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PURPOSE: To evaluate the blood glucose and renal function, determine the prevalence of hyperglycemia/diabetes mellitus (DM) and renal disease (nephropathy), and investigate the association between hyperglycemia/DM and renal disease in patients with viral hepatitis (VH). PATIENTS AND METHODS: A total of 491 subjects were included in the study. Patients with VH were further divided into the hepatitis B virus (HBV) infection, hepatitis C virus (HCV) infection, and HBV-HCV co-infection subgroups. Fasting blood glucose, glycated hemoglobin (HbA1c), glycated albumin (GA), glutamic oxaloacetic transaminase (GOT), creatinine (Cr), and cystatin C (Cys C) levels were measured. Urine microalbumin levels were also assessed. Formulas for estimated average glucose calculated using glycated albumin(eAG(GA)), estimated average glucose calculated using HbA1c (eAG(HbA1c)), and estimated glomerular filtration rate calculated using cystatin C (eGFRcys) were used to evaluate the average glucose and renal function. RESULTS: The prevalence of hyperglycemia/DM and renal disease was significantly higher in the VH group, especially in the HCV subgroup. The prevalence of renal disease was significantly higher in patients with VH with eAG(GA) ≥200 mg/dL. CONCLUSION: Our study used multiple parameters to evaluate blood glucose and renal function in patients with VH and found that hyperglycemia/DM and renal disease are closely associated with VH, especially in subjects with HCV infection. Patients with VH, especially those with HCV infection and hyperglycemia/DM, were particularly vulnerable to renal disease.
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BACKGROUND: Resistin, adipocyte-secreting adipokine, may play critical role in modulating cancer pathogenesis. The aim of this study was to investigate the effects of resistin on HCC adhesion to the endothelium, and the mechanism underlying these resistin effects. METHODS: Human SK-Hep1 cells were used to study the effect of resistin on intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expressions as well as NF-κB activation, and hence cell adhesion to human umbilical vein endothelial cells (HUVECs). 5-Aminoimidazole-4-carboxamide 1-ß-D-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, was used to determine the regulatory role of AMPK on HCC adhesion to the endothelium in regard to the resistin effects. RESULTS: Treatment with resistin increased the adhesion of SK-Hep1 cells to HUVECs and concomitantly induced NF-κB activation, as well as ICAM-1 and VCAM-1 expressions in SK-Hep1 cells. Using specific blocking antibodies and siRNAs, we found that resistin-induced SK-Hep1 cell adhesion to HUVECs was through NF-κB-regulated ICAM-1 and VCAM-1 expressions. Moreover, treatment with AICAR demonstrated that AMPK activation in SK-Hep1 cells significantly attenuates the resistin effect on SK-Hep1 cell adhesion to HUVECs. CONCLUSIONS: These results clarify the role of resistin in inducing HCC adhesion to the endothelium and demonstrate the inhibitory effect of AMPK activation under the resistin stimulation. Our findings provide a notion that resistin play an important role to promote HCC metastasis and implicate AMPK may be a therapeutic target to against HCC metastasis.
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Proteínas Quinasas Activadas por AMP/metabolismo , Carcinoma Hepatocelular/enzimología , Adhesión Celular/fisiología , Neoplasias Hepáticas/enzimología , Resistina/fisiología , Adhesión Celular/efectos de los fármacos , Activación Enzimática/efectos de los fármacos , Activación Enzimática/fisiología , Células Endoteliales de la Vena Umbilical Humana/efectos de los fármacos , Células Endoteliales de la Vena Umbilical Humana/enzimología , HumanosRESUMEN
Acute porphyrias are rare diseases with varying incidences worldwide. These diseases are disorders of heme biosynthesis characterized by acute attacks of neurological symptoms. Acute porphyria should be considered in patients with unexplained abdominal pain or neurological damage. Clinical manifestations of acute porphyria are nonspecific and are associated with multiple organ systems. This report examines a rare case of an uncommon type of acute porphyria in a patient with an initial presentation of abdominal pain and progressive polyneuropathy.
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Appendicitis is the most common abdominal disease that requires surgery in the emergency ward. It usually presents as right lower quadrant pain, but may rarely present as left upper quadrant (LUQ) pain due to congenital anatomical abnormalities of the intestine. We report a patient who complained of persistent LUQ abdominal pain and was finally diagnosed by computed tomography (CT) as congenital intestinal malrotation complicated with acute appendicitis. It is important to include acute appendicitis in the differential diagnosis of patients who complain of LUQ abdominal pain. Abdominal CT can provide significant information that is useful in preoperative diagnosis and determination of proper treatment.
