Relaxation Response Research Articles

Structural and Dynamical Studies of a Lipid-Nanoclay Composite Layer at the Air-Water Interface.

We modulate the adsorption affinities of nanoclay particles for the air-water interface by changing the cationic surface charge composition of the lipid monolayer and thereby tune the attractive electrostatic interaction between the positively charged lipid layer and the zwitterionic nanoclay particles in the water subphase. Our findings emphasize the significance of electrostatic interaction between lipids and the nanoclay, as well as its impact on the structural and viscoelastic features of the composite layer. We use surface pressure (Π)-mean molecular area (A) isotherms, atomic force microscope (AFM), Brewster angle microscopy (BAM), and energy dispersive X-ray spectrsocopy (EDXS) measurements to analyze the structure phases of lipid and lipid-nanoclay composite interfacial layer. The Π-A isotherm curve shows that the lipid-nanoclay composite layer has a larger lift-off area than the neat lipid layer, indicating that nanoparticles adsorb at the lipid layer via electrostatic interaction between lipid and nanoclay molecules. The surface density of the adsorbed nanoclay particles increases with an increase in the composition of the cationic lipid molecules. The stress relaxation response of the composite layer, measured using step compression measurements, exhibits exponential decay and ubiquitous dependence on the cationic dimyristoy-trimethylammonium propane (DMTAP) composition in the lipid layer with crossover to faster relaxation dynamics at DMTAP > 0.75. The power-law study of the frequency-dependent dynamic viscoelastic responses of the interfacial layer, measured using the barrier oscillation method, reveals a transition from glass-like response from neat lipid layer to gel-like dynamic response for the lipid-nanoclay composite layer. A solid-like behavior is evident for all the interface layers with dilation elastic modulus (E') > dilational viscous modulus (E″); however, the dynamic response of the neat layer is largely frequency-independent, whereas lipid-nanoclay composite layers with DMTAP > 0.75 reveal a frequency-dependent dynamic responses. The frequency-dependent power-law exponent of E', E″ increases on increasing the fractional composition of cationic DMTAP from 0.1 to 1.0, which forms a saturated interface of laponite particles and behaves as a viscoelastic gel in 2D.

A comparative study to show the improvement in quality of life by short-term and long-term meditation by raj yoga meditation to reduce stress

Background: Meditation brings certain biochemical and physical changes in the body namely changes in metabolism, heart rate, respiration, blood pressure and brain chemistry, collectively referred to as the ‘relaxation response. The present study was carried out to compare the improvement in quality of life by short term and long-term meditation by raj yoga meditation to reduce stress. Materials & Methods: 120 patients suffering from stress aged 18–50 years were included in the study. The patients suffering from stress were randomized to divide into two groups: Group I i.e. short term meditation by raj yoga meditation and Group II i.e. long term meditation by raj yoga meditation. Complete clinical examination, including general and systemic examination was done. Health-related quality of life (HRQOL) questions were rated. Data was collected and analysed by SPSS 22.P values of less than 0.05 was concerned significant.

Brain volumetric changes after sensory isolation: single case experimental design

This study aimed to investigate the cerebral volumetric changes measurable by brain magnetic resonance imaging, as well as the different physiological variables documented through neurobiofeedback equipment, before and after 30 serial sessions of guided meditations in a sensory isolation tank. A pilot test was carried out, with a single subject, and it was concluded that serial sessions of meditations in flotation tanks changed the brain structure, triggered the relaxation response, generating greater physical, psychological and mental well-being for the research participant.

Apelin-Induced Relaxation of Coronary Arteries Is Impaired in a Model of Second-Hand Cigarette Smoke Exposure.

