Frozen elephant trunk in acute type A aortic dissection: surgical techniques and the extracorporeal circuit management

Acute type A aortic dissection (ATAAD) is a challenging clinical condition with immediate and late complications. Frozen elephant trunk (FET) has been offered as a solution for it promises to address the late complications—false lumen thrombosis and aortic remodelling. Here, we describe the implantation of the FET in ATAAD with the surgical technique and extracorporeal circuit management. A 54-year-old male presented with retrograde type A aortic dissection with an entry point distal to the left subclavian artery. He underwent FET using Thoraflex™ hybrid vascular prosthesis (Vascutek, Inchinnan, Scotland). Three-month follow-up showed a complete obliteration of the false lumen in the descending thoracic aorta. FET in ATAAD is a valid option in the hands of experienced surgeons, while patient selection still remains the key in this surgery.     

Influence of preoptico-anterior and posterior hypothalamus on midline thalamic neurons

The present study was aimed at understanding the influence of the posterior hypothalamus (PH) and the preoptico-anterior hypothalamus (PO-AH) on the neurons of the midline thalamus (MTh) in encéphale isolé cats. A majority of the influenced neurons of the MTh showed increased firing on stimulation of the PH. Although the number of neurons showing increased or decreased firing on PO-AH stimulation were nearly equal, stimulus bound increased firing in many neurons was followed by a prolonged decreased firing. It is likely that the hypothalamo-thalamic circuit constitutes a parallel pathway to the reticulo-thalamic circuit for alteration of the cortical EEG.     

The effects of rapid eye movement sleep deprivation during late pregnancy on newborns' sleep

Sleep deprivation during pregnancy is an emerging concern, as it can adversely affect the development of the offspring brain. This study was conducted to evaluate the effects of deprivation of rapid eye movement (REM) sleep during the third term of pregnancy on the sleep–wake profiles of neonates in the Wistar rat model. Sleep–wake patterns were assessed through electrophysiological measures and behavioural observations during postnatal days 1–21 on pups born to REM sleep‐deprived dams and control rats. Pups of REM sleep‐deprived dams had active sleep that was not only markedly higher in percentage during all the days studied, but also had reduced latency during later postnatal days 15–21. Quiet sleep and wake periods were lower. These factors, along with less frequent but longer sleep–wake cycles, indicated maturational delay in the sleep–wake neural networks. The disruption of time‐bound growth of sleep–wake neural networks was substantiated further by the decreased slope of survival plots in the sleep bouts. Examination of altered sleep–wake patterns during early development may provide crucial information concerning deranged neural development in the offspring. This is the first report, to our knowledge, to show that maternal sleep deprivation during pregnancy can delay and impair the development of sleep–wake profile in the offspring.     

The fabrication and characterization of biodegradable HA/PHBV nanoparticle–polymer composite scaffolds

This study reports the fabrication and characterization of nano-sized hydroxyapatite (HA)/poly(hydroxyabutyrate-co-hydroxyvalerate) (PHBV) polymer composite scaffolds with high porosity and controlled pore architectures. These scaffolds were prepared using a modified thermally induced phase-separation technique. This investigation focuses on the effect of fabrication conditions on the overall pore architecture of the scaffolds and the dispersion of HA nanocrystals within the composite scaffolds. The morphologies, mechanical properties and in vitro bioactivity of the composite scaffolds were investigated. It was noted that the pore architectures could be manipulated by varying phase-separation parameters. The HA particles were dispersed in the pore walls of the scaffolds and were well bonded to the polymer. The introduction of HA greatly increased the stiffness and strength, and improved the in vitro bioactivity of the scaffolds. The results suggest these newly developed nano-HA/PHBV composite scaffolds may serve as an effective three-dimensional substrate in bone tissue engineering.     

Dietary homocysteine promotes atherosclerosis in apoE-deficient mice by inducing scavenger receptors expression

Elevated plasma homocysteine (Hcy) levels have been recognized as an independent risk factor for atherosclerosis leading to cardiovascular diseases. However, the mechanisms contributing to atherosclerosis have not been delineated. Since, scavenger receptors mediated uptake of oxidized-LDL (oxLDL) by macrophages resulting in foam cell formation is an early event in atherosclerosis, we hypothesized that atherogenic effects of Hcy may be mediated via regulating expression of scavenger receptor(s). We have tested this hypothesis using apoE-/- female mice fed normal rodent chow (NC) diet or NC supplemented with Hcy in drinking water (9 g/L). Hcy-fed mice showed increased fatty streak lesions in aortic sinus/root compared to NC group without alterations in plasma lipid profiles. Similar findings were observed in the enface analysis of the descending aorta. To determine the molecular mechanisms underlying Hcy-mediated progression of fatty streak lesions, expression of scavenger receptors such as CD36 and lectin-like oxidized LDL binding protein-1 (LOX-1) in the aortic lesions were analyzed. Interestingly, Hcy-fed mice had increased immuno-positive staining for CD36 and LOX-1 in the atherosclerotic lesions compared to NC-fed mice. In vitro analyses showed neither Hcy nor HcyLDL directly affect the expression of CD36 and LOX-1 on mouse macrophages. However, Hcy supplementation in apoE-/- mice resulted in elevated oxLDL levels in plasma. Since oxLDL has been shown to upregulate the expression of CD36 and LOX-1, these findings suggest that Hcy may exert its atherogenic effect in part by elevating the levels of oxLDL. Interestingly, interaction of monocytes with Hcy-activated endothelial cells resulted in upregulation of CD36 expression on monocytes, suggesting a possible mechanism by which Hcy may upregulate CD36 expression at the lesion site. Further, these findings suggest a novel mechanism by which Hcy may promote atherogenesis.     

