Furazolidone-induced pulmonary toxicity in Helicobacter pylori infection: Two case reports.

BACKGROUND: Helicobacter pylori (H. pylori) infection is a global problem, causing significant morbidity and mortality. Furazolidone is recommended to eradicate H. pylori infections in China owing to the highly associated antibiotic resistance. CASE SUMMARY: This article presents two cases of lung injury caused by furazolidone treatment of H. pylori infection and the relevant literature review. Two patients developed symptoms, including fever, cough, and fatigue after receiving a course of furazolidone for H. pylori infection. Chest computed tomography showed bilateral interstitial infiltrates. Laboratory studies revealed elevated blood eosinophil count. After discontinuing furazolidone with or without the use of corticosteroids, the symptoms improved rapidly. A PubMed database literature search revealed three reported cases of lung injury suggestive of furazolidone-induced pulmonary toxicity. CONCLUSION: Clinicians should be aware of the side effects associated with the administration of furazolidone to eradicate H. pylori infection.

Influences of dietary lipid and temperature on growth, fat deposition and lipoprotein lipase expression in darkbarbel catfish (Pelteobagrus vachellii).

Darkbarbel catfish (Pelteobagrus vachellii) is an important freshwater fish in China. Water temperature greatly influences the absorption and utilization of dietary lipid by fish. Response values (including growth, hepatic fat deposition, and gene expression) for darkbarbel catfish mediated by two factors (water temperature 20-34°C; dietary lipid level 2-17%) were the focus of this study. The relationship between the two factors and the response values was evaluated by the response surface method using the central composite design. The experiment was conducted under laboratory conditions and lasted for seven weeks. A total of 975 experimental fish (average weight 11.75 ± 0.17g) were selected and placed in 39 plastic tanks. The results showed that the linear effects of lipid level on feed conversion rate (FCR), hepatopancreas somatic index (HSI), hepatic triglycerides (TG), cholesterol (TC), and lipoprotein lipase (LPL) gene expression were significant (P < 0.05). The linear effects of water temperature on specific growth rate (SGR), HSI, TC level, and LPL mRNA expression were significant (P < 0.05). The quadratic effects of water temperature and lipid level on SGR and FCR were significant (P < 0.05). Low water temperature and low lipid diets significantly inhibited growth, increased HSI, and reduced hepatic TG and TC levels, and LPL mRNA expression. The adjusted R2 values for the SGR, FCR, HSI, TC, TG, and LPL mRNA regression models were 0.77, 0.85, 0.62, 0.73, 0.85, and 0.91, respectively. The optimal combination of water temperature and dietary lipid level was 27.5°C and 9.2%, at which the greatest growth and FCR were 2.13%.d-1 and 1.31 respectively, with desirability of 0.904. These results indicated that water temperature may mediate the requirement and utilization of dietary lipid, and intervene in hepatic fat deposition. The results of this study can be used to help optimize the culture conditions of darkbarbel catfish.

miR-29a modulates SCD expression and is regulated in response to a saturated fatty acid diet in juvenile genetically improved farmed tilapia (Oreochromis niloticus).

MicroRNAs (miRNAs) are small non-coding RNAs that regulate target gene expression by binding to the 3' untranslated region (3' UTR) of the target mRNA. MiRNAs regulate a large variety of genes, including those involved in liver biology and disease. Here, we report for the first time that miR-29a post-transcriptionally regulates stearoyl-CoA desaturase (SCD) by binding to its 3' UTR in genetically improved farmed tilapia (GIFT), Oreochromis niloticus, as shown by a 3' UTR luciferase reporter assay. miR-29a antagomir treatment in vivo resulted in significant upregulation of SCD expression. We found that miR-29a expression was negatively correlated with SCD expression in GIFT liver. Inhibition of miR-29a led to a significant increase in SCD expression on day 60 induced by a saturated fatty acid diet, thereby increasing conversion of 16:0 and 18:0 to 16:1 and 18:1, respectively, and activating serum insulin, which would favor glucose and lipid uptake by the liver. These results indicate that miR-29a regulates SCD levels by binding to its 3' UTR, and this interaction affects saturated fatty acid stress induction and insulin and lipid accumulation in serum. Our results suggest that miR-29a is critical in regulating lipid metabolism homeostasis in GIFT liver, and this might provide a basis for understanding the biological processes and therapeutic intervention encountered in fatty liver.

