Biomedical subjects

G Fritz

Publications and source records attributed to G Fritz.

At least 55 records · Page 3Linked to original sources

PubMed1998

Cytokine induction of NO synthase II in human DLD-1 cells: roles of the JAK-STAT, AP-1 and NF-kappaB-signaling pathways.

1. In human epithelial-like DLD-I cells, nitric oxide synthase (NOS) II expression was induced by interferon-gamma (100 u ml(-1)) alone and, to a larger extent, by a cytokine mixture (CM) consisting of interferon-gamma, interleukin-1beta (50 u ml(-1)) and tumor necrosis factor-alpha (10 ng ml(-1)). 2. CM-induced NOS II expression was inhibited by tyrphostin B42 (mRNA down to 1%; nitrite production down to 0.5% at 300 microM) and tyrphostin A25 (mRNA down to 24%, nitrite production down to 1% at 200 microM), suggesting the involvement of janus kinase 2 (JAK-2). Tyrphostin B42 also blocked the CM-induced JAK-2 phosphorylation (kinase assay) and reduced the CM-stimulated STAT1alpha binding activity (gel shift analysis). 3. CM reduced the nuclear binding activity of transcription factor AP-1. A heterogenous group of compounds, that stimulated the expression of c-fos/c-jun, enhanced the nuclear binding activity of AP-1. This group includes the protein phosphatase inhibitors calyculin A, okadaic acid, and phenylarsine oxide, as well as the inhibitor of translation anisomycin. All of these compounds reduced CM-induced NOS II mRNA expression (to 9% at 50 nM calyculin A; to 28% at 500 nM okadaic acid; to 18% at 10 microM phenylarsine oxide; and to 19% at 100 ng ml(-1) anisomycin) without changing NOS II mRNA stability. In cotransfection experiments, overexpression of c-Jun and c-Fos reduced promoter activity of a 7 kb DNA fragment of the 5'-flanking sequence of the human NOS II gene to 63%. 4. Nuclear extracts from resting DLD-1 cells showed significant binding activity for transcription factor NF-kappaB, which was only slightly enhanced by CM. The NF-kappaB inhibitors dexamethasone (1 microM), 3,4-dichloroisocoumarin (50 microM), panepoxydone (5 microg ml(-1)) and pyrrolidine dithiocarbamate (100 microM) produced no inhibition of CM-induced NOS II induction. 5. We conclude that in human DLD-1 cells, the interferon-gamma-JAK-2-STAT1alpha pathway is important for NOS II induction. AP-1 (that is downregulated by CM) seems to be a negative regulator of NOS II expression. NF-kappaB, which is probably important for basal activity of the human NOS II promoter, is unlikely to function as a major effector of CM in DLD-1 cells.

Cytokines↗

PubMed1998

Relationship of asthma severity and psychological problems in children.

OBJECTIVE: To determine whether physiological severity of asthma is associated with increased psychological symptoms in children. METHOD: Participants were 337 children, aged 7 to 19 years (mean 11.9, SE 0.13), and a parent of each child. Children's asthma severity was rated by experienced pediatric asthma specialists using current guidelines from the National Heart, Lung, and Blood Institute. Children filled out the Children's Manifest Anxiety Scale and the Weinberger Adjustment Inventory. Parents reported on their child's medical history, completed the Child Behavior Checklist (CBCL) about their child, and completed the Pennebaker Inventory of Linguid Languidness as a measure of their own physical symptoms. RESULTS: Child-rated anxiety symptoms were unrelated to asthma severity or to markers of asthma functional morbidity. Parental ratings of internalizing symptoms in their children were related to severity. Parent physical symptoms explained 10.2% of the variance in CBCL Internalizing symptoms, and asthma severity added an additional 6.7% to the variance. CONCLUSIONS: Asthma severity may be a more salient stressor to parents, who in turn report higher levels of child internalizing symptoms for children with severe asthma, than to children themselves. Contrary to prior hypotheses, children with severe asthma did not rate themselves as having higher levels of anxiety than those with mild or moderate asthma or than standardized norms.

