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Background Life-threatening basilar artery dissection (BAD) can be seen following subarachnoid hemorrhage (SAH), but it is not clear whether SAH causes dissection, or not. This study aims to investigate the relationship between degenerative changes in the superior cervical ganglia and the dissection rate of the basilar artery. Method In this study, after 3 weeks of experimental SAH, animals were decapitated. Eighteen rabbits were divided into three groups according to their vasospasm indices. The basilar arteries were examined by anatomical and histopathologic methods. Results Basilar dissection with high vasospasm index (VSI) value (VSI > 3) was detected in six animals (group I); severe basilar edema and moderate VSI value (>2.4) were detected in seven rabbits (group II); and slight VSI value (<1.5) was detected in five subjects (group III). The degenerated neuron densities of the superior cervical ganglia were 12 ± 4 n/mm 3 in group I, 41 ± 8 n/mm 3 in group II, and 276 ± 78 n/mm 3 in group III. The dissected surface values/lumen values were calculated as (42 ± 1)/(64 ± 11) in G-I, (21 ± 6)/(89 ± 17) in group II, and (3 ± 1)/(102 ± 24) in group III. If we look at these ratios as a percentage, it was 62% in group I, 23% in group II, and 5% in group III. Conclusion Inverse relationship between the degenerated neuron densities of the superior cervical ganglia and the dissected surface values of the basilar artery was observed. Common knowledge is that BAD may lead to SAH; however, this study indicates that SAH is the cause of BAD. [ABSTRACT FROM AUTHOR]

The relationship between damage to the liver and spleen by aging and the immune response status in these two organs, which are anatomically and immunologically interconnected, is unknown. The authors investigated the histopathological, ultrastructural, and immunological effects of aging in young and aged fibrotic mice by using an experimental model. Four groups were planned, with 10 mice in each experimental group. The levels of fibrosis and ultrastructural destruction in the liver were determined by α-SMA staining and TEM analysis. Expression levels of immunity genes (Il2, Il4, Il6, Il10, Il12, Il17, Tnf, Ifng, Tgfb1, Gata3, Rorc, Tbx21, Foxp3, Ccl2, Ccr2, Cxcr3, Pf4, Cxcl10) were carried out by qRT-PCR. While structural disorders were detected in the mitochondria of aged healthy group, cellular destruction in the fibrosis-induced elderly group was at a dramatic level. Fibrosis induction in aged mice caused an elevation in the expression of chemokines (CCl2, CXCL10, CCR2) and cytokine (IL-17a) genes that induce autoinflammatory response in the liver. Unlike the cellular pathology and genes activated in fibrosis in youth and the natural occurrence of fibrosis with aging, induction of fibrosis during aging causes deterioration in the liver and expression of genes responsible for autoimmunity in both the liver and spleen. [ABSTRACT FROM AUTHOR]

Traumas are the most important cause of mortality in the pediatric population. Bleeding is an important complication, especially in traumatic brain injuries with coagulation problem addition. Low-velocity penetrating brain injuries may be caused by sewing needles, nails, and knives. There are few studies in the literature for this injury type. This study presented a surgical technique and treatment to increase hemostasis in a 2-year-old patient after a sewing needle injury. [ABSTRACT FROM AUTHOR]

