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Abstract Aim To evaluate the effects of montelukast in smoke-induced lung injury. Methods 28 Wistar-Albino rats were enrolled into 4 groups with 7 rats per group. The healthy control group was exposed to fresh air while all rats in the 3 experimental groups were exposed to cigarette smoke for 20 weeks for 2 hours per day. After histopathological verification of smoke induced lung injury, montelukast (0.1 mg/kg) dissolved in Na2CO3 was given in one group (MON), Na2CO3 only was given in another group (MON control) and placebo was injected in the third group (COPD control) intraperitoneally for 21 days. At the end of this period blood samples were obtained for serum TNF-α assessment and light and electron microscopy analyses were performed on the lung tissues of sacrificed rats. Results Serum TNF-α levels in the MON group were significantly lower than in the MON control and COPD control groups (38.84 ± 4.9 pg/ml, 77.5 ± 5.8 pg/ml and 79.2 ± 6.9 pg/ml respectively, p < 0.05). Furthermore there was no statistically significant difference between the MON group and healthy controls with respect to serum TNF-α levels (38.84 ± 4.9 pg/ml vs. 29.5 ± 3.6 pg/ml, p > 0.05). Light and electron microscopic evaluation of the lungs demonstrated that the total histopathological damage score of the lung samples was significantly lower in the MON group than in MON controls and COPD controls (5.14 ± 0.5, 8.4 ± 0.6 and 8.7 ± 0.4 respectively, p < 0.05), while there was no significant difference between the MON group and healthy controls (5.1 ± 0.6 vs 2.3 ± 0.2, p > 0.05). Conclusion These findings suggest that montelukast might have a protective effect on smoke-induced lung injury in rats both from a histopathological and inflammatory point of view.

Objectives: Neurogenesis is the formation process of functional neurons from progenitor cells which continues during lifetime. Alterations in neurogenesis is associated with neurodegenerative disorders (ND). Different mechanisms underlie the ND in males and females which may be related to neurogenesis. In this study, we aimed to investigate the developmental process of neurogenesis in the hippocampus of male and female rats at different ages and shed light on the effect of gender difference on ND. Methods: Brains were obtained from 7, 14, 21 days and 3-month-old male and female Wistar rats following intracardiac perfusion and processed for immunohistochemical and immunoflorescence staining. Doublecortin protein (DCX) was used as a marker of newly-born neuroblasts to determine neurogenesis. Results: DCX immunoreactive (-ir) cells were dispersed throughout the granular and subgranular layers of DG in 7-days-old group in both genders. However, in the 14 and 21 days old groups, DCX-ir cells were observed only in the subgranular zone in the sections labelled with both immunohistochemistry (IHC) and immunoflourescent (IF) methods. In all age groups, female rats had a tendency to increase in DCX immunoreactivity when compared to that of male Wistar rats. Conclusion: DCX-ir cells may be localized in different parts of DG during development. The number of newly born neurons showed a tendency to increase in female rats in all groups. Further studies are needed to understand the reason for differences in the normal developmental neurogenesis process between two genders. [ABSTRACT FROM AUTHOR]

Primary ciliary dyskinesia (PCD) is composed of the diseases resulting from congenital defects of cilia. Diagnosis is reached on the basis of clinical history, abnormal ciliary beat frequency and specific axonemal defects observed by transmission electron microscopy. Electron microscopic assessment for the diagnosis of PCD comes into prominence in clinically and light microscopically undiagnosed cases. Microtubule defects, dynein arm deficiency and orientation disorders cannot be detected by light microscopy; electron microscopy is the method of choice in the diagnosis of such disorders. Ciliary orientation should be measured in patients having recurrent respiratory tract infections since disorientation can be the only defect in some patients. Ciliary disorders are classified as primary (congenital) and secondary (acquired) disorders. The latter are caused by environmental factors, such as infection, smoking and air pollution. The diagnosis of PCD may be difficult since the epithelial cell and ciliary defects can also be caused by acquired factors. Therefore, it is important to distinguish between primary and secondary structural and functional disorders. Electron microscopic analysis is the only option for diagnosing ultrastructural defects. Electron microscopic assessment in diagnosing PCD should be carried out only after excluding other probable causes of respiratory tract infections and after the appropriate treatment of infections responsible for secondary ciliary defects. In this manner, falsepositive diagnosis of PCD and high cost can be prevented. [ABSTRACT FROM AUTHOR]

We showed previously that genetic absence epilepsy rats from Strasbourg (GAERS) resist secondary generalization of focal limbic seizures after electrical kindling. We now investigate the effect of intra-amygdaloid injection of kainic acid, as another model of temporal lobe epilepsy, focusing on epileptogenesis, spike-and-wave discharges (SWDs), and the transition from basal to SWD states in GAERS. The EEG was recorded from the hippocampus and cortex of adult GAERS and Wistar rats before kainic acid injections into the basolateral amygdala and for 3 months thereafter. EEG and video recordings monitored SWDs and convulsive seizures. We analyzed spectral changes of the EEG during kainic acid-induced status epilepticus, SWDs, for 10 s before (silent period) and for 2 s before (transition period) SWDs. After the injection of kainic acid, all animals experienced convulsive seizures for at least 3 h. The first convulsive seizure was significantly delayed in GAERS compared with Wistar rats. SWDs and increases in power of the delta, alpha, and beta frequency ranges during the transition period disappeared after the kainic acid injection for 1-3 d and gradually reappeared. Power increases in the delta and alpha ranges were significantly correlated with the number of SWDs, in the beta and alpha ranges with their mean duration. Neo-Timm's staining at the end of experiments demonstrated that mossy fiber sprouting in GAERS is less pronounced than in Wistar rats. Our findings show that mechanisms underlying absence epilepsy and temporal lobe epilepsy interact with each other, although a site of this interaction remains to be defined. [ABSTRACT FROM AUTHOR]

Objective: In this study, we aimed to examine time-dependent morphologic changes and quantitative alterations in the density of basic fibroblast growth factor (bFGF)-immunoreactive (ir) astrocytes and CA2 pyramidal neurons in dorsal hippocampus of rats after status epilepticus (SE) induced by kainic acid (KA) injection. Methods: Wistar albino rats were injected with saline or KA i.p. to investigate time-dependent alterations in morphology and the number of bFGF-ir astrocytes and neurons in the dorsal hippocampus 15, 30 and 90 days after KA injection. Results: Fifteen days after KA injection, gliosis was present throughout the hippocampus and neuronal loss was evident in CA1 and CA3 regions, which was more severe after 30 and 90 days. KA-injected rats demonstrated significantly increased number of both bFGF-ir astrocytes throughout the hippocampus and pyramidal neurons in CA2 after 15 days and decreased number after 30 and 90 days. Conclusion: The decrease in the number of bFGF-ir astroglia and neurons in long term after KA injection may indicate a decrease in the production of bFGF and/or number of bFGF-ir cells, suggesting that protective effects of bFGF might be altered during epileptogenesis in the hippocampus. [ABSTRACT FROM AUTHOR]