A nomogram to predict exercise capacity from a specific activity questionnaire and clinical data

Recent investigations suggested that clinical exercise testing can be optimized by individualizing the protocol, depending on the purpose of the test and the subject tested. This requires some knowledge of a patient's exercise capacity before beginning the test. The accuracy of a simple physical activity questionnaire and readily available clinical data in predicting subsequent treadmill performance was examined. A brief, self-administered questionnaire (VSAQ) was developed for veterans who were referred to exercise testing for clinical reasons. The VSAQ was designed to determine which specific daily activities were associated with symptoms of cardiovascular disease (fatigue, chest pain and shortness of breath). Two hundred twelve consecutive patients (mean age 62 +/- 8 years) referred for maximal exercise testing were studied. Clinical and demographic variables were added to VSAQ responses in a stepwise regression model to determine their ability to predict treadmill performance. Only metabolic equivalents by VSAQ, and age were significant predictors of treadmill performance; these 2 variables yielded R = 0.82 (SEE 1.43; p < 0.001), and explained 67% of the variance in exercise capacity. The regression equation reflecting the relation between age, VSAQ and exercise capacity was: achieved metabolic equivalents = 4.7 + 0.97 (VSAQ) - 0.06 (age). Using this equation, a nomogram was developed. Incorporating the VSAQ with the nomogram requires only a few minutes, and yields a reasonably accurate estimate of a patient's exercise capacity. Although the present equation is population-specific, a similar approach in different populations may be useful for individualizing protocols for clinical exercise testing.     

A new method of infant monitoring: for use at home and hospital

AIM: To test a New Zealand originated, designed and funded remote infant heart rate monitor in the home and hospital settings (temporarily named the King Monitor) for accuracy and reliability. METHODS: The units were pretested using ECG simulators and on infants already being monitored in the neonatal unit. Longer term trials on hospital infants and infants being simultaneously monitored at home were then conducted. RESULTS: Interference and electrode problems were corrected during the pretesting phase. The unit worked accurately when compared with the standard neonatal heart and respiratory rate monitor in hospital and appeared in some infants to give earlier warning of problems than the standard home apnoea monitor. CONCLUSION: This simple to use monitor worked reliably and accurately under a wide variety of settings and with varying sized infants. In addition, the lack of direct connection between the infant and the control unit allowed freedom of movement of normal infants around the cot or bassinet. The monitor will require to be adapted for portable use at home and during travel.     

Interaction of short nucleotide derivatives with nucleic acids. IV. Modification of DNA by an alkylating tetranucleotide reagents in the presence of effectors in perfect and imperfect complexes

It was demonstrated that any mismatches in a complex formed by an ssDNA target and a tetranucleotide at 25 or 37 degrees C can be discriminated by alkylating the DNA with a tetranucleotide carrying a 4-[N-methyl-N-(2-chloroethyl)]aminobenzylethylamine residue at the 5'-terminal phosphate in the presence of a pair of flanking effectors, octanucleotide di-N-(2-hydroxyethyl)-phenazinium derivatives. The discrimination factor (ratio of the extent of the target modification in the perfect and mismatch-containing complexes) for a single mismatch in the tetranucleotide binding site at 25 degrees C varied between 4 and 500 depending on the type of mismatch and its location in the complex and exceeded 400 at 37 degrees C for all the investigated mismatches. The DNA target modification by the alkylating derivative of the 3'-estrone ester of tetranucleotide pCAGX (mean = C, T, A or G) was selective in the presence of a pair of hydrophobic effectors, octanucleotide 5'-cholesteryl-3'-phenazinium derivatives. The discrimination factors for 3'-terminal mismatches T.G, A.G, and G.G were 1,8,400, and 400, respectively.     

The status of the gastric and duodenal mucosa, biopsied from those who worked in the cleanup of the aftermath of the accident at the Chernobyl Atomic Electric Power Station, in an organotypic tissue culture

Biopsies of stomach and duodenum different regions mucosa obtained from patients with gastroduodenitis (liquidators of consequences of accident in Chernobyl nuclear station--LCA CNS-- and control patients) were studied cultured in vitro. The following are the differences found. Mononuclear cells, differentiating into macrophages were exposed from control biopsies. Mononuclear cells exposed from LCA CNS biopsies formed rosette-like accumulations after mitotic dividing on a distance from the explant. Part of cells within the rosettes acquired processes and formed syncytial structure.     

The ecological cause of the higher accumulation of 90Sr and 137Cs in the food of northern inhabitants

PURPOSE: To quantify S-antigen-specific (S-Ag) T cells in the retina after adoptive transfer, and to evaluate their role in the initiation and progress of destructive ocular inflammation in experimental autoimmune uveoretinitis (EAU). METHODS: Lewis rats were administered 10 x 10(6) S-Ag-specific T cells from the SP35 cell line or 10 x 10(6) concanavalin A-stimulated syngeneic spleen cell lymphoblasts labeled with lipophilic PKH26 fluorescent dye immediately before intravenous inoculation. Labeled cells in each retina were counted at various times from 4 to 120 hours after cell transfer by fluorescence microscopic analysis of each dissociated retina. Recipient eyes were examined within the same period by light and confocal microscope. RESULTS: SP35 T cells showed a biphasic distribution in the retina. The first peak of 160 cells/retina was noted at 24 hours. A steady decline of labeled cells at 48 and 72 hours was followed by a rapid increase at 96 and 120 hours. Concanavalin A-stimulated, control-labeled cell populations showed an identical peak at 24 hours but a persistent decline thereafter; only two or three T cells were present in each retina at 120 hours. Concurrent inoculation of SP35 cells and nonspecific T cell blasts did not produce more SP35 cells than control cells in the retina at any time. Microscopic analysis showed mononuclear cell infiltration of the iris, ciliary body, and aqueous humor at 48 hours, which intensified rapidly and persisted through 120 hours. Retinal inflammation did not begin until 80 hours. Mononuclear cell adherence to vascular endothelium and perivascular macrophage infiltration of the innermost layers progressed to edema, and profound destructive inflammation and loss of retinal stratification were observed at 120 hours. CONCLUSIONS: There is no evidence of a blood-ocular or blood-retinal barrier to activated T cell blasts. Autologous S-Ag does not provoke a more rapid entry of specific T cells at that site. The data confirm that anterior segment inflammation precedes retinal inflammation, even though S-Ag-specific T cells were present in the retina within a few hours after cell transfer. Because S-Ag is clearly present in the retina, delay in antigen presentation at that site may account for the temporal difference between retinal and anterior segment inflammation.     

