ABSTRACT
<p><b>OBJECTIVE</b>To study the value of 3D visualization technique in breast-preserving surgery for breast cancer with immediate breast reconstruction using laparoscopically harvested pedicled latissimus dorsi muscle flap.</p><p><b>METHODS</b>From January, 2015 to May, 2016, 30 patients with breast cancer underwent breast-preserving surgery with immediate breast reconstruction using pedicled latissimus dorsi muscle flap. The CT data of the arterial phase and venous phase were collected preoperatively and imported into the self-developed medical image 3D visualization system for image segmentation and 3D reconstruction. The 3D models were imported into the simulation surgery platform for virtual surgery to prepare for subsequent surgeries. The cosmetic outcomes of the patients were evaluated 6 months after the surgery. Another 18 patients with breast cancer who underwent laparoscopic latissimus dorsi muscle breast reconstruction without using 3D visualization technique from January to December, 2014 served as the control group. The data of the operative time, intraoperative blood loss and postoperative appearance of the breasts were analyzed.</p><p><b>RESULTS</b>The reconstructed 3D model clearly displayed the anatomical structures of the breast, armpit, latissimus dorsi muscle and vessels and their anatomical relationship in all the 30 cases. Immediate breast reconstruction was performed successfully in all the cases with median operation time of 226 min (range, 210 to 420 min), a median blood loss of 95 mL (range, 73 to 132 mL). Evaluation of the appearance of the breast showed excellent results in 22 cases, good appearance in 6 cases and acceptable appearance in 2 cases. In the control group, the median operation time was 283 min (range, 256 to 313 min) and the median blood loss was 107 mL (range, 79 to 147 mL) with excellent appearance of the breasts in 10 cases, good appearance in 4 cases and acceptable appearance in 4 cases.</p><p><b>CONCLUSION</b>3D reconstruction technique can clearly display the morphology of the latissimus dorsi and the thoracic dorsal artery, allows calculation of the volume of the breast and the latissimus dorsi, and helps in defining the scope of resection of the latissimus dorsi to avoid injuries of the pedicled vessels. This technique also helps to shorten the operation time, reduce intraoperative bleeding, and improve the appearance of the reconstructed breast using pedicled latissimus dorsi muscle flap.</p>
ABSTRACT
Objective To study the effect of pyrrolidine dithiocarbamate (PDTC) on the anti-tuberculosis drug-induced liver injury and the molecular mechanism. Methods Clean male SD rats were selected as experimental animals and randomly divided into normal group, model group, PDTC group and AG490 group. Animal model of anti-tuberculosis drug-induced liver injury was established by intragastric administration isoniazid + rifampicin. PDTC group received intraperitoneal injection of PDTC, and AG490 group received intraperitoneal injection of AG490. Twenty-eight days after intervention, the rats were executed, and the liver injury indexes, inflammation indexes and oxidative stress indexes in serum as well as JAK2/STAT3 expression, liver injury indexes, inflammation indexes and oxidative stress indexes in liver tissue were determined. Results p-JAK2, p-STAT3, TNF-α, IL-1β, IL-6, ROS, 8-OHdG and MDA expression in liver tissue as well as TBIL, ALT, AST, γ-GT, TNF-α, IL-1β, IL-6, 8-OHdG and MDA levels in serum of model group were significantly higher than those of normal group while p-JAK2, p-STAT3, TNF-α, IL-1β, IL-6, ROS, 8-OHdG and MDA expression in liver tissue as well as TBIL, ALT, AST, γ-GT, TNF-α, IL-1β, IL-6, 8-OHdG and MDA levels in serum of PDTC group and AG490 group were significantly lower than those of model group. Conclusions PDTC can inhibit the inflammation and oxidative stress mediated by JAK2/STAT3 signaling pathway to alleviate the anti-tuberculosis drug-induced liver injury.
