Platycodin D Reverses Pathological Cardiac Hypertrophy and Fibrosis in Spontaneously Hypertensive Rats.

Platycodin D (PD) is the main active saponin isolated from Platycodon grandiflorum (PG) and is reported to exhibit anticancer, anti-angiogenic, anti-inflammation and anti-obesity biological effects. The current study aims to evaluate the therapeutic efficacy of PD in cardiac fibrosis and for hypertrophy in spontaneous hypertension rats (SHRs) and to verify inhibition of the signaling pathway. Significant increases in the cardiac functional indices of left ventricular internal diameter end diastole (LVIDd) and left ventricular internal diameter end systole (LVIDs); the eccentric hypertrophy marker p-MEK5; concentric hypertrophy markers, such as CaMKII[Formula: see text] and calcineurin; and expression levels of NFATc3, p-GATA4 and BNP were observed in spontaneously hypertensive groups. PD treatment reversed these increases in SHRs. In addition, an increase in the fibrosis markers FGF2, uPA, MMP2, MMP9, TGF[Formula: see text]-1 and CTGF during cardiac hypertrophy was detected by western blotting analyses. These results demonstrated that PD treatment considerably attenuates cardiac fibrosis. Histopathological examination revealed that PD treatment remarkably reduced collagen accumulation in contrast to spontaneously hypertensive groups. This study clearly suggests that PD provides myocardial protection by alleviating two damaging responses to hypertension, fibrosis and hypertrophy, in the heart.

Effects of garlic oil on interleukin-6 mediated cardiac hypertrophy in hypercholesterol-fed hamsters.

Hypercholesterol diets are the major causes of cardiac hypertrophy and various cardiac disorders. The purpose of this study is to evaluate the effects of garlic oil on cardiac hypertrophy induced by hypercholesterol diets. Golden Syrian hamsters were fed with 2% cholesterol or 2% cholesterol plus 1% garlic oil for 2 months. Heart architecture changes were measured by hematoxylin-eosin staining and the molecular mechanism was determined by western blotting. Garlic oil reduced whole-heart weight to bone weight ratio, and left ventricle weight to bone weight ratio in the cholesterol-fed group. Moreover, the garlic oil group showed significantly reduced interleukin-6, phosphorylated (p)-extracellular signal-regulated kinase-5, p-mitogen-activated protein kinase-5, calcineurin, nuclear transcription factor of nuclear factor of activated T-cells-3 and p-GATA binding protein 4 when compared with the cholesterol group. However, no changes were observed in gp-130, signal transducer and activator of transcription-3, p-P38 and p-Jun N-terminal kinases protein levels in all groups. The results show that garlic oil may be useful in the treatment of hypertrophy-associated cardiovascular diseases.

Garlic oil attenuates the cardiac apoptosis in hamster-fed with hypercholesterol diet.

Hypercholesterolemia is a well established risk factor for cardiac cell apoptosis. The purpose of this study is to evaluate the effects of garlic oil on cardiac apoptosis induced by a hypercholesterol diet. Twenty-four male Golden-Syrian hamsters at 3 months of age were randomly divided into three groups, control, cholesterol and garlic oil groups received a chow diet, chow diet with 2% cholesterol, and chow diet with 2% cholesterol and 1% garlic oil for 8 weeks, respectively. The TUNEL-positive apoptotic cells, and several apoptotic proteins were significantly induced in the excised left ventricle in cholesterol group, whereas significant reduction was observed in cholesterol plus garlic oil group. The IGFI receptor dependent survival pathway was inhibited in cholesterol group whereas it was obviously reversed in cholesterol plus garlic oil group. Our results suggest that administration of garlic oil shows protective effects on cardiac apoptosis in rats with high cholesterol intake.

Ameliorate Effects of Li-Fu Formula on IL-6-Mediated Cardiac Hypertrophy in Hamsters Fed with a Hyper-Cholesterol Diet.