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Hyoscine N-butyl bromide, also known as scopolamine, is a type of antimuscarinic agent. This drug is associated with numerous common side effects, including abdominal fullness, constipation, urinary retention, blurred vision, skin flushing, tachycardia, decreased sweating, and salivation. The most unfavorable side effect is hemodynamic instability. In the present case, hypotension and acute myocardial infarction developed after intravenous hyoscine injection as a premedication therapy for colonoscopy. It was difficult to differentiate the cause-effect relationship between myocardial infarction and hypotension. Because both conditions were present under drug effects, we considered 2 possible diagnoses. One was coronary spasm with cardiogenic shock, and the other was myocardial ischemic sequela due to shock status. The latter diagnosis was confirmed after a series of examinations.
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Systemic lupus erythematosus (SLE) is a systemic autoimmune disorder with involvement of multiple organs. Various forms of serositis, including pleural effusion, pericardial effusion, and ascites, may be found during the course of SLE. Peritoneal involvement by ascites is common in the initial presentation of SLE. However, chylous ascites is uncommon in SLE patients. Here, we describe a 93-year-old female with initial presentation of chylous ascites during SLE flares. Marked distention and an ovoid shape of the abdomen were observed. Shifting dullness and central tympanic sounds were found on percussion. Rales were heard in bilateral breathing sounds, multiple oral ulcers appeared in the oral cavity, and chest images showed bilateral pleural effusion. Abdominal sonography revealed moderate ascites and pleural effusion. Neither organisms nor malignant cells were revealed in the culture or cytology of ascites and pleural effusion. The diagnosis of SLE was arrived at by positive antinuclear antibody (ANA), discoid rash, oral ulcers, serositis (pleural effusion and ascites), and proteinuria. The patient received intravenous methylprednisolone 250 mg/day for three days. The pleural effusion resolved dramatically after steroid therapy and abdominal distention related to ascites formation subsided obviously.
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Both the urokinase-type plasminogen activator (uPA) and the uPA receptor (uPAR) play important roles with regard to hepatocellular carcinoma (HCC) progression and metastasis. Notably, the stromal cell-derived factor-1 (SDF-1) is an important chemokine involved in HCC pathology. However, the influence of uPA on SDF-1 expression in human HCC cells remains unknown. We investigated the mechanisms underlying the modulation of SDF-1 expression through uPA stimulation in human HCC SK-Hep-1 cells. SK-Hep-1 cells stimulation with uPA induced increases in the expression and secretion of SDF-1. By using specific inhibitors and small interfering RNA, we have demonstrated that the activation of extracellular signal-related kinase (ERK) and c-Jun-NH(2)-terminal kinase (JNK) pathways are critical for uPA-induced SDF-1 expression. Transcription factor ELISA and chromatin immunoprecipitation assays suggest that uPA increase Sp1- and AP-1-DNA-binding activities in SK-Hep-1 cells. Inhibition of Sp1 and AP-1 activations by specific siRNAs blocked the uPA-induced SDF-1 promoter activity and expression. The effect of uPA on SK-Hep-1 signaling and SDF-1 expression is mediated by uPAR. In summary, our findings serve to elucidate the uPA/uPAR downstream signaling, providing new insight into the function of uPA in HCC cells.
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Carcinoma Hepatocelular/metabolismo , Quimiocina CXCL12/metabolismo , Regulación Neoplásica de la Expresión Génica/fisiología , Neoplasias Hepáticas/metabolismo , Activador de Plasminógeno de Tipo Uroquinasa/farmacología , Línea Celular Tumoral , Quimiocina CXCL12/genética , Quinasas MAP Reguladas por Señal Extracelular/genética , Quinasas MAP Reguladas por Señal Extracelular/metabolismo , Regulación Enzimológica de la Expresión Génica/fisiología , Humanos , MAP Quinasa Quinasa 4/genética , MAP Quinasa Quinasa 4/metabolismo , Fosforilación , Regiones Promotoras Genéticas , Interferencia de ARN , ARN Interferente Pequeño , Receptores del Activador de Plasminógeno Tipo Uroquinasa/metabolismo , Transducción de SeñalRESUMEN
CONTEXT: Tournefortia sarmentosa Lam. (Boraginaceae), a Chinese herbal medicine, is commonly used as a detoxicant or anti-inflammatory agent. OBJECTIVE: As acetaminophen (APAP) is a well-known hepatotoxin, we investigated the effect of the aqueous extract of the T. sarmentosa on APAP-induced hepatotoxicity in vivo and in vitro. MATERIALS AND METHODS: Levels of liver function markers serum glutamate oxaloacetate transaminase (SGOT), glutamate pyruvate transaminase (SGPT), and alkaline phosphatase (ALP), inflammatory markers tumor necrosis factor (TNF)-α, interleukin (IL)-1b, and IL-6 in serum, and antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), as well as lipid peroxidation were determined. RESULTS: T. sarmentosa significantly reduced the elevated liver function (SGOT, SGPT, and ALP, p < 0.01) and inflammatory markers (TNF-α, IL-1ß, and IL-6, p < 0.01) in serum of APAP-intoxicated rats. Malondialdehyde level (p < 0.05) and antioxidant enzyme levels (CAT, SOD, and GPx, p < 0.05) were also reduced in APAP-intoxicated rats treated with T. sarmentosa. Incubation of rat hepatocyte cell line clone-9 cells with APAP reduced cell viability and increased the extent of lipid peroxidation. APAP stimulation also reduced the level of glutathione (GSH) and caused reduction in the activities of the antioxidant enzymes, CAT, SOD, and GPx. Pretreatment of hepatocytes with T. sarmentosa aqueous extract before and during APAP stimulation attenuated the extent of lipid peroxidation, increased cell viability and GSH level, and enhanced the activities of antioxidant enzymes. DISCUSSION AND CONCLUSION: These data suggest that the aqueous extract of T. sarmentosa can prevent APAP-induced hepatotoxicity.
