RESUMEN
AIM: To investigate the therapeutic effects of hydrogel dressings on neurotrophic keratitis in rats. METHODS: Male Wistar rats, aged 42-56d, were randomly divided into control, experimental, and treatment groups, each consisting of five rats. The experimental and treatment groups underwent neurotrophic keratitis modeling in both eyes. After successful modeling, biomedical hydrogels formed with polyvinyl alcohol and polyvinyl pyrrolidone were used in treatment group for 7d. Ocular irritation response and keratitis index scores, Schirmer's test, tear film break-up time (BUT), sodium fluorescein staining, and hematoxylin and eosin (HE) staining were used to evaluate the effectiveness of the treatment. RESULTS: The neurotrophic keratitis model was successfully established in rats with severe ophthalmic nerve injury, characterized by keratitis, ocular irritation, reduced tear secretion measured by decreased BUT and Schirmer test values, corneal epithelial loss, and disorganized collagen fibers in the stromal layer. Following treatment with hydrogel dressings, significant improvements were observed in keratitis scores and ocular irritation symptoms in model eyes. Although the recovery of tear secretion, as measured by the Schirmer's test, did not show statistical differences, BUT was significantly prolonged. Fluorescein staining confirmed a reduction in the extent of corneal epithelial loss after treatment. HE staining revealed the restoration of the structural disorder in both the epithelial and stromal layers to a certain extent. CONCLUSION: Hydrogel dressing reduces ocular surface irritation, improves tear film stability, and promotes the repair and restoration of damaged epithelial cells by maintaining a moist and clean environment on the ocular surface in the rat model.
RESUMEN
We reported an 8-year-old boy with panscleritis in left eye and right epididymitis after falling on the ground. Etiologic diagnosis played a key role in this case. Systemic examinations ruled out systemic autoimmune diseases, tumors, and infections as the cause of scleritis and suggested that the disease was caused by a local delayed-type hypersensitivity (DTH) induced by ocular trauma and was non-infectious. Still, the right epididymitis was infectious. Both conditions were treated successfully using steroids and antibiotics, respectively. Thus, early etiologic diagnosis and reasonable treatment are crucial to prevent visual loss.
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Epididimitis , Lesiones Oculares , Escleritis , Heridas no Penetrantes , Masculino , Humanos , Niño , Epididimitis/etiología , Epididimitis/complicaciones , Lesiones Oculares/complicaciones , Heridas no Penetrantes/complicaciones , Escleritis/tratamiento farmacológico , Escleritis/etiología , CaraRESUMEN
Microwave ablation (MWA) is a new technology developed in recent years, which is widely used in various disciplines. Microwave ablation is an alternative to surgery in the management of various tumors, and it has been demonstrated to be effective in the management of primary tumors and metastatic tumors. Microwave ablation is widely used in the treatment of hepatocellular carcinoma with an obvious effect and less side effects, and only 2.7% had serious complications. Many studies have confirmed the complications are thermal damage, hemorrhage, pleural effusion, bile leak, tumor seeding, hepatic abscess, cholangitis, and so forth. But diaphragm perforation is rare, and it is probably the first case reported. This article describes diaphragmatic perforation secondary to MWA of the liver with subsequent pleural effusion and diaphragmatic hernia. We also describe its management via the laparoscopic approach.
