Empreendedorismo ambiental e preservacionismo compensatório: o turismo e as unidades de conservação Parque Estadual das Dunas e Área de Proteção Ambiental Jenipabu-RN

This doctoral thesis addresses the environmental issues and its vinculum with the tourism through the protected natural areas, in particular the conservation units, which consists in territorial areas created and demarcated by the government in order to protect ecosystems that have a high ecological and scenic-landscaped representativeness designed to the contemplation and controlled public visitation. In regard to its use for the touristic activities, are conceived while socio-environmental and symbolic materiality built around an imagery view of a nature-show, designed to attract visitors, aiming ensure the maintenance and reproduction of the capital in an entrepreneurial and preservationist way in the Metropolitan Region of Natal. It s a study about the Dunes State Park Jornalista José Maria Alves and the Jenipabu Environmental Protected Area, both created with the purpose of favor the implantation and empowerment of the touristic area through the State intervention as the main articulator agent of a new process of urbanization that uses the city marketing and the ideological discuss of environmental sustainability to recreate the imaginary of lost paradise and incorporate into the daily universe of tourists visiting the state of Rio Grande do Norte. The unveiling of this empirical reality made possible the construction and defense of the terms environmental entrepreneurship and compensatory preservationism, to explain how the formatting and idealization of this paradisiacal scenarios produce the commoditization of nature in an efficient and competitive way

Impaired Compensatory Beta-cell Function And Growth In Response To High-fat Diet In Ldl Receptor Knockout Mice.

In this study, we investigated the effect of low density lipoprotein receptor (LDLr) deficiency on gap junctional connexin 36 (Cx36) islet content and on the functional and growth response of pancreatic beta-cells in C57BL/6 mice fed a high-fat (HF) diet. After 60 days on regular or HF diet, the metabolic state and morphometric islet parameters of wild-type (WT) and LDLr-/- mice were assessed. HF diet-fed WT animals became obese and hypercholesterolaemic as well as hyperglycaemic, hyperinsulinaemic, glucose intolerant and insulin resistant, characterizing them as prediabetic. Also they showed a significant decrease in beta-cell secretory response to glucose. Overall, LDLr-/- mice displayed greater susceptibility to HF diet as judged by their marked cholesterolaemia, intolerance to glucose and pronounced decrease in glucose-stimulated insulin secretion. HF diet induced similarly in WT and LDLr-/- mice, a significant decrease in Cx36 beta-cell content as revealed by immunoblotting. Prediabetic WT mice displayed marked increase in beta-cell mass mainly due to beta-cell hypertrophy/replication. Nevertheless, HF diet-fed LDLr-/- mice showed no significant changes in beta-cell mass, but lower islet-duct association (neogenesis) and higher beta-cell apoptosis index were seen as compared to controls. The higher metabolic susceptibility to HF diet of LDLr-/- mice may be explained by a deficiency in insulin secretory response to glucose associated with lack of compensatory beta-cell expansion.

Anticipatory and compensatory postural adjustments in sitting in children with cerebral palsy

The aim of this study was to examine postural control in children with cerebral palsy performing a bilateral shoulder flexion to grasp a ball from a sitting posture. The participants were 12 typically developing children (control) without cerebral palsy and 12 children with cerebral palsy (CP). We analyzed the effect of ball mass (1 kg and 0.18 kg), postural adjustment (anticipatory, APA, and compensatory, CPA), and groups (control and CP) on the electrical activity of shoulder and trunk muscles with surface electromyography (EMG). Greater mean iEMG was seen in CPA, with heavy ball, and for posterior trunk muscles (p < .05). The children with CP presented the highest EMG and level of co-activation (p < .05). Linear regression indicated a positive relationship between EMG and aging for the control group, whereas that relationship was negative for participants with CP. We suggest that the main postural control strategy in children is based on corrections after the beginning of the movement. The linear relationship between EMG and aging suggests that postural control development is affected by central nervous disease which may lead to an increase in muscle co-activation. (C) 2011 Elsevier B.V. All rights reserved.

