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Background: This study aims to evaluate the effectiveness and safety of low-dose (1.5â mg) fondaparinux for venous thromboembolism (VTE) prophylaxis in patients post-total knee arthroplasty (TKA). Methods: We retrospectively identified 314 patients who carried out the primary TKAs and received fondaparinux for VTE chemoprophylaxis between July 2020 and December 2021. A total of 141 TKA patients were excluded according to the exclusion criteria. Two groups of patients were established: the low-dose group included 84 patients who injected 1.5â mg of fondaparinux, and the regular-dose group included 89 patients who injected 2.5â mg of fondaparinux. The pre-operative blood analysis and coagulation assays were performed. The surgical time, the incidence of symptomatic VET, blood loss, wound complication, bleeding, drainage, and mortality of patients were determined and assessed. Results: The pre-operative blood analysis, body mass index, sex, age, and coagulation assays of patients in both groups were comparable. In terms of symptomatic pulmonary embolism and deep vein thrombosis, there was no significant difference (variation) between the two groups. However, patients in both groups showed a substantial difference in terms of blood loss, drain volume, wound complication, and transfusion rate. Conclusion: In prevention of VET in patients post-TKA, low-dose fondaparin is as effective as conventional dose fondaparinux. A significant decrease in blood loss, post-surgical transfusion rates, and wound complications were detected in patients given low-dose fondaparinux compared to those receiving regular-dose fondaparinux.
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Treatment of adult tibiofibular fractures, especially severely comminuted fractures, is technically challenging due to the lack of reduction markers and difficulty in restoring the alignment. Fixation of the fibula can facilitate reduction of the tibia fracture and restoration of the lower-extremity alignment. However, there are few literatures mentioned using intramedullary nail fixation for fibular fractures. Twenty-three cases of tibiofibular fractures were treated with elastic nails fixation fibular fractures and intramedullary nail or plate stabilization tibial fractures between January 2012 and December 2012. Adult tibiofibular fractures with fibular neck fractures or fibular fracture line apart from the ankle joint surface within 8 cm was ruled out. There were 19 males and 4 females with an average age of 41 years (range, 21-59 years). The injury causes included 11 falls and 12 traffic accidents. The left side was involved in 11 cases and the right side was involved in 12 cases. Seventeen cases were closed fractures and 6 cases were open fractures, all were Gustilo type I and II fractures. According to the AO classification, six fractures were defined as type 42A, 11 as type 42B, and 6 as type 42C. The average interval between injury and surgery was 5.8 d (range, 3-22 d). The operation time of elastic nails fixation fibular fractures was 24 minutes (range, 15-42 minutes). Primary wound healing was achieved in all patients. No complications such as infection and wound necrosis occurred. Twenty-one patients were followed up for a mean follow-up period of 16.3 months (range, 12-26 months). The mean duration of fracture healing in the radiographs was 4.1 months (range, 3-8 months). No recurrent fracture dislocation and breakage of implant were observed. At the last follow-up visit, the lower-extremity alignment was excellent. Two degrees of varus deformity was found in 3 cases, and 2 degrees of valgus deformity was observed in 2 cases, but there were no serious varus or valgus deformity affecting the lower-extremity function or causing pain. The results of Tornetta's ankle function scoring were excellent in 17 cases, good in 3 cases, and fair in 1 case; and the good-to-excellent rate was 95.2%. In the case of adult tibiofibular fractures, elastic nails fixed fibular fracture is helpful to maintain and adjust the lower limbs axis, help tibial fracture reduction, and increase stability.
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OBJECTIVE: To investigate the expression of PTEN and loss of heterozygosity (LOH) of its epigenetic microsatellite in gastric carcinoma and explore their roles in progression of gastric carcinoma. METHODS: LOH of epigenetic microsatellites of PTEN (D10S541, D10S583 and D10S1687) in advanced gastric cancer was detected by PCR-SSCP. Expression of PTEN mRNA and protein in normal gastric mucosa and gastric cancer was evaluated by RT-PCR and SABC immunohistochemistry, respectively. The relationship between expression of PTEN mRNA and protein and lymph node metastasis or LOH of microsatellites was discussed. RESULTS: LOH of D10S541, D10S583 and D10S1687 was found in 37.5% (21/56) of advanced gastric cancers. The positive rates of PTEN mRNA expression were 80.4% (45/56), 45.5% (5/11) and 32.1% (18/56) in normal mucosa, early and advanced gastric carcinomas, respectively, while 78.6% (44/56), 44.5% (5/11) and 28.6% (16/56) at the protein level. PTEN mRNA and protein were less frequently expressed in early and advanced gastric carcinomas than that in normal gastric mucosa (P < 0.05). There was positive correlation between PTEN mRNA expression and LOH of microsatellites in advanced gastric carcinomas. PTEN protein expression paralleled with its mRNA expression (P < 0.05). The expression of PTEN mRNA and protein was negatively correlated with lymph node metastasis of advanced gastric carcinomas (P < 0.05). CONCLUSION: Down-regulated expression of PTEN gene is found in different stages of gastric carcinoma, and is closely correlated with LOH of its epigenetic microsatellites, which probably is its underlying molecular mechanisms. It suggests that altered PTEN gene contributes to tumorigenesis and progression of gastric carcinomas.