ABSTRACT
OBJECTIVE@#To study the effect of pyrrolidine dithiocarbamate (PDTC) on the anti-tuberculosis drug-induced liver injury and the molecular mechanism.@*METHODS@#Clean male SD rats were selected as experimental animals and randomly divided into normal group, model group, PDTC group and AG490 group. Animal model of anti-tuberculosis drug-induced liver injury was established by intragastric administration isoniazid + rifampicin. PDTC group received intraperitoneal injection of PDTC, and AG490 group received intraperitoneal injection of AG490. Twenty-eight days after intervention, the rats were executed, and the liver injury indexes, inflammation indexes and oxidative stress indexes in serum as well as JAK2/STAT3 expression, liver injury indexes, inflammation indexes and oxidative stress indexes in liver tissue were determined.@*RESULTS@#p-JAK2, p-STAT3, TNF-α, IL-1β, IL-6, ROS, 8-OHdG and MDA expression in liver tissue as well as TBIL, ALT, AST, γ-GT, TNF-α, IL-1β, IL-6, 8-OHdG and MDA levels in serum of model group were significantly higher than those of normal group while p-JAK2, p-STAT3, TNF-α, IL-1β, IL-6, ROS, 8-OHdG and MDA expression in liver tissue as well as TBIL, ALT, AST, γ-GT, TNF-α, IL-1β, IL-6, 8-OHdG and MDA levels in serum of PDTC group and AG490 group were significantly lower than those of model group.@*CONCLUSIONS@#PDTC can inhibit the inflammation and oxidative stress mediated by JAK2/STAT3 signaling pathway to alleviate the anti-tuberculosis drug-induced liver injury.
ABSTRACT
OBJECTIVE@#To study the effect of immune formulation-assisted conventional therapy on anti-infective ability of multidrug-resistant Mycobacterium tuberculosis infection mice.@*METHODS@#BALB/c mice were used as experimental animals, multidrug-resistant M. tuberculosis infection models were built, randomly divided into model group, moxifloxacin group, thymopentin group and combined treatment group and given corresponding drug intervention, and then colony numbers in the spleen and lung, T lymphocyte subset contents and programmed death-1 (PD-1) expression levels in peripheral blood were detected.@*RESULTS@#Colony numbers in lung and spleen of moxifloxacin group and thymopentin group were significantly lower than those of model group and colony numbers in lung and spleen of combined treatment group were significantly lower than those of moxifloxacin group and thymopentin group; contents of CD3(+)CD4(+)T cells, Th1 and Th17 in peripheral blood of moxifloxacin group and thymopentin group were higher than those of model group, and contents of CD3(+)CD8(+)T cells, Th2 and Treg were lower than those of model group; contents of CD3(+)CD4(+)T cells, Th1 and Th17 in peripheral blood of combined treatment group were higher than those of moxifloxacin group and thymopentin group, and contents of CD3(+)CD8(+)T cells, Th2 and Treg were lower than those of moxifloxacin group and thymopentin group; PD-1 expression levels on T lymphocyte, B lymphocyte and monocyte surface in peripheral blood of moxifloxacin group and thymopentin group were lower than those of model group, and PD-1 expression levels on T lymphocyte, B lymphocyte and monocyte surface in peripheral blood of combined treatment group were lower than those of moxifloxacin group and thymopentin group.@*CONCLUSIONS@#Immune formulation thymopentin can enhance the anti-infective ability of multidrug-resistant M. tuberculosis infection mice, decrease bacterial load in lung and spleen, and enhance immune function.
