Smartphones Helping Memory-Impaired Individuals Overcome Inconveniences During Daily Living.

The external compensatory means recommended for rehabilitation of memory disorder must consist of a means for storing information externally and a clue for accessing the externally stored information. Writing down the information on a paper pocketbook is usually used as an external compensatory means, but smartphones are overwhelmingly more useful in terms of the functions as compared to paper pocketbooks. The author, who has a memory disorder and works as an occupational therapist, has recently devised a method for utilizing a smartphone for overcoming the inconveniences during daily living and herein describes how to use it in daily life scenarios.

A Superinfection of Salmonella typhi and Hepatitis E Virus Causes Biphasic Acute Hepatitis.

A 47-year-old Japanese man was referred to our hospital because of a sustained high fever with diarrhea 12 days after a flight from India. Liver enzymes were elevated with rose spots, hepatosplenomegaly, relative bradycardia, and acute cholecystitis. A liver biopsy depicted the dense infiltration of lymphocytes and Kupffer cells in sinusoids and the granulomatous formation in the parenchyma. The liver damage was initially resolved with the administration of ceftriaxone for 16 days but flared up 1 week later. Laboratory tests yielded positive reactions for Salmonella typhi and hepatitis E virus RNA. The pathophysiological presentations of concurrent typhoid and type E hepatitis are discussed.

Spontaneous renal artery dissection.

Isolated spontaneous dissection of renal arteries or its branches are extremely rare. Most cases of renal artery dissection are associated with underlying pathology of the renal arteries. We report a case of spontaneous dissection of the left main renal artery and infarction of the left kidney with positive antiphospholipid antibody. Extensive work up of the patient including imaging studies confirmed the diagnosis of SRAD. Antiphospholipid antibodies may have a role in the pathogenesis of arterial dissection by causing endothelial dysfunction. This is a first literature report.

Inhibition of nuclear factor kappaB by IkappaB superrepressor gene transfer ameliorates ischemia-reperfusion injury after experimental lung transplantation.

OBJECTIVES: Ischemia-reperfusion injury after lung transplantation is associated with significant morbidity and mortality. The activation of the transcription factor nuclear factor kappaB is central to the 2 important pathways that characterize ischemia-reperfusion injury, namely the inflammatory response and apoptosis. The purpose of this study was to determine the effects of nuclear factor kappaB inhibition on experimental lung transplant ischemia-reperfusion injury with gene transfer of the nuclear factor kappaB inhibitor IkappaB in a superrepressor form (IkappaBSR). METHODS: An orthotopic left lung transplant model in isogeneic rats was used, with 18 hours of prolonged cold storage of donor lung grafts used to create severe ischemia-reperfusion injury. Donor rats underwent endobronchial gene transfection with saline alone or adenovirus encoding either beta-galactosidase control or IkappaBSR 48 hours before harvest. The function of transplanted lung grafts was assessed on the basis of isolated graft oxygenation, wet/dry lung weight ratio, and myeloperoxidase activity. Nuclear factor kappaB activation was assessed by means of enzyme-linked immunosorbent assay. Apoptotic cell death was assessed by evaluating the levels of histone-associated DNA fragments and caspase-3 activity. RESULTS: Treatment of donor lung grafts with IkappaBSR resulted in significantly improved oxygenation compared with that seen in control tissue 24 hours after transplantation. IkappaBSR-treated lungs also demonstrated less pulmonary edema and reduced neutrophil infiltration 24 hours after reperfusion. Nuclear factor kappaB activation and apoptotic cell death induction 2 hours after transplantation was significantly reduced in IkappaBSR-treated lungs compared with in control lungs. CONCLUSIONS: Inhibition of nuclear factor kappaB activation by IkappaBSR gene transfer improves transplanted lung graft oxygenation, decreases pulmonary edema and neutrophil sequestration, and reduces apoptotic cell death after experimental lung transplantation.

In vivo molecular imaging characterizes pulmonary gene expression during experimental lung transplantation.