Inhibition of miR-92d-3p enhances inflammation responses in genetically improved farmed tilapia (GIFT, Oreochromis niloticus) with Streptococcus iniae infection by modulating complement C3.

MicroRNAs (miRNAs) are small, non-coding RNAs that regulate target gene expression by binding to the 3'-untranslated regions (3'-UTRs) of their target mRNAs. The miR-92 family is an important miRNA family, which was discovered to be related to regulation of tumor proliferation, apoptosis, invasion, and metastasis. Inhibition of miR-92d-3p was found previously in head kidney of genetically improved farmed tilapia (GIFT, Oreochromis niloticus) exposed to Streptococcus iniae infection. In this study, we found that miR-92d-3p regulated complement C3 mRNA levels by binding to its 3'-UTR by 3'-UTR luciferase reporter assay, and reduced miR-92d-3p expression resulted in increased C3 mRNA levels. We detected a negative relationship between the expression levels of miR-92d-3p and C3 in GIFT injected with miRNA antagomir. We performed in vivo functional analysis by miR-92d-3p silencing. Inhibition of miR-92d-3p levels in GIFT head kidney caused a significant increase in C3 expression, which consequently increased the white blood cell counts and interleukin-1ß, tumor necrosis factor-α, and interferon-γ mRNA levels, all of which may help to activate the inflammatory response in GIFT post-infection with S. iniae. Our findings indicate that miR-92d-3p regulated C3 levels by binding with the C3 mRNA 3'-UTR, and this interaction affected S. iniae infection induction and the immune response in GIFT. We concluded that miR-92d-3p plays an important role in modulating the inflammatory response in GIFT head kidney. Our findings may contribute to understanding the mechanisms of miRNA-mediated gene regulation in tilapia in response to S. iniae infection.

miR-122 promotes hepatic antioxidant defense of genetically improved farmed tilapia (GIFT, Oreochromis niloticus) exposed to cadmium by directly targeting a metallothionein gene.

MicroRNAs (miRNAs) are small, non-coding RNAs that regulate target gene expression by binding to the 3'untranslated region (3'UTR) of the target mRNA. MiRNAs regulate a large variety of genes, including those involved in liver homeostasis and energy metabolism. Down-regulated levels of hepatic miR-122 were found in genetically improved farmed tilapia (GIFT, Oreochromis niloticus) exposed to cadmium (Cd) stress. Here, we report for the first time that reduction of miR-122 post-transcriptionally increased metallothionein (MT) mRNA levels by binding to its 3'UTR, as shown by a 3' UTR luciferase reporter assay. The expression levels of miR-122 were negatively related to MT levels in GIFT under Cd stress. We performed in vivo functional analysis of miR-122 by injecting the fish with a miR-122 antagomir. Inhibition of miR-122 levels in GIFT liver caused a significant increase in MT expression, affected white blood cell and red blood cell counts, and serum alanine and aspartate aminotransferase activities, and glucose levels, all of which may help to relieve Cd stress-related liver stress. miR-122 silencing modulated oxidative stress and stimulated the activity of antioxidant enzymes. Our findings indicate that miR-122 regulated MT levels by binding to the 3'UTR of MT mRNA, and this interaction affected Cd stress induction and the resistance response in GIFT. We concluded that miR-122 plays an important role in regulating the stress response in GIFT liver. Our findings may contribute to understanding the mechanisms of miRNA-mediated gene regulation in tilapia in response to environmental stresses.

The tracheobronchial foreign body in welder without the history of allotriophagy and foreign body aspiration.

The typical chest computed tomography (CT) finding of the arc welders is ill-defined micronodules diffusely distributed in the lung. We report a rare case of tracheobronchial foreign body in welder without the history of allotriophagy and foreign body aspiration. We used the CT and mineralogical analysis in diagnosis and the flexible fiberoptic bronchoscope in therapy. The CT showed bronchiectasis with pulmonary infiltration of the right lower lobe and high-density shadow in the basal bronchus of the right lower lobe. The foreign bodies were removed by a fibreoptic bronchoscope. Semiquantitative chemical analyses showed that the constituent of foreign body was similar to the dregs which were collected in the same garage. This is an unusual case of the welding-related respiratory diseases, which is different from Welder's siderosis and broncholith.

Proteomic analysis of energy metabolism and signal transduction in irradiated melanoma cells.

