Where has the lymphoma gone? Pericardial effusion adenosine deaminase may play a key role in diagnosing primary effusion lymphoma-like lymphoma: a case report.

Background: Primary effusion lymphoma (PEL) is a non-Hodgkin lymphoma that is exclusively generated by body cavity effusion. Primary effusion lymphoma develops in patients infected with human immunodeficiency virus (HIV) and is associated with the human herpes virus (HHV)-8 infection. However, there are sporadic cases without HHV-8 infections or any history of immunodeficiency, called 'PEL-like lymphoma'. Case summary: An 83-year-old man was admitted to our institution because of shortness of breath, fatigue, and facial oedema. Laboratory findings were unremarkable, including negative results for HIV antibodies. Transthoracic echocardiography revealed massive pericardial effusion surrounding the entire heart, which resulted in the early diastolic collapse of the right ventricular free wall, indicating elevated intra-pericardial pressure. He underwent pericardial centesis and 700 mL of pericardial fluid was drained. Adenosine deaminase (ADA) in the pericardial effusion showed an abnormally high value of 221 U/L. Cytological examination revealed a cellular population compatible with diffuse large B-cell lymphoma with prominent blastic characteristics and negative for HHV-8 latent nuclear antigens. Thus, the patient was diagnosed with HHV-8 unrelated HIV-negative PEL-like lymphoma. He was followed for more than 10 months in complete remission after a single pericardial drainage without any chemotherapy. Discussion: Exhaustive drainage of the lymphomatous effusion may induce complete remission in some patients with PEL-like lymphoma. Furthermore, the ADA value in the pericardial effusion may serve as a valuable guide to facilitate the accurate diagnosis of PEL-like lymphoma.

Interfacial biosilica coating of chitosan gel using fusion silicatein to fabricate robust hybrid material for biomolecular applications.

An enzyme-encapsulated silica-based hybrid material was developed using a chitosan gel. Fusion silicatein (InaKC-ChBD-Sil), silicatein fused with a soluble tag and chitin-binding domain, was employed as an interfacial catalyst to form silica on a chitosan gel matrix under physiological conditions, and horseradish peroxidase was immobilised on the hybrid material. Silica formation on the gel was verified via fluorescence microscopy using a designed fusion protein called TBP-mCherry, a fluorescent protein fused with a silica-binding peptide. We report a chitosan gel-silica hybrid material capable of encapsulating enzymes for biomedical and environmental applications.

Diastolic heart failure is a new clinical entity of trastuzumab-induced cardiotoxicity: a case report.

Background: Cancer therapy-related cardiac dysfunction (CTRCD) is defined as a decrease in the left ventricular ejection fraction (LVEF) of >10% to a value below the lower limit of normal or relative reduction in global longitudinal strain (GLS) >15% from baseline after cancer treatment. However, the possibility of the development of isolated diastolic dysfunction has never been considered in the clinical presentation of CTRCD. Case summary: An 81-year-old woman was admitted to our institution presenting with prominent bilateral leg oedema, orthopnoea, and 8 kg of weight gain after administration of the anti-human epidermal growth factor receptor 2 (HER-2) antibody, trastuzumab, for HER-2-positive breast cancer. Transthoracic echocardiography showed a preserved LVEF of 62% without a significant reduction in GLS compared with results obtained before anti-HER-2 targeted therapy. Doppler echocardiography distinctly revealed a newly developed significant left ventricular diastolic dysfunction with evidence of elevated filling pressure. After successful achievement of volume reduction, the patient underwent cardiac catheter examination, revealing an elevated pulmonary artery wedge pressure of 18 mmHg. Subsequently, trastuzumab was discontinued and the patient was treated with diuretics, arteriodilators, and venodilators, until the signs and symptoms of heart failure completely disappeared. Discussion: In the management of CTRCD, including pretreatment screening, cardiotoxicity monitoring, follow-up after anti-cancer agents, and evaluation of the effectiveness of the therapy, too much emphasis has been paid exclusively to the development of systolic dysfunction; however, perspectives for diastolic dysfunction may be needed. A comprehensive multidisciplinary team approach composed of breast surgeons, oncologists, onco-cardiologists, and echocardiography specialists is required.

A Ruptured Left Gastric Artery Aneurysm That Neoplasticized during the Course of Coronavirus Disease 2019: A Case Report.

