Surface Wave Cloak from Graded Refractive Index Nanocomposites.

Recently, a great deal of interest has been re-emerged on the possibility to manipulate surface waves, in particular, towards the THz and optical regime. Both concepts of Transformation Optics (TO) and metamaterials have been regarded as one of key enablers for such applications in applied electromagnetics. In this paper, we experimentally demonstrate for the first time a dielectric surface wave cloak from engineered gradient index materials to illustrate the possibility of using nanocomposites to control surface wave propagation through advanced additive manufacturing. The device is designed analytically and validated through numerical simulations and measurements, showing good agreement and performance as an effective surface wave cloak. The underlying design approach has much wider applications, which span from microwave to optics for the control of surface plasmon polaritons (SPPs) and radiation of nanoantennas.

The first patient with tandem duplication of 6q14q16: Molecular and phenotypic characterization.

Duplications of the long arm of chromosome 6 have been previously reported in a limited number of patients; however, most reported duplications encompass regions of chromosome 6 distal to band q21. Duplications restricted to the proximal portion of 6q are rare. We report an 8-year-old male with a 16.4 megabase (Mb) tandem duplication of chromosome 6q14.1q16.1 (chr6:78950191-95395865; hg19) who exhibited dysmorphic facial features, seizures, global developmental delay, intellectual disability, autism spectrum disorder, sensorineural hearing loss, and immune deficiency. This patient refines and potentially expands the current, poorly-characterized phenotype associated with duplication of this proximal 6q region. We recommend a low threshold for a hearing evaluation beyond newborn screening and for pursuing an immune work-up in patients with similar 6q duplications. © 2016 Wiley Periodicals, Inc.

Design and validation of immunological tests for the detection of Porcine endogenous retrovirus in biological materials.

The present study details the design and demonstrates function for a series of reagents and methods to allow the detection of exposure to antigens specific for Porcine endogenous retrovirus (PERV). The detection of PERV is carried out by the means of a variety of immunological screening methods including, indirect immunofluorescence, Western blotting and enzyme linked immunosorbent assay (ELISA) for the detection of antibodies in serum specific for PERV gag and env antigens. Alternatively, PERV-specific antisera for gag and env can be used to detect viral antigen in serum or other samples. PERV env peptides with potential specificity for the known PERV types are also described. Antisera against the peptides can be used to detect PERV antigens directly or to characterise viral type. Using electron microscopy coupled with labelled PERV-gag-specific antisera it was possible to visualise PERV virions.

The effect of submaximal exercise on recovery hemodynamics and thermoregulation in men and women.

Five women and 5 men were studied to examine the effects of submaximal exercise on thermoregulatory and hemodynamic variables during recovery in two environments: (a) control (C), 22 degrees C, 33% rh; and (b) hot humid (H), 32 degrees C. The participants exercised on a cycle ergometer at 60% of peak oxygen consumption for 35 min prior to 90 min of seated recovery. Sessions were identical, except for environment. Variables evaluated (p < .05) were: core temperature (TR), mean skin temperature (Ts), sweat rate (SR), heart rate (HR), stroke index (SI), cardiac index (CI), forearm blood flow (FBF), systolic blood pressure (SBP), and diastolic blood pressure (DBP). Men and women exhibited similar patterns of TR, Ts, and SR in both environments. Ts and SR (collapsed means for gender) were higher in the H than in the C. DBP was higher in men than in women throughout recovery in both environments. With combined means for gender, HR was higher in the H than in the C. CI, SI, FBF, and SBP were similar in both environments and returned to baseline within 15 min into recovery. These data suggest that heat dissipation during extended recovery was accomplished with similar contributions of cutaneous vasodilation and sweating in M and F. Furthermore, the moderate exercise level did not influence hemodynamics beyond 15 min of recovery in either environment.

Effect of dietary fat reduction and increased aerobic exercise on cardiovascular risk factors.

