THE TREATMENT OF ALLERGIC RHINITIS. (1/12)

Allergic inflammation of the nasal mucous membranes, like other atopic disorders, occurs primarily as the result of an antigenantibody reaction between external allergens and circulating skin-sensitizing antibodies. In addition, the disease process is frequently complicated by bacterial or viral infection. Effective treatment of allergic rhinitis, therefore, consists of: (1) changing the patient's environment in order to remove the offending allergens, (2) removing the patient from his environment, (3) altering the patient's response to environmental allergens by means of hyposensitization injections, (4) suppressing the allergic reaction with drugs, and (5) eliminating bacterial infection. Usually more than one of these therapeutic measures is required for the individual patient.  (+info)

Contribution of the histaminergic receptor subtypes to histamine-induced cerebellar granular neurotoxicity. (2/12)

In the present study, we investigated the effects of histamine and its specific H(1), H(2) and H(3) receptor blockers in cerebellar granular cell culture derived from rat pups. Histamine was applied at 10(-9),10(-8), 10(-7),10(-6), and 10(-5) M for 16 h into the cultures and the highest dose was found to be the most toxic one. Pheniramine (H(1) receptor blocker), ranitidine (H(2) receptor blocker) and thioperamide (H(3) receptor blocker) were applied at 10(-8), 10(-7), 10(-6), 10(-5) M into the flasks prior to histamine in the second step of the experiments. Also, the effect of all of the blockers together at 10(-5) M concentrations was tested on the toxicity induced by 10(-5) M histamine. The H(3) receptor blocker, thioperamide (10(-6) M) was demonstrated to be most effective histamine toxicity blocker. Histamine H(2) blocker, ranitidine, was found to attenuate histamine neurotoxicity at all doses tested, its most effective dose being the highest dose. On the other hand, H(1) blocker, pheniramine, was able to reverse the effect of histamine at 10(-6) and 10(-5) M, but it was found ineffective when given at 10(-9) and 10(-8) M. Combined application of H(1), H(2), and H(3) receptor blockers at 10(-5) M concentrations, 45 min before histamine addition into the flasks at 10(-5) M, was able to reduce cell death score but it was not as effective as H(3) blocker, thioperamide.  (+info)

Breakdown of the blood-brain barrier during dengue virus infection of mice. (3/12)

A breakdown of the blood-brain barrier occurred in mice inoculated intracerebrally (i.c.) or intraperitoneally (i.p.) with dengue virus type 2 (DEN2). This resulted in leakage of protein-bound Evans blue dye and 51Cr-labelled erythrocytes into the brain tissue. The leakage increased with time after infection and coincided with an increase of a DEN2-induced cytokine, the cytotoxic factor (CF), in the spleens of such mice. The titres of virus in the brain increased exponentially in i.c. inoculated mice but the virus was not detected in brains of mice given DEN2 by the i.p. route. Similar breakdown of the blood-brain barrier also occurred in mice inoculated intravenously with CF; the damage was dose-dependent and the vascular integrity was restored during the 3 h period after inoculation. Treatment of mice with antihistamine drugs, blocking H1 or H2 receptors, decreased the DEN2-induced protein leakage by up to 50% in i.c. inoculated mice and up to 92% in those inoculated i.p. Indomethacin, a prostaglandin synthetase inhibitor, had no effect. In i.c. inoculated mice protein leakage was inhibited by about 60% by treatment with CF-specific (CFA) or DEN2-specific antisera (DEN2A) whereas protection was complete with the combined treatment with both antisera. On the other hand, in i.p. inoculated mice the inhibition of protein leakage was 80 to 89% with CFA. These findings show a breakdown of the blood-brain barrier leading to cerebral oedema during DEN2 infection which is mediated via the release of histamine by a virus-induced cytokine.  (+info)

Antihistamine pretreatment to reduce incidence of withdrawal movement after rocuronium injection. (4/12)

 (+info)

Modulation of in vivo immunoglobulin production by endogenous histamine and H1R and H2R agonists and antagonists. (5/12)