Hypercholesterolemia diets are considered as major sources to cause cardiac hypertrophy. This study intends to evaluate the effects of Li-Fu formula on cardiac hypertrophy induced by hypercholesterolemia diet. Twenty-four male Golden Syrian hamsters were randomly divided into control, cholesterol and Li-Fu formula groups and fed with different experimental diets for 2 months. Histopathological analysis and western blotting were performed to measure the myocardial architecture, and various cardiac hypertrophy-associated molecules in the excised left ventricle from hamsters. The ratios of whole heart weight/body weight (BW) and left ventricle weight/BW were significantly higher in the cholesterol group but significantly lower in the Li-Fu formula group. The protein levels of both atrial natriuretic peptide and brain natriuretic peptide were significantly increased in the cholesterol group but significantly reduced in the Li-Fu formula group. Additionally, significantly increased interleukin-6, STAT3, MEK5, p-ERK5 and non-cardiomyocyte proliferate signal molecules such as p-MEK and p-ERK, were detected in the cholesterol group but significantly reduced in the Li-Fu formula group. Notably, no significant variations of inflammatory signaling molecules, including p-P38 and p-JNK, were detected in all groups. Our experimental results demonstrated the significant reductions of cardiac hypertrophy and related eccentric hypertrophy signaling, non-cardiomyocyte proliferate signaling in the excised left ventricle of hamsters from the Li-Fu formula. We suggested the protective effects of Li-Fu formula on cardiac hypertrophy that may be useful in prevention or treatment of hypertrophy-associated cardiovascular diseases.

Dilong: role in peripheral nerve regeneration.

Dilong, also known as earthworm, has been widely used in traditional Chinese medicine (TCM) for thousands of years. Schwann cell migration and proliferation are critical for the regeneration of injured nerves and Schwann cells provide an essentially supportive role for neuron regeneration. However, the molecular mechanisms of migration and proliferation induced by dilongs in Schwann cells remain unclear. Here, we discuss the molecular mechanisms that includes (i) migration signaling, MAPKs (mitogen-activated protein kinases), mediated PAs and MMP2/9 pathway; (ii) survival and proliferative signaling, IGF-I (insulin-like growth factor-I)-mediated PI3K/Akt pathways and (iii) cell cycle regulation. Dilong stimulate RSC96 cell proliferation and migration. It can induce phosphorylation of ERK1/2 and p38, but not JNK, and activate the downstream signaling expression of PAs (plasminogen activators) and MMPs (matrix metalloproteinases) in a time-dependent manner. In addition, Dilong stimulated ERK1/2 and p38 phosphorylation was attenuated by pretreatment with chemical inhibitors (U0126 and SB203580), and small interfering ERK1/2 and p38 RNA, resulting in migration and uPA-related signal pathway inhibition. Dilong also induces the phosphorylation of IGF-I-mediated PI3K/Akt pathway, activates protein expression of PCNA (proliferating cell nuclear antigen) and cell cycle regulatory proteins (cyclin D1, cyclin E and cyclin A) in a time-dependent manner. In addition, it accelerates G(1)-phase progression with earlier S-phase entry and significant numbers of cells entered the S-phase. The siRNA-mediated knockdown of PI3K that significantly reduces PI3K protein expression levels, resulting in Bcl(2) survival factor reduction, revealing a marked blockage of G(1) to S transition in proliferating cells. These results reveal the unknown RSC96 cell migration and proliferation mechanism induced by dilong, which find use as a new medicine for nerve regeneration.

IGF-II and MMP9 as surgical repair indicators of ventricular septal defects.

