Search

During recent years, diamond wire sawn (DWS) multicrystalline silicon (mc-Si) wafers have been widely used to reduce the production costs; however, these wafers need additional process treatments such as reactive ion etching (RIE) or metal-catalysed chemical etching (MCCE) to form a surface with relatively low reflectivity. Although the absolute power conversion efficiency of the solar cell could be improved by 0.3-0.5% through the introduction of such surface treatments, the production costs would also be increased. In this study, an improved production-scale acidic texturization with additives is used to texture the surfaces of DWS mc-Si wafers, giving a similar weighted averaged reflectance (WAR) of 19.69% as slurry-cut wafers. The effect of the texturization process on the surface morphology, WAR and performance of the DWS mc-Si cells is discussed. [ABSTRACT FROM AUTHOR]

Background Measuring fractional exhaled nitric oxide (FeNO) is a simple and non-invasive method for assessing airway inflammation. IL-17 plays an important role in T cell-dependent inflammatory response that occurs in allergic asthma, it could act as a potent activator of inducible nitric oxide synthase (iNOS) to amplify FeNO levels. Objectives To evaluate the differences in the CD4+IL-17A+ T cell counts, serum IL-17 levels, and FeNO levels in children with mild intermittent to moderate to severe persistent asthma classified by using the Global Initiative for Asthma (GINA). Methods One hundred and twenty asthmatic children divided into the mild intermittent ( n = 42), mild persistent ( n = 42), and moderate to severe persistent ( n = 36) groups, and 20 healthy controls were recruited for the study. Information obtained at visits included the assessment of asthma severity according to GINA guidelines and C-ACT, lung function parameters, FeNO levels, CD4+IL-17A+ T cells counts from PBMCs, iNOS production by sputum cells and serum IL-17 levels. Results Serum IL-17 and FeNO levels were significantly higher in mild to severe persistent asthmatic patients than in intermittent asthmatics or healthy controls ( P < 0.05). The percentage of CD4+IL-17A+ T cells was higher in moderate to severe persistent asthmatics than in mild asthmatics ( P < 0.01). Moderate to severe asthmatics ( n = 5) exhibited greater iNOS production in sputum cells than mild cases ( n = 5). Decreased iNOS expression in sputum cells was noted in all subjects after IL-17 neutralizing antibody ( P < 0.05). Serum IL-17 levels were positively correlated with FeNO ( rho = 0.74; P < 0.01), negatively correlated with C-ACT ( rho = −0.63; P < 0.01) in asthmatics. Conclusion and Clinical Relevance CD4+ IL-17A+ T cells counts and serum IL-17 levels in conjunction with augmented FeNO levels are systemic markers of childhood asthma, using these markers, prediction and potential therapeutics for persistent asthmatics may be developed. [ABSTRACT FROM AUTHOR]

Summary:The clinical significance of early airflow decline after myeloablative allogeneic hematopoietic SCT is uncertain. We performed a retrospective cohort analysis to determine if airflow decline by day 100 is associated with later development of transplant-related airflow obstruction (AFO) and increased mortality risk. Overall, 750 (40%) patients had airflow decline by day 100. Development of airflow decline by day 100 was associated with an increased risk for AFO at 1 year (relative risk 2.6, 95% confidence interval 2.1-3.1) but not with an increase in mortality risk (hazard ratio (HR) 0.86, P=0.05). However, patients with the fastest rate of decline between day 100 and 1 year (12.5% per year ±24) had the highest mortality risk (HR 3.2, P<0.001). In conclusion, airflow measurements made on day 100 do not predict the rate of airflow decline between day 100 and 1 year, and therefore are not useful as a single measurement for determining mortality risk associated with development of AFO. Closer monitoring of the rate of airflow decline during the first year may facilitate the timely detection and treatment of early airflow decline and prevent the development of fixed AFO and increased mortality risk after hematopoietic stem cell transplant.Bone Marrow Transplantation (2004) 33, 759-764. doi:10.1038/sj.bmt.1704422 Published online 16 February 2004 [ABSTRACT FROM AUTHOR]