Adolescent↗

PubMed1997

rhoB encoding a UV-inducible Ras-related small GTP-binding protein is regulated by GTPases of the Rho family and independent of JNK, ERK, and p38 MAP kinase.

The small GTPase RhoB is immediate-early inducible by DNA damaging treatments and thus part of the early response of eukaryotic cells to genotoxic stress. To investigate the regulation of this cellular response, we isolated the gene for rhoB from a mouse genomic library. Sequence analysis of the rhoB gene showed that its coding region does not contain introns. The promoter region of rhoB harbors regulatory elements such as TATA, CAAT, and Sp1 boxes but not consensus sequences for AP-1, Elk-1, or c-Jun/ATF-2. The rhoB promoter was activated by UV irradiation, but not by 12-O-tetradecanoylphorbol-13-acetate treatment. rhoB promoter deletion constructs revealed a fragment of 0.17 kilobases in size which was sufficient in eliciting the UV response. This minimal promoter fragment contains TATA and CAAT boxes but no other known regulatory elements. Neither MEK inhibitor PD98059 nor p38 kinase inhibitor SB203580 blocked stimulation of rhoB by UVC (UV light, 254 nm) which indicates that ERK or p38 mitogen-activated protein (MAP) kinase are not involved in the UV induction of rhoB. Also, phosphatidylinositol 3-kinase inhibitor wortmannin, which blocks UV stimulation of both JNK and p38 MAP kinase, did not inhibit rhoB activation. Furthermore, activation of JNK by interleukin-1beta did not affect rhoB expression. These data indicate that JNK is not involved in the regulation of rhoB. Overexpression of wild-type Rac as well as the Rho guanine-dissociation inhibitor caused activation of rhoB. Wild-type RhoB inhibited both basal and UV-stimulated rhoB promoter activity, indicating a negative regulatory feedback by RhoB itself. The data provide evidence both for a signal transduction pathway independent of JNK, ERK, and p38 MAP kinase to be involved in the induction of rhoB by genotoxic stress, and furthermore, indicate autoregulation of rhoB.

Animals↗

PubMed1997

High-dose selection with mafosfamide results in sensitivity to DNA cross-linking agents: characterization of hypersensitive cell lines.

One of the most frequently used alkylating drugs in the therapy of a broad spectrum of tumors is cyclophosphamide. To elucidate the mechanisms by which tumor cells acquire resistance to this agent, Chinese hamster ovary cells (CHO-K1) were treated with a high dose of the cyclophosphamide analogue mafosfamide, and survivors were analyzed as to their cell killing response, chromosomal aberrations, and DNA repair capacity. None of the surviving clones tested were mafosfamide resistant. Surprisingly, some of the isolated cell lines exhibited a mafosfamide-hypersensitive phenotype. Two of these cell variants (designated as CHO-K1-4 and CHO-K1-12) were analyzed in more detail and proved to be cross-sensitive to other DNA cross-linking antineoplastic drugs such as N-hydroxyethyl-N-chloroethylnitrosourea, treosulfan, melphalan, cisplatin, and mitomycin C. The hypersensitivity to the cytotoxic effect of mafosfamide was accompanied by a 2-3-fold increase in the frequency of chromosomal aberrations. The intracellular levels of glutathione and glutathione S-transferase activity of the hypersensitive variants as well as growth rate were comparable to wild-type cells. Both the variant and the parental cells did not exhibit an increase in the amount of p53 upon UV irradiation. Furthermore, sensitive cells displayed similar UV-induced unscheduled DNA synthesis and showed identical amounts of ERCC1 mRNA as wild-type cells, indicating that the hypersensitive phenotype is not due to a defect in nucleotide excision repair. The induction of DNA single-strand breaks upon mafosfamide treatment was very similar in wild-type and mutants, and the removal of mafosfamide-induced DNA cross-links was not reduced in hypersensitive cells. However, the hypersensitive cell variants exhibited a less severe drug-induced block to DNA replication. From the data obtained, we conclude that hypersensitivity to cross-linking agents upon mafosfamide selection is due to changes in cell cycle progression of drug-treated cells.

