ABSTRACT
Retinoblastoma (RB) is a pediatric malignancy, typically diagnosed at birth or during early childhood. The pathogenesis of RB is marked by the amplification of the Basic Helix-Loop-Helix (BHLH) Transcription Factor MYCN, which serves as a transcriptional regulator capable of binding to Dickkopf 3 (DKK3). However, the precise role of DKK3 in the malignant progression of RB cells caused by MYCN remains elusive. In the present study, the expression of MYCN was either overexpressed or interfered in RB cells. Subsequently, the expression level of DKK3 was assessed through quantitative real-time polymerase chain reaction and western blot analysis. Cell proliferation was evaluated using the Cell Counting Kit-8 assay and 5-ethynyl-2'-deoxyuridine staining, while cell cycle progression and apoptosis were analyzed by flow cytometry and western blot analysis, respectively. Additionally, the expression of proteins involved in the Wnt/ß-catenin/Fra-1/p53 signaling pathway was evaluated via western blot analysis. To gain further insights, Wnt agonists and the P53 inhibitor PFT-α were introduced into exploration. The current investigation revealed a negative correlation between the expression levels of MYCN and DKK3 in RB cells. Additionally, DKK3 overexpression inhibited cell proliferation, promoted cell apoptosis, and arrested cell cycle in RB cells with high expression of MYCN. Moreover, enhanced DKK3 expression inhibited proliferation, promoted cell cycle arrest and apoptosis of RB cells by modulating the wnt/ßcatenin/Fra-1/p53 signaling pathway. Furthermore, in vivo experiments revealed that overexpression of DKK3 inhibits the growth of RB tumors. Collectively, our findings elucidate that MYCN stimulates the Wnt/ß-catenin/Fra-1 pathway by suppressing DKK3 expression, ultimately suppressing p53 activity and contributing to malignant progression of RB.
Subject(s)
Adaptor Proteins, Signal Transducing , Cell Proliferation , N-Myc Proto-Oncogene Protein , Retinoblastoma , Tumor Suppressor Protein p53 , Wnt Signaling Pathway , Humans , N-Myc Proto-Oncogene Protein/genetics , N-Myc Proto-Oncogene Protein/metabolism , Retinoblastoma/metabolism , Retinoblastoma/genetics , Retinoblastoma/pathology , Tumor Suppressor Protein p53/metabolism , Tumor Suppressor Protein p53/genetics , Adaptor Proteins, Signal Transducing/genetics , Adaptor Proteins, Signal Transducing/metabolism , Cell Line, Tumor , Animals , Mice , Apoptosis , Intercellular Signaling Peptides and Proteins/genetics , Intercellular Signaling Peptides and Proteins/metabolism , Mice, Nude , beta Catenin/metabolismABSTRACT
BACKGROUND:Vitamin C,as an essential nutrient,has a wide range of biological effects and a variety of biological functions related to the pathogenesis of sarcopenia.Vitamin C supplementation is expected to be a novel prevention and treatment measure for sarcopenia. OBJECTIVE:To review recent research advances in the application of vitamin C in the pathogenesis and treatment of sarcopenia,and to discuss the potential role of vitamin C in the prevention and treatment of sarcopenia and possible mechanistic pathways based on published evidence. METHODS:The first author performed a computer search of PubMed,Web of Science,CNKI and other databases for relevant studies involving vitamin C in sarcopenia.The search keywords were"vitamin C,ascorbic acid,L-ascorbic acid,ascorbate,antioxidants,oxidative stress,sarcopenia,muscular atrophy,muscle weakness,muscle development,skeletal muscle regenerate,muscles,skeletal muscle"in English and Chinese,respectively.The search period was from each database inception to July 2023.After screening,85 articles were included for further review. RESULTS AND CONCLUSION:Ensuring adequate dietary vitamin C intake or maintaining normal circulating levels of vitamin C will help to reduce age-related muscle loss and decrease the prevalence of sarcopenia.In addition,vitamin C supplementation is also useful for improving skeletal muscle mass,strength and physical function with potential synergistic effects in exercise strategies for sarcopenia.The effects of vitamin C on sarcopenia may be via the following biological mechanisms:vitamin C limits the activation of the ubiquitin-proteasome pathway mainly by inhibiting oxidative stress and inflammatory responses in skeletal muscle,thus positively regulating protein metabolic homeostasis,and may enhance mitochondrial antioxidant defenses through its antioxidant effects to maintain healthy mitochondrial function.In addition,vitamin C affects myoblast proliferation,differentiation and myotube size,mainly by increasing the expression of myogenic regulatory factors and activating protein synthesis signaling pathways,which contribute to the promotion of muscle development as well as the repair and regeneration of damaged muscle tissue.The positive effects of vitamin C in sarcopenia need to be studied in large samples and with optimized designs for important influencing factors,such as the choice of supplementation dose and duration,the design of exercise prescription when vitamin C is combined with an exercise intervention,and the assessment of the redox status of the individual.It is recommended that future studies should be conducted in older patients with sarcopenia(<50 μmol/L)with suboptimal vitamin C status to investigate the efficacy of a combined intervention of long-term supplementation with 1 000 mg/d vitamin C(for 6 months or longer)with at least two or more types of multi-type combined exercise,with supplementation timed to take place at 1 hour after the end of the exercise,and with monitoring of markers of oxidative damage produced during the exercise such as malondialdehyde or protein hydroxyl levels were monitored.In conclusion,the optimal dose and timing of vitamin C supplementation for older adults with sarcopenia needs to be explored more,while the appropriate design of exercise prescriptions(especially the type and intensity of exercise)needs to be further determined.