Apelin, an endogenous ligand for APJ receptors, causes nitric oxide (NO)-dependent relaxation of coronary arteries. Little is known about the effects of apelin/APJ receptor signaling in the coronary circulation under pathological conditions. Here, we tested the hypothesis that the vasorelaxing effect of apelin is impaired by cigarette smoke extract (CSE), an established model for second-hand smoke exposure. Isolated rat coronary arteries were treated with 2% CSE for 4 hours. Apelin-induced relaxation of coronary arteries was abolished by CSE exposure, while relaxations to acetylcholine (ACh) (endothelium-dependent relaxation) and to diethyl amine NONOate (NO donor) were similar in control and CSE-treated arteries. Immunoblot analysis demonstrated that apelin increased eNOS ser1177 phosphorylation under control conditions but had no effect after exposure to CSE. Moreover, GRK2 expression was increased in CSE-exposed coronary endothelial cells. Pretreatment with CMPD101, a GRK2 inhibitor, improved the relaxation response to apelin in CSE-exposed coronary arteries. CSE treatment failed to inhibit relaxations evoked by CMF-019, an APJ receptor biased agonist that has little effect on GRK2. In arteries exposed to CSE, apelin impaired the response to ACh but not to diethyl amine NONOate. ACh-induced relaxation was unaffected by CMF-019 in either control or CSE-treated coronary arteries. The results suggest that APJ receptor signaling using the GRK2 pathway contributes to both loss of relaxation to apelin itself and the ability of apelin to inhibit endothelium-dependent relaxation to ACh in CSE-exposed coronary arteries, likely because of impaired production of NO from endothelial cells. These changes in apelin/APJ receptor signaling under pathological conditions (eg, exposure to second-hand smoke) could create an environment that favors increased vasomotor tone in coronary arteries.

Coronavirus pandemic in the Nordic countries: Health policy and economy trade-off.

BackgroundCountries making up the Nordic region – Denmark, Finland, Iceland, Norway, and Sweden – have minimal socioeconomic, cultural, and geographical differences between them, allowing for a fair comparative analysis of the health policy and economy trade-off in their national approaches towards mitigating the impact of the COVID-19 pandemic.MethodsThis study utilized publicly available COVID-19 data of the Nordic countries from January 2020 to January 3, 2021. COVID-19 epidemiology, public health and health policy, health system capacity, and macroeconomic data were analysed for each Nordic country. Joinpoint regression analysis was performed to identify changes in temporal trends using average monthly percent change (AMPC) and average weekly percent change (AWPC).ResultsSweden’s health policy, being by far the most relaxed response to COVID-19, was found to have the largest COVID-19 incidence and mortality, and the highest AWPC increases for both indicators (13.5, 95% CI = 5.6, 22.0, P < 0.001; 6.3, 95% CI = 3.5, 9.1, P < 0.001). Denmark had the highest number of COVID-19 tests per capita, consistent with their approach of increased testing as a preventive strategy for disease transmission. Iceland had the second-highest number of tests per capita due to their mass-testing, contact tracing, quarantine and isolation response. Only Norway had a significant increase in unemployment (AMPC = 2.8%, 95% CI = 0.7-4.9, P < 0.009) while the percentage change in real Gross Domestic Product (GDP) was insignificant for all countries.ConclusionsThere was no trade-off between public health policy and economy during the COVID-19 pandemic in the Nordic region. Sweden’s relaxed and delayed COVID-19 health policy response did not benefit the economy in the short term, while leading to disproportionate COVID-19 hospitalizations and mortality.

H2S releasing sodium sulfide protects against pulmonary hypertension by improving vascular responses in monocrotaline-induced pulmonary hypertension

Pulmonary arterial hypertension is caused by complex structural and functional changes in the endothelial and smooth muscle cells of pulmonary arteries. Hydrogen sulfide (H2S), a gasotransmitter, can potentially treat pulmonary hypertension by relaxing the pulmonary arteries and decreasing bronchial pressure. Although the role of H2S in systemic circulation has been examined, the H2S levels in pulmonary arteries, the role of H2S in endothelium-dependent vasorelaxation and the L-cysteine/H2S pathway in monocrotaline-induced pulmonary arterial hypertension have not been investigated. The rats were divided into control, monocrotaline, monocrotaline + Na2S, and Na2S groups. The right ventricular pressure and hypertrophy were evaluated. KCl, acetylcholine, and L-cysteine responses were obtained in the main pulmonary arteries by wire myograph. H2S levels were measured in pulmonary arteries and lungs by methylene blue assay. Right ventricular pressure and hypertrophy were increased by monocrotaline and ameliorated by Na2S. The KCl-induced contractions and relaxing responses to acetylcholine and L-cysteine in pulmonary arteries and H2S production in the lungs and pulmonary arteries were significantly attenuated in the monocrotaline group and augmented in the monocrotaline + Na2S group. These findings suggest that H2S levels were reduced, and L-cysteine-induced and endothelium-dependent relaxations were impaired in the pulmonary arteries in monocrotaline-induced pulmonary arterial hypertension. The H2S donor, Na2S, prevented endothelial dysfunction and increased pulmonary artery pressure and hypertrophy. Also, Na2S enhanced the L-cysteine-mediated responses and restored the diminished H2S levels in pulmonary arteries and the lungs. The treatments targeting H2S might be beneficial for promoting vascular alterations, i.e. endothelial dysfunction and impaired H2S-mediated relaxation in pulmonary arterial hypertension.

