HN1 is a novel dedifferentiation factor involved in regulating the cell cycle and microtubules in SH-SY5Y neuroblastoma cells.

Hematological and neurological expressed 1 (HN1), encoding a small protein, has been recently explored in different cancers owing to its higher expression in tumor samples as compared to adjacent normal. It was discovered and subsequently named because of its higher expression in hematological and neurological tissues in developing mice. Following discovery, it was considered a neuronal regeneration or dedifferentiation-related gene. However, since then, it has not been characterized in neuroblastoma or differentiated neurons. SH-SY5Y cell line presents a unique model of neuroblastoma often utilized in neurobiology research. In this study, first, we employed bioinformatics analysis along with in vitro evaluation using normal and retinoic acid (RA)-differentiated SH-SY5Y cells to determine the responses of HN1 and its function. The analysis revealed that HN1 expression is higher in neuroblastoma and lower in differentiated neurons and Parkinson's disease as compared to appropriate controls. Since HN1 coexpression network in neuroblastoma is found to be enriched in cell-cycle-related pathways, we have shown that HN1 expression increases in S-phase and remains lower in the rest of the cell cycle phases. Moreover, HN1 expression is also correlated with the microtubule stability in SH-SY5Y cells, which was investigated with nocodazole and taxol treatments. HN1 overexpression increased the ratio of S-type cells (undifferentiated), indicating that it acts as a dedifferentiating factor in neuroblastoma cells. Moreover, cell cycle dynamics also changed upon HN1 overexpression with alternating effects on SH-SY5Y and RA-differentiated (N-type) cells. Therefore, HN1 is a potential cell cycle regulatory element in the development of neuroblastoma or dedifferentiation of neurons, which requires further studies to decipher its mechanistic role.

Androgen receptor contributes to repairing DNA damage induced by inflammation and oxidative stress in prostate cancer.

Background: Androgen deprivation therapy remains the first-line therapy option for prostate cancer, mostly resulting in the transition of the disease to a castration-resistant state. The lack of androgen signaling during therapy affects various cellular processes, which sometimes paradoxically contributes to cancer progression. As androgen receptor (AR) signaling is known to contribute to oxidative stress regulation, loss of AR may also affect DNA damage level and the response mechanism in oxidant and inflammatory conditions of the prostate tumor microenvironment. Therefore, this study aimed to investigate the role of AR and AR-regulated tumor suppressor NKX3.1 upon oxidative stress-induced DNA damage response (DDR) in the inflammatory tumor microenvironment of the prostate. Materials and methods: Intracellular reactive oxygen species (ROS) level was induced by either inflammatory conditioned media obtained from lipopolysaccharide-induced macrophages or oxidants and measured by dichlorodihydrofluorescein diacetate. In addition to this, DNA damage was subsequently quantified by counting gH2AX foci using an immunofluorescence-based Aklides platform. Altered expression of proteins function in DDR detected by western blotting. Results: Cellular levels of ROS and ROS-induced DNA double-strand break damage were analyzed in the absence and presence of AR signaling upon treatment of prostate cancer cells by either oxidants or inflammatory microenvironment exposure. The results showed that AR suppresses intracellular ROS and contributes to DNA damage recognition under oxidant conditions. Besides, increased DNA damage due to loss of NKX3.1 under inflammatory conditions was alleviated by its overexpression. Moreover, the activation of the DDR mediators caused by AR and NKX3.1 activation in androgen-responsive and castration-resistant prostate cancer cells indicated that the androgen receptor function is essential both in controlling oxidative stress and in activating the ROS-induced DDR. Conclusion: Taken together, it is concluded that the regulatory function of androgen receptor signaling has a vital function in the balance between antioxidant response and DDR activation.

NKX3.1 Expression Contributes to Epithelial-Mesenchymal Transition of Prostate Cancer Cells.

