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BACKGROUND@#To achieve optimal bone marrow engraftment during bone marrow transplantation, migration of donor bone marrow cells (BMCs) toward the recipient’s bone marrow is critical. Despite the enhanced engraftment of BMCs by co-administration of mesenchymal stem cells (MSCs), the efficiency can be variable depending on MSC donor. The purpose of this study is to examine the functional heterogeneity of tonsil-derived MSCs (TMSCs) and to identify a marker to evaluate efficacy for the enhancement of BMC migration. @*METHODS@#To examine the donor-to-donor variation of TMSCs in potentiating BMC migration, we isolated TMSCs from 25 independent donors. Transcriptome of TMSCs and proteome of conditioned medium derived from TMSC were analyzed. @*RESULTS@#Enhanced BMC migration by conditioned medium derived from TMSCs was variable depending on TMSC donor. The TMSCs derived from 25 donors showed distinct expression profiles compared with other cells, including fibroblasts, adipose-derived MSCs and bone marrow–derived MSCs. TMSCs were distributed in two categories: high- and low-efficacy groups for potentiating BMC migration. Transcriptome analysis of TMSCs and proteome profiles of conditioned medium derived from TMSCs revealed higher expression and secretion of matrix metalloproteinase (MMP) 1 in the high-efficacy group. MMP1 knockdown in TMSCs abrogated the supportive efficacy of conditioned medium derived from TMSC cultures in BMC migration. @*CONCLUSION@#These data suggest that secreted MMP1 can be used as a marker to evaluate the efficacy of TMSCs in enhancing BMC migration. Furthermore, the strategy of analyzing transcriptomes and proteomes of the MSCs may be useful to set the standard for donor variation.
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BACKGROUND@#Mast cells are immune sentinels in the skin that respond to a wide range of pathological and environmental stimuli; they owe their function to the expression of Toll-like receptors (TLRs). We previously found that tonsilderived mesenchymal stem cells (T-MSCs) were able to effectively attenuate TLR7-mediated skin inflammation in mice, which was accompanied by an increase in mast cell number. The present study investigated whether T-MSC extracellular vesicles, such as exosomes, are able to regulate mast cell activation in response to TLR7 stimulation. @*METHODS@#The HMC-1 human mast cell line was treated with a TLR7 agonist in the presence or absence of T-MSC exosomes, and the levels of expressed inflammatory cytokines were assessed. Additionally, mice were repeatedly injected with a TLR7 agonist with or without interval treatments with T-MSC exosomes and assessed dermal distribution of mast cells and related immune cells. @*RESULTS@#We showed that T-MSC exosomes containing microRNAs that target inflammatory cytokines significantly reduced the expression of inflammatory cytokines in TLR7 agonist-treated HMC-1 cells. In addition, T-MSC exosomes inhibited the increase in the number of both dermal mast cells and CD14-positive cells in TLR7 agonist-treated mice. @*CONCLUSION@#Our data suggest that T-MSC exosomes have regulatory effects on mast cell activation under inflammatory conditions, including TLR7 stimulation.
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BACKGROUND@#Therapeutic strategies that can promote platelet production are in demand to enhance clinical outcomes of bone marrow transplantation (BMT). Our research group has studied human tonsil-derived mesenchymal stem cells (TMSCs) and their effectiveness in promoting bone marrow (BM) engraftment. Here, we analyzed the effects of T-MSCs on platelet production and hemostasis. @*METHODS@#Donor BM cells (BMCs) were isolated from C57BL/6 mice and transplanted with or without T-MSCs to BALB/c recipient mice. Mice were sacrificed and blood cells were counted using an Auto Hematology Analyzer. Femur sections were stained with CD41 antibody to analyze megakaryocytes in the BM. Growth factor secretion from MSCs was analyzed using the Quantibody Array. Effects of T-MSC conditioned medium (CM) on megakaryopoiesis were investigated using the MegaCult assay. In a mouse model of BMT, T-MSC CM was injected with or without anti-placental growth factor (a-PlGF) blocking antibody, and blood cell numbers and coagulation were analyzed. @*RESULTS@#T-MSC co-transplantation increased percent survival of BMT mice. Platelet numbers were significantly lower in the BMC-only group, whereas T-MSC co-transplantation restored circulating platelets to levels similar to those of the control group. Significantly reduced numbers of CD41 ? megakaryocytes in Bu-Cy and BMC groups were increased by T-MSC co-transplantation. PlGF secretion from T-MSCs were detected and enhanced megakaryopoiesis, platelet production, and coagulation by T-MCS CM were disrupted in the presence of the a-PlGF blocking antibody. @*CONCLUSION@#We demonstrated the effectiveness of T-MSC co-transplantation in promoting platelet production and coagulation after BMT. These findings highlight the potential therapeutic relevance of T-MSCs for preventing thrombocytopenia after BMT.
