Inflammation in cerebral ischemia reperfusion improved by avanafil via nod-like receptor protein-3 inflammasome: an experimental study in rats.

OBJECTIVE: The aim of study was to investigate the effect of avanafil, a second-generation phosphodiesterase-5 (PDE5) inhibitor, on cerebral ischemia reperfusion (CI/R) model. METHODS: 32 male albino Wistar rats were used. Four groups were constituted, as I: the healthy (sham), II: the CI/R group, III: the CI/R +I 10 mg/kg avanafil group, and IV: the CI/R + 20 mg/kg avanafil group. Avanafil was administered twice via oral gavage, first shortly after ischemia reperfusion and once more after 12 h. The rats were euthanized after 24 h. Histopathological and Real Time PCR analyzes were performed on cerebral tissues. RESULTS: IL-1ß, NLRP3 and TNF-α mRNA expressions were statistically higher in the CI/R group when compared to healthy (sham) group. Conversely, the IL-1ß, NLRP3, and TNF-α mRNA expressions were significantly decreased in both of the avanafil-treated groups when compared to CI/R group. Histopathological results showed that both doses of avanafil also decreased cellular damage in cerebral tissue that occurred after CI/R. CONCLUSION: Avanafil, was found to have ameliorated inflammatory response and cellular injury caused by CI/R. The mRNA expression of IL-1ß, NLRP3, and TNF-α decreased in the I/R groups and approached the control group levels with a high dose of avanafil.

Use of bee venom in preventive medicine: An experimental hepatic encephalopathy study in rats.

OBJECTIVES: Bee venom is used for medicinal purposes, including the treatment of neurological and liver diseases, but its use as a primary health care approach for preventive purposes requires further exploration. The aim of this study was to provide the first investigation into the possible protective effects of bee venom against hepatic encephalopathy, a serious neurodegenerative disease. MATERIALS AND METHODS: An experimental animal study was conducted in which healthy albino Sprague-Dawley rats were randomized into three groups: healthy, control and bee venom groups. All rats were tested for locomotor activity at the beginning and end of the study. No intervention was made in the healthy group, whereas hepatic encephalopathy was induced in the control and bee venom groups by the administration of thioacetamide (TAA) (200 mg/kg/day). The bee venom group also received bee venom (5 mg/kg/day) subcutaneously every day for 14 days prior to the TAA administration. RESULTS: The results for the final locomotor activity tests were statistically better in the bee venom group than in the control group, supporting a beneficial effect of prophylactic bee venom application. Blood ammonia levels and liver weights, determined as indicators of inflammation, were lower in the bee venom group than in the control group and were close to levels in the healthy group, but not statistically significant. CONCLUSIONS: Bee venom administration has protective effects against the development of hepatic encephalopathy and offers a promising therapeutic opportunity in preventive medicine.

Evaluation of the relationship among gene expressions and enzyme activities with antioxidant role and presenilin 1 expression in Alzheimer's disease.

It is known that oxidative stress originating from reactive oxygen species plays a role in the pathogenesis of Alzheimer's disease. In this study, the role of antioxidant status associated with oxidative stress in Alzheimer's disease was investigated. Peripheral blood samples were obtained from 28 healthy individuals (as control) and 28 Alzheimer's patients who met the National Institute of Neurological and Communicative Diseases and Stroke/Alzheimer's Disease and Related Disorders Association criteria. Catalase, glutathione S-transferase and paraoxonase 1 enzyme activities in blood plasma and glutathione S-transferase enzyme activities in erythrocytes were determined by spectrophotometer. Catalase, glutathione S-transferase and presenilin 1 gene expressions in leukocytes were determined using qRT-PCR. Data were analysed with SPSS one-way anova, a LSD post hoc test at p < 0.05. The activity of each enzyme was significantly reduced in Alzheimer's patients compared to control. The catalase gene expression level did not change compared to the control. Glutathione S-transferase and presenilin 1 gene expression levels were increased compared to the control.

How to diagnose COVID-19 in family practice? Usability of complete blood count as a COVID-19 diagnostic tool: a cross-sectional study in Turkey.

