ABSTRACT
In the original publication [...].
ABSTRACT
In rainy areas, sweet cherries are cultivated under plastic covers, preventing the cracking of the fruit but decreasing the firmness and acidity of the cherries. We evaluated the impact of plastic cover and pre-harvest K foliar application on quality parameters, antioxidant properties, and phenolic and organic acid compositions in fruits of sweet cherry cv. Regina of Southern Chile. Our results showed that K+ increased firmness, total soluble content, size, fruit weight, and titratable acidity at harvest, independent of the cover factor. The positive impacts of foliar K fertilization on anthocyanins, flavonoids, and phenolic acids could explain the higher antioxidant capacity of fruits. Our study revealed that the additional K doses applied increased malic acid, the main organic acid in cherry fruits, but only in fruits from uncovered trees. In covered trees, the effect was reversed. Citric acid was higher in fruit from covered trees. Our results indicated that tartaric acid also increased with the application of higher K doses; however, this acid was detectable only in uncovered tree fruit. Interestingly, all organic acids were lower in fruits produced in the lower canopy than those detected in fruits harvested from the upper canopy. This showed the positive impact of canopy light exposure on maintaining suitable acidity levels in sweet cherry fruits.
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In rainy locations, sweet cherry is cultivated under plastic covers, which are useful to prevent fruit cracking but decrease cherry quality such as firmness and acidity. Here we evaluate the impact of pre-harvest K foliar applications on harvest and post-harvest fruit quality and condition of sweet cherry cultivated under plastic covers in southern Chile orchards. The study was performed on two commercial orchards (cv. Regina), located in different regions, during two consecutive seasons. In all cases, a conventional K regime (four sprays) was compared to an intensive K regimen (seven sprays). Results showed that cherries from the most southern region revealed lower acidity but higher soluble solids content weight and size. The intensive K regime improved the firmness and acidity of fruits of covered trees at harvest and post-harvest. Moreover, we found that condition defects were higher in fruits from un-covered trees and that trees grown under intensive K regime showed lower levels of cracking at harvest and pitting at post-harvest compared to trees treated with the conventional K regime. Otherwise, pedicel browning was inconsistently affected by K sprays. Our results revealed that an intensive K regime could improve the quality and condition of fruits at harvest and post-harvest in covered orchards of sweet cherry cv. Regina; however, the impacts can significantly vary depending on season and locality.
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Gastric cancer (GC) is the fifth most prevalent type of cancer worldwide. Gastric tumor cells express MICA protein, a ligand to NKG2D receptor that triggers natural killer (NK) cells effector functions for early tumor elimination. MICA gene is highly polymorphic, thus originating alleles that encode protein variants with a controversial role in cancer. The main goal of this work was to study MICA gene polymorphisms and their relationship with the susceptibility and prognosis of GC. Fifty patients with GC and 50 healthy volunteers were included in this study. MICA alleles were identified using Sanger sequencing methods. The analysis of MICA gene sequence revealed 13 MICA sequences and 5 MICA-short tandem repeats (STR) alleles in the studied cohorts We identified MICA*002 (*A9) as the most frequent allele in both, patients and controls, followed by MICA*008 allele (*A5.1). MICA*009/049 allele was significantly associated with increased risk of GC (OR: 5.11 [95% CI: 1.39-18.74], p = 0.014). The analysis of MICA-STR alleles revealed a higher frequency of MICA*A5 in healthy individuals than GC patients (OR = 0.34 [95% CI: 0.12-0.98], p = 0.046). Survival analysis after gastrectomy showed that patients with MICA*002/002 or MICA*002/004 alleles had significantly higher survival rates than those patients bearing MICA*002/008 (p = 0.014) or MICA*002/009 (MICA*002/049) alleles (p = 0.040). The presence of threonine in the position MICA-181 (MICA*009/049 allele) was more frequent in GC patients than controls (p = 0.023). Molecular analysis of MICA-181 showed that the presence of threonine provides greater mobility to the protein than arginine in the same position (MICA*004), which could explain, at least in part, some immune evasion mechanisms developed by the tumor. In conclusion, our findings suggest that the study of MICA alleles is crucial to search for new therapeutic approaches and may be useful for the evaluation of risk and prognosis of GC and personalized therapy.