ABSTRACT
Objective: To study the effect of immune formulation-assisted conventional therapy on anti-infective ability of multidrug-resistant Mycobacterium tuberculosis infection mice. Methods: BALB/c mice were used as experimental animals, multidrug-resistant M. tuberculosis infection models were built, randomly divided into model group, moxifloxacin group, thymopentin group and combined treatment group and given corresponding drug intervention, and then colony numbers in the spleen and lung, T lymphocyte subset contents and programmed death-1 (PD-1) expression levels in peripheral blood were detected. Results: Colony numbers in lung and spleen of moxifloxacin group and thymopentin group were significantly lower than those of model group and colony numbers in lung and spleen of combined treatment group were significantly lower than those of moxifloxacin group and thymopentin group; contents of CD3
ABSTRACT
Objective To explore the expressions of inhibitors of DNA binding-1 (Id-1) and matrix metalloproteinase-9 (MMP-9) in colorectal carcinoma tissues and its correlation with microvessel density (MVD). Methods The expressions of Id-1 and MMP-9 as well as CD34-labelled MVD in colorectal adenocarcinoma tissues (n=50) and normal adjacent tissues (n=50) were examined by immunohistochemistry. Results The positive expressions of Id-1 and MMP-9 were seen in 72.00% (36/50) and 78.00%(39/50) of colorectal adenocarcinoma tissues,which were significantly higher than those [24.00%(12/50) and 28.00% (14/50)] in normal adjacent tissues (P=0.000). The MVD value (17.22±2.08) in colorectal adenocarcinoma tissues was significantly higher than that (5.36±2.17) in normal adjacent tissues (P=0.000). The expressions of Id-1 and MMP-9 and MVD were significantly correlated with serosa invasion,TNM stage,carcinoembryonic antigen(+),lymph node metastasis,vascular invasion,and liver metastasis (all P<0.05) but not with the patient's age,gender,tumor size,and differentiation degree (all P>0.05). The MVD value with Id-1 and MMP-9 positive expression were significantly higher than those with Id-1 and MMP-9 negative expression (all P=0.000). The expression of Id-1 in colorectal adenocarcinoma tissues showed significantly positive correlation with that of MMP-9 (r=0.429,P=0.000). Cox multivariate analysis showed that Id-1 and MMP-9 expressions were independent prognostic factors for colorectal carcinoma. Conclusions The high expressions of Id-1 and MMP-9 have high correlations with the development and progression of colorectal adenocarcinoma and have positive correlation with MVD. Both of them may be involved in the microvascular generation and the invasion and hematogenous metastasis of colorectal carcinoma.
Subject(s)
Humans , Adenocarcinoma , Metabolism , Colorectal Neoplasms , Metabolism , Disease Progression , Immunohistochemistry , Inhibitor of Differentiation Protein 1 , Metabolism , Liver Neoplasms , Lymphatic Metastasis , Matrix Metalloproteinase 9 , Metabolism , Microcirculation , Microvessels , Neovascularization, PathologicABSTRACT
OBJECTIVE@#To study the expression of caveolin-1 in colorectal adenocarcinoma tissues and its correlation with microlymphatic vessel density (LMVD), and to investigate the clinical pathological prognostic significance of caveolin-1 and LMVD in patients with colorectal cancer.@*METHODS@#The expression of caveolin-1 and LMVD in 45 specimens of normal colorectal tissues, and 90 specimens of colorectal adenocarcinoma tissues were detected by immunohistochemistry technique. The correlation between their expression and the clinicopathologic features was analyzed. Multivariable Cox regression was used to analyze the association between the laboratory indices and overall survival time.@*RESULTS@#The positive rates of caveolin-1 in colorectal adenocarcinoma tissues were significantly higher than those in normal colorectal tissues (P < 0.01). LMVD in colorectal adenocarcinoma tissues were significantly higher than those in normal colorectal tissues (P < 0.01). Mean LMVD in group with caveolin-1 positive was significantly higher than in that with caveolin-1 negative. The median survival time was 26.7 months. Cox regression analysis showed that the caveolin-1 expression, invation depth, lymph node metastasis, TNM stage, liver metastasis and LMVD were independent risk factors of overall survival time of patients with colorectal carcinoma.@*CONCLUSIONS@#Caveolin-1 may contribute to the lymphangiogenesis in the tumor. During the occurrence and development of colorectal adenocarcinoma, there is a close relationship between the expression of caveolin-1 and lymphatic microvessel of tumor. Caveolin-1 expression and microlymphatic vessel density are significant prognostic value of colorectal carcinoma.