The influence of a concurrent cognitive task on the compensatory stepping response to a perturbation in balance-impaired and healthy elders

This study investigated the influence of a concurrent cognitive task on the compensatory stepping response in balance-impaired elders and the attentional demand of the stepping response. Kinetic, kinematic and neuromuscular measures of a forward recovery step were investigated in 15 young adults, 15 healthy elders and 13 balance-impaired elders in a single task (postural recovery only) and dual task (postural recovery and vocal reaction time task) situation. Results revealed that reaction times were longer in all subjects when performed concurrently with a compensatory step, they were longer for a step than an in-place response and longer for balance-impaired older adults compared with young adults. An interesting finding was that the latter group difference may be related to prioritization between the two tasks rather than attentional demand, as the older adults completed the step before the reaction time, whereas the young adults could perform both concurrently. Few differences in step characteristics were found between tasks, with the most notable being a delayed latency and reduced magnitude of the early automatic postural response in healthy and balance-impaired elders with a concurrent task. (C) 2002 Elsevier Science B.V. All rights reserved.

Influence of an unstable shoe on compensatory postural adjustments: an experimental evaluation

This study attempted to evaluate the influence of using an unstable shoe in muscle re-cruitment strategies and center of pressure (CoP) displacement after the application of an external perturba-tion. Fourteen healthy female subjects participated in this study. The electromyographic activity of medial ga-strocnemius, tibialis anterior, rectus femoris, biceps femoris, rectus abdominis and erector spinae muscles and the kinetic values to calculate the CoP were collected and analyzed after the application of an external pertur-bation with the subject in standing position, with no shoes and using unstable footwear. The results showed increased in medial gastrocnemius activity during the first compensatory postural adjustments and late com-pensatory postural adjustments when using an unstable shoe. There were no differences in standard deviation and maximum peak of anteroposterior displacement of CoP between measurements. From the experimental findings, one can conclude that the use of an unstable shoe leads to an increase in gastrocnemius activity with no increase in CoP displacement following an unexpected external perturbation.

Influence of wearing an unstable shoe construction on compensatory control of posture

This study investigated the influence of wearing unstable shoe construction (WUS) on compensatory postural adjustments (CPA) associated with external perturbations. Thirty-two subjects stood on a force platform resisting an anterior-posterior horizontal force applied to a pelvic belt via a cable, which was suddenly released. They stood under two conditions: barefoot and WUS. The electromyographic (EMG) activity of gastrocnemius medialis, tibialis anterior, rectus femoris, biceps femoris, rectus abdominis, and erector spinae muscles and the center of pressure (CoP) displacement were acquired to study CPA. The EMG signal was used to assess individual muscle activity and latency, antagonist co-activation and reciprocal activation at joint and muscle group levels. Compared to barefoot, WUS led to: (1) increased gastrocnemius medialis activity, (2) increased total agonist activity, (3) decreased antagonist co-activation at the ankle joint and muscle group levels, (4) increased reciprocal activation at the ankle joint and muscle group levels, and (5) decrease in all muscle latencies. No differences were observed in CoP displacement between conditions. These findings demonstrate that WUS led to a reorganization of the postural control system associated to improved performance of some components of postural control responses.

Influence of long-term wearing of unstable shoes on compensatory control of posture: An electromyography-based analysis

Purpose: This study investigated the influence of long-term wearing of unstable shoes (WUS) on compensatory postural adjustments (CPA) to an external perturbation. Methods: Participants were divided into two groups: one wore unstable shoes while the other wore conventional shoes for 8 weeks. The ground reaction force signal was used to calculate the anterior– posterior (AP) displacement of the centre of pressure (CoP) and the electromyographic signal of gastrocnemius medialis (GM), tibialis anterior (TA), rectus femoris (RF) and biceps femoris (BF) muscles was used to assess individual muscle activity, antagonist co-activation and reciprocal activation at the joint (TA/GM and RF/(BF + GM) pairs) and muscle group levels (ventral (TA + RF)/dorsal (GM + BF) pair) within time intervals typical for CPA. The electromyographic signal was also used to assess muscle latency. The variables described were evaluated before and after the 8-week period while wearing the unstable shoes and barefoot. Results: Long-term WUS led to: an increase of BF activity in both conditions (barefoot and wearing the unstable shoes); a decrease of GM activity; an increase of antagonist co-activation and a decrease of reciprocal activation level at the TA/GM and ventral/dorsal pairs in the unstable shoe condition. Additionally, WUS led to a decrease in CoP displacement. However, no differences were observed in muscle onset and offset. Conclusion: Results suggest that the prolonged use of unstable shoes leads to increased ankle and muscle groups’ antagonist co-activation levels and higher performance by the postural control system.