Subject(s)
Alleles , Genetic Predisposition to Disease , Histocompatibility Antigens Class I/genetics , Microsatellite Repeats , Neoplasm Proteins/genetics , Polymorphism, Genetic , Stomach Neoplasms/genetics , Aged , Female , Histocompatibility Antigens Class I/immunology , Humans , Male , Middle Aged , Neoplasm Proteins/immunology , Stomach Neoplasms/immunologyABSTRACT
BACKGROUND: Helicobacter pylori is detected by pathogen recognition receptors including toll-like receptors (TLR) and nucleotide-binding oligomerization domain (NOD)-like receptors, eliciting an innate immune response against this bacteria. The aim of this study was to assess if polymorphisms of TLR2, TLR4, TLR5, NOD1 and NOD2 genes are associated with gastric cancer, in particular in individuals infected with H. pylori. RESULTS: A case-control study of 297 gastric cancer patients and 300 controls was performed to assess the association of 17 polymorphisms. Analyses performed under the allele model did not find association with gastric cancer. However, NOD1 rs2075820 (p.E266K) showed association with intestinal-type gastric cancer among H. pylori infected subjects (OR = 2.69, 95% CI 1.41-5.13, p = 0.0026). The association was not statistically significant in diffuse-type gastric cancer cases (OR = 1.26, 95% CI 0.63-2.52, p = 0.51). When the analyses were performed in patients carrying H. pylori strains harboring the cag pathogenicity island (cagPAI), we noticed significant association with NOD1 rs2075820 (OR = 4.90, 95% CI 1.80-3.36, p = 0.0019), in particular for intestinal-type gastric cancer cases (OR = 7.16, 95% CI 2.40-21.33, p = 4.1 × 10- 4) but not among diffuse-type gastric cancer cases (OR = 3.39, 95% CI 1.13-0.10, p = 0.03). CONCLUSIONS: NOD1 rs2075820 increases the risk of intestinal-type gastric cancer among individuals infected with H. pylori, particularly in those harboring the cagPAI.
Subject(s)
Helicobacter Infections , Nod1 Signaling Adaptor Protein/genetics , Stomach Neoplasms , Case-Control Studies , Genomic Islands , Helicobacter Infections/genetics , Helicobacter pylori , Humans , Stomach Neoplasms/geneticsABSTRACT
BACKGROUND: Helicobacter pylori is detected by pathogen recognition receptors including toll-like receptors (TLR) and nucleotide-binding oligomerization domain (NOD)-like receptors, eliciting an innate immune response against this bacteria. The aim of this study was to assess if polymorphisms of TLR2, TLR4, TLR5, NOD1 and NOD2 genes are associated with gastric cancer, in particular in individuals infected with H. pylori. RESULTS: A case-control study of 297 gastric cancer patients and 300 controls was performed to assess the association of 17 polymorphisms. Analyses performed under the allele model did not find association with gastric cancer. However, NOD1 rs2075820 (p.E266K) showed association with intestinal-type gastric cancer among H. pylori infected subjects (OR = 2.69, 95% CI 1.41-5.13, p = 0.0026). The association was not statistically significant in diffuse-type gastric cancer cases (OR = 1.26, 95% CI 0.63-2.52, p = 0.51). When the analyses were performed in patients carrying H. pylori strains harboring the cag pathogenicity island (cagPAI), we noticed significant association with NOD1 rs2075820 (OR = 4.90, 95% CI 1.80-3.36, p = 0.0019), in particular for intestinal-type gastric cancer cases (OR = 7.16, 95% CI 2.40-21.33, p = 4.1 × 10- 4) but not among diffuse-type gastric cancer cases (OR = 3.39, 95% CI 1.13-0.10, p = 0.03). CONCLUSIONS: NOD1 rs2075820 increases the risk of intestinal-type gastric cancer among individuals infected with H. pylori, particularly in those harboring the cagPAI.
