Education of parents of infants and very young children with asthma: a developmental evaluation of the Wee Wheezers program

A randomized control trial of the Wee Wheezers asthma education program was conducted with 76 children < 7 years of age, 31% of whom were on a medication regimen consistent with mild, 51% with moderate, and 18% with moderately severe/severe asthma. Treatment children showed improved morbidity at 3-month follow-up relative to the changes in the controls: increased symptom-free days in the preceding 2 weeks (mean change of +2.2 vs. -2.6 in the controls; p = .004) and month (+2.0 vs. -3.8; p < .02), fewer nights of parental sleep interruption in a typical week (+0.7 vs. +1.8; p < or = .05), and a trend toward fewer asthma sick days (-0.2 vs +0.7; p = ns). These improvements were accompanied by significantly better parental asthma management compared with controls (more consistent use of preventive medications, p < or = .01; early symptom intervention, [corrected] p < or = .05) and trends toward more restrictions on smoking in the home (p < .07) and decreased parental confusion about asthma treatment (p < .11). This study provides evidence that a multisession program of asthma education for parents can improve parental asthma management and clinical outcomes in very young children and provides information on the validity and sensitivity of various asthma outcome measures in this age group.     

Magnetic resonance imaging scanning in the diagnosis of zone II flexor tendon rupture

This study was undertaken to determine the usefulness of magnetic resonance imaging (MRI) in the diagnosis of flexor tendon rupture in patients who had prior surgery. Magnetic resonance imaging scans were performed on 11 digits (16 tendons) with the clinical diagnosis of flexor tendon rupture. Clinical suspicion correlated with MRI and surgical findings. Clinical examination yielded a 60% accuracy in diagnosis. MRI differentiated rupture from adhesions with a 100% accuracy rate. The MRI scan is a valuable tool in diagnosing tendon ruptures and may help reduce the incidence of unnecessary tendon explorations.     

Intraarticular foot and ankle injections to identify source of pain before arthrodesis

OBJECTIVE: The purpose of our study was to evaluate the usefulness of diagnostic joint injections in patients with foot and ankle pain when the radiologist attempts to identify the source of pain. This study also correlated the results of injection with outcome after arthrodesis. MATERIAL AND METHODS: We retrospectively reviewed the records of 22 patients who had a foot or ankle joint injected to identify a source of pain and who later underwent arthrodesis of the painful joint. All patients had long-term foot and ankle symptoms of variable causes. Twenty-four joints were assessed: 13 subtalar, five talonavicular, four ankle, one calcaneocuboid, and one metatarsocuneiform. All patients had plain radiographs, 11 had CT studies, and five had bone scans. Contrast material was used to assess adequate positioning of the needle inside the joint before injection. All joints were injected under fluoroscopic control. Steroid was added in eight joints. After injection, patients were assessed for relief of symptoms. Patients subsequently underwent arthrodesis on the basis of the results of the injection. RESULTS: In 20 patients (22 joints), long-term follow-up showed that injections allowed us to correctly identify the source of pain and successfully guide arthrodesis. Of these 20 patients, 17 had significant pain relief after injection and fusion, whereas three patients had mild or no response. With one of these patients, we injected other joints and changed surgical plans. One of the two remaining patients had more pain relief after injection than after arthrodesis. The other patient had no relief after injection, but subsequent fusion because of persistent pain was successful. We found imaging studies to be less useful than diagnostic injections when we were attempting to identify the source of pain. CONCLUSION: Intraarticular injection of anesthetic in painful foot and ankle joints helped us confirm the source of pain in 20 of 22 patients, which in turn led to successful arthrodesis and good outcomes for these patients.     

