International and Japanese guidelines classify childhood asthma as mild, moderate, or severe, and recommend treatment with "as needed" bronchodilators, inhaled sodium cromoglycate, and inhaled corticosteroids, respectively. Alternatively, some investigators proposed inhaled corticosteroids as first-line therapy to prevent airway inflammatory obstruction. This article describes a clinical study assessing the effect of early intervention with inhaled sodium cromoglycate in childhood asthma. This was a retrospective study of 189 asthmatic children treated with inhaled sodium cromoglycate for five years and whose age of onset of asthma was six year of age or younger. An end-of-study questionnaire completed the examination. Children administered oral or inhaled corticosteroids simultaneously with sodium cromoglycate, were excluded. Asthma scores as defined by the Japanese Pediatric Allergic Committee, were reduced continuously during the five years after the start of sodium cromoglycate treatment. The frequency of emergency department visits and hospitalizations also decreased. Significant between-period intervention differences showed improvement of clinical outcomes for children with severe asthma during the five years of sodium cromoglycate inhalation. The early intervention regime of starting sodium cromoglycate inhalation within two years of the onset of asthma shows a large improvement in the long-term prognosis of childhood asthma, especially for children with severe asthma. It is possible that starting inhaled sodium cromoglycate earlier than the present recommendation of corticosteroids could further improve clinical outcomes, but a prospective study should be performed to verify our results.

Administration, Inhalation↗

PubMedDate not supplied

Local tissue irritating effects and adjuvant activities of calcium phosphate and aluminium hydroxide with different physical properties.

Effects of calcium phosphate and aluminium hydroxide adjuvants with different physical properties were examined in guinea pigs for local histopathological reactions, electron-microscopical changes of macrophages and adjuvanticity on total IgG antibody response to subcutaneously administered ovalbumin (OVA) and tetanus toxoid (TT). Calcium phosphate gel (Ca-gel) induced active inflammatory reactions consisting of neutrophils (pseudoeosinophils) and foamy macrophages associated with many multinuclear giant cells for at least 4 weeks. Aluminium hydroxide gel (Al-gel) also elicited granulomatous inflammatory reactions consisting mainly of macrophages with foamy cytoplasm, small lymphocytes and giant cells at the injection sites for up to 8 weeks or longer. Severity of local tissue irritation due to calcium phosphate gel (Ca-gel) was similar to that due to Al-gel except for the duration of the inflammatory reactions. Calcium phosphate suspension (Ca-sus)-induced local reactions completely ceased by the 4th week, while aluminium hydroxide suspension (Al-sus)-induced reactions were seen up to the 8th week. Electron-microscopical observations showed that both Al-gel and Al-sus caused damage of macrophages. The adjuvant activity of Al-gel for OVA or TT was significantly stronger than that of any other adjuvant material, whereas those of Ca-gel and Ca-sus were not seen at a dose of 3 mg calcium phosphate per millilitre. Al-sus-TT at a dose of 3 mg aluminium hydroxide per millilitre induced very low levels of antibody. These results suggest that calcium phosphate adjuvant may not be an useful alternative to Al adjuvant.

Adjuvants, Immunologic↗

PubMedDate not supplied

Analysis of the prognosis and the recovery process of profound facial nerve paralysis secondary to acoustic neuroma resection.

The prognosis and the recovery process of facial nerve paralysis were reviewed in 74 patients who, despite preservation of nerve continuity, showed no facial movement after acoustic neuroma resection. In 50 or 67.6% of patients, facial movement recovered sufficiently so as not to require any reanimation procedures. However, no apparent sign of remission was observed for 7-49 months in the other 24 patients (32.4%), and hypoglossal-facial nerve anastomosis was performed in 20 of these patients. When remission was seen, the first sign of muscle movement appeared most frequently after 3-4 months but, in a small number of patients, it was also seen within 1.5 months or after 5-10 months. Based upon these results, the timing of reanimation procedures for facial nerve paralysis following acoustic neuroma resection is discussed.

Adult↗

PubMedDate not supplied

Hypoglossal-facial nerve anastomosis after acoustic neuroma resection: influence of the time anastomosis on recovery of facial movement.

Facial movement following hypoglossal-facial nerve anastomosis was investigated in 29 acoustic neuroma patients. The amount of facial movement was assessed using both the grading system of House and Brackmann and the revised grading scale of Yanagihara. The data were analyzed to determine the influence of the time elapsed between tumor resection and anastomosis upon recovery of facial movement. A slightly larger number of patients with delayed anastomosis (7-23 months) showed minimally poorer results than those with early anastomosis (within 3 months). However, these differences were not statistically significant. Moreover, there was no apparent relationship between the duration of facial nerve paralysis and the recovery of facial movement within either of these two groups. These results showed that hypoglossal-facial nerve anastomosis can be delayed up to 2 years following tumor resection with only minimal effect on the recovery of facial movement.

Adult↗

PubMedDate not supplied

Electromyographic analysis of profound facial nerve paralysis following acoustic neuroma resection.