Animals↗

PubMed1996

Active site mutation of the C3-like ADP-ribosyltransferase from Clostridium limosum--analysis of glutamic acid 174.

Clostridium limosum ADP-ribosyltransferase modifies low molecular mass GTP-binding proteins of the Rho subtype family. Here we cloned and sequenced the gene of the transferase and expressed it in Escherichia coli. The gene encodes a protein of 250 amino acids (M(r) = 27,840), with a putative signal peptide of 45 amino acids, that shows about 60-65% identity with C3 transferases from Clostridium botulinum. The mature C. limosum transferase was expressed as a maltose-binding fusion protein in E. coli and purified to apparent homogeneity. To study the functional role of Glu174 of C. limosum transferase, which was recently photoaffinity-labeled with [carbonyl-14C]NAD [Jung, M., et al. (1993) J. Biol. Chem. 268, 23215-23218], two mutants E174D and E174Q were constructed by a polymerase chain reaction-based system. The E174D and E174Q mutants showed a dramatic decrease in kcat, but no major changes in Km,NAD. Furthermore, replacement of Glu174 by aspartic acid and glutamine largely reduced and completely blocked UV-induced incorporation of [carbonyl-14C]NAD into the transferase. The data indicate that Glu174 is an active site residue of C. limosum transferase.

ADP Ribose Transferases↗

PubMed1996

Radiographic assessment of the second metatarsal: measure of first ray hypermobility.

Hypermobility of the first metatarsal cuneiform joint has been implicated as a cause of the hallux valgus deformity. The objective definition of hypermobility at this joint, however, has not been clearly defined. We used a modified Coleman block test to accentuate motion at the first metatarsal cuneiform joint in order to measure physiologic limits of motion in vivo. This motion was compared with radiographic analysis of the feet, which included the hallux valgus angle, intermetatarsal angle, and medial cortical thickening at the midshaft of the second metatarsal. This assessment was performed on 100 feet (50 right feet and 50 left feet in 50 patients). The average intermetatarsal angle was 8.7 degrees (range, 4-14 degrees), the average hallux valgus angle was 11 degrees (range, 4 degrees of varus to 30 degrees of valgus), and the average midshaft medial cortical thickness was 3.2 mm (range, 2.0-5.5 mm). Pearson's correlation coefficient was calculated to compare these factors. The relationship between variables was found to be small (r < or = 0.2). Motion was noted to occur in the normal foot at this joint and a range of normal values for medial cortical thickness was identified.

Adult↗

PubMed1996

Abnormal sperm morphology and function in the fathers of hypospadiacs.

A lower motility of spermatozoa and a higher incidence of abnormal sperm morphology were found in 25 fathers of hypospadiacs compared with those of 50 fathers who produced children who were not hypospadiacs. Subfertility of fathers may result in a higher risk of hypospadias in offspring and as subfertile males now represent a higher proportion among fathers, owing to the improved efficacy of infertility treatment, this may explain the increased occurrence of hypospadias. Our relaxed-selection hypothesis, which states that there is a redistribution in the number of children born to fertile and infertile (subfertile) couples, may account for the increasing number of other defects and cancers of male genitalia observed today and the fall in sperm counts.

Adult↗

PubMed1995

The ras-related small GTP-binding protein RhoB is immediate-early inducible by DNA damaging treatments.