OBJECTIVE: The insulin-like growth factor-I (IGF-I), insulin-like growth factor binding protein-3 (IGFBP-3) and human growth hormone (h-GH) have been recognized as therapeutic targets for the heart disease therapy. The bioavailability and actions of insulin-like growth factors-II (IGF-II) and matrix metalloproteinase-9 (MMP9) are important for embryonic development and cardiomyocyte differentiation as well. However, the clinical manifestations following the change in the serum IGF-II and MMP9 in infants with isolated ventricular septal defect (VSD) undergoing surgical repair have not been clearly defined. STUDY DESIGN: Serum samples were collected from 72 infants: Twenty normal infants (group I) and 51 consecutive infants with echocardiography established isolated VSD (aged from 3 months to 1 year) were investigated. Among the 51 infants with VSD, 28 with shunt fraction, Qp/Qs < or = 1.5 were free of congestive heart failure symptoms (group II); 23 with shunt fraction, Qp/Qs > or = 2.0 were in congestive heart failure (group IIIa); and 23 of these 23 infants had undergone VSD repair 6 months before their second study (group IIIb). All insulin-like growth factors-II (IGF-II) and human growth hormone (h-GH), insulin like growth factor binding protein-3 (IGFBP-3) and its specific serum protease-MMP9 concentration were analyzed using ELISA and zymography, respectively. RESULTS: Serum IGF-II and MMP9 exhibited significant decreasing trends among the three groups and significantly lower concentrations of IGF-II, IGF-II/IGFBP-3 ratio and MMP9, were found only in the severe group whereas h-GH/IGF-II ratio became significantly higher in this group. Moreover, there were no significant differences in these parameters between the infants after surgical correction and the normal ones. CONCLUSIONS: The improvement in IGF-II and MMP9 serum concentration was identified in infants with VSD after surgical repair. These findings also indicate a significant relationship between IGF-II, MMP9 and VSD which might be used as diagnosis and prognosis indicators for this defect. Slight reductions in IGF-II/IGFBP3 ratio and slight increase in the h-GH/IGF-II ratio indicate mild VSD. The reductions in the MMP9, IGF-II, and IGF-II/IGFBP3 ratio plus high increase in the h-GH/IGF-II ratio indicate severe VSD.

Carthamus tinctorius L. prevents LPS-induced TNFalpha signaling activation and cell apoptosis through JNK1/2-NFkappaB pathway inhibition in H9c2 cardiomyoblast cells.

AIM OF THE STUDY: Severe and potentially fatal hypotension and cardiac contractile dysfunction are common symptoms in patients with sepsis. In our previous study, we found that estradiol and estrogen-receptor alpha have cardio-protective effects in myocardial cells exposed to LPS. Estradiol supplementation has been shown to induce breast and cervical cancers. Flos Carthami, the flower of Carthamus tinctorius L. (Compositae) is an important traditional Chinese medicine used for the treatment of heart disease and inflammation, and therefore might be a potential alternative to Estradiol in the prevention of heart damage. This study investigated the effect of Flos Carthami (FC(EtOH)) ethanolic extract on LPS-induced apoptosis in H9c2 cardiomyoblast cells. MATERIALS AND METHODS: H9c2 cells induced apoptosis with LPS administration (1 microg/mL). H9c2 cells were divided into five groups: Control, LPS (1 microg/mL), and three FC(EtOH) (31.25, 62.5,and 125 microg/mL). We detected apoptosis using MTT, LDH, TUNEL assay. JC-1 staining and Western blot were used to detect pro-apoptosis proteins, anti-apoptosis proteins, MAPK proteins (JNK, ERK, and P38), and NFkappaB expression. RESULTS: FC(EtOH) (62.5 microg/mL) inhibited LPS-induced apoptosis by suppressing JNK1/2 activity, which resulted in the reduction of both IkappaB degradation and NFkappaB activation. In addition, FC(EtOH) led to the activation of anti-apoptotic proteins, Bcl-2 and Bcl-xL, the stabilization of the mitochondria membrane and the down-regulation of extrinsic and intrinsic pro-apoptotic proteins, such as TNFalpha, active caspase-8, t-Bid, Bax, active caspases-9, and -3. CONCLUSIONS: Carthamus tinctorius L. possesses the ability to suppress JNK activity and inhibit LPS-induced TNFalpha activation and apoptosis in H9c2 cardiomyoblast cells. Carthamus tinctorius L could potentially serve as a cardio-protective agent against LPS-induced apoptosis.

