Exhaled nitric oxide as an indicator of severity of asthmatic inflammation

Traditional assessment of severity of asthma relies on an evaluation of signs and symptoms and pulmonary function tests. These pulmonary function tests, such as peak expiratory flow rates, forced vital capacity, and forced expiratory flow rates, are indirect measures of airway caliber only, and not inflammation. Since asthma is an inflammatory disease, a measure of the degree of inflammation would be helpful in quantitating severity and titrating of anti-inflammatory therapy. A noninvasive method for measuring pulmonary inflammation would therefore be helpful to assist the emergency physician in initial treatment and assist in titration of anti-inflammatory therapy during repeat visits. Exhaled nitric oxide (NO) assays are convenient and practical and may fulfill this role. In this review, we discuss the role of NO in asthmatic inflammation and the role that exhaled NO values may play in the emergency management of asthma.     

Altering the NICU and measuring infants' responses

The aim of the study was to measure the impact of a designated Quiet period on the NICU environment and its influence on the infants' physiological and movement responses. The study group comprised 10 preterm infants on assisted ventilation (mean gestational age 28.7 wk (range 24-32 wk), mean birthweight 1,322 g (range 600-2,060 g), mean age 5.2 d). The environment in which the infants were nursed was altered in terms of reduced light, noise, staff activity and infant handling. The infants' heart rate, blood pressure, oxygen saturation and movement responses were recorded during this Quiet period and compared with a period of Normal activity. When the Quiet period was compared with the Normal period (median values), the NICU environment had significantly altered in terms of Light: Quiet period 3.0 Lux, Normal period 254.5 Lux (p < 0.01); Noise: Quiet period 54.0 dB, Normal period 58.0 dB (p < 0.01); Alarm events: Quiet period 491.5 sec, Normal period 1,180.5 sec (p < 0.01); Staff conversation: Quiet period 16.0 occasions per hour, Normal period 60.0 occasions per hour (p < 0.01); Staff activity: Quiet period 25.5 occasions per hour, Normal period 59.0 occasions per hour (p <0.01); Infant handling: Quiet period 0.0 events per hour, Normal period 4.5 events per hour (p < 0.01). Infants' diastolic blood pressure and mean arterial pressure: median reduction of 2 mmHg for both during the Quiet period (p < 0.05). Infants' movements: Quiet period 14.5 movements per hour, Normal period 84.0 movements per hour (p < 0.05). DISCUSSION: This study demonstrates that Quiet periods are feasible for infants undergoing neonatal intensive care. The NICU environment was altered significantly for light, noise, infant handling and staff activity for a specified time period. These changes were associated with a reduced median diastolic blood pressure and mean arterial pressure and a decrease in infant movements.     

Meningococcal disease in Dallas County, Texas: results of a six-year population-based study

OBJECTIVE: Neisseria meningitidis is an important cause of serious bacterial infection in children and adults in the US. From 1992 to 1997 invasive disease caused by N. meningitidis was studied among 1.9 million residents of Dallas County, TX METHODS: The demographic characteristics and diagnoses of 151 patients were identified through active, population-based surveillance and review of medical records. Serogroups were determined for strains infecting 129 (85%) patients. RESULTS: The average annualized incidence rate was 1.3 cases per 100,000 person years and was highest for children <1 year (13 cases/100,000 person years). Older patients (50+ years old) were more likely to present with pneumonia and less likely to present with meningitis than younger patients. Neither the fatality rate nor the duration of hospitalization for surviving patients was associated with age. Among patients with a known serogroup, serogroup C disease was found in 35% of cases <1 year old, 64% of those 1 to 49 years old and 44% of those 50+ years old. Serogroup B strains were isolated from 26% of patients <1 year, 17% of patients 1 to 49 years old and none of the patients 50+ years old. Serogroup Y disease increased from 22% to 35% of cases between 1992 and 1997 (P = 0.03). This serogroup was identified in 26% of patients <1 year old, 17% of patients 1 to 49 years old and in 50% of patients 50+ years old. Serogroup C and Y accounted for 61% of cases in children <1 year old and for 79% of cases in all age groups. CONCLUSION: The results underscore the importance of conjugate vaccines for serogroups C and Y.     

