Objective:To investigate the clinicopathological features and molecular characteristics of β-catenin-deficient colorectal cancer.Methods:The clinical, pathological and molecular features of 11 colorectal cancers with β-catenin protein loss diagnosed at the 960th Hospital of People′s Liberation Army of China, from January 2012 to November 2022 were analyzed.Results:Among the 11 patients, 3 were males and 8 were females. Their age ranged from 43 to 74 years, with the median age of 59 years. Six were in the left colon and 5 were in the right colon. One of the 11 cases had lymph node metastasis, 10 cases were well and moderately differentiated adenocarcinoma, and 1 was mucinous adenocarcinoma. Eight cases were of TNM stage T4, 2 of T1 stage and 1 of Tis stage. β-catenin protein was not detected using immunohistochemistry. Sanger sequencing revealed the presence of fragment-deletion mutation in exon 3 of CTNNB1 gene, resulting in loss of β-catenin protein expression.Conclusion:β-catenin deficiency is present in a small number of colorectal cancers and may be associated with exon 3 mutations of CTNNB1 gene.

OBJECTIVETo observe the pathological changes in rabbits with spinal cord injury induced by decompression sickness (DCS), and to investigate the role of tumor necrosis factor-alpha (TNF-α) in spinal cord injury induced by DCS.

METHODSRabbits were randomly divided into normal control group, DCS group, and safe decompression group. The rabbit model of DCS was established. Light microscopy, real-time PCR, and immunohistochemical method were used to observe the pathomorphological changes in the thoracolumbar spinal cord and the mRNA and protein expression of TNF-α, respectively. The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) was used to observe the apoptosis in the spinal cord.

RESULTSIn the DCS group, cavities formed in the white matter of spinal cord and gliosis occurred around necrotic areas. Moreover, the mRNA and protein expression of TNF-α was significantly higher in the DCS group than in the normal control group and the safe decompression group (P<0.01). The results of TUNEL showed that the number of positive apoptotic cells was significantly larger in the DCS group than in the normal control group and the safe decompression group (P<0.05).

CONCLUSIONApoptosis plays an important role in spinal cord injury induced by DCS. In the early stage of DCS, the massive release of TNF-α initiates apoptosis and contributes to the pathological changes in spinal cord injury induced by DCS.

Animals ; Apoptosis ; Decompression Sickness ; metabolism ; pathology ; Disease Models, Animal ; In Situ Nick-End Labeling ; RNA, Messenger ; Rabbits ; Spinal Cord ; pathology ; Spinal Cord Injuries ; metabolism ; pathology ; Tumor Necrosis Factor-alpha ; metabolism

Objective To investigate the effects of astrocyte and microglia on spinal cord injury of the rabbits in decompression sickness (DCS).Methods Twenty-one healthy adult male New Zealand rabbits were averagely divided into 3 groups according to random number table:control group,safety relief group and DCS group.Experimental animals were placed in the pressure cabin.Safety relief group model referred to the Chinese Navy diving decompression tables when decompression applied.In DCS group,the pressure equably was increased to 0.8 MPa (absolute pressure) within 5 min by compressed air,maintained for 60 min and then equably decompressed to normal pressure within 5 min.The change of pathology morphology in the spinal cord of thoracolumbar vertebra was observed by light microscope.The expression of tumor necrosis factor-a (TNF-a) and Glial Fibrillary Acidic Protein (GFAP) mRNA were measured by real-time polymerase chain reaction (real-time PCR) and the expression of TNF-α,GFAP,ionized calcium binding adapter molecule 1 (IBA1) protein was measured by immunohistochemistry method.Results There were some cavity formations on white matter of spinal cord in DCS group.The relative expression of TNF-α mRNA was higher in DCS (6.28±1.73) than that in control group (1.00±0.14) and in safety relief group (1.34±0.42) (P＜0.01).The relative expression of GFAP mRNA was higher in DCS (7.39±2.04) than in that control group (1.02±0.26) and in safety relief group (1.63±0.90) (P＜ 0.01).The expression of TNF-α protein was significantly higher in DCS group (24.14± 2.61) than that in control group (6.71±1.25) and in safety relief group (8.28 ± 1.11) (P＜0.01).The expression of GFAP protein was also significantly higher in DCS (18.20±4.38) than that in control group (4.30±2.70) and in safety relief group (6.20±2.92) (P＜0.01).The expression of IBA1 protein was also significantly higher in DCS (21.53±1.37) than that in control group (5.94±0.36) and in safety relief group (6.69 ± 0.81) (P＜0.01).Conclusions The astrocyte and microglia may play a key role in pathophysiology of spinal cord injury.They are activated in the early stage of DCS and accompanied with massive release of TNF-α,which causes excessive inflammation reaction and induces the spinal cord injury finally.