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Bone marrow adipose tissue (BMAT) increases with aging and once disregarded as a passive marrow space filler. However, accumulating evidence suggests that BMAT is an active modulator of bone, hematopoiesis, and metabolism. Characterization of BMAT in molecular and cellular levels identified that it is distinct from white or brown adipose tissue. This review summarizes current knowledge on changes of BMAT under physiological and pathophysiological conditions of bone and marrow. Expansion of BMAT is closely linked with increased fracture risk, therefore regulation of BMAT can be considered as a novel therapeutic approach to enhance bone strength. Regarding hematopoiesis, increase in BMAT is negatively associated with the marrow function, but it is indispensable for maintaining myelopoiesis in acute myeloid leukemia. In addition, BMAT expansion is paradoxically identified in obesity as well as anorexia nervosa. It is considered that BMAT performs a different function in different nutritional states. Future studies would involve more detailed research about regulatory factors of BMAT and its functions in health and diseases. Enhancing our understanding about BMAT would open a new avenue for combating BMAT-related diseases.
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Background@#Mast cells are skin immune sentinels located in the upper dermis, where wheal formation and sensory nerve stimulation take place. Skin inflammation is occasionally accompanied by mast cell-driven responses with wheals, angioedema, or both. Immunoglobulin E (IgE) antibodies are regarded as typical stimuli to drive mast cell activation. However, various causative factors, including microbial infections, can drive IgE-independent mast cell response. When infected, the innate immunity orchestrates an immune response by activating receptor signaling via Toll-like receptors (TLRs). @*Objective@#In this study, we determined the effect of TLR7 stimulation on mast cells to investigate the possible mechanism of IgE-independent inflammatory response. @*Methods@#Human mast cell (HMC) line, HMC-1 cells were treated with TLR7 agonist and the morphologic alteration was observed in transmission electron microscopy. Further, TLR7 agonist treated HMC-1 cells were conducted to RNA sequencing to compare transcriptomic features. @*Results@#HMC-1 cells treated with TLR7 agonist reveals increase of intracellular vesicles, lipid droplets, and ribosomes. Also, genes involved in pro-inflammatory responses such as angiogenesis are highly expressed, and Il12rb2 was the most highly upregulated gene. @*Conclusion@#Our data suggest that TLR7 signaling on mast cells might be a potential therapeutic target for mast cell-driven, IgE-independent skin inflammation.
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BACKGROUND@#The advantages of tonsil-derived mesenchymal stem cells (TMSCs) over other mesenchymal stem cells (MSCs) include higher proliferation rates, various differentiation potentials, efficient immune-modulating capacity, and ease of obtainment. Specifically, TMSCs have been shown to differentiate into the endodermal lineage. Estrogen deficiency is a major cause of postmenopausal osteoporosis and is associated with higher incidences of ischemic heart disease and cerebrovascular attacks during the postmenopausal period. Therefore, stem cell-derived, estrogen-secreting cells might be used for estrogen deficiency. @*METHODS@#Here, we developed a novel method that utilizes retinoic acid, insulin-like growth factor-1, basic fibroblast growth factor, and dexamethasone to evaluate the differentiating potential of TMSCs into estrogen-secreting cells. The efficacy of the novel differentiating method for generation of estrogen-secreting cells was also evaluated with bone marrow- and adipose tissue-derived MSCs. @*RESULTS@#Incubating TMSCs in differentiating media induced the gene expression of cytochrome P450 19A1 (CYP19A1), which plays a key role in estrogen biosynthesis, and increased 17b-estradiol secretion upon testosterone addition. Furthermore, CYP11A1, CYP17A1, and 3b-hydroxysteroid dehydrogenase type-1 gene expression levels were significantly increased in TMSCs. In bone marrow-derived and adipose tissue-derived MSCs, this differentiation method also induced the gene expression of CYP19A1, but not CYP17A1, suggesting TMSCs are a superior source for estrogen secretion. @*CONCLUSION@#These results imply that TMSCs can differentiate into functional estrogen-secreting cells, thus providing a novel, alternative cell therapy for estrogen deficiency.