AIM: To analyze proteomic and signal transduction alterations in irradiated melanoma cells. METHODS: We combined stable isotope labeling with amino acids in cell culture (SILAC) with highly sensitive shotgun tandem mass spectrometry (MS) to create an efficient approach for protein quantification. Protein-protein interaction was used to analyze relationships among proteins. RESULTS: Energy metabolism protein levels were significantly different in glycolysis and not significantly different in oxidative phosphorylation after irradiation. Conversely, tumor suppressor proteins related to cell growth and development were downregulated, and those related to cell death and cell cycle were upregulated in irradiated cells. CONCLUSION: Our results indicate that irradiation induces differential expression of the 29 identified proteins closely related to cell survival, cell cycle arrest, and growth inhibition. The data may provide new insights into the pathogenesis of uveal melanoma and guide appropriate radiotherapy.

Up-regulation of calcitonin gene-related peptide protects streptozotocin-induced diabetic hearts from ischemia/reperfusion injury.

BACKGROUND: Diabetic hearts are vulnerable to ischemia/reperfusion (I/R) injury. Pretreatment with exogenous calcitonin gene-related peptide (CGRP) exerts a cardioprotective effect against myocardial I/R injury. Our previous study found that the CGRP level was decreased in diabetic hearts. This study aimed to investigate whether up-regulation of CGRP could reduce I/R injury in diabetic hearts. METHODS AND RESULTS: Adenovirus encoding the CGRP gene (Ad-CGRP) was injected intramyocardially in mice with or without streptozotocin (STZ) treatment. Three days after injection, the hearts were subjected to in vivo and in vitro I/R. Myocardial infarct size, cardiac function, lactate dehydrogenase (LDH) level in plasma and effluents, and cell mitochondrial function were measured. After ischemia (30 min) and reperfusion (24h) in vivo, diabetes mellitus (DM) mice had greater myocardial infarct size than their nondiabetic counterparts, and released more LDH in plasma. However, CGRP gene transfer reduced myocardial infarct size and plasma LDH level in both non-DM and DM hearts. After 30 min global ischemia and 40 min reperfusion in vitro, the DM hearts demonstrated increased left ventricular end-diastolic pressure (LVEDP) and effluent LDH level, and decreased left ventricular developed pressure (LVDP), coronary flow (CF), as well as cell mitochondrial function, when compared with the non-DM hearts. Again, CGRP gene transfer could protect against I/R injury in both non-DM and DM hearts. CONCLUSIONS: Adenovirus-mediated up-regulation of CGRP gene expression protects diabetic hearts against I/R injury.

Effect of beta-blockers on cardiac function and calcium handling protein in postinfarction heart failure rats.

OBJECTIVES: The normal expression of Ca2+-handling protein is critical for efficient myocardial function. The present study was designed to test the hypothesis that beta-blocker treatment may attenuate left ventricular (LV) remodeling and cardiac contractile dysfunction in the failing heart, which may be associated with alterations of Ca2+-handling protein METHODS: We investigated the change of LV remodeling and function in a rat model of heart failure due to myocardial infarction (MI) with or without carvedilol (30 mg/kg/d) or metoprolol (60 mg/kg/d) treatment for 6 weeks (n = 9 in the MI plus carvedilol group, and n = 8 in every other group). The expression of messenger RNA and proteins of sarcoplasmic reticulum Ca2+-adenosine triphosphatase (SERCA) and phospholamban in cardiomyocytes of all rats were also measured RESULTS: There was significant LV remodeling and cardiac contractile dysfunction in MI rats. The messenger RNA and protein expression of SERCA were down-regulated (p < 0.01), but the expression of phospholamban messenger RNA and protein were up-regulated (p < 0.01) in MI rats compared to sham-operated rats. After the treatment with beta-blockers, LV remodeling and function were clearly improved. Carvedilol was better in attenuating the weight of the LV and the relative weight of the right ventricle than metoprolol (p < 0.05). beta-Blockers restored the low expression of SERCA (p < 0.05) but showed no effect on phospholamban expression (p > 0.05). Moreover, carvedilol induced a more significant improvement of SERCA expression than metoprolol (p < 0.05) CONCLUSIONS: Beta-blockers are effective in preventing LV remodeling and cardiac contractile dysfunction in the failing heart. The molecular mechanism may be related to normalization of SERCA expression.