Adults with end-stage of chronic liver diseases have lower antibody titers after hepatitis-B vaccination. We have less amount of knowledge about the effect of non-viral cause chronic liver fibrosis on vaccination. In this study, we investigated the effect of non-viral chronic liver fibrosis on hepatitis B vaccine and the effect of tetanous toxoid co-administration at the level of humoral and cellular immune responses in an experimental model. Hepatitis B vaccine was administered either alone or in combination with tetanus toxoid in thioacetamide-induced fibrotic BALB/c mice. Fibrosis level was determined by Knodell scoring. Anti-HBsAg, biochemical parameters, inflammatory (IL-1β, TNF-α), and anti-inflammatory (IL-10) cytokine levels were investigated in serum samples by automated systems and ELISA; respectively. Frequencies of activated lymphocytes were determined in flow cytometer. Antibody titers significantly decreased after immunization of fibrotic mice. However, co-administration of toxoid significantly elevated antibody titer. The percentage of CD19+CD69+ B lymphocytes was found to be lower in vaccinated fibrotic group compared to vaccinated naive group. Simultaneous administration of toxoid significantly increased the frequencies of CD4+ and CD8+ T cells expressing CD69 and CD127. Interestingly, CD19+CD5+CD1high Breg cells were significantly reduced in the group vaccinated with hepatitis B vaccine and toxoid, simultaneously. The reduction in Breg percentage did not expose a significant decrease in the level of IL-10. Non-viral chronic liver fibrosis causes a reduction on specific antibody level after vaccination. Reduction on Breg cell frequency may have an effect on elevation of antibody level after co-administration of tetanus toxoid. [ABSTRACT FROM AUTHOR]

Objective: We investigated the presence of thromboembolism that may develop in hippocampal arteries due to decreased cerebrospinal fluid volume because of choroid plexus damage caused by subarachnoid hemorrhage. Materials and Methods: Twenty-four rabbits were included as test subjects in this study. The study group comprised 14 test subjects administered autologous blood (0.5 mL). Coronary sections of the temporal uncus were prepared to observe the choroid plexus and the hippocampus together. Cellular shrinkage, darkening, halo formation, and ciliary element loss were considered criteria for degeneration. Blood--brain barriers were also examined in the hippocampus. The density of degenerated epithelial cells in the choroid plexus (n/mm³) and thromboembolisms in the hippocampal arteries (n/cm²) were compared statistically. Results: Histopathological examination revealed that the number of degenerated epithelial cells in the choroid plexus and the number of thromboembolisms in the hippocampal arteries were 7 ± 2 and 1 ± 1 in group 1, 16 ± 4 and 3 ± 1 in group 2, and 64 ± 9 and 6 ± 2 in group 3, respectively. The significance levels were P < .005 for group 1 vs. group 2, P < .0005 for group 2 vs. group 3, and P < .00001 for group 1 vs. group 3. Conclusion: This study demonstrates that decreased cerebrospinal fluid volume induced by choroid plexus degeneration causes cerebral thromboembolism following subarachnoid hemorrhage, which has not been previously described. [ABSTRACT FROM AUTHOR]

Background/aim: In this study, we evaluate sciatic nerve injuries due to intramuscular injections, which is an important medicolegal problem frequently encountered in medical practice, with an extended experimental rat model of peripheral nerve injury. Materials and methods: A total of 78 male Wistar albino rats were divided into five main groups, including a control group, a sham saline group, and groups that received benzathine penicillin G, diclofenac sodium, and dexamethasone, respectively. These pharmaceutical agents were applied to the sciatic nerves of all rats after exploration in the epineurial, endoneurial, and intrafascicular compartments, excluding the control group. Outcomes were evaluated for all rats and their sciatic nerves according to functional, electrophysiological, and histopathological results. Results: Injuries were most evident in the groups that received penicillin G and diclofenac sodium, and this finding was statistically significant. It was also found that endoneurial and intrafascicular injections may cause more harm than epineurial injections. Conclusion: We have demonstrated that any medical injections applied to the epineurial, endoneurial, or intrafascicular compartments of the sciatic nerve may cause functional and electrophysiological loss with or without deterioration of the peripheral nerve architecture. [ABSTRACT FROM AUTHOR]