OBJECTIVE: COVID-19 is currently diagnosed in hospital settings. An easy and practical diagnosis of COVID-19 is needed in primary care. For this purpose, the usability of complete blood count in the diagnosis of COVID-19 was investigated. DESIGN: Retrospective, cross-sectional study. SETTING: Single-centre study in a tertiary university hospital in Erzurum, Turkey. PARTICIPANTS: Between March 2020 and February 2021, patients aged 18-70 years who applied to the hospital and underwent both complete blood count and reverse-transcription-PCR tests for COVID-19 were included and compared. Conditions affecting the test parameters (oncological-haematological conditions, chronic diseases, drug usage) were excluded. OUTCOME MEASURE: The complete blood count and COVID-19 results of eligible patients identified using diagnostic codes [U07.3 (COVID-19) or Z03.8 (observation for other suspected diseases and conditions)] were investigated. RESULTS: Of the 978 patients included, 39.4% (n=385) were positive for COVID-19 and 60.6% (n=593) were negative. The mean age was 41.5±14.5 years, and 53.9% (n=527) were male. COVID-19-positive patients were found to have significantly lower leucocyte, neutrophil, lymphocyte, monocyte, basophil, platelet and immature granulocyte (IG) values (p<0.001). Neutrophil/lymphocyte, neutrophil/monocyte and IG/lymphocyte ratios were also found to be significantly decreased (p<0.001). With logistic regression analysis, low lymphocyte count (OR 0.695; 95% CI 0.597 to 0.809) and low red cell distribution width-coefficient of variation (RDW-CV) (OR 0.887; 95% CI 0.818 to 0.962) were significantly associated with COVID-19 positivity. In receiver operating characteristic analysis, the cut-off values of lymphocyte and RDW-CV were 0.745 and 12.35, respectively. CONCLUSION: Although our study was designed retrospectively and reflects regional data, it is important to determine that low lymphocyte count and RDW-CV can be used in the diagnosis of COVID-19 in primary care.

Predictive role of trigeminal ganglion ischemia on scalp survival affected by temporal artery diameters: The first experimental study.

Scalp arteries are mainly innervated by trigeminal, facial, and vagal nerves. The ischemic neurodegeneration of the trigeminal ganglion can impede scalp circulation via vasospasm-creating effects. This study was designed to investigate whether there is any link between the vasospasm index of deep temporal arteries and ischemic neuron densities of the trigeminal ganglion after subarachnoid hemorrhage. The study subjects included five normal control rabbits, six sham rabbits, and nine rabbits chosen from a formerly established experimental subarachnoid hemorrhage group created by cisternal homologous blood injection (0.75 mL). These rabbits, all male, were followed up for 3 weeks. The trigeminal ganglion and deep temporal artery vasospasm indexes were examined by stereological methods. Ischemic neuron densities of the trigeminal ganglion and vasospasm index values of deep temporal arteries were compared statistically. Postmortem examinations showed important vasospasms of deep temporal arteries, foramen magnum herniations, and neurodegeneration of the trigeminal ganglion. The mean vasospasm index values and degenerated neuron densities of the trigeminal ganglion were determined as 1.03 ± 0.13 and 10 ± 3/mm3 (p > 0.5) in the control group, 1.21 ± 0.18 and 35 ± 9/mm3 in the sham group (p < 0.005 for sham vs. control), and 2.54 ± 0.84 and 698 ± 134/mm3 in the experimental group (p < 0.0005 for sham vs. control and p < 0.00001 for study vs. control). There was an inverse relationship between the vasospasm index values and the degenerated neuronal density of the trigeminal ganglion. The high degenerated neuron density in the trigeminal ganglion had a facilitative effect on temporal artery vasospasm. Trigeminal ganglion neurodegeneration may promote temporal artery vasospasms after subarachnoid hemorrhage, which has not been previously mentioned in the literature.

Does Intravitreal Dopamine Agonist and Antagonist Administration Have Effects on the Brain? An Experimental Study in Rats.

