The Fasciocapsular Flap in Capsular Herniation

After augmentation mammaplasty, either subglandular or submuscular, the most typical complication to occur is capsule formation or its advanced form, capsular contracture. Even the less severe capsule formation can cause a feeling of discomfort because the breast starts to be fixed to the rear chest wall, thus resulting in a feeling of slight tightening. In extreme cases, a painful, distorted knot appears, which can immobilize the implant, resulting in the development of the so-called tennis ball phenomenon. Currently, because of high-quality mammary prostheses, the occurrence of the aforementioned extreme capsulation is rare (2–3%). The development of a soft, thin, but strong capsule, which neither distorts the shape of the breast nor fixes the breast to the rear chest wall, is much more frequent. However, the capsule does exist, and even if barely noticeable, it puts the implant under considerable pressure. It does not harm the prosthesis, but it is possible that the capsule itself is weakened, leading to the development of a hernia in which the implant may become visible. In the early phase, the hernia cannot be seen at rest, but when the implant is pressed, a small tumescence occurs on the breast. When the pressure is released, the herniated part of the implant withdraws, and the bulge disappears. At later stages, however, the bulge becomes permanent, and the implant protrudes along the weakened capsule. Thus, the overall image of the breast has lost its smooth continuity. The new tissue has developed around the implant, and the fascia of the pectoral muscle should be used to strengthen the weak point of the breast because the blood supply of both the capsule and the fascia is sufficient to allow their use as flaps.     

Gastroesophageal variceal haemorrhage--new advances in pathophysiology

Ruptured gastroesophageal varices are the most severe and frequent causes of upper gastrointestinal bleeding in patients suffering from liver cirrhosis, accounting for 80% of all bleeding episodes. Despite recent progress in treatment strategies, variceal bleeding is still considered the most severe type of gastrointestinal bleeding associated with a mortality of 20% at 6 weeks. The most widely accepted explanation for the rupture is the "explosion hypothesis": bleeding is a result of the elevated intravariceal pressure and increased wall-straining due to a rapid increase in the portal pressure gradient. The rupture of the varices and the early rebleeding cannot be attributed solely to mechanical changes. Furthermore, the factors involved in the sudden increase of portal pressure gradient are yet to be discovered. Recently it was postulated that various humoral factors may also play an important role in the pathomechanism of the rupture. The pivotal role of bacterial infection and consequent endotoxaemia must be emphasized. Passage of both viable microbes and microbial products, such as endotoxins from the intestinal lumen to peripheral and portal circulation in cirrhotic patients can be explained by the intestinal bacterial overgrowth, the intestinal dysmotility and the increased intestinal permeability. Endotoxaemia can be a critical factor that triggers a cascade of humoral events, resulting in a further increase of portal pressure, impairment of liver function and worsening of haemostasis, and eventually leads to variceal bleeding. Early administration of prophylactic antibiotics to variceal bleeders recently became an integral and important part of therapeutic strategy. Antibiotics are not only useful in the prevention of early rebleeding but also they are proven to significantly decrease the rate of mortality. The improvement in mortality is equivalent to that seen with terlipressine.     

Drosophila melanogaster Rac2 is necessary for a proper cellular immune response

It has been reported that during Drosophila embryonic development, and in cell culture, that the Rac GTPases are redundant. To better elucidate Rac function in Drosophila, we decided to study the role of Rac2 in larval cellular defense reactions against the parasitiod Leptopilina boulardi. Here we show a dramatic effect in the context of cellular immunity where, unlike embryonic development, Rac2 appears to have a non-redundant function. When an invading parasitoid is recognized as foreign, circulating hemocytes (blood cells) should recognize and attach to the egg chorion. After attachment the hemocytes should then spread to form a multilayered capsule surrounding the invader. In Rac2 mutants this process is disrupted. Immune surveillance cells, known as plasmatocytes, adhere to the parasitoid egg but fail to spread, and septate junctions do not assemble, possibly due to mislocalization of the Protein 4.1 homolog Coracle. Finally, larger cells known as lamellocytes attach to the capsule but also fail to spread, and there is a lack of melanization. From these results it appears that Rac2 is necessary for the larval cellular immune response.     

