Sepsis and Brain-Derived Neurotrophic Factor (BDNF): Exploring the Complex Connection

In recent studies, brain-derived neurotrophic factor (BDNF) become a very important position. Because it is now known that it is not just a hormone that is released from the hippocampus and which supports the differentiation and growth of newly formed nerve cells and synapses while maintaining the vitality of existing neurons. Today BDNF was used as an indicator of severe sepsis and also in the follow-up of the disease. Moreover, BDNF is a potential anti-inflammatory agent which can be given like a medicament. In some studies, antiinflammatory effect was proven “in acute lung injury, in myocardial injury, in hepatorenal injury” triggered by sepsis. In this chapter, we will try to explain the BDNF effect in sepsis according to recent literature and update our knowledge

Vazoaktif ıntestinal peptid ve vinposetinin embriyonik nöral kök hücrelerdeki mangan toksisitesi üzerine etkisi

Increased concentration of Manganese in the brain is known to be associated with excitotoxicity and neuroinflammation. Vinpocetine, an alkaloid derived from the plant Vinca minor L. , basicly shows its effect via phosphodiesterase inhibition and voltage dependent Na+ channels. Vasoactive intestinal peptide (VIP) has gastrointestinal, vasomotor, muscular and neuroprotective effects. The aim of this study was to examine the potential protective effects of vinpocetine and VIP against Mn2+ toxicity in neural stem cells (NSCs). VIP treatment at 1000 nM and vinpocetine treatment at 2 ?M concentrations were sufficient to yield maximum protection and these concentrations were adopted in the following experiments. In this study, Mn2+ treatment significantly increased LDH leakage, ROS production and triggered cell death in NSCs. However, significant reduction in LDH release was observed following vinpocetine or VIP treatments when compared with control. Similar to these findings, Vinpocetine or VIP treatments significantly reduced membrane degradation induced by Mn2+ (p0.0001). Moreover, Vinpocetine attenuated Mn2+ induced decrease of mitochondrial membrane potential (p0.0001). Similarly, ROS production significantly decreased in cells after incubation with vinpocetine (p=0.01) or VIP in the presence of Mn2+ (p0.0001). On the other hand, we did not observe any significant changes in ATP levels following VIP or vinpocetine treatments. Our study provides the evidence that Vinpocetine and VIP may exert protective effects via modulating free radical production, mitochondrial membrane potential and oxidative stress in Mn2+ induced neurodegeneration. Keywords: Manganese, Neural Stem Cell, Vinpocetine, VIP, Toxicity, Neuroprotective, AntioxidantManganın beyinde artmış konsantrasyonlarının eksitotoksisite ve nöro inflamasyonla ilişkili olduğu bilinmektedir. Vinposetin Vincaminor L. yapraklarından elde edilen alkaloidvinkaminden sentezlenmiştir. Nöroprotektif etkilerini temelde voltaj bağımlı Na+ kanalları ve Fosfodiesteraz enzimi üzerinden göstermektedir. Vazoaktif intestinal peptid 28 aminoasit' ten oluşan gastrointestinal, muskuler ve vazomotor etkilerinin yanısıra nöroprotektif etkiside bilinen bir peptidtir. Bu çalışmada embriyonel nöral kök hücrelerde Mangan toksisitesi sonrası vazoaktif intestinal peptid (VIP) ve vinposetin uygulamasının potansiyel koruyucu etkinliği incelenmiştir. Hücresel toksisiteyi saptamak için hücre canlılık analizi WST-1' den faydalanılmış olup IC50 Mangan dozu 50?M olarak saptanmıştır. Hücre canlılık analizi metodu ile 50?M Mn+2 toksistesi sonrası nöroproteksyon sağlayan etkin VIP dozu 1000nM, vinposetin dozu ise 2?M olarak bulunmuştur. LDH membran bütünlüğü testinde kontrol grubuna göre vinposetin ve vazoaktif intestinal peptid gruplarında anlamlı LDH azalması bulunmuştur (p0,0001). 50?M Mn+2grubu ile 50?M Mn+2 /Vinposetin ve 50?M Mn+2 / VIP gruplarındada kontrole göre anlamlı LDH azalması gözlendi (p 0.0001). Mitokondri Membran Potansiyeli deneyinde 2 ?M/ 50 ?M Mn+2 eklenen gruptaki membran potansiyeli 50 ?M Mangan içeren gruba göre anlamlı gerilemiştir (p 0,0001). Fakat 1000nM VIP + 50 ?M Mn+2 eklenen gruptaki membran potansiyeli ile 50 ?M Mangan'lı gruptaki membran düzeyindeki fark anlamlı olarak sonuç vermemiştir (p > 0.05). Reaktif Oksijen Türleri tespitinde DCF-DA uygulamasında 2 ?M vinposetin + 50 ?M Manganlı grup ile sadece 50 ?M Mangan'lı grup arasında ROT üretiminde anlamlı fark bulunmuştur (p=0.01). Aynı şekilde 1000nM VIP + 50 ?M Manganlı grup ile sadece 50 ?M Mangan'lı grup arasında anlamlı fark bulunmuştur (p0.0001). ATP düzeyleri karşılaştırıldığında, sadece 50 ?M Manganlı gruba göre 1000nM VIP/Mn+2 için istatistiksel olarak anlamlı olmayan (p>0.005) fakat daha yüksek ATP düzeyi, Vinposetin/Mn+2grupta ise yine istatistiksel olarak anlamlı olmayan (p>0.005) fakat kontrolden daha yüksek bir ATP düzeyi saptanmıştır. Bu çalışmalarda Vinposetin ve VIP' in saptadığımız etkin dozlarda antioksidan ve antiapoptotik etkileri mitokondri ve oksidatif stres ile ilişkili parametrelerdeki değişimler ile gösterilmiştir. Literatüre bakıldığında VIP ve vinposetinin Mangan toksisitesi üzerine etkisi çalışılmamıştır. Bu açıdan çalışmamız örnek teşkil etmektedir

