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Background and Objectives: Lymphedema is a progressive, chronic condition. Traumatic damage to the lymphatics, removal of lymph nodes, and/or radiation are the major causes of fibrosis and a subsequent pathological cascade. Macrophages play a crucial role in wound healing, with M1 macrophages known for their pro-inflammatory effects and M2 macrophages recognized for their anti-inflammatory effects, including improved angiogenesis, lymph angiogenesis, and tissue healing. This study aims to assess the use of calcitriol to alter the M2/M1 macrophage balance, reduce tissue fibrosis in a lymphedema model, promote new micro-lymphatic vessel formation, and evaluate the benefits of active vitamin D. Material and Methods: Forty-five rats were randomly divided into three groups: control surgery (group A), surgery with preoperative–postoperative calcitriol (group B), and postoperative calcitriol (group C). One week after the surgical ablation a total dose of 20 Gy radiation therapy was administered to the operated groin region. Micro-computed tomography was used for limb volume calculation, fluorescence lymphatic imaging was used to assess the presence of lymphedema, and histopathological analyses were conducted to evaluate the M1/M2 macrophage ratio, fibrosis accumulation, and lymph angiogenesis. Results: The micro-computed tomography evaluation revealed that 75% of the rats of group A exhibited long-lasting lymphedema. In group B, the initial lymphedema ratio was the lowest, affecting only 25% of the rats. After ligating the main vessels, a linear lymphatic microvascular structure was observed in groups B and C. Group B had a significant increase in M2 macrophages and newly formed lymphatic vessels (p < 0.05). However, group A showed a significant elevation of M1 macrophages and collagen accumulation (p < 0.05) in the surgically treated hind limb. Conclusions: Both histological analyses and clinical results reported a relevant influence of calcitriol administration. Among all groups, the most favorable outcomes were seen in group B (prophylaxis group). Hence, calcitriol administration could play a crucial role in enhancing the migration of M2 macrophages to the damaged tissue. Such migration may contribute to lymphedema resolution either by enhancing the organization of superficial lymphatic vessels or resolving fibrosis, or with a combination of both these mechanisms.

ABSTRACT Introduction: Custodiol (histidine-tryptophan-ketoglutarate) and repetitive blood cardioplegia are the solutions for myocardial protection and cardiac arrest. In this study, we aimed to compare immunohistochemical analysis, clinical outcomes, and cardiac enzyme values of Custodiol and blood cardioplegia groups. Methods: This was a randomized prospective study consisting of 2 groups and 20 patients, 10 patients for each group, who underwent mitral and mitral/tricuspid valve surgery. Group 1 was formed for Custodiol cardioplegia and group 2 for blood cardioplegia. Perioperative and postoperative cardiac events were recorded, cardiac enzymes were analyzed with intervals, and myocardial samples were taken for immunohistochemical analysis. Recorded data were statistically evaluated. Results: There was no significant difference for the Custodiol and blood cardioplegia groups in perioperative and postoperative cardiac performance and adverse events. Cardiac enzyme analysis showed no significant difference between groups. However, two parameters (eNOS, Bcl-2) were in favor of the Custodiol group in immunohistochemical studies. Custodiol performed better in cellular oxidative stress resistance and cellular viability. Conclusion: Clinical outcomes and cardiac enzyme analysis results were similar regarding myocardial protection. However, Custodiol performed better in the immunohistochemical analysis.

Objective: Autosomal recessive cutis laxa type IIA (ARCL2A) is a rare congenital disorder characterized by loose and elastic skin, growth and developmental delay, and skeletal anomalies. It is caused by biallelic mutations in ATP6V0A2. Those mutations lead to increased pH in secretory vesicles and thereby to impaired glycosyltransferase activity and organelle trafficking. We aimed to identify the genetic and molecular cause of the unexpected hematological findings in a Turkish family. Materials and Methods: We performed clinical, genetic, and histological analyses of a consanguineous family afflicted with wrinkled and loose skin, microcephaly, intellectual disability, cleft lip and palate, downslanting palpebral fissures, ectopia lentis, bleeding diathesis, and defective wound healing. Results: Linkage analysis using SNP genotype data yielded a maximal multipoint logarithm of odds score of 2.59 at 12q24.21-24.32. Exome sequence analysis for the proband led to the identification of novel homozygous frameshift c.2085_2088del (p.(Ser695Argfs*12)) in ATP6V0A2, within the linked region, in the two affected siblings. Conclusion: Our patients do not have gross structural brain defects besides microcephaly, strabismus, myopia, and growth or developmental delay. Large platelets were observed in the patients and unusual electron-dense intracytoplasmic inclusions in fibroblasts and epidermal basal cells were observed in both affected and unaffected family members. The patients do not have any genetic defect in the VWF gene but von Willebrand factor activity to antigen ratios were low. Clinical findings of bleeding diathesis and defective wound healing have not been reported in ARCL2A and hence our findings expand the phenotypic spectrum of the disease.

Objective: It is widely known that myocardial damage is not immediately terminated after the elimination of epicardial occlusion in cases of myocardial infarction. In situ thrombosis during epicardial occlusion might contribute to poor myocardial perfusion after reperfusion of an occluded epicardial artery. In the current study, we sought to determine the effects of ischemia and reperfusion on microvascular thrombotic occlusion. Methods: Thirty male Wistar rats were included in the study. After the rats had been anesthetized and thoracotomized, the left coronary artery was occluded for 30 minutes in the first group, and it was occluded for 30 minutes and reperfused for an additional 20 minutes in the second group. Ten rats were used as a sham-operated control group. After completion of the study protocol, excised heart preparations were analyzed by immunohistochemistry and electron microscopy. Results: A significant difference was found between the infarction plus reperfusion group and the other 2 groups, with respect to microvascular fibrin and thrombocyte deposition in immunohistochemistry analysis. These results were confirmed by morphological examination with electron microscopy. Conclusion: In situ fibrin formation accompanies microvascular obstruction in acute myocardial infarction. Our results indicate that additional therapeutic approaches are needed in order to achieve better tissue perfusion in contemporary treatment of acute myocardial infarction after successful reopening of the infarct-related artery.