The present study was designed to delineate the immunomodulatory role of histamine receptors (H1R and H2R) and their antibody generation in a rabbit model. Six groups containing 18 rabbits each received either vehicle (sterile distilled water, 1 ml/kg x b.i.d), histamine (100 mug/kg x b.i.d.), H1R agonist (HTMT, 10 mug/kg x b.i.d.), H2R agonist (amthamine, 10 mug/kg x b.i.d.), H1R antagonist (pheniramine, 10 mg/kg x b.i.d.) or H2R antagonist (ranitidine, 10 mg/kg x b.i.d.). All animals were subsequently immunized with an intravenous injection of sheep red blood cells (SRBC). Estimations of total serum immunoglobulins (Igs), immunoglobulin M (IgM) and immunoglobulin G (IgG) were performed by ELISA and hemagglutination assay (HA) at days 0 (pre-immunization), 7, 14, 21, 28 and 58 (post-immunization). Both the ELISA and the HA showed similar production of Igs, IgM and IgG but the results were found comparatively more significant by ELISA as opposed to HA. Results showed that histamine could influence a detectable antibody response to SRBC early (i.e., at day 7), which lasted until day 58. Immunomodulatory processes showed suppression of an Ig generation in the H1R-antagonist group with enhancement in the H2R-antagonist group. The H1R-agonist group showed an increased Ig production in comparison to the H2R-agonist group. The IgM production was inhibited in the H1R-antagonist group as compared to the H2R-antagonist group, and it was also suppressed in H1R-agonist group as compared to H2R-agonist group. IgG production was inhibited in the H1R-antagonist group as opposed to the H2R-antagonist group. In contrast, the H1R-agonist group increased IgG production as compared to the H2R-agonist group. All the results were found to be statistically significant (p < 0.05 or p < 0.01). In conclusion, histamine and its receptor (H1R and H2R) agonists enhance antibody production by triggering the histamine receptors (H1R and H2R), and both the H1R antagonist and the H2R antagonist positively or negatively regulate the antibody production. The findings of this study may have clinical significance.  (+info)

Artificial neural network combined with principal component analysis for resolution of complex pharmaceutical formulations. (6/12)

A chemometric approach based on the combined use of the principal component analysis (PCA) and artificial neural network (ANN) was developed for the multicomponent determination of caffeine (CAF), mepyramine (MEP), phenylpropanolamine (PPA) and pheniramine (PNA) in their pharmaceutical preparations without any chemical separation. The predictive ability of the ANN method was compared with the classical linear regression method Partial Least Squares 2 (PLS2). The UV spectral data between 220 and 300 nm of a training set of sixteen quaternary mixtures were processed by PCA to reduce the dimensions of input data and eliminate the noise coming from instrumentation. Several spectral ranges and different numbers of principal components (PCs) were tested to find the PCA-ANN and PLS2 models reaching the best determination results. A two layer ANN, using the first four PCs, was used with log-sigmoid transfer function in first hidden layer and linear transfer function in output layer. Standard error of prediction (SEP) was adopted to assess the predictive accuracy of the models when subjected to external validation. PCA-ANN showed better prediction ability in the determination of PPA and PNA in synthetic samples with added excipients and pharmaceutical formulations. Since both components are characterized by low absorptivity, the better performance of PCA-ANN was ascribed to the ability in considering all non-linear information from noise or interfering excipients.  (+info)

C7a, a biphosphinic cyclopalladated compound, efficiently controls the development of a patient-derived xenograft model of adult T cell leukemia/lymphoma. (7/12)

 (+info)

Effect of dengue virus-induced cytotoxin on capillary permeability. (8/12)

Capillary permeability is increased in cases of dengue haemorrhagic fever (DHF) and dengue shock syndrome (DSS) but its genesis is not known. Dengue type 2 virus (DV) induces production of a cytokine (CF2) by mouse macrophages. The present study was undertaken to investigate the effect of CF2 on capillary permeability. It was observed that intraperitoneal inoculation of CF2 in mice increased the capillary permeability in a dose-dependent manner, as shown by leakage of intravenously injected radioactive iodine (125I) or Evan's blue dye in the peritoneal cavity. Peak leakage occurred at 30 min and the vascular integrity was restored by 1-2 h. The increase in capillary permeability was abrogated by pretreatment of mice with avil (H1 receptor blocker) but not by ranitidine (H2 receptor blocker). The findings thus show that DV-induced CF2 increases the capillary permeability via release of histamine.  (+info)

• 1
• 2