The low molecular weight GTP-binding proteins RhoA, RhoB, and RhoC are characterized as specific substrates for the ADP-ribosyltransferase C3 from Clostridium botulinum and are supposed to be involved in the organization of the microfilamental network and transformation. rhoB is known to be immediate-early inducible by growth factors and protein-tyrosine kinases. Since increasing evidence indicates overlapping of growth factor- and UV-induced signal pathways, we studied the effect of UV light and other genotoxic agents on early rhoB transcription. Within 30 min after UV irradiation of NIH3T3 cells, the amount of rhoB mRNA increased 3-4-fold. Elevated rhoB mRNA was accompanied by an increase in RhoB protein, as detected by C3-mediated [32P]ADP-ribosylation. The transcription inhibitor actinomycin D prevented the UV-induced increase in rhoB mRNA and proved rhoB mRNA to be unstable with a half-life of approximately 20 min. Transcriptional activation of rhoB by UV light was confirmed by run-on analysis. The increase in rhoB mRNA after UV irradiation was prevented by inhibitors of protein kinase A (H9) and C (H7, Gö18). The tyrosine kinase inhibitor genistein did not affect UV induction of rhoB. In addition to UV, N-methyl-N-nitrosourea and the cytostatic drug cisplatin evoked rhoB response. Cycloheximide was likewise effective in increasing the amount of rhoB mRNA, whereas Bt2cAMP, 12-O-tetradecanoylphorbol-13-acetate, and retinoic acid were without effect. Prior down-regulation of signaling by 12-O-tetradecanoylphorbol-13-acetate and serum pretreatment reduced UV-stimulated rhoB expression. The data indicate that rhoB represents a novel DNA damage-inducible function involved in early steps of signal transduction upon genotoxic stress.

3T3 Cells↗

PubMed1995

Studies on the active-site structure of C3-like exoenzymes: involvement of glutamic acid in catalysis of ADP-ribosylation.

Various C3-like ADP-ribosyltransferases like Clostridium botulinum exoenzyme C3, C limosum transferase, B cereus transferase and a transferase from Staphylococcus aureus (EDIN) selectively modify the low-molecular mass GTP-binding proteins RhoA,B,C. UV-irradiation of C limosum transferase in the presence of [carbonyl-14C]NAD resulted in radiolabeling of Glu-174. Concomitantly, ADP-ribosyltransferase and NAD glycohydrolase activities were inhibited. Site-directed mutagenesis of Glu-174 (E174D, E174Q) which resulted in more than 1000-fold reduction of enzyme activity, suggests that the glutamic acid residue is essentially involved in the catalytic action of C3-like transferases. These findings support the view that all bacterial ADP-ribosyltransferases share a similar active-site structure.

ADP Ribose Transferases↗

PubMed1995

Isolation and characterization of a Clostridium botulinum C2 toxin-resistant cell line: evidence for possible involvement of the cellular C2II receptor in growth regulation.

Clostridium botulinum C2 toxin, which consists of the binding component C2II and the enzyme component C2I, acts on eukaryotic cells by selective ADP-ribosylation of G-actin. To obtain C2 toxin-resistant cells, we mutagenized CHO-K1 cells with N-nitroso-N-methylurea and selected for C2 resistance. Cells which survived the selection procedure with 50 ng of C2I and 100 ng of C2II per ml were obtained with a frequency of 30 x 10(-6). The colony-forming ability of CHO wild-type cells was reduced to 50% with 10 ng of C2I and 20 ng of C2II per ml. In contrast, the colony-forming ability of the isolated CHO mutant cells was not influenced by up to 200 ng of C2I and 400 ng of C2II per ml. Toxin-induced ADP-ribosylation of G-actin was not impaired in lysates of mutant cells. The C2 toxin-resistant phenotype remained sensitive to the cell-rounding activities of cytotoxins from C. perfringens (iota-toxin), C. novyi, C. difficile, and C. botulinum (C3) and to cytochalasin D. Binding of component C2II was impaired in resistant CHO cells, suggesting mutation of the toxin cell surface receptor. Serum factors protected wild-type cells against the cytotoxic effect of C2 toxin. Furthermore, the C2-resistant phenotype correlated with an increased serum dependency. The data suggest that the action of C. botulinum C2 toxin is mediated by its binding and uptake via a cell surface receptor which might be involved in growth regulation.

