ABSTRACT
Inguinal hernia is one of the common diseases in general surgery, and tension-free hernia repair is the most common treatment for inguinal hernia. Patch infection is the common complication after hernia repair, confuses many of the general surgeons for its complex condition and long duration. The pathogenetic factors of patch infection can be roughly divided into three aspects, which include patients' physical condition, operation details, material and structure of patch. Prevention in advance of the susceptible factors of mesh infection can significantly improve the prognosis of patients. As for the treatment of patch infection, there is no unified standard yet, and individual treatment plans should be formulated according to the patient's condition and experience of the clinician. This article reviews the latest research progress of the occurrence, diagnosis, prevention and treatment of patch infection after tension-free hernia repair.
ABSTRACT
Emerging evidence indicates that microglia activation plays an important role in spinal cord injury (SCI) caused by trauma. Studies have found that inhibiting the Rho/Rho-associated protein kinase (ROCK) signaling pathway can reduce inflammatory cytokine production by microglia. In this study, Western blotting was conducted to detect ROCK2 expression after the SCI; the ROCK Activity Assay kit was used for assay of ROCK pathway activity; microglia morphology was examined using the CD11b antibody; electron microscopy was used to detect microglia phagocytosis; TUNEL was used to detect tissue cell apoptosis; myelin staining was performed using an antibody against myelin basic protein (MBP); behavioral outcomes were evaluated according to the methods of Basso, Beattie, and Bresnahan (BBB). We observed an increase in ROCK activity and microglial activation after SCI. The microglia became larger and rounder and contained myelin-like substances. Furthermore, treatment with fasudil inhibited neuronal cells apoptosis, alleviated demyelination and the formation of cavities, and improved motor recovery. The experimental evidence reveals that the ROCK inhibitor fasudil can regulate microglial activation, promote cell phagocytosis, and improve the SCI microenvironment to promote SCI repair. Thus, fasudil may be useful for the treatment of SCI.
Subject(s)
Animals , Male , Rats , 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine , Pharmacology , Therapeutic Uses , Apoptosis , Microglia , Metabolism , Myelin Basic Protein , Metabolism , Myelin Sheath , Metabolism , Phagocytosis , Protein Kinase Inhibitors , Pharmacology , Therapeutic Uses , Rats, Sprague-Dawley , Spinal Cord Injuries , Drug Therapy , rho-Associated Kinases , MetabolismABSTRACT
Emerging evidence indicates that microglia activation plays an important role in spinal cord injury (SCI) caused by trauma. Studies have found that inhibiting the Rho/Rho-associated protein kinase (ROCK) signaling pathway can reduce inflammatory cytokine production by microglia. In this study, Western blotting was conducted to detect ROCK2 expression after the SCI; the ROCK Activity Assay kit was used for assay of ROCK pathway activity; microglia morphology was examined using the CD11b antibody; electron microscopy was used to detect microglia phagocytosis; TUNEL was used to detect tissue cell apoptosis; myelin staining was performed using an antibody against myelin basic protein (MBP); behavioral outcomes were evaluated according to the methods of Basso, Beattie, and Bresnahan (BBB). We observed an increase in ROCK activity and microglial activation after SCI. The microglia became larger and rounder and contained myelin-like substances. Furthermore, treatment with fasudil inhibited neuronal cells apoptosis, alleviated demyelination and the formation of cavities, and improved motor recovery. The experimental evidence reveals that the ROCK inhibitor fasudil can regulate microglial activation, promote cell phagocytosis, and improve the SCI microenvironment to promote SCI repair. Thus, fasudil may be useful for the treatment of SCI.