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Background@#Mast cells are skin immune sentinels located in the upper dermis, where wheal formation and sensory nerve stimulation take place. Skin inflammation is occasionally accompanied by mast cell-driven responses with wheals, angioedema, or both. Immunoglobulin E (IgE) antibodies are regarded as typical stimuli to drive mast cell activation. However, various causative factors, including microbial infections, can drive IgE-independent mast cell response. When infected, the innate immunity orchestrates an immune response by activating receptor signaling via Toll-like receptors (TLRs). @*Objective@#In this study, we determined the effect of TLR7 stimulation on mast cells to investigate the possible mechanism of IgE-independent inflammatory response. @*Methods@#Human mast cell (HMC) line, HMC-1 cells were treated with TLR7 agonist and the morphologic alteration was observed in transmission electron microscopy. Further, TLR7 agonist treated HMC-1 cells were conducted to RNA sequencing to compare transcriptomic features. @*Results@#HMC-1 cells treated with TLR7 agonist reveals increase of intracellular vesicles, lipid droplets, and ribosomes. Also, genes involved in pro-inflammatory responses such as angiogenesis are highly expressed, and Il12rb2 was the most highly upregulated gene. @*Conclusion@#Our data suggest that TLR7 signaling on mast cells might be a potential therapeutic target for mast cell-driven, IgE-independent skin inflammation.
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BACKGROUND@#The advantages of tonsil-derived mesenchymal stem cells (TMSCs) over other mesenchymal stem cells (MSCs) include higher proliferation rates, various differentiation potentials, efficient immune-modulating capacity, and ease of obtainment. Specifically, TMSCs have been shown to differentiate into the endodermal lineage. Estrogen deficiency is a major cause of postmenopausal osteoporosis and is associated with higher incidences of ischemic heart disease and cerebrovascular attacks during the postmenopausal period. Therefore, stem cell-derived, estrogen-secreting cells might be used for estrogen deficiency. @*METHODS@#Here, we developed a novel method that utilizes retinoic acid, insulin-like growth factor-1, basic fibroblast growth factor, and dexamethasone to evaluate the differentiating potential of TMSCs into estrogen-secreting cells. The efficacy of the novel differentiating method for generation of estrogen-secreting cells was also evaluated with bone marrow- and adipose tissue-derived MSCs. @*RESULTS@#Incubating TMSCs in differentiating media induced the gene expression of cytochrome P450 19A1 (CYP19A1), which plays a key role in estrogen biosynthesis, and increased 17b-estradiol secretion upon testosterone addition. Furthermore, CYP11A1, CYP17A1, and 3b-hydroxysteroid dehydrogenase type-1 gene expression levels were significantly increased in TMSCs. In bone marrow-derived and adipose tissue-derived MSCs, this differentiation method also induced the gene expression of CYP19A1, but not CYP17A1, suggesting TMSCs are a superior source for estrogen secretion. @*CONCLUSION@#These results imply that TMSCs can differentiate into functional estrogen-secreting cells, thus providing a novel, alternative cell therapy for estrogen deficiency.