Objective To investigate the effects of astrocyte and microglia on spinal cord injury of the rabbits in decompression sickness (DCS).Methods Twenty-one healthy adult male New Zealand rabbits were averagely divided into 3 groups according to random number table:control group,safety relief group and DCS group.Experimental animals were placed in the pressure cabin.Safety relief group model referred to the Chinese Navy diving decompression tables when decompression applied.In DCS group,the pressure equably was increased to 0.8 MPa (absolute pressure) within 5 min by compressed air,maintained for 60 min and then equably decompressed to normal pressure within 5 min.The change of pathology morphology in the spinal cord of thoracolumbar vertebra was observed by light microscope.The expression of tumor necrosis factor-a (TNF-a) and Glial Fibrillary Acidic Protein (GFAP) mRNA were measured by real-time polymerase chain reaction (real-time PCR) and the expression of TNF-α,GFAP,ionized calcium binding adapter molecule 1 (IBA1) protein was measured by immunohistochemistry method.Results There were some cavity formations on white matter of spinal cord in DCS group.The relative expression of TNF-α mRNA was higher in DCS (6.28±1.73) than that in control group (1.00±0.14) and in safety relief group (1.34±0.42) (P＜0.01).The relative expression of GFAP mRNA was higher in DCS (7.39±2.04) than in that control group (1.02±0.26) and in safety relief group (1.63±0.90) (P＜ 0.01).The expression of TNF-α protein was significantly higher in DCS group (24.14± 2.61) than that in control group (6.71±1.25) and in safety relief group (8.28 ± 1.11) (P＜0.01).The expression of GFAP protein was also significantly higher in DCS (18.20±4.38) than that in control group (4.30±2.70) and in safety relief group (6.20±2.92) (P＜0.01).The expression of IBA1 protein was also significantly higher in DCS (21.53±1.37) than that in control group (5.94±0.36) and in safety relief group (6.69 ± 0.81) (P＜0.01).Conclusions The astrocyte and microglia may play a key role in pathophysiology of spinal cord injury.They are activated in the early stage of DCS and accompanied with massive release of TNF-α,which causes excessive inflammation reaction and induces the spinal cord injury finally.

OBJECTIVETo investigate the changes in expression of tumor necrosis factor-alpha (TNF-α) and glial fibrillary acidic protein (GFAP) in rabbits with decompression disease (DCS), and to investigate the functioning mechanism.

METHODSA total of 21 healthy adult rabbits were randomly divided into 3 groups: normal control group, DCS group, and safe relief group, with 7 rabbits in each group. A rabbit DCS model was established by quick decompression. The changes in pathological morphology and mRNA and protein expression of TNF-α and GFAP in the brain and spinal cord of rabbits with DCS were determined by light microscopy, real-time PCR, and immunohistochemistry, respectively.

RESULTSCavity formation was observed in the white matter of spinal cord in DCS group. The mRNA and protein expression of TNF-α and GFAP was significantly higher in the DCS group than in the normal control group and safe relief group (P < 0.01), while no significant differences were observed in the brain (P > 0.05).

CONCLUSIONSpinal cord is the main part of central nervous system injury in DCS. Activation of TNF-α and GFAP genes accompanied by increase in their protein expression can be observed at the early stage of DCS. The astrocytes and TNF-α play important roles in the process of spinal cord injury in DCS.