ABSTRACT
Acute myeloid leukemia (AML) is a malignant clonal disease of hematopoietic stem cells, characterized by the proliferation of abnormal primordial cells of myeloid origin in bone marrow, blood and other tissues. At present, the standard induction therapy for AML mainly includes “3+7” standard treatment(anthracycline combined with cytarabine), allogeneic hematopoietic stem cell transplantation (Allo-HSCT) and targeted drug therapy. However, AML cells usually express high levels of P-glycoprotein, which mediates the efflux of chemotherapeutic drugs, which makes AML cells resistant to chemotherapy, resulting in many patients who are not sensitive to chemotherapy or relapse after complete remission. And some patients can not tolerate intensive therapy or lack of donors and can not use Allo-HSCT therapy. Therefore, it is of great clinical significance to find new drugs to improve the efficacy of AML patients. Epigenetic disorders play a key role in the pathogenesis of many diseases, especially cancer. Studies have shown that most AML patients have epigenetic regulatory gene mutations, such as DNMT3A, IDH and TET2, and these mutations are potentially reversible, which has become one of the therapeutic targets of AML. Histone deacetylase inhibitors (HDACi) can regulate the balance between histone acetylation and deacetylation, change the expression of proto-oncogenes or tumor suppressor genes that control cancer progression from epigenetics, and play an important role in many kinds of tumor therapy. At present, HDACi has shown the ability to induce differentiation, cell cycle arrest and apoptosis of AML cells. The mechanism may be mainly related to HDACi inducing chromatin conformation opening of tumor suppressor gene by inhibiting HDAC activity, promoting oncogene damage and preventing oncogene fusion protein from recruiting HDAC. Although the preclinical outcome of HDACi is promising, it is not as effective as the conventional therapy of AML. However, the combination strategy with various anticancer drugs is in clinical trials, showing significant anti-AML activity, improving efficacy through key targeting pathways in a typical synergistic or additive way, increasing AML sensitivity to chemotherapy, reducing tumor growth and metastasis potential, inhibiting cell mitotic activity, inducing cell apoptosis, regulating bone marrow microenvironment, which provides a good choice for the treatment of AML. Especially for those AML patients who are not suitable for intensive therapy and drug resistance to chemotherapy. This review introduces the relationship between HDAC and cancer; the classification of HDAC and its function in AML; the correlation between HDAC and AML; the clinical application of five types of HDACi; preclinical research results and clinical application progress of six kinds of HDACi in AML, such as Vrinota, Belinostat, Panobinostat, Valproic acid, Entinostat, and Chidamide, the mechanism of HDACi combined with other anticancer drugs in AML indicates that the current HDACi is mainly aimed at various subtypes of pan-HDAC inhibitors, with obvious side effects, such as fatigue, thrombocytopenia, nausea, vomiting, diarrhea. In recent years, the next generation of HDACi is mainly focused on the selectivity of analogues or isomers. Finding the best combination of HDACi and other drugs and the best timing of administration to balance the efficacy and adverse reactions is a major challenge in the treatment of AML, and the continued development of selective HDACi with less side effects and more accurate location is the key point for the development of this drug in the future. It is expected to provide reference for clinical treatment of AML.