Effect of High Testosterone Levels on Endothelial Function in Aorta and Erectile Function in Rats.

BackgroundTestosterone is an important hormone for the physical and mental health of men; however testosterone administration has also been suggested to adversely affect the cardiovascular system.AimTo investigate the effects of excessive testosterone administration on vascular endothelial and erectile function in rats.MethodsA total of seventy-five 12-week-old rats were divided into the following groups: Sham, castrated (Cast), castrated with subcutaneous administration of 100 mg/kg/month testosterone (Cast + T1), and castrated with subcutaneous administration of 100 mg/kg/week testosterone (Cast + T4). To observe the changes in testosterone level after the administration, rats were further divided into the following groups: control; T(6.25), wherein the rats were subcutaneously injected with 6.25 mg/kg testosterone; T(25) per week, wherein the rats were subcutaneously injected with 25 mg/kg testosterone per week; and T(100), wherein the rats were subcutaneously injected with 100 mg/kg testosterone per week. The relaxation responses of aorta were measured in these rats using standardized methods, and their erectile function was also evaluated. Statistical analysis of the obtained data was performed using two-way analysis of variance (ANOVA), Tukey-Kramer's multiple comparison test, or Student's t-test.OutcomesAt the end of the study period, endothelial function was evaluated through measurement of isometric tension, while erectile function was assessed using intracavernosal pressure (ICP), mean arterial pressure (MAP), and the expression of endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), sirtuin 1 (Sirt1) and vascular endothelial growth factor A.ResultsThe ICP/MAP ratio in the Cast group (0.42 ± 0.04) was significantly lower than that in the Sham group (0.79 ± 0.07). The ICP/MAP ratio in the Cast + T1 group (0.73 ± 0.06) was significantly higher than that in the Cast group (P < .01) and that of the Cast + T4 (0.38 ± 0.01) group was unchanged (P > .05). The T(25) and T(100) groups exhibited significantly lower responses to ACh than the control group at 4 weeks (P < .01). Meanwhile, the ICP/MAP ratios in the T(25) group (0.44 ± 0.07) and T(100) group (0.47 ± 0.03) were significantly lower than that in the control group (0.67 ± 0.05) at stimulation frequencies of 16 Hz (P < .05). The expression of androgen receptor, Sirt1, and eNOS were significantly lower while that of iNOS was higher in the T(25) group compared with the control group (P < .05).Clinical TranslationThe results based on this animal model indicate that extremely high testosterone levels may affect endothelial and erectile function.Strengths and LimitationsWe found that high-dose testosterone administration decreased endothelial function in aorta and erectile function in rats. A major limitation of this study is that the blood concentration may not be representative of that in humans, and further research is needed.ConclusionThe findings suggest that high doses of testosterone may cause endothelial dysfunction in the aorta and erectile dysfunction in rats and that the blood concentration should be monitored after testosterone administration.Kataoka T, Fukamoto A, Hotta Y, et al. Effect of High Testosterone Levels on Endothelial Function in Aorta and Erectile Function in Rats. Sex Med 2022;10:100550.

Endothelial dysfunction of the mesenteric arteries of rats in the early obesity induced by high-fat diet