1. The combined effect of dietary fat reduction and increased aerobic exercise on coronary heart disease (CHD) risk factors was investigated in healthy, normolipidaemic, normotensive, sedentary individuals. 2. After a baseline period of 2 weeks, 21 subjects were randomly allocated to one of two intervention groups (low fat exercise (LFEX) or low fat control (LFC)) for 8 weeks. Both groups were counselled to reduce their dietary fat intake to 20-25% energy from fat. The LFEX group was also required to commence an aerobic exercise programme (4 x 45 min per week). 3. In both groups, the falls in total cholesterol seen at week 4 were not maintained at the end of the study; however, the LFEX group maintained a fall in low-density lipoprotein (LDL) of 0.21 +/- 0.11 mmol/L. At the end of the study, the LFC group experienced a fall in high-density lipoprotein (HDL)-cholesterol of 0.16 +/- 0.05 mmol/L, due to a 0.19 +/- 0.07 mmol/L fall in the HDL2 subfraction. The LFEX group experienced no change in HDL (-0.09 +/- 0.06 mmol/L) or HDL2 (-0.09 +/- 0.05 mmol/L). 4. At the end of the study the LFEX and LFC groups experienced a 7 +/- 3 and 5 +/- 1 mmHg fall in systolic blood pressure, respectively, while the LFEX group also observed a 4 +/- 2 mmHg fall in diastolic blood pressure. 5. The benefits of a low-fat diet combined with aerobic exercise include a reduction in LDL and blood pressure, while maintaining HDL through the HDL2 subfraction.

Release of endothelium-derived relaxing factor from resistance arteries in hypertension.

Aortic rings from SHR are reported to have a decreased relaxation response to the endothelium-dependent agent acetylcholine compared with rings from WKY rats. Thus, a reduced EDRF (nitric oxide) response could contribute to hypertension. We found that in mesenteric small resistance arteries (200 microns I.D.) taken from 5- to 50-week old rats and mounted in a Mulvany-Halpern myograph, that the concentration-response curves to acetylcholine were similar in range and sensitivity (EC50) in arteries from SHR and WKY rats at the same age. Similarly, in small resistance arteries from human buttock skin, the relaxation to acetylcholine was not different between vessels from normotensive volunteers (mean BP = 95.2 +/- 1.5 mm Hg) and patients with untreated essential hypertension (mean BP = 116.5 +/- 2.5 mm Hg). In rabbits with chronic renovascular hypertension (cellophane renal wrap), acetylcholine and adenosine infusions into the lower abdominal aorta caused falls in hindquarter resistance that were enhanced in range, but with no change in sensitivity compared with normotensive rabbits. In normotensive rabbits, nitric oxide synthase inhibition with N omega-nitro-L-arginine infusion caused a rise in blood pressure, fall in hindquarter conductance and blockade of the acetylcholine responses. These experiments suggest that at the level of resistance arteries in vivo and in vitro, a defect in the receptor-stimulated response to EDRF associated with hypertension could not be detected. Apparently, basal nitric oxide is important in resting vasodilator tone, but its role in chronic hypertension is still unclear.

Manual reduction of displaced disk.

Early use of manual disk reduction procedures was significant in providing a functional disk-condyle relationship. Ninety-three percent of the 41 patients with anterior medial displaced disk without recapture did not require surgical correction using manual disk reduction procedures. All reductions were done within a six- to eight-week time period from the date of onset.

Depletion of serotonin in the nervous system of Aplysia reduces the behavioral enhancement of gill withdrawal as well as the heterosynaptic facilitation produced by tail shock.

Noxious stimuli, such as electrical shocks to the animal's tail, enhance Aplysia's gill- and siphon-withdrawal reflex. Previous experimental work has indicated that this behavioral enhancement, known as dishabituation (if the reflex has been habituated) or sensitization (if it has not been habituated), might be mediated, at least in part, by the endogenous monoaminergic transmitter serotonin (5-HT). To assess 5-HT's role in dishabituation and sensitization of Aplysia withdrawal reflex, we treated Aplysia with the serotonergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT). We found that 5,7-DHT treatment significantly reduced the dishabituation of the withdrawal reflex produced by tail shock. Treatment with the neurotoxin also blocked the heterosynaptic facilitation of monosynaptic connections between siphon sensory neurons and their follower cells, which contributes to the behavioral enhancement. Analysis by high-performance liquid chromatography indicated that 5,7-DHT treatment significantly reduced 5-HT levels in the Aplysia CNS. Moreover, the neurotoxic effects of 5,7-DHT appeared to be relatively specific for serotonergic pathways. Thus, 5,7-DHT treatment did not disrupt the ability of nonserotonergic facilitatory interneurons, the L29 cells, to facilitate the connections of siphon sensory neurons. Also, 5,7-DHT reduced 5-HT-dependent, but not dopamine-dependent, histofluorescence in Aplysia central ganglia. Finally, 5,7-DHT does not reduce the levels of the facilitatory peptides SCPA and SCPB within the Aplysia CNS. Our results, together with those of Mackey et al. (1989), indicate that 5-HT plays a major role in mediating dishabituation and sensitization of Aplysia's withdrawal reflex.

A functional study of the development of the cardiac sympathetic neuroeffector junction in the SHR.

