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Prevention of patch infection after abdominal external hernia repair

specific mechanism underlying patch infection remains unclear to date because of its complex origin. Factors that increase the risk for patch infection include patients, chronic obstructive pneumonia, diabetes, morbid obesity, malnutrition, history of coronary heart disease, smoking history, immunodeficiencies, and American Society of Anesthesiologists score ≥3 [ 3 , 4 , 5 , 6 ]. In addition, recent studies have discovered other factors related to the occurrence of patch infection. These factors are discussed below. |1 The pore size of the patch material and the

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Research progress on human microecology and infectious diseases

. Ahluwalia et al . [ 22 ] found that intestinal flora is associated with neuronal damage in patients with hepatic encephalopathy, and a model for end-stage liver disease scores in patients with hepatic encephalopathy is negatively correlated with the abundance of intestinal ancestral Lachnospiraceae, rumen family, and Incertae sedis XIV (Spirulina) but is positively correlated with the abundance of the potential pathogenic bacteria Enterococcus . The gut microbiota of patients with associated acute-on-chronic liver failure is significantly imbalanced. 16S rDNA

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Treatment of tuberculosis infection complicated with liver transplant

in the anti-TB treatment. Therefore, anti-TB treatment should be postponed until after the transplant [ 9 , 29 , 30 ]. However, other researchers have different views and maintained that such patients were safe to undergo anti-TB treatment [ 29 , 30 , 31 ]. Singh et al . [ 30 ]. enrolled 18 LTBI patients waiting for liver transplant (average Child–Pugh scoring: 8 points), wherein liver function test results showed that the treatment with isoniazid for 12 months was not significantly different from that of the untreated control group, and the patients did not

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Polymorphisms of AZIN1 rs2679757 and TRPM5 rs886277 are Associated with Cirrhosis Risk in Chinese Patients with Chronic Hepatitis B

2007;46:297-306. 7 Marcolongo M, Young B, Dal Pero F, Fattovich G, Peraro L, Guido M, et al. A seven-gene signature (cirrhosis risk score) predicts liver fibrosis progression in patients with initially mild chronic hepatitis C. Hepatology 2009;50:1038-1044. 8 Curto TM, Lagier RJ, Lok AS, Everhart JE, Rowland CM, Sninsky JJ, et al. Predicting cirrhosis and clinical outcomes in patients with advanced chronic hepatitis C with a panel of genetic markers (CRS7). Pharmacogenet Genomics 2011;21:851-860. 9 Shepard CW, Simard EP

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The Relationship between Intrahepatic Distribution of Hepatitis B Virus Core Antigen and Serum ALT, HBV DNA Levels and HBeAg Status


Objective The clinical significance of differential distribution of hepatitis B virus (HBV) nucleocapsid antigen in hepatocytes remains unknown. The goal of this study is to determine the relationship between distinct HBV core antigen distribution pattern and alanine transaminase (ALT), liver histological inflammatory activity grades, serum HBeAg status and HBV DNA level.

Methods Total of 958 cases with chronic hepatitis B were recruited into this study. Liver function tests, serum HBV DNA level, serological HBV markers and liver immunohistochemistry were examined according to the conventional instructions. Chi Square tests were performed to analyze the differences among these groups.

Results It was found that 552 (58%) cases were tested positive for HBV core antigen by immunohistochemical staining. Cytoplasmic hepatitis B core antigen (HBcAg) expression correlated with ALT level and serum HBV DNA and liver inflammatory activity scores, however, nuclear HBcAg expression in hepatocytes was associated with normal ALT level, lower liver inflammatory activity score and higher serum HBV DNA level and rate of HBeAg positivity. Both nuclear and cytoplasmic HBcAg expression in hepatocytes associated with a middle ALT level and liver inflammatory activity score, higher rate of serum detectable HBeAg and a higher HBV DNA level. However, undetectable core antigen was related to a lower ALT level and histological inflammatory activity grade, lower positive HBeAg rate and HBV DNA level.

Conclusions Undetectable liver HBcAg is associated with HBV clearance, ALT normalization and hepatitis B e antigen (HBeAg) seroconversion, and cytoplasmic HBcAg expression associated with higher hepatic inflammatory activity. However, nuclear HBcAg expression correlates with immune tolerance characterized with normal ALT and lower liver inflammatory activity, higher HBV replication level and higher rate of HBeAg positivity.