Sleep, stress and compensatory behaviors in Australian nurses and midwives

OBJECTIVE: To describe sleep, stress and compensatory behaviors in nurses and midwives. METHODS: The study included 41 midwives and 21 nurses working in Australian hospitals between 2005 and 2009. Participation was voluntary. All participants recorded on a daily basis their work and sleep hours, levels of stress and exhaustion, caffeine intake and use of sleep aids for a month (1,736 days, 1,002 work shifts). RESULTS: Participants reported moderate to high levels of stress and exhaustion on 20-40% of work days; experienced sleep disruption on more than 50% of work days; struggled to remain awake on 27% of work days; and suffered extreme drowsiness or experienced a near accident while travelling home on 9% of workdays. Age, perceived sleep duration and work hours were significant predictors of caffeine intake. About 60% of participants reported using sleep aids (about 20% reported taking prescription medications and 44% of nurses and 9% of midwives reported alcohol use as a sleep aid at least once during the study). Stress and workdays were significant predictors of sedative use. Overall, 22% reported being indifferent or mildly dissatisfied with their job. CONCLUSIONS: Sleep problems, high levels of stress and exhaustion and low job satisfaction are prevalent among nurses and midwives. The use of alcohol and sleeping pills as sleep aids, and the use of caffeine to help maintain alertness is also common. Nurses and midwives may use caffeine to compensate for reduced sleep, especially on workdays, and sleeping pills to cope with their daily work-related stress.

Arterial distensibility as a possible compensatory mechanism in chronic aortic regurgitation

OBJECTIVE: To evaluate elastic properties of conduit arteries in asymptomatic patients who have severe chronic aortic regurgitation. METHODS: Twelve healthy volunteers aged 30±1 years (control group) and 14 asymptomatic patients with severe aortic regurgitation aged 29±2 years and left ventricular ejection fraction of 0.61±0.02 (radioisotope ventriculography) were studied. High-resolution ultrasonography was performed to measure the systolic and diastolic diameters of the common carotid artery. Simultaneous measurement of blood pressure enabled the calculation of arterial compliance and distensibility. RESULTS: No differences were observed between patients with aortic regurgitation and the control group concerning age, sex, body surface, and mean blood pressure. Pulse pressure was significantly higher in the aortic regurgitation group compared with that in the control group (78±3 versus 48±1mmHg, P<0.01). Arterial compliance and distensibility were significantly greater in the aortic regurgitation group compared with that in the control group (11.0±0.8 versus 8.1±0.7 10-10 N-1 m4, P=0.01 e and 39.3±2.6 versus 31.1±2.0 10-6 N-1 m², P=0.02, respectively). CONCLUSION: Patients with chronic aortic regurgitation have increased arterial distensibility. Greater vascular compliance, to lessen the impact of systolic volume ejected into conduit arteries, represents a compensatory mechanism in left ventricular and arterial system coupling.

Compensatory β-cell mass expansion: a big role for a tiny actor.

Comment on: Jacovetti C, et al. J Clin Invest 2012; 122:3541-51.

Cardiac dysfunction and impaired compensatory response to pressure overload in mice deficient in stem cell antigen-1.

