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At least 73 records · Page 4Linked to original sources
PubMed2001

Pennsylvania's early discharge legislation: effect on maternity and infant lengths of stay and hospital charges in Philadelphia.

OBJECTIVE: To assess the effect of maternal length of stay (LOS) legislation on LOS and hospital charges associated with Philadelphia resident live births from 1994 through 1997. DATA SOURCE/STUDY SETTING: This was a descriptive epidemiological study involving secondary data analyses of linked birth record and hospital discharge data pertaining to all Philadelphia resident live births occurring between January 1, 1994 and December 31, 1997. STUDY DESIGN: Using these linked data, trends in median and mean maternal and infant LOS and hospital charges were described for three distinct time periods: (1) a "prelegislative" period (January 1, 1994 through June 30, 1995); (2) a one-year period during which LOS legislation was introduced, debated, modified, and eventually passed by Pennsylvania lawmakers (July 1, 1995 through June 30, 1996); and (3) a "post-LOS law" period immediately following enactment of Act 85 mandating minimum LOS for mothers and their newborns (July 1, 1996 through December 31, 1997). LOS variables for both mothers and infants were calculated based on the actual number of hours elapsing between birth and discharge; hospital charges were obtained directly from information available in the Hospital Discharge Survey data. PRINCIPAL FINDINGS: Maternal median charges and LOS per delivery for vaginal births rose from 5,270 dollars to 6,333 dollars and from 35 to 47 hours following the enactment of Pennsylvania maternal minimum LOS legislation. Median infant cost and LOS per delivery mirrored these trends. CONCLUSIONS: Pennsylvania LOS legislation had a profound effect on maternal and infant discharge practices in Philadelphia. As much as $20 million may have been added to annual health care costs associated with Philadelphia resident births.

Adult↗
PubMed2004

Trisomy 8 in Philadelphia-negative cells during imatinib therapy.

Targeted therapy with imatinib selectively suppresses Philadelphia-positive cells in chronic myeloid leukemia cells, with reappearance of apparently normal hemopoiesis in a considerable number of patients. Recently, clonal abnormalities have been observed in Philadelphia-negative cells during imatinib therapy, the biologic and prognostic significance of which is actually unknown. A case of trisomy 8 occurring in Philadelphia-negative cells, which was treated by bone marrow transplantation, is reported. Chromosomal abnormalities in Philadelphia-negative cells do not seem to herald disease transformation, but the long-term prognosis may be influenced by an increased incidence of myelodysplasia in younger patients.

Benzamides↗
PubMed1982

Identification of hemoglobin G-Philadelphia (alpha 68 Asn replaced by Lys) and hemoglobin Matsue-Oki (alpha 75 Asp replaced by Asn) in a black infant.

Two alpha-chain variants, Hb G-Philadelphia and Hb Matsue-Oki, were present in members of a relatively large black family from South Carolina. The four Hb G-Philadelphia heterozygotes averaged 35.6% Hb G, suggesting the presence of an alpha-thalassemia-2 condition in cis to the Hb G mutation, which was confirmed by DNA structural analysis. The seven Hb Matsue-Oki heterozygotes averaged 22.2% Hb MO and likely have four active alpha-chain genes. One infant was a compound heterozygote for the two Hb variants which could not be separated from each other. The quantity of Hb G plus Hb MO was 58% by DEAE-cellulose chromatography and 69% by chain analyses. These results and the family data indicate that this child had three active alpha-chain genes, of which one regulated the synthesis of the normal alpha chain, one was mutated to give the alpha G chain, and one to give the alpha MO chain. The amino acid substitutions in Hb G-Philadelphia and Hb Matsue-Oki are located in the tryptic peptide alpha T-9, which is 29 amino acid residues long. Structural analyses of these abnormalities made use of high-pressure liquid chromatography for the separation of both tryptic and thermolytic peptides and of a highly sensitive ultra-micro sequencing procedure. Although the alpha 68 Asn replaced by Lys substitution is readily demonstrable in Hb G-Philadelphia the elucidation of the alpha 75 Asp replaced by Asn replacement in Hb Matsue-Oki was greatly facilitated by the use of these microprocedures.

Adolescent↗
PubMed1974

Fibrinogen Philadelphia. A hereditary hypodysfibrinogenemia characterized by fibrinogen hypercatabolism.