Studies demonstrate that inflammation synergizes with high-grade aggressive prostate tumor development and ultimately metastatic spread, in which a lot of work has been done in recent years. However, the clear mechanism of inflammation inciting prostate cancer remains largely uncharacterized. Our previous study has shown that the conditioned media (CM)-mediated LNCaP cell migration is partially correlated with the loss of expression of the tumor suppressor NKX3.1. Here, we continue to investigate the inflammation-mediated migration of prostate cancer cells, and the role of NKX3.1 in this process to gain insights into cell migration-related changes comprehensively. Earlier, the model of inflammation in the tumor microenvironment have been optimized by our research group; here, we continue to investigate the time-dependent effect of CM exposure together with NKX3.1 changes, in which we observed that these changes play important roles in gaining heterogeneous epithelial-to-mesenchymal transition (EMT) phenotype. Hence, this is an important parameter of tumor progression; we depleted NKX3.1 expression using the CRISPR/Cas9 system and examined the migrating cell clusters after exposure to inflammatory cytokines. We found that the migrated cells clearly demonstrate reversible loss of E-cadherin expression, which is consistent with subsequent vimentin expression alterations in comparison to control cells. Moreover, the data suggest that the AR-mediated transcriptional program also contributes to mesenchymal-to-epithelial transition (MET) in prostate cancer progression. Furthermore, the quantitative proteomic analysis showed that migrated subpopulations from the same cell line presented different phenotypes in which the proteins overexpressed are involved in cell metabolism and RNA processing. According to KEGG pathway analysis, the ABC transporters were found to be the most significant. Thus, the dynamic process of cellular migration favors diverse genetic compositions under changing tumor microenvironments. The different levels of invasiveness are supported by shifting the cells in between these EMT and MET phenotypes.

Mitotic kinase inhibitors as Therapeutic Interventions for Prostate Cancer: Evidence from In vitro Studies.

Prostate cancer is one of the devastating diseases characterized by genetic changes leading to uncontrolled growth and metastasis of the cells of the prostate gland and affects men worldwide. Conventional hormonal and chemotherapeutic agents are effective in mitigating the disease if diagnosed at an early stage. All dividing eukaryotic cells require mitotic progression for the maintenance of genomic integrity in progeny populations. The protein kinases, upon activation and de-activation in an ordered fashion, lead to spatial and temporal regulation of the cell division process. The entry into mitosis along with the progression into sub-phases of mitosis is ensured due to the activity of mitotic kinases. These kinases include Polo-Like-Kinase 1 (PLK1), Aurora kinases, and Cyclin-Dependent-Kinase 1 (CDK1), among others. The mitotic kinases, among others, are usually overexpressed in many cancers and can be targeted using small molecule inhibitors to reduce the effects of these regulators on mechanisms, such as regulation of genomic integrity and mitotic fidelity. In this review, we attempted to discuss the appropriate functions of mitotic kinases revealed through cell culture studies and the impact of their respective inhibitors derived in pre-clinical studies. The review is designed to elucidate the growing field of small molecule inhibitors and their functional screening or mode of action at the cellular and molecular level in the context of Prostate Cancer. Therefore, studies performed specifically on cells of Prostatic-origin are narrated in this review, culminating in a comprehensive view of the specific field of mitotic kinases that can be targeted for therapy of Prostate cancer.

The Regulation of Cyclins and Cyclin-Dependent Kinases in the Development of Gastric Cancer.

Gastric cancer predominantly occurs in adenocarcinoma form and is characterized by uncontrolled growth and metastases of gastric epithelial cells. The growth of gastric cells is regulated by the action of several major cell cycle regulators including Cyclins and Cyclin-dependent kinases (CDKs), which act sequentially to modulate the life cycle of a living cell. It has been reported that inadequate or over-activity of these molecules leads to disturbances in cell cycle dynamics, which consequently results in gastric cancer development. Manny studies have reported the key roles of Cyclins and CDKs in the development and progression of the disease in either in vitro cell culture studies or in vivo models. We aimed to compile the evidence of molecules acting as regulators of both Cyclins and CDKs, i.e., upstream regulators either activating or inhibiting Cyclins and CDKs. The review entails an introduction to gastric cancer, along with an overview of the involvement of cell cycle regulation and focused on the regulation of various Cyclins and CDKs in gastric cancer. It can act as an extensive resource for developing new hypotheses for future studies.

HN1 Is Enriched in the S-Phase, Phosphorylated in Mitosis, and Contributes to Cyclin B1 Degradation in Prostate Cancer Cells.