Aim: The c-Jun NH2-terminal kinases (JNK) signaling pathway is an important signaling pathway in liver regeneration. it was planned to investigate the expression levels of Mitogen Activated Protein Kinase Kinase (MKK)-4 and -7 (MKK7), which are mediator molecules involved in the JNK signaling pathway and Activating Transcription Factor (ATF) 2 transcription factor genes, which are in the last stage of the signaling pathway, in liver tissues in young and old mice. In addition, it was aimed to examine the ultrastructural changes caused by aging in hepatocytes. Material and Methods: We examined MKK4, MKK7 and ATF2 expression levels by using Real Time Polymerase Chain Reaction (RT-qPCR) method. Transmission electron microscopy (TEM) was used to observe the ultrastructural changes of hepatocytes. Results: While MKK4 and ATF2 gene expressions reduced in the liver of aged mice, MKK7 gene expression did not change. In TEM examinations, granular endoplasmic reticulum loss and mitochondrial damage were observed in elderly individuals. Conclusion: According to these results, spontaneous liver damage that can be seen in aged subjects may be caused by disruption in cellular signaling pathways and organelle damage in hepatocytes. [ABSTRACT FROM AUTHOR]

Objective: Lipoxins are anti-inflammatory, pro-resolving molecules that are secreted by immune cells such as neutrophils and macrophages. Lipoxins are a metabolite of the arachidonic acid pathway that resolve inflammation in fibrotic liver by producing several anti-inflammatory molecules. In this study, phenotypic distribution activation markers of lymphocytes in the spleen and expression levels of chemokines (chemokine (C-X-C motif) receptor 3, chemokine (C-X-C motif) ligand 10) cytokines (interferon gamma, tumor necrosis factor alpha, interleukin-6, interleukin-10) in the liver of lipoxin A4-treated fibrotic mice were investigated. Materials and methods: Liver fibrosis was induced in BALB/c mice by thioacetamide administration. Lipoxin A4 was administered during last 2 weeks of induction. Fibrosis level was determined by using Knodell scoring. Lymphocytes were identified by flow-cytometry. Expression levels of genes were measured by quantitative real time polymerase chain reaction in liver homogenates. Results: Lipoxin A4 treatment caused an elevation of T-lymphocyte percentage in the spleen. Interestingly, administration of lipoxin A4 significantly reduced B-lymphocyte population in spleen of fibrotic group. CD8+ cytotoxic T cell frequency significantly reduced in thioacetamide-induced mice; however, lipoxin A4 administration increased that percentage significantly. Lipoxin A4 treatment significantly reduced frequency of activated (CD8+CD69+) cytotoxic T cells. Expression levels of chemokines significantly reduced in the liver after lipoxin A4 treatment. While expression levels of interferon gamma, tumor necrosis factor alpha, and interleukin-6 significantly reduced in the liver after lipoxin A4 treatment, an anti-inflammatory cytokine interleukin- 10 expression was almost at similar levels in all experimental groups. Conclusion: Lipoxin A4 performs its anti-inflammatory effect by reducing the frequency of activated T cells and expression levels of chemokines cytokines responsible from inflammatory immune response in the liver. [ABSTRACT FROM AUTHOR]

Aim: Panel Reactive Antibodies (PRA) analysis is important not only in virtual cross-match of donors and recipients but also in follow-up of recipients immune response after transplantation. Although bead based tests give faster and more reliable, it may have false positive and negative results. We investigated HLA groups of patients with false negative results and the frequencies of anti- HLA antibodies in all three false negative situations. Materials and Methods: PRA results of all patients were divided into 3 groups according to negative controls and samples results. First one is negative controls were false negative and samples were false negative (1st Situation); second one is negative controls were false negative but samples were true negative (2nd Situation); third one is negative controls were true negative but samples were false negative (3rd Situation). All serum samples were tested by bead based Luminex assay. Results: While anti-HLA-A68, A24, A32 were the most frequent antibodies for the first situation, anti-HLA-A03,24,32 were the most frequent three antibodies for the second situation. In case of anti-HLA-B antibodies; anti-HLA-B38, B44, B48 were detected for the first situation, and anti-HLA-B44, B58, B49 were detected for the second situation. In case of class II antibodies; we detected anti-HLA-DRB110, DRB115 and DRB151 antibodies as the most frequent three antibodies at 1st situation. Frequencies of anti-HLA antibodies of 120 patients with false negative results were determined in serum samples. In case of 3rd situation, while anti-A23, A68, A24; anti-B06, B04, B39 and anti-Cw07 were the most frequent anti-HLA Class I antibodies, anti-HLA DQ07, DQ05, DQ04 and anti-HLA-DRB152, DRB113, DRB153 were the most frequent HLA-Class II antibodies detected in serum samples. Conclusion: Samples with false negative PRA results should be repeated and these samples should be recorded in the laboratory for internal control system. [ABSTRACT FROM AUTHOR]