Background: Disturbance of the morphological and functional properties of the vascular bed in obesity are a serious clinical problem. Basis to their development is endothelial dysfunction. The developed models of obesity in animals using various diets indicate a change in vascular reactivity, however, questions about the stage at which this occurs and what mechanisms are involved in this process remain open, while they are decisive for choosing the correct tactics for correcting dysfunctions.Aim: The aim of the present study is to determine the changes in acetylcholine (ACh)-induced vasodilation of isolated arteries from rats after six weeks of administration of a high-fat diet (HFD).Materials and methods: The experiments were performed on Sprague-Dawley males, which at the age of 8 weeks were divided into 2 experimental groups that were treated for the next 6 weeks in the following manner: 1 - control) with standard dry food; 2 - a group fed with a HFD, the total amount of fat in which was 50%. At finish of the diet, the degree of obesity, biochemical parameters in the blood, and blood pressure were measured. Intravital microscopy of the rat mesentery with video recording was used to study the reactivity of the vessels. The contractile and relaxant responses of the vessels were determined by changes in their diameter.Results: The rats after treatment with the HFD (n=15) had higher body weight and amount of visceral fat, significantly increased blood triglycerides, moderate increases in glucose level in blood and systolic pressure compared with the control (n=15). Relaxation responses of mesenteric arteries, having a diameter of 140 to 300 μm in PSS, were recorded after precontraction by phenylephrine. A decrease in ACh-induced vasorelaxation was obtained, which manifests itself before the development of significant changes in carbohydrate metabolism. Incubation of drugs with the inhibitor of endothelial NO synthase L-NAME led to a pronounced weakening of relaxation in animals on a standard diet, and had little effect on vasodilation in the arteries of rats with the HFD. Vasodilation induced by the administration of sodium nitroprusside (NO donor) did not differ significantly in control and experimental animals, which indicates that the sensitivity of vascular smooth muscle to NO remained practically unchanged. ACh-induced relaxation of arteries in dietary rats did not change when the cyclooxygenase pathway was blocked by diclofenac.Conclusion: Functional changes in the contractile activity of the mesenteric arteries, manifested in the form of a decrease in ACh-induced vasorelaxation, occur after treatment with the HFD when animals had an early stage of obesity development before the onset of pronounced disorders of carbohydrate metabolism. This decrease is mainly due to the disruption of the NO-dependent mechanism underlying ACh-induced relaxation in the norm.

Sodium butyrate ameliorates erectile dysfunction through fibrosis in a rat model of partial bladder outlet obstruction.

In different animal models, a histone deacetylase (HDAC) inhibitor, sodium butyrate (NaBu) reduced inflammation, oxidative stress and fibrosis which were involved in the pathogenesis of erectile dysfunction (ED), but whether NaBu could improve ED in an experimental animal model of benign prostate hyperplasia (BPH) was not known. To investigate the preventive effect of NaBu on ED in a partial bladder outlet obstruction (PBOO) rat model. PBOO was induced by partial urethral obstruction. NaBu (20mg/kg/day) was administered orally to rats for 6 weeks after creation of PBOO. In vivo erectile responses, in vitro relaxation and contraction responses in cavernosal tissue were measured. Real-time polymerase chain reaction (RT-PCR) and Western blot were performed to determine the gene and protein expression. Inflammation, fibrosis, and localization of proteins were evaluated using histological techniques. HDAC activity and tumor necrosis factor (TNF)-α levels were measured in penile tissues. NaBu improved decreased intracavernosal pressure/mean arterial pressure, nitrergic and endothelium-dependent relaxation responses, and contractile responses to phenylephrine and electrical field stimulation in the PBOO group without affecting increased bladder weight. Increased endothelial nitric oxide synthase (eNOS), transforming growth factor (TGF)-β1, and nuclear factor kappa B (NF-κB) gene levels in PBOO group were ameliorated by NaBu treatment. The administration of NaBu to PBOO rats significantly increased neuronal NOS (nNOS) and decreased TGF-β1 protein expression. The nuclear/cytosolic ratio of NF-κB demonstrated a decrease in PBOO and all treatment groups compared to control. A significant increase in the nuclear-to-cytoplasmic ratio of nuclear factor erythroid 2-related factor 2 (Nrf2) after PBOO was reduced by the treatment. Both eNOS and inducible NOS (iNOS) protein expression, together with TNF-α levels did not differ in the penile tissue of all groups. In histological analysis, increased TGF-β1 protein expression and fibrosis, as well as decreased nNOS protein in PBOO, were reversed by the treatment. NaBu did not normalize moderate inflammation in obstructed rats. An increase in the HDAC activity in PBOO was significantly suppressed by NaBu. Inhibition of the HDAC activity by NaBu in penile tissue could ameliorate fibrosis-associated changes induced by PBOO. NaBu promotes recovery of erectile function, and also significantly prevents penile fibrosis and normalizes TGF-β1 and nNOS protein expression in a rat model of PBOO. The HDAC pathway may present a promising target to prevent ED in patients with BPH.