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BACKGROUND: The liver is an organ with remarkable regenerative capacity; however, once chronic fibrosis occurs, liver failure follows, with high mortality and morbidity rates. Continuous exposure to proinflammatory stimuli exaggerates the pathological process of liver failure; therefore, immune modulation is a potential strategy to treat liver fibrosis. Mesenchymal stem cells (MSCs) with tissue regenerative and immunomodulatory potential may support the development of therapeutics for liver fibrosis. METHODS: Here, we induced hepatic injury in mice by injecting carbon tetrachloride (CCl₄) and investigated the therapeutic potential of conditionedmedium from tonsil-derivedMSCs (T-MSCCM). In parallel, we used recombinant human IL-1Ra,which, as we have previously shown, is secreted exclusively from T-MSCs and resolves the fibrogenic activation of myoblasts. Hepatic inflammation and fibrosis were determined by histological analyses using H&E and Picro-Sirius Red staining. RESULTS: The results demonstrated that T-MSC CM treatment significantly reduced inflammation as well as fibrosis in the CCl₄-injured mouse liver. IL-1Ra injection showed effects similar to T-MSC CM treatment, suggesting that T-MSC CM may exert anti-inflammatory and anti-fibrotic effects via the endogenous production of IL-1Ra. The expression of genes involved in fibrosis was evaluated, and the results showed significant induction of alpha-1 type I collagen, transforming growth factor beta, and tissue inhibitor of metalloproteases 1 upon CCl₄ injection, whereas treatment with T-MSC CM or IL-1Ra downregulated their expression. CONCLUSION: Taken together, these data support the therapeutic potential of T-MSC CM and/or IL-1Ra for the alleviation of liver fibrosis, as well as in treating diseases involving organ fibrosis.
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Animales , Humanos , Ratones , Tetracloruro de Carbono , Colágeno Tipo I , Medios de Cultivo Condicionados , Fibrosis , Inflamación , Proteína Antagonista del Receptor de Interleucina 1 , Cirrosis Hepática , Fallo Hepático , Hígado , Células Madre Mesenquimatosas , Metaloproteasas , Mortalidad , Mioblastos , Factor de Crecimiento Transformador betaRESUMEN
Gut microbiota inhabit the host gastrointestinal (GI) tract and play roles in many aspects of metabolic and immunologic homeostasis. Understanding about gut microbiota composition in health and disease is accumulating with the advances in gene sequencing technology. Graft-versus-host disease (GVHD) is a major complication after allogenic bone marrow transplantation (allo-BMT), a gold standard clinical procedure to treat hematologic disorders such as leukemia and lymphomas. Recent studies have shown that a disturbance in the gut microbiota affects GVHD prognosis. Decrease in a compositional diversity is suggested as an independent predictor of GVHD and colonization of noncommensal Enterococcus is shown to be involved in unpleasant treatment outcomes. This article describes current understanding about allo-BMT-induced gut microbiota changes and its involvement in the incidence of GVHD. In addition, several putative therapeutic strategies to decrease GVHD-related mortality after allo-BMT are discussed.
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Trasplante de Médula Ósea , Colon , Enterococcus , Microbioma Gastrointestinal , Enfermedad Injerto contra Huésped , Homeostasis , Incidencia , Leucemia , Linfoma , Mortalidad , PronósticoRESUMEN
B cell activation factor (BAFF) is a novel member of the TNF ligand superfamily, mainly produced by myeloid cells. BAFF has been shown to participate in B-cell survival and B- and T-cell maturation. BAFF expression in adipocytes has been recently demonstrated. In the current study, we verified that BAFF expression is increased during adipocyte differentiation. BAFF expression was augmented by TNF-alpha treatment and was decreased by rosiglitazone treatment. BAFF secretion in lean and in ob/ob mice sera were compared and smaller amount of BAFF was secreted in ob/ob mice. mRNA and protein expression were different between epididymal and visceral adipose tissue. BAFF expression was also increased in ob/ob mouse adipose tissue. We sought to identify known BAFF receptors (BAFF-R, BCMA, and TACI) in adipocytes, and determined that all three were present and upregulated during adipocyte differentiation. However, the expression of TACI was distinct from that of BAFF-R and BCMA under TNF-alpha and BAFF ligand treatment. BAFF-R and BCMA expression levels were upregulated under pro-inflammatory conditions, but TACI was reduced. Conversely, BAFF-R and BCMA expression levels were downregulated by rosiglitazone treatment, but TACI was increased. Taken together, our results suggest that BAFF may be a new adipokine, representing a link between obesity and inflammation.
