Assessment of mean platelet volume in chronic obstructive pulmonary disease during stable period and acute exacerbation

Objective: Chronic obstructive pulmonary disease (COPD) is an important public health problem and it is associated with systemic inflammation. Mean platelet volume (MPV) is one of the markers indicating platelet activation, and it was found to be high in many diseases related to inflammation. In previous studies reported different results evaluating of MPV in COPD. In this study, we aimed to evaluate of C-reactive protein (CRP), white blood cell (WBC), and MPV in acute exacerbation of COPD and stable COPD patients. Methods: In this retrospective study, data of 40 patients with acute exacerbation of COPD, 43 stable COPD patients and 40 healthy subjects were evaluated. Results: The mean MPV, CRP and WBC were found in control, stable COPD and acute exacerbation of COPD groups, 7.9±1.1; 8.2±1.3 and 8.7±1.6 fL; 3.4±1.2; 5.2±3.5 and 27.5±23.6 mg/L; 7.8±1.6; 8.1±2.1 and 11.4±4.5 x103/ ϻL, respectively. The mean WBC and CRP in the acute exacerbation of COPD group were significantly higher than the other groups (for both values p ˂0.001). The mean MPV in the acute exacerbation of COPD group was found higher than in the other groups. The mean MPV values were significantly higher in patients of acute exacerbation than control subjects (p=0.030). Conclusion: The results of this study suggest that the increased MPV may be a marker for the evaluation acute exacerbation of COPD as well as the classic acute phase reactant CRP. J Clin Exp Invest 2013; 4 (4): 483-48

Relationship between Hba1c and blood glucose level in hemodialysis patients with diabetes mellitus

Within in the scope of this study, a researchwas aimed at the relationship between HbA1c markersand blood glucose levels with DM, chronic renal failureand receiving dialysis treatment.Methods: In this study, monthly glucose levels and quarterlyHbA1c markers of 131 patients (53 female, 78 male)receiving dialysis treatment in a private dialysis centerbetween January 1, 2009-July 31, 2010 were evaluatedretrospectively.Results: The average age of 131 cases was 63.3±11.2years (range, 30-91). Gender distribution of the cases: 53female (40.5%), 78 male (59.5%). While the age averageof the females was 62.2±11.2 and the males’ was64.1±11.2. The average glucose level of the females andmales have a correlation to average HbA1c (Female:p<0.001, r=0.761, Males: p<0.001, r=0.743). The averageglucose level of the both case groups have a correlationto average HbA1c (p<0.001, r=0.755). While 32.8%of the examined HbA1c results were observed underthe level 6,5%, and 67.2% of the examined results wereobserved above the level 6.5%. While 18.3% of the preprandialblood glucose levels were obtained under 126mg/dl level, and 81.3% of the results were obtained above126 mg/dl level. It has been observed that the mean bloodglucose level has a correlation to average HbA1c level.Conclusion: The measurement of HbA1c and blood glucose(pre-prandial and postprandial) and the correlationbetween them, by virtue of the fact that, are vitally importantin cardiovascular mortality and morbidity, monitorof DM for the dialysis patients with diabetic nephropathy.Key words: Hemodialysis, diabetes mellitus, HbA1

Histopathologic investigation of the protective effects of omega-3 fatty acids against boric acid-induced injury in kidney and testis tissue

Objective: In this study, it was aimed to evaluate the effects of boric acid on rat kidney and testis tissues histopathologically. Secondly, the protective effects of omega-3 fatty acid against boric acid-induced renal and testicular toxicity were investigated. Methods: 32 wistar albino rats were divided into 4 groups as follows: Control, Omega-3 (400 mg/kg/day for 10 days), Boric acid (375 mg/kg/day for 10 days) and Boric acid+omega-3 (both drugs same dosage for same day). Kidney and testis tissues were evaluated using a scoring system based on the extent of certain histopathological changes. Results: In histopathological examination, boric acid caused significant degeneration in both testis and kidney tissues. Most evident findings were glomerular shrinkage and necrosis, hemorrhage and tubular cell degeneration in kidneys, and exfoliation of seminiferous tubule cells, detachement of epithelium from basement membrane, decreased cellularity and degeneration in epithelial cells in testis tissues. Omega-3 administration significantly attenuated these changes. Conclusion: To our literature search, this is the first study reporting protective effects of omega-3 fatty acid against boric-acid-induced testicular and renal injury