ABSTRACT
Obstructive sleep apnea hypopnea syndrome (OSAHS) is a sleep breathing disorder caused by obstruction of the upper airway during sleep from various causes. At present, the diagnosis and treatment of OSAHS are insufficient. OSAHS causes cognitive decline due to excessive oxidative stress and inflammatory response caused by sleep breathing disorder, and its alteration of the brain gray matter area may be related to cognitive dysfunction. This review investigates the correlation between cognitive dysfunction and brain gray matter areas changes in OSAHS, and elucidates the underlying mechanisms, which provide a theoretical basis for early clinical diagnosis and treatment.
ABSTRACT
Purpose@#This study was performed to analyze the rule of confluence of the caudate lobe bile duct (CLD) into the left hepatic duct (LHD) and to discuss the protective strategy during left hemihepatectomy. @*Methods@#MRI of 400 patients and T-tube angiography images of 100 patients were collected, and the imaging rules of the confluence of the CLD into the LHD were summarized. The clinical data of 33 patients who underwent left hemihepatectomy using the protective strategy were analyzed. @*Results@#MRI and T-tube angiography images showed that the length from the confluence point of the CLD into the LHD to the confluence of the left and right hepatic ducts was 1.19 ± 0.40 cm and 1.26 ± 0.39 cm, respectively. The average angle between the longitudinal axis of the 2 bile ducts was 68.27° ± 22.59° and 66.58 ± 22.88°, respectively. Coronal and cross-sectional images showed that inflow from the foot side to the cranial side was noted in 79.8% and 82.0% of patients, respectively, and inflow from the dorsal to the ventral side was observed in 84.5% and 88.0%, respectively. Based on these imaging rules, the safe transection length and plane were summarized, and the CLD was effectively protected in 33 cases of left hemihepatectomy. @*Conclusion@#In left hemihepatectomy, the LHD should be transected at least 1.5 cm away from the confluence of the left and right hepatic ducts, and the plane of transection should be oblique to the dorsal side at an angle of 45° with the LHD, these parameters represent an effective strategy to protect the CLD.
ABSTRACT
Pancreatic cancer is an aggressive malignant tumor with poor prognosis.On the one hand,it has a narrow therapeutic window due to the lack of specific markers and obvious clinical symptoms.Once diagnosed,it has often developed to an advanced stage.On the other hand,located in a vital region of the body,pancreatic operation is difficult and the postoperative recurrence rate is high.Therefore,surgical treatment is only suitable for a small number of early patients.Pancreatic cancer has a tumor microenvironment with the characteristic of dense stroma,hypoxia,paucity of blood vessels and highly immunosuppression.It is often insensitive to traditional radiation and chemotherapy.Therefore,strategies targeting on tumor microenvironment have a potential prospect.This article reviews the research progress in tumor microenvironment of pancreatic cancer,in order to provide the references in the further research and treatment of oancreatic cancer.
ABSTRACT
Objective::To establish a rapid evaluation method for Cinnamomi Cortex decoction pieces by near infrared spectroscopy. Method::The contents of coumarin, cinnamalol, cinnamic acid and cinnamaldehyde in 86 batches of Cinnamomi Cortex of different origins were determined by HPLC. And the NIR spectra of different batches of Cinnamomi Cortex were also collected. With NIR spectrum as independent variable and coumarin, cinnamalol, cinnamic acid and cinnamaldehyde as dependent variables, a quantitative analysis model of four components in cinnamon was established by partial least squares method. Result::The correlation coefficients (r) of coumarin, cinnamic alcohol, cinnamic acid and cinnamaldehyde near infrared quantitative analysis models were 0.952 8, 0.977 7, 0.961 9, 0.992 2, root mean square error of cross(RMSEC) were 0.012 2, 0.006 1, 0.004 3, 0.82 g·g-1, root mean square errorof cross-validation(RMSECV) were 0.015 8, 0.011 2, 0.002 0, 1.481 1 g·g-1, and root mean square error of prediction(RMSEP) were 0.017 8, 0.010 3, 0.010 3, 0.005 5, 1.63 g·g-1. Conclusion::The established NIR quantitative analysis model of four active ingredients in Cinnamomi Cortex slices has a good accuracy, and provides a basis for rapid evaluation of the quality of Cinnamomi Cortex slices.
