Diving behavior reduces genera richness of lice (Insecta,Phthiraptera) of mammals

Lice of mammals spend the entire life cycle in the host hair, thus, the microclimate found near the mammal skin is likely to influence the structure of louse communities. Here we use a comparative approach to examine the effect of mammals’ diving behavior on the taxonomic richness of their lice. We compared the mean genera richness of lice, and — as potential confounding variables — the mean species richness of host, and the mean body mass of host between diving clades and their non-diving sister clades. Louse genera richness was significantly lower in clades of aquatic mammals than on their non-diving sister clades. Host species richness was not significantly different between these clades. Body mass was significantly higher in clades of aquatic mammals, however, the direction of this difference cannot explain the difference in parasite taxonomic richness. This study suggests that mammals’ diving behavior can effectively shape their ectoparasite communities.     

Decreased oligodendrocyte nuclear diameter in Alzheimer's disease and lewy body dementia

To better understand the pathogenesis of dementia, it is important to understand histopathologic changes in neurodegenerative diseases because they might highlight key aspects of the degenerative process. In this study, the nuclear diameter of neurons and oligodendrocytes in selected temporal lobe areas were determined in autopsy tissue sections from patients with Alzheimer's disease (AD), Lewy body dementia (LBD) and controls. Our morphometric studies targeted neurons in the CA4 region of the pyramidal cell layer of the hippocampus, neurons in the granular layer of the dentate gyrus and oligodendrocytes in parahippocampal white matter. Mean neuronal nuclear diameters were not different among the studied groups. However, our studies revealed a statistically significant reduction of mean oligodendrocyte nuclear diameter in AD and LBD relative to controls. The reduction of the mean nucleus diameter of oligodendrocytes in LBD was independent of the presence of associated AD pathology in LBD. These findings for the first time identify decreased oligodendrocyte nucleus diameter as a morphologic feature of AD and LBD and may lead to a better understanding of the role of oligodendrocytes in AD and LBD pathogenesis.     

Induction of heat shock proteins for protection against oxidative stress

Heat shock proteins (Hsps) have been studied for many years and there is now a large body of evidence that demonstrates the role of Hsp upregulation in tissue and cell protection in a wide variety of stress conditions. Oxidative stress is known to be involved in a number of pathological conditions, including neurodegeneration, cardiovascular disease and stroke, and even plays a role in natural aging. In this review we summarize the current understanding of the role of Hsps and the heat shock response (HSR) in these pathological conditions and discuss the therapeutic potential of an Hsp therapy for these disorders. However, although an Hsp based therapy appears to be a promising approach for the treatment of diseases that involve oxidative damage, there are some significant hurdles that must be overcome before this approach can be successful. For example, to be effective an Hsp based therapy will need to ensure that the upregulation of Hsps occurs in the right place (i.e. be cell specific), at the right time and to a level and specificity that ensures that all the important binding partners, namely the co-chaperones, are also present at the appropriate levels. It is therefore unlikely that strategies that involve genetic modifications that result in overexpression of specific Hsps will achieve such sophisticated and coordinated effects. Similarly, it is likely that some pharmaceutical inducers of Hsps may be too generic to achieve the desired specific effects on Hsp expression, or may simply fail to reach their target cells due to delivery problems. However, if these difficulties can be overcome, it is clear that an effective Hsp based therapy would be of great benefit to the wide range of depilating conditions in which oxidative stress plays a critical role.     

Clinical Manifestations and Epigenetic Regulation of Oral Herpesvirus Infections

The oral cavity is often the first site where viruses interact with the human body. The oral epithelium is a major site of viral entry, replication and spread to other cell types, where chronic infection can be established. In addition, saliva has been shown as a primary route of person-to-person transmission for many viruses. From a clinical perspective, viral infection can lead to several oral manifestations, ranging from common intraoral lesions to tumors. Despite the clinical and biological relevance of initial oral infection, little is known about the mechanism of regulation of the viral life cycle in the oral cavity. Several viruses utilize host epigenetic machinery to promote their own life cycle. Importantly, viral hijacking of host chromatin-modifying enzymes can also lead to the dysregulation of host factors and in the case of oncogenic viruses may ultimately play a role in promoting tumorigenesis. Given the known roles of epigenetic regulation of viral infection, epigenetic-targeted antiviral therapy has been recently explored as a therapeutic option for chronic viral infection. In this review, we highlight three herpesviruses with known roles in oral infection, including herpes simplex virus type 1, Epstein–Barr virus and Kaposi’s sarcoma-associated herpesvirus. We focus on the respective oral clinical manifestations of these viruses and their epigenetic regulation, with a specific emphasis on the viral life cycle in the oral epithelium.     