Hinokitiol produces vasodilation in aortae from normal and angiotensin II- induced hypertensive rats via endothelial-dependent and independent pathways

Hinokitiol is a natural bioactive compound with numerous pharmacological properties. Here, we aimed to examine hinokitiol's effects on vascular relaxation. Cumulative relaxation responses to hinokitiol were assessed in isolated aortae from normotensive and angiotensin II-induced hypertensive rats in the presence and absence of selective inhibitors. Hinokitiol produced vasodilation of phenylephrine preconstricted aortae using both normotensive and hypertensive rats. In normotensive rats, hinokitiol's vasodilation was reduced by endothelial denudation and nitric oxide synthase (NOS), guanylate cyclase, and cyclooxygenase inhibition. Also, hinokitiol vasodilation was attenuated by β-receptors, adenylate cyclase, Ca2+-activated K+ channels and hyperpolarization inhibition. Moreover, hinokitiol exhibited a blocking activity on Ca2+ mobilization through voltage dependent Ca2+ channels (VDCC). However, its effect was not changed by muscarinic receptor and Sarc-K+ ATP channels blocking but was enhanced by blocking voltage-dependent K+ channels. However, in angiotensin II-induced hypertension, hinokitiol vasodilating activity was attenuated by NOS inhibition and it blocked Ca2+ mobilization through VDCC, while its vasodilation was partially attenuated by Sarc-K+ ATP channels blocking. However, the vasodilating effect of hinokitiol was not attenuated by either cyclooxygenase, β-receptor, Ca2+-activated K+ channels, or voltage-dependent potassium channels inhibition, but was enhanced by blocking hyperpolarization. Hinokitiol's vasodilating effect in normotensive and hypertensive vessels is mediated through both endothelium-dependent and endothelium-independent mechanisms.

Supplementation with Spirulina platensis Prevents Damage to Rat Erections in a Model of Erectile Dysfunction Promoted by Hypercaloric Diet-Induced Obesity.

Erectile dysfunction (ED) is the inability to achieve and/or maintain a penile erection sufficient for sexual satisfaction. Currently, many patients do not respond to the pharmacotherapy. The effects of a supplementation with Spirulina platensis, were evaluated in a model of ED induced by hypercaloric diet consumption. Wistar rats were divided into groups fed with standard diet (SD) or hypercaloric diet (HD) and supplemented with this alga at doses of 25, 50 or 100 mg/kg. Experimental adiposity parameters and erectile function were analyzed. In SD groups, Spirulina platensis reduced food intake, final body mass and adiposity index, and increased the total antioxidant capacity (TAC) of adipose tissue. However, no change was observed in erectile function. In the HD group, without Spirulina supplementation, a decrease in food intake was observed, in addition to an increase of final body mass, weight gain, adipose reserves, and adiposity index. Additionally, reduction in the number and increase in the latency of penile erection and adipose malondialdehyde levels, as well as a reduction in TCA was noted. Furthermore, cavernous contractility was increased, and the relaxing response was decreased. Interestingly, these deleterious effects were prevented by the algae at doses of 25, 50 and/or 100 mg/kg. Therefore, the supplementation with S. platensis prevents damages associated to a hypercaloric diet consumption and emerges as an adjuvant the prevention of ED.

Involvement of a neutrophil-mast cell axis in the effects of Piper malacophyllum (C. PESL) C. DC extract and its isolated compounds in a mouse model of dysmenorrhoea.

