Heat Sink Effect on Tumor Ablation Characteristics as Observed in Monopolar Radiofrequency,Bipolar Radiofrequency,and Microwave,Using Ex Vivo Calf Liver Model

Thermal ablation of liver tumors near large blood vessels is affected by the cooling effect of blood flow, leading to incomplete ablation. Hence, we conducted a comparative investigation of heat sink effect in monopolar (MP) and bipolar (BP) radiofrequency ablation (RFA), and microwave (MW) ablation devices.With a perfused calf liver, the ablative performances (volume, mass, density, dimensions), with and without heat sink, were measured. Heat sink was present when the ablative tip of the probes were 8.0 mm close to a major hepatic vein and absent when >30 mm away. Temperatures (T1 and T2) on either side of the hepatic vein near the tip of the probes, heating probe temperature (T3), outlet perfusate temperature (T4), and ablation time were monitored.With or without heat sink, BP radiofrequency ablated a larger volume and mass, compared with MP RFA or MW ablation, with latter device producing the highest density of tissue ablated. MW ablation produced an ellipsoidal shape while radiofrequency devices produced spheres.Percentage heat sink effect in Bipolar radiofrequency : Mono-polar radiofrequency : Microwave was (Volume) 33:41:22; (mass) 23:56:34; (density) 9.0:26:18; and (relative elipscity) 5.8:12.9:1.3, indicating that BP and MW devices were less affected.Percentage heat sink effect on time (minutes) to reach maximum temperature (W) = 13.28:9.2:29.8; time at maximum temperature (X) is 87:66:16.66; temperature difference (Y) between the thermal probes (T3) and the temperature (T1 + T2)/2 on either side of the hepatic vessel was 100:87:20; and temperature difference between the (T1 + T2)/2 and temperature of outlet circulating solution (T4), Z was 20.33:30.23:37.5.MW and BP radiofrequencies were less affected by heat sink while MP RFA was the most affected. With a single ablation, BP radiofrequency ablated a larger volume and mass regardless of heat sink.     

An unusual parasagittal tumour with acute blindness and response to cerebrospinal fluid shunting.

We report a seven-year-old girl who presented with a sudden tumor apoplexy due to a parasagittal hemangiopericytoma. Following tumor excision, the child was noted to have bilateral optic nerve dysfunction and progressive papilledema, despite rapid overall neurological improvement. Based on the clinical features, we feel that this case represents an unusual form of visual deterioration related to impaired CSF absorption somehow precipitated by the acute tumour apoplexy. This unusual case of blindness responded significantly to CSF shunting. Several reports exist describing raised intracranial pressure with papilledema caused by nonthrombotic sinus occlusion due to tumors in proximity to the posterior superior sagittal sinus, torcular herophili and the jugular outlet. Communicating hydrocephalus, pseudotumor syndrome or intracranial venous sinus obstruction should be considered when otherwise inexplicable visual loss coexists with optic nerve dysfunction and papilledema. We emphasize the importance of a thorough search for the cause of visual loss.     

Bilateral sino-orbital pseudotumour

The authors present a case of histopathologically proved bilateral idiopathic inflammatory pseudotumour of the orbits with involvement of the paranasal sinuses in a child. Clinically, the bilateral proptosis was manifest at the age of 5 years. While extraorbital manifestations are rare, orbital pseudotumour should be considered in such cases.     

Myoblast fusion in Drosophila melanogaster is mediated through a fusion-restricted myogenic-adhesive structure (FuRMAS).

During myogenesis in Drosophila embryos, a prominent adhesive structure is formed between precursor cells and fusion-competent myoblasts (fcms). Here, we show that Duf/Kirre and its interaction partners Rols7 (found in founder myoblasts and growing myotubes) and Sns (found in fcms) are organized in a ring-structure at the contact points of fcms with precursor cells, while cytoskeletal components like F-actin and Titin are centered in this ring in both cell types. The cytoplasmic protein Blow colocalizes with the actin plugs in fcms after cell adhesion. Furthermore, the requirement of additional as yet unidentified components was demonstrated by using mammalian C2C12 myoblasts. In this study, we propose that the fusion-restricted myogenic-adhesive structure (FuRMAS) is pivotal in linking cell adhesion as well as local F-actin assembly and dynamics to downstream events that ultimately lead to plasma membrane fusion. Moreover, we suggest that the FuRMAS may restrict the area of membrane breakdown.     