Coronavirus disease 2019 (COVID-19) is an acute respiratory syndrome caused by SARS-CoV-2 and is known to cause respiratory and systemic symptoms. A SARS-CoV-2 infection is involved in aneurysm formation, enlargement, and rupture in medium-sized vessels, such as the cerebral and coronary arteries and the aorta. In contrast, its involvement in forming aneurysms in medium-sized vessels other than the cerebral and coronary arteries has not been reported. An 84-year-old Japanese man with COVID-19 was admitted to our hospital. The treatment course was favorable, and the COVID-19 treatment was completed by the 10th day. On day 14, pancreatic enzymes increased mildly. An abdominal computed tomography revealed a ruptured left gastric aneurysm after spontaneous hemostasis. Arterial embolization was performed. In this patient, a new left gastric aneurysm was suspected of having formed and ruptured during the course of the COVID-19 treatment. To the best of our knowledge, this is the first report of abdominal visceral aneurysm formation caused by COVID-19 in a medium-sized vessel, and it is necessary to remember that aneurysms can be formed at any site when treating this syndrome.

A case report of myocarditis combined with hepatitis caused by herpes simplex virus.

BACKGROUND: Viral myocarditis presents with various symptoms, including fatal arrhythmia and cardiogenic shock, and may develop into chronic myocarditis and dilated cardiomyopathy in some patients. We report a case of viral myocarditis and hepatitis caused by herpes simplex virus. CASE PRESENTATION: A 20-year-old woman was admitted to our hospital with fever, fatigue, and anorexia. The initial investigation showed elevated liver enzyme levels and elevated creatine phosphokinase, and computed tomography showed diffuse swelling and internal heterogeneous image in the liver. These findings were consistent with acute hepatitis; therefore, we performed a liver biopsy, which showed parenchymal necrosis and lymphocytic infiltration. The night that the liver biopsy was performed, blood pressure gradually decreased and revealed cardiogenic shock. Electrocardiography showed diffuse ST-segment elevation, and echocardiography showed a dilated, spherical ventricle with reduced systolic function and pericardial effusion. An endomyocardial biopsy revealed lymphocyte infiltration of the myocardium, confirming acute myocarditis. After a few days, tests for immunoglobin M and immunoglobin G antibodies against herpes simplex virus were positive. CONCLUSIONS: We presented a rare case of myocarditis combined with hepatitis that was caused by herpes simplex virus. Acute myocarditis can occur concurrently with hepatitis, pancreatitis, nephritis, and encephalitis; thus, determining the presence of other infectious lesions is necessary to provide appropriate treatment for the patient.

Expression of Toll-like receptors on human platelets.

INTRODUCTION: Platelets play a crucial role in arterial thrombosis, which is the main cause of acute coronary syndrome. Some mycobacteriums, such as Chlamydia pneumoniae, were associated with progression of atherosclerosis and they are interacted with Toll-like receptors (TLRs), which have been defined as pathogen-associated molecular pattern recognition molecules in innate immunity. In the present study, we examined whether human platelets express TLRs. MATERIALS AND METHODS: Human platelets were obtained from healthy volunteers and the mRNA and protein level of TLRs on platelets and Meg-01 cells, megakaryoblastic cell line, were investigated. RESULTS: Reverse transcription-polymerase chain reaction (RT-PCR) demonstrated that TLR1 and TLR6 mRNA were expressed in platelets and Meg-01 cells. Furthermore, interferon-gamma up-regulated their mRNA levels in dose and time dependent manners after stimuli. Both TLR1 and TLR6 proteins in platelets were detected by Western blotting, and their expression of platelets was more than that of Meg-01 cells. Flow cytometry analysis revealed the expression of TLR1 and TLR6 on the cell surface of Meg-01 cells. Furthermore, immunohistochemical analysis using human coronary thrombi obtained from patients with acute coronary syndrome confirmed the expression of TLR1 and TLR6 on platelets. CONCLUSION: In summary, we demonstrated that human platelets and Meg-01 cells expressed a family of TLRs for the first time, and our findings indicated that platelets might recognize antigens directly via TLRs. Our findings suggest a possibility that platelets have the ability to recognize the antigens via TLRs and that there are mechanistic relations between infectious inflammation and atherosclerotic vascular diseases.