Subject(s)
Humans , Stomach Neoplasms/genetics , Helicobacter Infections/genetics , Nod1 Signaling Adaptor Protein/genetics , Case-Control Studies , Helicobacter pylori , Genomic IslandsABSTRACT
Genetic variants are considered risk factors for gastric cancer. To date, 61 polymorphisms have been identified as associated with this disease. The aim of the present study was to analyze the association of some of those polymorphisms with GC in Chile. We performed a case-control study including 310 gastric cancer cases and 311 controls to assess the association of 36 single-nucleotide polymorphisms genotyped by Global Screening Array (GSA). Three polymorphisms was significantly associated: PSCA rs2294008 (allele model, OR = 1.49, 95%CI 1.17-1.88, P = 1.08 × 10-3), IL-4 rs2243250 (allele model, OR = 1.28, 95%CI 1.01-1.62, P = 0.04), and MUC1 rs4072037 (allele model, OR = 0.78, 95%CI 0.61-0.99, P = 0.04).PSCA rs2294008, IL-4 rs2243250 and MUC1 rs4072037 are associated with gastric cancer in Chile. It suggests that those polymorphisms could be used as biomarkers to assess the genetic risk for this cancer outside of the previously studied populations, not only for East Asians and Caucasians populations.
Subject(s)
Antigens, Neoplasm/genetics , Genetic Predisposition to Disease/genetics , Interleukin-4/genetics , Mucin-1/genetics , Neoplasm Proteins/genetics , Polymorphism, Single Nucleotide , Stomach Neoplasms/genetics , Adolescent , Adult , Aged , Aged, 80 and over , Alleles , Case-Control Studies , Chile , Female , GPI-Linked Proteins/genetics , Gene Frequency , Genotype , Humans , Male , Middle Aged , Risk Factors , Young AdultABSTRACT
Gastric cancer (GC) is the third most common cause of cancer-related death worldwide. Invariant natural killer T (iNKT) cells are innate-like cytotoxic T lymphocytes involved in tumor immune surveillance. They can be activated either through CD1d-presented glycolipid antigens recognized by their invariant T-cell receptor, cytokines or by sensing tumor-associated stress-induced ligands through the natural killer group 2, member D (NKG2D) receptor. Although the number and functionality of iNKT cells may be decreased in several types of cancer, here we show that GC patients presented a mild increase in iNKT cell frequencies and numbers in the blood compared with healthy donors. In GC patients, iNKT cells, expanded in vitro with α-galactosyl ceramide and stimulated with phorbol 12-myristate 13-acetate and ionomycin, produced higher levels of interleukin-2 and transforming growth factor-beta, while their capacity to degranulate remained preserved. Because tumor-derived epithelial cell adhesion molecule-positive epithelial cells did not display surface CD1d, and NKG2D ligands (NKG2DLs) were detected in the gastric tumor milieu, we envisioned a role for NKG2D in iNKT cell functions. Peripheral iNKT cells from GC patients and controls presented similar levels of NKG2D; nevertheless, the percentages of interferon-γ-producing and CD107a-positive iNKT cells from patients were reduced upon challenge with CD1d-negative, NKG2DL-positive K562 cells, suggesting a compromised response by iNKT cells in GC patients, which may not result from impaired NKG2D/NKG2DL signaling. The decreased response of iNKT cells may explain the fact that higher frequencies of circulating iNKT cells did not confer a survival benefit for GC patients. Therefore, functional impairment of iNKT cells in GC may contribute to tumor immune escape and favor disease progression.