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Animales , Ratones , Adipocitos/citología , Adipoquinas/biosíntesis , Factor Activador de Células B/biosíntesis , Receptor del Factor Activador de Células B/metabolismo , Diferenciación Celular , Hipoglucemiantes/farmacología , Inflamación/metabolismo , Obesidad/metabolismo , Tiazolidinedionas/farmacología , Factor de Necrosis Tumoral alfa/farmacologíaRESUMEN
In our previous study, we have shown that berberine has both anti-adipogenic and anti-inflammatory effects on 3T3-L1 adipocytes, and the anti-adipogenic effect is due to the down-regulation of adipogenic enzymes and transcription factors. Here we focused more on anti-inflammatory effect of berberine using real time RT-PCR and found it changes expressions of adipokines. We hypothesized that anti-adipogenicity of berberine mediates anti-inflammtory effect and explored leptin as a candidate mediator of this signaling. We studied this hypothesis by western blot analysis, but our results showed that berberine has no effect on the phosphorylations of STAT-3 and ERK which have important roles on leptin signaling. These results led us to conclude that the anti-inflammatory effect of berberine is not mediated by the inhibition of leptin signal transduction. Moreover, we have found that berberine down-regulates NF-kappaB signaling, one of the inflammation-related signaling pathway, through western blot analysis. Taken together, the anti-inflammatory effect of berberine is not mediated by leptin, and berberine induces anti-inflammatory effect independent of leptin signaling.
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Adipocitos , Adipoquinas , Berberina , Western Blotting , Regulación hacia Abajo , Inflamación , Leptina , FN-kappa B , Fosforilación , Transducción de Señal , Factores de TranscripciónRESUMEN
BACKGROUND: Adipose tissues were initially introduced as energy storages, but recently they have become famous as an endocrine organ which produces and secretes various kinds of molecules to make physiologic and metabolic changes in human body. It has been studied that these molecules are secreted in abundance as the adipose tissue becomes bigger along with obesity. Furthermore, it has been found that they are mediating systemic inflammation and generation of metabolic diseases such as type 2 diabetes and atherosclerosis. On the basis of these, we studied previous papers which have been researched about the interaction between preadipocytes and macrophages, adipose tissues and lymph nodes, and adipose tissue secreting molecules. RESULTS: Firstly, preadipocytes and macrophages are expressing similar transcriptomes and proteins, and preadipocytes can be converted to mature macrophages which have phagocytic activity. Moreover, the monocytes, which initially located in the bone marrow, are filtrated to the adipose tissue by monocyte chemotatic protein-1 and are matured to macrophages by colony stimulating factor-1. Secondly, adipose tissues and their associated lymph nodes are interacting each other in terms of energy efficiency. Lymph nodes promote lipolysis in adipose tissues, and polyunsaturated fatty acids in adipocytes become energy sources for dendritic cells. Lastly, adipose tissues produce and secrete proinflammatory molecules such as leptin, adiponectin, TNF-alpha, IL-6, and acute phase proteins, which induce the inflammation and potentially generate metabolic diseases. CONCLUSION: According to these, we can link adipose tissues to inflammation, but we need to affirm the actual levels and roles of adipose tissue-derived proinflammatory molecules in human body.
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Proteínas de Fase Aguda , Adipocitos , Adiponectina , Tejido Adiposo , Aterosclerosis , Médula Ósea , Células Dendríticas , Ácidos Grasos Insaturados , Cuerpo Humano , Sistema Inmunológico , Inflamación , Interleucina-6 , Leptina , Lipólisis , Ganglios Linfáticos , Macrófagos , Enfermedades Metabólicas , Monocitos , Negociación , Obesidad , Transcriptoma , Factor de Necrosis Tumoral alfaRESUMEN
Berberine (BBR), an isoquinoline alkaloid, has a wide range of pharmacological effects, yet its exact mechanism is unknown. In order to understand the anti-adipogenic effect of BBR, we studied the change of expression of several adipogenic enzymes of 3T3-L1 cells by BBR treatment. First, we measured the change of leptin and glycerol in the medium of 3T3-L1 cells treated with 1 micrometer, 5 micrometer and 10 micrometer concentrations of BBR. We also measured the changes of adipogenic and lipolytic factors of 3T3-L1. In 3T3-L1 cells, both leptin and adipogenic factors (SREBP-1c, C/EBP-alpha, PPAR-gamma, fatty acid synthase, acetyl-CoA carboxylase, acyl-CoA synthase and lipoprotein lipase) were reduced by BBR treatment. Glycerol secretion was increased, whereas expression of lipolytic enzymes (hormone-sensitive lipase and perilipin) mRNA was slightly decreased. Next, we measured the change of inflammation markers of 3T3-L1 cells by BBR treatment. This resulted in the down-regulation of mRNA level of inflammation markers such as TNF-alpha, IL-6, C- reactive protein and haptoglobin. Taken together, our data shows that BBR has both anti-adipogenic and anti-inflammatory effects on 3T3-L1 adipocytes, and the anti-adipogenic effect seems to be due to the down-regulation of adipogenic enzymes and transcription factors.
