An Overview of Rhinoplasty Practices: European Academy of Facial Plastic Surgery, Collaborative Cross-Sectional Study.

This collaborative European Academy of Plastic Surgery (EAFPS) study aimed to provide an overview of rhinoplasty practices, informing clinician and patient decision making. It is a multicenter cross-sectional study, reported as per Strengthening the Reporting of Observational Studies in Epidemiology guidelines. All EAFPS members were contacted via email, inviting them to participate. Members expressing an interest to participate were asked to anonymously complete a questionnaire, related to rhinoplasties that they performed as first/supervising surgeon over a period from January 1, 2019 to January 1, 2022. A descriptive analysis was performed. One hundred and fifteen surgeons submitted data on 41,259 rhinoplasties from 33 countries. Eighty percent of rhinoplasties were primary, and 20% were secondary. Thirty five percent of primary rhinoplasties were closed and 65% were open. Thirty one percent of primary rhinoplasties were for cosmetic indications, 11% functional and 58% were for both. Of the 8147 secondary rhinoplasties, 44% were closed and 56% were open. Thirty percent were for cosmetic indications, 11% functional, and 59% for both cosmetic and functional. Ninety-one percent of rhinoplasties were performed by ENT surgeons, 3% by plastic surgeons, 5% by maxillofacial surgeons, and 1% were dual (maxillofacial and ENT) trained. One-thousand seven-hundred thirty primary rhinoplasties underwent revision surgery (5%) and 102 secondary rhinoplasties underwent revision surgery (1%). The most commonly reported indications for revision surgery were dorsal asymmetry, nasal blockage, and dissatisfaction with nasal tip. Three percent of rhinoplasties underwent preoperative psychological assessment. To the authors knowledge, this is the largest published rhinoplasty dataset. This study provides an overview of rhinoplasty practices that can be used for benchmarking and to guide clinician and patient decision making. Psychological assessment of prerhinoplasty appears insufficient with higher levels recommended to minimize unsuccessful outcomes. This study showcases the power of collaborative research and may serve as a catalyst for future collaborative facial plastic surgery research.

Marula oil nanoemulsion improves motor function in experimental parkinsonism via mitigation of inflammation and oxidative stress.

Introduction: Parkinson's disease (PD) is a neurologic condition exhibiting motor dysfunction that affects old people. Marula oil (M-Oil) has been used longley in cosmetics and curing skin disorders. M-Oil is particularly stable due to its high concentration of monounsaturated fatty acids and natural antioxidants. The current study formulated M-Oil in an o/w nanoemulsion (M-NE) preparations and tested its anti-inflammatory and antioxidant actions against experimental parkinsonism. Methods: Four experimental groups of male albino mice were used and assigned as vehicle, PD, PD + M-Oil and PD + M-NE. Locomotor function was evaluated using the open field test and the cylinder test. Striatal samples were used to measure inflammatory and oxidative stress markers. Results: The results indicated poor motor performance of the mice in PD control group then, improvements were recorded after treatment with crude M-Oil or M-NE. In addition, we found high expression and protein of inflammatory markers and malondialdehyde levels in PD group which were downregulated by using doses of crude M-Oil or M-NE. Hence, formulating M-Oil in form of M-NE enhanced its physical characters. Discussion: This finding was supported by enhanced biological activity of M-NE as anti-inflammatory and antioxidant agent that resulted in downregulation of the inflammatory burden and alleviation of locomotor dysfunction in experimental PD in mice.

Betanin improves motor function and alleviates experimental Parkinsonism via downregulation of TLR4/MyD88/NF-κB pathway: Molecular docking and biological investigations.

