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PurposeDue to its increased volume, polycystic ovarian tissue is more prone to torsion than normal ovarian tissue. In treating ovarian torsion, detorsion is applied to ensure oxygenation of hypoxic tissues. However, the resulting oxygen radicals cause tissue damage. Bromelain is a substance obtained from pineapple, and studies in the literature show it is used as an antioxidant. This study aimed to evaluate the damage caused by ischemia-reperfusion (I/R) in the torsion-detorsion model created in normal and polycystic ovarian tissue and investigate the role of bromelain in this damage.MethodsPolycystic ovarian tissue was created by applying dihydroepiandrosterone sulfate to rats. Afterward, a torsion-detorsion model was used for all rats. The rats were divided into six groups: the polycystic ovary sham-operated group (P-S), the normal ovary sham-operated group (N-S), the polycystic ovary ischemia/reperfusion group (P-IR), the normal ovary ischemia/reperfusion group (N-IR), the polycystic ovary ischemia/reperfusion group treated with bromelain (P-IRB), and the normal ovary ischemia/reperfusion group treated with bromelain (N-IRB). After the procedure, tissues were collected for histopathological examination, and MDA, TUNEL, and NF-κB levels were measured.ResultsThis study detected significant decreases in MDA and NF-κB levels and apoptotic cell numbers assessed by TUNEL staining in groups with IR damage and given bromelain compared to the control groups. The number of TUNEL-positive cells was found to be highest in the P-IR group (8.80 ± 2.98) and significantly lower in the bromelain-administered P-IRB (1.04 ± 1.09) and N-IRB (0.52 ± 0.58) groups (p< 0.05). NF-κB expression was also high in P-IR and N-IR groups, while it was significantly decreased in bromelain-treated groups (P-IRB and N-IRB) (p< 0.05). In addition, IR damage was more pronounced in polycystic ovary tissue than in normal ovary tissue.ConclusionIschemia perfusion damage may be more pronounced in polycystic ovarian tissue than in normal ovarian tissue. Bromelain may be preferred to prevent I/R injury caused by ovarian torsion. It is also thought that bromelain may function in treating polycystic ovaries, and further studies can be conducted on this subject.

Recently, we described the alteration of six miRNAs in the serum of autistic children, their fathers, mothers, siblings, and in the sperm of autistic mouse models. Studies in model organisms suggest that noncoding RNAs participate in transcriptional modulation pathways. Using mice, approaches to alter the amount of RNA in fertilized eggs enable in vivo intervention at an early stage of development. Noncoding RNAs are very numerous in spermatozoa. Our study addresses a fundamental question: can the transfer of RNA content from sperm to eggs result in changes in phenotypic traits, such as autism? To explore this, we used sperm RNA from a normal father but with autistic children to create mouse models for autism. Here, we induced, in a single step by microinjecting sperm RNA into fertilized mouse eggs, a transcriptional alteration with the transformation in adults of glial cells into cells affected by astrogliosis and microgliosis developing deficiency disorders of the ‘autism-like’ type in mice born following these manipulations. Human sperm RNA alters gene expression in mice, and validates the possibility of non-Mendelian inheritance in autism.

The aim of this study was to investigate the tissue damage created by the two commonly used percutaneous tracheostomy methods of multiple dilatational tracheostomy and the controlled rotating dilation technique. A total of 21 sheep trachea samples were obtained from the slaughterhouse. The tracheas were separated into 3 groups of 7 samples in each. In Group 1, only an incision was made. In Group 2, the multiple dilatational tracheostomy method was applied, and in Group 3, the controlled rotating dilation technique. The tissue samples taken were separated into 2 equal pieces. One piece was used for histopathological examination and the other was examined under electron microscope. When the hematoxylin-eosin staining results and the electron microscope images of the sheep trachea slices were evaluated, cartilage integrity was observed to have been preserved in Groups 1 and 2. In Group 3, there was seen to be epithelial injury and disruption of the cartilage integrity. To reduce the complications of percutaneous tracheostomy techniques to a minimum, the protection of tissue integrity is important. The multiple dilatational tracheostomy method was seen to be superior to the controlled rotating dilation technique in respect of protecting tissue integrity. [Med-Science 2019; 8(4.000): 870-4]