Subject(s)
Natural Killer T-Cells , Stomach Neoplasms , Antigens, CD1d , Cytokines/immunology , Humans , K562 Cells , Lymphocyte Activation , NK Cell Lectin-Like Receptor Subfamily K/immunology , Natural Killer T-Cells/immunology , Receptors, Antigen, T-Cell/immunology , Stomach Neoplasms/immunologyABSTRACT
BACKGROUND/AIM: Inflammation is a key process in gastric carcinogenesis. Cytokines are mediators of inflammation and are involved in metastasis and tumorigenicity. We previously assessed the role of cytokine gene polymorphisms in gastric cancer risk in Chile. In the present study, we aimed to analyze whether these polymorphisms are associated with overall survival (OS) in gastric cancer (GC) patients. PATIENTS AND METHODS: A total of 153 individuals with GC diagnosis were followed-up for at least 2 years. Hazard ratios (HR) were estimated from Cox regression models using SNPs as predictor variables. The following SNPs were genotyped for study using a TaqMan assay: rs16944 (IL1B -511C>T); rs4073 (IL8 -251 T>A); rs2275913 (IL-17 -197G>A); rs1800872 (IL10 -592 C>A); rs1800896 (IL10 -1082A>G); rs28372698 (IL32). RESULTS: Interleukin-8 rs4073 (IL-8 -251T>A) showed association with OS under the dominant model (TA + AA) only when adjusted by clinicopathological variables (HR=1.64, 95%CI=1.05-2.55, p=0.030, q-value=0.18), but not with the univariate model (HR=1.51, 95%CI=0.98-2.31, p=0.062, q-value=0.37). No significant differences were observed after adjusting for population stratification (PC1 and PC2 from Principal Component Analysis using genotypes from Infinium Global Screening Array). After stratification by clinicopathological variables, the association with shorter overall survival was higher among patients with diffuse-type tumors (HR=2.24, 95%CI=1.16-4.45) and patients with tumor size >5 cm (HR=1.79, 95%CI=1.08-2.97). CONCLUSION: These results suggest a role of IL-8 rs4073 in cancer prognosis. Its use as a prognostic marker of GC survival warrants further investigation.
Subject(s)
Adenocarcinoma/genetics , Interleukin-8/genetics , Polymorphism, Single Nucleotide , Stomach Neoplasms/genetics , Adenocarcinoma/pathology , Adenocarcinoma/surgery , Biomarkers, Tumor , Humans , Prognosis , Stomach Neoplasms/pathology , Stomach Neoplasms/surgery , Survival RateABSTRACT
BACKGROUND/AIM: Epithelial-mesenchymal transition (EMT) program has been linked as a driver of metastatic dissemination by conferring migratory and invasive capacity to cancer cells. Gastric cancer (GC) patients with tumors expressing altered levels of EMT markers have low survival. This study aimed to assess if polymorphisms of CDH1, TWIST1, SNAIL2, ZEB1 and ZEB2 genes are associated with survival in GC patients. PATIENTS AND METHODS: A total of 153 individuals with diagnosis of GC were recruited in Santiago, Chile. All patients were genotyped using Infinium Global Screening Array (GSA). Twenty Tag SNPs of the studied genes were retrieved. RESULTS: Three SNPs were associated with survival: rs2526614 (TWIST1) (genotype CA + AA, adjusted HR=0.58, 95%CI=0.37-0.93), rs6953766 (TWIST1) (genotype GG, crude HR=2.02, 95%CI=1.06-3.82, adjusted HR=2.14, 95%CI=1.07-4.25), and rs431073 (ZEB1) (genotype AC + CC, crude HR=1.62, 95%CI=1.01-2.59, adjusted HR=1.96, 95%CI=1.18-3.25). CONCLUSION: To the best of our knowledge, this is the first study proposing a role of these SNPs in cancer prognosis. Their use as prognostic markers of GC survival warrants further investigation.