Parkinson's disease (PD) is a progressive neuroinflammatory and degenerative disease. In this study, we investigated the neuroprotective action of betanin in the rotenone-induced Parkinson-like mice model. Twenty-eight adult male Swiss albino mice were divided into four groups: Vehicle, Rotenone, Rotenone + Betanin 50 mg/kg, and Rotenone + Betanin 100 mg/kg. Parkinsonism was induced by subcutaneous injection of 9 doses of rotenone (1 mg/kg/48 h) plus betanin at 50 and 100 mg/kg/48 h in rotenone + betanin groups for twenty days. Motor dysfunction was assessed after the end of the therapeutic period using the pole, rotarod, open-field, grid, and cylinder tests. Malondialdehyde, reduced glutathione (GSH), Toll-like receptor 4 (TLR4), myeloid differentiation primary response-88 (MyD88), nuclear factor kappa- B (NF-κB), neuronal degeneration in the striatum were evaluated. In addition, we assessed the immunohistochemical densities of tyrosine hydroxylase (TH) in Str and in substantia nigra compacta (SNpc). Our results showed that rotenone remarkably decreased (results of tests), increased decreased TH density with a significant increase in MDA, TLR4, MyD88, NF-κB, and a decrease in GSH (p < 0.05). Treatment with betanin significantly results of tests), increased TH density. Furthermore, betanin significantly downregulated malondialdehyde and improved GSH. Additionally, the expression of TLR4, MyD88, and NF-κB was significantly alleviated. Betanin's powerful antioxidative and anti-inflammatory properties can be related to its neuroprotective potential as well as its ability to delay or prevent neurodegeneration in PD.

Impact of weight loss on sexual and psychological functions and quality of life in females with sexual dysfunction: A forgotten avenue.

Objectives: This study aimed to evaluate the impact of weight loss on sexual and psychological health as well as quality of life in females with sexual dysfunction. Materials and methods: The study was done at Delta University for Science and Technology in Gamasa, Egypt, on 40 obese married females having sexual dysfunction. Their age ranged from 20 to 40 years old, with a mean of 28.98 ± 4.96 years. They followed a weight loss program in the form of diet regimen and physical training for 6 months. Anthropometric measures, Arabic Female Sexual Function Index (FSFI), Arabic version of Hospital Anxiety and Depression Scale (HADS), and Arabic version of Short-Form 36 Health Survey (SF-36) were evaluated prior to starting the study, after 3 and 6 months of the study. Results: Statistical analysis revealed significant reductions in anthropometric measures, as well as significant improvements in HADS and SF-36 scores after both 3 and 6 months of weight loss intervention compared to the baseline measurements, while there were significant improvements in sexual arousal, lubrication, patient satisfaction as well as the total score of FSFI after 3 months and contrarily there were no statistically significant changes in any of the FSFI's domains or overall score after 6 months of the weight loss program compared to baseline. Conclusion: Weight loss improves females' anthropometric measures, psychological function and quality of life; however, it has no direct effect on female sexual dysfunction (FSD) after 6 months compared to baseline, so increased awareness of FSD is necessary as this issue suffers from inadequate identification and management.

Comparative Study of the Neurotoxic Effects of Pregabalin Versus Tramadol in Rats.

In Egypt, both pregabalin and tramadol misuse increased in the last decade. Although many studies have confirmed the neurotoxic effects of tramadol, those of pregabalin are understudied. The aim of the study is to evaluate the neurotoxic effects of pregabalin compared with tramadol. Thirty male albino rats were included in this experimental study, and they were randomly allocated into three equal groups: group I (normal saline), group II (tramadol misuse), and group III (pregabalin misuse). All rats received the commenced drugs for 1 month. Open field tests were performed on the day of scarification, and after that, cortical samples were taken for immunohistochemical analysis and quantification of dopamine receptors' gene expression. The drug misuse groups showed a significant decrease in weight gain at the end of the study. Open field testing showed the upper hand of controls regarding all of the tested parameters. Tramadol has a more negative impact on the locomotor parameters compared with pregabalin. Both drugs induced relatively low dopamine-1 receptor (D1Rs) expression to dopamine-2 receptors (D2Rs), mimicking the schizophrenia model. Both tramadol and pregabalin were associated with neurotoxic effects in male albino rats. These effects were less noticed with pregabalin. It is suggested that long-term abuse may end in psychosis.

The Anti-Rheumatic Drug, Leflunomide, Induces Nephrotoxicity in Mice via Upregulation of TGFß-Mediated p53/Smad2/3 Signaling.