A new, autosomally inherited abnormal fibrinogen associated with hypofibrinogenemia has been described in several members of a family. Plasma fibrinogen measured either as thrombin-clottable protein or by immunodiffusion revealed a fibrinogen level ranging between 60 and 90 mg/100 ml. The thrombin time of plasma or purified fibrinogen was prolonged and only partially corrected by the addition of calcium. Purified fibrinogen prolonged the thrombin time of normal plasma. Fibrinopeptide release by thrombin was normal in rate and amount, but fibrin monomer aggregation was grossly disturbed, especially in a high ionic strength medium. We have designated this fibrinogen "fibrinogen Philadelphia." Acrylamide gel electrophoresis of mixtures of [121I]normal and [125I]abnormal fibrinogens revealed a slight increase in the anodal mobility of fibrinogen Philadelphia. Similarly, DEAE-cellulose chromatography showed slightly stronger binding of fibrinogen Philadelphia than normal. To elucidate the mechanism responsible for the low plasma fibrinogen concentration, simultaneous metabolic studies of autologous (patient) and homologous (normal) fibrinogen, labeled with 125I and 121I, respectively, were performed in two affected subjects. Autologous fibrinogen half-life was short and the fractional catabolic rate was markedly increased in both family members. In contrast, homologous fibrinogen half-life and fractional catabolic rate were normal. These metabolic studies demonstrate that rapid degradation of fibrinogen Philadelphia is largely responsible for the depressed levels of a plasma fibrinogen. This represents the first example of a mutant plasma protein in which the molecular defect is associated with an altered catabolism.

Adolescent↗
PubMed1988

Generation of a monoclonal antibody specific for Hb G-Philadelphia [alpha 2(68)(E17)Asn----Lys beta 2] and development of an immunoassay.

A murine hybridoma was generated which secreted a monoclonal antibody (Mab) that specifically recognized the alpha 2(68)(E17)Asn----Lys beta 2 substitution of Hb G-Philadelphia. Hybridomas were produced by fusion of RBF/DnJ immune splenic lymphocytes with FOX-NY murine myeloma cells and selected in adenine-aminopterin-thymidine (AAT) medium. Culture fluids were screened by ELISA for antibody reacting with Hb G-Philadelphia but not Hb A. One such culture was cloned by limiting dilution, expanded and injected into pristane-primed, cyclophosphamide-suppressed BALB/c mice for ascites production. An enzyme-linked immunoassay was developed by conjugating hemoglobin in hemolysates or purified hemoglobins to the plastic surface of wells of a microtiter plate. The ascites fluid containing the Hb G-Philadelphia Mab was added to the wells followed by goat anti-mouse IgG conjugated with horseradish peroxidase. After the addition of substrate (tetramethylbenzidine), a deep blue color developed, signifying a positive reaction. We analyzed 58 hemolysates (17 adult, 41 cord) containing a G-variant along with 28 control hemolysates (12 cords comprising FA, FAC, FAS, FSS, FCC phenotypes; 16 adults consisting of AA, AS, SS, SC, S-beta thal, AD-Los Angeles phenotypes). Of the 58 hemolysates containing a G-variant, 53 were positive by ELISA and confirmed by radioimmunoassay (RIA). Four of the five hemolysates negative for Hb G-Philadelphia were shown to be Hb G-Montgomery by RIA. None of the control hemolysates were positive. The assay could be completed in 1 hr and represents a technological advance in hemoglobin identification.

Animals↗
PubMed1999

Molecular and phenotypic spectrum of de novo Philadelphia positive acute leukemia.

The Philadelphia chromosome is present in a heterogeneous group of leukemias. It is most commonly associated with chronic myelogenous leukemia (CML) and B-lineage acute lymphoblastic leukemia (ALL) being found in more than 95% and 15-25% of cases respectively. We undertook a study to determine the morphologic, phenotypic and molecular diversity of Philadelphia positive de novo acute leukemia patients seen at our institution over the past 3 1/2 years. Twenty-one patients with de novo acute leukemia were found to have the Philadelphia chromosome by cytogenetic studies. They consisted of 3 patients with acute myelogenous leukemia (AML), 1 biphenotypic leukemia and 17 ALL patients. Of the patients with ALL, 16 were of B-lineage while 1 had a T-cell phenotype. Ten patients expressed the p210 BCR-ABL transcript alone and 10 expressed only the p190 BCR-ABL transcript. One patient had co-expression of p190 and p210 b3a2 BCR-ABL transcripts. Thus the Philadelphia chromosome can be found in a diverse cohort of morphologic and immunologic subtypes of de novo acute leukemia reflecting the heterogeneity of lineage involvement in this disease.