Multi Groups Cooperation based Symbiotic Evolution for TSK-type Neuro-Fuzzy Systems Design.

In this paper, a TSK-type neuro-fuzzy system with multi groups cooperation based symbiotic evolution method (TNFS-MGCSE) is proposed. The TNFS-MGCSE is developed from symbiotic evolution. The symbiotic evolution is different from traditional GAs (genetic algorithms) that each chromosome in symbiotic evolution represents a rule of fuzzy model. The MGCSE is different from the traditional symbiotic evolution; with a population in MGCSE is divided to several groups. Each group formed by a set of chromosomes represents a fuzzy rule and cooperate with other groups to generate the better chromosomes by using the proposed cooperation based crossover strategy (CCS). In this paper, the proposed TNFS-MGCSE is used to evaluate by numerical examples (Mackey-Glass chaotic time series and sunspot number forecasting). The performance of the TNFS-MGCSE achieves excellently with other existing models in the simulations.

Role of ERK signaling in the neuroprotective efficacy of magnesium sulfate treatment during focal cerebral ischemia in the gerbil cortex.

Magnesium sulfate (MgSO4) ameliorates focal ischemia-induced neuronal death in the rat and gerbil models. However, the molecular mechanisms for this neuroprotection are not known. Focal cerebral ischemia was produced by unilateral occlusion of the right common carotid artery and the right middle cerebral artery (CCAO + MCAO) for 30 min or 60 min. Treatment with MgSO4 significantly increased the level of mitogen-activated protein kinase/extra-cellular signal-regulated kinase kinase 1/2 (MEK1/2), extra-cellular signal-regulated kinase 1/2 (ERK1/2), cyclic-AMP response element binding protein (CREB) phosphorylation and the anti-apoptotic protein Bcl-2 both in the non-ischemic (contralateral) and ischemic (ipsilateral) cortex. However, these effects were reversed by administration of U0126, a MEK kinase inhibitor. In the ipsilateral cortex, a significant increase in the level of the proapoptotic proteins Bax, Bad, BNIP3 and activated caspase 3 were detected at the end of focal ischemia compared to the non-ischemic cortex. Treatment of MgSO4 prevented these ischemia-induced activations of the death cascade. Collectively, these data indicate that the ERK-CREB-Bcl-2 signaling pathway might be involved in MgSO4-induced neuroprotection following focal ischemia. Moreover, MgSO4 treatment also resulted in a reduction in pro-apoptotic proteins. These results enhance our understanding on the role of MgSO4 in treating cerebral ischemia.

Proliferative effects of Chishao on Schwann cells are FGF-uPA, and ERK- and JNK-dependent.

This study evaluated the proliferative effects of chishao on RSC96, Schwann cells. A dose-dependent proliferative effect of chishao was obtained by methylthiazol tetrazolium (MTT), proliferating cell nuclear antigen (PCNA) Western blotting, and wound healing assays in Schwann cells administered with chishao (0-500 mg/ml), except at 500 mg/ml concentration. The chishao-treated cells also showed a dose-dependent activated fibroblast growth factor-2 (FGF-2) signaling with increased urokinase plasminogen activator (uPA) and decreased plasminogen activator inhibitor-1 (PAI-1), enhanced proliferative proteins, extracellular signal regulated kinase (ERK) and c-Jun N-terminal kinase (JNK)-signaling. Using mitogen-actvated protein kinase (MAPK)-signaling chemical inhibitors, U0126, SB203580, and SP600125, the proliferative effects of chishao on RSC cells were identified to be ERK- and JNK- signaling dependent. Based on the results, applying appropriate doses of chishao to Schwann cells would be a potential approach for enhancing neuron regeneration.

Reappraisal of the management and outcome of emphysematous pyelonephritis.