Recent studies indicated renal toxicity and interstitial nephritis in patients receiving leflunomide (LEFN), but the exact mechanism is still unknown. The transforming growth factor ß (TGFß)/p53/Smad2/3 pathway crucially mediates renal fibrosis. We aimed to assess the nephrotoxic effect of LEFN in mice and the possible role of TGFß-stimulated p53/SMAD2/3 signaling. The study design involved distributing sixty male albino mice into four groups: (i) vehicle-treated mice, (ii) LEFN (2.5 mg/kg), (iii) LEFN (5 mg/kg), and (iv) LEFN (10 mg/kg). The drug was given orally every 48 h and continued for 8 weeks. Blood samples were then taken from mice for the determination of kidney function parameters. Right kidneys were used for histopathologic staining and immunohistochemistry, whereas left kidneys were frozen and used for Western blot analysis of the target proteins, p-p53 and Smad2/3. Results indicated that chronic administration of LEFN in mice resulted in a four- and nine-fold increase in serum urea and creatinine levels, respectively. Kidney specimens stained with hematoxylin and eosin or periodic acid-Schiff showed significant histopathological manifestations, such as cellular irregularity, interstitial congestion, and moderate lymphocytic inflammatory infiltrate in mice treated with LEFN. Western blotting indicated upregulation of the p-p53/Smad2/3 proteins. LEFN, especially in the highest dose (10 mg/kg), produced prominent nephrotoxicity in mice. This toxicity is mediated through stimulating fibrotic changes through TGFß-stimulated p53/Smad2/3 signaling and induction of glomerular and tubular apoptosis. An improved understanding of LEFN-induced nephrotoxicity would have great implications in the prediction, prevention, and management of leflunomide-treated rheumatic patients, and may warrant further clinical studies for following up these toxidromes.

Discovery of varlaxins, new aeruginosin-type inhibitors of human trypsins.

Low-molecular weight natural products display vast structural diversity and have played a key role in the development of novel therapeutics. Here we report the discovery of novel members of the aeruginosin family of natural products, which we named varlaxins. The chemical structures of varlaxins 1046A and 1022A were determined using a combination of mass spectrometry, analysis of one- and two-dimensional NMR spectra, and HPLC analysis of Marfey's derivatives. These analyses revealed that varlaxins 1046A and 1022A are composed of the following moieties: 2-O-methylglyceric acid 3-O-sulfate, isoleucine, 2-carboxy-6-hydroxyoctahydroindole (Choi), and a terminal arginine derivative. Varlaxins 1046A and 1022A differ in the cyclization of this arginine moiety. Interestingly, an unusual α-D-glucopyranose moiety derivatized with two 4-hydroxyphenylacetic acid residues was bound to Choi, a structure not previously reported for other members of the aeruginosin family. We sequenced the complete genome of Nostoc sp. UHCC 0870 and identified the putative 36 kb varlaxin biosynthetic gene cluster. Bioinformatics analysis confirmed that varlaxins belong to the aeruginosin family of natural products. Varlaxins 1046A and 1022A strongly inhibited the three human trypsin isoenzymes with IC50 of 0.62-3.6 nM and 97-230 nM, respectively, including a prometastatic trypsin-3, which is a therapeutically relevant target in several types of cancer. These results substantially broaden the genetic and chemical diversity of the aeruginosin family and provide evidence that the aeruginosin family is a source of strong inhibitors of human serine proteases.

Protective effect of chronic caffeine intake on gene expression of brain derived neurotrophic factor signaling and the immunoreactivity of glial fibrillary acidic protein and Ki-67 in Alzheimer's disease.

Alzheimer's disease (AD) is a neurodegenerative disorder with progressive degeneration of the hippocampal and cortical neurons. This study was designed to demonstrate the protective effect of caffeine on gene expression of brain derived neurotrophic factor (BDNF) and its receptor neural receptor protein-tyrosine kinase-ß (TrkB) as well as glial fibrillary acidic protein (GFAP) and Ki-67 immunoreactivity in Aluminum chloride (AlCl3) induced animal model of AD. Fifty adult rats included in this study were classified into 5 group (10 rats each); negative and positive control groups (I&II), AD model group (III), group treated with caffeine from the start of AD induction (IV) and group treated with caffeine two weeks before AD induction (V). Hippocampal tissue BDNF and its receptor (TrkB) gene expression by real time RT-PCR in addition to immunohistochemical study of GFAP and Ki67 immunoreactivity were performed for all rats in the study. The results of this study revealed that caffeine has protective effect through improving the histological and immunohistochemical findings induced by AlCl3 as well as BDNF and its receptor gene expression. It could be concluded from the current study, that chronic caffeine consumption in a dose of 1.5 mg/kg body weight daily has a potentially good protective effect against AD.

Possible effects of metallosis on spermatozoal apoptotic genes expression in individuals with intramedullary nailing prosthesis.