DİYET VE DİYABET

Being a metabolic syndrome component, Type 2 Diabetes Mellitus is characterized with progressive insuline secretion defect induced by insuline resistance. Type 2 diabetes patients are mostly obese and obesity is, to a certain extent, the reason of insuline resistance. Obesity is also closely associated with diet. In diet originated obesity, the blame is particularly put on ready-made food. High fat and high fructose diet can lead to obesity and insuline resistance. The purpose of the presented compilation is to emphasize the importance of the habits of diet in the patogenesis of diabetes mellitu

Protective effect of inhibition of nitric oxide synthase on iron-induced purkinje cell loss

Amaç: Demir, nöronal hiperaktivite ve oksidatif stresi indüklemek için sıklıkla kullanılan bir metaldir. Nitrik oksit sentaz (NOS) tarafından sentezlenen nitrik oksit ile hücre ölümü arasındaki ilişkiyi ortaya koyan bulgular da mevcuttur. Bu çalışmada, intraserebroventriküler olarak injekte edilen demirin sıçan serebellar Purkinje hücrelerinde oluşturduğu nörotoksisiteye karşı bir indüklenebilir NOS inhibitörü olan aminoguanidin ve non-selektif NOS inhibötörü olan N-nitro-L- arjinin metil ester’in (L-NAME) etkisi araştırıldı. Gereç ve Yöntem: Sıçanlar; kontrol, demir, demir+aminoguanidin ve demir+L-NAME grupları olmak üzere dört gruba ayrıldı. Demir, demir+aminoguanidin ve demir+L-NAME gruplarındaki sıçanlara intraserebroventriküler olarak demir verildi. Operasyonu takiben on gün süreyle, demir+aminoguanidin ve demir+L-NAME gruplarındaki sıçanlara sırasıyla 30 mg/kg aminoguanidin ve 60 mg/kg L-NAME intraperitoneal olarak verildi. Onuncu günün sonunda, bütün gruplardaki hayvanlar üretan anestezi altında intrakardiyak yolla perfüze edildi. Toplam Purkinje hücre sayımları için tarafsız sayım metodu olan stereolojik yöntem kullanıldı. Bulgular: Demir+aminoguanidin ve demir+L- NAME grupları demir grubu ile karşılaştırıldığında, aminoguanidin ve L-NAME demirin indüklediği Purkinje hücre kaybını %24.9’dan sırasıyla %12.3 ve %11.3’e gerilettiği bulundu (p<0.05). Sonuç: Bu çalışmanın sonuçları, aminoguanidin ve L-NAME’nin demirin indüklediği Purkinje hücre kaybını anlamlı olarak azalttığını ve NOS inhibisyonunun demirin zararlı etkilerini önleyebileceğini gösterdi.Objective: Iron is commonly used as a metal to induce neuronal hyperactivity and oxidative stress. A body of evidence also indicates a link between nitric oxide synthase (NOS) and neuronal death. In this study, we investigated the effects of aminoguanidine, an inducible NOS inhibitor and NG-nitro-L-arginine methyl ester (L-NAME), a nonselective NOS inhibitor, against intracerebroventricular-injected iron induced neurotoxicity on the cerebellar Purkinje cells in rats. Methods: Rats were divided into four groups: control, iron, iron+aminoguanidine and iron+L- NAME. Animals in iron, iron+aminoguanidine and iron+L-NAME groups received intracerebroventricular iron injection. All animals were kept alive for ten days following the operation and animals in iron+aminoguanidine and iron+L- NAME groups received intraperitoneally 30 mg/kg aminoguanidine and 60 mg/kg L-NAME, respectively. At the end of the tenth day, rats were perfused intracardially under urethane anesthesia. Unbiased stereological technique was used to estimate the total number of Purkinje cells. Results: It was found that aminoguanidine and L- NAME decreased iron induced Purkinje cell loss from 24.9% to 12.3% and 11.3%, respectively (p&lt;0.05), when iron+aminoguanidine and iron+L- NAME groups compared with iron group. Conclusion: Results of the present study showed that aminoguanidine and L-NAME significantly attenuate iron-induced Purkinje cell loss and inhibition of NOS can prevent the deleterious effects of iron

