Using satellite-based measurements to explore spatiotemporal scales and variability of drivers of new particle formation.

New particle formation (NPF) can potentially alter regional climate by increasing aerosol particle (hereafter particle) number concentrations and ultimately cloud condensation nuclei. The large scales on which NPF is manifest indicate potential to use satellite-based (inherently spatially averaged) measurements of atmospheric conditions to diagnose the occurrence of NPF and NPF characteristics. We demonstrate the potential for using satellite-based measurements of insolation (UV), trace gas concentrations (sulfur dioxide (SO2), nitrogen dioxide (NO2), ammonia (NH3), formaldehyde (HCHO), and ozone (O3)), aerosol optical properties (aerosol optical depth (AOD) and Ångström exponent (AE)), and a proxy of biogenic volatile organic compound emissions (leaf area index (LAI) and temperature (T)) as predictors for NPF characteristics: formation rates, growth rates, survival probabilities, and ultrafine particle (UFP) concentrations at five locations across North America. NPF at all sites is most frequent in spring, exhibits a one-day autocorrelation, and is associated with low condensational sink (AOD × AE) and HCHO concentrations, and high UV. However, there are important site-to-site variations in NPF frequency and characteristics, and in which of the predictor variables (particularly gas concentrations) significantly contribute to the explanatory power of regression models built to predict those characteristics. This finding may provide a partial explanation for the reported spatial variability in skill of simple generalized nucleation schemes in reproducing observed NPF. In contrast to more simple proxies developed in prior studies (e.g., based on AOD, AE, SO2, and UV), use of additional predictors (NO2, NH3, HCHO, LAI, T, and O3) increases the explained temporal variance of UFP concentrations at all sites.

Sta-Peg arthroereisis for treatment of the planovalgus foot in cerebral palsy.

The Sta-Peg procedure is most effective in the non-rigid foot in which reasonable muscle balance can be attained. Where such balance cannot be attained or where rigid deformity exists, this procedure will not solve the problem and should not be used. The authors want to emphasize that this study pertains to the use of Sta-Peg in the valgus foot caused by cerebral palsy. The procedure is rarely needed in the flexible flatfoot of a normal child.

Elevated expression of the junB proto-oncogene is essential for v-fos induced transformation of Rat-1 cells.

We previously described the isolation of non-tumorigenic revertants from mutagenized populations of v-fos-transformed Rat-1 cells (Zarbl et al., 1987). In the present study we examined the possibility that the revertant phenotype resulted from mutations that altered the expression or activities of the c-jun or junB proto-oncogenes. The results demonstrated that levels of the c-jun mRNA and protein were unchanged in the revertants when compared to the transformed parental cells, and ectopic overexpression of c-jun failed to retransform the revertants. Although one mutant allele was detected in revertant EMS-1-19, overexpression of this mutant allele failed to inhibit v-fos induced cell transformation. Together these results indicated that the revertant phenotype did not result from altered expression or mutations in the c-jun gene. In contrast to the results obtained with c-jun, the levels of junB mRNA and protein were found to be reduced two- or threefold in revertant EMS-1-19. Ectopic overexpression of junB induced transformation of revertant EMS-1-19, but failed to transform Rat-1 cells. Moreover, about 10% of v-fos transformed cells transfected with vectors that express antisense junB mRNA acquired a non-transformed phenotype. Together these results indicate that expression of junB above a threshold level is essential for v-fos-induced transformation of Rat-1 fibroblasts.

Functional in vitro assays for the isolation of cell transformation effector and suppressor genes.

Malignant transformation may be viewed as an imbalance between signals inducing cell growth and signals leading to growth inhibition, differentiation, or senescence. A basic understanding of how these counterbalancing forces interact to regulate normal cell growth is the prerequisite to comprehending the mechanisms of tumorigenesis. Identification and characterization of the gene products implicated in these regulatory pathways is the first step toward understanding the disease process. The studies outlined here provide the potential basis for isolating and molecularly characterizing transformation effector and suppressor genes, which must respectively function in the positive and negative regulation of normal cell growth. The general strategy used involves the isolation and molecular characterization of nontransformed variants (revertants) from populations of tumor cells. The selection of revertants is facilitated by the ability to separate normal from transformed cells by fluorescence-activated sorting. The basis for this separation is the differential retention of the fluorescent dye rhodamine 123 in the mitochondria of normal versus transformed cells. Using this approach, we have isolated revertants from a mutagenized population of v-fos-transformed Rat-1 fibroblasts. Characterization of these clones indicated that they had sustained causal mutations in transformation effector genes. The unmutated effector genes are being identified and molecularly cloned by isolating retransformed clones from revertant cell lines that have been transfected with DNA or cDNA from normal primary cells. The same selection protocol has also been used to isolate revertants from tumor cell lines that have been transfected with DNA or cDNA from primary cells. The putative tumor-suppressor genes present in these revertants are currently being analyzed.

Sacral ribs. A case report.

Supernumerary ribs are a rare anatomic curiosity usually discovered as an incidental finding on routine radiographs. The occurrence of sacrococcygeal ribs are extremely rare. Sacral ribs develop as a consequence of the failure of the rib anlage to fuse with the vertebral centers. The present case is unique from previous reports because of the associated scoliosis and hypoplasia of the ipsilateral gluteal musculature and foramina within the accessory rib.