Seminal quality could be affected by metallosis caused by intramedullary nailing (IMN). Our objectives were to estimate metal ion levels in the seminal plasma of subjects with IMN, to determine their effects on semen parameters and on spermatozoal apoptotic gene expression, and to determine whether these expressed genes could be used as candidate biomarkers of seminal deterioration in individuals with IMN or not. Semen samples were collected from 60 subjects with IMN and 30 age-matched healthy controls. Seminal plasma contents of cobalt (Co), chromium (Cr), and molybdenum (Mo) were assayed. Spermatozoal Bcl-2 and Bax gene expressions were determined. Studied semen parameters were significantly lower in subjects with IMN for ≥5 years in relation to controls while the concentrations of Co, Cr, and Mo in the seminal plasma samples were significantly higher. There were significantly lower spermatozoal Bcl-2 expression, higher Bax expression, and lower Bcl-2/Bax ratio in subjects with IMN for ≥5 years than in controls. In subjects with IMN for ≥5 years, receiver operating characteristic (ROC) curve analysis of studied gene expressions and Bcl-2/Bax ratio were done showing priority of the ratio with 86.7 % sensitivity, 100 % specificity, 100 % positive predictive value, and 93.8 % negative predictive value at cutoff values ≤0.777. Co, Cr, and Mo metals are found at high concentrations in the seminal plasma of individuals with IMN leading to increased spermatozoal apoptotic activity. Spermatozoal Bcl-2/Bax ratio could be used as a candidate biomarker of reproductive disorders in individuals with intramedullary nailing.

[Peripartum cardiomyopathy: incidence, pathogenesis, diagnosis, treatment and prognosis]. / Myocardiopathie du péripartum : incidence, physiopathologie, manifestations cliniques, prise en charge thérapeutique et pronostic.

INTRODUCTION: Peripartum cardiomyopathy (PPCM) is a rare and life-threatening disease of unknown aetiology. The primary objective of this review was to analysed aetiopathogeneses, clinical presentation and diagnosis, as well as pharmacological, perioperative and intensive care management and prognosis of this pathology. METHODS: We undertook a systematic review of the literature using Medline, Google Scholar and PubMed searches. RESULTS: Unlike other parts of the world in which cardiomyopathy are rare, dilated cardiomyopathy is a major cause of heart failure throughout Africa. Its aetiopathogenesis is still poorly understood, but recent evidence supports inflammation, viral infection and autoimmunity as the leading causative hypotheses. This diagnosis should be limited to previously healthy women who present with congestive heart failure (CHF) and decreased left ventricular systolic function in the last month of pregnancy or within 5 months after delivery. Recently, introduction of echocardiography has made diagnosis of PPCM easier and more accurate. Conventional treatment consists of diuretics, vasodilators, and sometimes digoxin and anticoagulants, usually in combination. Patients who fail to recover may require inotropic therapy. In resistant cases, newer therapeutic modalities such as immunomodulation, immunoglobulin and immunosuppression may be considered. Prognosis is highly related to reversal of ventricular dysfunction. Compared to historically higher mortality rates, recent reports describe better outcome, probably because of advances in medical care. Based on current information, future pregnancy is usually not recommended in patients who fail to recover normal heart function. CONCLUSION: PPCM is a rare but serious form of cardiac failure affecting women in the last months of pregnancy or early puerperium. Its aetiopathogenesis is still poorly understood. Introduction of echocardiography has made diagnosis of PPCM easier and more accurate. Prognosis is highly related to reversal of ventricular dysfunction.

Breast cancer: incidence, mortality, and early detection in Louisiana, 1988-1997.

Breast cancer is the most commonly diagnosed cancer and the second leading cause of cancer death among Louisiana women. The incidence data from Louisiana Tumor Registry were used to calculate breast cancer incidence rates, which were compared with the combined rates from the National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) program. Breast cancer mortality rates for Louisiana were compared with the US death rates from the National Center for Health Statistics (NCHS). Our data revealed that Louisiana women were not at a higher risk for developing breast cancer than women in the SEER areas, but that mortality rates in Louisiana were not correspondingly low. Although the percentage of cases diagnosed at an early stage (in situ and localized) increased in Louisiana from 1988 through 1997, the average in Louisiana was still below the level for the SEER areas (65.9% and 71.6%) in 1993-1997. The rates of in situ breast cancer significantly increased (on average 5.3% for whites per year and 7.1% for blacks), and localized breast cancer also significantly increased (2.6% for whites and 2.5% for blacks), while the incidence of distant stage breast cancer significantly decreased (3.4% for whites and 2.0% for blacks). Compared with white women, black women still were less likely to be diagnosed with early stage breast cancer in 1993-1997 (56.4% and 68.9%). Women residing in the parishes with high percentages of persons in poverty were less likely to be diagnosed with early stage of disease.