Ventral ve Dorsal Kök Aksonları Üzerine 4-Aminopiridinin Farklı Etkileri

Aim: Rat motor and sensory nerve fibers may responses differently to the potassium channelblocking agent, 4-aminopyridine (4-AP). In this study we examined the electrophysiological properties of rat ventral and dorsal root axons with 4-AP and compound action potentials (CAP’s). Materials-Methods: Male Wistar rats were sacrificed by rapid carotid exsanguinations’ under ether anesthesia. Lumbar (L-4) ventral and dorsal roots were excised with laminectomy and immediately placed in a modified chilly Krebs solution saturated with 95% 02, and 5% CO2. To evaluate effect of 4-AP on the roots, CAP’s were recorded in a modified sucrose gap chamber in vitro. All experiments were performed at 20-22 oC. Results: The total duration of CAP obtained from the ventral root was prolonged by 4-AP and the return to baseline was delayed. The duration of CAP of the dorsal root more broadened than ventral roots at least two fold. The CAP of the dorsal roots developed a distinct hump when return to baseline. This phenomenon was not observed in ventral roots. The latency of ventral and dorsal root were 256 ± 24 and 508 ± 69 µs, conduction velocity 20.4 ± 2.4 and 10.8 ± 1.4 m/s, respectively. Conclusion: In this study we showed that 4-AP has entirely different effects on rat motor and sensory axons. The differential effect of 4-AP on motor and sensory fibers may be due to differences in ratio of myelinated-unmyelinated axons and its diameters. In addition there may be differences node or paranode’s potassiumsodium channels diversity in ventral and dorsal root

Klodronat Periferik Sinirlerde Yaralanma Sonrası Rejenerasyon Sürecini Hızlandırır mı?

Aim: In this study, we aimed of the effects of LEC (LEC; Liposome Encapsulated Clodronate) an agent, to selectively deplete or reduce resident and systemic macrophages population during the degeneration-regeneration cycle after peripheral nerve injury. Materials-Methods: In our experiments, eight weeks old male wistar rats randomly divided into 5 groups as control (Group A), crush (Group B4 and B8) and crush+received LEC treatment (Groups C4 and C8) (n=40). Nerve crush injury model was performed on right sciatic nerve of the animals except the control group. Immediately after injury, LEC was intravenously injected after the days of postoperation 5, 10 and 15th (Group C). After 4-8 weeks following the injury, before EMG measurement was recorded than sciatic nerve dissected from Group B and C. Before and after 4-Aminophyridine (4-Ap) administration, the Compound Action Potential (CAP) were recorded with modified sucrose-gap system which is an in-vitro electrophysiological method from these branches Results: Our data show that LEC administration on damaged nerve did not significantly change CAP's parameters which are CV (CV; Conduction Velocity), amplitude of CAP, depolarization time (DT), latency and half width of CAP (p>0.05). However, LEC significantly changed the amplitude of delayed depolarization (del-dep) when occuring after administration of 4- Ap (

Efficacy of resuscitation with Intralipid in a levobupivacaine-induced cardiac arrest model

Aim: Cardiac toxicity due to the administration of local anesthetics may be fatal. In this study, we evaluated the efficacy of a 20% lipid solution combined with epinephrine in a levobupivacaine-induced cardiac arrest model. Materials and methods: A total of 14 New Zealand rabbits were sedated and mechanically ventilated. Asystole was induced with intravenous levobupivacaine injection. The rabbits were randomized into groups receiving the same volume of either 0.9% saline (CR group) or a 20% lipid solution (LE group) along with a 100 &micro;g/kg epinephrine bolus, which were administered immediately upon asystole. Standard advanced cardiac life support protocols were performed. Results: Four subjects in the LE group as well as 3 subjects in the CR group had a spontaneous recovery (P = 0.592). In the 20th minute after arrest, 3 subjects in the LE group had maintained spontaneous circulation, while there was only 1 subject from the CR group with the same outcome. Conclusion: We found that adding a lipid solution to epinephrine for the resuscitation of rabbits that underwent levobupivacaineinduced cardiac arrest increased recovery rates of circulation and therefore the likelihood of survival. Further studies are needed to develop clinical therapies for the systemic toxicity of local anesthetics.Aim: Cardiac toxicity due to the administration of local anesthetics may be fatal. In this study, we evaluated the efficacy of a 20% lipid solution combined with epinephrine in a levobupivacaine-induced cardiac arrest model. Materials and methods: A total of 14 New Zealand rabbits were sedated and mechanically ventilated. Asystole was induced with intravenous levobupivacaine injection. The rabbits were randomized into groups receiving the same volume of either 0.9% saline (CR group) or a 20% lipid solution (LE group) along with a 100 &micro;g/kg epinephrine bolus, which were administered immediately upon asystole. Standard advanced cardiac life support protocols were performed. Results: Four subjects in the LE group as well as 3 subjects in the CR group had a spontaneous recovery (P = 0.592). In the 20th minute after arrest, 3 subjects in the LE group had maintained spontaneous circulation, while there was only 1 subject from the CR group with the same outcome. Conclusion: We found that adding a lipid solution to epinephrine for the resuscitation of rabbits that underwent levobupivacaineinduced cardiac arrest increased recovery rates of circulation and therefore the likelihood of survival. Further studies are needed to develop clinical therapies for the systemic toxicity of local anesthetics

