All infected HCW whose condition had progressed severely and who had failed to respond to the available treatment, survived after transfusion with convalescent plasma.

BackgroundA comprehensive analysis has not been performed on patients with thyrotoxic periodic paralysis (TPP) characterized by acute hypokalemia and paralysis in the setting of thyrotoxicosis.PurposeThe aim of this study was to analyze the detailed symptomatology of thyrotoxicosis and precipitating factors for the attack in a large cohort of TPP patients.Patients and methodsA prospective observational study enrolled patients with TPP consecutively over 10 years at an academic medical center. Clinical features, including signs/symptoms of thyrotoxicosis and precipitating factors, were analyzed. The Wayne's index was used to assess the severity of thyrotoxicosis at presentation. Patients who agreed to receive an oral glucose-loading test after recovery were evaluated.ResultsAmong the 135 TPP patients (male:female, 130:5), 70% of paralytic attacks occurred in the morning, especially during the seasons of summer and fall. Two-thirds of patients did not have a known family or personal history of hyperthyroidism. Only 17% of TPP patients manifested overt signs/symptoms of thyrotoxicosis (Wayne's index >19). A clear precipitating factor, such as high carbohydrate load, acute upper respiratory tract infection, strenuous exercise, high-salt diet, or the use of steroids or bronchodilators, was identified in only 34% of TPP patients. A glucose load to stimulate insulin secretion induced acute hypokalemia (K+2.47±0.6 mmol/l) with reparalysis in only 18% (10/55) of TPP patients.ConclusionsMost TPP patients have only subtle clinical signs/symptoms of thyrotoxicosis and only a small fraction has clear precipitating factors. In addition to the effects of hyperinsulinemia, other insulin-independent mechanisms may participate in the pathogenesis of TPP.

We have constructed a series of plasmids encoding premembrane (prM) and envelope (E) protein genes of dengue virus type 2 (DEN-2). These plasmids included an authentic DEN-2 prM-E construct (pCBD2-14-6), and two chimeric constructs, 90% DEN-2 E-10% Japanese encephalitis (JE) virus E (pCB9D2-1J-4-3) and 80% DEN-2 E-20% JE E (pCB8D2-2J-2-9-1). Monoclonal antibody (MAb) reactivity indicated that all three plasmids expressed authentic DEN-2 virus E protein epitopes representative of flavivirus domains 1, 2, and 3. However, only the pCB8D2-2J-2-9-1 construct secreted high levels of prM, M (membrane), and E proteins into the culture fluid of plasmid-transformed COS-1 cells. The major portion of the prM and E proteins expressed by COS-1 cells transformed by pCBD2-14-6 or pCB9D2-4-3 plasmids remained membrane-bound. The results supported the notion that an unidentified membrane retention sequence is located between E-397 and E-436 of DEN-2 virus E protein. Replacing the carboxyl-terminal 20% of DEN-2 E (397-450) with the corresponding JE sequence had no effect on anti-DEN-2 MAb reactivity, indicating that this region is antigenically inert, although it is required for antigen secretion. Plasmid pCBD2-2J-2-9-1, which expressed secreted forms of prM/M and E that have the potential to form subviral particles, was superior to other constructs in stimulating an antibody response. Ninety percent neutralization titers ranging from 1:40 to >1:1000 were observed in seven of nine serum specimens from pCB8D2-2J-2-9-1-immunized mice. Eleven of twelve 2-day-old neonatal mice, derived from a pCB8D2-2J-2-9-1 immunized female mouse, survived intraperitoneal challenge of DEN-2 New Guinea C virus.

We have investigated the plasma proteome by using 2D gel electrophoresis and MS from patients with severe acute respiratory syndrome (SARS). A complete proteomic analysis was performed on four patients with SARS in different time courses, and a total of 38 differential spots were selected for protein identification. Most of the proteins identified are acute phase proteins, and their presence represents the consequence of serial cascades initiated by SARS-coronavirus infection. There are several proteins that have never been identified in plasma before using 2D gel electrophoresis, among which peroxiredoxin II was chosen for further study by analyzing additional 20 plasma samples from patients with probable and suspected SARS and patients with fever, respectively. The results showed that the level of plasma peroxiredoxin II in patients with SARS is significantly high and could be secreted by T cells. Taken together, our findings indicate that active innate immune responses, along with the oxidation-associated injuries, may play a major role in the pathogenesis of SARS.proteomic techniques ͉ acute phase proteins ͉ peroxiredoxin II S evere acute respiratory syndrome (SARS) was first recognized at the end of 2002 in Guangdong, China, and since then the disease has spread to several countries. By late July 2003, Ͼ8,000 SARS cases and Ͼ700 SARS-related deaths were reported from Ͼ25 countries around the world, and no effective treatment has been established so far. Through extensive studies, the causative agent of SARS has been identified as a human SARS-coronavirus (SARS-CoV) (1-3). Although the complete genome sequence of SARS-CoV, the structure of the main protease (3CL protease), and the possible receptor have been determined (4-7), the pathogenesis of SARS is still not fully understood.Plasma proteins are useful targets for diagnostic, prognostic, and͞or therapeutic development. With proteomic tools available recently, profiling of human plasma proteome becomes more feasible in searching for disease-related markers (8). To explore the possible pathogenetic mechanisms involving the progression of SARS, we have analyzed the plasma proteins of 22 different plasma samples from four SARS patients in different time courses by using 2D gel electrophoresis (2DE) in combination with MS. The results showed that most of the plasma proteins found in patients with SARS are acute phase proteins (APPs) generated by inflammatory reactions during SARS-CoV-induced acute lung injuries. Materials and MethodsHuman Subjects. Four SARS patients with a total of 22 plasma samples were selected for complete proteomic analysis. These patients were infected by SARS-CoV through nosocomial transmission during one major SARS outbreak in one municipal hospital in Taipei. For comparison, plasma samples from six healthy individuals were used as controls. The protein concentration of each sample was determined by the standard Bradford method. The use of these samples was approved by the Review Board of the Tri-Service General Hospital, National Def...