We studied the function of the cardiac sympathetic nerve varicosity in isolated right atrial preparations of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats at 4, 9, 14, 20 and 50 weeks of age. Cumulative concentration-atrial period response (C-R) curves to isoprenaline showed similar maximum response and sensitivity (EC50) at all ages but there was an age-related fall in resting atrial rate. Similar results were found for methoxamine (alpha 1-adrenoceptor agonist) although the maximum response was significantly less than for isoprenaline. The time-dependent recovery (T 1/2) of the fall in atrial period in response to sympathetic nerve stimulation from electrical field pulses (1-32 at 1 Hz) was enhanced by neuronal uptake inhibition by desipramine (0.1-1 mumol/l), to a similar degree at all ages. Pre-junctional alpha 2-adrenoceptor stimulation by clonidine caused progressively more inhibition of the number of field pulses-fall in period relationship with age. SHR atria were similar to WKY rat atria at all ages except for a further impairment of the development of pre-junctional alpha 2-adrenoceptors. These studies indicate that the function of the cardiac sympathetic varicosity matures early (by 4 weeks) and overall there is very little impairment in SHR versus WKY rat atria.

[False chordae tendineae: incidence and clinical meaning]. / False corde tendinee: incidenza e significato clinico.

The presence of false tendons (FT) was sought with M-mode and 2-D echocardiography in a consecutive series of 316 patients with a wide age range (13-73 yrs). FT were observed in 13 patients (4.1%), all of them in the left ventricular cavity. Their clinical significance is pointed out together with the possibility of diagnostic error with other pathological formations, particularly intracavitary thrombi.

Comparative assay of neuronal uptake and autoinhibitory feedback in guinea-pig and rat atria.

1. The roles of neuronal uptake and autoinhibitory feedback were studied in guinea-pig and rat isolated right atria. Tachycardia was used as a measure of noradrenaline concentration at the post-junctional beta-adrenoreceptors in response to electrical field stimulation, 1-16 pulses at 1 Hz, or to exogenous noradrenaline. 2. The EC50 values for noradrenaline concentration-response curves were similar (7.3, -log M) in the two species when neuronal uptake was inhibited by desipramine (DMI, 1 microM). In the absence of DMI, however, the EC50 values were different for the rat (7.0) and guinea-pig (6.3). 3. DMI (0.01-1 microM) caused a substantial increase in half-response time (t 1/2), an integrated measure of tachycardia, in the rat during field stimulation but only caused modest increases in the guinea-pig atria. Following pretreatment with the irreversible alpha 2-adrenoceptor antagonist benextramine, the t 1/2 values were substantially raised in guinea-pig atria with no further change to t 1/2 in the rat atria. 4. The existence of presynaptic inhibitory alpha 2-adrenoceptors in the rat was established using clonidine which caused parallel rightward shifts of field stimulation-tachycardia curves. 5. These results suggest that in the guinea-pig atria blockade of both autoinhibitory feedback and neuronal uptake cause a very large increase in tachycardia compared with blockade of either system alone. In rat atria the most important modulation is from neuronal uptake, which suggests that in this species autoinhibitory feedback is of little consequence.

Tail shock produces inhibition as well as sensitization of the siphon-withdrawal reflex of Aplysia: possible behavioral role for presynaptic inhibition mediated by the peptide Phe-Met-Arg-Phe-NH2.

Recent studies have shown that, in addition to being modulated by presynaptic facilitation, the sensory neurons of the gill- and siphon-withdrawal reflex of Aplysia are also capable of being modulated by transient presynaptic inhibition produced by the peptide Phe-Met-Arg-Phe-NH2. These two modulatory effects involve different second-messenger systems: the facilitation is mediated through cAMP-dependent protein phosphorylation, and the inhibition is mediated through the lipoxygenase pathway of arachidonic acid. To explore the behavioral function of this inhibition, we have carried out a parametric analysis of the effect of tail shock on the siphon-withdrawal reflex. In addition to producing sensitization of the withdrawal reflex, tail shock also transiently inhibits the reflex. The inhibition is produced by relatively weak shock, whereas sensitization is more prominent and may mask the inhibition with stronger shock. Furthermore, inhibition is not observed after habituation training. Cellular studies suggest that the behavioral inhibition is mediated, at least in part, by presynaptic inhibition of transmitter release from the siphon sensory neurons. Moreover, we have identified an interneuron within the left pleural ganglion (LPL16) that shows Phe-Met-Arg-Phe-NH2 immunoreactivity, is activated by tail shock, and simulates the presynaptic inhibitory actions produced by tail shock. Therefore, our results suggest that presynaptic inhibition mediated by Phe-Met-Arg-Phe-NH2 and its lipoxygenase second messenger contributes to behavioral inhibition of the siphon-withdrawal reflex.