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Carcinoma Hepatocelular/cirugía , Ablación por Catéter/efectos adversos , Diafragma/cirugía , Hernia Diafragmática/cirugía , Neoplasias Hepáticas/cirugía , Microondas/efectos adversos , Microondas/uso terapéutico , Complicaciones Posoperatorias/cirugía , Carcinoma Hepatocelular/diagnóstico por imagen , Diafragma/diagnóstico por imagen , Diafragma/lesiones , Hernia Diafragmática/diagnóstico por imagen , Hernia Diafragmática/etiología , Humanos , Laparoscopía/métodos , Neoplasias Hepáticas/diagnóstico por imagen , Imagen por Resonancia Magnética , Masculino , Persona de Mediana Edad , Derrame Pleural/etiología , Complicaciones Posoperatorias/diagnóstico por imagen , Complicaciones Posoperatorias/etiología , Tomografía Computarizada por Rayos XRESUMEN
Recent evidence shows that excess nicotinamide can cause epigenetic changes in developing rats. The aim of the present study was to investigate the effects of maternal nicotinamide supplementation on the fetus. Female rats were randomised into four groups fed a standard chow diet (control group) or diets supplemented with 1 g/kg of nicotinamide (low-dose group), 4 g/kg of nicotinamide (high-dose group) or 4 g/kg of nicotinamide plus 2 g/kg of betaine (betaine group) for 14-16 d before mating and throughout the study. Fetal tissue samples were collected on the 20th day of pregnancy. Compared with the control group, the high-dose group had a higher fetal death rate, and the average fetal body weight was higher in the low-dose group but lower in the high-dose group. Nicotinamide supplementation led to a decrease in placental and fetal hepatic genomic DNA methylation and genomic uracil contents (a factor modifying DNA for diversity) in the placenta and fetal liver and brain, which could be completely or partially prevented by betaine. Moreover, nicotinamide supplementation induced tissue-specific alterations in the mRNA expression of the genes encoding nicotinamide N-methyltransferase, DNA methyltransferase 1, catalase and tumour protein p53 in the placenta and fetal liver. High-dose nicotinamide supplementation increased fetal hepatic α-fetoprotein mRNA level, which was prevented by betaine supplementation. It is concluded that maternal nicotinamide supplementation can induce changes in fetal epigenetic modification and DNA base composition. The present study raises the concern that maternal nicotinamide supplementation may play a role in the development of epigenetic-related diseases in the offspring.
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Metilación de ADN , Suplementos Dietéticos , Regulación hacia Abajo , Feto/metabolismo , Regulación del Desarrollo de la Expresión Génica , Fenómenos Fisiologicos Nutricionales Maternos , Niacinamida/metabolismo , Animales , Betaína/metabolismo , Betaína/uso terapéutico , Encéfalo/embriología , Encéfalo/metabolismo , ADN/biosíntesis , Suplementos Dietéticos/efectos adversos , Epigénesis Genética , Femenino , Muerte Fetal/etiología , Muerte Fetal/prevención & control , Desarrollo Fetal , Hígado/embriología , Hígado/metabolismo , Neuronas/metabolismo , Niacinamida/administración & dosificación , Niacinamida/efectos adversos , Niacinamida/antagonistas & inhibidores , Placenta/metabolismo , Placentación , Embarazo , Distribución Aleatoria , Ratas , Ratas Sprague-Dawley , Uracilo/metabolismoRESUMEN
Ecological evidence suggests that niacin (nicotinamide and nicotinic acid) fortification may be involved in the increased prevalence of obesity and type 2 diabetes, both of which are associated with insulin resistance and epigenetic changes. The purpose of the present study was to investigate nicotinamide-induced metabolic changes and their relationship with possible epigenetic changes. Male rats (5 weeks old) were fed with a basal diet (control group) or diets supplemented with 1 or 4 g/kg of nicotinamide for 8 weeks. Low-dose nicotinamide exposure increased weight gain, but high-dose one did not. The nicotinamide-treated rats had higher hepatic and renal levels of 8-hydroxy-2'-deoxyguanosine, a marker of DNA damage, and impaired glucose tolerance and insulin sensitivity when compared with the control rats. Nicotinamide supplementation increased the plasma levels of nicotinamide, N1-methylnicotinamide and choline and decreased the levels of betaine, which is associated with a decrease in global hepatic DNA methylation and uracil content in DNA. Nicotinamide had gene-specific effects on the methylation of CpG sites within the promoters and the expression of hepatic genes tested that are responsible for methyl transfer reactions (nicotinamide N-methyltransferase and DNA methyltransferase 1), for homocysteine metabolism (betaine-homocysteine S-methyltransferase, methionine synthase and cystathionine ß-synthase) and for oxidative defence (catalase and tumour protein p53). It is concluded that nicotinamide-induced oxidative tissue injury, insulin resistance and disturbed methyl metabolism can lead to epigenetic changes. The present study suggests that long-term high nicotinamide intake (e.g. induced by niacin fortification) may be a risk factor for methylation- and insulin resistance-related metabolic abnormalities.
