ORCID Profile
0000-0002-6911-7018
Current Organisations
Second Military Medical University
,
Universidade do Oeste Paulista
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Publisher: Wiley
Date: 05-09-2013
DOI: 10.1002/OBY.20534
Abstract: Peptide YY (PYY3-36) and pancreatic polypeptide (PP) potently inhibit food intake in rodents and humans, however, it is unclear whether they have any synergistic/additive interaction in decreasing food intake. Fasted WT, Y2(-) (/) (-) , Y4(-) (/) (-) , or Y2Y4(-) (/) (-) mice were i.p. administrated with saline, PYY3-36, and/or PP. Combined injection of PYY3-36 and PP reduces food intake in an additive manner was demonstrated in this study. This effect is mediated via Y2 and Y4 receptors, respectively. It was demonstrated that PYY3-36 and PP activate distinct neuronal pathways in the hypothalamus, as demonstrated by immunostaining for c-fos, which shows distinct patterns in response to either hormone. After PYY3-36 injection, neurons in the dorsal aspect of the arcuate nucleus (Arc), paraventricular nucleus, and dorso-medial nucleus of the hypothalamus (DMH) are activated with minimal responses seen in the ventro-medial nucleus of the hypothalamus (VMH) and lateral hypothalamic area (LHA) of WT mice. These effects are absent in Y2(-) (/) (-) mice. PP activates preferably the lateral aspect of the Arc, the DMH, VMH, and LHA in a Y4 receptor-dependent manner. Importantly, the expression pattern of c-fos immunoreactive neurons induced by combined treatment appears to be the sum of the effects of single treatments rather than a result of synergistic interaction. These findings demonstrate that PYY3-36 and PP activate distinct pathways in the hypothalamus to reduce food intake in an additive manner.
Publisher: Oxford University Press (OUP)
Date: 22-09-2011
DOI: 10.1093/NDT/GFR575
Abstract: Elevated macrophage inhibitory cytokine-1 (MIC-1/GDF15) levels in serum mediate anorexia and weight loss in some cancer patients and similarly elevated levels occur in chronic kidney disease (CKD). Serum MIC-1/GDF15 is also elevated in chronic inflammatory diseases and predicts atherosclerotic events independently of traditional risk factors. The relationship between chronic inflammation, decreasing body mass index (BMI) and increased mortality in CKD is not well understood and is being actively investigated. MIC-1/GDF15 may link these features of CKD. Cohorts of incident dialysis patients from Sweden (n = 98) and prevalent hemodialysis patients from the USA (n = 381) had serum MIC-1/GDF15, C-reactive protein (CRP) levels and BMI measured at study entry. Additional surrogate markers of nutritional adequacy, body composition and inflammation were assessed in Swedish patients. Patients were followed for all-cause mortality. In the Swedish cohort, serum MIC-1/GDF15 was associated with decreasing BMI, measures of nutrition and markers of oxidative stress and inflammation. Additionally, high serum MIC-1/GDF15 levels identified patients with evidence of protein-energy wasting who died in the first 3 years of dialysis. The ability of serum MIC-1/GDF15 to predict mortality in the first 3 years of dialysis was confirmed in the USA cohort. In both cohorts, serum MIC-1/GDF15 level was an independent marker of mortality when adjusted for age, CRP, BMI, history of diabetes mellitus and/or cardiovascular disease and glomerular filtration rate or length of time on dialysis at study entry. MIC-1/GDF15 is a novel independent serum marker of mortality in CKD capable of significantly improving the mortality prediction of other established markers. MIC-1/GDF15 may mediate protein-energy wasting in CKD and represent a novel therapeutic target for this fatal complication.
Publisher: Public Library of Science (PLoS)
Date: 27-06-2014
Publisher: Oxford University Press (OUP)
Date: 07-2021
Abstract: Imaging for low back pain is widely regarded as a target for efforts to reduce low-value care. We aimed to estimate the prevalence of the overuse and underuse of lumbar imaging in patients presenting with low back pain to the emergency department (ED). This was a retrospective chart review study of five public hospital EDs in Sydney, Australia, in 2019–20. We reviewed the clinical charts of consecutive adult patients who presented with a complaint of low back pain and extracted clinical features relevant to a decision to request lumbar imaging. We estimated the proportion of encounters where a decision to request lumbar imaging was inappropriate (overuse) or where a clinician did not request an appropriate and informative lumbar imaging test when indicated (underuse). Six hundred and forty-nine patients presented with a complaint of low back pain, of which 158 (24.3%) were referred for imaging. Seventy-nine (12.2%) had a combination of features suggesting that lumbar imaging was indicated according to clinical guidelines. The prevalence of overuse and underuse of lumbar imaging was 8.8% (57 of 649 cases, 95% CI 6.8–11.2%) and 4.3% (28 of 649 cases, 95% CI 3.0–6.1%), respectively. Thirteen cases were classified as underuse because the patients were referred for uninformative imaging modalities (e.g. referred for radiography for suspected cauda equina syndrome). In this study of emergency care, there was evidence of not only overuse of lumbar imaging but also underuse through failure to request lumbar imaging when indicated or referral for an uninformative imaging modality. These three issues seem more important targets for quality improvement than solely focusing on overuse.