The aim of our retrospective study was to determine whether electromyographic findings (motor unit action potentials, MUAPs) can be used in long-term prognosis for profound facial nerve paralysis in patients whose nerve continuity is preserved during surgery for acoustic neuroma. The orbicularis oris, frontal, and orbicularis oculi muscles were examined for the occurrence of MUAPs in 48 such patients. In 30 patients who recovered from complete paralysis within 10 months after surgery, MUAPs in the first two muscles tended to precede the first sign of facial movement. MUAPs appeared in the orbicularis muscle in 80% of these patients at 1 month and in all at 5 months. In the frontal and orbicularis oculi muscles, MUAPs occurred in only 0-20% of these patients in the first month; within 3-5 months the number increased rapidly, and MUAPs were present in 95% of these patients at 10 months. In the remaining 18 patients with long-term complete paralysis (at least 1 year), MUAPs appeared solely in the orbicularis oris muscle: in 20% of these patients in the first month after surgery. While this number slowly rose, there was no period of rapid increase later. We conclude that the occurrence of MUAPs in the orbicularis oris and frontal muscles within 3 months of surgery indicates a good prognosis for reversal of facial nerve paralysis.

Anastomosis, Surgical↗

PubMedDate not supplied

Comparison of the metabolism of parathion by a rat liver reconstituted mixed-function oxidase enzyme system and by a system containing cumene hydroperoxide and purified rat liver cytochrome P-450.

The metabolism of parathion by a reconstituted mixed-function oxidase enzyme system (rat liver cytochrome P-450, NADPH-cytochrome c reductase, dilauroyl phosphatidylcholine, deoxycholate, and NADPH) or a cumene hydroperoxide system (cytochrome P-450, dilauroyl phosphatidylcholine, and cumene hydroperoxide) have been compared. The products formed on incubation of parathion with both systems were paraoxon, diethyl phosphorothioic acid, diethyl phosphoric acid, p-nitrophenol, and atomic sulfur. The apparent KM values for parathion for formation of paraoxon and diethyl phosphorothioic acid with the cumene hydroperoxide system were 55 and 39 X 10(-6) M, respectively. These KM values are not significantly different. When the reconstituted system was used, apparent KM values of 2.8 x 10(-6) M for formation of paraoxon and 3.9 x 10(-6) M for The formation of diethyl phosphorothioic acid and diethyl phosphoric acid were determined. These KM values are also not significantly different. covalent binding of the sulfur atom, released in the metabolism of parathion to paraoxon, to the proteins of the reconstituted system and to cytochrome P-450 of the cumene hydroperoxide system was also examined. With both the reconstituted system and the cumene hydroperoxide system approximately 65% of the sulfur released became bound to the proteins of these enzyme systems. The binding of the sulfur atome resulted in a progressive inhibition of the metabolism of parathion by these two systems.

Animals↗

PubMedDate not supplied

Protection against chicken leucocytozoonosis provided by immunization with spleen homogenate infected with Leucocytozoon caulleryi.

Protection against chicken leucocytozoonosis was assessed in chickens immunized with spleen homogenates from chickens that had received sporozoites of Leucocytozoon caulleryi 7 or 13 days previously. Chickens immunized with the homogenate were challenged with sporozoites of L. caulleryi and observed for changes in clinical signs, parasitemia, serum-soluble antigen, and antibody responses. In chickens immunized with either the 7-day or 13-day homogenate, clinical signs and parasitemia were moderate, mild or absent. This was the case both after immunization with the homogenate and after sporozoite challenge. Immunization with spleen homogenates demonstrated protection against chicken leucocytozoonosis.

Animals↗

PubMedDate not supplied

Metabolism of diphenyl sulfoxide in perfused guinea pig liver. Involvement of aldehyde oxidase as a sulfoxide reductase.

To evaluate the metabolic capacity of intact guinea pig liver under normoxic and hypoxic conditions, oxidative and reductive metabolism of diphenyl sulfoxide (DPSO) was studied by the nonrecirculating perfusion method in situ. DPSO was exclusively converted into diphenyl sulfone (DPSO2), an oxidative metabolite, under normoxia. When diphenyl sulfide (DPS) was infused, DPSO was eliminated as a predominant metabolite. Judging from the susceptibility toward selective inhibitors of cytochrome P-450, both oxidative steps appear to be catalyzed by cytochrome P-450-dependent monooxygenase rather than flavin adenine dinucleotide-containing monooxygenase. Under hypoxic conditions, however, DPSO2 formation was decreased in parallel with reduced oxygen concentration in the influent perfusate, whereas only a trace amount of DPS, a reductive metabolite, was detected. On the other hand, coinfusion of an electron donor for aldehyde oxidase such as 2-hydroxypyrimidine and benzaldehyde, but not xanthine, markedly stimulated the formation of DPS during hypoxia. These results indicate that the oxidative pathway catalyzed by cytochrome P-450-dependent monooxygenase is predominant in DPSO metabolism under normoxic conditions, whereas only under hypoxia does the reductive pathway become the major one if an electron donor for aldehyde oxidase exists in intact guinea pig liver.

Aldehyde Oxidase↗