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Factors Associated with Death Due to 2009 Influenza A (H1N1) Virus Infection and Acute Respiratory Distress Syndrome in Beijing, 2009 - 2011


Objective Patients with H1N1 virus infection were hospitalized and quarantined, and some of them developed into acute respiratory failure, and were transfered to the medical intensive care unit of Beijing Ditan Hospital, Capital Medical University in Beijing, China.

Methods The clinical features and preliminary epidemiologic findings among 30 patients with confirmed H1N1 virus infection who developed into acute respiratory failure for ventilatory support were investigated.

Results A total of 30 patients (37.43 ± 18.80 years old) with 2009 influenza A (H1N1) related acute respiratory distress syndrome (ARDS) received treatment with mechanical ventilation, 15 cases of whom were male and 17 cases died of ARDS. Fatal cases were significantly associated with an APACHE Ⅱ score (P = 0.016), but not with PaO2/FIO2 (P = 0.912) and chest radiograph (P = 0.333). The most common complication was acute renal failure (n = 9). Five patients received extracorporeal membrane oxygenation (ECMO), 3 of whom died and the others survived. The major causes of death were multiple organ dysfunction syndrome (MODS) (39%), intractable respiratory failure (27%) and sepsis (20%).

Conclusions Most patients with respiratory failure due to influenza A (H1N1) virus infection were young, with a high mortality, particularly associated with APACHE ∥ score, secondary infection of lung or type 2 diabetes mellitus.

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The Serum NT-proBNP in Patients with Cirrhosis: Relationship to Cardiac Dysfunction and Liver Function


Objective To detect the values of NT-proBNP and evaluate its relationship with liver function, cardiac structure, and cardiac function which was evaluated by echocardiography in patients with liver cirrhosis.

Methods A total of 50 liver cirrhotic patients and 11 healthy controls were studied by two dimensional Doppler echocardiography. Liver cirrhotic patients were divided into group A, B and C according to the Child-Pugh score. Cardiac dimensions and left and right ventricular functions were also evaluated. At the same time, the serum NTproBNP of liver cirrhotic patients and healthy controls were detected, respectively.

Results By Comparison between two groups, we found that the values of LVd, LAs, LVPW, AAO, A Wave, RVOTs, PV and NT-proBNP in liver cirrhosis group were higher than those in control group, whereas the value of E/A decreased. As for the value of LAs and serum NT-proBNP, A and B group were all lower than C group. With LAs > 35 mm, the number of cases in liver cirrhosis group was higher than that in control group. So did that With E/A < 1.

Conclusions The cardiac dysfunction confirmed the existence of cirrhotic cardiomyopathy. More clinical implications were found in liver cirrhotic patients with increased values of serum NT-proBNP.

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Biomolecular changes and cortical neurodegenerative lesions in Trichinella spiralis infected BALB/c mice: a preliminary study elucidating a potential relationship between systemic helminthic infections and idiopathic Parkinson’s


Idiopathic Parkinson’s (IP) is a neurodegenerative disease that is suspected to be due to exposure to infections during early life. Toxoplasmosishas been the only suspected parasitic infection in IP (Celik et al., 2010). Recently, some non-central nervous system bacterial and viral infections have been incriminated in IP (Çamcı & Oğuz, 2016). So in the current study, we tried to explore if the systemic infl ammatory reactions triggered by some helminths like Trichinella spiralis can induce Parkinsonian lesions in the brain, especially that the cerebral complications have been reported in 10-20% of Trichinella spiralis infected patients . An experimental study was designed to assess the neurodegenerative and biomolecular changes that may occur in Trichinella spiralis infected BALB/C mice in comparison to rotenone induced PD model and apparently healthy ones. The motor affection was significantly lesser in the Trichinella infected mice than the Parkinson’s model, but when the catalepsy score was calculated (through the grid and bar tests) it was found to be significantly higher in the infected mice than in the healthy ones. A significant increase in the blood advanced oxidative protein products (AOPP), IFN-γ, TGF-β, and brain DNA fragmentation was also detected in the Trichinella spiralis infected mice. After histopathological examination, a significant increase in the cortical apoptotic neurons and Lewy’s body were observed in the Trichinella infected and the rotenone induced Parkinson’s model sections. A significant decrease in the immunohistochemical expression of the tyrosine hydroxylase expression in the brain sections and the ELISA measured dopamine level in the brain homogenate was also reported in the infected mice group. This study findings may collectively suggest that the systemic inflammatory reactions and the oxidative stresses associated with some systemic helminthic infections like trichinellosis are possible to precipitate neurodegenerative lesions and biomolecular changes in the brain , and manifest with IPD later in life.