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Acetaminofén/toxicidad , Boraginaceae/química , Enfermedad Hepática Inducida por Sustancias y Drogas/prevención & control , Extractos Vegetales/farmacología , Analgésicos no Narcóticos/toxicidad , Animales , Antioxidantes/metabolismo , Línea Celular , Supervivencia Celular/efectos de los fármacos , Enfermedad Hepática Inducida por Sustancias y Drogas/patología , Hepatocitos/efectos de los fármacos , Hepatocitos/patología , Técnicas In Vitro , Peroxidación de Lípido/efectos de los fármacos , Pruebas de Función Hepática , Masculino , Medicina Tradicional China , Estrés Oxidativo/efectos de los fármacos , Ratas , Ratas WistarRESUMEN
Internal hernia is an unusual cause of intestinal obstruction, and the through sites of hernias may include the paraduodenum, transmesenteric region, foramen of Winslow, paracecum, the broad ligament of the uterus, and the transomental region. Transomental hernia is the rarest type of internal hernia and accounts for fewer than 1% of internal hernias. Transmesenteric and transomental hernias are different from the other types of internal hernia, and usually present acute intestinal obstruction with strangulation of the small bowel. We report a 74-year-old male with initial manifestation of peritonitis. Internal hernia-induced intestinal obstruction with strangulation was highly suspected from the image study. After an urgent exploratory laparotomy, transomental hernia was diagnosed.
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Hernia Abdominal/diagnóstico por imagen , Obstrucción Intestinal/diagnóstico por imagen , Epiplón , Tomografía Computarizada por Rayos X , Anciano , Diagnóstico Diferencial , Hernia Abdominal/complicaciones , Hernia Abdominal/cirugía , Humanos , Obstrucción Intestinal/etiología , Obstrucción Intestinal/cirugía , MasculinoRESUMEN
Berberine is the major constituent of Coptidis Rhizoma with multiple pharmacological activities, including anti-inflammation, promotion of apoptosis and anticancer potential effect. Mitogen-activated protein kinase (MAPK) and reactive oxygen species (ROS) may contribute to the causal relationship between tumorigenesis and pro-apoptotic function. Berberine is studied for the mechanism of its action in apoptotic pathway in human colonic carcinoma cell. Treatment of SW620 cells with 50 microM berberine resulted in activation of the caspase 3 and caspase 8, cleavage of poly ADP-ribose polymerase (PARP) and the release of cytochrome c; whereas, the expression of BID and anti-apoptosis factor c-IAP1, Bcl-2, and Bcl-(XL) were decreased markedly. Berberine-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of JNK and p38 MAPK, as well as generation of the ROS. Furthermore, the induction of apoptosis was alleviated by inhibitors specific for JNK and p38. In addition, there was an increase in the cellular levels of phospho-c-Jun, FasL and t-BID in the berberine-induced apoptosis via the activation of JNK and p38 signaling modules. NAC administration, a scavenger of ROS, reversed berberine-induced apoptosis effects via inhibition of JNK, p38 and c-jun activation, and FasL and t-BID expression. These results leads us to speculate that berberine may play an apoptotic cascade in SW620 cells by activation of the JNK/p38 pathway and induction of ROS production, providing a new mechanism for berberine-induced cell death in human colon cancer cells.