The effects of Piper malacophyllum (C. Pesl) C. DC extracts and its isolated compounds were analysed in a mouse model of primary dysmenorrhoea (PD). Female Swiss mice (6-8weeks old) on proestrus were intraperitoneally treated with estradiol benzoate for 3days, to induce PD. Twenty-four hours later, animals were treated 24h later with vehicle, plant extract, gibbilimbol B, 4,6-dimethoxy-5-E-phenylbutenolide, mixture of 4,6-dimethoxy-5-E-phenylbutenolide and 4,6-dimethoxy-5-Z-phenylbutenolide, or ibuprofen. One hour later, oxytocin was injected and the numbers of abdominal writhing were counted. Then, mice were euthanized and uteri were collected for morphometrical and histological analyses. The effects of P. malacophyllum in inflammation were investigated in mouse peritoneal neutrophils culture stimulated with LPS or fMLP (chemotaxis and mediator release). Finally, uterus contractile and relaxing responses were assessed. Similar to ibuprofen, P. malacophyllum extract and isolated compounds reduced abdominal writhing in mice with PD. Histology indicated a marked neutrophil and mast cell infiltrate in the uterus of PD animals which was attenuated by the extract. The compounds and the extract reduced neutrophil chemotaxis and inflammatory mediator release by these cells. Reduced TNF levels were also observed in uteri of PD mice treated with P. malacophyllum. The extract did not affect spontaneous uterine contractions nor those induced by carbachol or KCl. However, it caused relaxation of oxytocin-induced uterine contraction, an effect blunted by H1 receptor antagonist. Overall the results indicate that P. malacophyllum may represent interesting natural tools for reliving PD symptoms, reducing the triad of pain, inflammation and spasmodic uterus behaviour.

Maternal perfluorooctane sulfonic acid exposure during rat pregnancy causes hypersensitivity to angiotensin II and attenuation of endothelium-dependent vasodilation in the uterine arteries †.

Epidemiological studies show a strong association between environmental exposure to perfluorooctane sulfonic acid (PFOS) and preeclampsia and fetal growth restriction; however, the underlying mechanisms are unclear. We tested the hypothesis that gestational PFOS exposure leads to pregnancy complications via alterations in uterine vascular endothelium-independent angiotensin II-related mechanisms and endothelium-derived factors such as nitric oxide. Pregnant Sprague-Dawley rats were exposed to PFOS 0.005, 0.05, 0.5, 5, 10, and 50μg/mL through drinking water from gestational day 4 to 20, and dams with PFOS 50μg/mL were used to assess mechanisms. PFOS exposure dose dependently increased maternal blood pressure but decreased fetal weights. Uterine artery blood flow was lower and resistance index was higher in the PFOS dams. In PFOS dams, uterine artery contractile responses to angiotensin II were significantly greater, whereas contractile responses to K+ depolarization and phenylephrine were unaffected. Plasma angiotensin II levels were not significantly different between control and PFOS dams; however, PFOS exposure significantly increased Angiotensin II type 1 receptor (AGTR1) and decreased AGTR2 protein levels in uterine arteries. Endothelium-dependent relaxation response to acetylcholine was significantly reduced with decreased endothelial nitric oxide synthase expression in the uterine arteries of PFOS dams. Left ventricular hypertrophy and fibrosis were observed, along with increased ejection fraction and fractional shortening in PFOS dams. These results suggest that elevated maternal PFOS levels decrease uterine blood flow and increase vascular resistance via heightened angiotensin II-mediated vasoconstriction and impaired endothelium-dependent vasodilation, which provides a molecular mechanism linking elevated maternal PFOS levels with gestational hypertension and fetal growth restriction.

A Bayesian Optimization Approach to the Simultaneous Extraction of Intrinsic Physical Parameters fromT1 andT2 Relaxation Responses

SummaryNuclear magnetic resonance (NMR) relaxation responses in porous media provide a sensitive probe of the microstructure and yet are influenced by a number of factors which are not easily detangled. Low-field T2 transverse relaxation measurements can be carried out quickly and are frequently used as pore size distributions, while adding T1 longitudinal relaxation measurements provides additional insights into surface properties and fluid content. Here we present an inverse solution workflow extracting related intrinsic physical parameters of the system by fitting experiment and numerical simulation(s). An efficient NMR forward solver for the simultaneous calculation of T1 and T2 responses is introduced, which honors existing inequality relationships between T1 and T2 parameters. We propose a Bayesian optimization approach that jointly identifies T1- and T2-related properties satisfying physical constraints by simultaneously fitting T1 and T2 experiments to simulations. This dual-task inverse solution workflow (DT-ISW) identifies the solution by minimizing the sum of the L2 norm of the fitting residuals of both T1 and T2 distributions into a single objective and jointly models the two highly correlated objectives with high efficiency using the vector-valued Gaussian process (GP) kernel for transfer learning. A multimodal search strategy is used to identify nonunique solution sets of the problem. The workflow is demonstrated on Bentheimer sandstone, identifying five intrinsic physical parameters. The performance of the joint DT-ISW (DT-ISW-J) is compared to a sequential DT-ISW (DT-ISW-S) approach as well as an independent single-task ISW (ST-ISW) of the T1 and T2 responses. Both dual-task versions converge more than two times faster than the single-task version. DT-ISW-J equally minimizes the L2 norm of T1 and T2 fitting residuals whereas DT-ISW-S only preferentially minimizes the objective assigned higher importance. A Pareto optimal solution (POS) is provided to allow operators to subjectively balance the preference of T1 and T2 data fits for the slightly conflicting objectives. The ability to extract five intrinsic physical parameters simultaneously provides new techniques for tracking wettability alteration and assessing the influence of clay amount and distribution on petrophysical property estimates.