Abstract Background An ideal aesthetic restorative material should be attached to the tooth tissues by adhesion, have a smooth surface as possible, should not cause toxic reactions in the pulp and discoloration and microleakage. This study aims at comparatively assess the cytotoxicity of current adhesive systems on human dental pulp cells. Materials and methods The adequate density of human pulp cells was observed from the ready cell line. The passaging was performed and the 3rd passage cells were selected. Adhesive systems and MTA were used on the cultures. Trypan blue staining was conducted on the cells at the 1st, 2nd, 3rd days and a count of live and dead cells using a light microscope. The dead cells whose membrane integrity was impaired by staining with trypan blue and the viability rate was determined using live and dead cell numbers. Data analysis was performed using IBM SPSS Statistics 22. Results A significant difference in vialibity rates between adhesive systems was observed on the first day. No significant statistical differences were observed on the 2nd and 3rd days (p

Background: Spinal administration of dexmedetomidine has been proposed as an adjuvant in spinal anesthesia. However, there is limited information about its possible neurotoxic effect after its neuraxial administration. Potential spinal neurotoxicity should be investigated in animals before administering drugs through the spinal cord. Our aim was to investigate the neurotoxic effects of intrathecal dexmedetomidine in rats. Methods: Two groups were performed: the dexmedetomidine (D) group (n = 10) received 10 μg (0.5 ml), whereas the control (C) group (n = 10) received 0.9% (0.5 ml) sodium chloride through indwelling intrathecal catheter. Seven days after the injection, the medulla spinalis was extracted. Samples were withdrawn from both groups for histologic, electron microscopic examination. The histologic examination was performed separately on each of the four sites. The findings were categorized as follows: 0 - normal neuron; 1 - intermediate neuron damage; and 2 - neurotoxicity. Results: Intrathecal administration of dexmedetomidine sensorial block was seen in the dexmedetomidine group and significant differences in the dexmedetomidine group than control group in 15th and 30th min (P < 0.05). Histological examination did not show evidence suggestive of neuronal body or axonal lesion, gliosis, or myelin sheath damage in any group. In all animals, there were observed changes compatible with unspecific inflammation at the tip of the needle location. On the four-area scoring histologic examination, the scores of both groups were 0–1, and no statistical difference was observed between the groups. Conclusions: A single dose of intrathecal dexmedetomidine did not produce histologic evidence of neurotoxicity.

Purpose: In this experimental study, the effects of systemic memantine administration on the retinal ultrastructure of experimentally induced glaucomatous rats were investigated. Methods: Twenty-four Wistar albino rats were included in this study. Glaucoma was induced by injecting sodium hyaluronate into the anterior chamber of the rats for a period of three weeks. As a control, 8 rats were sham treated (Group C). Glaucoma induced animals were divided into two groups; Group M (n = 8) received a single daily dose of 10 mg/kg memantine, and Group G received the same volume of saline (n = 8), via intraperitoneal route for a period of six weeks, starting with the induction of glaucoma. Then, all rats were sacrificed and the retinas were prepared for electron microscopic examination. Electron microscopic damage findings were graded between 0 and 4 and mean damage scores for each cell or layer was calculated for each group. Statistical comparison was made between group G and group M. Results: Including the photoreceptor cells, marked ultrastructural changes were observed in the retinas of the animals in group G. The ultrastructural changes in group M were modest and there was no significant cell death. Statistical findings indicated these results. Conclusion: Results of the present study suggest that memantine treatment, when started in the early phase of glaucomatous process, may help to preserve the retinal ultrastructure and thus prevent neuronal injury in experimentally induced glaucoma.

Purpose: This study investigates the effects of semaphorin 3A on new bone formation in an experimental rat model., Materials and Methods: Cortical bone defects, 5 mm, were created in the calvaria of 40 Wistar rats, which were then separated into three groups: empty defect (control) group, collagen group, collagen + semaphorin 3A group. The bone blocks were harvested after 4 and 8 weeks. New bone formation was assessed by micro-computed tomography (micro-CT), histology, histomorphometry, transmission electron microscope (TEM) and immunohistochemistry., Results: Increased bone formation was observed in collagen + semaphorin 3A groups both histologically and with micro-CT. In the histomorphometic analysis, the control group had significantly less bone formation compared to both the collagen and collagen + semaphorin 3A group at 4 weeks (p = 0.0001) and 8 weeks (p = 0.0001). The collagen group had significantly less bone formation compared to collagen + semaphorin 3A group both at 4 weeks (p = 0.002) and 8 weeks (p = 0.005). Immunohistochemical analysis revealed that semaphorin 3A inhibited receptor activator of nuclear factor-kB ligand (RANKL) expression and increased the expressions of osteoblastic bone markers at 4 weeks. In TEM analysis, the collagen + semaphorin 3A group had an increased proliferation and bone formation rate at 4 weeks, whereas bone quantity and maturation were enhanced at 8 weeks., Conclusion: Locally applied semaphorin 3A increases callus formation at 4 weeks and bone formation at 8 weeks. Semaphorin 3A prevents bone resorption by inhibiting osteoclasts and increases bone formation by inducing osteoblasts., (Copyright © 2018 European Association for Cranio-Maxillo-Facial Surgery. Published by Elsevier Ltd. All rights reserved.)