Inhibition of G1 cyclin-dependent kinase activity during growth arrest of human breast carcinoma cells by prostaglandin A2

Prostaglandin A2 (PGA2) potently inhibits cell proliferation and suppresses tumor growth in vivo, but little is known regarding the molecular mechanisms mediating these effects. Here we demonstrate that treatment of breast carcinoma MCF-7 cells with PGA2 leads to G1 arrest associated with a dramatic decrease in the levels of cyclin D1 and cyclin-dependent kinase 4 (cdk4) and accompanied by an increase in the expression of p21. We further show that these effects occur independent of cellular p53 status. The decline in cyclin D and cdk4 protein levels is correlated with loss in cdk4 kinase activity, cdk2 activity is also significantly inhibited in PGA2-treated cells, an effect closely associated with the upregulation of p21. Immunoprecipitation experiments verified that p21 was indeed complexed with cdk2 in PGA2-treated cells. Additional experiments with synchronized MCF-7 cultures stimulated with serum revealed that treatment with PGA2 prevents the progression of cells from G1 to S. Accordingly, the kinase activity associated with cdk4, cyclin E, and cdk2 immunocomplexes, which normally increases following serum addition, was unchanged in PGA2-treated cells. Furthermore, the retinoblastoma protein (Rb), a substrate of cdk4 and cdk2 whose phosphorylation is necessary for cell cycle progression, remains underphosphorylated in PGA2-treated serum-stimulated cells. These findings indicate that PGA2 exerts its growth-inhibitory effects through modulation of the expression and/or activity of several key G1 regulatory proteins. Our results highlight the chemotherapeutic potential of PGA2, particularly for suppressing growth of tumors lacking p53 function.     

The imprinted domain in mouse distal Chromosome 7: reagents for mutagenesis and sequencing

BACKGROUND: Right lower quadrant abdominal pain may pose a diagnostic problem in patients with cystic fibrosis. Abdominal ultrasound examination, used commonly in the diagnostic work-up, may reveal abnormalities of the appendix. However, interpretation of such findings is problematic, because the appearance of the gastrointestinal system during routine examination has not been documented in patients with cystic fibrosis. The purpose of this study was to investigate the findings during routine abdominal ultrasound scans in our cohort of patients with cystic fibrosis and in control subjects. METHODS: Abdominal ultrasound scans were performed prospectively during routine clinic visits in a cohort of patients with cystic fibrosis. RESULTS: Fifty patients aged 10+/-6 years, (range, 0.5-28 years) were examined; 45 had pancreatic insufficiency. Four patients (3 with pancreatic insufficiency) reported right lower quadrant pain at the time of the scan. According to standard ultrasound criteria, the appearance of the appendix was abnormal in 8 patients (16%), 6 had a mucoid appendix, and 2 had a pathologically thickened appendiceal wall. Only 1 of these 8 patients mentioned abdominal pain at the time of the study. Other incidental findings included gallstones (3 patients), intussusception (2 patients), and pancreatic cyst (1 patient). CONCLUSIONS: Abnormalities can be observed during routine abdominal ultrasonographic studies in cystic fibrosis. These findings may not be associated with abdominal pain; their clinical relevance needs further investigation.     

A gene for autosomal recessive symmetrical spastic cerebral palsy maps to chromosome 2q24-25

Cerebral palsy has an incidence of approximately 1/500 births, although this varies between different ethnic groups. Genetic forms of the disease account for approximately 1%-2% of cases in most countries but contribute a larger proportion in populations with extensive inbreeding. We have clinically characterized consanguineous families with multiple children affected by symmetrical spastic cerebral palsy, to locate recessive genes responsible for this condition. The eight families studied were identified from databases of patients in different regions of the United Kingdom. After ascertainment and clinical assessment, we performed a genomewide search for linkage, using 290 polymorphic DNA markers. In three families, a region of homozygosity at chromosome 2q24-q25 was identified between the markers D2S124 and D2S148. The largest family gave a maximum LOD score of 3.0, by multipoint analysis (HOMOZ). The maximum combined multipoint LOD score for the three families was 5.75. The minimum region of homozygosity is approximately 5 cM between the markers D2S124 and D2S2284. We have shown that a proportion of autosomal recessive symmetrical spastic cerebral palsy maps to chromosome 2q24-25. The identification of genes involved in the etiology of cerebral palsy may lead to improved management of this clinically intractable condition.