Uncontrolled repetitive generalized tonic-clonic seizures (GTCS) are the main risk factor for sudden unexpected death in epilepsy (SUDEP). GTCS can be observed in models such as Pentylenetetrazole kindling (PTZ-K) or pilocarpine-induced Status Epilepticus (SE-P), which share similar alterations in cardiac function, with a high risk of SUDEP. Terminal cardiac arrhythmia in SUDEP can develop as a result of a high rate of hypoxic stress-induced by convulsions with excessive sympathetic overstimulation that triggers a neurocardiogenic injury, recently defined as “Epileptic Heart” and characterized by heart rhythm disturbances, such as bradycardia and lengthening of the QT interval. Recently, an iron overload-dependent form of non-apoptotic cell death called ferroptosis was described at the brain level in both the PTZ-K and SE-P experimental models. However, seizure-related cardiac ferroptosis has not yet been reported. Iron overload cardiomyopathy (IOC) results from the accumulation of iron in the myocardium, with high production of reactive oxygen species (ROS), lipid peroxidation, and accumulation of hemosiderin as the final biomarker related to cardiomyocyte ferroptosis. Iron overload cardiomyopathy is the leading cause of death in patients with iron overload secondary to chronic blood transfusion therapy; it is also described in hereditary hemochromatosis. GTCS, through repeated hypoxic stress, can increase ROS production in the heart and cause cardiomyocyte ferroptosis. We hypothesized that iron accumulation in the “Epileptic Heart” could be associated with a terminal cardiac arrhythmia described in the IOC and the development of state-potentially in the development of SUDEP. Using the aforementioned PTZ-K and SE-P experimental models, after SUDEP-related repetitive GTCS, we observed an increase in the cardiac expression of hypoxic inducible factor 1α, indicating hypoxic-ischemic damage, and both necrotic cells and hemorrhagic areas were related to the possible hemosiderin production in the PTZ-K model. Furthermore, we demonstrated for the first time an accumulation of hemosiderin in the heart in the SE-P model. These results suggest that uncontrolled recurrent seizures, as described in refractory epilepsy, can give rise to high hypoxic stress in the heart, thus inducing hemosiderin accumulation as in IOC, and can act as an underlying hidden mechanism contributing to the development of a terminal cardiac arrhythmia in SUDEP. Because iron accumulation in tissues can be detected by non-invasive imaging methods, cardiac iron overload in refractory epilepsy patients could be treated with chelation therapy to reduce the risk of SUDEP.

Epilepsy is characterized by an imbalance in neurotransmitter activity; an increased excitatory to an inhibitory activity. Acetylcholine (ACh), serotonin, and norepinephrine (NE) may modulate neural activity via several mechanisms, mainly through its receptors/transporter activity and alterations in the extracellular potassium (K+) concentration via K+ ion channels. Seizures may disrupt the regulation of inwardly rectifying K+ (Kir) channels and alter the receptor/transporter activity. However, there are limited data present on the immunoreactivity pattern of these neurotransmitter receptors/transporters and K+ channels in chronic models of epilepsy, which therefore was the aim of this study. Changes in the immunoreactivity of epileptogenesis-related neurotransmitter receptors/transporters (M2, 5-HT2B, and NE transporter) as well as Kir channels (Kir3.1 and Kir6.2) were determined in the cortex, hippocampus and medulla of adult Wistar rats by utilizing a Pentylenetetrazol (PTZ)-kindling chronic epilepsy model. Increased immunoreactivity of the NE transporter, M2, and 5-HT2B receptors was witnessed in the cortex and medulla. While the immunoreactivity of the 5-HT2B receptor was found increased in the cortex and medulla, it was decreased in the hippocampus, with no changes observed in the M2 receptor in this region. Kir3.1 and Kir6.2 staining showed increase immunoreactivity in the cerebral cortex, but channel contrasting findings in the hippocampus and medulla. Our results suggest that seizure kindling may result in significant changes in the neurotransmitter system which may contribute or propagate to future epileptogenesis, brain damage and potentially towards sudden unexpected death in epilepsy (SUDEP). Further studies on the pathogenic role of these changes in neurotransmitter receptors/transporters and K+ channel immunoreactivity may identify newer possible targets to treat seizures or prevent epilepsy-related comorbidities.

Epilepsy is a group of neurological disorders characterized by abnormal electrical activity in the central nervous system (CNS) and recurrent seizures representing the principal clinical manifestation. Sudden unexpected death in epilepsy (SUDEP) is the predominant cause of death in young epileptic patients. SUDEP patients displayed an increased cardiovascular (CV) risk, probably due to an impaired autonomic control of CV functions, but the underlying mechanisms need to be explored yet. Therefore, we aimed to examine the cardiac morphological alterations in a pentylenetetrazol (PTZ)-kindled rat model, a well-established tool for studying chronic epilepsy. To complete this, the distance between the atria, between the atrium and ventricle were measured, the heart was weighed, and the pathological morphology of dissected hearts was analyzed by histological assessment with hematoxylin and eosin staining. A significantly decreased distance between atria and a significant increase in heart weight were observed in PTZ-kindled rats which interestingly also displayed increased hemorrhagic content when compared with controls. Our findings provided evidence that changes in cardiac morphology may be related to autonomic CV dysfunctions occurring during SUDEP while also opening up more avenues to better develop novel drugs for the treatment of this disorder.

The aim of this project was the determination of the effect of bee bread supplement in diets of obese rats on interleukin 6 immunreactivity. This study has been shown that bee bread against obesity with a high-fat diet reduces IL-6 expression in the stomach.