Stem cell antigen-1 (Sca-1) has been used to identify cardiac stem cells in the mouse heart. To investigate the function of Sca-1 in aging and during the cardiac adaptation to stress, we used Sca-1-deficient mice. These mice developed dilated cardiomyopathy [end-diastolic left ventricular diameter at 18 wk of age: wild-type (WT) mice, 4.2 mm ± 0.3; Sca-1-knockout (Sca-1-KO) mice, 4.6 mm ± 0.1; ejection fraction: WT mice, 51.1 ± 2.7%; Sca-1-KO mice, 42.9 ± 2.7%]. Furthermore, the hearts of mice lacking Sca-1 demonstrated exacerbated susceptibility to pressure overload [ejection fraction after transaortic constriction (TAC): WT mice, 43.5 ± 3.2%; Sca-1-KO mice, 30.8% ± 4.0] and increased apoptosis, as shown by the 2.5-fold increase in TUNEL(+) cells in Sca-1-deficient hearts under stress. Sca-1 deficiency affected primarily the nonmyocyte cell fraction. Indeed, the number of Nkx2.5(+) nonmyocyte cells, which represent a population of cardiac precursor cells (CPCs), was 2-fold smaller in Sca-1 deficient neonatal hearts. In vitro, the ability of CPCs to differentiate into cardiomyocytes was not affected by Sca-1 deletion. In contrast, these cells demonstrated unrestricted differentiation into cardiomyocytes. Interestingly, proliferation of cardiac nonmyocyte cells in response to stress, as judged by BrdU incorporation, was higher in mice lacking Sca-1 (percentages of BrdU(+) cells in the heart after TAC: WT mice, 4.4 ± 2.1%; Sca-1-KO mice, 19.3 ± 4.2%). These data demonstrate the crucial role of Sca-1 in the maintenance of cardiac integrity and suggest that Sca-1 restrains spontaneous differentiation in the precursor population. The absence of Sca-1 results in uncontrolled precursor recruitment, exhaustion of the precursor pool, and cardiac dysfunction.

MicroRNAs contribute to compensatory β cell expansion during pregnancy and obesity.

Pregnancy and obesity are frequently associated with diminished insulin sensitivity, which is normally compensated for by an expansion of the functional β cell mass that prevents chronic hyperglycemia and development of diabetes mellitus. The molecular basis underlying compensatory β cell mass expansion is largely unknown. We found in rodents that β cell mass expansion during pregnancy and obesity is associated with changes in the expression of several islet microRNAs, including miR-338-3p. In isolated pancreatic islets, we recapitulated the decreased miR-338-3p level observed in gestation and obesity by activating the G protein-coupled estrogen receptor GPR30 and the glucagon-like peptide 1 (GLP1) receptor. Blockade of miR-338-3p in β cells using specific anti-miR molecules mimicked gene expression changes occurring during β cell mass expansion and resulted in increased proliferation and improved survival both in vitro and in vivo. These findings point to a major role for miR-338-3p in compensatory β cell mass expansion occurring under different insulin resistance states.

Role of Endogenous GLP-1 and GIP in Beta Cell Compensatory Responses to Insulin Resistance and Cellular Stress.

Role of GLP-1 and GIP in beta cell compensatory responses to beta cell attack and insulin resistance were examined in C57BL/6 mice lacking functional receptors for GLP-1 and GIP. Mice were treated with multiple low dose streptozotocin or hydrocortisone. Islet parameters were assessed by immunohistochemistry and hormone measurements were determined by specific enzyme linked immunoassays. Wild-type streptozotocin controls exhibited severe diabetes, irregularly shaped islets with lymphocytic infiltration, decreased Ki67/TUNEL ratio with decreased beta cell and increased alpha cell areas. GLP-1 and GIP were co-expressed with glucagon and numbers of alpha cells mainly expressing GLP-1 were increased. In contrast, hydrocortisone treatment and induction of insulin resistance increased islet numbers and area, with enhanced beta cell replication, elevated mass of beta and alpha cells, together with co-expression of GLP-1 and GIP with glucagon in islets. The metabolic responses to streptozotocin in GLP-1RKO and GIPRKO mice were broadly similar to C57BL/6 controls, although decreases in islet numbers and size were more severe. In contrast, both groups of mice lacking functional incretin receptors displayed substantially impaired islet adaptations to insulin resistance induced by hydrocortisone, including marked curtailment of expansion of islet area, beta cell mass and islet number. Our observations cannot be explained by simple changes in circulating incretin concentrations, suggesting that intra-islet GLP-1 and GIP make a significant contribution to islet adaptation, particularly expansion of beta cell mass and compensatory islet compensation to hydrocortisone and insulin resistance.