Recovery after chronic stress fails to reverse amygdaloid neuronal hypertrophy and enhanced anxiety-like behavior

The hippocampus and amygdala are important components of the neural circuitry mediating stress responses. While structural plasticity in the hippocampus may mediate cognitive aspects of behavioral impairments caused by severe stress, changes in the amygdala are more likely to contribute to the affective aspects of stress disorders. Recent reports have identified cellular and molecular correlates of stress-induced amygdaloid plasticity that may underlie anxiety. Hence, we examined the impact of chronic stress, in terms of its duration, at the cellular and behavioral levels in rats. We found that, even after 21 days of stress-free recovery, animals exposed to chronic immobilization stress (CIS) continue to exhibit enhanced anxiety, as manifested by a significant reduction in open-arm exploration and risk-assessment behavior in the elevated plus-maze. At the cellular level, we tested if CIS-induced dendritic remodeling in the amygdala is also as long-lasting as enhanced anxiety after 21 days of recovery. Indeed, long-lasting facilitation of CIS-induced anxiety is accompanied by a persistent increase in dendritic arborization of basolateral amygdala (BLA) spiny neurons. Moreover, CIS-induced BLA hypertrophy is distinct from hippocampal CA3 atrophy, which is reversible within the same period of stress-free recovery. These findings on persistent dendritic remodeling in the amygdala, in addition to highlighting important differences with hippocampal structural plasticity, may provide a cellular basis for examining anxiety and mood disorders triggered by chronic stress.     

Comparison of four erythrocyte fragility tests as indicators of vitamin E status in adult dogs.

Plasma alpha-tocopherol (alpha-T) concentrations, erythrocyte osmotic fragility and detergent sensitivity were measured at 8 week intervals in two 1-year-old male beagle dogs fed a vitamin E-deficient diet (< 0.08 mg per kg alpha-T) and in two control beagles fed the same diet supplemented with vitamin E (> 90 mg per kg alpha-T). Beginning at 24 weeks, dialuric acid haemolysis and spontaneous haemolysis were evaluated also. In the vitamin E-deficient dogs, plasma alpha-T concentrations declined progressively from baseline values of 20.5 and 31.3 micrograms per ml to 0.11 and 0.07 micrograms per ml, respectively, by 90 weeks. The supplemented dogs maintained alpha-T concentrations between 18.3 and 38.4 micrograms per ml. Both dialuric acid haemolysis (R = -0.89) and spontaneous haemolysis (R = -0.91) increased with declining plasma alpha-T concentration. In the dialuric acid haemolysis assay, 50 per cent haemolysis occurred when plasma alpha-T declined to 1.7 micrograms per ml, compared with spontaneous haemolysis in which 50 per cent haemolysis occurred when plasma alpha-T declined to 0.5 micrograms per ml. Osmotic fragility and detergent sensitivity remained unchanged in the vitamin E-deficient dogs throughout the study. Of the four tests, dialuric acid haemolysis was the most sensitive in-vitro assay for vitamin E deficiency in adult dogs.     

Hyperpolarization of myenteric neurons by opioids does not involve cyclic adenosine-3',5'-monophosphate.

To investigate the role of cyclic adenosine-3'5'-monophosphate on the inhibitory actions of opioids in guinea-pig ileum, we made intracellular recordings from the two electrophysiologically defined classes of neurons (S and AH) in the myenteric plexus. The selective opioid mu agonist (D-Ala2,N-Me-Phe4,Gly5-ol)-enkephalin caused a membrane hyperpolarization in 34 out of 67 S neurons but did not affect the membrane potential of AH neurons. The mean amplitude (+/- S.E.M.) of the hyperpolarization was 8.2 +/- 0.8 mV. Forskolin, which activates adenylate cyclase and increases intracellular cyclic adenosine-3',5'-monophosphate levels, caused a membrane depolarization in AH neurons (9.4 +/- 1.9 mV) but did not alter the resting membrane potential of S neurons. Similarly, neither the phosphodiesterase inhibitor, isobutylmethylxanthine, nor the membrane permeable analogue of cyclic adenosine-3',5'-monophosphate, dibutyryl cyclic adenosine-3'-5'-monophosphate, altered the resting membrane properties of S neurons. Furthermore, none of these agents affected significantly the amplitude of the hyperpolarization of S neurons by (D-Ala2,N-Me-Phe4,Gly5-ol)-enkephalin. The experiments indicate that changes in intracellular cyclic adenosine-3',5'-monophosphate are not important in the processes that link occupation of mu receptors to the opening of potassium channels on myenteric neurons.