Browsing by Author "Vučević, Danijela (55881342600)"

Objective: The alcoholic liver disease (ALD)/nonalcoholic fatty liver disease (NAFLD) (ANI) scoring system was constructed as a response to a clinical need for avoiding the risks of liver biopsy in diagnosing the etiology of fatty liver disease. The aim of this study was to test the reliability of ANI as a noninvasive method to distinguish ALD from NAFLD. Materials and Methods: One hundred and thirty-five patients were classified into two groups, ALD and NAFLD, according to the pathohistological results. Parameters for ANI are aspartate aminotransferase, alanine aminotransferase, mean corpuscular volume, BMI, and sex. ANI was calculated using an online calculator, official site of Mayo Clinic. Results: ANI was significantly higher in patients with ALD than NAFLD (P<0.01). The cutoff point of ANI is-0.66. ANI greater than-0.66 indicates ALD, whereas ANI less than-0.66 yields a higher probability of NAFLD with high specificity (96.7%) and sensitivity (84.1%). The mean corpuscular volume and aspartate aminotransferase/alanine aminotransferase ratio were higher, whereas BMI was lower in patients with ALD than in NAFLD (P<0.01). Conclusion: The ANI scoring system may be used for the estimation of alcoholic origin of steatosis/steatohepatitis and may help in triaging patients for liver biopsy. ANI less than-0.66 indicates NAFLD, whereas ANI greater than-0.66 confirms the alcoholic etiology, but does not exclude the contribution of associated factors toward the development of fatty liver in a Serbian population. © 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins.

Binging is a behavior with undesirable outcomes for drinkers and those around them. A debate over recent years has focused on how this harmful and potentially life threatening pattern of drinking should be defined and how many drinks make up a binge. From a clinician's stand-point, a binge refers to a pattern of drinking to intoxication, usually a solitary activity lasting up to several days and involving loss of control over consumption. The National Institute of Alcohol Abuse and Alcoholism (Bethesda, Maryland, US) defines binge drinking episodes as consumption of five or more drinks (male) or four or more drinks (female) in the space of about 2 hours. However, this definition does not consider the amount of alcohol intake in one binge episode, nor the possibility that some individuals may go on several binges during the same day. Generally speaking, binge drinking implies "drinking too much too fast." Periods of binge drinking (several consecutive days, weeks or months) are typically followed by periods of abstinence or, in some cases, significantly lower levels of consumption. Thus, the nature and severity of the problems that binge drinking causes depends on how frequently it occurs and over how long a period it is maintained. This pattern of drinking is extremely common, especially among young adults, and remains the leading cause of death among college-aged students in the US, with similar worldwide rates of problematic alcohol use across Europe, South America and Australia. Due to the physiological and psychological changes occurring in adolescence and youth, binge drinking may have lasting harmful consequences, including greater risk for the development of alcohol dependence. It is known that alcohol affects virtually every organ system in the body, and in high doses, can cause coma and death. Namely, in the brain it affects several neurotransmitter systems, including opiates, γ-aminobutyric acid (GABA), glutamate, serotonin and dopamine. Increased opiate levels help explain the euphoric effect of alcohol, while its effects on GABA cause anxiolytic and sedative effects. Additionally, binge drinking increases the risk of acute hemorrhagic and ischemic strokes by up to ten-fold. It also leads to cardiovascular problems (atrial fibrillation, known as "holiday heart", sudden cardiac death, etc.). Repeated binge drinking can cause damage to the esophagus resulting in acute hemorrhage, gastritis, pancreatitis and myopathy. For pregnant women, binge drinking has been correlated with harm to the developing fetus, especially during the early stages of pregnancy. This pattern of drinking combined with smoking is responsible for a rise in oral cancer in men and women in their twenties and thirties. Additionally, it is feared that the increase in binge drinking among young women will lead to a significant increase in breast cancer in the next half century. It is well established that binge drinking causes a higher level of psychological morbidity, particularly anxiety and neurosis, than the same amount of alcohol consumed more steadily over a longer period. Interestingly, young binge drinkers are substantially more likely than non-binge drinkers to take illegal drugs. © 2009 Nova Science Publishers, Inc.