Acute Disease↗
PubMed1989

Engulfment of the Philadelphia strain of Legionella pneumophila within pseudopod coils in human phagocytes. Comparison with other Legionella strains and species.

In this paper we report our ultrastructural studies of the early phagocytosis of two different strains of L. pneumophila serogroup (SG) 1 (Philadelphia 1 and Knoxville 1) and of L. micdadei. These bacteria replicate, in vivo as well as in vitro, in eukaryotic cells e.g. in monocytes and macrophages. Whether or not the mode of entry of these organisms in phagocytes contributes to their intracellular survival is presently unknown. Whilst internalization of bacteria of the Philadelphia 1 strain occurred within a pseudopod coil, organisms of the Knoxville 1 strain and L. micdadei were phagocytized in the classical manner, i.e. between pseudopods. No ultrastructural differences were observed between the two strains of L. pneumophila SG 1 whereas L. micdadei appeared as shorter rods with an extracellular layer of relatively low electron density. The phenomenon of coiling phagocytosis was not affected by heat-killing the bacteria or preopsonization with specific antibody. Formation of phagolysosomes was seen when cells of the Knoxville strain and L. micdadei were used but not with the Philadelphia strain. In our experiments, the occurrence of coiling phagocytosis was specific for the Philadelphia 1 strain of L. pneumophila and independent of bacterial virulence. Thus, it seems most unlikely that the coiling phenomenon plays any important role in the resistance of Legionella to the killing abilities of phagocytic cells.

Humans↗
PubMedDate not supplied

[Clinical, structural and functional studies of HbG Philadelphia detected in a Moroccan newborn].

Hb G Philadelphia (alpha68 Asn leads to Lys) is widely distributed in black people but is uncommon in North-Africa. Only one case has been previously described in an Arab immigrant. The latter and our propositus originated from North-East morocco. Hb G alpha Philadelphia is stable. The abnormal hemoglobin represented 28% of total hemoglobin in the hemolysate of the propositus, a 7 month old child. At birth, 4 fractions were detected on electrophoresis: Hb A, Hb F, Hb G Philadelphia, which migrated like Hb S, and a mutant alpha2Ggamma2. The oxygen affinity of Hb G Philadelphia was slightly elevated. Cooperativity and Bohr effect were normal. The abnormal hemoglobin was also detected in the father of the propositus in the heterozygote state: its clinical and hematological data were normal. No evidence of thalassemia trait was found in the family. The percentage of abnormal hemoglobin obtained in the propositus and his father is in accordance with the presence of two loci for the alpha chain on the homologous chromosome.

Electrophoresis, Cellulose Acetate↗
PubMed2026

Cytogenetic Diversity of Variant Philadelphia Translocations in Chronic Myeloid Leukemia.

INTRODUCTION: Chronic myeloid leukemia (CML) is a disease characterized by Philadelphia (Ph) translocations. These translocations can be classical or variant. The structural features and diagnostic implications of variant Philadelphia translocations remain incompletely defined, and they display considerable cytogenetic heterogeneity. METHODS: In this retrospective study, variant Ph translocations identified by conventional cytogenetic analysis and fluorescence in situ hybridization (FISH) were systematically classified among 639 patients diagnosed with CML. A total of 35 patients with variant Ph translocations were included in the analysis. Molecular follow-up data, when available, were assessed using RT-qPCR analyses in a subset of patients. RESULTS: Chromosome analysis revealed 2 simple and 33 complex variant Ph translocations. FISH analysis, performed in 20 patients, identified deletions involving BCR, ABL1, or both in a limited number of cases. Additional chromosomal abnormalities and secondary translocations accompanied variant Ph translocations in four patients. The partner chromosomes involved in variant Ph translocations showed marked diversity, involving multiple chromosomal loci. CONCLUSION: Variant Philadelphia chromosome translocations in CML exhibit substantial cytogenetic diversity, reflecting the complexity of their underlying genomic architecture. The rarity and heterogeneity of these rearrangements complicate their classification and interpretation in routine diagnostic practice. Descriptive reporting of variant Ph translocations may contribute to a better understanding of their diagnostic complexity and support more accurate cytogenetic interpretation in CML.

Humans↗
PubMed2005

Every case of essential thrombocythemia should be tested for the Philadelphia chromosome.