Use of size-exclusion and ion-exchange high-performance liquid chromatography for the isolation of biologically active growth factors.

Size-exclusion and ion-exchange high-performance liquid chromatography were used to purify biologically active growth factors as measured by the ability of the factors to stimulate DNA synthesis in 3T3 cells. Chromatography was performed in aqueous buffer and at neutral pH to avoid possible inactivation of biological activity. The growth factors analyzed were chondrosarcoma growth factor (CHSA-GF), human milk growth factor (HMGF), retinal-derived growth factor (RDGF) and mouse epidermal growth factor (EGF). CHSA-GF, HMGF, and RDGF were eluted from TSK 2000 columns as well-defined peaks of activity with molecular weights of 12,000-15,000, 5000-6000, and 16,000-18,000, respectively. EGF was found to have an abnormally low molecular weight after chromatography on TSK 2000. However, incorporation of guanidine . HCl into the TSK column resulted in the elution of EGF at its known molecular weight of ca. 6000. Anion-exchange high-performance liquid chromatography on AX 300 was used for the purification of HMGF and RDGF, and cation-exchange high-performance liquid chromatography on CM 300 was used for the purification of CHSA-GF. The results show that size-exclusion and ion-exchange chromatography can be used without organic solvents or extremes in pH to purify a number of different growth factors successfully with retention of biological activity.

Orthopaedic management of lumbosacral agenesis. Long-term follow-up.

Twenty-two patients with lumbosacral agenesis were treated at the Shriners Hospital for Crippled Children, Chicago Unit, from 1953 to 1979. At the time of this study, ten of the patients were skeletally mature after an average follow-up of 24.1 years. Two patients had died, twelve could be examined, and eight who were unable to return for examination responded to a questionnaire. Eleven of the patients had diabetic mothers. Of the orthopaedic problems in these patients, knee-flexion contractures with popliteal webbing were the most difficult to correct. These deformities varied in severity with the level of the agenesis and the resulting loss of motor power. Other problems were dislocations and flexions contractures of the hips, scoliosis, equinovarus deformities of the foot, and instability at the spinal-pelvic junction. When there was inadequate quadriceps function it was difficult to correct knee-flexion contractures and to prevent them from recurring. For severe knee deformity, knee disarticulation and prosthetic fitting were the most effective treatment. Spinal-pelvic instability was not a problem in eighteen of the twenty surviving patients. Unreduced dislocated hips also did not cause any problems.

Binding of bovine thyrotropin to receptors in rat testis and its interaction with gonadotropins.

Previously, we have shown that preparations of hCG bind to bovine thyroid membranes, as judged from their ability both to inhibit the binding of 125I-labeled bovine TSH (bTSH) and to activate adenylate cyclase (Amir, S.M., H. Uchimura, and S.H. Ingbar, J Clin Endocrinol Metab 45: 280, 1977). In the present studies, 125I-labeled, highly purified bTSH ([125I]bTSH) has been shown to bind specifically and saturably to receptors in a particulate fraction from rat testis. At 37 C, binding was rapid, reaching a maximum level in less than 15 min, but then declining markedly during the next several hours. At 22 C, binding reached a steady state after 2 h and remained unchanged for another 22 h. Binding of [125I]bTSH was greatest at pH 5.5, at which pH more than 50% of [125I]bTSH was bound in the presence of 330 microgram/ml particulate protein, the concentration of protein that yielded maximum binding. Nevertheless, the majority of experiments were conducted at lesser protein concentrations and at physiological pH (7.45), under which conditions total binding was only 25% of that measured at pH 5.5. Scatchard plots indicated the presence of a single binding site with a dissociation constant of 5.8 X 10(-8) M and a binding capacity of 0.22 nmol/mg protein on the basis of data obtained at 22 C and pH 7.45. Both crude and highly purified preparations of hCG inhibited the binding of [125I]bTSH to testis particulate fraction; crude hCG had 46 times the activity, and purified hCG had only one-tenth the activity of bTSH itself in this respect. This was true despite the fact that with respect to the displacement of [125I]hCG, crude and purified hCG were almost equally active. Bovine LH had one-third the activity of bTSH in displacing [125I]bTSH. Human FSH inhibited [125I]bTSH binding only slightly at the highest concentration tested, while glucagon, insulin, PRL, and GH were inactive. Purified bTSH inhibited the binding of [125I]hCG to testis particulate fraction but contained only about 2% of the activity of purified hCG. Lineweaver-Burk analysis suggested that inhibition of [125I]hCG binding by bTSH was competitive in nature. Purified bTSH stimulated cAMP production in Leydig cells, but with only about 0.1% of the activity of purified hCG. It is concluded that bTSH binds reversibly, saturably, and with relatively high affinity to receptors in rat testis that are either the same as receptors for hCG and LH or that interact therewith. bTSH, like hCG, is capable of stimulating the production of cAMP in rat Leydig cells, but is much less potent than hCG in this regard. Preparations of crude hCG contain a factor lacking hCG activity in bioassay, immunoassay, and receptor assay that is especially potent in displacing [125I]bTSH from receptors in testis, as has earlier been described for bTSH receptors in bovine thyroid membranes.