Publisher: Public Library of Science (PLoS)
Date: 28-02-2013
Publisher: Wiley
Date: 28-11-2016
DOI: 10.1002/ACR.22919
Abstract: To investigate whether physical activity interventions increase objectively measured physical activity levels of patients with chronic musculoskeletal pain (e.g., osteoarthritis, low back pain) compared to no/minimal intervention. We performed a systematic review with meta-analysis searching the Medline, Embase, Cumulative Index to Nursing and Allied Health Literature, SportDiscus, and Physiotherapy Evidence Database (PEDro) databases, and the main clinical trials registries. Quasirandomized or randomized controlled trials investigating the effect of physical activity interventions on objectively measured physical activity levels (e.g., using accelerometers or pedometers) of patients with chronic musculoskeletal pain compared with no/minimal intervention were considered eligible. Analyses were conducted separately for short-term (≤3 months), intermediate (>3 months and <12 months), and long-term (≥12 months) followups. Pooled effects were calculated using the standardized mean difference (SMD), and the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach was used in summary conclusions. Eight published trials and 6 registered trials were included. For the short-term followup, pooling of 6 trials showed no significant effect (SMD 0.34, 95% confidence interval -0.09, 0.77) between a physical activity intervention and no/minimal intervention. Similarly nonsignificant results were found for the intermediate and long-term followups. The overall evidence according to the GRADE approach was classified as low quality. Our findings suggest that physical activity-based interventions may lead to little or no difference in objectively measured physical activity levels of patients with chronic musculoskeletal pain compared with no/minimal interventions. Given the number of registered trials, the pooled effect found in this review is likely to change once the results of these trials become available.
Publisher: Wiley
Date: 09-04-2020
Publisher: Wiley
Date: 05-02-2020
DOI: 10.1111/CPF.12619
Abstract: Meta-analyses have shown that isometric handgrip training reduces blood pressure in normotensive and hypertensive subjects. However, the effects on cardiac autonomic modulation are still controversial. Thus, the aim of this systematic review and meta-analysis was to analyse the effects of isometric handgrip training on cardiac autonomic modulation in normotensive and hypertensive subjects. For this, Medline, Cinhal, Embase, Spordiscus and PEdro were searched for relevant studies published until December 2018. Randomized controlled trials investigating the effect of isometric handgrip training on heart rate variability parameters were considered eligible. Parameters were obtained in time (standard deviation of all the RR intervals-SDNN, root mean square of successive differences between the normal adjacent RR intervals-RMSSD and the percentage of adjacent intervals with more than 50 ms-PNN50) and frequency domain (low frequency-LF, high frequency-HF and sympathovagal balance-LF/HF). Mean difference (MD) and 95% confidence interval (95% CI) were calculated using an inverse variance method with a random effects model. Seven trials were included in the systematic review and meta-analysis, totalling 86 participants. No significant effect was observed in heart rate variability parameters after isometric handgrip training (4 trials to SDNN: MD = -1.44 ms and 95% CI = -8.02, 5.14 ms RMSSD: MD = -1.48 ms and 95% CI = -9.41, 6.45 ms PNN50: MD = 0.85% and 95% CI = -1.10, 2.81% 7 trials to LF: -0.17 n.u. and 95% CI = -6.32, 5.98 n.u. HF: MD = 0.17 n.u. and 95% CI = -5.97, 6.30 n.u. and LF/HF: MD = 0.13 and 95% CI = -0.34, 0.59). In conclusion, current literature indicates that isometric handgrip training does not improve heart rate variability.
Publisher: Wiley
Date: 26-09-2014
DOI: 10.1002/JBMR.2205
Abstract: Chronic stress and depression have adverse consequences on many organ systems, including the skeleton, but the mechanisms underlying stress-induced bone loss remain unclear. Here we demonstrate that neuropeptide Y (NPY), centrally and peripherally, plays a critical role in protecting against stress-induced bone loss. Mice lacking the anxiolytic factor NPY exhibit more anxious behavior and elevated corticosterone levels. Additionally, following a 6-week restraint, or cold-stress protocol, Npy-null mice exhibit three-fold greater bone loss compared to wild-type mice, owing to suppression of osteoblast activity. This stress-protective NPY pathway acts specifically through Y2 receptors. Centrally, Y2 receptors suppress corticotropin-releasing factor expression and inhibit activation of noradrenergic neurons in the paraventricular nucleus. In the periphery, they act to control noradrenaline release from sympathetic neurons. Specific deletion of arcuate Y2 receptors recapitulates the Npy-null stress response, coincident with elevated serum noradrenaline. Importantly, specific reintroduction of NPY solely in noradrenergic neurons of otherwise Npy-null mice blocks the increase in circulating noradrenaline and the stress-induced bone loss. Thus, NPY protects against excessive stress-induced bone loss, through Y2 receptor-mediated modulation of central and peripheral noradrenergic neurons.