HN1 has previously been shown as overexpressed in various cancers. In Prostate cancer, it regulates AR signaling and centrosome-related functions. Previously, in two different studies, HN1 expression has been observed as inversely correlated with Cyclin B1. However, HN1 interacting partners and the role of HN1 interactions in cell cycle pathways have not been completely elucidated. Therefore, we used Prostate cancer cell lines again and utilized both transient and stable inducible overexpression systems to delineate the role of HN1 in the cell cycle. HN1 characterization was performed using treatments of kinase inhibitors, western blotting, flow cytometry, immunofluorescence, cellular fractionation, and immunoprecipitation approaches. Our findings suggest that HN1 overexpression before mitosis (post-G2), using both transient and stable expression systems, leads to S-phase accumulation and causes early mitotic exit after post-G2 overexpression. Mechanistically, HN1 interacted with Cyclin B1 and increased its degradation via ubiquitination through stabilized Cdh1, which is a co-factor of the APC/C complex. Stably HN1-expressing cells exhibited a reduced Cdt1 loading onto chromatin, demonstrating an exit from a G1 to S phenotype. We found HN1 and Cdh1 interaction as a new regulator of the Cyclin B1/CDK1 axis in mitotic regulation which can be explored further to dissect the roles of HN1 in the cell cycle.

HN1 interacts with γ-tubulin to regulate centrosomes in advanced prostate cancer cells.

Prostate cancer is one of the most common cancer for men worldwide with advanced forms showing supernumerary or clustered centrosomes. Hematological and neurological expressed 1 (HN1) also known as Jupiter Microtubule Associated Homolog 1 (JPT1) belongs to a small poorly understood family of genes that are evolutionarily conserved across vertebrate species. The co-expression network of HN1 from the TCGA PRAD dataset indicates the putative role of HN1 in centrosome-related processes in the context of prostate cancer. HN1 expression is low in normal RWPE-1 cells as compared to cancerous androgen-responsive LNCaP and androgen insensitive PC-3 cells. HN1 overexpression resulted in differential response for cell proliferation and cell cycle changes in RWPE-1, LNCaP, and PC-3 cells. Since HN1 overexpression increased the proliferation rate in PC-3 cells, these cells were used for functional characterization of HN1 in advanced prostate carcinogenesis. Furthermore, alterations in HN expression led to an increase in abnormal to normal nuclei ratio and increased chromosomal aberrations in PC-3 cells. We observed the co-localization of HN1 with γ-tubulin foci in prostate cancer cells, further validated by immunoprecipitation. HN1 was observed as physically associated with γ-tubulin and its depletion led to increased γ-tubulin foci and disruption in microtubule spindle assembly. Higher HN1 expression was correlated with prostate cancer as compared to normal tissues. The restoration of HN1 expression after silencing suggested that it has a role in centrosome clustering, implicating a potential role of HN1 in cell division as well as in prostate carcinogenesis warranting further studies.

Oxidative DNA Damage-Mediated Genomic Heterogeneity Is Regulated by NKX3.1 in Prostate Cancer.

The 8-hydroxy-2'-deoxyguanosine (8-OHdG) damages are base damages induced by reactive oxygen species. We aimed to investigate the role of Androgen Receptor and NKX3.1 in 8-OHdG formation and repair activation by quantitating the DNA damage using Aklides.NUK system. The data demonstrated that the loss of NKX3.1 resulted in increased oxidative DNA damage and its overexpression contributes to the removal of menadione-induced 8-OHdG damage even under oxidative stress conditions. Moreover, 8-oxoguanine DNA glycosylase-1 (OGG1) expression level positively correlates to NKX3.1 expression. Also in this study, first time a reliable cell-based quantitation method for 8-OHdG damages is reported and used for data collection.

Cycloartane-type sapogenol derivatives inhibit NFκB activation as chemopreventive strategy for inflammation-induced prostate carcinogenesis.

Chronic inflammation is associated to 25% of cancer cases according to epidemiological data. Therefore, inhibition of inflammation-induced carcinogenesis can be an efficient therapeutic approach for cancer chemoprevention in drug development studies. It is also determined that anti-inflammatory drugs reduce cancer incidence. Cell culture-based in vitro screening methods are used as a fast and efficient method to investigate the biological activities of the biomolecules. In addition, saponins are molecules that are isolated from natural sources and are known to have potential for tumor inhibition. Studies on the preparation of analogues of cycloartane-type sapogenols (9,19-cyclolanostanes) have so far been limited. Therefore we have decided to direct our efforts toward the exploration of new anti-tumor agents prepared from cycloastragenol and its production artifact astragenol. The semi-synthetic derivatives were prepared mainly by oxidation, condensation, alkylation, acylation, and elimination reactions. After preliminary studies, five sapogenol analogues, two of which were new compounds (2 and 3), were selected and screened for their inhibitory activity on cell viability and NFκB signaling pathway activity in LNCaP prostate cancer cells. We found that the astragenol derivatives 1 and 2 as well as cycloastragenol derivatives 3, 4, and 5 exhibited strong inhibitory activity on NFκB signaling leading the repression of NFκB transcriptional activation and suppressed cell proliferation. The results suggested that these molecules might have significant potential for chemoprevention of prostate carcinogenesis induced by inflammatory NFκB signaling pathway.