We report a study on the relation between open-field behavior and electroencephalographic (EEG) changes during lindane-induced seizures in 2-month-old adult male Wistar rats. For chronic EEG recordings and power spectra analysis, 3 electrodes were implanted into the skull. Three groups of animals, (i) saline-injected control (n = 6), (ii) DMSO-treated (n = 6), and (iii) lindane intraperitoneally administered: L4 (4 mg/kg,n = 10), L 6 (6 mg/kg, n = 11), and L8 (8 mg/kg, n = 11), were observed for 30 min for the occurrence of convulsive behavior. It was assessed by incidence of motor seizures, and seizure severity grade was determined by a descriptive rating scale (0, no response; 1, head nodding, lower jaw twitching; 2, myoclonic body jerks, bilateral forelimb clonus with full rearing; 3, progression to generalized clonic convulsions followed by tonic extension of fore and hind limbs and tail; 4, status epilepticus). EEG signal and spectral analyses were suitable to describe the dynamics of complex behavioral responses. Incidence and severity of epileptic manifestations, recorded as high voltage spike-wave complexes, polyspikes, sleep-like patterns in EEG, and power spectra changes, were greater in lindane-treated groups in a dose-dependent manner compared with control or DMSO-treated groups. Our results suggest good correlation between lindane-induced epileptiform activity and behavioral changes. © 2008 NRC.

We report a study on the relation between open-field behavior and electroencephalographic (EEG) changes during lindane-induced seizures in 2-month-old adult male Wistar rats. For chronic EEG recordings and power spectra analysis, 3 electrodes were implanted into the skull. Three groups of animals, (i) saline-injected control (n = 6), (ii) DMSO-treated (n = 6), and (iii) lindane intraperitoneally administered: L4 (4 mg/kg,n = 10), L 6 (6 mg/kg, n = 11), and L8 (8 mg/kg, n = 11), were observed for 30 min for the occurrence of convulsive behavior. It was assessed by incidence of motor seizures, and seizure severity grade was determined by a descriptive rating scale (0, no response; 1, head nodding, lower jaw twitching; 2, myoclonic body jerks, bilateral forelimb clonus with full rearing; 3, progression to generalized clonic convulsions followed by tonic extension of fore and hind limbs and tail; 4, status epilepticus). EEG signal and spectral analyses were suitable to describe the dynamics of complex behavioral responses. Incidence and severity of epileptic manifestations, recorded as high voltage spike-wave complexes, polyspikes, sleep-like patterns in EEG, and power spectra changes, were greater in lindane-treated groups in a dose-dependent manner compared with control or DMSO-treated groups. Our results suggest good correlation between lindane-induced epileptiform activity and behavioral changes. © 2008 NRC.

Chronic ethanol consumption is a major risk factor for epilepsy, and seizures frequently occur during the withdrawal period. The aim of our study was to investigate effects of ethanol on lindane-induced seizures in rats. Male Wistar rats were injected i.p. with one of the following 5 treatments: (i) saline, (ii) dimethylsulfoxide, (iii) lindane (8 mg/kg) (L), (iv) ethanol in doses of 0.5 g/kg (E0.5), 1 g/kg (E1), and 2 g/kg (E 2), and (v) groups that received ethanol 30 min before lindane (LE0.5, LE1, and LE2). Behavioral changes were described by using a descriptive scale as follows: 0, no response; 1, head nodding, lower jaw twitching; 2, myoclonic body jerks, bilateral forelimb clonus; 3, generalized tonic-clonic convulsions; 4, status epilepticus. The incidence of convulsions in the LE2 group was significantly lower than the incidence in the L (p < 0.01) and LE0.5 groups (p < 0.05). The median grade of convulsive behavior was significantly lower in the LE2 (p < 0.01) and LE1 groups (p < 0.05) compared with the L group. Latencies to the first seizure response were not significantly different among groups. ED50 of ethanol was 1.40 (1.19-1.65). Our findings suggest that ethanol decreased severity and incidence of lindane-induced seizures in a dose-dependent manner. © 2008 NRC Canada.