Publisher: Wiley
Date: 21-03-2012
DOI: 10.1111/J.1463-1326.2012.01592.X
Abstract: Both the neuronal-derived neuropeptide Y (NPY) and the gut hormone peptide YY (PYY) have been implicated in the regulation of energy balance and glucose homeostasis. However, despite similar affinities for the same Y receptors, the co-ordinated actions of these two peptides in energy and glucose homeostasis remain largely unknown. To investigate the mechanisms and possible interactions between PYY with NPY in the regulation of these processes, we utilized NPY/PYY single and double mutant mouse models and examined parameters of energy balance and glucose homeostasis. PYY(-/-) mice exhibited increased fasting-induced food intake, enhanced fasting and oral glucose-induced serum insulin levels, and an impaired insulin tolerance, - changes not observed in NPY(-/-) mice. Interestingly, whereas PYY deficiency-induced impairment in insulin tolerance remained in NPY(-/-) PYY(-/-) mice, effects of PYY deficiency on fasting-induced food intake and serum insulin concentrations at baseline and after the oral glucose bolus were absent in NPY(-/-) PYY(-/-) mice, suggesting that NPY signalling may be required for PYY's action on insulin secretion and fasting-induced hyperphagia. Moreover, NPY(-/-) PYY(-/-) , but not NPY(-/-) or PYY(-/-) mice had significantly decreased daily food intake, indicating interactive control by NPY and PYY on spontaneous food intake. Furthermore, both NPY(-/-) and PYY(-/-) mice showed significantly reduced respiratory exchange ratio during the light phase, with no additive effects observed in NPY(-/-) PYY(-/-) mice, indicating that NPY and PYY may regulate oxidative fuel selection via partly shared mechanisms. Overall, physical activity and energy expenditure, however, are not significantly altered by NPY and PYY single or double deficiencies. These findings show significant and erse interactions between NPY and PYY signalling in the regulation of different aspects of energy balance and glucose homeostasis.
Publisher: BMJ
Date: 09-10-2020
DOI: 10.1136/EMERMED-2020-209588
Abstract: Most low back pain trials have limited applicability to the emergency department (ED) because they provide treatment and measure outcomes after discharge from the ED. We investigated the efficacy and safety of pharmacological and non-pharmacological interventions delivered in the ED to patients with non-specific low back pain and/or sciatica on patient-relevant outcomes measured during the emergency visit. Literature searches were performed in MEDLINE, EMBASE and CINAHL from inception to week 1 February 2020. We included all randomised controlled trials investigating adult patients (≥18 years) with non-specific low back pain and/or sciatica presenting to ED. The primary outcome of interest was pain intensity. Two reviewers independently screened the full texts, extracted the data and assessed risk of bias of each trial using the Physiotherapy Evidence Database (PEDro) scale. The overall quality of evidence, or certainty, provided by a set of trials evaluating the same treatment was evaluated using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach, which considers imprecision, inconsistency, indirectness and bias in the evidence. Fifteen trials (1802 participants) were included with 12 of 15 at low risk of bias (ie, PEDro score ). Based on results from in idual trials and moderate quality evidence, ketoprofen gel was more effective than placebo for non-specific low back pain at 30 min (mean difference (MD) −15.0, 95% confidence interval (CI) −21.0 to −9.0). For those with sciatica (moderate quality evidence), intravenous paracetamol (acetaminophen) (MD −15.7, 95% CI −19.8 to −11.6) and intravenous morphine (MD −11.4, 95% CI −21.6 to −1.2) were both superior to placebo at 30 min. Based on moderate quality of evidence, corticosteroids showed no benefits against placebo at emergency discharge for non-specific low back pain (MD 9.0, 95% CI −0.71 to 18.7) or sciatica (MD −6.8, 95% CI −24.2 to 10.6). There were conflicting results from trials comparing different pharmacological options (moderate quality evidence) or investigating non-pharmacological treatments (low quality evidence). Ketoprofen gel for non-specific low back pain and intravenous paracetamol or morphine for sciatica were superior to placebo, whereas corticosteroids were ineffective for both conditions. There was conflicting evidence for comparisons of different pharmacological options and those involving non-pharmacological treatments. Additional trials measuring important patient-related outcomes to EDs are needed.