In vitro anti-HBs antibody synthesis from anti-hepatitis B vaccine recipients.

Peripheral blood mononuclear cells (PBMC) from 'responders' recently boosted with hepatitis B vaccine, were studied for synthesis in vitro of antibody to hepatitis B surface antigen (anti-HBs Ab) when stimulated with pokeweed mitogen (PWM) or HBsAg. HBsAg alone can induce an antigen-specific anti-HBs Ab response in vitro; this antibody synthesis is T cell-dependent. In some responders both allogeneic T4+ cells (in absence of PWM or HBsAg) and mixed leucocyte culture supernatants (MLC/SN) (without T cells and antigen) can help responder B cells to produce anti-HBs Ab. Thus, in some immunized subjects, B lymphocytes involved in anti-HBs Ab synthesis are in an advanced phase of differentiation and require only non-antigen specific T cell signals (B cell growth factor or B cell differentiation factor or interleukin 2, etc) to differentiate into antibody-secreting cells. Moreover, the concentration of the antigen necessary to suppress anti-HBs Ab production induced by HBsAg was five times lower than that necessary to suppress antibody production induced by PWM. T cell help for antigen induced anti-HBs Ab could be different from T cell help for the PWM-induced anti-HBs Ab response. Moreover, the finding that the low HBsAg doses inhibiting specific response did not affect the PWM-driven anti-HBs response suggests that antigen-specific T suppressor cells could play a role in this context.

Characterization of post-junctional alpha-adrenoceptors in the rat isolated perfused femoral artery.

A comparison was made of contractile responses to alpha-adrenoceptor agonists in the rat aorta and in the rat isolated perfused femoral artery. Dose-response curves were constructed to noradrenaline (alpha 1/alpha 2), methoxamine (alpha 1-selective) and B-HT 920 (alpha 2-selective). Methoxamine behaved as a full agonist in both tissues as compared with noradrenaline, while B-HT 920 was only a partial agonist in the aorta and produced small responses in the femoral artery preparation which were not dose-dependent. pA2 or -log KB values were calculated for prazosin and idazoxan against noradrenaline and methoxamine. Similar -log KB values for prazosin against both agonists were obtained in both tissues, while idazoxan was approximately ten times more potent in the femoral artery preparation than in the aorta. These results suggest that the aorta contains a single population of alpha 1-adrenoceptors, while the perfused femoral artery preparation contains predominantly alpha 1-adrenoceptors but also a small population of alpha 2-adrenoceptors.

Release of growth hormone, prolactin and somatostatin during perifusion of anterior pituitary and preoptic-medial basal hypothalamus from male and female rats.

These experiments were designed to determine whether it is possible using in vitro perifusion to identify a sex difference in anterior pituitary (AP) release of growth hormone (GH) and, if so, to determine whether this difference is correlated with a sex difference in hypothalamic release or content of somatostatin (SRIF). Age-matched rats of both sexes were decapitated at approximately 09.00 h, and blood was collected for determination of non-stress plasma concentrations of GH. Each pituitary was rapidly removed and prepared for perifusion of the AP, and each preoptic-medial basal hypothalamus (PO-MBH) was removed and placed in a separate perifusion chamber. The effluent fractions from perifused APs were assayed for GH and prolactin (Prl), and those from PO-MBH blocks were assayed for SRIF. Non-stress plasma GH concentrations were similar in males and females. During perifusion, baseline GH release was higher (P less than 0.001) from male than from female APs. Release of GH from the APs of both sexes was similarly inhibited (P less than 0.001) by a 1-h administration of SRIF (10(-7) M), and high K+ (50 mM) caused larger (P less than 0.05) GH responses from male than from female APs. In contrast, baseline Prl release was higher (P less than 0.01) from female than from male glands, and Prl release was not affected by SRIF. Male and female PO-MBH tissues showed similar baseline release of SRIF and similar responses to high K+. After perifusion, GH content and concentration were higher in APs from males than from females, but SRIF content in the perifused male and female PO-MBH tissues was similar.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of periventricular lesions on the release of somatostatin during perifusion.