This study compared the management, prognostic factors and outcomes of patients with emphysematous pyelonephritis (EPN). Twenty-one patients with EPN were studied between September 1996 and August 2005, and were assigned to two groups. Patients in Group 1 received conservative treatment with/without percutaneous catheter drainage (PCD) while patients in Group 2 underwent nephrectomy following medical treatment and PCD. A post hoc analysis of the prognostic factors was performed between survivors and nonsurvivors, and between the survivors in Group 1 and Group 2. There were 14 patients in Group 1, and seven in Group 2. The mortality in Group 1 was 35.7% (5/14) and in Group 2 was 0% (p = 0.12). There were no statistically significant differences in prognostic factors between the two groups, though patients in Group 1 had relatively lower platelet counts (p = 0.07) and Group 2 patients had a higher incidence of dialysis after nephrectomy (p = 0.03). Comparing the survivors and nonsurvivors, patients with comorbid congestive heart failure and patients initially presenting with consciousness disturbances had higher mortalities (p = 0.02 and p < 0.01, respectively). Nonsurvivors also had lower platelet counts (p = 0.06). In conclusion, medical treatment with/without PCD can be used to manage patients with EPN. More agressive drainage is needed in patients with congestive heart failure who initially present with consciousness disturbances or thrombocytopenia.

Lipopolysaccharide upregulates uPA, MMP-2 and MMP-9 via ERK1/2 signaling in H9c2 cardiomyoblast cells.

Upregulation of urokinase plasminogen activator (uPA), tissue plasminogen activator (tPA), and matrix metallopeptidases (MMPs) is associated with the development of myocardial infarction (MI), dilated cardiomyopathy, cardiac fibrosis, and heart failure (HF). Evidences suggest that lipopolysaccharide (LPS) participates in the inflammatory response in the cardiovascular system; however, it is unknown if LPS is sufficient to upregulate expressions and/or activity of uPA, tPA, MMP-2, and MMP-9 in myocardial cells. In this study, we treated H9c2 cardiomyoblasts with LPS to explore whether LPS upregulates uPA, tPA, MMP-2, and MMP-9, and further to identify the precise molecular and cellular mechanisms behind this upregulatory responses. Here, we show that LPS challenge increased the protein levels of uPA, MMP-2 and MMP-9, and induced the activity of MMP-2 and MMP-9 in H9c2 cardiomyoblasts. However, LPS showed no effects on the expression of tissue inhibitor of metalloproteinase-1, -2, -3, and -4 (TIMP-1, -2, -3, and -4). After administration of inhibitors including U0126 (ERK1/2 inhibitor), SB203580 (p38 MAPK inhibitor), SP600125 (JNK1/2 inhibitor), CsA (calcineurin inhibitor), and QNZ (NFkappaB inhibitor), the LPS-upregulated expression and/or activity of uPA, MMP-2, and MMP-9 in H9c2 cardiomyoblasts are markedly inhibited only by ERK1/2 inhibitors, U0126. Collectively, these results suggest that LPS upregulates the expression and/or activity of uPA, MMP-2, and MMP-9 through ERK1/2 signaling pathway in H9c2 cardiomyoblasts. Our findings further provide a link between the LPS-induced cardiac dysfunction and the ERK1/2 signaling pathway that mediates the upregulation of uPA, MMP-2 and MMP-9.

ZAK induces MMP-2 activity via JNK/p38 signals and reduces MMP-9 activity by increasing TIMP-1/2 expression in H9c2 cardiomyoblast cells.

Leucine-zipper and sterile-alpha motif kinase (ZAK) is the key intra-cellular mediator protein in cardiomyocyte hypertrophy induction by transforming growth factor beta 1 (TGF-beta1) which has also been identified as a profibrotic cytokine involved in cardiac fibrosis progression. We hypothesized whether ZAK over-expression causes cardiac scar formation due to the extra-cellular matrix (ECM) degraded enzyme regulation in this paper. Using immuno-histochemical analysis of the human cardiovascular tissue array, we found a positively significant association between ZAK over-expression and myocardial scars. ZAK over-expression in H9c2 cardiomyoblast cells increases the metalloproteinase tissue inhibitor 1/2 (TIMP-1/2) protein level, which reduces matria metalloproteinase-9 (MMP-9) activity and also activates c-JNK N-terminal kinase 1/2 (JNK1/2) and p38 signaling, which induces MMP-2, possibly resulting in cardiac fibrosis. Taken together, ZAK activity inhibition may be a good strategy to prevent the cardiac fibrosis progression.