High energy phosphate abnormalities normalize after antipsychotic treatment in schizophrenia: A longitudinal 31P MRS study of basal ganglia

We reported increased high-energy phosphate metabolism in the basal ganglia of antipsychotic-naïve schizophrenia patients using ³¹P Magnetic Resonance Spectroscopy (MRS). These patients were followed up for 1 year and and reassessed using ³¹P MRS. Fourteen (8 males) patients with DSM-IV schizophrenia and 14 (11 males) healthy controls underwent ³¹P MRS of sub-cortical structures (predominantly basal ganglia) twice (mean ± S.D. interscan interval 1.15 ± 0.17 year) on a 1.5 T scanner. Total scores on the Positive and Negative Syndrome Scale (PANSS) decreased significantly after treatment in schizophrenia patients. Patients had significantly lower mean PCr/ATP ratios than healthy controls at baseline but not during the follow-up. In patients, there was a significant positive correlation between the magnitude of improvement in PANSS total scores and the extent of change in the PCr/ATP ratio. Findings support the hypothesis that reduction of energy demand or induction of decreased energy-demanding processes might underlie the mechanism of action of antipsychotics in schizophrenia.     

Changes in sleep-wakefulness in the medial preoptic area lesioned rats: role of thermal preference

Changes in sleep-wakefulness (S-W) were studied in adult male Wistar rats, along with body temperature (T(b)), locomotor activity (LMA) and thermal preference, after the lesion of the medial preoptic area (mPOA) with N-methyl-D-aspartic acid (NMDA). The sleep was decreased after the lesion of the mPOA, but there was recovery when the rats were given freedom to stay in an ambient temperature (T(amb)) which they preferred. When given a choice between three T(amb) (24, 27 and 30 degrees C), the rats preferred 27 degrees C before the mPOA lesion, and 24 degrees C during the initial days after the lesion. There was a shift in the thermal preference to 30 degrees C, on the fourth week after the lesion, which coincided with the considerable recovery of sleep. The preference for higher T(amb) probably helped to improve sleep, as T(amb) of 30 degrees C is known to promote sleep. When the lesioned rats were not given the freedom to select the T(amb), there was no recovery in sleep. The mPOA seems to be essential for increasing the durations of slow wave sleep (SWS) episodes, especially the light SWS (S1), as they remained shorter than the pre-lesion value, even when the rats were given freedom to stay in a preferred T(amb). The homeostatic recovery of sleep, especially the night time sleep, resulted in the disruption of circadian sleep rhythm. But, the LMA, T(b) and thermal preference maintained their diurnal variation. T(b) and LMA were elevated after the mPOA lesion and they remained so till the end of the study.     

Enhanced C-terminal truncation of alphaA- and alphaB-crystallins in diabetic lenses

PURPOSE: To investigate the influence of diabetes on the cleavage of C-terminal amino acid residues of alphaA- and alphaB-crystallins in human and rat lenses. METHODS: The human lenses were diabetic or age-matched control lenses from donors 57, 59, 69, and 72 years of age. Lenses were also obtained from streptozotocin-induced diabetic rats. Individual lens crystallins in water-soluble fractions were separated by gel-permeation chromatography. The high (alphaH)- and low (alphaL)-molecular-weight fractions were analyzed by electrospray ionization mass spectrometry. RESULTS: A typical mass spectrum of alphaA-crystallin from human lenses showed intact unmodified alphaA-crystallin, truncated alphaA(1-172), and monophosphorylated alphaA-crystallin. Diabetic lenses showed nearly twofold higher levels of alphaA(1-172) than did the control lenses. Also, the alphaH fraction consistently showed significantly higher levels of alphaA(1-172) than the alphaL fraction. Human alphaB-crystallin showed no evidence of C-terminal truncation. Rat alphaA-crystallin had five C-terminal-truncated components, most of which showed substantial increases in diabetes. Truncated alphaA(1-162) appeared only in the diabetic rat lenses, suggesting specific activation of m-calpain in diabetes. alphaB-crystallin had only one C-terminal-truncated component, alphaB(1-170), which also showed increased levels in diabetes. CONCLUSIONS: These data suggest that diabetic stress causes either enzymatic or nonenzymatic cleavage of peptide bonds between specific C-terminal amino acid residues. Such truncated alpha-crystallins appear to contribute to an increased level of the alphaH fraction generally present in diabetic lenses. Loss of alphaA-crystallin chaperone activity seems to be related to truncation of the C-terminal amino acid residues.