ABSTRACT
Although previous reports showed drug-eluting stent (DES) could effectively inhibit neointima formation, in-stent restenosis (ISR) remains an important obstacle. The purpose of this study was to investigate different effects of paclitaxel on proliferation and cell cycle regulators between vascular smooth muscle cells (VSMCs) and vascular endothelial cells (VECs) of rats in vitro. The cultured VSMCs and VECs of rats from the same tissues were examined by using immunohistochemistry, flow cytometry and Western blotting in control and paclitaxel-treated groups. The results showed paclitaxel could effectively inhibit proliferation of VSMCs and VECs. However, as compared with VECs, proliferation of VSMCs in paclitaxel-treated group decreased less rapidly. The percentage of cells in G0-G1 and G2-M phases was reduced, and that in S phase increased after treatment for 72 h. The expression of cyclin D1 and B1, p27 and PCNA in VSMCs of paclitaxel-treated group was up-regulated, but that of p21 down-regulated as compared with VECs. It is concluded that there are significant differences in the expression of cell cycle regulators and proliferation rate between paclitaxel-treated VSMCs and paclitaxel-treated VECs, suggesting that the G1-S checkpoint regulated by paclitaxel may play a critical role in the development of complications of DES, which provides new strategies for treatments of ISR.
Subject(s)
Animals , Rats , Blotting, Western , Cell Cycle , Cell Cycle Proteins , Metabolism , Cell Proliferation , Cells, Cultured , Cyclin B1 , Metabolism , Cyclin D1 , Metabolism , Cyclin-Dependent Kinase Inhibitor p21 , Metabolism , Cyclin-Dependent Kinase Inhibitor p27 , Metabolism , Endothelial Cells , Metabolism , Flow Cytometry , G1 Phase Cell Cycle Checkpoints , Immunohistochemistry , Microscopy, Fluorescence , Muscle, Smooth, Vascular , Cell Biology , Myocytes, Smooth Muscle , Metabolism , Paclitaxel , Pharmacology , Proliferating Cell Nuclear Antigen , Metabolism , Tubulin Modulators , PharmacologyABSTRACT
RhoA, a small GTPase, is involved in a wide array of cellular functions in the central nervous system, such as cell motility, cytoskeleton rearrangement, transcriptional regulation, phagocytosis and cell growth. It is not known how spinal cord injury (SCI) affects the expression of RhoA in different nerve cells. In the present study, we investigated the changes of RhoA expression in remote areas of the injury at the 3rd, 7th and 30th day after SCI, which was established by T10 contusion method. Moreover, we examine its expression profile in neurons, astrocytes and microglia. RhoA was found to be weakly expressed in these nerve cells in normal spinal cord. Western blotting showed that, after SCI, the total RhoA expression was up-regulated, and the RhoA expression was increased and peaked at the 7th day. Double immunostaining revealed specific and temporal expression patterns of RhoA in different nerve cells. The expression of RhoA in neurons started to increase at day 3, peaked at day 7 and then decreased slightly at day 30. Expression of RhoA in astrocytes increased moderately after SCI and peaked at day 7. There was no obvious change in RhoA expression in microglia after SCI in remote areas. This study demonstrated that, after SCI, RhoA expression exhibited different patterns with different nerve cells of spinal cord. RhoA expression patterns also changed with time after SCI, and among different nerve cells in the injured spinal cord. These findings can help us better understand the roles of RhoA in SCI.
Subject(s)
Animals , Male , Astrocytes , Metabolism , Blotting, Western , Immunohistochemistry , Microglia , Metabolism , Microscopy, Confocal , Neurons , Metabolism , Rats, Sprague-Dawley , Spinal Cord Injuries , Metabolism , Time Factors , rhoA GTP-Binding Protein , MetabolismABSTRACT
RhoA, a small GTPase, is involved in a wide array of cellular functions in the central nervous system, such as cell motility, cytoskeleton rearrangement, transcriptional regulation, phagocytosis and cell growth. It is not known how spinal cord injury (SCI) affects the expression of RhoA in different nerve cells. In the present study, we investigated the changes of RhoA expression in remote areas of the injury at the 3rd, 7th and 30th day after SCI, which was established by T10 contusion method. Moreover, we examine its expression profile in neurons, astrocytes and microglia. RhoA was found to be weakly expressed in these nerve cells in normal spinal cord. Western blotting showed that, after SCI, the total RhoA expression was up-regulated, and the RhoA expression was increased and peaked at the 7th day. Double immunostaining revealed specific and temporal expression patterns of RhoA in different nerve cells. The expression of RhoA in neurons started to increase at day 3, peaked at day 7 and then decreased slightly at day 30. Expression of RhoA in astrocytes increased moderately after SCI and peaked at day 7. There was no obvious change in RhoA expression in microglia after SCI in remote areas. This study demonstrated that, after SCI, RhoA expression exhibited different patterns with different nerve cells of spinal cord. RhoA expression patterns also changed with time after SCI, and among different nerve cells in the injured spinal cord. These findings can help us better understand the roles of RhoA in SCI.