ABSTRACT
This study aimed to establish an animal model of decompression-induced lung injury (DILI) secondary to repetitive diving in mice and explore the role of macrophages in DILI and the protective effects of high-concentration hydrogen (HCH) on DILI. Mice were divided into three groups: control group, DILI group, and HCH group. Mice were exposed to hyperbaric air at 600 kPa for 60 min once daily for consecutive 3 d and then experienced decompression. In HCH group, mice were administered with HCH (66.7% hydrogen and 33.3% oxygen) for 60 min after each hyperbaric exposure. Pulmonary function tests were done 6 h after decompression; the blood was harvested for cell counting; the lung tissues were harvested for the detection of inflammatory cytokines, hematoxylin and eosin (HE) staining, and immunohistochemistry; western blotting and polymerase chain reaction (PCR) were done for the detection of markers for M1 and M2 macrophages. Our results showed that bubbles formed after decompression and repeated hyperbaric exposures significantly reduced the total lung volume and functional residual volume. Moreover, repetitive diving dramatically increased proinflammatory factors and increased the markers of both M1 and M2 macrophages. HCH inhalation improved lung function to a certain extent, and significantly reduced the pro-inflammatory factors. These effects were related to the reduction of M1 macrophages as well as the increase in M2 macrophages. This study indicates that repetitive diving damages lung function and activates lung macrophages, resulting in lung inflammation. HCH inhalation after each diving may be a promising strategy for the prevention of DILI.
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Methane is the simplest hydrocarbon, consisting of one carbon atom and four hydrogen atoms. It is abundant in marsh gas, livestock rumination, and combustible ice. Little is known about the use of methane in human disease treatment. Current research indicates that methane is useful for treating several diseases including ischemia and reperfusion injury, and inflammatory diseases. The mechanisms underlying the protective effects of methane appear primarily to involve anti-oxidation, anti-inflammation, and anti-apoptosis. In this review, we describe the beneficial effects of methane on different diseases, summarize possible mechanisms by which methane may act in these conditions, and discuss the purpose of methane production in hypoxic conditions. Then we propose several promising directions for the future research.
Subject(s)
Humans , Antioxidants/pharmacology , Apoptosis/drug effects , Inflammation/drug therapy , Ischemia/drug therapy , Methane/therapeutic use , Reperfusion Injury/drug therapyABSTRACT
This study aimed to establish an animal model of decompression-induced lung injury (DILI) secondary to repetitive diving in mice and explore the role of macrophages in DILI and the protective effects of high-concentration hydrogen (HCH) on DILI. Mice were divided into three groups: control group, DILI group, and HCH group. Mice were exposed to hyperbaric air at 600 kPa for 60 min once daily for consecutive 3 d and then experienced decompression. In HCH group, mice were administered with HCH (66.7% hydrogen and 33.3% oxygen) for 60 min after each hyperbaric exposure. Pulmonary function tests were done 6 h after decompression; the blood was harvested for cell counting; the lung tissues were harvested for the detection of inflammatory cytokines, hematoxylin and eosin (HE) staining, and immunohistochemistry; western blotting and polymerase chain reaction (PCR) were done for the detection of markers for M1 and M2 macrophages. Our results showed that bubbles formed after decompression and repeated hyperbaric exposures significantly reduced the total lung volume and functional residual volume. Moreover, repetitive diving dramatically increased proinflammatory factors and increased the markers of both M1 and M2 macrophages. HCH inhalation improved lung function to a certain extent, and significantly reduced the pro-inflammatory factors. These effects were related to the reduction of M1 macrophages as well as the increase in M2 macrophages. This study indicates that repetitive diving damages lung function and activates lung macrophages, resulting in lung inflammation. HCH inhalation after each diving may be a promising strategy for the prevention of DILI.
Subject(s)
Animals , Male , Mice , Cell Polarity , Diving/adverse effects , Lung/physiology , Lung Injury/etiology , Macrophages/physiology , Mice, Inbred BALB C , Pulmonary Edema/etiologyABSTRACT
Pancreatic cancer is an aggressive malignant tumor with poor prognosis. On the one hand, it has a narrow therapeutic window due to the lack of specific markers and obvious clinical symptoms. Once diagnosed, it has often developed to an advanced stage. On the other hand, located in a vital region of the body, pancreatic operation is difficult and the postoperative recurrence rate is high. Therefore, surgical treatment is only sui-table for a small number of early patients. Pancreatic cancer has a tumor microenvironment with the characteristic of dense stroma, hypoxia, paucity of blood vessels and highly immunosuppression. It is often insensitive to traditional radiation and chemotherapy. Therefore, strategies targeting on tumor microenvironment have a potential prospect. This article reviews the research progress in tumor microenvironment of pancreatic cancer, in order to provide the references in the further research and treatment of pancreatic cancer.