The Functional Effects of Visfatin on Human Left Internal Mammary Artery.

Visfatin may play a role in vascular dysfunction in metabolic disorders. Apart from its insulin-mimetic actions, it has divergent actions in the cardiovascular system with discordant results in the literature. Thus, we aimed to study the effects of visfatin on vascular responses of the human left internal mammary artery. Sections of redundant human left internal mammary artery were cut into 3-mm wide rings and hung in 20-mL organ baths containing physiologic salt solution and attached to an isometric force transducer connected to a computer-based data acquisition system. Removing endothelium caused an increase in pD2 values for visfatin-induced relaxation responses (10 -12 -10 -7 M) (9.06 ± 0.21 and 11.08 ± 0.92, respectively). Nicotinamide phosphoribosyltransferase inhibitor FK866 (10 µM) reversed the visfatin-induced relaxations (10 -12 -10 -7 M) ( P = 0.024). Incubations with nitric oxide synthase inhibitor nitro- l -arginine methylester and guanylate cyclase inhibitor 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (ODQ) caused significant reductions in relaxation responses of visfatin ( P = 0.011 and 0.008, respectively). Visfatin incubations decreased relaxation responses to acetylcholine but not to sodium nitroprusside. Incubations with visfatin did not change contractile responses to angiotensin II, endothelin-1, noradrenalin, and phenylephrine. In this study, visfatin caused endothelium-dependent relaxations mediated by nitric oxide-cyclic guanosine monophosphate pathway and nicotinamide phosphoribosyltransferase activity. Furthermore, visfatin-induced decreases in relaxation responses were also related to endothelium-derived nitric oxide.

Adapting, testing, and refining a resilience intervention for older women with HIV: An open pilot study

Half of persons with HIV in the United States (US), many of whom are women, are over age 50. Aging women with HIV (WWH) face unique biopsychosocial challenges, including stigma, the physiological effects of aging, and illness-associated stressors. Resilience interventions can build awareness of such stressors and aid in facilitating the relaxation response; however, no existing interventions specifically cater to the needs of older WWH. The content of the Relaxation Response Resiliency Program, which teaches positive psychology strategies, relaxation techniques, and cognitive behavioral skills, was adapted for older WWH. Thirteen WWH over 50 participated in an open pilot of the adapted intervention to iteratively refine the program and its procedures. Participants attended either 8 or 10 weekly group sessions; three groups were conducted in total. Pre- and post-intervention assessments and qualitative exit interviews were conducted. Among completers, an increase in resilience was observed. Though significance testing was not conducted, social support also increased, and depression, anxiety, and HIV stigma decreased from pre- to post-intervention. Over half of eligible women enrolled; completers reported high satisfaction with the program. However, retention was difficult; six participants withdrew or were lost to follow-up. Mean number of sessions attended was 3.5 in the 8-session group and 5 in the 10-session groups. In this small sample, the adapted intervention led to a clinically meaningful increase in resilience, though recruitment and retention were challenging. Further refinements to the intervention are needed to minimize attrition and increase acceptability before additional testing is initiated.