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Genes Supresores de Tumor , Pérdida de Heterocigocidad , Repeticiones de Microsatélite/genética , Monoéster Fosfórico Hidrolasas/biosíntesis , Neoplasias Gástricas , Proteínas Supresoras de Tumor/biosíntesis , Mucosa Gástrica/metabolismo , Mucosa Gástrica/patología , Regulación Neoplásica de la Expresión Génica , Humanos , Metástasis Linfática/genética , Estadificación de Neoplasias , Fosfohidrolasa PTEN , Monoéster Fosfórico Hidrolasas/genética , ARN Mensajero/biosíntesis , ARN Mensajero/genética , Neoplasias Gástricas/genética , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patología , Proteínas Supresoras de Tumor/genéticaRESUMEN
To investigate the role of PTEN and matrix metalloproteinase-7 (MMP-7) expression in tumorigenesis and progression of gastric carcinoma, their expression in 113 gastric carcinomas was studied by immunohistochemistry. Microvessel density (MVD) was counted using the anti-CD34 antibody. The expressions of PTEN and MMP-7, and MVD were compared with the clinicopathological parameters of tumors, and the relationship between PTEN and MMP-7 expression and MVD was analyzed. It was found that PTEN was expressed less frequently in primary gastric carcinoma cells than in adjacent epithelial cells (P < 0.05), whereas this was reversed for MMP-7 (P < 0.05). PTEN expression was negatively correlated with invasion, metastasis, growth pattern, Lauren's classification and histological classification (P < 0.05). Matrix metalloproteinase-7 expression was positively associated with tumor size, Borrmann's classification, invasive depth, metastasis and TNM staging (P < 0.05), but negative with PTEN expression (P < 0.05). A positive correlation of MVD with tumor size, invasive depth, metastasis and TNM staging was found (P < 0.05). Microvessel density depended on decreased PTEN expression and increased MMP-7 expression (P < 0.05). The results of the present study suggested that down-regulated PTEN expression and up-regulated MMP-7 expression were greatly implicated in tumorigenesis and progression of gastric carcinoma. Close correlation between PTEN on MMP-7 expression provided a novel insight into the regulatory effects of PTEN on MMP-7 expression in gastric carcinoma.
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Adenocarcinoma/enzimología , Metaloproteinasa 7 de la Matriz/metabolismo , Neovascularización Patológica/enzimología , Monoéster Fosfórico Hidrolasas/metabolismo , Neoplasias Gástricas/enzimología , Proteínas Supresoras de Tumor/metabolismo , Adenocarcinoma/irrigación sanguínea , Adenocarcinoma/clasificación , Adenocarcinoma/secundario , Adulto , Anciano , Anciano de 80 o más Años , Núcleo Celular/metabolismo , Núcleo Celular/patología , Femenino , Regulación Neoplásica de la Expresión Génica , Humanos , Técnicas para Inmunoenzimas , Masculino , Metaloproteinasa 7 de la Matriz/genética , Microcirculación , Persona de Mediana Edad , Invasividad Neoplásica , Estadificación de Neoplasias , Neovascularización Patológica/patología , Fosfohidrolasa PTEN , Monoéster Fosfórico Hidrolasas/genética , Neoplasias Gástricas/irrigación sanguínea , Neoplasias Gástricas/clasificación , Neoplasias Gástricas/patología , Proteínas Supresoras de Tumor/genéticaRESUMEN
AIM: To investigate expression of PTEN in gastric cancer and to explore its roles in tumorigenesis and progression of gastric cancer. METHODS: Formalin-fixed and paraffin-embedded tissues of adjacent non-tumor mucosa and primary foci from 113 cases of gastric cancers were studied for the expression of PTEN and Caspase-3 and microvessel density (MVD) by streptavidin-peroxidase (S-P) immunohistochemistry with antibodies against PTEN, Caspase-3, and CD34. The relationship between PTEN and Caspase 3 expression and clinicopathological parameters of tumors was compared. RESULTS: Primary gastric cancer cells expressed PTEN less frequently than adjacent epithelial cells of primary foci (54.9 % vs 89.4 %; P=0.000, chi(2)=33.474). PTEN expression was significantly associated with invasive depth (P=0.003, rs=0.274), metastasis (P=0.036, rs=0.197), growth pattern (P=0.008, rs=0.282), Lauren's classification (P=0.000, rs=0.345), and histological classification (P=0.005, rs=0.262) of tumors, but not with tumor size (P=0.639, rs=0.045), Borrmann's classification (P=0.544, rs=0.070) or TNM staging (P=0.172, rs=0.129). PTEN expression was negatively correlated with MDV in primary gastric cancer (P=0.020, F=5.558). Primary gastric cancer cells showed less frequent immunoreactivity to Caspase-3 than adjacent epithelial cells of primary foci (32.7 % vs 50.4 %; P=0.007, chi(2)=7.286). Caspase-3 expression was dependent of PTEN expression in primary gastric cancer cells (P=0.000, chi(2)=15.266). CONCLUSION: Down-regulated expression of PTEN plays an important role in tumorigenesis, progression, growth, differentiation and angiogenesis of gastric cancer. Low expression of PTEN can decrease expression of Caspase-3 to disorder apoptosis of tumor cells, which might explain the molecular mechanisms of PTEN contributions to tumorigenesis and progression of gastric cancer.