Essential thrombocythemia (ET) and chronic myelogenous leukemia (CML) usually present with distinctive features. Citing experience with cases that overlap, the Polycythemia Vera Study Group recommends that negative tests for the Philadelphia chromosome be obtained before diagnosing ET. We describe two young women presenting with features absolutely typical for ET, including extreme thrombocytosis, no leukocytosis, no basophilia, no peripheral immature cells, and no splenomegaly. Severe thrombotic complications ensued: multiple cerebrovascular thromboemboli, pulmonary emboli, and miscarriage in one and myocardial infarction in the other. By 4 years, both developed leukocytosis, extreme basophilia, and circulating blasts, typical of accelerated CML. Cytogenetic studies were then performed, revealing the Philadelphia chromosome. Imatinib produced rapid clearing of blasts and basophils, but one woman later succumbed after allogeneic bone marrow transplant and the other has not achieved a major cytogenetic response. We conclude that CML can present in identical fashion as ET. The mandate for routine Philadelphia chromosome testing is magnified by the availability of targeted therapy and its greater efficacy in early stage disease.

Adult↗
PubMed1990

Neutrophilic myelofibrosis presenting as Philadelphia chromosome negative BCR non-rearranged chronic myeloid leukemia.

Chronic myeloid leukemia consists of Philadelphia chromosome positive disease in 90% of cases, and a further 5%, although Philadelphia chromosome negative, exhibit bcr gene rearrangements consistent with the disease. The remaining 5% of cases have a heterogeneous clinical picture with a course unlike that of classical chronic myeloid leukemia, and may belong to different pathologic entities. We report five cases belonging to the latter group, initially identified as Philadelphia chromosome negative, bcr non-rearranged chronic myeloid leukemia, that developed progressive leucocytosis, absolute monocytosis, myelodysplasia, extramedullary hematopoiesis, and had evidence of myelofibrosis. These cases may represent a distinct clinical entity characterized by neutrophilic myelofibrosis, which can be identified prospectively by clinical and pathologic criteria. Standard therapy for treating chronic myeloid leukemia or idiopathic myelofibrosis may not be appropriate for this group.

Adult↗
PubMed1986

Two apparent Philadelphia chromosomes arising from translocations with different chromosomes in a patient with CML: 46,XY,t(7;22)(p22;q11),t(9;22)(q34;q11).

Chromosome studies on bone marrow cells and unstimulated peripheral lymphocytes from a patient with chronic myelogenous leukemia revealed the presence in all cells of two apparent Philadelphia chromosomes: one resulting from the classical translocation with a chromosome #9, and the other arising from a translocation between chromosomes #22 and #7. There was no normal chromosome #22. Some of the cells also had an i(17q), indicative of blast crisis. Repeated chromosome studies at different times during the course of the disease revealed the evolution of additional karyotypic changes. All cells from later samples had an extra #8; some of these cells had a third Philadelphia chromosome, whereas, others had a second Y chromosome. Although a few normal cells were seen in PHA-stimulated lymphocyte cultures, indicating that the patient has a normal constitutional karyotype, most of the cells had a karyotype identical to that found in unstimulated cultures. This unusual karyotype, 46,XY,t(7;22)(p22;q11),t(9;22)(q34;q11), represents the first case in which two apparent Philadelphia chromosomes are present in the leukemic cells from a patient in the absence of a normal #22 chromosome.

Chromosome Banding↗
PubMed1987

Philadelphia chromosome positive essential thrombocythemia evolving into lymphoid blast crisis.

The Philadelphia chromosome with the classic translocation t(9;22) was detected in all metaphases of a patient with essential thrombocythemia who presented without hematologic signs of chronic myeloid leukemia (CML). After 12 months of treatment with hydroxyurea followed by 6 months of busulfan, the disease transformed into lymphoid blast crisis with the immunophenotype of pre-pre-B cells frequently seen in lymphoid blast crisis of CML. This progression was not associated with karyotypic evolution because lymphoblasts contained only the Philadelphia chromosome. Further clinical course in this patient confirmed the development of a Philadelphia chromosome positive stem cell with predominantly megakaryocytic committment through partially megakaryocytic/lymphoid differentiation to purely lymphoid committment, a previously unreported transformation.

Adult↗
PubMed2000

Variant intra philadelphia translocation with rearrangement of BCR-ABL and ABL-BCR within the same chromosome in a patient with cALL.