Background: Systemic lupus erythematosus (SLE) is a complex autoimmune disease with various clinical and serological manifestations. Previous studies have shown the association of SLE and anti-Ro, anti-La and anti-dsDNA autoantibodies with various clinical manifestations. We investigated the relationship between these autoantibodies and clinical findings of our patients with SLE., Methods: Eighty patients with SLE at Department of Pediatrics, Taipei Veterans General Hospital, Taiwan from October 1999 to March 2000 were enrolled in the study. Frequencies of various clinical manifestations were calculated. Autoantibodies to Ro, La and dsDNA were measured using ELISA method., Results: The most frequent clinical findings were arthritis (92.3%), photosensitivity (90.9%) and malar rash (86.1%). The most frequent laboratory findings were positive anti-nuclear antibody (ANA) (94.9%), low serum CH50 hemolytic titer (88.6%) and positive anti-dsDNA level (72.5%). Patients with anemia or photosensitivity had higher titers of anti-Ro antibody (Ab) than those without the respective clinical findings (p = 0.001 and 0.002, respectively). However, patients with proteinuria had lower anti-Ro Ab titers (p < 0.05). There was no correlation between clinical findings and anti-La Ab titers. Patients have higher titers of anti-dsDNA Ab if they had clinical findings of Raynauld's phenomenon, photosensitivity, arthritis, hypocomplementemia (p < 0.001), thrombocytopenia, proteinuria, or serositis (p < 0.05). No correlation was found between renal involvement and titers of various autoantibodies., Conclusions: Neither anti-Ro, anti-La nor anti-dsDNA antibodies was correlated with renal involvement in patients with SLE. However, patients with proteinuria had significantly lower titers of anti-Ro Ab than those without proteinuria.

Lipopolysaccharide (LPS) has been implicated in the pathogenesis of graft-versus-host disease (GVHD). The toll-like receptor (TLR)-4 has been recently identified as a major receptor for LPS. Mutations of TLR4 have been associated with LPS hyporesponsiveness. We hypothesized that TLR4 mutations reduce the risk of acute GVHD in allogeneic marrow transplant recipients. In a preliminary study to determine the frequency of TLR4 mutations and their possible association with GVHD, we tested 237 patients and their HLA-identical sibling donors for 2 TLR4 polymorphisms. All patients received methotrexate and cyclosporine for GVHD prophylaxis. One or more mutants were detected in 10.8% of patients and 10.6% of donors. Multivariable logistic regression models were used to analyze the association between TLR4 mutations and probability (1-sided) of GVHD. The odds ratio (adjusted for advanced disease, total body irradiation dose, and patient age) for development of grades II to IV GVHD when a mutation was present in the recipient was 0.63 (95% confidence interval [CI], 0.25-1.60; P = .16). When a mutation was present in the donor, the adjusted odds ratio was 0.88 (95% CI, 0.36-2.17; P = .40). When a mutation was present in both recipient and donor, the odds ratio was 0.72 (95% CI, 0.22-2.32; P = .29). Among 24 patients with TLR4 mutations in either donor or recipient, 4 (16.7%) developed gram-negative bacteremia. Among 213 patients without mutations, 14 (6.6%) developed gram-negative bacteremia (P = .09). The data indicate that a reduced risk of acute GVHD is associated with TLR4 mutations and that TLR4 mutations may increase the risk for gram-negative bacteremia. However, these associations are not statistically significant in recipients of HLA-matched sibling marrow transplants who are prophylactically treated for infections and GVHD. A much larger study population would be needed to confirm the role of LPS in the pathogenesis of GVHD in humans.

Influenza, respiratory syncytial, and parainfluenza viruses usually cause mild, self-limited illness in adults. However, elderly and immunocompromised persons are at increased risk for development of severe pneumonia. Clinical and radiographic features of epidemic viral pneumonias are often nonspecific. Newer and faster methods of viral culture and viral antigen detection have improved the capability for definitive diagnosis in recent years. Preventive measures for influenza virus pneumonia center on limiting exposure of high-risk patients to active cases of influenza, administering annual vaccinations, and providing chemoprophylaxis. Prophylaxis against RSV is effective in preventing complications. No effective vaccines have been developed against RSV or parainfluenza. Therapy for viral pneumonia is primarily supportive. Amantadine may be beneficial for influenza virus pneumonia, and ribavirin may be useful for RSV and parainfluenza virus disease. However, further definitive studies are necessary to determine their roles in these viral pneumonias.