Self-face recognition activates a frontoparietal "mirror" network in the right hemisphere: an event-related fMRI study

Self-recognition has been demonstrated by a select number of primate species and is often used as an index of self-awareness. Whether a specialized neural mechanism for self-face recognition in humans exists remains unclear. We used event-related fMRI to investigate brain regions selectively activated by images of one's own face. Ten right-handed normal subjects viewed digital morphs between their own face and a gender-matched familiar other presented in a random sequence. Subjects were instructed to press a button with the right hand if the image looked like their own face, and another button if it looked like a familiar or scrambled face. Contrasting the trials in which images contain more "self" with those containing more familiar "other" revealed signal changes in the right hemisphere (RH) including the inferior parietal lobule, inferior frontal gyrus, and inferior occipital gyrus. The opposite contrast revealed voxels with higher signal intensity for images of "other" than for "self" in the medial prefrontal cortex and precuneus. Additional contrasts against baseline revealed that activity in the "self" minus "other" contrasts represent signal increases compared to baseline (null events) in "self" trials, while activity in the "other" minus "self" contrasts represent deactivations relative to baseline during "self" trials. Thus, a unique network involving frontoparietal structures described as part of the "mirror neuron system" in the RH underlies self-face recognition, while regions comprising the "default/resting state" network deactivate less for familiar others. We provide a model that reconciles these findings and previously published work to account for the modulations in these two networks previously implicated in social cognition.     

Exploring the contributions of premotor and parietal cortex to spatial compatibility using image-guided TMS

Functional brain imaging studies have demonstrated increased activity in dorsal premotor and posterior parietal cortex when performing spatial stimulus-response compatibility tasks (SRC). We tested the specific role of these regions in stimulus-response mapping using single-pulse transcranial magnetic stimulation (TMS). Subjects were scanned using functional magnetic resonance imaging (fMRI) prior to the TMS session during performance of a task in which spatial compatibility was manipulated. For each subject, the area of increased signal within the regions of interest was registered onto their own high-resolution T1-weighted anatomic scan. TMS was applied to these areas for each subject using a frameless stereotaxic system. Task accuracy and reaction time (RT) were measured during blocks of compatible or incompatible trials and during blocks of real TMS or sham stimulation. On each trial, a single TMS pulse was delivered at 50, 100, 150, or 200 ms after the onset of the stimulus in the left or right visual field. TMS over the left premotor cortex produced various facilitatory effects, depending on the timing of the stimulation. At short intervals, TMS appeared to prime the left dorsal premotor cortex to select a right-hand response more quickly, regardless of stimulus-response compatibility. The strongest effect of stimulation, however, occurred at the 200-ms interval, when TMS facilitated left-hand responses during the incompatible condition. Facilitation of attention to the contralateral visual hemifield was observed during stimulation over the parietal locations. We conclude that the left premotor cortex is one of the cortical regions responsible for overriding automatic stimulus-response associations.     

Decreased oral self-administration of alcohol in kappa-opioid receptor knock-out mice

BACKGROUND: Although a large body of evidence suggests a role for the opioid system in alcoholism, the precise role of mu-, delta-, kappa-, and ORL1-opioid receptors and the physiological significance of their natural genetic variation have not been identified. The method of targeted gene disruption by homologous recombination has been used to knock out (KO) genes coding for opioid receptors, and study their effects on alcohol self-administration. Here we examined the effects of targeted disruption of kappa-opioid receptor (KOR) on oral alcohol self-administration and other behaviors. METHODS: Oral alcohol, saccharin and quinine self-administration was assessed in a two-bottle choice paradigm using escalating concentrations of alcohol, or tastant solutions. In preference tests 12% alcohol, 0.033% and 0.066% saccharin, and 0.03 mM and 0.1 mM quinine solutions were used. Open-field activity was determined in an arena equipped with a computer-controlled activity-detection system. Subjects were tested for three consecutive days. Locomotor activity was assessed on days 1 and 2 (after saline injection, i.p.) and on day 3 (after alcohol injection, i.p.). Alcohol-induced locomotor activity was determined as the difference in activity between day 3 and day 2. RESULTS: Male KOR KO mice in preference tests with 12% alcohol consumed about half as much alcohol as wild-type (WT) or heterozygous (HET) mice, showed lower preference for saccharin (0.033% and 0.066%) and higher preference to quinine (0.1 mM) than WT mice. Female KOR KO mice showed similar reduction in alcohol consumption in comparison to WT and HET mice. Partial deletion of KOR in HET mice did not change alcohol consumption in comparison to WT mice. In all genotype-groups females drank significantly more alcohol than males. MANOVA of locomotor activity among KO, WT, and HET mice indicated that strain and sex effects were not significant for alcohol-induced activation (p > 0.05), while strain x sex interaction effects on alcohol-induced activation could be detected (F(1,55) = 6.07, p < 0.05). CONCLUSION: Our results indicating decreased alcohol consumption, lower saccharin preference, and higher quinine preference in KOR KO mice are in line with previous observations of opioid involvement in maintenance of food intake and raise the possibility that the deficient dynorphin/KOR system affects orosensory reward through central mechanisms which reduce alcohol intake and disrupt tastant responses, either as direct effects of absence of kappa-opioid receptors, or as effects of indirect developmental compensatory changes.     