ADP Ribose Transferases↗

PubMed1995

Recent advances in the treatment of ARDS.

Despite more than 25 years of extensive research the mortality of ARDS patients remains high. Besides the often deleterious course of the underlying disease, another reason for this high mortality lies in the aggressive ventilatory regimen which is required to maintain arterial blood gases in a more or less normal range. Therapeutic methods which are used to reduce iatrogenic damage to the lungs are pressure controlled ventilation with permissive hypercapnia, differential lung ventilation, positioning therapy, dehydration, and extracorporeal gas exchange with membrane lungs. Nevertheless, many of these patients still die following hypoxaemia or multiple organ failure. Therefore, the need remains to develop new therapeutic strategies and to investigate their influence on the morbidity and mortality of this life-threatening disease. First experiences with nitric oxide (NO) inhalation, intravenous application of antioxidants, intratracheal instillation of surfactant, tracheal gas insufflation and combined fluid/gas ventilation with perfluorocarbon are presented. All these new methods have proved their efficacy, at least in animal studies, however, they should still be regarded as experimental.

Animals↗

PubMed1994

Differentiation-induced increase in Clostridium botulinum C3 exoenzyme-catalyzed ADP-ribosylation of the small GTP-binding protein Rho.

The specific [32P]ADP-ribosylation by Clostridium botulinum exoenzyme C3 was used to study differentiation-dependent changes in the regulation of the low-molecular-mass GTP-binding protein Rho. Differentiation of F9 teratocarcinoma cells to neuronal-like cells by treatment with retinoic acid and dibutyryl-adenosine 3',5'-monophosphate [(Bt)2cAMP] increased the C3-catalyzed ADP-ribosylation of RhoA proteins in cytosolic and membrane fractions by about threefold and sixfold, respectively. Phenotypical differentiation of F9 cells was not required for increase in ADP-ribosylation. Increase in ADP-ribosylation after (Bt)2cAMP and retinoic acid treatments was blocked by cycloheximide, indicating the requirement of protein biosynthesis. As deduced from specific rho mRNA amounts and from Western analysis with a monoclonal RhoA antibody, the stimulation in the [32P]ADP-ribosylation of Rho was not caused by an increased de-novo synthesis of Rho proteins. GDP increased the ADP-ribosylation of membrane-associated Rho from non-differentiated, but not from differentiated F9 cells. GTP[S] decreased ADP-ribosylation of membranous Rho from differentiated and much less from non-differentiated F9 cells. Differentiation-dependent increase in ADP-ribosylation of cytosolic Rho was reversed by protein phosphatase type-1. Treatment with SDS (0.01%) which releases Rho from complexation with guanine nucleotide dissociation inhibitor, increased ADP-ribosylation both in differentiated and non-differentiated cells, indicating no differentiation-specific change of such complexes. In total, our data indicate that the induction of the differentiation process in F9 cells is accompanied by changes in the regulation of cytosolic and membrane-associated Rho proteins.

ADP Ribose Transferases↗

PubMed1994

Tissue-specific variations in the expression and regulation of the small GTP-binding protein Rho.

Rho proteins are involved in the regulation of the assembly of the microfilamental cellular network and are known to be specific substrates for the ADP-ribosyltransferase C3 from Clostridium botulinum. Here, we studied the distribution of Rho and Rho-regulating proteins in extracts from various rabbit tissues. The highest amounts of [32P]ADP-ribosylated proteins were detected in cell extracts from lung and kidney. Compared to these tissues, 50-95% reduced labeling of Rho proteins was observed in extracts from liver, spleen, brain, heart and muscle. The level of the C3-mediated [32P]ADP-ribosylation of Rho did not correlate with the amount of RhoA proteins detected by Western analysis. The relative amounts of [32P]ADP-ribosylated proteins located in cytosolic or membrane fractions, respectively, depended on the type of tissue investigated, indicating a tissue-specific variation in the subcellular distribution of Rho proteins. The same was true for the complexation of Rho with other factors and the expression of diverse Rho species. In respect to Rho-regulating proteins, extracts from lung and brain contained the highest amounts of guanine nucleotide dissociation-inhibitor proteins (Rho-GDI). The association of Rho with Rho-GDI however showed tissue specificity and did not correlate with Rho-GDI amounts. The highest Rho-GAP (GAP = GTPase-activating protein) activities were observed in extracts from lung, kidney and spleen, the lowest ones in extracts from muscle and heart. In total, our data demonstrate tissue-specific differences in the expression of RhoA, [32P]ADP-ribosylated proteins and Rho-regulating factors, indicating a tissue-specific variation in the activity and regulation of Rho proteins.