Tartrazine finds widespread application in the realms of alimentation, pharmaceuticals, cosmetic formulations, and textile manufacturing. Tartrazine has a negative effect on human health such as hyperactivity, allergies and asthma in children. Substances such as tartrazine might effect the embryo in a kind of aspects, containing physical or mental disorders, and a decrease in the child's intellectual memory. In this study, Sprague dawley female rats, 70–100 days old, weighing 250–300 g, with confirmed pregnancy, were divided into two groups of 5: control and tartrazine group. Rats were sacrificed on the 20th day and heart, lung, kidney and liver tissues were removed from the fetuses. The effect of tartrazine on fetal bone development was assessed by double skeletal staining, histological analysis on organs, and IL-6, IL-1β, TNF-α, and TRPM2 gene levels. It has been observed that tartrazine, which is frequently used as a food dye, damages important fetal tissues such as liver, kidney, lung and heart. A statistically meaningful reduce was observed in the total length, total area, bone length and bone area values of the limb bones in the tartrazine group compared to the control group (p

Objective:Experimental and clinical studies indicate that cardiovascular system diseases have the highest mortality rate. One of the major factors underlying this high mortality rate is hypoxia. The inward rectifying potassium channel 6.2 (Kir6.2) plays a key role in the adaptation and metabolic regulation of cardiac tissue to hypoxia. In this study, the effect of chloroquine on Kir6.2 expression in heart tissue exposed to moderate chronic hypoxia was investigated.Methods:In this study, 32 8-12-week-old male Wistar albino rats weighing 200-300 g were used in 4 groups. Accordingly, the first group exposed to a normoxic (at 21% O2 concentration) environment, the second group was administered daily chloroquine (50 mg/kg intraperitoneal) injection in a normoxic environment, the third group exposed to a moderately hypoxic environment (10% O2 concentration), and the fourth group in the hypoxic environment had chloroquine (50 mg/kg intraperitoneal) injection. At the end of the 28-day period, the heart tissues were dissected with anesthesia. Immunohistochemical analysis was performed for Kir6.2 channels.Results:In hypoxic heart tissue, a significant decrease in Kir6.2 immunoreactivity was observed due to chloroquine administration compared to the control group (p

Introduction:Ischemia/reperfusion damage (IRD) is one of the most important factors in the success of organ transplantation. IRD plays a role in both acute and chronic rejection. This study aims to evaluate the effects of lycopene, which is known to be a powerful antioxidant, on experimental uterine IRD.Methods:Twenty-four albino Wistar rats were included in the study and divided into three groups. No substances were administered the sham and ischemia/reperfusion groups. The ischemia/reperfusion and ischemia/reperfusion + lycopene groups were administered ischemia for 1 h and reperfusion for 2 h. The ischemia/reperfusion + lycopene group was administered 2.5 mg/kg lycopene reperfusion intraperitoneally half an hour before ischemia/reperfusion. Both uterine horns were extracted at the end of the procedure. Oxidative stress, inflammation, and apoptosis in the tissues were assessed.Results:The malondialdehyde level, nuclear factor kappa-B immunoreactivity, and apoptotic cell number in the lycopeneadministered group (ischemia/reperfusion + lycopene) were significantly decreased compared with those in the ischemia/ reperfusion group (p

Objective: This study evaluated the biochemical and histopathological effects of propolis oil extract on liver and testicular tissue in rats subjected to alcohol toxicity. Materials and Methods: Sixty Wistar albino rats were randomly assigned into 6 groups: Control, Ethanol (EtOH: 20% ethanol) Propolis-1 (PR1: 100 mg/kgbw) Propolis-2 (PR2: 200 mg/kgbw) EtOH+PR1, and EtOH+PR2. Rats were administered ethanol and propolis by gastric tube for 15 days. Hematological, biochemical, and histopathological (liver and testes) parameters were examined. In addition, sperm concentration and motility were determined. Results: Increased deterioration of complete blood count parameters was statistically significant in the EtOH group when compared to the control group. Propolis was preventative for some effects of EtOH. The most pronounced preventive effect of propolis on ethanol-induced damage was observed in nucleated red blood cells (NRBC) and mean corpuscular hemoglobin concentration (MCHC) parameters (p

Experimental and clinical studies of cardiac pathology associated with epilepsy have demonstrated an impact on the autonomic nervous system (ANS). However, the underlying molecular mechanism has not been fully elucidated. Molecular investigation of the neurotransmitters related receptor and ion channel directing ANS might help in understanding the associated mechanism. In this paper, we investigated the role of acetylcholine (ACh), which demonstrates both sympathetic and parasympathetic roles in targeted expression in terms of the relevant receptor and ion channel. Inwardly rectifying potassium (Kir) channels play a significant role in maintaining the resting membrane potential and controlling cell excitability and are prominently expressed in both the excitable and non-excitable tissues. The immunoreactivity of ACh-activated Kir3.1 channel and muscarinic ACh receptors (M2) in autonomic centers such as the brainstem, vagus nerve (VN) and atria of heart was confirmed by both histological staining and pathological tissue analysis. Significant upregulations of Kir3.1 and M2 receptors were observed in pentylenetetrazol (PTZ)-kindled epileptic rats for all related tissues investigated, whereas no pathological difference was observed. These findings provide proof-of-concept that changes in ACh-associated immunoreactivity might be linked to the ANS dysfunctions associated with epilepsy.