Estrogen and estrogen receptor-{beta} (ER{beta})-selective ligands induce galanin expression within gonadotropin hormone-releasing hormone-immunoreactive neurons in the female rat brain

Among the many factors that integrate the activity of the GnRH neuronal system, estrogens play the most important role. In females, estrogen, in addition to the negative feedback, also exhibits a positive feedback influence upon the activity and output of GnRH neurons to generate the preovulatory LH surge and ovulation. Until recently, the belief has been that the GnRH neurons do not contain estrogen receptors (ERs) and that the action of estrogen upon GnRH neurons is indirect involving several, estrogen-sensitive neurotransmitter and neuromodulator systems that trans-synaptically regulate the activity of the GnRH neurons. Based on our recent findings that GnRH neurons of the female rat coexpress galanin, that galanin is a potent GnRH-releasing peptide, and that ERbeta is present in GnRH neurons, we have evaluated the effect of 17beta-estradiol and two ERbeta-selective agonists (WAY-200070, WAY-166818) on the expression of galanin within GnRH neurons. By combining immunocytochemistry for GnRH and in situ hybridization histochemistry for galanin, we demonstrate that 17beta-estradiol (20 mug/kg, sc) stimulates galanin expression within GnRH-immunoreactive neurons in a time-dependent manner. A significant increase was observed 2 h after its administration to ovariectomized rats. However, a more robust expression required 3-d treatment regimen. Treatment with the beta-selective ligands resulted in similar observations, although no statistical analysis is available for the 2 hr survival. These observations strongly suggest that estrogen and the ERbeta-selective ligands stimulate galanin expression within GnRH neurons via ERbeta, although an indirect mechanism via interneurons still cannot be ruled out.     

Energy Analysis of Flow Induced Harmonic Motion in Blood Vessel Walls

Energy is transferred between the flowing blood and the vessel walls during pulsatile blood flow (a normal pulse cycle) resulting in storage and dissipation of elastic energy. This allows the elastic and muscular arteries to act as an auxiliary pump to propel the blood fluid forward during systole and maintain a basal blood pressure during diastole. The pulsatile flow pattern caused by the contraction of the left ventricle sets up a state of harmonic motion in the blood vessel walls throughout the arterial vasculature. In this paper, we report on a kinetic energy analysis of pressure and flow velocity waveforms, which characterize energy transfer between the blood and the blood vessel walls at different frequencies of pulsatile flow and pressure. Porcine carotid arteries were tested under simulated physiologic pulsatile flow and pressure conditions in a model water bath system and compared to measurements in vivo on human carotid arteries. Fluid and wall pressures were monitored on the porcine vessels in situ using an absolute differential pressure transducer (fluid) and by a low-pressure volumetric balloon transducer (wall), respectively. A continuous-wave Doppler ultrasonic transducer monitored flow velocity and measurements were made both in vitro and in vivo at frequencies of 1.2 Hz (72 cycles per minute) and 2.1 Hz (125 cycles per minute) for comparison purposes. The areas under the pressure versus time and flow velocity versus time curves were used to calculate the relative change in work and kinetic energies. The calculations of the ratios of the relaxation slopes versus the impact slopes showed that the vessel wall absorbed more energy at the frequency of 1.2 Hz than at the 2.1 Hz frequency. The results of these calculations indicate that energy of the pulse pressure at rest pulse rates is absorbed and dissipated in the vessel wall and the surrounding extracellular matrix. At higher pulse rates and pressures, the vessel wall becomes increasingly elastic, and therefore, transmits or reflects most of the energy of the pressure pulse back to the blood fluid. As the vessel wall becomes less compliant with aging or disease, the energy absorbing and dissipating properties of the arterial wall at rest pulse rate diminish.