed until their discharge from hospital. Results There were 13 patients (7 women and 6 men). Four had massive and 9 had submassive pulmonary embolism. There was one mortality. Postoperative echocardiography showed no evidence of pulmonary hypertension in 7. Conclusions Open pulmonary embolectomy can be performed in patients with major pulmonary embolism with minimal mortality and morbidity. It may prevent the development of chronic thromboembolic pulmonary hypertension and should be a part of the algorithm in the treatment of major pulmonary embolism.

Pseudoaneurysms in the ascending aorta most commonly occur as a complication of surgical procedures at this site. They have also been reported in association with trauma, infection, aortitis, and other disorders. Pseudoaneurysm formation in the descending aorta or arch may occur as a result of penetrating ulcers in the presence of severe atherosclerotic plaque. Pseudoaneurysm as a result of atherosclerotic disease has only rarely been noted in the ascending aorta, where complex plaque is less common. We report here the finding with transesophageal echocardiography of a pseudoaneurysm in the ascending aorta as a result of atherosclerotic disease and penetrating ulcer.

A 70-year-old man, who had undergone a radical nephrectomy for localized renal cell carcinoma (RCC) three years ago, was recently evaluated for shortness of breath. During his work-up, a transesophageal echocardiogram and magnetic resonance imaging indicated an extensive vena caval thrombus originating from the renal vein stump. Successful vena caval thrombectomy with cardiopulmonary bypass confirmed that the thrombus was comprised of RCC. This is a rare type of RCC recurrence with an unusual timing (3 years after a nephrectomy), alerting the importance of strict follow-up on all patients even after complete surgical excision of all suspected tumors.

Cavernous hemangioma is a rare tumor with infrequent cardiac involvement. Preoperative or antemortem diagnosis may be difficult. Several prior case reports have described echocardiographic findings of cavernous hemangioma. We report here a 50-year-old white female patient with this tumor. Transesophageal echocardiography detected a mass with an echocardiographic appearance not previously described for cavernous hemangioma. The tumor appeared as a large echolucent unilocular cystic mass, leading to an erroneous preoperative diagnosis of pericardial cyst. This previously unreported finding should be recognized by echocardiographers in the evaluation of cardiac masses. (J Am Soc Echocardiogr 1997;10:579-81.)

Delftia acidovorans (Comamonas acidovorans) is an aerobic, non-fastidious, non-fermentative gram-negative bacillus classified in the Pseudomonas rRNA homology group III that is generally regarded as an environmental organism found in soil and water and as a non-pathogen. We report the first case of systemic D. acidovorans infection in a patient without a long-term immunosuppressive condition where D. acidovorans has been recovered in pure culture as a primary pathogen.

As survival improves in patients with sickle cell anemia, the prospects of performing cardiac surgical procedures on older patients with this genetic defect increase. We describe the successful management of a 52-year-old patient with sickle cell disease (homozygous for hemoglobin S) and a history of multiple sickle crisis undergoing cardiopulmonary bypass for mitral valve repair. Preoperative partial exchange transfusion followed by total exchange transfusion at the time of operation was performed to reduce the level of hemoglobin S to 5.4% during bypass. Other management strategies included high-flow normothermic bypass with aortic crossclamping, topical hypothermia, and cold crystalloid cardioplegia.

The integration of the diagnostic and treatment skills of both the orthodontist and the maxillofacial surgeon has become a standard procedure in the treatment of severe dentofacial dysplasias. Orthognathic surgery, surgery without prior tooth movement, is being replaced by an interdisciplinary approach as the treatment of choice. When a proper tooth-to-denture-base relationship is obtained, an ideal maxillomandibular relationship can be achieved surgically. The quadrilateral analysis enables the practitioner to obtain an individualized skeletal, dental, and soft-tissue assessment of each patient requiring treatment. It determines the direction and extent of the skeletal dysplasia in millimeter measurements and allows the clinician to outline the appropriate surgical orthodontic procedures. The quadrilateral analysis indicates that in a balanced facial pattern a 1:1 ratio exists between the maxillary bony base length (Max.Lth.) and the mandibular bony base length (Mand.Lth.); also that the average of the anterior lower facial height (ALFH) and the posterior lower facial height (PLFH) equals these bony base lengths. Simply stated, the Max.Lth. = Mand.Lth. = (formula; see text) An accurate diagnosis locates the area and quantifies the magnitude of skeletal dysplasia. Then the correct placement of a dentition within the denture bases and the appropriate surgery in the area of dysplasia can produce an individualized, balanced facial pattern.

Rattlesnake poisoning frequently produces a severe tissue damaging effect including myonecrosis and hemorrhage. In this investigation, viriditoxin was isolated from the venom of the prairie rattlesnake (Crotalus viridis viridis), and its chemical properties and biological activities associated with tissue damage were investigated. The toxin has a molecular weight of approximately 115 000 with an isoelectric point of 4.8. Amino acid composition analyses indicate that the toxin consists of approximately 1018 residues with high content of acidic amino acid residues. Circular dichroism was used to examine the conformation of viriditoxin. Although there is some indication of a high beta-sheet content, it is not possible to identify the exact conformation due to the anomalous CD spectra. Viriditoxin has both myotoxic and hemorrhagic activities. High serum creatine kinase activity of mice injected with the toxin substantiates the destructive action of viriditoxin on muscle. Viriditoxin has an LD50 value of approximately 5.0 microgram/g in mice indicating the protein is also moderately lethal in addition to its tissue damaging effect.

N umerous techniques have appeared over the past three decades for analyzing the roentgenographic cephalogram, each attempting to depict certain skeletal or dental disharmonies contributing to the malocclusion. Using the earlier techniques of Downs,2, 3 Tweed,lll I2 and Steiner,lO orthodontists attempted to find standards of the ideal or normal occlusion to which the malocclusion case could be compared. Later analyses shifted the emphasis from the horizontal to the vertical dimension. Using the methods of Wylie,13s I4 Scott,s Schudy,71 * and Sassouni,4-6 orthodontists again tried to find vertical norms or standards which would serve as guides for treatment. Today, however, orthodontists are becoming increasingly aware that many cases do not fit the standard categories and that the combination of variables is too complex to treat to an average. It was this desire for an individualized approach to treatment that led to the development of the quadrilateral analysis. This analysis, as designed by DiPaolo,l concerns itself with the effects of the overlying skeletal configuration on the relationships of the bony arches, in the horizontal as well as the vertical dimensions, regardless of the superimposed dentoalveolar relat,ionships. Since this analysis is individualized, there is no need for standards or norms to relate the patient under treatment to another so-called “ideal” patient. The purpose of the present art,iclc is, therefore, to show that this analysis has the capability of depicting any facial disharmony in either the horizontal or the vertical dimension.