Iron status and cardiovascular risk factors in patients with haemodialysis versus patients with ischaemic heart disease.

AIM: The study aimed to investigate whether imbalanced iron status in patients with haemodialysis coexisted with abnormal lipid profile, higher inflammatory status and altered growth hormone-insulin-like growth factor (GH-IGF)-I axis and to compare these biochemical markers with patients with ischaemic heart disease. METHODS: Serum samples for biochemical and immunological analyses were collected from 74 normal subjects, 138 patients with ischaemic heart disease (IHD) and 115 patients on haemodialysis (HD). RESULTS: Compared with normal subjects, lower serum iron, lower total iron-binding capacity (TIBC) and higher ferritin in HD patients coexisted with decreases in high-density lipoprotein cholesterol and total bilirubin as well as increases in lactate dehydrogenase (LDH), interleukin (IL)-6, C-reactive protein (CRP) and IL-10. Decreased IGF-I and increased GH were found in HD patients whereas unchanged GH-IGF axis were found in IHD patients. Compared with IHD, much higher ferritin, lower TIBC, lower bilirubin and higher LDH levels were found in HD patients. CONCLUSION: Imbalanced iron status in patients on HD coexisted with abnormal lipid profiles, increased anaerobic activity and higher inflammatory status, which suggests that imbalanced iron status in HD patients may play a deleterious role in cardiovascular pathophysiology. Altered GH-IGF axis found in HD patients was more obvious than in IHD patients. This may imply that the GH-IGF axis system is modulated or adapted by HD.

IGF-II/mannose-6-phosphate receptor signaling induced cell hypertrophy and atrial natriuretic peptide/BNP expression via Galphaq interaction and protein kinase C-alpha/CaMKII activation in H9c2 cardiomyoblast cells.

The role played by IGF-II in signal transduction through the IGF-II/mannose-6-phosphate receptor (IGF2R) in heart tissue has been poorly understood. In our previous studies, we detected an increased expression of IGF-II and IGF2R in cardiomyocytes that had undergone pathological hypertrophy. We hypothesized that after binding with IGF-II, IGF2R may trigger intracellular signaling cascades involved in the progression of pathologically cardiac hypertrophy. In this study, we used immunohistochemical analysis of the human cardiovascular tissue array to detect expression of IGF2R. In our study of H9c2 cardiomyoblast cell cultures, we used the rhodamine phalloidin staining to measure the cell hypertrophy and western blot to measure the expression of cardiac hypertrophy markers atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in cells treated with IGF-II. We found that a significant association between IGF2R overexpression and myocardial infarction. The treatment of H9c2 cardiomyoblast cells with IGF-II not only induced cell hypertrophy but also increased the protein level of ANP and BNP. Using Leu27IGF-II, an analog of IGF-II which interacts selectively with the IGF2R, to specifically activate IGF2R signaling cascades, we found that binding of Leu27IGF-II to IGF2R led to an increase in the phosphorylation of protein Kinase C (PKC)-alpha and calcium/calmodulin-dependent protein kinase II (CaMKII) in a Galphaq-dependent manner. By the inhibition of PKC-alpha/CaMKII activity, we found that IGF-II and Leu27IGF-II-induced cell hypertrophy and upregulation of ANP and BNP were significantly suppressed. Taken together, this study provides a new insight into the effects of the IGF2R and its downstream signaling in cardiac hypertrophy. The suppression of IGF2R signaling pathways may be a good strategy to prevent the progression of pathological hypertrophy.

Lipopolysaccharide induces cellular hypertrophy through calcineurin/NFAT-3 signaling pathway in H9c2 myocardiac cells.