ABSTRACT
Synaptic vesicle protein 2A (SV2A) involvement has been reported in the animal models of epilepsy and in human intractable epilepsy. The difference between pharmacosensitive epilepsy and pharmacoresistant epilepsy remains poorly understood. The present study aimed to observe the hippocampus SV2A protein expression in amygdale-kindling pharmacoresistant epileptic rats. The pharmacosensitive epileptic rats served as control. Amygdaloid-kindling model of epilepsy was established in 100 healthy adult male Sprague-Dawley rats. The kindled rat model of epilepsy was used to select pharmacoresistance by testing their seizure response to phenytoin and phenobarbital. The selected pharmacoresistant rats were assigned to a pharmacoresistant epileptic group (PRE group). Another 12 pharmacosensitive epileptic rats (PSE group) served as control. Immunohistochemistry, real-time PCR and Western blotting were used to determine SV2A expression in the hippocampus tissue samples from both the PRE and the PSE rats. Immunohistochemistry staining showed that SV2A was mainly accumulated in the cytoplasm of the neurons, as well as along their dendrites throughout all subfields of the hippocampus. Immunoreactive staining level of SV2A-positive cells was 0.483 ± 0.304 in the PRE group and 0.866 ± 0.090 in the PSE group (P < 0.05). Real-time PCR analysis demonstrated that 2(-ΔΔCt) value of SV2A mRNA was 0.30 ± 0.43 in the PRE group and 0.76 ± 0.18 in the PSE group (P < 0.05). Western blotting analysis obtained the similar findings (0.27 ± 0.21 versus 1.12 ± 0.21, P < 0.05). PRE rats displayed a significant decrease of SV2A in the brain. SV2A may be associated with the pathogenesis of intractable epilepsy of the amygdaloid-kindling rats.
Subject(s)
Animals , Male , Rats , Amygdala , Metabolism , Anticonvulsants , Pharmacology , Disease Models, Animal , Drug Resistance , Electric Stimulation , Epilepsy , Drug Therapy , Genetics , Metabolism , Pathology , Gene Expression Regulation , Hippocampus , Metabolism , Kindling, Neurologic , Genetics , Metabolism , Pathology , Membrane Glycoproteins , Genetics , Metabolism , Nerve Tissue Proteins , Genetics , Metabolism , Phenobarbital , Pharmacology , Phenytoin , Pharmacology , RNA, Messenger , Genetics , Metabolism , Rats, Sprague-Dawley , Synaptic Transmission , Synaptic Vesicles , Metabolism , PathologyABSTRACT
Objective: To study the expression of caveolin-1 in colorectal adenocarcinoma tissues and its correlation with microlymphatic vessel density (LMVD), and to investigate the clinical pathological prognostic significance of caveolin-1 and LMVD in patients with colorectal cancer. Methods: The expression of caveolin-1 and LMVD in 45 specimens of normal colorectal tissues, and 90 specimens of colorectal adenocarcinoma tissues were detected by immunohistochemistry technique. The correlation between their expression and the clinicopathologic features was analyzed. Multivariable Cox regression was used to analyze the association between the laboratory indices and overall survival time. Results: The positive rates of caveolin-1 in colorectal adenocarcinoma tissues were significantly higher than those in normal colorectal tissues (P < 0.01). LMVD in colorectal adenocarcinoma tissues were significantly higher than those in normal colorectal tissues (P < 0.01). Mean LMVD in group with caveolin-1 positive was significantly higher than in that with caveolin-1 negative. The median survival time was 26.7 months. Cox regression analysis showed that the caveolin-1 expression, invation depth, lymph node metastasis, TNM stage, liver metastasis and LMVD were independent risk factors of overall survival time of patients with colorectal carcinoma. Conclusions: Caveolin-1 may contribute to the lymphangiogenesis in the tumor. During the occurrence and development of colorectal adenocarcinoma, there is a close relationship between the expression of caveolin-1 and lymphatic microvessel of tumor. Caveolin-1 expression and microlymphatic vessel density are significant prognostic value of colorectal carcinoma.