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Ratones , Animales , ARN Mensajero/genética , Leptina/metabolismo , Mediadores de Inflamación/metabolismo , Inflamación/genética , Glicerol/metabolismo , Regulación de la Expresión Génica/efectos de los fármacos , Citocinas/genética , Berberina/farmacología , Adipogénesis/efectos de los fármacos , Adipocitos/efectos de los fármacos , Células 3T3-L1RESUMEN
Despite advances in our understanding of venous thromboembolic disease, the prevention, diagnosis and treatment of pulmonary thromboembolism remain a clinical challenged. In western country, pulmonary thromboembolism is common : its antemortem diagnosis is not. Its frequency in routine hospital autopsies is 5%~10%. Especially, pregnancy and orthopedic surgery are widely recognized to be physiologic states with markedly elevated risk for thromboembolic complication. Deep venous thrombosis is very frequent after surgery, and its major comlpication, pulmonary thromboembolism, is the most frequent cause of postoperative death. The reduction of this cause of mortality is mainly based on its prevention rather than its therapy. All of these 40 cases were autopsied between 1997~1999 in National Institute of Scientific Investigation(NISI) and the causes of death were verified pulmonary thromboembolism. The aims of study were to investigate post-mortem verified causes of death, pulmonary thromboembolism, to cirrelate these with clinical practice, to identify the potential for prevention according to the literature and to contribute to decrease the mortality rate due to pulmonary thromboembolism.
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Embarazo , Autopsia , Causas de Muerte , Diagnóstico , Mortalidad , Ortopedia , Embolia Pulmonar , Trombosis de la VenaRESUMEN
Despite advances in our understanding of venous thromboembolic disease, the prevention, diagnosis and treatment of pulmonary thromboembolism remain a clinical challenged. In western country, pulmonary thromboembolism is common : its antemortem diagnosis is not. Its frequency in routine hospital autopsies is 5%~10%. Especially, pregnancy and orthopedic surgery are widely recognized to be physiologic states with markedly elevated risk for thromboembolic complication. Deep venous thrombosis is very frequent after surgery, and its major comlpication, pulmonary thromboembolism, is the most frequent cause of postoperative death. The reduction of this cause of mortality is mainly based on its prevention rather than its therapy. All of these 40 cases were autopsied between 1997~1999 in National Institute of Scientific Investigation(NISI) and the causes of death were verified pulmonary thromboembolism. The aims of study were to investigate post-mortem verified causes of death, pulmonary thromboembolism, to cirrelate these with clinical practice, to identify the potential for prevention according to the literature and to contribute to decrease the mortality rate due to pulmonary thromboembolism.
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Embarazo , Autopsia , Causas de Muerte , Diagnóstico , Mortalidad , Ortopedia , Embolia Pulmonar , Trombosis de la VenaRESUMEN
BACKGROUND: Pulmonary embolism can occur in various clinical situation and its diagnosis is difficult to be made but once it happens it can be a fatal disease to cause a death. We investigated 27 autopsied cases in the recent three years at National Institute of Scientific Investigation (NISI) who received anesthesia and diagnosed as pulmonary thromboembolism as cause of death and evaluated clinial situation and mortality by reviewing medical records. METHODS: Among 6848 autopsied cases in NISI from 1/1997 to 12/1999, 27 cases who were recieved anesthesia and whose cause of death were confirmed as pulmonary thromboembolism were investigated through its autopsy record, clinical record and statement. RESULTS: The type of anesthesia of 17 cases was general anesthesia, 4 cases was local anesthesia and 6 cases was unknown. As clinical distribution, obstetric were 17 cases, orthopedic 7 cases and thoracic surgery, general surgery and urology were 1 cases. By comparing the time interval between operation and death, 7 cases of obstetric were on postoperative 1 2 days. Deep thromboembolism was observed on lower extremities by 22 cases and anatomocally heart lesion was observed by 14 cases by autopsy. CONCLUSIONS: Pulmonary thromboembolism is one of the leading causes of sudden postoperative death, but because reliable symptoms, signs and diagnostic methods were absent, physician have to be aware of the problem and make effort to diagnose if possible.