Evaluation of Brain Nuclear Medicine Imaging Tracers in a Murine Model of Sepsis-Associated Encephalopathy

Purpose

The purpose of this study was to evaluate a set of widely used nuclear medicine imaging agents as possible methods to study the early effects of systemic inflammation on the living brain in a mouse model of sepsis-associated encephalopathy (SAE). The lipopolysaccharide (LPS)-induced murine systemic inflammation model was selected as a model of SAE.

Procedures

C57BL/6 mice were used. A multimodal imaging protocol was carried out on each animal 4 h following the intravenous administration of LPS using the following tracers: [^99mTc][2,2-dimethyl-3-[(3E)-3-oxidoiminobutan-2-yl]azanidylpropyl]-[(3E)-3-hydroxyiminobutan-2-yl]azanide ([^99mTc]HMPAO) and ethyl-7-[¹²⁵I]iodo-5-methyl-6-oxo-4H-imidazo[1,5-a][1,4]benzodiazepine-3-carboxylate ([¹²⁵I]iomazenil) to measure brain perfusion and neuronal damage, respectively; 2-deoxy-2-[¹⁸F]fluoro-d-glucose ([¹⁸F]FDG) to measure cerebral glucose uptake. We assessed microglia activity on another group of mice using 2-[6-chloro-2-(4-[¹²⁵I]iodophenyl)-imidazo[1,2-a]pyridin-3-yl]-N-ethyl-N-methyl-acetamide ([¹²⁵I]CLINME). Radiotracer uptakes were measured in different brain regions and correlated. Microglia activity was also assessed using immunohistochemistry. Brain glutathione levels were measured to investigate oxidative stress.

Results

Significantly reduced perfusion values and significantly enhanced [¹⁸F]FDG and [¹²⁵I]CLINME uptake was measured in the LPS-treated group. Following perfusion compensation, enhanced [¹²⁵I]iomazenil uptake was measured in the LPS-treated group’s hippocampus and cerebellum. In this group, both [¹⁸F]FDG and [¹²⁵I]iomazenil uptake showed highly negative correlation to perfusion measured with ([^99mTc]HMPAO uptake in all brain regions. No significant differences were detected in brain glutathione levels between the groups. The CD45 and P2Y12 double-labeling immunohistochemistry showed widespread microglia activation in the LPS-treated group.

Conclusions

Our results suggest that [¹²⁵I]CLINME and [^99mTc]HMPAO SPECT can be used to detect microglia activation and brain hypoperfusion, respectively, in the early phase (4 h post injection) of systemic inflammation. We suspect that the enhancement of [¹⁸F]FDG and [¹²⁵I]iomazenil uptake in the LPS-treated group does not necessarily reflect neural hypermetabolism and the lack of neuronal damage. They are most likely caused by processes emerging during neuroinflammation, e.g., microglia activation and/or immune cell infiltration.

     

Stimulation of substantia nigra pars reticulata suppresses neocortical seizures

The effects of unilateral electrical stimulation of the substantia nigra pars reticulata (SNpr) on the electrocorticographic (ECoG) manifestations of seizures were studied in anesthetized rats. Epileptiform activity was provoked in the primary focus (Pf) by unilateral, local application of 3-aminopyridine which induced secondary focus in the homologous area of the contralateral cortex (mirror focus, Mf). The position of the electrode for stimulation of SNpr was contralateral to the Pf. The results showed a strong suppressive nigral effect on cortical seizure propagation and on seizure susceptibility in both hemispheres. Stimulation of the SNpr prevented the manifestation of sustained epileptiform events, decreased the rate of seizure appearance in the Mf, delayed the onset of paroxysmal activity and markedly reduced the amplitude and duration of ictal episodes at both foci. Seizure potentials of lower frequencies disappeared, while the relative proportion of those of higher frequency increased in SNpr-stimulated animals. SNpr stimulation had no significant effect on fully developed seizures. Our observations support the idea that SNpr might be involved in the control of cortical seizure susceptibility, regulating other structures which are possibly involved in the generation and propagation of seizure.     

Platelet arachidonate cascade of migraineurs in the interictal phase

Morphological and functional alterations of platelets in migraineurs may be linked to the development of migraine. We examined the eicosanoid synthesis of platelets of untreated female migraineurs in a headache-free period and compared it to that of age- and blood group-matched healthy female volunteers. In the platelets of headache-free migraineurs significantly less amounts of anti-aggregatory prostaglandin D 2 and prostacyclin, as well as of 12-L-hydroxy–5,8,10-heptadecatrienoic acid (a potent endogenous inducer of endothelial prostacyclin production) were produced, while the synthesis of platelet aggregatory thromboxane did not differ when compared to that of healthy women. These results suggest that the platelet eicosanoids of migraineurs in the headache-free period might promote the development of cellular, vascular and neurological events inducing headache.