Is it necessary to administer anti‐D to prevent RhD immunization after the transfusion of RhD‐positive platelet concentrates?

Serology for the presence of anti-D after RhD-incompatible platelet transfusions was performed in 24 RhD-negative patients with haematological disease and 59 RhD-negative patients with non-haematological disease. None of the patients were given prophylaxis with anti-D to prevent RhD immunization. Eight out of 59 (13.5%) non-haematology patients developed detectable anti-D, whereas 0 out of 24 (0%) of the haematology patients formed anti-D (P = 0.06). The risk of alloimmunization after RhD-incompatible platelet transfusions using platelet concentrates prepared by modern technical methods appears to be small in patients with haematological disease, but is significant in non-immunocompromised patients.     

Effects of alcohol and saccharin deprivations on concurrent ethanol and saccharin operant self-administration by alcohol-preferring (P) rats

Consumption of sweet solutions has been associated with a reduction in withdrawal symptoms and alcohol craving in humans. The objective of the present study was to determine the effects of ethanol and saccharin (SACC) deprivations on operant oral self-administration. Alcohol-preferring (P) rats were allowed to lever press concurrently self-administer ethanol (15% vol/vol) and SACC (0.0125% g/vol) for 8 weeks. Rats were then maintained on daily operant access (nondeprived), deprived of both fluids (2 weeks), deprived of SACC and given 2 ml of ethanol daily, or deprived of ethanol and given 2 ml of SACC daily. All groups were then given 2 weeks of daily operant access to ethanol and SACC, followed by an identical second deprivation period. P rats responded more for ethanol than SACC. All deprived groups increased responding on the ethanol lever, but not on the SACC lever. Daily consumption of 2 ml ethanol decreased the duration of the alcohol deprivation effect (ADE). Home cage access to 2 ml of SACC also decreased the ADE but to a lesser extent than access to ethanol. A second deprivation period further increased and prolonged the expression of an ADE. These results show ethanol is a more salient reinforcer than SACC. With concurrent access to ethanol and SACC, P rats do not display a saccharin deprivation effect. Depriving P rats of both ethanol and SACC had the most pronounced effect on the magnitude and duration of the ADE, suggesting that there may be some interactions between ethanol and SACC in their CNS reinforcing effects.     

MNNG-induced gastric carcinoma in ferrets infected with Helicobacter mustelae

N-Methyl-N-nitro-N'-nitrosoguanidine (MNNG) is a gastric carcinogenin several animal species and has been used in a number of systemsto dissect the co-carcinogenic potential of various compoundsin the induction of gastric adeno-carcinoma. Recent epidemiologicalevidence suggests that Helicobacter pylori may play a role asa co-carcinogen in the etiology of this tumor in humans andwe have been interested in developing an animal model to studythis possibility. A related organism, H.mustelae, naturallycolonizes the ferret stomach and causes persistent chronic gastritis.The pathology elicited by H.mustelae in ferrets has many similaritieswith the human disease including different stages of multifocalatrophic gastritis which underlie the gastric ulcer and gastriccarcinoma syndrome. There is little evidence, however, demonstratingthe susceptibility of ferrets toward chemical carcinogenesis.We have consequently undertaken a study to ascertain whether10 6-month-old female ferrets given a single oral dose of MNNG(50–100 mg/kg) would develop adeno-carcinoma of the stomach.Five age-matched unmanipulated control animals were includedfor comparative purposes. All 15 ferrets were infected withH.mustelae. Nine of 10 ferrets dosed with MNNG developed gastricadenocarcinoma (29–55 months after dosing), while noneof the five historical control ferrets examined an average of63 months after the initiation of the study developed gastrictumors. By comparison, we have not observed gastric adenocarcinoma,nor has it been reported, in >10 years of observation ofuntreated ferrets naturally infected with H.mustelae. The H.mustelae-infectedferret, with demonstrated susceptibility to a gastric carcinogen,plus the recent availability of specific pathogen-free ferrets,should now allow longitudinal studies in vivo to probe the roleof Helicobacter in the development of gastric cancer.