Chronic ethanol consumption is a major risk factor for epilepsy, and seizures frequently occur during the withdrawal period. The aim of our study was to investigate effects of ethanol on lindane-induced seizures in rats. Male Wistar rats were injected i.p. with one of the following 5 treatments: (i) saline, (ii) dimethylsulfoxide, (iii) lindane (8 mg/kg) (L), (iv) ethanol in doses of 0.5 g/kg (E0.5), 1 g/kg (E1), and 2 g/kg (E 2), and (v) groups that received ethanol 30 min before lindane (LE0.5, LE1, and LE2). Behavioral changes were described by using a descriptive scale as follows: 0, no response; 1, head nodding, lower jaw twitching; 2, myoclonic body jerks, bilateral forelimb clonus; 3, generalized tonic-clonic convulsions; 4, status epilepticus. The incidence of convulsions in the LE2 group was significantly lower than the incidence in the L (p < 0.01) and LE0.5 groups (p < 0.05). The median grade of convulsive behavior was significantly lower in the LE2 (p < 0.01) and LE1 groups (p < 0.05) compared with the L group. Latencies to the first seizure response were not significantly different among groups. ED50 of ethanol was 1.40 (1.19-1.65). Our findings suggest that ethanol decreased severity and incidence of lindane-induced seizures in a dose-dependent manner. © 2008 NRC Canada.

We investigated the effects of hypothermia on the incidence and EEG signs of audiogenic seizures in rats treated with metaphit (1- [1(3isothiocyanatophenyl)-cyclohexyl] piperidine), an experimental model of generalized reflex epilepsy. After i.p. injection with metaphit (10 mg/kg) Wistar rats were exposed to audiogenic stimulation at hourly intervals during the time course of the experiment. After intermittent use of an ice pack 8 h after the metaphit treatment, when seizure was fully developed, the body temperature was reduced to 30 ± 0.5°C in one half of the rats, and maintained at 37 ± 0.5°C in the other half. Saline-injected rats served as a control group. In the hypothermia group, the incidence of audiogenic seizures induced by metaphit was completely suppressed during the 3 consecutive testing times, while no signs of epileptiform activity were noted in EEG tracings. The termination of hypothermic treatment resulted in the recovery of seizure susceptibility, and during audiogenic stimulation, bursts of spiking activity were recorded in the EEGs of metaphit-treated rats. These findings indicate that moderate body hypothermia is an effective anticonvulsant treatment for audiogenic seizures in metaphit-treated rats. © 2007 NRC.

We investigated the effects of hypothermia on the incidence and EEG signs of audiogenic seizures in rats treated with metaphit (1- [1(3isothiocyanatophenyl)-cyclohexyl] piperidine), an experimental model of generalized reflex epilepsy. After i.p. injection with metaphit (10 mg/kg) Wistar rats were exposed to audiogenic stimulation at hourly intervals during the time course of the experiment. After intermittent use of an ice pack 8 h after the metaphit treatment, when seizure was fully developed, the body temperature was reduced to 30 ± 0.5°C in one half of the rats, and maintained at 37 ± 0.5°C in the other half. Saline-injected rats served as a control group. In the hypothermia group, the incidence of audiogenic seizures induced by metaphit was completely suppressed during the 3 consecutive testing times, while no signs of epileptiform activity were noted in EEG tracings. The termination of hypothermic treatment resulted in the recovery of seizure susceptibility, and during audiogenic stimulation, bursts of spiking activity were recorded in the EEGs of metaphit-treated rats. These findings indicate that moderate body hypothermia is an effective anticonvulsant treatment for audiogenic seizures in metaphit-treated rats. © 2007 NRC.

