Effect of platelet-rich fibrin on epidural fibrosis and comparison to ADCON® Gel and hyaluronic acid

Objective

In this experimental study, PRF (Platelet Rich Fibrin), HA (Hyaluronic Acid) gel and ADCON® Gel were compared in terms of preventing epidural fibrosis.

Heavy metal levels in patients with ineffective erythropoiesis

Objectives

Iron is taken into enterocytes at the duodenum via apical divalent metal-ion transporter 1 protein. Besides iron, divalent metal-ion transporter 1 also transports other divalent metals. We aimed to investigate blood heavy metal levels in patients with ineffective erythropoiesis.

Venous thromboembolism in intensive care unit patients

In intensive care units, venous thromboembolism (VTE) is a life threatening, clinically important issue. The diagnosis of VTE is significantly complicated, even in patients except intensive care units and there is no consensus between clinicians about its treatment. The factors such as heterogeneity of intensive care units patients, the association of thrombosis and bleeding risks in the majority of patients, the non-specific signs and symptoms of VTE, the feasibility limitations of diagnostic methods are caused difficulties in the diagnosis and treatment of VTE. In this review, it has been aimed to remind VTE issue in the intensive care units, by review the investigations about the diagnosis, treatment and thromboprophylaxis of VTE.     

The effectiveness of thrombolytic therapy in patients with massive and submassive pulmonary thromboembolism

Thrombolytic therapy is the most effective therapy for massive pulmonary embolism (PTE). In this study we evaluated the symptoms, clinical and radiologic features and response to thrombolytic therapy in patients who had massive or submassive PTE. Thrombolytic therapy was administered for a mean period of 3 (1-5) hours to 19 patients with a mean age of 63.7 years who had the diagnosis of PTE based on symptoms which lasted for an average of 72 (2-240) hours and findings of echocardiography, spiral computed tomography (CT) angiography and perfusion scan. The patients to whom heparin infusion and oral anticoagulant treatment were given after thrombolytic therapy were evaluated. Bleeding as a complication was noted in six patients after thrombolytic therapy. Two patients died due to this complication. Control spiral CT angiography was performed to 12 of 15 (80%) patients who were initially diagnosed PTE by spiral CT angiography. While marked regression was noted in 5 (41.7%) patients in the early phase (second week), in 7 (58.3%) patients in the late phase (sixth month) PTE findings were completely disappeared. The median value of pulmonary artery pressure was 65 (45-70) mmHg before and 39.5 (30-45) mmHg after the treatment. Of the genetic factors studied before thrombolytic therapy, antithrombin III deficiency was found as the most common one. This study demonstrates that spiral thorax CT angiography is a very accurate diagnostic tool for the definitive diagnosis and transthoracic echocardiography is very useful for the rapid diagnosis and to decide for thrombolytic therapy, in especially patients who are not hypotensive and have submassive to massive PTE, and support the idea that thrombolytic therapy is life saving after reaching the certain diagnosis.     

Visualization of degenerating axons in a dysmyelinating mouse mutant with axonal loss

Mice homozygously deficient for the myelin component P0 show loss of axons in peripheral nerves. In order to investigate the morphological characteristics of degenerating axons, we crossbred the myelin mutants with a transgenic mouse line expressing yellow fluorescent protein (YFP) in a small proportion of neurons. Peripheral nerves of the double mutants were prepared into small fiber bundles and investigated by fluorescence microscopy. We could identify the tips of degenerating axon as bulb-like structures. Additionally, by electron microscopy, these structures were characterized as axoplasmic extensions containing numerous membraneous compartments. By immunoelectron microscopy, the degenerating end bulbs were in contact with ensheathing Schwann cells that contained YFP-immunoreactivity possibly reflecting phagocytosis of axon material by these cells. Immunohistochemistry using antibodies against macrophages revealed that YFP-positive bulbs, but also other axonal swellings, were often associated with macrophages supporting our previous findings that myelin-related axonal loss is partially mediated by these cells.     

Diffuse alveolar hemorrhage as an unusual presentation of systemic lupus erythematosus

Diffuse alveolar hemorrhage (DAH) is rarely seen in patients with systemic lupus erythematosus (SLE), often associated with a poor outcome. It almost affects young women and it is an unusual initial manifestation of SLE. We report a case of SLE presenting with DAH. The patient was a male. He had no history of photosensitivity, malar rash, discoid rash, arthritis, and oral ulcer. Antinuclear antibody, and anti-double stranded DNA (dsDNA) were positive with very high titers, and serum complement levels (C3, C4) were low. He also had renal dysfunction and pericardial effusion. He was diagnosed as DAH due to SLE. He had to undergo hemodialysis for several weeks. DAH and renal dysfunction were improved with intensive treatment including corticosteroid, cyclophosphamide, and mycophenolate mophetil.     

A case of chronic eosinophilic pneumonia with atypical clinical and radiological progress

Eosinophilic lung disease is characterised by eosinophilic infiltration of lung tissue besides peripherical blood and bronchoalveolar lavage (BAL) fluid eosinophilia. A 48 year-old male who attended our clinics with cough and sputum lasting for 2-3 months, has been evaluated for micronodular interstitial infiltration bilaterally in all lung areas. Eosinophilia was detected in hemogram but BAL fluid was not diagnostic. Transbronchial lung parenchymal biopsy was compliant with chronic eosinophilic pneumonia. No special cause has been found after evaluation and the case was accepted to be idiopathic. Because of unfamiliar clinical, radiological and pathological findings, we decided to present this case.     

Sunitinib impedes brain tumor progression and reduces tumor‐induced neurodegeneration in the microenvironment

Malignant gliomas can be counted to the most devastating tumors in humans. Novel therapies do not achieve significant prolonged survival rates. The cancer cells have an impact on the surrounding vital tissue and form tumor zones, which make up the tumor microenvironment. We investigated the effects of sunitinib, a small molecule multitargeted receptor tyrosine kinase inhibitor, on constituents of the tumor microenvironment such as gliomas, astrocytes, endothelial cells, and neurons. Sunitinib has a known anti‐angiogenic effect. We found that sunitinib normalizes the aberrant tumor‐derived vasculature and reduces tumor vessel pathologies (i.e. auto‐loops). Sunitinib has only minor effects on the normal, physiological, non‐proliferating vasculature. We found that neurons and astrocytes are protected by sunitinib against glutamate‐induced cell death, whereas sunitinib acts as a toxin towards proliferating endothelial cells and tumor vessels. Moreover, sunitinib is effective in inducing glioma cell death. We determined the underlying pathways by which sunitinib operates as a toxin on gliomas and found vascular endothelial growth factor receptor 2 (VEGFR2, KDR/Flk1) as the main target to execute gliomatoxicity. The apoptosis‐inducing effect of sunitinib can be mimicked by inhibition of VEGFR2. Knockdown of VEGFR2 can, in part, foster the resistance of glioma cells to receptor tyrosine kinase inhibitors. Furthermore, sunitinib alleviates tumor‐induced neurodegeneration. Hence, we tested whether temozolomide treatment could be potentiated by sunitinib application. Here we show that sunitinib can amplify the effects of temozolomide in glioma cells. Thus, our data indicate that combined treatment with temozolomide does not abrogate the effects of sunitinib. In conclusion, we found that sunitinib acts as a gliomatoxic agent and at the same time carries out neuroprotective effects, reducing tumor‐induced neurodegeneration. Thus, this report uncovered sunitinib's actions on the brain tumor microenvironment, revealing novel aspects for adjuvant approaches and new clinical assessment criteria when applied to brain tumor patients.