Endovascular Repair of Peripheral Arterial Disease: Midterm Results From a Single Center.

OBJECTIVE: One thousand consecutive patients who underwent endovascular repair in an 8-year period were studied retrospectively to evaluate technical success, freedom from reinterventions, early clinical outcome, and risk factors for restenosis/occlusion. METHODS: Mean ± SD Rutherford class was 3.29 ± 0.8. A total of 755 patients have claudication, 423 from rest pain, and 569 from ischemic ulceration. RESULTS: A total of 552 men and 448 women (mean ± SD = 69.84 ± 8 years; range = 19-89 years) underwent endovascular repair. A total of 698 patients received local anesthesia and 302 general anesthesia. A total of 447 patients received percutaneous transluminal angioplasty, 650 stents were placed; 231 atherectomies were performed and 171 patients received hybrid approach. The procedure was successful in 847 patients (84%). There was no early death. There were 151 early occlusions (95 underwent surgery, 56 received stents), 121 dissections (39 underwent surgery, 56 received stents and 26 medical treatment), 32 hematoma, and 13 early leaks. Mean ± SD Rutherford class improved to 3.02 ± 0.9. Freedom from reintervention rate at 8 years was 76%. A total of 63 patients underwent surgery and 59 cellular therapy. A total of 134 finger, 142 below-knee, and 29 above-knee amputations were reported. CONCLUSIONS: Endovascular interventions can be performed with a satisfactory technical success and low complication rates; however, nonfatal complications and catheter-based reinterventions are frequent.

Synthesis and Topoisomerase I inhibitory properties of klavuzon derivatives.

Klavuzon is a naphthalen-1-yl substituted α,ß-unsaturated δ-lactone derivative, and is one of the anti-proliferative members of this class of compounds. Asymmetric and racemic syntheses of novel α,ß-unsaturated δ-lactone derivatives are important to investigate their potential for the treatment of cancer. In this study, asymmetric and racemic syntheses of heteroatom-substituted klavuzon derivatives are reported. The syntheses were completed by a well-known three-step procedure. Anti-proliferative activity of seven novel racemic klavuzon derivatives were reported against MCF-7, PC3, HCT116 p53+/+ and HCT116 p53-/- cancer cell lines. Topoisomerase I inhibitory properties of 5,6-dihydro-2H-pyran-2-one derivatives were also studied.

Automated Cell-Based Quantitation of 8-OHdG Damage.

Detection of 8-OHdG-base damage has been a big challenge for decades, though different analytical methods are developed. The recent approaches that are used for quantitating either the total amount of base damage or the amount of base damage per cell from different sources of samples are not automated. We have developed a method for automated damage detection from a single cell and applied it to 8-OHdG quantitation.

Early Mortality and Long-term Survival after Repair of Post-infarction Ventricular Septal Rupture: An Institutional Report of Experience.

BACKGROUND: To determine predictors of mortality after surgical management of post-infarction ventricular septal rupture repair. METHODS: A total of 63 patients (73.2%, mean age 67.22±7.71 years, male:female ratio; 35:28) underwent open heart surgery for post-infarction ventricular septal rupture repair. Patient demographics, operative data and postoperative parameters were analysed to reveal predictors of early mortality and long-term survival. RESULTS: In-hospital mortality was 54.0% (34/63). Time from myocardial infarction to operation ≤ 14 days (OR: 4.10, 95% CI 1.16-14.46, p=0.02), systolic pulmonary artery pressure > 45 mmHg (OR: 4.14, 95% CI 1.110-15.496, p=0.03) and age (years) (OR: 1.09, 95% CI 1.002-1.194, p=0.04) were found to be independent predictors of in-hospital mortality. In multivariate Cox regression analysis, presence of pulmonary oedema on admission (HR: 4.95, 95% CI 1.58-15.54, p=0.006), age (years) (HR: 1.09, 95% CI 1.009-1.180, p= 0.02) and cross-clamp time <60 min (HR: 3.93, 95% CI 1.13-13.64, p=0.03) were found to be independent predictors of long-term survival. Within a follow-up of a median of 60.0 months, five-year survival rate was 67±9.0%. CONCLUSION: In line with the previous studies, our study demonstrated the benefits of delaying the repair for post-infarction ventricular septal rupture to allow adequate myocardial healing if haemodynamic status of the patient allows.