Experimental gene therapy is a promising strategy to prevent ischemia-reperfusion (I/R) injury and allograft rejection after lung transplantation, and methods will eventually be needed to characterize pulmonary transgene expression in vivo in humans. Therefore, we studied positron emission tomography (PET) as a means of performing in vivo molecular imaging in rodent models of lung transplantation. Rats were transfected endotracheally with adenovirus encoding a fusion gene of a mutant Herpes simplex virus-1 thymidine kinase and the green fluorescent protein gene (the former serving as an imaging reporter gene). Twenty-four hours after transfection, lungs were transplanted in groups representing normal transplantation, I/R injury and acute allograft rejection. Imaging was obtained either 24 h after transplantation to study reperfusion injury or 4 days after transplantation to study graft rejection. After imaging, lungs were excised and analyzed for thymidine kinase activity. Imaging detected transgene expression in transplanted lungs even in the presence of acute rejection or I/R injury. The PET imaging signal correlated with in vitro lung tissue assays of thymidine kinase activity (r(2) = 0.534). Thus, noninvasive molecular imaging with PET is a feasible, sensitive and quantitative method for characterizing pulmonary transgene expression in experimental lung transplantation.

Endobronchial gene transfer of soluble type I interleukin-1 receptor ameliorates lung graft ischemia-reperfusion injury.

BACKGROUND: Soluble type I interleukin-1 receptor is a competitive inhibitor of interleukin-1 and may reduce its proinflammatory actions. The objective of this experiment was to demonstrate that endobronchial gene transfer of soluble type I interleukin-1 receptor IgG to donor lung grafts reduces posttransplant ischemia-reperfusion injury. METHODS: All experiments utilized an orthotopic left lung isograft transplant model. Donors were divided into three groups (n = 6 each) for endobronchial transfection: group I received 2 x 10(7) plaque-forming units of adenovirus encoding soluble type I interleukin-1 receptor IgG; group II received 2 x 10(7) plaque-forming units of nonfunctional control adenovirus encoding beta-galactosidase; and group III received 0.1 mL of saline. Left lungs were harvested 24 hours after transfection and stored for 18 hours before transplantation. Graft function was assessed 24 hours after reperfusion using three measurements: isolated graft oxygenation, wet-to-dry lung weight ratio, and tissue myeloperoxidase activity. Transgene expression of soluble type I interleukin-1 receptor IgG was also evaluated using enzyme-linked immunosorbent assay and immunohistochemistry. RESULTS: Isolated graft arterial oxygenation was significantly improved in group I compared with groups II and III (281.8 +/- 134.8 versus 115.7 +/- 121.5 and 88.0 +/- 58.9 mm Hg, p = 0.0197 and p = 0.0081, respectively). Myeloperoxidase activity was also significantly reduced in group I compared with groups II and III (0.083 +/- 0.044 versus 0.155 +/- 0.043 and 0.212 +/- 0.079 optical density units per minute per milligram protein, p = 0.0485 and p = 0.0016, respectively). Expression of soluble type I interleukin-1 receptor IgG was detected only in lungs from group I. CONCLUSIONS: Endobronchial gene transfer of soluble type I interleukin-1 receptor IgG to donor lung grafts subjected to prolonged cold ischemia ameliorates ischemia-reperfusion injury by improving graft oxygenation and reducing lung edema and neutrophil sequestration.

Microcystic variant of localized malignant mesothelioma accompanying an adenomatoid tumor-like lesion.

The case of a 70-year-old man with a hitherto undescribed pleural mesothelioma is reported. The tumor was localized in the left lung apex and had invaded the parietal pleura. Histologically, the tumor was characterized by a proliferation of epithelioid cells and the formation of microcysts. The tumor cells were positive for calretinin and vimentin, and possessed abundant microvilli, indicating a mesothelial cell origin for the tumor. A high Ki-67 index and mitotic index, and the recurrence of the tumor after surgery, indicated malignancy. Based on the evidence, we propose that the tumor is a microcystic variant of a localized malignant mesothelioma.