Comparison of low and high doses of carvedilol on restoration of cardiac function and calcium-handling proteins in rat failing heart.

1. The beta-adrenoceptor antagonist carvedilol reverses cardiac dysfunction in the failing heart. A recent study showed that beta-adrenoceptor antagonists indirectly normalize Ca(2+)-regulatory proteins. The relationship between these two phenomena and the suitable dosage of carvedilol remains unclear. 2. We investigated the change in left ventricular (LV) remodelling and function in a rat model of heart failure due to myocardial infarction (MI) with or without carvedilol (30 or 2 mg/kg per day) treatment for 6 weeks. The expression of mRNA and proteins of sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) and phospholamban (PLB) in cardiomyocytes was also measured. 3. There was significant LV remodelling and cardiac contractile dysfunction in MI rats. The expression of SERCA mRNA and protein were downregulated (P < 0.01), but the expression of PLB mRNA and protein were upregulated (P < 0.01) in MI rats compared with sham-operated rats. After treatment with carvedilol, LV remodelling and cardiac contractile dysfunction were clearly improved. Low-dose carvedilol was better at improving some parameters of LV remodelling and function than the high dose. Carvedilol partially restored the low expression of SERCA (P < 0.05), but had no effect on PLB expression (P > 0.05). Moreover, low-dose carvedilol induced a more significant improvement in SERCA expression than did the high dose (P < 0.05). 4. The results of the present study suggest that carvedilol is effective in improving LV remodelling and cardiac contractile dysfunction after MI. This may be related to the normalization of SERCA expression.

Statins reduce connexin40 and connexin43 expression in atherosclerotic aorta of rabbits.

BACKGROUND: Gap junction protein connexin43 (Cx43) expression was enhanced in proliferating smooth muscle cells (SMCs) in the neointima of atherosclerotic lesions. HMG-CoA Reductase Inhibitors (statins) can reduce Cx43 expression in vivo and in vitro. Connexin40 (Cx40) is also a very important connexin in SMCs of arterial wall. METHODS: We observed the expression of Cx40 and Cx43 in a rabbit model of a high-cholesterol diet and investigated the effect of lovastatin (10 mg.kg-1.d-1, 2 weeks) or fluvastatin (10 mg.kg-1.d-1, 2 weeks) on these changes by the methods of western blotting, RT-PCR, immunohistochemistry, and transmission electron microscope. RESULTS: There was abundant expression of Cx40 mRNA and protein in SMCs of rabbit aorta. Besides Cx43, Cx40 expression was also obviously upregulated in atherosclerotic plaques. Treatment with statins reduced the over-expression of Cx43 and Cx40 in atherosclerotic lesion. Cx40 and Cx43 gap junction quantity from each of the arteries obtained at the different drug treatment levels revealed no significant difference. Neointimal SMCs had abundant, large gap junctions, whereas normal SMCs had smaller, less frequent junctions. Statins also normalized the enlarged gap junctions. CONCLUSIONS: These results provide novel in vivo evidence for the key role of gap junctions in atherogenesis and the possible mechanism in antiatherogenic effect of statins.

[Mid- to long-term effects of delayed percutaneous coronary intervention on left ventricular function and prognosis in patients with acute myocardial infarction].

OBJECTIVE: To investigate the mid- to long-term effects of delayed percutaneous coronary intervention (PCI) on the left ventricular function and clinical outcome of patients with acute myocardial infarction (AMI). METHODS: PCI (including percutaneous transluminal coronary angioplasty and stenting) was performed in 42 patients within 1 to 2 weeks following the onset of AMI (PCI group), with another 31 patients who were admitted within the same period to receive medication for AMI serving as the control group. The patients in both groups were observed for comparison of the occurrence of reinfarction and angina, mortality at 1 and 6 months, and findings by ultrasound cardiograms (UCG). RESULTS: In PCI group, the left ventricular function were obviously improved as compared with the control group (P<0.01) 1 month after the onset of AMI, showing greater improvement at 6 months (P<0.01). No death or reinfarction occurred in the PCI group, with only 1 patients experiencing angina 5 months after PCI. In control group, death occurred in 2 cases, reinfarction in 1 case, recurrent angina in 4 cases (include 2 cases of early postinfarction angina). CONCLUSION: Delayed PCI may significantly improve the prognosis of patients with AMI and prolong their survival without cardiovascular accidents and ameliorate their left ventricular functions, with high success rate of the operation.