OBJECTIVE: There might be dopaminergic connections between the retina and the brain. In this context, the study was aimed to investigate the possible interaction between the retina and basal ganglia through the dopaminergic system. MATERIALS AND METHODS: In total, 32 healthy rats were randomized into 4 groups: healthy, Sham, dopamine antagonist injected group (risperidone, 0.04 mg/kg intravitreally), and dopamine agonist injected group (apomorphine, 0.4 mg/kg intravitreally). The locomotor activity and Morris water maze tests were applied to all rats twice, before the injection and 28 days after, to detect changes in movement, memory, and attention. Histopathologically, the basal ganglia and hippocampus regions were removed and examined. RESULTS: In the locomotor activity test, a statistical significance was found between the first and last measurement values of the apomorphine group and a decrease in activities and an increase in resting times (P < .05). In the Morris water maze test, a statistical significance was detected between the first and last tests of the control group and the apomorphine groups and showed significantly shorter learning times (P < .05). Histological analyses of the substantia nigra and hippocampus were noteworthy in that the number of damaged neurons in the risperidone group was considerably higher than the other groups. The number of damaged neurons in the apomorphine group was significantly lower than in the healthy group. CONCLUSION: Intravitreal administration of dopamine agonists and antagonists has given rise to alterations in the cerebral dopaminergic system, leading to changes in locomotor activity and memory and histopathological changes.

An antihypertensive agent benidipine is an effective neuroprotective and antiepileptic agent: an experimental rat study.

BACKGROUND: Benidipine is an L, N and T type calcium channel blocker drug that is widely used as an antihypertensive drug. OBJECTIVE: For the first time in the literature, it was aimed to investigate the effectiveness of benidipine in controlling epileptic seizure and preventing the development of neurodegeneration in epilepsy. METHODS: An experimentally epilepsy model was produced with pentylenetetrazole, and rats were divided into seven groups, in different benidipine treatment doses or with valproic acid combinations. The epileptic activities of all rats were recorded according to the Fisher&Kittner classification. Biochemical parameters, histopathological Caspase-3 activity, Wyler hippocampal sclerosis, gliosis and neuronal degenerations were investigated. RESULTS: It was found that in the post-hoc analysis of epileptic activities, there was a similar antiepileptic scores among the treatment groups. IL-1 level was found to be significantly lower in the benidipine 4 mg/kg group, and TNF-alpha was lower in the group given valproic acid+benidipine 2 mg/kg (p<0.05). The other biochemical parameters were not found to be significant. Neural degeneration levels in the brain tissues were statistically significant (p<0.001). Compared with the healthy group, the most neural degeneration was in the control group, the least neural degeneration was in the valproic acid+benidipine 4 mg/kg group. CONCLUSIONS: For the first time in the literature, benidipine, alone or combined with valproic acid, were found to have a statistically significant antiepileptic efficacy, and provided neuroprotection when combined with valproic acid. Benidipine will be a promising agent in the treatment of epilepsy with its antiepileptic and neuroprotective effects.

A new experimental evidence that olfactory bulb lesion may be a causative factor for substantia nigra degeneration; preliminary study.

Background: Anosmia has been considered as the first diagnostic criteria of Parkinson disease (PD), we investigated the effect of the olfactory bulbectomy (OBX) on histopathological features of the substantia nigra in an animal model.Methods: Twenty-seven male rats were used in this study. Animals were divided into three groups as five (control), six SHAM and sixteen study (OBL) groups. Nothing was done in the control group, the only burr hole was done in the SHAM group, OBL was not applied, and bilateral OBL was performed in the study group, and followed ten weeks, then animals were decapitated. Olfactory bulb volumes were measured by macro anatomically. The olfactory bulbs and substantia nigra sections were analyzed by a stereological method to evaluate olfactory glomerulus and neuron density of substantia nigra per cubic centimeter and compared with statistically.Results: The mean olfactory bulb volume, degenerated olfactory glomerulus density and degenerated neuron density of substantia nigra were measured as:(4.14 ± 0.20) mm3, (1 ± 1)/mm3 and (7 ± 2)/mm3 in control (Group I); (3.6 ± 0.16)/mm3, (4 ± 1)/mm3 and(32 ± 7)/mm3 in SHAM (Group II) and (2.2 ± 0.9)/mm3, (112 ± 18)/mm3 and (1543 ± 115)/mm3in study group (Group III). Diminished olfactory bulb volume was observed in Group III animals.Conclusions: We concluded that OBL may lead to the degeneration of substantia nigra.

Differential Diagnosis of Ischemic Vertigo by Optical Coherence Tomography.