Animals↗

PubMed1994

Effect of transfection of human poly(ADP-ribose)polymerase in Chinese hamster cells on mutagen resistance.

Poly(ADP-ribose)polymerase (PARP) is a DNA-binding protein that is activated upon induction of DNA breaks and supposed to play a role in DNA repair. To elucidate the effect of overexpression of PARP on the resistance of cells to mutagens, Chinese hamster ovary cells (both the line CHO-9 and the mutagen-hypersensitive derivative 27-1) were transfected with the human PARP cDNA along with pSV2neo. Treatment of the transfected cell population with a high dose of MNNG and selection with G418 gave rise to a significant increase of neo+ clones, as compared to the control transfection with pSV2neo + salmon sperm DNA. The frequency of survivors in these mass culture experiments was lower, however, than after transfection with the bacterial ada gene encoding the DNA repair protein O6-alkylguanine-DNA alkyltransferase. Thus transfection of PARP cDNA in CHO cells is only weakly effective in inducing alkylation resistance. This was confirmed by analyzing the mutagen resistance of individual PARP transfectant clones derived from CHO-9 and 27-1 cells that expressed increased levels of PARP mRNA, protein and PARP activity. These strains were slightly more resistant to the toxic effect of MMS and showed a reduced frequency of MMS-induced chromosomal aberrations. CHO-9-PARP transfectants also gained resistance to UV. From these data we conclude that, in CHO cells, PARP is limiting in handling critical lesions during the repair process and that increase of the amount of PARP protein can elicit some protection against genotoxic effects of mutagens.

Animals↗

PubMed1994

ADP-ribosylation of Rho proteins by Clostridium botulinum exoenzyme C3 is influenced by phosphorylation of Rho-associated factors.

Specific [32P]ADP-ribosylation by Clostridium botulinum exoenzyme C3 was used to study the involvement of phosphorylation in the regulation of the low-molecular-mass GTP-binding protein Rho. Dephosphorylation of CHO cell extracts by alkaline phosphatase treatment resulted in a 80-90% reduction in the C3-catalysed [32P]ADP-ribosylation of Rho proteins in both cytosolic and membrane fractions. Similar results were obtained after dephosphorylation with protein phosphatase type-1 from bovine retina, whereas type-2B and type-2C phosphatases had no effect on the level of subsequent [32P]ADP-ribosylation of Rho by C3. Incubation of CHO cell lysate under phosphorylation conditions increased the subsequent C3-mediated [32P]ADP-ribosylation of Rho proteins. The protein kinase inhibitors H7 and H9 had no effect on [32P]ADP-ribosylation at concentrations which are specific for inhibition of protein kinase A or C. Recombinant glutathione S-transferase-RhoA fusion protein (GST-RhoA) was phosphorylated by protein kinase A; however, the phosphorylation had no stimulatory effect on the ADP-ribosylation of GST-RhoA by C3. An approx. 48 kDa phosphoprotein was identified which bound specifically to recombinant GST-RhoA fusion protein. By gel-permeation chromatography, Rho-containing complexes of approx. 50 kDa and 130-170 kDa were detected. The ADP-ribosylation of Rho in the 130-170 kDa complex was reduced by alkaline phosphatase pretreatment. The data suggest that Rho activity is influenced by phosphorylation of Rho-associated regulatory factors. Phosphorylation/dephosphorylation of these Rho-regulating factors appears to alter the ability of Rho to serve as a substrate for C3-induced [32P]ADP-ribosylation.

