Risk factors in IVIG-resistant Kawasaki disease and correlation with Japanese scoring systems — a study from Eastern India

Clinical Rheumatology - To assess the risk factors of intravenous immunoglobulin (IVIG)-resistant Kawasaki disease (KD) and to evaluate the performance of the three Japanese risk-scoring systems,...     

Lethal factor toxemia and anti-protective antigen antibody activity in naturally acquired cutaneous anthrax

Cutaneous anthrax outbreaks occurred in Bangladesh from August to October 2009. As part of the epidemiological response and to confirm anthrax diagnoses, serum samples were collected from suspected case patients with observed cutaneous lesions. Anthrax lethal factor (LF), anti-protective antigen (anti-PA) immunoglobulin G (IgG), and anthrax lethal toxin neutralization activity (TNA) levels were determined in acute and convalescent serum of 26 case patients with suspected cutaneous anthrax from the first and largest of these outbreaks. LF (0.005-1.264 ng/mL) was detected in acute serum from 18 of 26 individuals. Anti-PA IgG and TNA were detected in sera from the same 18 individuals and ranged from 10.0 to 679.5 μg/mL and 27 to 593 units, respectively. Seroconversion to serum anti-PA and TNA was found only in case patients with measurable toxemia. This is the first report of quantitative analysis of serum LF in cutaneous anthrax and the first to associate acute stage toxemia with subsequent antitoxin antibody responses.     

Anthrax outbreaks in Bangladesh, 2009-2010

During August 2009-October 2010, a multidisciplinary team investigated 14 outbreaks of animal and human anthrax in Bangladesh to identify the etiology, pathway of transmission, and social, behavioral, and cultural factors that led to these outbreaks. The team identified 140 animal cases of anthrax and 273 human cases of cutaneous anthrax. Ninety one percent of persons in whom cutaneous anthrax developed had history of butchering sick animals, handling raw meat, contact with animal skin, or were present at slaughtering sites. Each year, Bacillus anthracis of identical genotypes were isolated from animal and human cases. Inadequate livestock vaccination coverage, lack of awareness of the risk of anthrax transmission from animal to humans, social norms and poverty contributed to these outbreaks. Addressing these challenges and adopting a joint animal and human health approach could contribute to detecting and preventing such outbreaks in the future.     

Anatomical relationship between the foramen ovale and the lateral plate of the pterygoid process: application to percutaneous treatments of trigeminal neuralgia

Neurosurgical Review - Our aim was to clarify the variations in the positional relationship between the base of the lateral plate of the pterygoid process and the foramen ovale (FO), which block...     

Protection of mice against brucellosis by intranasal immunization with Brucella melitensis lipopolysaccharide as a noncovalent complex with Neisseria meningitidis group B outer membrane protein

Intranasal immunization of mice with purified Brucella melitensis lipopolysaccharide (LPS) as a noncovalent complex with Neisseria meningitidis group B outer membrane protein (GBOMP) elicited a high-titer anti-LPS systemic antibody response and a significant mucosal antibody response. The anti-LPS immunoglobulin G (IgG) antibody was predominantly of the IgG1 subtype, although there was some response of the IgG2a, IgG2b, and IgG3 subtypes. The antibody titer remained high for 16 weeks postimmunization. Immunized mice and sham-immunized control mice were challenged intranasally with 10(4) CFU of virulent B. melitensis strain 16 M 4 weeks after the second dose of vaccine. The numbers of bacteria in lungs, livers, and spleens at 3 days, 9 days, and 8 weeks postchallenge were determined. Bacteria were found in lungs of all mice on day 3, but there was no disseminated infection of liver or spleen. By day 9, 40% of the mice had infected spleens and livers. At 8 weeks postchallenge, spleens of 25 of 62 immunized mice were infected, compared to 61 of 62 control mice (P < 0.0001). The livers of 12 of 43 immunized mice were infected, compared to 22 of 36 control mice (P = 0.005). In contrast, the lungs of 26 of 46 immunized mice were still infected, compared to 27 of 44 control mice. The numbers of bacterial CFU in lungs of immunized and control animals were identical. These studies show that intranasal immunization with B. melitensis LPS-GBOMP subunit vaccine significantly protects mice against intranasal challenge with virulent B. melitensis. Vaccination reduces bacterial dissemination to spleen and liver but has no effect on the course of lung infection.     

Self-assembled peptide-based hydrogels as scaffolds for anchorage-dependent cells

We report here the design of a biomimetic nanofibrous hydrogel as a 3D-scaffold for anchorage-dependent cells. The peptide-based bioactive hydrogel is formed through molecular self-assembly and the building blocks are a mixture of two aromatic short peptide derivatives: Fmoc-FF (Fluorenylmethoxycarbonyl-diphenylalanine) and Fmoc-RGD (arginine-glycine-aspartate) as the simplest self-assembling moieties reported so far for the construction of small-molecule-based bioactive hydrogels. This hydrogel provides a highly hydrated, stiff and nanofibrous hydrogel network that uniquely presents bioactive ligands at the fibre surface; therefore it mimics certain essential features of the extracellular matrix. The RGD sequence as part of the Fmoc-RGD building block plays a dual role of a structural component and a biological ligand. Spectroscopic and imaging analysis using CD, FTIR, fluorescence, TEM and AFM confirmed that FF and RGD peptide sequences self-assemble into β-sheets interlocked by π–π stacking of the Fmoc groups. This generates the cylindrical nanofibres interwoven within the hydrogel with the presence of RGDs in tunable densities on the fibre surfaces. This rapid gelling material was observed to promote adhesion of encapsulated dermal fibroblasts through specific RGD–integrin binding, with subsequent cell spreading and proliferation; therefore it may offer an economical model scaffold to 3D-culture other anchorage-dependent cells for in-vitro tissue regeneration.     

Chronic Arsenic Exposure Impairs Macrophage Functions in the Exposed Individuals

Introduction  Owing to the established roles of human macrophages in immune defense, we investigated the effect of chronic arsenic exposure upon these major hematopoietic cells in 70 arsenic-exposed individuals with skin lesions and 64 unexposed individuals. Methods  Human monocyte-derived macrophages were prepared from peripheral blood mononuclear cells, by culture of the adherent cells for 6 days in medium supplemented with granulocyte–monocyte colony stimulating factor. Parameters studied included cell adhesion capacity, expression of CD54 and F-actin, nitric oxide production, phagocytic capacity, and effect of arsenic on Rho A-ROCK pathway. Results  In macrophages of exposed individuals when compared to unexposed group, there was cell rounding accompanied with a significant (p < 0.001) loss of cell adhesion capacity, decrease in nitric oxide production, impaired phagocytic capacity, and decreased CD 54 and F-actin expression. Additionally, chronic arsenic exposure affected Rho A-ROCK pathway which in turn impaired macrophage functions. Discussion and Conclusion  These altogether could contribute significantly to arsenic-induced immunosuppression observed in the arsenic-exposed individuals.