Thrombolytic use in patients with a history of recent trauma: a case report

Masif emboli submasif emboliden farklı olarak trombolitik tedavi verilmesi gereken bir durumdur. Yakın zamanda travma öyküsü olan hastalarda trombolitik kullanımı kanama açısından tartışmalıdır. Majör embolide trombolitik tedavinin majör kontrendikasyonları arasında “yakın zamanda geçirilmiş travma/cerrahi girişim/kafa yaralanması” yer almaktadır. Mutlak kontrendikasyonların dipnotu ise miyokard enfarktüsünde mutlak olduğu düşünülen trombolitik kontrendikasyonları yaşamı tehdit eden yüksek riskli pulmoner emboli olan bir hastada görece kontrendikasyona dönüşebilir şeklindedir. Hastamızda travma yarar/zarar hesabı göz önünde bulundurulduğunda görece kontrendikasyon kabul edilmiş ve hastanın kliniği hızla düzelmiştir. Bu durum majör kontrendikasyonların görece kontrendikasyona dönüştüğü bir olgu örneği olup travmanın çeşitliliği ile tartışmaya açık konu olarak düşünülmüştür.Massive embolism, unlike submassive embolism, is a condition that should be given thrombolytic therapy. Thrombolytic use in patients with a history of recent trauma is controversial in terms of bleeding. “Recent history of trauma/surgery/head injury” are among the major contraindications of thrombolytic therapy in major embolism. The note of absolute contraindications is that absolute contraindications of thrombolytic therapy in myocardial infarction can be thought relative contraindications in high-risk patients with pulmonary embolism. Considering profit and loss account, trauma is regarded as relative contraindication in our patient and the clinic is improved rapidly. This case, an example of the transition of majör contraindication to relative contraindication, is thought to be questionable according to the variety of the trauma

A rare complication of cardiopulmonary resuscitation applied during transportation by ambulance: A case report of flail chest

Cardiopulmonary resuscitation (CPR) to be applied during patient transfer by ambulance differs from CPR applied in the field or in the hospital in terms of physical condition. Especially the deeper and faster chest compressions recommended in the latest CPR guidelines, when administered during ambulance transport, may result in a further increase in traumatic CPR complications. However, in the current CPR guidelines, there are no clear recommendations regarding additional measures that can be taken to reduce the complications and increase the efficiency of CPR during patient transport. In this study, a case of flail chest that developed after short-term CPR application during ambulance transport is presented. The aim of this study was to evaluate the flail chest complication and solution suggestions that may occur due to chest compressions applied during transportation

Roxadustat protects rats from cisplatin-induced acute kidney injury

Purpose: To investigate the potential protective effect of roxadustat against cisplatin-induced acute kidney injury (AKI) by evaluating biochemical markers, inflammatory parameters, renal function tests, and histopathological changes. Methods: Thirty female Wistar rats were randomized into control group, cisplatin with tap water group, and cisplatin with roxadustat group. Cisplatin-induced AKI was established by intraperitoneal injection of cisplatin at 10 mg/kg for seven days. Roxadustat was administered orally at 20 mg/kg/day to the treatment group. Blood and kidney samples were collected for biochemical and histopathological analyses respectively. Results: Roxadustat treatment significantly reduced markers of renal injury (malondialdehyde (MDA), kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), transforming growth factor-beta 1 (TGF-beta1)), inflammatory cytokines (tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-18 (IL-18)) compared to the cisplatin group (p 0.05). Conclusion: Roxadustat significantly prevents cisplatin-induced AKI by attenuating renal injury, reducing inflammation, and improving renal function. This evidence suggests that roxadustat may be a promising preventive option for patients receiving cisplatin chemotherapy

Vinpocetine attenuates manganese-induced toxicity in neural stem cells

Conference of the Society-for-Free-Radical-Research-Europe (SFRR-E) -- JUN 08-11, 2016 -- Budapest, HUNGARYWOS: 000377617900113Soc Free Rad Res Europ