Introduction: Olfaction and its relation to human health is an area of growing interest. Although olfaction disorders have been considered a part of Kallmann syndrome, the role of olfactory dysfunction on spermatogenesis has not been studied yet. We studied if olfactory bulbectomy (OBX) causes dysfunction in spermatogenesis as a result of Onuf's nucleus damage. Methods: Twenty-eight male rats were divided into three groups: six as the control (G-1; n = 6), six as the only frontal burr hole applied animals SHAM (G-2; n = 6), and 16 as the study group (G-3; n = 16) in which OBX was performed. The animals were followed for 2 months. After the decapitation of the animals, olfactory bulb (OB) volumes (mm3), the neuron density of the Onuf's nucleus (n/mm3), and sperm density (n/mm3) were estimated stereologically and analyzed. Results: OB volumes (mm3), degenerated neuron density of Onuf's nucleus (n/mm3), and sperm numbers of control, SHAM, and study groups were estimated as: 4 ± 0.5; 6 ± 2 and 103.245 ± 10.841 in G-1; 3.5 ± 0.7; 14 ± 4 and 96.891 ± 9.569 in G-2; and 1.3 ± 0.3; 91 ± 17 and 73.561 ± 6.324 in G-3. The statistical results of degenerated neuron density of Onuf's nucleus and sperm numbers between groups are p < 0.005 for G-1/G-2; p < 0.0005 for G-2/G-3; and p < 0.00001 for G-1/G-3. Discussion: This study first time indicates that Onuf's nucleus degeneration secondary to OBX seems to be responsible for reduced sperm numbers. [ABSTRACT FROM AUTHOR]

Hydatid cyst of the posterior cranial fossa is rarely seen. We report the case of a 13-year-old girl with extradural hydatid cyst of the posterior cranial fossa presenting with the symptoms of high intracranial pressure. Diagnosis was made by radiological investigations and confirmed during surgery and by histological examination. Cranial hydatid cyst must be considered especially in children presenting with the symptoms of raised intracranial pressure and living in endemic areas. [ABSTRACT FROM AUTHOR]

Objective: Cerebral hydatid disease is a rare manifestation of echinococcosis but it constitutes a significant part of all intracranial mass lesions. This study aims to determine the clinical, radiological and surgical features of brain hydatidosis and share our experience. Method: Medical records of ten patients with cerebral hydatid disease were retrospectively reviewed. Clinical presentations, radiological examinations, treatment modalities and outcomes of the patients were analyzed. Results: All patients were admitted from the rural areas. Nine patients had E. Granulosus cyst and one patient had E. Multilocularis cyst. The cyst was solitary in nine patients and multiple in one. Multiple organ involvement was found in one patient. Cysts were located in the right cerebral hemisphere in five patients, left cerebral hemisphere in four patients and posterior fossa in one. All patients were treated surgically. Complications related to surgery were observed in four patient. All patients improved after the treatment. There were no recurrences or residual cysts among the patients. Conclusion: Hydatic disease should considered in the differential diagnosis of intracranial space occupying lesions in developing countries. Early diagnosis of cerebral hydatid cysts may prevent serious life-threatening complications of this disease. Outcome is favourable when the cyst is completely removed without rupture. [ABSTRACT FROM AUTHOR]