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Anestesia , Anestesia General , Anestesia Local , Autopsia , Causas de Muerte , Diagnóstico , Corazón , Sistemas de Distribución en Hospital , Extremidad Inferior , Registros Médicos , Mortalidad , Ortopedia , Embolia Pulmonar , Cirugía Torácica , Tromboembolia , UrologíaRESUMEN
BACKGROUND: Pulmonary embolism can occur in various clinical situation and its diagnosis is difficult to be made but once it happens it can be a fatal disease to cause a death. We investigated 27 autopsied cases in the recent three years at National Institute of Scientific Investigation (NISI) who received anesthesia and diagnosed as pulmonary thromboembolism as cause of death and evaluated clinial situation and mortality by reviewing medical records. METHODS: Among 6848 autopsied cases in NISI from 1/1997 to 12/1999, 27 cases who were recieved anesthesia and whose cause of death were confirmed as pulmonary thromboembolism were investigated through its autopsy record, clinical record and statement. RESULTS: The type of anesthesia of 17 cases was general anesthesia, 4 cases was local anesthesia and 6 cases was unknown. As clinical distribution, obstetric were 17 cases, orthopedic 7 cases and thoracic surgery, general surgery and urology were 1 cases. By comparing the time interval between operation and death, 7 cases of obstetric were on postoperative 1 2 days. Deep thromboembolism was observed on lower extremities by 22 cases and anatomocally heart lesion was observed by 14 cases by autopsy. CONCLUSIONS: Pulmonary thromboembolism is one of the leading causes of sudden postoperative death, but because reliable symptoms, signs and diagnostic methods were absent, physician have to be aware of the problem and make effort to diagnose if possible.
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Anestesia , Anestesia General , Anestesia Local , Autopsia , Causas de Muerte , Diagnóstico , Corazón , Sistemas de Distribución en Hospital , Extremidad Inferior , Registros Médicos , Mortalidad , Ortopedia , Embolia Pulmonar , Cirugía Torácica , Tromboembolia , UrologíaRESUMEN
The principal manifestation of poisoning induced by the alkaline substance is a corrosive effects in tissues. The alkalies combine with protein and fat of the tissue, causing deep penetrating injury and liquefactive necrosis of the organs. Liquid lye is the most frequently ingested form of corrosive agents and causes most of the deaths associated with corrosive agent ingestion. We have experienced 5 fatal cases which were accidentally administered liquid lye as soap-saline enema in the hospital during 30 days. the 3 cases of them were autopsied at this institute. At autopsy, the digestive tract including rectum, colon and small intestine revealed hemorrhagic necrosis with multiple area of perforation. Because these were the first proved cases that the liquid lye was used as enema solution, we report here.
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Álcalis , Autopsia , Colon , Corrosión , Ingestión de Alimentos , Enema , Tracto Gastrointestinal , Intestino Delgado , Lejía , Necrosis , Intoxicación , RectoRESUMEN
Upper gastrointestinal (UGI) hemorrhage remains one of the more common cause of emergency hospital admissions. The majority of patients with ulcer bleeding will not have recurrent bleeding, but 25% of patients will have recurrent or continuous bleeding and require further therapy. Endoscopy is the preferred investigative procedure for UGI bleeding because of its accuracy and low complication rate. Although no study has clearly demonstrated improved mortality rates attributable specifically to the use of endoscopy, it is likely that improved therapeutic outcome lags behind diagnostic advances. All of these 4 patients died eventually due to the massive UGI bleeding in hospital and autopsy was done between September, 1997. and May, 1998. in National Institute of Scientific Investigation (NISI). Despite major advances in diagnostic and therapeutic capabilities, mortality from this often devastating condition remains unacceptably high. The optimal balance between operative and non-operative therapy has yet to be determined. So the close cooperation between internist and surgeon is required.