Cytogenetics and mechanisms of spontaneous abortions: increased apoptosis and decreased cell proliferation in chromosomally abnormal villi.

Genetic defects of the zygote, such as chromosome aberrations, are the most frequent causes of abnormal embryonic development and spontaneous abortion. However, the underlying mechanisms remain unknown. Chromosome aberrations likely cause changes in placental morphology and function (such as size, shape, vascularity, and the presence of trophoblastic inclusion). We postulated that chromosome aberrations may affect rates of cell proliferation or programmed cell death (apoptosis) during the differentiation of chorionic villi. To address these questions, we evaluated cell proliferation using a monoclonal antibody to Ki-67 (a cell-cycle marker) and apoptosis using the in situ end-labeling method (TUNEL) on paraffin-embedded placental tissues. Tissues were obtained from spontaneous abortions in early gestational periods with normal (11 cases) and abnormal karyotypes (15 cases), as well as eight normal control placentas from elective abortions. Apoptotic cells were found in the stroma of all cases, but were significantly higher in number in the stroma of chromosomally abnormal versus chromosomally normal spontaneous abortions. The apoptotic index of the trophoblasts was not significantly different between groups. Cell proliferation was higher in muscularized blood vessels in chromosomally normal placentas (both elective and spontaneous abortions) versus chromosomally abnormal spontaneous abortions. Cell proliferation was different in the trophoblast and stroma between the groups but to a lesser degree than in blood vessels. The morphological and biological data presented here suggest that: (1) chromosomally abnormal spontaneous abortions may occur because of different mechanisms than chromosomally normal spontaneous abortions, (2) apoptosis of the stromal cells and cell proliferation in blood vessels and stroma play an important role in the differentiation and functioning of villi, and (3) these changes could explain the etiology of spontaneous abortion and growth retardation of chromosomally abnormal embryos.

Comparative genomic hybridization studies in hydatidiform moles and choriocarcinoma: amplification of 7q21-q31 and loss of 8p12-p21 in choriocarcinoma.

Comparative genomic hybridization (CGH) was utilized to investigate genetic changes from archived cases of choriocarcinoma (n = 12) and hydatidiform moles (n = 7). Test DNA was extracted from paraffin-embedded tissues, amplified using total universal PCR, and co-hybridized with control DNA to normal metaphases. Comparative genomic hybridization findings showed chromosomal imbalances in 9 of 12 cases of choriocarcinoma. By contrast, all hydatidiform moles showed normal CGH profiles. Consistent findings in choriocarcinoma included deletion at 8p (5 cases) and amplification at 7q (4 cases). A tumor suppressor gene (e.g., N33) at 8p and/or a growth regulator at 7q could play a role in the initiation of choriocarcinoma and its progression. This is the first study showing specific alterations in choriocarcinomas by CGH, and illustrates the utility of this technique in elucidating genetic changes in gynecological tumors.

Induction of DNA replication in adult rat neurons by deregulation of the retinoblastoma/E2F G1 cell cycle pathway.

In adult organisms, a range of proliferative capacities are exhibited by different cell types. Stem cell populations in many tissues readily enter the cell cycle when presented with serum growth factors or other proliferative cues, whereas "terminally" postmitotic cells, such as cardiac myocytes and neurons, fail to do so. Although they rarely show evidence of a proliferative capacity in vivo, there is accumulating evidence to suggest that DNA synthesis can be triggered in postmitotic cells. We now show that cultured adult rat sensory neurons can replicate DNA in response to ectopic expression of E2F1 or E2F2 and that this is augmented by expression of cyclin-dependent kinase activities. We also find that addition of serum and laminin inhibits the E2F-induced S-phase in neurons but not in nonneuronal cells in the same cultures. We conclude that, although terminally differentiated neurons possess the capacity to reinitiate DNA replication in response to G1 regulatory activities, they fail to do so in the presence of signals that do not inhibit S-phase in other cell types in the same cultures. This suggests the existence of cell type-specific inhibitory pathways induced by these signals.

Cancer of the colon and rectum in Louisiana.