ABSTRACT
Pancreas metabonomic profiles of the type 2 diabetic rats' induced by streptozotocin(STZ) and high-sugar, high fat diet on the treatment of Renshenjian decoction(RSJD) after 8 weeks were investigated.In this study, 48 Rats were randomly divided into four groups: normal control (NC), Pathological model (PM), Renshenjian decoction(RSJD 3.76 g·kg⁻¹) and glimepiride control (GC 0.04 mg·kg⁻¹). They are induced insulin resistance model of type 2 diabetes mellitus by streptozotocin(STZ) after 4 weeks' high-sugar, high fat diet except for NC. After sucessful modeling, they are given intragastric administration respectively with same amount of saline, RSJD and glimepiride in 4 weeks. At the end of the 8th week, the pancreatic tissue of rats in each group was collected, and the ¹H-NMR spectrum was collected after being treated by certain method, and analyzed by principal component analysis (PCA). Compared with NC's rats, we found PM's a significant elevation in the level of leucine/isoleucine, valine, lactic acid, creatine but reduction in the level of inose and less obvious changes in the level of creatine, cholic acid, taurine in pancreatic extract. After having been recieved RSJD, reduction level in leucine/isoleucine, valine, alanine, creatine, choline, taurine are also found in pancreatic extract of RSJD's rats, together with the increase of creatinine and tryptophan levels. The results showed that RSJD could regulate the level of amino acids in pancreas of IR rats, promoting a recovery in the process of metabolism. It's helpful to simulate the metabolic changes of IR rats via ¹H-NMR for a further understanding to study the mechanism how RSJD treat IR rats.
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Sleep deficiency is a common public health problem associated with many diseases, such as obesity and cardiovascular disease. In this study, we established a sleep deprivation (SD) mouse model using a ‘stick over water’ method and observed the effect of sleep deficiency on ocular surface health. We found that SD decreased aqueous tear secretion; increased corneal epithelial cell defects, corneal sensitivity, and apoptosis; and induced squamous metaplasia of the corneal epithelium. These pathological changes mimic the typical features of dry eye. However, there was no obvious corneal inflammation and conjunctival goblet cell change after SD for 10 days. Meanwhile, lacrimal gland hypertrophy along with abnormal lipid metabolites, secretory proteins and free amino-acid profiles became apparent as the SD duration increased. Furthermore, the ocular surface changes induced by SD for 10 days were largely reversed after 14 days of rest. We conclude that SD compromises lacrimal system function and induces dry eye. These findings will benefit the clinical diagnosis and treatment of sleep-disorder-related ocular surface diseases.
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Stellate ganglion blockade (SGB) protects patients from focal cerebral ischemic injury, and transection of the cervical sympathetic trunk (TCST) in a rat model can mimic SGB in humans. The purpose of this study was to investigate the mechanisms underlying the neuroprotective effects of TCST on neuronal damage in the hippocampus in a rat model of middle cerebral artery occlusion (MCAO) in an attempt to elucidate the neuroprotective effects of SGB. The modified method of Zea Longa was used to establish the permanent MCAO model. Male Wistar rats were randomly divided into three groups: sham-operated group, MCAO group, and TCST group. The animals in TCST group were sacrificed 48 h after TCST which was performed after the establishment of the MCAO model. Proteins were extracted from the ipsilateral hippocampus and analyzed by two-dimensional difference gel electrophoresis (2D-DIGE) and peptide mass fingerprinting (PMF). The levels of N-ethylmaleimide-sensitive factor (NSF) were measured as well. The results showed that 11 types of proteins were identified by 2D-DIGE. The expressions of eight proteins were changed both in the sham-operated and TCST groups, and the expressions of the other three proteins were changed in all three groups. Moreover, the expression of NSF was higher in the TCST group than in the MCAO group but lower in the MCAO group than in sham-operated group. The ratio of NSF expression between the MCAO group and shamoperated group was -1.37 (P<0.05), whereas that between the TCST group and MCAO group was 1.35 (P<0.05). Our results imply that TCST increases the expression of NSF in the hippocampus of adult rats with focal cerebral ischemia, which may contribute to the protection of the injured brain. Our study provides a theoretical basis for the therapeutic application of SGB to patients with permanent cerebral ischemia.