Subject(s)
Nuclear Proteins/genetics , Polymorphism, Single Nucleotide , Stomach Neoplasms/pathology , Twist-Related Protein 1/genetics , Zinc Finger E-box-Binding Homeobox 1/genetics , Adult , Aged , Aged, 80 and over , Epithelial-Mesenchymal Transition/genetics , Female , Humans , Male , Middle Aged , Prognosis , Stomach Neoplasms/genetics , Survival RateABSTRACT
The RAS/RAF/MEK/ERK pathway regulates certain cellular functions, including cell proliferation, differentiation, survival, and apoptosis. Dysregulation of this pathway leads to the occurrence and progression of cancers mainly by somatic mutations. This study aimed to assess if polymorphisms of the RAS/RAF/MEK/ERK pathway are associated with gastric cancer. A case-control study of 242 gastric cancer patients and 242 controls was performed to assess the association of 27 single nucleotide polymorphisms (SNPs) in the RAS/RAF/MEK/ERK pathway genes with gastric cancer. Analyses performed under the additive model (allele) showed four significantly associated SNPs: RAF1 rs3729931 (Odds ratio (OR) = 1.54, 95%, confidence interval (CI): 1.20â»1.98, p-value = 7.95 × 10-4), HRAS rs45604736 (OR = 1.60, 95% CI: 1.16â»2.22, p-value = 4.68 × 10-3), MAPK1 rs2283792 (OR = 1.45, 95% CI: 1.12â»1.87, p-value = 4.91 × 10-3), and MAPK1 rs9610417 (OR = 0.60, 95% CI: 0.42â»0.87, p-value = 6.64 × 10-3). Functional annotation suggested that those variants or their proxy variants may have a functional effect. In conclusion, this study suggests that RAF1 rs3729931, HRAS rs45604736, MAPK1 rs2283792, and MAPK1 rs9610417 are associated with gastric cancer.
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Resumen Introducción: La resección quirúrgica ha demostrado ser la única opción curativa para el cáncer gástrico, al incluir linfadenectomía D2 como estándar de seguridad. Sin embargo, el beneficio de extender la resección a la bursa omentalis sigue siendo controvertido. La investigación publicada no ha arrojado evidencia categórica definiendo la eficacia. Realizamos una revisión sistemática de ensayos clínicos aleatorizados publicados (ECA), para evaluar el beneficio de la bursectomía en la sobrevida global (OS) y la sobrevida libre de enfermedad (SLE) de los pacientes. Como resultado secundario se consideró la seguridad del procedimiento. Métodos: Se realizó una búsqueda bibliográfica en las bases de datos de Pubmed, Cochrane, Scielo, Metabuscador PUC, Epistemonikos, Tripdatabase, Sciencedirect y Lilacs para ECA que compararan la bursectomía con la no bursectomía, publicados antes de marzo de 2016. Se establecieron y aplicaron criterios de inclusión y exclusión. Resultados: Se encontraron 3 ECA correspondientes a diferentes informes de la misma cohorte de pacientes. Se incluyeron 210 pacientes (104 en el grupo de bursectomía y 106 en el grupo de no bursectomía). La bursectomía no tuvo un efecto significativo ni en la OS a 5 años (HR: 1,4; IC del 95%: 0,87-2,25) ni en la SLE (HR: 1,25; IC del 95% 0,80-1,97). No se observó diferencia estadísticamente significativa en la tasa de complicaciones al comparar el grupo de bursectomía y el grupo de no bursectomía. Conclusión: La gastrectomía con bursectomía no es superior a la no bursectomía, ya sea en términos de OS a 5 años o de SLE.
Abstract Introduction: The surgical resection has proved to be the only curative option for Gastric Cancer, when including D2 linfadenectomy as security standard. The benefit of extending the resection to the bursa omentalis, however, is still controversial. The published research has not yielded categorical evidence on defining the efficacy of bursectomy. We conducted a systematic review of published randomized controlled trials (RCT), to evaluate the benefit of bursectomy in the overall survival (OS) and disease-free survival (DFS) of patients. As secondary outcome, was considered the safety of the procedure. Methods: A literature search was conducted in Pubmed, Cochrane library databases, Scielo, Metabuscador PUC, Epistemonikos, Tripdatabase, Sciencedirect, and Lilacs for randomized clinical trials comparing bursectomy with non-bursectomy, published before March 2016. Inclusion and exclusion criteria were established and applied. Results: We found three RCT corresponding to different reports of the same cohort of randomized patients. They included 210 patients (104 in the bursectomy group, and 106 in the non-bursectomy group). The bursectomy did not have a significant effect either on 5-years OS (HR: 1.4; 95%CI: 0,87-2,25), or on DFS (HR: 1.25; 95% CI: 0,80-1,97). No statistically significant difference was observed in the rate of complications, when comparing the bursectomy group and the non-bursectomy group. Conclusion: Gastrectomy with bursectomy is not superior to non-bursectomy either in terms of 5 years OS or on DFS.