OBJECTIVE: This study aimed to evaluate the differences in the mean retinal nerve fiber layer (RNFL) thickness using optical coherence tomography (OCT) in patients with early stage central vertigo with or without vertebrobasilar stenosis detected by Doppler ultrasound. MATERIALS AND METHODS: A total of 50 patients with ischemic vertigo and 50 healthy individuals were included in the study. The distinction between central and peripheral vertigo was determined by physical and neurological examinations and the Dix-Hallpike maneuver. For all patients, the mean RNFL thickness was determined using OCT performed by 2 independent ophthalmologists. RESULTS: There were no significant differences between the groups in terms of age and sex distribution (p>0.05). On average, in superior, inferior, and temporal quadrants, there was a statistically significant difference between the control and patient groups (p<0.001). CONCLUSION: The retina may be affected in patients with ischemic vertigo because of atherosclerotic ischemic lesions in the carotid and vertebral arteries. Neuroimaging methods and OCT were evaluated together to develop a new diagnostic approach. With OCT, which is a non-invasive method, early and more objective differential diagnosis will be possible.

A Rare Neurologic Disease that Mimics Cranial Hydatid Cyst: Leukoencephalopathy, Cerebral Calcifications, and Cysts.

A 33-year-old male patient was admitted to the clinic with seizures and progressive neurologic symptoms. In the family history of the patient, a first degree relative had a history of hydatid cyst surgery. Cranial computed tomography images showed intracranial cysts and calcifications. Thus, it was suspected that it might be hydatid cyst. However, the patient was diagnosed with leukoencephalopathy with intracranial calcifications and cysts, a rare neurologic entity by advanced radiologic imaging, serologic and pathologic evaluation.

New determinants for casual peripheral mechanism of neurogenic lung edema in subarachnoid hemorrhage due to ischemic degeneration of vagal nerve, kidney and lung circuitry. Experimental study1.

PURPOSE: To evaluate whether there is a relationship between renal artery vasospasm related low glomerular density or degeneration and neurogenic lung edema (NLE) following subarachnoid hemorrhage. METHODS: This study was conducted on 26 rabbits. A control group was formed of five animals, a SHAM group of 5 to which saline and a study group (n=16) injected with homologous blood into the sylvian cisterna. Numbers of degenerated axons of renal branches of vagal nerves, atrophic glomerulus numbers and NLE scores were recorded. RESULTS: Important vagal degeneration, severe renal artery vasospasm, intrarenal hemorrhage and glomerular atrophy observed in high score NLE detected animals. The mean degenerated axon density of vagal nerves (n/mm2), atrophic glomerulus density (n/mm3) and NLE scores of control, SHAM and study groups were estimated as 2.40±1.82, 2.20±1.30, 1.80±1.10, 8.00±2.24, 8.80±2.39, 4.40±1.14 and 154.38±13.61, 34.69±2.68 and 12.19±1.97 consecutively. Degenerated vagal axon, atrophic glomerulus and NLE scores are higher in study group than other groups and the differences are statistically meaningful (p<0.001). CONCLUSION: Vagal complex degeneration based glomerular atrophy have important roles on NLE following SAH which has not been extensively mentioned in the literature.

Predeterminative role of Onuf's nucleus ischemia on mesenteric artery vasospasm in spinal subarachnoid hemorrhage: A preliminary experimental study.

BACKGROUND: Although posttraumatic mesenteric artery ischemia is attributed to various etiologies, sacral parasympathetic network/mesenteric artery relations have not been studied so far. The primary objective of this study is to elucidate whether there is a relationship between Onuf's nucleus ischemia and mesenteric artery vasospasm following subarachnoid hemorrhage (SAH). METHODS: This study was conducted on 22 rabbits. The animals were grouped as follows: 5 of animals control, 5 SHAM which saline was given, and 12 animals study group that was homologous blood injected into the spinal subarachnoid space at the Li level. Neurodegeneration in Onuf's nucleus, axonal degeneration of S2 roots, and mesenteric arteries vasospasm indexes (VSI; Wall surface/Lumen surface), brachias of mesentery arteries in various tissues and ischemic mucosal changes of intestines of all animals were determined histopathologically. Important degenerative changes were detected in axons in S2 roots and Onuf's nucleus in severe mesenteric artery vasospasm observed. RESULTS: The mean degenerated neuron density of Onuf's nucleus (n/mm3), degenerated axon density in S2 roots (n/mm2), and VSI values of mesenteric arteries of control, SHAM, and study groups were estimated as 5.00 ± 1.58, 4.00 ± 1.58, 1.76 ± 0.13; 18.29 ± 4.31, 11.00 ± 2.24, 2.23 ± 0.20; and 135.21 ± 30.75, 117.33 ± 22.11, 2.81 ± 0.44, respectively. Statistical analyses between the VSI values, mucosal ischemic changes degenerated neurons in Onuf's nucleus, and axons in S2 levels were meaningful (p < 0.005). CONCLUSION: We interestingly noticed that Onuf's nucleus-S2 roots complex degeneration plays an important role in mesenteric artery vasospasm and the development of intestinal ischemic mucosal changes following SAH which has not been extensively mentioned in the literature.