ABSTRACT
This study investigated the effect of advanced glycation end products (AGEs) on differentiation of naïve CD4(+) T cells and the role of the receptor of AGEs (RAGE) and peroxisome proliferator-activated receptors (PPARs) activity in the process in order to gain insight into the mechanism of immunological disorders in diabetes. AGEs were prepared by the reaction of bovine serum albumin (BSA) with glucose. Human naïve CD4(+) T cells, enriched from blood of healthy adult volunteers with negative selection assay, were cultured in vitro and treated with various agents including AGEs, BSA, high glucose, PGJ2 and PD68235 for indicated time. In short hairpin (sh) RNA knock-down experiment, naïve CD4(+) T cells were transduced with media containing shRNA-lentivirus generated from lentiviral packaging cell line, Lent-X(TM) 293 T cells. Surface and intracellular cytokine stainings were used for examination of CD4(+) T cell phenotypes, and real-time PCR and Western blotting for detection of transcription factor mRNA and protein expression, respectively. The suppressive function of regulatory T (Treg) cells was determined by a [(3)H]-thymidine incorporation assay. The results showed that AGEs induced higher pro-inflammatory Th1/Th17 cells differentiated from naïve CD4(+) T cells than the controls, whereas did not affect anti-inflammatory Treg cells. However, AGEs eliminated suppressive function of Treg cells. In addition, AGEs increased RAGE mRNA expression in naïve CD4(+) T cells, and RAGE knock-down by shRNA eliminated the effect of AGEs on the differentiation of CD4(+) T cells and the reduction of suppressive function of Treg cells. Furthermore, AGEs inhibited the mRNA expression of PPARγ, not PPARα PPARγ agonist, PGJ2, inhibited the effect of AGEs on naïve CD4(+) T cell differentiation and reversed the AGE-reduced suppressive function of Treg cells; on the other hand, PPARγ antagonist, PD68235, attenuated the blocking effect of RAGE shRNA on the role of AGEs. It was concluded that AGEs may promote CD4(+) T cells development toward pro-inflammatory state, which is associated with increased RAGE mRNA expression and reduced PPARγ activity.
ABSTRACT
This study investigated the effect of advanced glycation end products (AGEs) on differentiation of naïve CD4(+) T cells and the role of the receptor of AGEs (RAGE) and peroxisome proliferator-activated receptors (PPARs) activity in the process in order to gain insight into the mechanism of immunological disorders in diabetes. AGEs were prepared by the reaction of bovine serum albumin (BSA) with glucose. Human naïve CD4(+) T cells, enriched from blood of healthy adult volunteers with negative selection assay, were cultured in vitro and treated with various agents including AGEs, BSA, high glucose, PGJ2 and PD68235 for indicated time. In short hairpin (sh) RNA knock-down experiment, naïve CD4(+) T cells were transduced with media containing shRNA-lentivirus generated from lentiviral packaging cell line, Lent-X(TM) 293 T cells. Surface and intracellular cytokine stainings were used for examination of CD4(+) T cell phenotypes, and real-time PCR and Western blotting for detection of transcription factor mRNA and protein expression, respectively. The suppressive function of regulatory T (Treg) cells was determined by a [(3)H]-thymidine incorporation assay. The results showed that AGEs induced higher pro-inflammatory Th1/Th17 cells differentiated from naïve CD4(+) T cells than the controls, whereas did not affect anti-inflammatory Treg cells. However, AGEs eliminated suppressive function of Treg cells. In addition, AGEs increased RAGE mRNA expression in naïve CD4(+) T cells, and RAGE knock-down by shRNA eliminated the effect of AGEs on the differentiation of CD4(+) T cells and the reduction of suppressive function of Treg cells. Furthermore, AGEs inhibited the mRNA expression of PPARγ, not PPARα PPARγ agonist, PGJ2, inhibited the effect of AGEs on naïve CD4(+) T cell differentiation and reversed the AGE-reduced suppressive function of Treg cells; on the other hand, PPARγ antagonist, PD68235, attenuated the blocking effect of RAGE shRNA on the role of AGEs. It was concluded that AGEs may promote CD4(+) T cells development toward pro-inflammatory state, which is associated with increased RAGE mRNA expression and reduced PPARγ activity.