A unique variant Philadelphia translocation accompanied by the loss of the short arm of chromosome 9 in a 32-year-old female with common acute lymphoblastic leukemia (cALL) is described. Furthermore, supernumerary chromosome 8 material was found as an insertion into the long arm of chromosome 2 and/or as ring chromosomes in addition to two normal chromosomes 8. The chromosomal abnormalities were identified by combined conventional chromosome banding analysis and fluorescence in situ hybridization (FISH). The BCR-ABL rearrangement was confirmed by FISH and reverse transcriptase-polymerase chain reaction (RT-PCR) studies. Possible mechanisms leading to this variant intra Philadelphia translocation are discussed. The aberrations found have prognostic implications, because 9p anomalies confer an adverse effect to the already poor prognosis of Philadelphia-positive ALL.

Adult↗
PubMed2000

Three-dimensional spectral precision distance microscopy of chromatin nanostructures after triple-colour DNA labelling: a study of the BCR region on chromosome 22 and the Philadelphia chromosome.

Topological analysis of the three-dimensional (3D) chromatin nanostructure and its function in intact cell nuclei implies the use of high resolution far field light microscopy, e.g. confocal laser scanning microscopy (CLSM). However, experimental evidence indicates that, in practice, under biologically relevant conditions, the spatial resolution of CLSM is limited to about 300 nm in the lateral direction and about 700 nm in the axial direction. To overcome this shortcoming, the use of a recently developed light microscopical approach, spectral precision distance microscopy (SPDM) is established. This approach is based on the precise localization of small labelling sites of a given target in spectrally differential images. By means of quantitative image analysis, the bary centres (intensity weighted centroid analogous to the centre of mass) of these independently registered labelling sites can be used as point markers for distance and angle measurements after appropriate calibration of optical aberrations (here, polychromatic shifts). In combination with specific labelling of very small chromatin target sites with dyes of different spectral signatures by fluorescence in situ hybridization (FISH), SPDM presently allows us to analyse the nuclear topology in three-dimensionally conserved nuclei with a 'resolution equivalent', many times smaller than the conventional optical resolution. Chronic myelogeneous leukaemia (CML) is genetically characterized by the fusion of parts of the BCR and ABL genes on chromosomes 22 and 9, respectively. In most cases, the fusion leads to a translocation t(9; 22) producing the Philadelphia chromosome. SPDM was applied to analyse the 3D chromatin structure of the BCR region on the intact chromosome 22 and the BCR-ABL fusion gene on the Philadelphia chromosome (Ph) by using a new triple-colour FISH protocol: two different DNA probes were used to detect the BCR region and the third DNA probe was used to identify the location of the ABL gene. Consistent 3D distance measurements down to values considerably smaller than 100 nm were performed. The angle distributions between the three labelled sites on the Philadelphia chromosome territory were compared to two state-of-the-art computer models of nuclear chromatin structure. Significant differences between measured and simulated angle distributions were obtained, indicating a complex and non-random angle distribution.

Bone Marrow Cells↗
PubMed1997

Treatment of Philadelphia leukemia in severe combined immunodeficient mice by combination of cyclophosphamide and bcr/abl antisense oligodeoxynucleotides.