ABSTRACT
Although previous reports showed drug-eluting stent (DES) could effectively inhibit neointima formation, in-stent restenosis (ISR) remains an important obstacle. The purpose of this study was to investigate different effects of paclitaxel on proliferation and cell cycle regulators between vascular smooth muscle cells (VSMCs) and vascular endothelial cells (VECs) of rats in vitro. The cultured VSMCs and VECs of rats from the same tissues were examined by using immunohistochemistry, flow cytometry and Western blotting in control and paclitaxel-treated groups. The results showed paclitaxel could effectively inhibit proliferation of VSMCs and VECs. However, as compared with VECs, proliferation of VSMCs in paclitaxel-treated group decreased less rapidly. The percentage of cells in G0-G1 and G2-M phases was reduced, and that in S phase increased after treatment for 72 h. The expression of cyclin D1 and B1, p27 and PCNA in VSMCs of paclitaxel-treated group was up-regulated, but that of p21 down-regulated as compared with VECs. It is concluded that there are significant differences in the expression of cell cycle regulators and proliferation rate between paclitaxel-treated VSMCs and paclitaxel-treated VECs, suggesting that the G1-S checkpoint regulated by paclitaxel may play a critical role in the development of complications of DES, which provides new strategies for treatments of ISR.
ABSTRACT
<p><b>BACKGROUND</b>Long-term peritoneal dialysis (PD) requires that the peritoneal membrane remain effective for dialysis. Research directed toward human peritoneal morphology and structure is limited. The present study was performed to investigate morphological changes of the human peritoneal membrane during PD and to elucidate the possible mechanisms of its functional deterioration.</p><p><b>METHODS</b>A total of 32 peritoneal biopsies were performed in normal subjects (n = 10), uremic nondialysis patients (n = 12) at the time of catheter insertion, and PD patients (n = 10) at the time of catheter removal or reinsertion or at the time of renal transplantation. Peritoneal morphology was examined by light microscopy, scanning electron microscopy, and transmission electron microscopy.</p><p><b>RESULTS</b>The peritoneal membrane in normal subjects consisted of a monolayer of mesothelial cells on a basement membrane and a layer of connective tissue containing cells, blood vessels, and lymphatic vessels. Mesothelial cells were polygonal, often elongated, and had numerous microvilli on their luminal surface. There were lots of oval or roundish pinocytotic vesicles in the cytoplasm of the mesothelial cells. The peritoneal morphology of uremic nondialysis patients was similar to that of normal subjects. However, significant abnormalities of the peritoneal membrane were observed in PD patients, and the changes were found to be progressive. Microvilli were the first site of damage which involved microvilli shortening, a gradual reduction in their number, and, eventually, the total disappearance of microvilli. Mesothelial cells then detached from the basement membrane, disappearing completely in some cases. In the end, the peritoneal membrane consisted only of submesothelial connective tissue without any cells.</p><p><b>CONCLUSIONS</b>PD can modify peritoneal morphology and structure. The morphological change is progressive and may be one of the important causes of peritoneal failure. Peritoneal biopsies can provide lots of valuable information about the effects of PD. Studying the relationship between peritoneal structure and its function proved very useful for understanding the physiopathology of the peritoneum during PD.</p>