Subject(s)
Adult , Animals , Cattle , Humans , Blotting, Western , CD4-Positive T-Lymphocytes , Metabolism , Cell Differentiation , Cells, Cultured , Glucose , Pharmacology , Glycation End Products, Advanced , Pharmacology , HEK293 Cells , Interferon-gamma , Metabolism , Interleukin-17 , Metabolism , PPAR gamma , Genetics , Metabolism , Prostaglandin D2 , Pharmacology , RNA Interference , Receptor for Advanced Glycation End Products , Receptors, Immunologic , Genetics , Metabolism , Reverse Transcriptase Polymerase Chain Reaction , Serum Albumin, Bovine , Pharmacology , T-Lymphocytes, Regulatory , Metabolism , Th1 Cells , Metabolism , Th17 Cells , MetabolismABSTRACT
<p><b>BACKGROUND</b>Endothelin-1 (ET-1) has deleterious effects on water homeostasis, cerebral edema, and blood-brain barrier (BBB) integrity. Highly expressed ET-1 was observed after intracerebral hemorrhage (ICH); however, ET-1 changes and their relationship with BBB disruption within 24 hours of ICH have not been thoroughly investigated. The aim of the present study was to observe the changes in perihematomal ET-1 levels in various phases of ICH and their correlation with the BBB integrity in a rabbit model of ICH.</p><p><b>METHODS</b>Twenty-five rabbits (3.2-4.3 kg body weight) were randomly divided into a normal control group (five rabbits) and a model group (20 rabbits). Animals in the model group were equally divided into four subgroups (five rabbits each to be sacrificed at 6, 12, 18, and 24 hours following ICH establishment). An ICH model was prepared in the model group by infusing autologous arterial blood into the rabbit brain. ET-1 expression in perihematomal brain tissues was determined using immunohistochemistry and color image analysis, and the permeability of the BBB was assayed using the Evan's Blue (EB) method. A repeated measures analysis of variance was used to make comparisons of the ET-1 and EB content across the entire time series.</p><p><b>RESULTS</b>The number of perihematomal endothelial cells with ET-1 positive expressions following 6, 12, 18, and 24 hours ICH model establishment was 9.32, 13.05, 15.90, and 20.44, respectively, but as low as 6.67 in the control group. The average transmittance of ET-1-positive cell bodies at 6, 12, 18, and 24 hours after ICH was 99.10, 97.40, 85.70, and 80.80, respectively, but 100.12 in the control group. These data reveal that the expression of ET-1 was significantly increased at 6, 12, 18, and 24 hours after ICH compared with the control group, and a marked decrease in the average transmittance of ET-1-positive cell bodies was noted (P < 0.05). Similarly, the perihematomal EB content at 6, 12, 18, and 24 hours after ICH was 29.39 ± 1.16, 32.20 ± 0.73, 33.63 ± 1.08, and 35.26 ± 1.12, respectively, in the model group and 28.06 ± 0.80 in the control group. The results indicate that a significant increase in the EB content in the model group was observed compared with that of the control group (P < 0.05). Moreover, a positive correlation between the number of ET-1-positive endothelial cells and BBB permeability was observed (r = 0.883, P < 0.05).</p><p><b>CONCLUSIONS</b>High levels of ET-1 are closely associated with BBB disruption. ET-1 may play an important role in the pathogenesis of secondary brain injury after ICH.</p>