Cancer of the colon and rectum ranks fourth for incidence and second for mortality among Louisiana residents. Incidence rates calculated from Louisiana Tumor Registry data for 1991-95 show that whites in Louisiana were diagnosed with colon cancer at approximately the same rates as those in the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) program, but rates for African Americans were significantly lower in Louisiana than nationally. For rectal cancer, Louisiana incidence rates approximate the national rates for all but African-American males, whose rate was significantly lower. Mortality rates for colon and rectal cancer in Louisiana were comparable to the SEER rates, suggesting Louisiana blacks, once diagnosed, have a poorer survival than their national counterparts. Risk factors for colorectal cancer and guidelines for screening are discussed, as is an upcoming study of patient care for colon cancer.

Louisiana Tumor Registry: new developments and activities.

New developments in the Louisiana Tumor Registry (LTR) over the past 3 years have enhanced the operation of the LTR and broadened its functions. Recent funding for numerous special studies and research collaborations have expanded the registry activities from data collection and special etiologic studies to more completely address the mandates of registry law, which require the LTR to participate in studies of cancer causes, treatment, and survival in order to reduce cancer morbidity and mortality in Louisiana.

Unconjugated estriol as an indication for prenatal diagnosis of steroid sulfatase deficiency by in situ hybridization.

BACKGROUND: Undetectable or very low unconjugated estriol (E3) levels in routine maternal serum screening are associated with steroid sulfatase deficiency, miscarriages, and anencephaly. CASES: Fluorescence in situ hybridization techniques were used in the diagnosis of steroid sulfatase deficiency prenatally in three cases with low or undetectable unconjugated E3 levels. Results showed a male fetus with a deleted steroid sulfatase region, but intact Kallmann syndrome region in all three cases. One mother was studied by fluorescence in situ hybridization and showed a similar deletion for steroid sulfatase gene in one copy of X chromosome (carrier). CONCLUSION: Women with undetectable or very low levels of estriol on serum screening should be counseled regarding steroid sulfatase deficiency with evaluation by fluorescence in situ hybridization.

Familial subepithelial corneal amyloidosis (gelatinous drop-like corneal dystrophy): exclusion of linkage to lactoferrin gene.

PURPOSE: Because corneal tissue with familial subepithelial corneal amyloidosis (FSCA; gelatinous drop-like dystrophy of the cornea) contains lactoferrin the possibility that the FSCA gene was the human lactoferrin (hLF) gene was investigated. Due to contradictory published information we also mapped the hLF gene. METHODS: We mapped the hLF gene using a genomic clone of the entire hLF gene as a probe by fluorescence in situ hybridization (FISH). Utilizing PCR primers that are specific to the hLF gene, we also mapped the hLF via radiation somatic cell hybrid analysis. Linkage of the FSCA gene to the hLF gene was evaluated by genetic linkage analysis using polymorphic markers within and in the vicinity of the hLF gene. RESULTS: The hLF gene mapped to the short arm of chromosome 3 at 3p21. Linkage analysis using polymorphic markers for hLF and haplotype analysis of the 3p21 loci indicates that the FSCA gene is not linked to the 3p21 locus. CONCLUSIONS: The gene for FSCA is not the hLF gene in these families.

Genomic structure and chromosomal localization of the novel ETS factor, PE-2 (ERF).

The members of the ETS family of transcription factors are grouped because they share a highly conserved DNA binding domain. These factors are involved in growth factor pathways and regulate both proliferation and differentiation. To identify ETS factors that may be involved in early hematopoietic progenitor regulation, we isolated a novel member of the ETS family by reverse transcriptase-PCR of the conserved DNA binding domain using degenerate oligonucleotides. This gene directs the synthesis of a 2704-nucleotide transcript whose largest open reading frame encodes a 548-amino-acid protein. Northern blot analysis reveals ubiquitous expression in all human tissues and cell lines tested, with highest levels in the testis, ovary, pancreas, and heart. Comparison of this gene with the available databases reveals very significant homology to the ETS factor PE-1 and probable near-identity with the recently cloned factor ERF. The PE-2 gene is composed of four exons spanning over 9 kb of genomic DNA. Sequence analysis of the promoter region reveals a GC-rich sequence without a TATA motif and with putative binding motifs for CREB, c-myb, and AP-1 factors. Using mouse-human somatic hybrids and FISH analysis, the PE-2 gene is localized to human chromosome 19q13.2, a region involved in translocations and deletions in leukemias and several solid tumors, suggesting that this novel ETS factor may play a role in carcinogenesis.