Subject(s)
Humans , Stomach Neoplasms/surgery , Gastrectomy/methods , Peritoneal Cavity/surgery , Postoperative Complications , Stomach Neoplasms/mortality , Survival Analysis , Disease-Free SurvivalABSTRACT
Gastric cancer (GC) is the third most common cause of cancer death worldwide. Natural killer cells play an important role in the immune defense against transformed cells. They express the activating receptor NKG2D, whose ligands belong to the MIC and ULBP/RAET family. Although it is well established that these ligands are generally expressed in tumors, the association between their expression in the tumor and gastric mucosa and clinical parameters and prognosis of GC remains to be addressed. In the present study, MICA and MICB expression was analyzed, by flow cytometry, in 23 and 20 pairs of gastric tumor and adjacent non-neoplasic gastric mucosa, respectively. Additionally, ligands expression in 13 tumors and 7 gastric mucosa samples from GC patients were evaluated by immunohistochemistry. The mRNA levels of MICA in 9 pairs of tumor and mucosa were determined by quantitative PCR. Data were associated with the clinicopathological characteristics and the patient outcome. MICA expression was observed in 57% of tumors (13/23) and 44% of mucosal samples (10/23), while MICB was detected in 50% of tumors (10/20) and 45% of mucosal tissues (9/20). At the protein level, ligand expression was significantly higher in the tumor than in the gastric mucosa. MICA mRNA levels were also increased in the tumor as compared to the mucosa. However, clinicopathological analysis indicated that, in patients with tumors >5 cm, the expression of MICA and MICB in the tumor did not differ from that of the mucosa, and tumors >5 cm showed significantly higher MICA and MICB expression than tumors ≤5 cm. Patients presenting tumors >5 cm that expressed MICA and MICB had substantially shorter survival than those with large tumors that did not express these ligands. Our results suggest that locally sustained expression of MICA and MICB in the tumor may contribute to the malignant progression of GC and that expression of these ligands predicts an unfavorable prognosis in GC patients presenting large tumors.
Subject(s)
Histocompatibility Antigens Class I/biosynthesis , Stomach Neoplasms/genetics , Adult , Aged , Aged, 80 and over , Female , Flow Cytometry , Gene Expression Regulation, Neoplastic , Histocompatibility Antigens Class I/immunology , Humans , Killer Cells, Natural/immunology , Killer Cells, Natural/metabolism , Male , Middle Aged , NK Cell Lectin-Like Receptor Subfamily K/biosynthesis , NK Cell Lectin-Like Receptor Subfamily K/immunology , RNA, Messenger/biosynthesis , Stomach Neoplasms/immunology , Stomach Neoplasms/pathologyABSTRACT
AIM: To assess the role of pro- and anti-inflammatory polymorphisms in gastric cancer susceptibility. PATIENTS AND METHODS: We genotyped 12 polymorphisms in eight cytokine genes (Interleukin-1ß -IL1B-, IL8, IL17A, IL17F, IL32, tumor necrosis factor-α -TNF-, IL1RN, IL10) in a case-control study of 147 patients with gastric cancer and 172 controls. RESULTS: Single polymorphism analysis revealed an association between the IL10 -592C>A single nucleotide polymorphism and cases with moderately- or well-differentiated tumors [AA vs. GG, odds ratio (OR)=3.01; 95% confidence interval (CI)=1.08-8.50]. We further analyzed gene-gene interactions using a combined attribute network implemented in multifactor dimensionality reduction software. The analysis revealed an interaction between IL8 -251A>T and IL32 rs28372698 SNPs among cases with moderately- or well-differentiated tumors. Homozygosity for both IL8 -251T and IL32 T alleles increases the odds for developing gastric cancer up to 2.63-fold (OR=2.63; 95% CI=1.15-6.03). This association was higher compared to the homozygosity for the IL8-251 T allele alone (OR=1.11; 95% CI=0.51-2.43) or the IL32 T allele alone (OR=1.21; 95% CI=0.54-2.72). CONCLUSION: These findings suggest that IL10 -592C>A increases the odds for developing gastric cancer. An interaction between IL8 -251A>T and IL32 rs28372698 SNPs is also proposed.