Functional characterization of transforming growth factor beta type II receptor mutants in human cancer

We recently identified missense mutations at amino acid residues 526 and 537 located within the highly conserved subdomain XI of the transforming growth factor beta type II receptor (TbetaR-II) serine-threonine kinase in two human squamous carcinoma cell lines. These cell lines are resistant to transforming growth factor beta-mediated inhibition of growth. Moreover, treatment with transforming growth factor beta fails to increase the levels of type 1 plasminogen activator inhibitor and fibronectin synthesis. To test the effects of the mutations on receptor function, mutant TbetaR-II cDNAs were expressed in TbetaR-II-deficient T47D cells. Cyclin A promoter activity was reduced by 50% in cells expressing wild-type TbetaR-II but increased 2-fold in cells transfected with either of the two mutant receptors. Conversely, plasminogen activator inhibitor type 1 promoter activity was increased 6-fold in cells transfected with wild-type receptor but not with either of the two mutant receptors. Moreover, the activity of both mutant serine-threonine kinases was strongly reduced compared to that of the wild-type receptor. Thus, the amino acid residues at positions 526 and 537 seem to be essential for kinase function and signaling activity of the TbetaR-II.     

Mutational analysis of N-RAS and GAP-related domain of the neurofibromatosis type 1 gene in chronic myelogenous leukemia

RAS mutations can be detected in a variable number of patients with myeloproliferative disorders such as myelodysplastic syndromes and acute myeloid leukemia, but are rare events in chronic myelogenous leukemia in chronic phase. However, there is good evidence supporting the involvement of RAS signalling pathway in CML and this could be due to alterations in RAS activity regulatory proteins. The neurofibromatosis (NF1) gene down-regulates the RAS signal transduction pathway through the inhibitory function of its GAP-related domain (GRD) on RAS protein. The loss or alteration of neurofibromin (the NF1 protein) may produce a disfunction similar to point mutations in the RAS gene resulting in the permanent stimulation of the RAS signal transduction pathway. Mutations involving the GRD region of the NF1 gene (GRD-NF1) have been described in a variety of tumors such as colon carcinoma and astrocytoma. Germline mutations and deletions in the NF1 gene, as seen in neurofibromatosis type 1, are also associated with certain myeloid disorders. In the present work, we sought to identify mutations in the codons 12/13 and 61 of RAS gene and in the Lys-1423 codon of GRD-NF1, which are well known hot spots in these genes, in a group of 36 adults and ten children with chronic myelogenous leukemia in chronic phase and blast crisis. Using the PCR-SSCP and the allele-specific restriction assay (ASRA) techniques, we were not able to observe any RAS or NF1 detectable mutation. These findings suggest that RAS and GRD-NF1 mutations are not involved either in chronic phase or in the progression to blast crisis in chronic myelogenous leukemia in adults and children.     

Long-term results after reoperation for failed antireflux procedures

From January 1960 to June 1995, 185 patients underwent reoperation without esophageal resection for symptoms of recurrent gastroesophageal reflux disease. There were 102 men and 83 women. Median age was 58 years (range 20 to 84 years). A single previous antireflux operation had been performed in 147 patients, two in 33, and three in 5. The median interval between the reoperation and the previous operation was 36 months (range 1 to 291 months). Indications for reoperation were symptoms in 184 patients and a large paraesophageal hernia in one patients. The surgical approach was by means of a thoracotomy in 133 patients (71.9%), laparotomy in 27 (14.6%), and a thoracoabdominal incision in 25 (13.5%). A Nissen fundoplication was performed in 107 patients (57.8%), Belsey fundoplication in 47 (25.4%), truncal vagotomy and antrectomy with Roux-en-Y reconstruction in 17 (9.2%), anatomic hernia repair in 12 (6.5%), and Hill gastropexy in 2 (1.1%). A Collis gastroplasty was added to the fundoplication in 116 patients (62.7%), and a pyloroplasty was performed in 17 (9.2%). There was one operative death (0.5%). Complications occurred in 47 patients (25.4%). Median postoperative hospitalization was 9 days (range 5 to 58 days). Follow-up was complete in 156 patients (84.3%) and ranged from 3 to 283 months (median 44 months). Improvement occurred in 137 patients (87.8%). Functional results were classified as excellent in 65 patients (41.6%), good in 29 (18.6%), fair in 43 (27.6%), and poor in 19 (12.2%). No single operative approach or procedure proved to be functionally superior. We conclude that reoperation with esophageal preservation after a failed antireflux procedure will result in significant functional benefit and can be performed with low mortality and acceptable morbidity. The type of repair should be tailored to the individual patient.