Effect of Montelukast on Spinal Cord Ischemia- Reperfusion Injury.

AIM: Paraplegia due to ischemia-reperfusion (I/R) injury of the spinal cord is a devastating complication of thoracoabdominal aortic surgery. Cysteinyl leukotrienes are potent mediators of inflammation that are associated with I/R injury. The present study was designed to investigate the role of montelukast, a selective reversible CysLT1 receptor antagonist, on spinal cord I/R injury in an experimental model. MATERIAL AND METHODS: Twenty-one male Sprague-Dawley rats were randomly assigned to three groups (n=7 per group) as G1 (no aortic occlusion and montelukast administration), G2 (45 min. aortic occlusion; no montelukast administration) and G3 (45 min. aortic occlusion, 10 mg/kg montelukast administration). After neurologic evaluation using the Motor Deficit Index (MDI) score at the 48th hour of reperfusion, lumbar spinal cords were removed for histopathological evaluation and immunohistochemical staining for HSP70, interleukin-6 and myeloperoxidase (MPO). RESULTS: All rats in the G1 group had a normal neurological status and their MDI score was 0 (p < 0.05). The MDI score of G3 was significantly lower than G2 group (2.8 vs. 5.5; p < 0.05). Vacuolar congestion was found to be significantly lower in G1 than the other groups (p=0.0001). The interleukin-6 receptor level was found to be significantly lower in G3 group than the control group (p=0.013). There was no statistically significant difference found among the groups in terms of the degree of HSP70 and MPO staining. CONCLUSION: Increased generation of leukotrienes in postischemic organs play an important role in I/R injury. The findings of the current study demonstrated that montelukast improved motor recovery and decreased IL-6 levels in spinal cord I/R injury.

The redox biology network in cancer pathophysiology and therapeutics.

The review pinpoints operational concepts related to the redox biology network applied to the pathophysiology and therapeutics of solid tumors. A sophisticated network of intrinsic and extrinsic cues, integrated in the tumor niche, drives tumorigenesis and tumor progression. Critical mutations and distorted redox signaling pathways orchestrate pathologic events inside cancer cells, resulting in resistance to stress and death signals, aberrant proliferation and efficient repair mechanisms. Additionally, the complex inter-cellular crosstalk within the tumor niche, mediated by cytokines, redox-sensitive danger signals (HMGB1) and exosomes, under the pressure of multiple stresses (oxidative, inflammatory, metabolic), greatly contributes to the malignant phenotype. The tumor-associated inflammatory stress and its suppressive action on the anti-tumor immune response are highlighted. We further emphasize that ROS may act either as supporter or enemy of cancer cells, depending on the context. Oxidative stress-based therapies, such as radiotherapy and photodynamic therapy, take advantage of the cytotoxic face of ROS for killing tumor cells by a non-physiologically sudden, localized and intense oxidative burst. The type of tumor cell death elicited by these therapies is discussed. Therapy outcome depends on the differential sensitivity to oxidative stress of particular tumor cells, such as cancer stem cells, and therefore co-therapies that transiently down-regulate their intrinsic antioxidant system hold great promise. We draw attention on the consequences of the damage signals delivered by oxidative stress-injured cells to neighboring and distant cells, and emphasize the benefits of therapeutically triggered immunologic cell death in metastatic cancer. An integrative approach should be applied when designing therapeutic strategies in cancer, taking into consideration the mutational, metabolic, inflammatory and oxidative status of tumor cells, cellular heterogeneity and the hypoxia map in the tumor niche, along with the adjoining and systemic effects of oxidative stress-based therapies.

Application of radiofrequency ablation procedure on a morbidly obese patient with a venous ulcer and large saphenous vein.

Venous ulcers that occur due to chronic venous insufficiency are seen on the upper medial malleol of the ankle. Treatment of venous ulcers is protracted and generally the success rate is low. Co-morbid factors play an important role in the success of treatment of venous ulcers. In this case report, we demonstrate successful venous ulcer treatment in a morbidly obese patient with co-morbid conditions.

Inflammation contributes to NKX3.1 loss and augments DNA damage but does not alter the DNA damage response via increased SIRT1 expression.