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Apoptosis , Neovascularización Patológica , Monoéster Fosfórico Hidrolasas/genética , Neoplasias Gástricas/irrigación sanguínea , Neoplasias Gástricas/patología , Proteínas Supresoras de Tumor/genética , Adulto , Anciano , Anciano de 80 o más Años , Caspasa 3 , Caspasas/metabolismo , Diferenciación Celular , Femenino , Mucosa Gástrica/metabolismo , Humanos , Masculino , Persona de Mediana Edad , Invasividad Neoplásica , Fosfohidrolasa PTEN , Monoéster Fosfórico Hidrolasas/metabolismo , Neoplasias Gástricas/fisiopatología , Neoplasias Gástricas/secundario , Proteínas Supresoras de Tumor/metabolismoRESUMEN
AIM: To study the role of Fas ligand (FasL) and Caspase-3 expression in carcinogenesis and progression of gastric cancer and molecular mechanisms of relevant immune escape. METHODS: FasL and Caspase-3 expression was studied in adjacent epithelial cells, cancer cells and lymphocytes of primary foci, and cancer cells of metastatic foci from 113 cases of gastric cancer by streptavidin-biotin-peroxidase (S-P) immunohistochemistry. Expression of both proteins in cancer cells of primary foci was compared with clinicopathological features of gastric cancer. The relationship between FasL expression in cancer cells and Caspase-3 expression in cancer cells or infiltrating lymphocytes of primary foci was investigated. RESULTS: Cancer cells of primary foci expressed FasL in 53.98 % (61/113) of gastric cancers, more than their adjacent epithelial cells (34.51 %, 39/113) (P=0.003, chi(2)=8.681), while the expression of Caspase-3 in cancer cells of primary foci was detected in 32.74 % (37/113) of gastric cancers, less than in the adjacent epithelial cells (50.44 %, 57/113) (P=0.007, chi(2)=7.286). Infiltrating lymphocytes of the primary foci showed positive immunoreactivity to Caspase-3 in 70.80 % (80/113) of gastric cancers, more than their corresponding adjacent epithelial cells (P=0.001, chi(2)=10.635) or cancer cells of primary foci (P=0.000, chi(2)=32.767). FasL was less expressed in cancer cells of metastases (51.16 %, 22/43) than in those of the corresponding primary foci (81.58 %, 31/38) (P=0.003, chi(2)=9.907). Conversely, Caspase-3 was more expressed in cancer cells of metastases (58.14 %, 25/43) than in those of the corresponding primary foci (34.21 %, 13/38) (P=0.031, chi(2)=4.638). FasL expression was significantly correlated with tumor size (P=0.035,rs=0.276), invasive depth (P=0.039, rs=0.195), metastasis (P=0.039, rs=0.195), differentiation (P=0.015, rs=0.228) and Lauren's classification (P=0.038, rs=0.196), but not with age or gender of patients, growth pattern or TNM staging of gastric cancer (P>0.05). In contrast, Caspase-3 expression showed no correlation with any clinicopathological parameters described above in cancer cells of the primary foci (P>0.05). Interestingly, FasL expression in primary gastric cancer cells paralleled to Caspase-3 expression in infiltrating lymphocytes of the primary foci (P=0.016, chi(2)=5.825). CONCLUSION: Up-regulated expression of FasL and down-regulated expression of Caspase-3 in cancer cells of primary foci play an important role in gastric carcinogenesis. As an effective marker to reveal the biological behaviors, FasL is implicated in differentiation, growth, invasion and metastasis of gastric cancer by inducing apoptosis of infiltrating lymphocytes. Chemical substances derived from the primary foci and metastatic microenvironment can inhibit the growth of metastatic cells by enhancing Caspase-3 expression and diminishing FasL expression.