Thymoquinone attenuates trauma induced spinal cord damage in an animal model

BACKGROUND: Spinal cord injury (SCI) is one of the most devastating conditions leading to neurological impairment and disabilities. The aim of the study was to investigate the potential neuroprotective effect of thymoquinone (TQ) histopathologically in an experimental model of traumatic spinal cord injury (SCI). METHODS: Twenty-four male Wistar albino rats were randomly divided into 4 groups: control group; SCI group; SCI-induced and 10 mg/kg/day TQ administered group; SCI-induced and 30 mg/kg/day TQ administered group. TQ was given as intraperitoneal for three days prior to injury and four days following injury. Spinal cord segment between T8 and T10 were taken for histopathologic examination. Hemorrhage, spongiosis and liquefactive necrosis were analyzed semiquantatively for histopathological changes. RESULTS: Administration of TQ at a dose of 10 mg/kg did not cause any significant change on the histological features of neuronal degeneration as compared to the SCI group (p=0.269); however, 30 mg/kg TQ significantly decreased the histological features of spinal cord damage below that of the SCI group (p=0.011). CONCLUSION: Data from this study suggest that TQ supplementation attenuates trauma induced spinal cord damage. Thus, TQ needs to be taken into consideration, for it may have a neuroprotective effect in trauma induced spinal cord damageBACKGROUND: Spinal cord injury (SCI) is one of the most devastating conditions leading to neurological impairment and disabilities. The aim of the study was to investigate the potential neuroprotective effect of thymoquinone (TQ) histopathologically in an experimental model of traumatic spinal cord injury (SCI). METHODS: Twenty-four male Wistar albino rats were randomly divided into 4 groups: control group; SCI group; SCI-induced and 10 mg/kg/day TQ administered group; SCI-induced and 30 mg/kg/day TQ administered group. TQ was given as intraperitoneal for three days prior to injury and four days following injury. Spinal cord segment between T8 and T10 were taken for histopathologic examination. Hemorrhage, spongiosis and liquefactive necrosis were analyzed semiquantatively for histopathological changes. RESULTS: Administration of TQ at a dose of 10 mg/kg did not cause any significant change on the histological features of neuronal degeneration as compared to the SCI group (p=0.269); however, 30 mg/kg TQ significantly decreased the histological features of spinal cord damage below that of the SCI group (p=0.011). CONCLUSION: Data from this study suggest that TQ supplementation attenuates trauma induced spinal cord damage. Thus, TQ needs to be taken into consideration, for it may have a neuroprotective effect in trauma induced spinal cord damag

Effect of clozapine on locomotor activity and anxiety-related behavior in the neonatal mice administered MK-801

Atypical antipsychotics have been used to treat fear and anxiety disturbance that are highly common in schizophrenic patients. It is suggested that disruptions of N-methyl-d-aspartate (NMDA)-mediated transmission of glutamate may underlie the pathophysiology of schizophrenia. The present study was conducted to analyze the effectiveness of clozapine on the anxiety-related behavior and locomotor function of the adult brain, which had previously undergone NMDA receptor blockade during a developmental period. In order to block the NMDA receptor, male mice were administered 0.25 mg/kg of MK-801 on days 7 to 10 postnatal. In adulthood, they were administered intraperitoneally 0.5 mg/kg of clozapine and tested with open-field and elevated plus maze test, to assess their emotional behavior and locomotor activity. In the group receiving MK-801 in the early developmental period the elevated plus maze test revealed a reduction in the anxiety-related behavior (p<0.05), while the open-field test indicated a decrease in locomotor activity (p<0.01). Despite these reductions, clozapine could not reverse the NMDA receptor blockade. Also, as an atypical antipsychotic agent, clozapine could not reverse impairment in the locomotor activity and anxiety-related behavior, induced by administration of the MK-801 in neonatal period