3T3 Cells↗

PubMed1994

Clostridium difficile toxin B acts on the GTP-binding protein Rho.

Clostridium difficile toxin B exhibits cytotoxic activity that is characterized by the disruption of the microfilamental cytoskeleton. Here we studied whether the GTP-binding Rho protein, which reportedly participates in the regulation of the actin cytoskeleton, is involved in the toxin action. Toxin B treatment of Chinese hamster ovary cells reveals a time- and concentration-dependent decrease in the ADP-ribosylation of Rho by Clostridium botulinum C3 exoenzyme in the cell lysate. Disruption of the microfilament system induced by C. botulinum C2 toxin or cytochalasin D does not cause impaired ADP-ribosylation of Rho. Toxin B exhibits its effects on Rho not only in intact cells but also when added to cell lysates. Besides endogenous Rho, RhoA-glutathione S-transferase (Rho-GST) fusion protein added to cell lysate showed decreased ADP-ribosylation after toxin B treatment. Immunoblot analysis reveals identical amounts of Rho-GST and no change in molecular mass after toxin B treatment compared with controls. ADP-ribosylation of Rho-GST purified from toxin B-treated cell lysate is inhibited, indicating a modification of Rho itself. Finally, transfection of rhoA DNA under the control of a strong promoter into cells protects them from the activity of toxin B. Altogether, the data indicate that C. difficile toxin B acts directly or indirectly on Rho proteins to inhibit ADP-ribosylation and suggest that the cytotoxic effect of toxin B involves Rho.

3T3 Cells↗

PubMed1994

Emergency department assessment of adolescent suicide attempters: factors related to short-term follow-up outcome.

Empirical data to help gauge risk for repeat suicide attempts and noncompliance with outpatient psychiatric care among adolescent suicide attempters discharged from emergency departments is scarce. In this study, 62 adolescent suicide attempters discharged from a regional trauma center serving an urban/suburban area with a broad range of social classes were followed up at three months after their attempts to assess treatment compliance and repeat attempts. Information regarding suicidal intent and characteristics of the attempt were collected by emergency physicians at the time of the attempt. Parental ratings of adolescent functioning were also collected. At three-month follow-up, none of the adolescents had completed suicide; 7% made a repeat suicide attempt, 16% never followed through with outpatient psychiatric appointments, 15% attended one session, and 21% went to only two appointments. A prior suicide attempt, alcohol use at the time of the attempt, and greater planning of the suicide attempt were associated with better compliance with outpatient psychiatric treatment. None of the variables predicted repeat attempts. Parental reports of an adolescent's physical fighting and health problems of a family member were related to referral failure. Clinical implications are discussed.

Adolescent↗

PubMed1994

A pictorial visual analog scale for rating severity of childhood asthma episodes.

The purpose of this study was to determine whether the use of pictorial anchors improved a visual analog scale (VAS) designed to assess asthma episodes. The sample consisted of 77 children with moderate to severe asthma attending a summer camp. They rated one of two VASs, either nonpictorial (39 subjects in year 1) or pictorial (38 subjects in year 2), three times a day for 2 weeks to report the severity of their asthma symptoms. Immediately after the subjects rated the VAS, pulmonary function testing was obtained. The mean VAS scores increased 64% using the pictorial VAS while the mean PEFRs in the 2 years were almost identical, suggesting that changes on the VAS were not due to differences in pulmonary functioning. For boys, the increase in individual mean VAS score in year 2 using the pictorial VAS was 44%; for girls, the increase in individual mean VAS scores was 112%. Use of a pictorial VAS increases the range of severity of symptoms reported by children with asthma. The instrument may be a useful tool in the systematic quantifiable assessment of subjective symptomatology in pediatric asthma.

Adolescent↗