Hyperimmunoglobulin E syndrome

Hyperimmunoglobulin E (HIE) syndrome is a primary immunodeficiency disorder characterized by recurrent bacterial infections in presence of very high serum Ig E levels. We are reporting a nine-year-old child with HIE syndrome and reviewing literature on this disease.     

Contrast study of the nasopharynx

A contrast study of the nasopharynx in nasopharyngeal space occupying lesions was conducted. Both the lateral as well as the submento-vertical-views were taken prior to and after filling the nasopharynx with the contrast medium (Micropaque). The contrast study was also carried out in ten normal cases to observe the anatomical details. The posterior wall of the nasopharynx measured 15–21 mm irrespective of sex and roof 7–10 mm in males and 5–8 mm in females. The contrast study of nasopharynx was of immense help in defining the site, extent and nature of the mass. The results were compared with plain X-ray and the Contrast medium X-ray diagnosis of the cases were confirmed on histopathology.     

Anti-inflammatory activity of quinazolinoformazans

Eight substituted quinazolonoformazans were synthesized and evaluated for anti-inflammatory activity. The degree of protection provided by seven of these compounds, at a dose of 100 mg/kg, po, against carrageenin-induced edema in rat paw ranged from 26 to 57%. The four active substituted quinazolonoformazans (1, 2, 6, 8), on further evaluation for antiwrithmogenic activity, provided 10-80% protection against the aconitine-induced writhing response in mice. The ulcerogenic liabilities of two of the most active compounds were also determined. The doses producing ulcers in 50% of the treated rats (UD50) were 155 and 260 mg/kg, ip, for 2 and 8, respectively. The low toxicities possessed by these substituted quinazolonoformazans were indicated by their LD50 values which ranged from 600 to 1300 mg/kg, ip, in mice.     

Role of Putative Neurotransmitters in Bradykinin-Induced Catalepsy in the Rat

Intracerebroventricular administration of bradykinin produced a dose-related cataleptic response in rats. Bradykinin-induced catalepsy was significantly attenuated following pretreatment with pharmacologic agents that decrease central prostaglandin, serotonin, and acetylcholine activity, as well as by the opioid receptor antagonist naloxone. Conversely, pharmacologic treatments that enhance central catecholamine levels and, specifically, central dopaminergic activity also inhibited bradykinin-induced catalepsy. The prostaglandin precursor, arachidonic acid, and prostaglandin E₂, as well as met- and leu-enkephalin showed a synergistic effect with bradykinin catalepsy. Much evidence indicates that several actions of bradykinin, in the central nervous system and the periphery, are likely to be prostaglandin mediated. Further, the recent report from this laboratory that centrally administered bradykinin specifically augments rat brain prostaglandin E₂ levels, together with the proposed role of central prostaglandins as modulators of central synaptic transmission, suggests that bradykinin-induced catalepsy is mediated and modulated through PGE effects on serotonergic, cholinergic, and dopaminergic neurotransmitter systems. The study also indicates that endogenous opioid peptides may be involved in braydkinin catalepsy.