Subject(s)
Cytokines/genetics , Stomach Neoplasms/genetics , Adult , Aged , Aged, 80 and over , Alleles , Case-Control Studies , Chile , Female , Genetic Predisposition to Disease , Humans , Interleukins/genetics , Male , Middle Aged , Polymorphism, Single Nucleotide , Stomach Neoplasms/immunology , Tumor Necrosis Factor-alpha/geneticsABSTRACT
BACKGROUND: Gastric cancer is the first cause of death by cancer in Chile. Quality of Life is a multidimensional construct that explores functionality and well-being, including physiological, psychological and social aspects. AIM: To assess Quality of Life of patients operated for gastric cancer. PATIENTS AND METHODS: The European Organization Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ-30), translated into Spanish, was applied to 33 patients, aged 42 to 82 years (25 males), subjected to curative total or subtotal gastrectomy for gastric cancer, between January 2004 and December 2006. RESULTS: The average lapse from the moment of the surgical intervention to the interview, was 52.2 weeks. Fifty five percent perceived their Quality of Life in the "good" category. Male patients and those with less than 6 months of surgery, obtained better scores in psychological aspects of quality of life. CONCLUSIONS: A high percentage of patients operated for gastric cancer qualified their quality of life as good in spite of the severity of the underlying disease and invasiveness of the intervention. This is probably explained by the importance of psychological factors that influence quality of life.
Subject(s)
Gastrectomy/psychology , Quality of Life/psychology , Stomach Neoplasms/surgery , Adult , Aged , Aged, 80 and over , Chile , Female , Humans , Male , Middle Aged , Statistics, Nonparametric , Stomach Neoplasms/psychology , Surveys and Questionnaires , Time FactorsABSTRACT
Background: Gastric cancer is the first cause of death by cáncer in Chile. Quality of Life is a multidimensional construct that explores functionality and well-being, including physiological, psychological and social aspects. Aim: To assess Quality of Life of patients operated for gastric cancer. Patients and methods: The European Organization Research and Treatment of Cáncer Quality of Life Questionnaire (EORTC QLQ-30), translated into Spanish, was applied to 33 patients, aged 42 to 82 years (25 males), subjected to curative total or subtotal gastrectomy for gastric cancer, between January 2004 and December 2006. Results: The average lapse from the moment of the surgical intervention to the interview, was 52.2 weeks. Fifty five percent perceived their Quality of Life in the "good" category. Male patients and those with less than 6 months of surgery, obtained better scores in psychological aspects of quality of life. Conclusions: A high percentage of patients operated for gastric cancer qualified their quality of life as good in spite of the severity of the underlying disease and invasiveness of the intervention. This is probably explained by the importance of psychological factors that influence quality of life.
Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Gastrectomy/psychology , Quality of Life/psychology , Stomach Neoplasms/surgery , Chile , Surveys and Questionnaires , Statistics, Nonparametric , Stomach Neoplasms/psychology , Time FactorsABSTRACT
Analiza que la tuberculosis esofágica es una entidad clínica rara. Esta puede ser sitio excepcional de una reactivación tuberculosa o más frecuentemente puede coexistir con la tuberculosis mediastinal extraesofágica. Debido a que clínicamente simula a la neoplasia esofágica, pero difiere en su tratamiento, su diagnóstico correcto es crucial. Presentamos un caso de tuberculosis de reactivación esofágica sin otros signos radiográficos visibles de actividad tuberculosa. La disfagia progresiva y los hallazgos endoscópicos-radiológicos sugerían cáncer esofágico por lo que se decidió el procedimiento quirúrgico: resección-anatomosis. El examen patológico de la pieza anátomo-quirúrgica reveló granulomas con bacilos ácido-resistentes en la pared del esófago y tuberculosis caseosa ganglionar periesofágica...