BACKGROUND: Philadelphia cells are human chronic myelogenous leukemia (CML) cells that contain the BCR/ABL oncogene (a fusion of the BCR and ABL genes). Selective eradication of these cells in vitro can be achieved by combined treatment with antisense phosphorothioate oligodeoxynucleotides ([S]ODNs) specifically targeted to this oncogene (bcr/abl [S]ODNs) and a suboptimal (for use as a single agent) dose of mafosfamide (the in vitro active form of cyclophosphamide). PURPOSE: We evaluated the ability of bcr/abl antisense [S]ODNs, alone or subsequent to treatment with a single injection of cyclophosphamide, to suppress the leukemic process induced in severe combined immunodeficient (SCID) mice by Philadelphia cells (i.e., primary CML-blast crisis [CML-BC] cells). In addition, we studied potential mechanisms that might explain the efficacy of the bcr/abl antisense [S]ODN-mafosfamide combination against Philadelphia cells in vitro. METHODS: The effects of treating leukemic mice with cyclophosphamide (25 mg/kg body weight; 25% of the dose required to eradicate evidence of leukemia in SCID mice) and/or bcr/abl antisense [S]ODNs were assessed by analysis of survival, by examination of bone marrow for the presence of leukemia cells (using a colony formation assay or using coupled reverse transcription and the polymerase chain reaction to screen for bcr/abl messenger RNA), and by examination of a variety of tissues for the presence of infiltrating leukemia cells. The induction of apoptosis (a cell death program) in vitro in primary CML-BC cells following treatment with bcr/abl antisense [S]ODNs plus or minus prior treatment with mafosfamide was monitored by use of a commercial assay. Relative cellular uptake of [S]ODNs by CML-BC cells treated in vitro with or without prior treatment with mafosfamide was determined by use of confocal microscopy and flow cytometry (for fluorescent [S]ODNs) or by use of blotting techniques that employed radioactively labeled probes (for extracted, unlabeled [S]ODNs). Levels of specific proteins in treated and untreated cells were determined by use of western blotting methods. Reported P values are two-sided. RESULTS: The disease process in leukemic mice was retarded substantially by combination treatment with cyclophosphamide and specific bcr/abl antisense [S]ODNs (P < .001, relative to treatment with specific antisense [S]ODNs alone, cyclophosphamide alone, or cyclophosphamide plus nonspecific [i.e., control] antisense [S]ODNs); 50% of the mice treated with cyclophosphamide and specific antisense [S]ODNs appeared to be cured of leukemia. The combination treatment was associated with increased induction of apoptosis. In addition, cellular uptake of bcr/abl antisense [S]ODNs appeared to be increased twofold to sixfold by prior treatment with mafosfamide. This increased uptake of [S]ODNs was associated with enhanced suppression of p210bcr/abl protein levels. CONCLUSIONS AND IMPLICATIONS: Combination therapy with antisense [S]ODNs targeted to specific oncogenes and less toxic doses of anticancer drugs may represent a rational strategy to purpose for the treatment of human leukemias.

Animals↗
PubMed1997

Air pollution and mortality in Philadelphia, 1974-1988.

Analyses involving data from many locations throughout the world have now been conducted to assess the association between air pollution and mortality. To date, six independent analyses of mortality data for Philadelphia, Pennsylvania, have been reported. In this new analysis of Philadelphia data for 1974-1988, Poisson regression models were developed to estimate the increased risk of daily mortality associated with air pollution while controlling for longer-term time trends and season and for weather. Model development was based on prior understanding of the effects of these factors on mortality and on consideration of model fit. The authors found moderate correlations of daily concentrations of total suspended particles (TSP), sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO), and only slight correlations of ozone (O3) with other pollutants. When included individually in the model, the means of current and previous days' levels of TSP, SO2, and O3 had statistically significant effects on total mortality; pollutant increases of an interquartile range (34.5 micrograms/m3, 12.9 ppb, and 20.2 ppb, respectively) were associated with increases in mortality of around 1% for TSP and SO2, and of around 2% for O3. The effects of TSP and SO2 were diminished when both pollutants were simultaneously included in the model, whether pairwise or in the full multi-pollutant model. These analyses confirm the association between TSP and mortality found in previous studies in Philadelphia and show that the association is robust to consideration of other pollutants in the model.

Aged↗
PubMedDate not supplied

Fire fatalities among children: an analysis across Philadelphia's census tracts.

OBJECTIVE: This study investigates the possible causes of high levels of residential fire deaths to children younger than 15 years of age in Philadelphia from 1989 to 2000. METHODS: The authors analyzed 246 deaths from 146 residential fires by census tract in Philadelphia using both individual level data and aggregate level data drawn from the records of the Fire Marshall's Office. Death rates by age and sex were calculated using the 1990 Census. Data on fires from official records were combined with aggregate level data by census tract from the 1990 Census and analyzed using logistic regression. Newspaper articles on the fires analyzed were used to identify residences with possible fire code violations. The authors used data from the Philadelphia Bureau of Licenses and Inspections to provide evidence of code violations. RESULTS: The statistically significant variables that resulted from the logistic regression were census tracts in the highest quartile for low income households, census tracts in the highest quartile for single-parent households with children younger than age 18, census tracts in the highest quartile for houses built before 1939, and the number of children younger than 15 years of age in a census tract. CONCLUSION: Population characteristics by census tract are useful in identifying risk factors for residential fire deaths of children. Census tracts identified as at highest risk can provide fire prevention units with opportunities to take preventative measures such as the distribution of smoke detectors, and the education of residents about the dangers of careless smoking and planning for the rescue of children in the event of a fire.

Adolescent↗