Increase in pulse transit time to the foot after epidural anaesthesia treatment

Epidurally induced anaesthetic treatment is a routine treatment for pain relief during surgical procedure, based on blocking the sensory and sympathetic fibres that mediate pain. The epidural sympathetic block results in relaxation of the muscle walls in the lower limbs, which can be assessed by the resultant haemodynamic changes. In the current study, the difference t_t,f in the transit time of the blood pressure pulses between the toe and the finger is measured by photoplethysmography (PPG). Fifteen patients are administered 10 ml 0.25% of bupivacaine, ten patients are administered 10 ml 0.5%, and 17 patients are administered 40 ml 0.0625%. t_t,f decreases as a function of the patient's age and blood pressure, both before and after the sympathetic block, owing to the decrease in arterial compliance with age and blood pressure. The time delay t_t,f increases after the epidural treatment by 10.1±7.0 and by 16.8±10.8 ms for the 0.25% and the 0.5% concentrations, respectively. The time delay increase for the lowest concentration is not statistically significant. The toe-finger time delay change is found to reflect the haemodynamic changes induced by the sympathetic block with higher reliability than the routine methods of skin temperature or arterial blood pressure.     

Neural crest and Schwann cell progenitor-derived melanocytes are two spatially segregated populations similarly regulated by Foxd3

Skin melanocytes arise from two sources: either directly from neural crest progenitors or indirectly from neural crest-derived Schwann cell precursors after colonization of peripheral nerves. The relationship between these two melanocyte populations and the factors controlling their specification remains poorly understood. Direct lineage tracing reveals that neural crest and Schwann cell progenitor-derived melanocytes are differentially restricted to the epaxial and hypaxial body domains, respectively. Furthermore, although both populations are initially part of the Foxd3 lineage, hypaxial melanocytes lose Foxd3 at late stages upon separation from the nerve, whereas we recently found that epaxial melanocytes segregate earlier from Foxd3-positive neural progenitors while still residing in the dorsal neural tube. Gain- and loss-of-function experiments in avians and mice, respectively, reveal that Foxd3 is both sufficient and necessary for regulating the balance between melanocyte and Schwann cell development. In addition, Foxd3 is also sufficient to regulate the switch between neuronal and glial fates in sensory ganglia. Together, we propose that differential fate acquisition of neural crest-derived cells depends on their progressive segregation from the Foxd3-positive lineage.     

Unilateral pulmonary edema: a rare presentation of congestive heart failure

The authors present a case of an 85-year-old woman known to suffer from severe congestive heart failure who presented with dyspnea and a unilateral infiltrate in the right lung on chest x-ray. Following clinical judgment, she was diagnosed with unilateral pulmonary edema and was treated accordingly, with rapid improvement of symptoms and disappearance of the infiltrate within 12 hours. The patient had been hospitalized many times during the previous years with pulmonary edema affecting both lung fields. Unilateral pulmonary edema is an unusual clinical condition that has been reported as a manifestation of left heart failure, mostly affecting the right lung. The authors emphasize the possible presentation of unilateral pulmonary edema in a patient with heart failure and recurrent bilateral pulmonary edema.     

Alterations in segmentary branch pulmonary artery blood flow velocimetry in fetuses of diabetic mothers.

OBJECTIVE: To evaluate pulmonary blood flow in fetuses of diabetic mothers by measuring changes in fetal segmentary pulmonary artery blood flow velocimetry throughout pregnancy. METHODS: Thirty-eight women with pregestational diabetes between weeks 18 and 38 were compared with 99 women with singleton low-risk gestations as controls. Flow velocity waveforms at the proximal middle and distal segments of the right pulmonary artery were obtained with power and color Doppler sonography in all fetuses. The pulsatility index of each segment was compared between the 2 groups. The mean value and 95% confidence interval for each segment were determined in correlation with gestational age for both groups. RESULTS: The highest mean pulsatility indices were obtained in the proximal segment of the pulmonary artery and were 2.25 in the diabetes group and 2.36 in controls. The mean pulsatility indices were significantly decreased in the middle and distal segments to 1.59 and 1.10 in the diabetes group and to 1.57 and 1.02 in controls (P < .05). There were no significant differences in pulsatility indices measured at the proximal and middle segments between the study and control groups. However, the mean pulsatility index +/- SD measured at the distal segment in the diabetic group was 9% higher than in controls (1.10 +/- 0.13 versus 1.02 +/- 0.12; P = .01). The mean pulsatility index (in the study and control groups) in each arterial segment did not change significantly throughout gestation (P > .1). CONCLUSIONS:. In human fetuses throughout gestation, the pulmonary circulation maintains stable vascular resistance in both diabetic and normal pregnancies. However, in all gestations, the pulsatility index in each segment of the pulmonary artery is unique and reflects the proximity to the heart and the impedance at each location. The significantly higher pulsatility index in the diabetes group might be related to alterations in the microcirculation of diabetic patients.     