Exploring of the Unpredicted Effects of Olfactory Network Injuries on Mammary Gland Degeneration: A Preliminary Experimental Study.

Purpose of the study: Hypofunctioning breasts are typically considered a dysfunction of higher brain centers that regulate hormonal feedback, and olfactory information has been proposed as a triggering factor for lactation in the maternal body. However, there are no substantive studies regarding whether olfaction disorders and/or loss of olfactory sense may result in breast gland atrophy by causing diminished olfactory stimulation. To fill this gap in the literature, we studied the histologic features of breast glands as a sample model in animals that had undergone an olfactory bulb lesion (OBL). Materials and methods: This study was conducted on 22 rats. Six, eight, and six of them were used as control, SHAM, and OBL groups, respectively. After 10 weeks, the animals were decapitated. Olfactory bulbs and breast glands were stained with Hematoxylin-eosin and tunnel dye. Specimens were analyzed stereologically to evaluate the loss in volume of the olfactory bulbs, total breast follicle volume (TBFV) and Meissner's corpuscles per cubic centimeter, and these two senior metrics were compared with each other statistically. Results: Olfactory bulb volume loss and breast gland atrophy were both detected in study group. Mean TBFV and OB volumes were measured as: (296 ± 89) × 106 µm3/cm3 and 4.43 ± 0.98 mm3 in control (Group I); (264 ± 63) × 106 µm3/cm3 and 3.86 ± 0.81 mm3 in SHAM (Group II) and (194 ± 52) × 106 µm3/cm3 and 1.52 ± 0.36 mm3 in OBL group (Group III). It was noted that the TBFV was significantly diminished, with apoptotic degradation in the olfactory bulbs and breast glands of OBL-applied animals (p < 0.001). Conclusion: It seems that diminished milk secretion is attributable to the degradation of breast glands that results from olfaction loss in OBL animals.

New determinants for casual peripheral mechanism of neurogenic lung edema in subarachnoid hemorrhage due to ischemic degeneration of vagal nerve, kidney and lung circuitry. Experimental study

Abstract Purpose: To evaluate whether there is a relationship between renal artery vasospasm related low glomerular density or degeneration and neurogenic lung edema (NLE) following subarachnoid hemorrhage. Methods: This study was conducted on 26 rabbits. A control group was formed of five animals, a SHAM group of 5 to which saline and a study group (n=16) injected with homologous blood into the sylvian cisterna. Numbers of degenerated axons of renal branches of vagal nerves, atrophic glomerulus numbers and NLE scores were recorded. Results: Important vagal degeneration, severe renal artery vasospasm, intrarenal hemorrhage and glomerular atrophy observed in high score NLE detected animals. The mean degenerated axon density of vagal nerves (n/mm2), atrophic glomerulus density (n/mm3) and NLE scores of control, SHAM and study groups were estimated as 2.40±1.82, 2.20±1.30, 1.80±1.10, 8.00±2.24, 8.80±2.39, 4.40±1.14 and 154.38±13.61, 34.69±2.68 and 12.19±1.97 consecutively. Degenerated vagal axon, atrophic glomerulus and NLE scores are higher in study group than other groups and the differences are statistically meaningful (p<0.001). Conclusion: Vagal complex degeneration based glomerular atrophy have important roles on NLE following SAH which has not been extensively mentioned in the literature.