Survival, re-expansion, and pregnancy outcome following vitrification of dromedary camel cloned blastocysts: A possible role of vitrification in improving clone pregnancy rate by weeding out poor competent embryos.

There is a clinical demand for efficient cryopreservation of cloned camel embryos with considerable logistic and economic advantage. Vitrification of in vivo derived embryos has been reported in camels, but there is no study on vitrification of cloned embryos. Moreover, whether characteristic differences between cloned and in vivo derived embryos imply different vitrification requirement is unresolved. Here, we compared survival, re-expansion and pregnancy rates of cloned embryos vitrified using two commercial vitrification kits (Cryotec and Kitazato), developed basically for human embryos, and a vitrification protocol developed for in vivo camel embryos (CVP). Cloned embryos responded dynamically to vitrification-warming steps in commercial kits, with a flat shrinkage in the final vitrification solution and a quick re-expansion to the original volume immediately after transferring to the isotonic warming solution. Contrarily, full shrinkage was not observed in CVP method, and majority of embryos were still collapsed post-warming. The immediate re-expansion was highly associated and predictive of higher survival and total cell number, and also better redox state of embryos vitrified by Cryotec and Kitazato kits compared to CVP method. Importantly, while 30% blastomere loss, verified by differential dye exclusion test, was tolerated in vitrified embryos, >50% blastomeres loss in non-expanded blastocysts implied the minimal essential cell survival rate for blastocoelic cavity re-expansion in vitrified cloned camel blastocysts, irrespective of vitrification method. A protocol-based exposure of embryos to cryoprotectants indicated that cryoprotectant toxicity, per se, may not be involved in lower cryosurvival of embryos in CVP vs. Cryotec and Kitazato. The initial pregnancy rates were numerically higher in Cryotec and Kitazato frozen transfers compared to fresh transfer (56.3, 60 and 33.3%, respectively), and importantly, a higher percentage of established pregnancies in vitrified groups passed the critical 3 months period of early embryonic loss compared to sibling fresh clone pregnancies (50, 40, and 10%, respectively). Results confirmed the suitability of Cryotec and Kitazato kits for vitrification of cloned camel embryos and that vitrification may improve pregnancy outcome by weeding out poor competent embryos.

Prophylactic Role of Oral Melatonin Administration on Neurogenesis in Adult Balb/C Mice during REM Sleep Deprivation.

Purpose. The aim of this study was to assess the effect of melatonin in the proliferation of neural progenitors, melatonin concentration, and antiapoptotic proteins in the hippocampus of adult mice exposed to 96 h REM sleep deprivation (REMSD) prophylactic administration of melatonin for 14 days. Material and Methods. Five groups of Balb/C mice were used: (1) control, (2) REMSD, (3) melatonin (10 mg/kg) plus REMSD, (4) melatonin and intraperitoneal luzindole (once a day at 5 mg/kg) plus REMSD, and (5) luzindole plus REMSD. To measure melatonin content in hippocampal tissue we used HPLC. Bcl-2 and Bcl-xL proteins were measured by Western Blot and neurogenesis was determined by injecting 5-bromo-2-deoxyuridine (BrdU) and BrdU/nestin expressing cells in the subgranular zone of the dentate gyrus were quantified by epifluorescence. Results. The melatonin-treated REMSD group showed an increased neural precursor in 44% with respect to the REMSD group and in 28% when contrasted with the control group (P < 0.021). The melatonin-treated REMSD group also showed the highest expression of Bcl-2 and Bcl-xL as compared to the rest of the groups. Conclusion. The exogenous administration of melatonin restores the tissue levels of sleep-deprived group and appears to be an efficient neuroprotective agent against the deleterious effects of REMSD.

Rapid Eye Movement Sleep Deprivation Produces Long-Term Detrimental Effects in Spatial Memory and Modifies the Cellular Composition of the Subgranular Zone.

Sleep deprivation (SD) affects spatial memory and proliferation in the dentate gyrus. It is unknown whether these deleterious effects persist in the long run. The aim of this study was to evaluate the proliferation, differentiation and maturation of neural progenitors as well as spatial memory 21 days after suffering SD. Sixty-day old male Balb/C mice were exposed to 72-h REM-SD. Spatial memory, cell fate, apoptosis and expression levels of insulin-like growth factor 1 receptor (IGF-1R) were evaluated in the hippocampus at 0, 14, and 21 days after SD or control conditions. After 21-days recovery period, memory performance was assessed with the Barnes maze, we found a significant memory impairment in SD mice vs. control (94.0 ± 10.2 s vs. 25.2 ± 4.5 s; p < 0.001). The number of BrdU+ cells was significantly decreased in the SD groups at day 14 (controls = 1.6 ± 0.1 vs. SD mice = 1.2 ± 0.1 cells/field; p = 0.001) and at day 21 (controls = 0.2 ± 0.03 vs. SD mice = 0.1 ± 0.02 cells/field; p < 0.001). A statistically significant decrease was observed in neuronal differentiation (1.4 ± 0.1 cells/field vs. 0.9 ± 0.1 cells/field, p = 0.003). Apoptosis was significantly increased at day 14 after SD (0.53 ± 0.06 TUNEL+ cells/field) compared to controls (0.19 ± 0.03 TUNEL+ cells/field p < 0.001) and at 21-days after SD (SD mice 0.53 ± 0.15 TUNEL+ cells/field; p = 0.035). At day 0, IGF-1R expression showed a statistically significant reduction in SD animals (64.6 ± 12.2 units) when compared to the control group (102.0 ± 9.8 units; p = 0.043). However, no statistically significant differences were found at days 14 and 21 after SD. In conclusion, a single exposition to SD for 72-h can induce deleterious effects that persist for at least 3 weeks. These changes are characterized by spatial memory impairment, reduction in the number of hippocampal BrdU+ cells and persistent apoptosis rate. In contrast, changes IGF-1R expression appears to be a transient event. Highlight Sleep deprivation affects spatial memory and proliferation in the dentate gyrus. To date it is unknown whether these deleterious effects are persistent over a long period of time. We analyzed the effects of sleep deprivation in the hippocampus after 21 days of recovery sleep. Our findings indicate that after sleep recovery, the detrimental effects of SD can be observed for at least 2 weeks, as shown by a reduction in memory performance, changes in the hippocampal cellular composition and higher apoptotic rate over a long period of time.