Study Objectives: To determine if 100% oxygen administration adversely influences gas exchange in acutely ill asthmatic subjects., Design: Prospective preinterventional and postinterventional comparison., Setting: University hospital emergency department., Patients: Thirty-seven asthmatic subjects seeking care for symptomatic exacerbations., Interventions: Twenty minutes of 100% oxygen administration by face mask., Measurements and Results: Arterial blood gases and FEV(1) were measured before and during the last minute of oxygen administration. On presentation, the subjects had moderately severe airway obstruction (FEV(1), 49.1 +/- 3.6% of predicted); hypocarbia (PaCO(2), 36.8 +/- 1.1 mm Hg); hypoxemia (PaO(2), 70.2 +/- 2.5 mm Hg); and respiratory alkalosis (pH, 7.43 +/- 0.01). During oxygen breathing, 25 patients (67.6%) experienced elevations in PaCO(2) ranging from 1 to 10 mm Hg (mean, 4.1 +/- 0.6 mm Hg; p = 0.0003). The increase was considered to be a physiologic manifestation of the Haldane effect (ie, < or = 2 mm Hg) in 10 subjects, but in the remaining 15 subjects (40.5% of the total studied), the elevation represented worsening gas exchange. In seven of these patients (46.7%), hypercapnic respiratory failure developed (PaCO(2) before oxygen, 39.6 +/- 0.6; during oxygen, 44.7 +/- 0.7 mm Hg; p = 0.005), and in six patients (40%), it worsened (PaCO(2) before oxygen, 46.8 +/- 1.9; during oxygen, 52.0 +/- 3.1 mm Hg; p = 0.03). In general, the tendency toward hypercarbia was the greatest in the participants with the most severe airway obstructions., Conclusions: Our data demonstrate that the administration of 100% oxygen to acutely ill asthmatics may adversely influence carbon dioxide elimination.

Three herpesviruses--herpes simplex, varicella-zoster, and cytomegalovirus--commonly cause respiratory tract infections in immunocompromised patients. Adenoviruses and measles virus are also significant causes of respiratory disease in this population. Diagnosis of herpesvirus infections is difficult because these viruses can establish latency and are often shed intermittently in the absence of invasive disease. A positive respiratory tract culture of herpesviruses alone is not diagnostic of active invasive disease. Preventive measures should focus on limiting the patient's exposure to active infection, broad use of available vaccines in children and susceptible adults, and use of hyperimmune globulin and chemoprophylaxis in high-risk patients. Adenovirus pneumonia is diagnosed by viral culture and rapid antigen detection assays, whereas measles pneumonia is often identifiable by the characteristic rash. Treatment of either adenovirus or measles pneumonia is primarily supportive.

Despite enhanced laboratory techniques such as viral culture, rapid antigen detection, and gene amplification, a confident diagnosis of viral pneumonia continues to be a challenge. The nonspecific nature of clinical characteristics and the extreme sensitivity of laboratory techniques make the diagnosis difficult, even when a viral agent is detected. Understanding the limitations of these technological advances and the use of histopathologic techniques can greatly enhance a skilled clinician's ability to make an accurate diagnosis.

To explore the relation between levels of HIV-1 in the cerebrospinal fluid (CSF) and plasma, simultaneously obtained samples from twelve patients who were receiving or had received lamivudine were examined. HIV-1 RNA levels were measured by nucleic acid sequence-based amplification procedure (NASBA). HIV-1 pol gene was amplified and sequenced. Median plasma and CSF HIV-1 RNA levels were 4.98 log and 2.93 log respectively. In total, 5 patients had CSF levels <100 copies/ml. A significant correlation between plasma and CSF HIV-1 RNA levels was found; 3 patients with disproportionately elevated CSF HIV-1 RNA levels had clinical evidence of central nervous system disease. Genotypic analysis was available for 9 plasma/CSF pairs. In 4, the lamivudine (3TC)-resistance mutation M184V was found in both CSF and plasma. Discordance was found in 2 pairs. In both, M184V was found in plasma but not CSF. These data suggest that CSF and plasma levels of HIV-1 may be correlated.

We present a case of paradoxical clinical deterioration during antituberculosis therapy in an HIV-infected adult with pulmonary TB. The clinical course was characterized by marked cervical and mediastinal adenopathy accompanied by fever and weight loss during simultaneous treatment of TB and HIV disease. After extensive investigation for causes of therapeutic failure, the paradoxical reaction was attributed to partial immune reconstitution related to highly effective antiretroviral therapy. Due to the high prevalence of TB in HIV-infected patients, it is important to recognize this phenomenon and understand that it is usually self-limited.

When bacteremia is suspected, the physician's first step is to determine the most likely source by using all available data from the history, physical examination, and laboratory studies. When evaluation for bacteremia is warranted, two or three sets of blood cultures should be carefully obtained using strict procedure guidelines, and empirical antibiotic therapy should be initiated. If the source of bacteremia has not been identified, blood culture results must be correlated with the clinical situation so that further investigations may be pursued and antimicrobial therapy may be initiated or modified. A high index of suspicion must be maintained for unusual or fastidious pathogens in immunocompromised patients.