Hypothalamic periventricular (PV) nucleus lesions reduce median eminence (ME) SRIF content by approximately equal to 80% without affecting non-stress plasma growth hormone (GH) levels or the GH response to stress. Our aim was to study the effects of PV lesions on SRIF released during perifusion of preoptic-anterior hypothalamic (PO-AH) tissue. Female rats received anterior or posterior PV lesions; sham-lesioned and intact rats served as controls. Non-stress and stress plasma GH levels were similar in all groups at 2, 4 and 16 weeks after surgery. At 18 weeks after surgery, the perifused PO-AHs of the PV- and sham-lesioned rats released similar amounts of SRIF, and these were higher (P less than 0.001) than amounts released from PO-AHs of intact rats. The PO-AHs from all groups showed similar increases in SRIF release after 56 mM K+. Two rats were chosen randomly from each group to assess ME SRIF content; PV lesions caused almost 80% depletion of SRIF, sham lesions did not. These results confirm that most SRIF neurons in the PV nucleus and 80% of ME SRIF content are not essential for the control of GH levels under non-stress conditions or for the GH response to stress and indicate that PV or sham lesions in the rostral forebrain enhance in vitro SRIF release, perhaps from neurons outside the PV nucleus.

Effect of 28 consecutive days lymphoblastoid interferon (alpha-IFN) administration on hepatitis B virus related chronic liver disease.

Eight HBsAg, HBeAg, DNA-p, HBV-DNA-positive patients with biopsy-proven chronic hepatitis were treated with human lymphoblastoid interferon (Wellferon) given for 28 consecutive days at a dosage ranging from 2.5 to 7.5 MU/m2 i.m.; 10 patients were used as controls. Our results suggest that certain chronic carriers may respond to the treatment with this agent. In fact, the treated patients showed a permanent inhibition of HBV replication sooner and in higher percentage with respect to untreated patients (37.5% vs 20%). IFN administration does not induce any important changes in the immunoregulatory wetwork, but is able to increase significantly the cytolytic activity of NK cells in the patients who respond to the therapy with a permanent inhibition of HBV replication.

Immunoregulation of the in vitro anti-HBs antibody synthesis in chronic HBsAg carriers and in recently boosted anti-hepatitis B vaccine recipients.

We report a study on immunoregulation of in vitro antibody to hepatitis B surface antigen (anti-HBs) synthesis induced by pokeweed mitogen (PWM) from peripheral blood mononuclear cells (PBMC) in chronic hepatitis B surface antigen (HBsAg) carriers and in 'high responders', (anti-HBs RIA ratio greater than or equal to 20 in serum), recently boosted with anti-hepatitis B vaccine. Anti-HBs was detected in 11 days PBMC supernatants (SN) from 24 out of 36 'high responders', but in none from 31 chronic HBsAg carriers, despite detectable amounts of polyclonal IgG and antibody to hepatitis B core antigen (anti-HBc) were produced. The lack of anti-HBs production by chronic HBsAg carriers did not seem to be determined by suppressor influences because T lymphocytes from the majority of chronic HBsAg carriers, co-cultured with 'high responders' PBMC did not suppress anti-HBs production. Co-cultures between HBsAg carriers T4 positive (helper/inducer) cells and allogenic 'high responder' non-T cells produced anti-HBs antibody, indicating that HBsAg carrier T cells are not deficient in this allogenic helper function under PWM stimulation. Allogenic cocultures between HBsAg carrier non-T cells and 'high responder' T4 positive cells failed in anti-HBs production: a specific B lymphocyte defect might be involved in the lacking anti-HBs synthesis in chronic HBV patients. Antigen-induced specific anti-HBs synthesis experiments indicate that B cells themselves seem to be the target for HBsAg-induced suppression of anti-HBs antibody response.

T-cell subsets in the hyporesponsiveness to hepatitis B surface antigen (HBsAg) and antigen-specific suppressor lymphocytes in chronic hepatitis B virus (HBV) infection.

In contrast to convalescent hepatitis B patients, who exhibit the ability to elicit a specific immune response to HBsAg, patients with chronic hepatitis B virus (HBV) infection are markedly hyporesponsive to HBsAg and show a decrease in the normal ratio of OKT4-positive (helper/inducer) to OKT8-positive (suppressor/cytotoxic) lymphocytes. In this study the role of OKT4-positive and OKT8-positive cells on cellular immune response to HBsAg was evaluated in patients with chronic HBV infection and the ability of such patients to develop antigen-specific suppressor lymphocytes after in vitro sensitization to HBsAg. Elimination of OKT8-positive cells markedly improved the in vitro lymphocyte proliferative response to HBsAg without altering the reactivity of cells from the same donor to PPD or Candida. In contrast, the degree of responsiveness to HBsAg was not affected by the depletion of OKT4-positive cells. In vitro co-culture experiments, performed in the seven chronically HBV-infected patients who showed a proliferative response when their PBM were cultured with purified HBsAg or PPD, have demonstrated that lymphocytes from chronic HBV carriers, stimulated with HBsAg, inhibit the response of autologous PBM to HBsAg but not to the unrelated antigen PPD.