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The fine structures of Cystocaulus ocreatus (Nematoda: Protostrongylidae) and the related lung pathology

(Protostronglylidae, Nematoda) using macroscopic lesion scores. Vet. Res., 28: 143–148 [4] Guttekova, A., Zmoray, I. (1974): Comparative study of the ultrastructure of muscle cells in pneumohelminths. Helminthologia, 15: 585–602 [5] Hernandez de Lujan, S., Muela De la, N., Ferre, I. (2001): Helminth parasites in goats in Valencia region. Med. Vet., 18: 476–482 [6] Levine, N. D. (1968): Nematode Parasites of Domestic Animals and of Man. Burgess Publishing Company, USA. [7

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Effects of Interleukin-18 and Anti-interleukin- 18-mAb on Experimental Immunological Liver Fibrosis Induced by Repeatedly Administered Concanavalin A and Its Mechanism


Objective To explore the prevention of IL-18 or anti-IL-18-mAb to the immune liver fibrosis model induced by repeated injection of concanavalin A in BALB/c mice and its mechanism.

Methods Total of 120 BALB/c mice were divided into four groups, control group mice (Ga) were injected weekly with normal saline, concanavalin A group was divided into Gb, Gc, Gd. All mice were injected with concanavalin A (15 mg/kg) once a week. Moreover, Gc, Gd mice were injected weekly with IL-18 (7.5 mg/kg) and anti-IL-18-mAb (10 mg/kg) 2 hours before treatment with concanavalin A, respectively. Twenty-four hours after concanavalin A challenge at 1, 5, 12 and 20 weeks, 3 mice were killed by vena orbitalis, repectively. The sera were storaged at 4° for detecting of up TNF-α and IFN-γ by ELISA. The liver of mice in different groups were excised and fixed in 10% formalin for HE staining and Masson staining or frozen in liquid nitrogen for immunohistochemical staining for α-SMA. After extracting of total RNA from liver tissue, MMP-2 and TIMP-1 A messenger RNA were amplified by reverse transcription polymerase chain reaction (PCR). products were electrophoresed on agrose gel containing ethidium bromide and visualized under ultraviolet light. Densitometric RT-PCR data were standardized with β-actin signals.

Results After experiment, the number of dead mice of Ga, Gb, Gc and Gd were 0, 6, 15 and 3, respectively. There were significant difference on each group (P < 0.05). At the fifth week of experiment, hepatocellular necrosis in IL-18 administered group mice had become widespread throughout the lobule. Evidence of liver fibrosis was observed during this period. However, at the twelfth week of experimemt, bridging fibrosis and large fibrosis strip in the parenchyma with hepatocellular necrosis was detectable in Gb, but at twentieth week, only the small fibrosis strip had been found in anti-IL-18-mAb administered group mice by HE staining and Masson staining. The serum levels of TNF-α and IFN-γ in IL-18 administered group were higher than that in concanavalin A group and anti-IL-18 administered groups (P < 0.05). Moreover, immunohistochemical staining for α-SMA indicated that the semi-quantu scores in IL-18 administered group were more than concanavalin A group and anti-IL-18- mAb administered groups (P < 0.05). MMP-2-mRNA, TIMP-1- mRNA expression levels increased signifigantly compared with concanavalin A group and anti-IL-18-mAb administered group (P < 0.05).

Conclusions The immune liver fibrosis model induced by repeated injection of concanavalin A in BALB/c mice could be worsened by IL-18 administration and block by anti-IL-18 mAb administraion.

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