Epilepsia del lóbulo temporal y neurocisticercosis activa: dos casos representativos / Temporal lobe epilepsy and active neurocysticercosis: two representative case reports

Introducción. Existen pocas evidencias notificadas de casos de epilepsia del lóbulo temporal asociadas a cisticercosis activa en su fase quística. El objetivo es presentar la correlación entre cisticercosis activa en zonas topográficas asociadas a epilepsia del lóbulo temporal, con las manifestaciones neuropsiquiátricas y el patrón de crisis parciales secundariamente generalizadas. Casos clínicos. Dos casos de pacientes adultos con manifestaciones neuropsiquiátricas de un año de evolución, refractarios a tratamiento farmacológico antipsicótico, y en quienes posteriormente aparecen crisis convulsivas parciales secundariamente generalizadas de inicio tardío. Se identifica la presencia de cisticercosis activa en el lóbulo temporal en un paciente, y en la ínsula, en el otro. Buen control clínico posterior al tratamiento con albendazol, pero se mantiene el mismo tratamiento anticonvulsionante para considerar la pertinencia de su retirada farmacológica. Conclusiones. La neurocisticercosis activa puede ser causa de trastornos neuropsiquiátricos adquiridos y de epilepsia del lóbulo temporal de inicio tardío cuando su topografía se encuentra en el circuito mesolímbico. El diagnóstico etiológico oportuno y el tratamiento apropiado permiten el control adecuado de su sintomatología y, potencialmente, su curación definitiva (AU)

Introduction. There are limited evidences reported of temporal lobe epilepsy associated with active cysticercosis in cystic stage. The objective is to present the correlation between active cysticercosis in topographical zones associated with temporal lobe epilepsy, with neuropsychiatric manifestations and pattern of secondarily generalized partial seizures. Case reports. Two cases of adult patients with neuropsychiatric manifestations of one year evolution, refractory to antipsychotic drug treatment, and who subsequently appear late onset partial-secondarily generalized seizures. Cysticercosis active presence in the temporal lobe in one patient, and the insula in the other, is identified. A better clinical control after albendazol treatment and subsequently anticonvulsant therapy only remained to evaluate pertinence of pharmacological withdrawal criteria. Conclusions. Active neurocysticercosis, may be the cause of acquired neuropsychiatric disorders and temporal lobe epilepsy of late onset when the topography is in the mesolimbic circuit. Early etiologic diagnosis and appropriate treatment allows adequate control of their symptoms and potentially final cure (AU)

[Temporal lobe epilepsy and active neurocysticercosis: two representative case reports]. / Epilepsia del lobulo temporal y neurocisticercosis activa: dos casos representativos.

INTRODUCTION: There are limited evidences reported of temporal lobe epilepsy associated with active cysticercosis in cystic stage. The objective is to present the correlation between active cysticercosis in topographical zones associated with temporal lobe epilepsy, with neuropsychiatric manifestations and pattern of secondarily generalized partial seizures. CASE REPORTS: Two cases of adult patients with neuropsychiatric manifestations of one year evolution, refractory to antipsychotic drug treatment, and who subsequently appear late onset partial-secondarily generalized seizures. Cysticercosis active presence in the temporal lobe in one patient, and the insula in the other, is identified. A better clinical control after albendazol treatment and subsequently anticonvulsant therapy only remained to evaluate pertinence of pharmacological withdrawal criteria. CONCLUSIONS: Active neurocysticercosis, may be the cause of acquired neuropsychiatric disorders and temporal lobe epilepsy of late onset when the topography is in the mesolimbic circuit. Early etiologic diagnosis and appropriate treatment allows adequate control of their symptoms and potentially final cure.

TITLE: Epilepsia del lobulo temporal y neurocisticercosis activa: dos casos representativos.Introduccion. Existen pocas evidencias notificadas de casos de epilepsia del lobulo temporal asociadas a cisticercosis activa en su fase quistica. El objetivo es presentar la correlacion entre cisticercosis activa en zonas topograficas asociadas a epilepsia del lobulo temporal, con las manifestaciones neuropsiquiatricas y el patron de crisis parciales secundariamente generalizadas. Casos clinicos. Dos casos de pacientes adultos con manifestaciones neuropsiquiatricas de un año de evolucion, refractarios a tratamiento farmacologico antipsicotico, y en quienes posteriormente aparecen crisis convulsivas parciales secundariamente generalizadas de inicio tardio. Se identifica la presencia de cisticercosis activa en el lobulo temporal en un paciente, y en la insula, en el otro. Buen control clinico posterior al tratamiento con albendazol, pero se mantiene el mismo tratamiento anticonvulsionante para considerar la pertinencia de su retirada farmacologica. Conclusiones. La neurocisticercosis activa puede ser causa de trastornos neuropsiquiatricos adquiridos y de epilepsia del lobulo temporal de inicio tardio cuando su topografia se encuentra en el circuito mesolimbico. El diagnostico etiologico oportuno y el tratamiento apropiado permiten el control adecuado de su sintomatologia y, potencialmente, su curacion definitiva.