Animals ; Brain ; metabolism ; Decompression Sickness ; metabolism ; Disease Models, Animal ; Glial Fibrillary Acidic Protein ; metabolism ; Male ; Rabbits ; Spinal Cord ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism

Objective To investigate the mechanism of brain and spinal cord injury in experimental rabbits with decompression sickness (DCS) and the effect of hyperbaric oxygen (HBO).Methods Twentyeight adult male healthy New Zealand rabbits were randomly divided into 4 groups:the normal control group,the DCS group,the safe decompression group and the HBO group,each consisting of 7 animals.The rabbits in the DCS group were compressed with air in 5 minutes to a pressure 0.8 MPa and maintained at the said pressure for 60 min,and then were decompressed to normal pressure within 5 min.The animals in the HBO group underwent the same compression and decompression procedures,as the animals in the DCS group,but were immediately put into the hyperbaric chamber to receive HBO therapy.The safe decompression group was compressed and decompressed with the profile of the Chinese Navy Diving Decompression Tables.Changes in pathological morphology and apoptosis of brain and spinal cord tissue cells in the thoracic and lumbar segments were observed with light microscopy and terminal deoxynucleotidyl transferase-mediated DUTP nick end labeling (TUNEL) method.Results For the animals in the DCS group,cavity in the white matter of the spinal cord and proliferation of gliocytes around the damaged tissue could obviously be observed.TUNEL results showed that more positive apoptotic cells were detected in the DCS group (28.29 ± 2.56)/HP,as compared with those of the normal control group (0.57 ± 0.54)/HP,the safe decompression group (2.29 ± 1.11)/HP and the HBO group (3.71 ± 1.11)/HP,with statistical significance (P ＜ 0.05).More positive apoptotic cells were also seen in the HBO group (3.71 ± 1.1 1)/HP,as compared with those of the normal control group (P ＜0.05),but were significantly less,as compared with those of the DCS group (P ＜ 0.05),also with statistical significance (P ＜ 0.05).Slightly more positive apoptotic cells were detected in the animals of the HBO group,when compared with those of the safe decompression group,but without statistical significance (P ＜ 0.05).No significant apoptosis of cells could be seen in the brain tissue.Conclusions Spinal core was the main site involved in the central nervous system injury induced by rapid decompression.The spinal cord injury induced by rapid decompression was the result of the apoptosis of gliocytes,and gliocytes might play a key role in the recovery of spinal cord injury.HBO therapy could obviously inhibit the apoptosis of gliocytes,following spinal cord injury.

Objective To investigate the mechanism of brain and spinal cord injury in experimental rabbits with decompression sickness (DCS) and the effect of hyperbaric oxygen (HBO).Methods Twentyeight adult male healthy New Zealand rabbits were randomly divided into 4 groups:the normal control group,the DCS group,the safe decompression group and the HBO group,each consisting of 7 animals.The rabbits in the DCS group were compressed with air in 5 minutes to a pressure 0.8 MPa and maintained at the said pressure for 60 min,and then were decompressed to normal pressure within 5 min.The animals in the HBO group underwent the same compression and decompression procedures,as the animals in the DCS group,but were immediately put into the hyperbaric chamber to receive HBO therapy.The safe decompression group was compressed and decompressed with the profile of the Chinese Navy Diving Decompression Tables.Changes in pathological morphology and apoptosis of brain and spinal cord tissue cells in the thoracic and lumbar segments were observed with light microscopy and terminal deoxynucleotidyl transferase-mediated DUTP nick end labeling (TUNEL) method.Results For the animals in the DCS group,cavity in the white matter of the spinal cord and proliferation of gliocytes around the damaged tissue could obviously be observed.TUNEL results showed that more positive apoptotic cells were detected in the DCS group (28.29 ± 2.56)/HP,as compared with those of the normal control group (0.57 ± 0.54)/HP,the safe decompression group (2.29 ± 1.11)/HP and the HBO group (3.71 ± 1.11)/HP,with statistical significance (P ＜ 0.05).More positive apoptotic cells were also seen in the HBO group (3.71 ± 1.1 1)/HP,as compared with those of the normal control group (P ＜0.05),but were significantly less,as compared with those of the DCS group (P ＜ 0.05),also with statistical significance (P ＜ 0.05).Slightly more positive apoptotic cells were detected in the animals of the HBO group,when compared with those of the safe decompression group,but without statistical significance (P ＜ 0.05).No significant apoptosis of cells could be seen in the brain tissue.Conclusions Spinal core was the main site involved in the central nervous system injury induced by rapid decompression.The spinal cord injury induced by rapid decompression was the result of the apoptosis of gliocytes,and gliocytes might play a key role in the recovery of spinal cord injury.HBO therapy could obviously inhibit the apoptosis of gliocytes,following spinal cord injury.