Students’ Perception of the Educational Environment at Hawler College of Medicine, Erbil, Iraq

BACKGROUND: Medical education and training vary considerably across the world. Various teaching methodologies have been adopted in medical education. AIM: This study aimed to elicit the perception of medical students at Hawler College of Medicine about their educational environment. METHODS: The study participants included all 152 students in their final year of study at Hawler College of Medicine, Erbil, Iraq. An anonymous questionnaire containing 27 items about the quality of their education, preparedness for residency, students’ affairs, and behaviors experienced or witnessed during medical school with a five-point Likert scale was used for data collection. The Statistical Package for the Social Sciences program was used for data analysis. RESULTS: Of 140 students participated in the study, 73 (52.1%) said that the final year was helpful in their preparation for residency, 67 (47.8%) were satisfied with the quality of their education, and 65 (46.4%) said that basic science coursework had sufficient illustrations of clinical relevance. Overall the students mostly were dissatisfied with the relaxation spaces, study space, health services, and response to their problems. Fifty-six (40%) were frequently publicly embarrassed, 45 (32.1%) believed that they received lower evaluations or grades solely based on gender rather than performance, and 27 (19.1%) were denied opportunities for training or rewards based on gender. CONCLUSIONS: Most of the students were satisfied with their education but unsatisfied with study space, relaxation space, and health services in the college.

Effect of Benson’s Relaxation Response on Anorexia in Cancer Patients Undergoing Chemotherapy

Effect of Benson’s Relaxation Response on Anorexia in Cancer Patients Undergoing Chemotherapy

Midgestation Leptin Infusion Induces Characteristics of Clinical Preeclampsia in Mice, Which Is Ablated by Endothelial Mineralocorticoid Receptor Deletion.

Patients with preeclampsia demonstrate increases in placental leptin production in midgestation, and an associated increase in late gestation plasma leptin levels. The consequences of mid-late gestation increases in leptin production in pregnancy is unknown. Our previous work indicates that leptin infusion induces endothelial dysfunction in nonpregnant female mice via leptin-mediated aldosterone production and endothelial mineralocorticoid receptor (ECMR) activation, which is ablated by ECMR deletion. Therefore, we hypothesized that leptin infusion in mid-gestation of pregnancy induces endothelial dysfunction and hypertension, hallmarks of clinical preeclampsia, which are prevented by ECMR deletion. Leptin was infused via miniosmotic pump (0.9 mg/kg per day) into timed-pregnant ECMR-intact (WT) and littermate-mice with ECMR deletion (KO) on gestation day (GD)11-18. Leptin infusion decreased fetal weight and placental efficiency in WT mice compared with WT+vehicle. Radiotelemetry recording demonstrated that blood pressure increased in leptin-infused WT mice during infusion. Leptin infusion reduced endothelial-dependent relaxation responses to acetylcholine (ACh) in both resistance (second-order mesenteric) and conduit (aorta) vessels in WT pregnant mice. Leptin infusion increased placental ET-1 (endothelin-1) production evidenced by increased PPET-1 (preproendothelin-1) and ECE-1 (endothelin-converting enzyme-1) expressions in WT mice. Adrenal aldosterone synthase (CYP11B2) and angiotensin II type 1 receptor b (AT1Rb) expression increased with leptin infusion in pregnant WT mice. KO pregnant mice demonstrated protection from leptin-induced reductions in pup weight, placental efficiency, increased BP, and endothelial dysfunction. Collectively, these data indicate that leptin infusion in midgestation induces endothelial dysfunction, hypertension, and fetal growth restriction in pregnant mice, which is ablated by ECMR deletion.

The Effects of a Single Relaxation Hypnosis Session on Mental Stress in Chronically Stressed Individuals

Abstract. Background: Chronically stressed people often suffer from anxiety and depressive mood. Hypnosis is a technique that can induce a relaxation response and reduce negative stress symptoms. Objective: This explorative study investigated the impact of a single relaxation hypnosis session on stress-related psychological symptoms. Method: 47 suggestible, stressed individuals (87 % female) were randomized to a hypnosis group ( n = 23, 20-minute hypnosis) or a control group ( n = 24, 20-minute scientific documentary). Before and after the intervention, we assessed perceived stress, negative affect, anxiety, and depressive mood. Results: After the hypnosis intervention, depressive mood ( d = 0.36) and state anxiety ( d = 1.00) decreased, while negative affect remained stable ( d = 0.04). Perceived stress was reduced in both groups. Conclusion: A single relaxation hypnosis session decreased stress-related symptoms in chronically stressed individuals. Our results substantiated the stress-alleviating effects of hypnosis.