Evidences suggest that lipopolysaccharide (LPS) participates in the inflammatory response in the cardiovascular system; however, it is unknown if LPS is sufficient to cause the cardiac hypertrophy. In the present study, we treated H9c2 myocardiac cells with LPS to explore whether LPS causes cardiac hypertrophy, and to identify the precise molecular and cellular mechanisms behind hypertrophic responses. Here we show that LPS challenge induces pathological hypertrophic responses such as the increase in cell size, the reorganization of actin filaments, and the upregulation of hypertrophy markers including atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in H9c2 cells. LPS treatment significantly promotes the activation of GATA-4 and the nuclear translocation of NFAT-3, which act as transcription factors mediating the development of cardiac hypertrophy. After administration of inhibitors including U0126 (ERK1/2 inhibitor), SB203580 (p38 MAPK inhibitor), SP600125 (JNK1/2 inhibitor), CsA (calcineurin inhibitor), FK506 (calcineurin inhibitor), and QNZ (NFkappaB inhibitor), LPS-induced hypertrophic characteristic features, such as increases in cell size, actin fibers, and levels of ANP and BNP, and the nuclear localization of NFAT-3 are markedly inhibited only by calcineurin inhibitors, CsA and FK506. Collectively, these results suggest that LPS leads to myocardiac hypertrophy through calcineurin/NFAT-3 signaling pathway in H9c2 cells. Our findings further provide a link between the LPS-induced inflammatory response and the calcineurin/NFAT-3 signaling pathway that mediates the development of cardiac hypertrophy.

Emergency department response to SARS, Taiwan.

How emergency departments of different levels and types cope with a large-scale contagious infectious disease is unclear. We retrospectively analyzed the response of 100 emergency departments regarding use of personal protective equipment (PPE) and implementation of infection control measures (ICMs) during the severe acute respiratory syndrome outbreak in Taiwan. Emergency department workers in large hospitals were more severely affected by the epidemic. Large hospitals or public hospitals were more likely to use respirators. Small hospitals implemented more restrictive ICMs. Most emergency departments provided PPE (80%) and implemented ICMs (66%) at late stages of the outbreak. Instructions to use PPE or ICMs more frequently originated by emergency department administrators. The difficulty of implementing ICMs was significantly negatively correlated with their effectiveness. Because ability to prepare for and respond to emerging infectious diseases varies among hospitals, grouping infectious patients in a centralized location in an early stage of infection may reduce the extent of epidemics.

The impact of the SARS outbreak on an urban emergency department in Taiwan.

OBJECTIVE: Emergency departments (ED) were on the front lines for possible cases of transmission during the severe acute respiratory syndrome (SARS) epidemic. The purpose of this study was to investigate the impact of the SARS catastrophe on an urban ED. METHODS: The patients' characteristics in an urban ED were collected from March to May 2003 during the SARS outbreak in Taiwan. The crisis period was divided into 2 periods: 30 days before (period 1) and after (period 2) April 21, the date of the first hospital-associated transmission. Problem severity in the ED and stress levels of ED staff during the SARS catastrophe were rated from mild (1 point) to severe (5 points). RESULTS: The number of ED patients declined 33.4% in period 2. There was a 2.1% (95%CI, 0.4-3.8) increase in the percentage of male patients, a 2.5% (95% CI, 1.5-3.7) increase in percentage of fever (>38 degrees C), and a 4.0% (95% CI, 2.6-5.4%) increase in chief complaint of fever in period 2. The number of nontrauma patients younger than 18 years had declined by 44.5% in period 2. The total charge for reimbursement from an insurance institution declined 21.7%. During the SARS outbreak, the most severe stress experienced by either physicians or nurses occurred during emergency resuscitation (median stress rating point, 4; interquartile range, 1). CONCLUSION: The SARS catastrophe affected the ED visit volume, finances, various patient characteristics, and stress levels in the ED physicians and nurses. EDs must be fully prepared to face the challenges of the next outbreak of SARS or other infectious disease.