In high-fat diet (HFD) induced nonalcoholic fatty liver disease (NAFLD), there is an increase in the endocannabinoid system activity, which significantly contributes to steatosis development. The aim of our study was to investigate the effects of cannabinoid receptor type 1 blockade on adipokine and proinflammatory cytokine content in adipose and hepatic tissue in mice with NAFLD. Male mice C57BL/6 were divided into a control group fed with a control diet for 20 weeks (C, n = 6) a group fed with a HFD for 20 weeks (HF, n = 6), a group fed with a control diet and treated with rimonabant after 18 weeks (R, n = 9), and a group fed with HFD and treated with rimonabant after 18 weeks (HFR, n = 10). Rimonabant significantly decreased leptin, resistin, apelin, visfatin, interleukin 6 (IL-6), and interferon-γ (IFN-γ) concentration in subcutaneous and visceral adipose tissue in the HFR group compared to the HF group (p < 0.01). Rimonabant reduced hepatic IL-6 and IFN-γ concentration as well as plasma glucose and insulin concentration and the homeostatic model assessment index in the HFR group compared to the HF group (p < 0.01). It can be concluded that the potential usefulness of CB1 blockade in the treatment of HFD-induced NAFLD is due to modulation of the adipokine profile and proinflammatory cytokines in both adipose tissues and liver as well as glucose metabolism. © 2019, Published by NRC Research Press.

In high-fat diet (HFD) induced nonalcoholic fatty liver disease (NAFLD), there is an increase in the endocannabinoid system activity, which significantly contributes to steatosis development. The aim of our study was to investigate the effects of cannabinoid receptor type 1 blockade on adipokine and proinflammatory cytokine content in adipose and hepatic tissue in mice with NAFLD. Male mice C57BL/6 were divided into a control group fed with a control diet for 20 weeks (C, n = 6) a group fed with a HFD for 20 weeks (HF, n = 6), a group fed with a control diet and treated with rimonabant after 18 weeks (R, n = 9), and a group fed with HFD and treated with rimonabant after 18 weeks (HFR, n = 10). Rimonabant significantly decreased leptin, resistin, apelin, visfatin, interleukin 6 (IL-6), and interferon-γ (IFN-γ) concentration in subcutaneous and visceral adipose tissue in the HFR group compared to the HF group (p < 0.01). Rimonabant reduced hepatic IL-6 and IFN-γ concentration as well as plasma glucose and insulin concentration and the homeostatic model assessment index in the HFR group compared to the HF group (p < 0.01). It can be concluded that the potential usefulness of CB1 blockade in the treatment of HFD-induced NAFLD is due to modulation of the adipokine profile and proinflammatory cytokines in both adipose tissues and liver as well as glucose metabolism. © 2019, Published by NRC Research Press.

Bronchial asthma is a chronic inflammatory disorder of the airways in which many cells play a role, in particular mast cells, eosinophils, neutrophils, T-lymphocytes and epithelial cells. In susceptible individuals this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness and cough, particularly at night and/or in the early morning. These symptoms are usually associated with variable and extensive limitations of airflow in the bronchi reversible spontaneously or by treatment. It has been shown that restrain of the effectors of stress response participate in the pathogenesis of bronchial asthma. Anger that is not expressed and frustrations may activate the limbic stress pathway. Thus, the released neurotransmitters followed by excitation thus causing psychogenic (mental or emotional) stress. It is also known that emotional stress may be responsible for the exacerbation of asthma. Namely, pronounced emotions cause hyperventilation and hypocapnia inducing bronchospasm. Certain psychological personality features are related to adaptive or inadequate body response to numerous life events. Thus, until the beginning of the last century, bronchial asthma was referred to as asthma nervosa, because clinicians clearly observed the psychological profile of patients with predominant fear of asphyxia and recurrent attacks of paroxysmal dyspnoea. Besides, increased sensitivity, repression of aggressive feelings and expressive empathy have been identified as the most frequent psychological characteristics of asthmatic patients. However, scientists are still far from a full understanding of bronchial asthma pathogenesis. The contribution of psychic factors has become meaningful in the understanding of the development of bronchial asthma. Having in mind that in the majority of patients asthma is a lifelong condition, there is a hope that further investigations of bronchial asthma psychogenesis will improve prevention and treatment of this disease.