MicroRNAs as a potential prognostic factor in gastric cancer

AIM:To compare the microRNA (miR) profiles in the primary tumor of patients with recurrent and non-recurrent gastric cancer.METHODS:The study group included 45 patients who underwent curative gastrectomies from 1995 to 2005 without adjuvant or neoadjuvant therapy and for whom adequate tumor content was available.Total RNA was extracted from formalin-fixed paraffin-embedded tumor samples,preserving the small RNA fraction.Initial profiling using miR microarrays was performed to identify potential biomarkers o...     

TGF-β signaling through SMAD2/3 induces the quiescent microglial phenotype within the CNS environment

Microglia are myeloid-derived cells that colonize the central nervous system (CNS) at early stages of development and constitute up to 20% of the glial populations throughout life. While extensive progress has been recently made in identifying the cellular origin of microglia, the mechanism whereby the cells acquire the unique ramified and quiescent phenotype within the CNS milieu remains unknown. Here, we show that upon co-culturing of either CD117(+) /Lin(-) hematopoietic progenitors or CD11c(+) bone marrow derived cells with organotypic hippocampal slices or primary glia, the cells acquire a ramified morphology concomitant with reduced levels of CD86, MHCII, and CD11c and up-regulation of the microglial cell-surface proteins CX(3) CR1 and Iba-1. We further demonstrate that the transforming growth factor beta (TGF-β) signaling pathway via SMAD2/3 phosphorylation is essential for both primary microglia and myeloid-derived cells in order to acquire their quiescent phenotype. Our study suggests that the abundant expression of TGF-β within the CNS during development and various inflammatory processes plays a key role in promoting the quiescent phenotype of microglia and may thus serve as a target for therapeutic strategies aimed at modulating the function of microglia in neurodegenerative diseases such as Alzheimer's and prion.     

Is glucose-6-phosphate dehydrogenase deficiency a risk factor for hyperbaric oxygen exposure?

Divers and patients lacking glucose-6-phosphate dehydrogenase (G6PD) may face a serious threat of central nervous system oxygen toxicity (CNS-OT) during exposure to hyperbaric oxygen (HBO), due to the important part played by G6PD in cellular redox balance. Our objective was to investigate G6PD deficiency as a risk factor for CNS-OT. We exposed G6PD-deficient (G6PDdef) and wild type (WT) mice to HBO at 405 kPa. Latency to CNS-OT was measured by observing the animal and monitoring the time to appearance of convulsions. Changes in glutathione peroxidase (GPx) and catalase activity were measured in red blood cells, and levels of endothelial and neuronal nitric oxide synthase (eNOS and nNOS) and 3-nitrotyrosine (NT) were measured in extracts of whole brain tissue by Western blot analysis. Unexpectedly, latency to CNS-OT was more than twice as long in G6PDdef mice compared with WT (36.9 ± 15.4 and 15.6 ± 13.2 min, respectively, P < 0.005). No significant differences were found in GPx and catalase activity or in protein levels of eNOS. However, nNOS and NT levels were lower in G6PDdef mice compared with WT (50.6%, P < 0.01 and 52.8%, P < 0.05, respectively). Our results suggest that the enhanced resistance of G6PDdef mice to HBO is due in part to a reduction in nNOS and NT levels in the brain. We conclude that G6PD deficiency at the level of the animals in the present study may not be a risk factor for developing CSN-OT, but this remains to be verified for human subjects.     

Combined treatment with Pseudomonas aeruginosa toxin and interferon on mouse and human cells

The combined biological effect of Pseudomonas toxin and beta-interferon on mammalian cells was studied on two cell lines. The first was a virus-producing clone derived from NIH/3T3 mouse fibroblasts transformed by Moloney murine sarcoma virus. The second was a clone derived from human amnion cells. The parameters examined were either retrovirus release from the mouse cells or the rate of protein synthesis in both cell lines. When applied together with Pseudomonas toxin, interferon inhibits virus release even at a Pseudomonas toxin concentration that by itself does not exhibit any biological effect on NIH/3T3 cells. This enhancement phenomenon is both Pseudomonas toxin and interferon dose-dependent. Likewise, the combined treatment of either mouse or human cells with Pseudomonas toxin and the appropriate species-specific interferon, inhibits protein synthesis to a much greater extent than either of these agents alone. The kinetics of the inhibition of virus release is different from that seen with protein synthesis indicating that the enhancement phenomenon observed on virus release is not a result of the inhibition of total cellular protein synthesis. Interferon potentiates the effect of Pseudomonas toxin in a species-specific manner, thus suggesting that this process does not occur at the level of cell receptors but is a consequence of a subsequent intracellular event. It is concluded that the enhancement phenomenon does not reflect a direct interaction between interferon and Pseudomonas toxin, since Pseudomonas incubated together with interferon retained its normal biological activity as indicated by the ability of the toxin molecule to transfer the adenine diphosphoribose (ADP-ribose) moiety of nicotinamide-adenine dinucleotide (NAD) onto elongation factor 2 (EF-2).