ABSTRACT
Stellate ganglion blockade (SGB) protects patients from focal cerebral ischemic injury, and transection of the cervical sympathetic trunk (TCST) in a rat model can mimic SGB in humans. The purpose of this study was to investigate the mechanisms underlying the neuroprotective effects of TCST on neuronal damage in the hippocampus in a rat model of middle cerebral artery occlusion (MCAO) in an attempt to elucidate the neuroprotective effects of SGB. The modified method of Zea Longa was used to establish the permanent MCAO model. Male Wistar rats were randomly divided into three groups: sham-operated group, MCAO group, and TCST group. The animals in TCST group were sacrificed 48 h after TCST which was performed after the establishment of the MCAO model. Proteins were extracted from the ipsilateral hippocampus and analyzed by two-dimensional difference gel electrophoresis (2D-DIGE) and peptide mass fingerprinting (PMF). The levels of N-ethylmaleimide-sensitive factor (NSF) were measured as well. The results showed that 11 types of proteins were identified by 2D-DIGE. The expressions of eight proteins were changed both in the sham-operated and TCST groups, and the expressions of the other three proteins were changed in all three groups. Moreover, the expression of NSF was higher in the TCST group than in the MCAO group but lower in the MCAO group than in sham-operated group. The ratio of NSF expression between the MCAO group and shamoperated group was -1.37 (P<0.05), whereas that between the TCST group and MCAO group was 1.35 (P<0.05). Our results imply that TCST increases the expression of NSF in the hippocampus of adult rats with focal cerebral ischemia, which may contribute to the protection of the injured brain. Our study provides a theoretical basis for the therapeutic application of SGB to patients with permanent cerebral ischemia.
Subject(s)
Animals , Male , Rats , Brain Injuries , Genetics , Metabolism , Pathology , Brain Ischemia , Genetics , Metabolism , Pathology , Gene Expression Regulation , Hippocampus , Metabolism , Pathology , N-Ethylmaleimide-Sensitive Proteins , Genetics , Rats, Wistar , Stellate Ganglion , Metabolism , Pathology , TransfectionABSTRACT
<p><b>OBJECTIVE</b>To investigate the value of susceptibility weighted imaging(SWI)in the diagnosis of hemorrhagic foci early after blast injury and its role in the outcome prediction.</p><p><b>METHODS</b>Totally 30 rabbits with blast-induced cerebral blast injury were used in this study. After routine CT/MRI and SWI scanning,quantified analysis was performed in regions of interest using post-processing technology. After dissecting the brains of the experimental rabbits,the cerebral histopathological changes were observed,and the results were compared with SWI findings.</p><p><b>RESULTS</b>In these 30 rabbits,22,102,221,and 738 hemorrhagic foci were detected by CT,T1WI,T2WI,and SWI,respectively. The number of cerebral microbleeds detected by SWI was significantly larger than those revealed by conventional T1WI and T2WI(Χ(2)=10.00,P<0.01). Furthermore,the SWI imaging displayed the punctiform(n=315,42.7%),lamellar(n=218,29.5%),slinar(n=205,27.8%)hypointense foci,with clear margin. The number of hemorrhagic foci detected by SWI was positively correlated with survival(r=-0.667,P<0.05).</p><p><b>CONCLUSIONS</b>SWI remarkably increases the detection rate of hemorrhagic foci(particularly microbleeds)in rabbits with cerebral blast injury. The number of cerebral microbleeds and location of foci are closely related with the outcomes and therefore may facilitate clinical managment.</p>
Subject(s)
Animals , Female , Male , Rabbits , Blast Injuries , Diagnosis , Brain , Pathology , Brain Injuries , Diagnosis , Cerebral Hemorrhage , Diagnosis , Image Enhancement , Magnetic Resonance Imaging , Methods , PrognosisABSTRACT
Objective To analyze the X ray findings of enema unreduced (including 4 perforations ) intussusception so as to improve the knowledge about the difficulty of reduction by air enema or the risk of perforation. Methods Of the 552 cases, 506 cases were successfully reduced by air enema. The range of air pressure was 6.67 to 14.67 kPa(60~110 mm Hg). Forty six unreduced cases were cured by operation. The films were taken before and during the reduction period. X ray findings were analyzed compared with that of the operative pathology. Results (1)Abdominal plain films showed total obstruction in 26 cases and asctis in 4 cases; (2) Air enema showed big and lobular masses in 36 cases and the location of masses in distal part of colon in 22 cases; (3)Operation pathology: ileoilecolic intussusception in 35 cases, 15 cases with intestinal necrosis (including 4 perforation cases). In 3 cases, perforations were in the intussusceptum,the other in the intussuscipiens. Conclusion 92% of intussusceptions can be reducted by pressure of air enema. Complex intussusception, with intestinal necrosis and primary intussusceptum, are difficult to reduce, and these patients ought to be operated on time.