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Metilación de ADN/efectos de los fármacos , Suplementos Dietéticos/efectos adversos , Epigénesis Genética/efectos de los fármacos , Enfermedades Metabólicas/inducido químicamente , Niacina/efectos adversos , Niacinamida/efectos adversos , Complejo Vitamínico B/efectos adversos , Animales , Betaína/sangre , Colina/sangre , Islas de CpG/efectos de los fármacos , ADN/metabolismo , Daño del ADN , Intolerancia a la Glucosa/inducido químicamente , Intolerancia a la Glucosa/genética , Intolerancia a la Glucosa/metabolismo , Homocisteína/genética , Homocisteína/metabolismo , Resistencia a la Insulina/genética , Hígado/efectos de los fármacos , Hígado/metabolismo , Masculino , Enfermedades Metabólicas/genética , Enfermedades Metabólicas/metabolismo , Niacinamida/análogos & derivados , Niacinamida/sangre , Estrés Oxidativo/genética , Regiones Promotoras Genéticas/efectos de los fármacos , Ratas , Ratas Sprague-Dawley , Factores de Tiempo , Uracilo/metabolismo , Aumento de Peso/efectos de los fármacosRESUMEN
Methylation, a methyl group-consuming reaction, plays a key role in the degradation (i.e., inactivation) of monoamine neurotransmitters, including catecholamines, serotonin and histamine. Without labile methyl groups, the methylation-mediated degradation cannot take place. Although high niacin (nicotinic acid and nicotinamide) intake, which is very common nowadays, is known to deplete the body's methyl-group pool, its effect on monoamine-neurotransmitter degradation is not well understood. The aim of this article was to investigate the effect of excess nicotinamide on the levels of plasma serotonin and histamine in healthy subjects. Urine and venous blood samples were collected from nine healthy male volunteers before and after oral loading with 100 mg nicotinamide. Plasma N(1)-methylnicotinamide, urinary N(1)-methyl-2-pyridone-5-carboxamide (2-Py), and plasma betaine levels were measured by using high-performance liquid chromatography (HPLC). Plasma concentrations of choline, serotonin and histamine were measured using commercial kits. The results showed that the plasma N(1)-methylnicotinamide level and the urinary excretion of 2-Py significantly increased after oral loading with 100 mg nicotinamide, which was accompanied with a decrease in the methyl-group donor betaine. Compared with those before nicotinamide load, five-hour postload plasma serotonin and histamine levels significantly increased. These results suggest that excess nicotinamide can disturb monoamine-neurotransmitter metabolism. These findings may be of significance in understanding the etiology of monoamine-related mental diseases, such as schizophrenia and autism (a neurodevelopmental disorder).
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Histamina/sangre , Niacinamida/análogos & derivados , Niacinamida/administración & dosificación , Serotonina/sangre , Betaína/sangre , Colina/sangre , Cromatografía Líquida de Alta Presión , Humanos , Masculino , Niacinamida/sangre , Piridonas/orinaRESUMEN
The skin, the body's largest organ, plays an important role in the biotransformation/detoxification and elimination of xenobiotics and endogenous toxic substances, but its role in oxidative stress and insulin resistance is unclear. We investigated the relationship between skin detoxification and oxidative stress/insulin resistance by examining burn-induced changes in nicotinamide degradation. Rats were divided into four groups: sham-operated, sham-nicotinamide, burn, and burn-nicotinamide. Rats received an intraperitoneal glucose injection (2 g/kg) with (sham-nicotinamide and burn-nicotinamide groups) or without (sham-operated and burn groups) coadministration of nicotinamide (100 mg/kg). The results showed that the mRNA of all detoxification-related enzymes tested was detected in sham-operated skin but not in burned skin. The clearance of nicotinamide and N(1)-methylnicotinamide in burned rats was significantly decreased compared with that in sham-operated rats. After glucose loading, burn group showed significantly higher plasma insulin levels with a lower muscle glycogen level than that of sham-operated and sham-nicotinamide groups, although there were no significant differences in blood glucose levels over time between groups. More profound changes in plasma H(2)O(2) and insulin levels were observed in burn-nicotinamide group. It may be concluded that decreased skin detoxification may increase the risk for oxidative stress and insulin resistance.