The oxidative stress response is a cellular defense mechanism that protects cells from oxidative damage and cancer development. The exact molecular mechanism by which reactive oxygen species (ROS) contribute to DNA damage and increase genome instability in prostate cancer merits further investigation. Here, we aimed to determine the effects of NKX3.1 loss on antioxidant defense in response to acute and chronic inflammation in an in vitro model. Oxidative stress-induced DNA damage resulted in increased H2AX((S139)) phosphorylation (a hallmark of DNA damage), along with the degradation of the androgen receptor (AR), p53 and NKX3.1, upon treatment with conditioned medium (CM) obtained from activated macrophages or H2O2. Furthermore, the expression and stability of SIRT1 were increased by CM treatment but not by H2O2 treatment, although the level of ATM((S1981)) phosphorylation was not changed compared with controls. Moreover, the deregulated antioxidant response resulted in upregulation of the pro-oxidant QSCN6 and the antioxidant GPX2 and downregulation of the antioxidant GPX3 after CM treatment. Consistently, the intracellular ROS level increased after chronic treatment, leading to a dose-dependent increase in the ability of LNCaP cells to tolerate oxidative damage. These data suggest that the inflammatory microenvironment is a major factor contributing to DNA damage and the deregulation of the oxidative stress response, which may be the underlying cause of the increased genetic heterogeneity during prostate tumor progression.

Use of a superficial femoral artery autograft as a femoral vein replacement.

Posttraumatic arteriovenous fistulas (AVFs) are common complications of vascular penetrating trauma. Here we present a case of a 59-year-old woman who had a history of gunshot injury 42 years ago causing AVF between superficial femoral artery (SFA) and superficial femoral vein (SFV). SFV was resected. Ipsilateral SFA was used to restore SFV. SFA was reconstituted using a 7-mm polytetrafluorethylene graft. The patient has normal venous and arterial flow at 3- and 15-month follow-up.

HN1 negatively influences the ß-catenin/E-cadherin interaction, and contributes to migration in prostate cells.

Previously, it has been reported that HN1 is involved in cytoplasmic retention and degradation of androgen receptor in an AKT dependent manner. As HN1 is a hormone inducible gene, and has been shown that it is upregulated in various cancers, we studied the importance of HN1 function in ß-catenin signaling in prostate cancer cell line, PC-3 and mammary cancer cell line MDA-MB231. Here, we demonstrated that HN1 physically associates with GSK3ß/ß-catenin destruction complex and abundantly localizes to cytoplasm, especially when the GSK3ß is phosphorylated on S9 residue. Further, ectopic HN1 expression results an increase in the ß-catenin degradation leading to loss of E-cadherin interaction, concurrently contributing to actin re-organization, colony formation and migration in cancer cell lines. Thus, we report that HN1 is an essential factor for ß-catenin turnover and signaling, augments cell growth and migration in prostate cancer cells.

Relationship of admission neutrophil-to-lymphocyte ratio with in-hospital mortality in patients with acute type I aortic dissection.

AIM: Acute aortic dissection is a life-threatening cardiovascular emergency. Neutrophil-to-lymphocyte ratio is proposed as a prognostic marker and found to be related to worse clinical outcomes in various cardiovascular diseases. The aim of the present study was to evaluate the relationship between admission neutrophil-to-lymphocyte ratio and in-hospital mortality in acute type I aortic dissection. MATERIALS AND METHODS: We retrospectively evaluated 123 consecutive patients who had undergone emergent surgery for acute type I aortic dissection. Patients were divided into 2 groups as patients dying in the hospital (Group 1) and those discharged alive (Group 2). All parameters, including neutrophil-to-lymphocyte ratio, were compared between the 2 groups and predictors of mortality was estimated by using multivariate analysis. RESULTS: A total of 104 patients (79 males, mean age: 55.2 + 14 years) were included in the final analysis. In multivariate analyses, cross- clamp time, cardiopulmonary bypass time, intensive care-unit duration, platelet count, and neutrophil-to-lymphocyte ratio were found to be independent predictors of mortality. Patients with higher neutrophil-to-lymphocyte ratios had a significantly higher mortality rate (hazard ratio: 1.05; 95% CI: 1.01-1.10; P = 0.033). Receiver operating characteristic analysis revealed that using a cut-off point of 8, neutrophil-to-lymphocyte ratio predicts mortality with a sensitivity of 70% and specificity of 53%. CONCLUSION: This study suggests that admission neutrophil-to-lymphocyte ratio is a potential predictive parameter for determining the in-hospital mortality of acute type I aortic dissection.