Publisher: Wiley
Date: 13-06-2022
DOI: 10.1002/EJP.1977
Abstract: To investigate whether the sedentary behaviour contributes to the development of new episodes of low back pain in adults. Searches were performed in five electronic databases from their inception to March 2022. Prospective cohort studies with people without low back pain at baseline investigating the effect of sedentary behaviour on the development of new episodes of low back pain at follow-up were considered eligible. Two independent authors screened, extracted the data and assessed the risk of bias of included studies. An adapted version of the Quality In Prognosis Studies (QUIPS) tool was used to assess the risk of bias. Meta-analyses were performed using random effect models to obtain a pooled risk ratio (RR) and 95% confidence intervals (CIs). Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach was used to assess the overall certainty of the evidence. Ten studies were included in this review, with a total s le ranging from 107 to 57,504 participants and mean age ranging from 21.7 to 53.6 years. Most studies (n = 9) assessed sedentary behaviour using self-reported methods, including validated questionnaires or single questions, except for one study that used video recording. The overall risk of bias of the included studies was low. Pooled analysis showed that people classified as sedentary or spending more time in sedentary activities were not likely to develop a new episode of low back pain (RR 1.01, 95% CI 0.98-1.04, I Sedentary behaviour probably does not contribute to the development of new episodes of low back pain in an adult population. Sedentary behaviour does not appear to increase the chances of developing a new episode of low back pain. This might imply that health lifestyle contributors seem to be more related to the amount and type of physical activity, but not the amount of sedentary time. However, studies evaluating the relationship of the sedentary and physical activity with the development of a new episode of low back pain are still needed.
Publisher: Springer Science and Business Media LLC
Date: 02-11-2022
DOI: 10.1007/S11064-022-03785-9
Abstract: Postoperative neurocognitive disorder (PND) is a disease that frequently develops in older patients during the perioperative period. It seriously affects the quality of life of the affected patients. Despite advancements in understanding PND, this disorder's mechanisms remain unclear, including pathophysiological processes such as central synaptic plasticity and function, neuroinflammation, excitotoxicity, and neurotrophic support. Growing evidence suggests that microenvironmental changes are major factors for PND induction in older in iduals. Exosomes are carriers for transporting different bioactive molecules between nerve cells in the microenvironment and maintaining intercellular communication and tissue homeostasis. Studies have shown that exosomes and microRNAs (miRNAs) are involved in various physiological and pathological processes, including neural processes related to PND, such as neurogenesis and cell death, neuroprotection, and neurotrophy. This article reviews the effects of exosomes and miRNAs on the brain microenvironment in PND and has important implications to improve PND diagnosis, as well as to develop targeted therapy of this disorder.
Publisher: Elsevier BV
Date: 06-2007
Publisher: Public Library of Science (PLoS)
Date: 29-06-2010
Publisher: Elsevier BV
Date: 12-2012
DOI: 10.1016/J.NPEP.2012.08.010
Abstract: Chronic opiate usage, whether prescribed or illicit, has been associated with changes in bone mass and is a recognized risk factor for the development of osteoporosis however, the mechanism behind this effect is unknown. Here we show that lack of dynorphin, an endogenous opioid, in mice (Dyn-/-), resulted in a significantly elevated cancellous bone volume associated with greater mineral apposition rate and increased resorption indices. A similar anabolic phenotype was evident in bone of mice lacking dynorphin's cognate receptor, the kappa opioid receptor. Lack of opioid receptor expression in primary osteoblastic cultures and no change in bone cell function after dynorphin agonist treatment in vitro indicates an indirect mode of action. Consistent with a hypothalamic action, central dynorphin signaling induces extracellular signal-regulated kinase (ERK) phosphorylation and c-fos activation of neurons in the arcuate nucleus of the hypothalamus (Arc). Importantly, this signaling also leads to an increase in Arc NPY mRNA expression, a change known to decrease bone formation. Further implicating NPY in the skeletal effects of dynorphin, Dyn-/-/NPY-/- double mutant mice showed comparable increases in bone formation to single mutant mice, suggesting that dynorphin acts upstream of NPY signaling to control bone formation. Thus the dynorphin system, acting via NPY, may represent a pathway by which higher processes including stress, reward/addiction and depression influence skeletal metabolism. Moreover, understanding of these unique interactions may enable modulation of the adverse effects of exogenous opioid treatment without directly affecting analgesic responses.
Publisher: Springer Science and Business Media LLC
Date: 14-03-2019
DOI: 10.1007/S13346-019-00627-0
Abstract: Myocardial infarction (MI) remains one of the leading cause of mortality over the world. However, current treatments are more palliative than curative, which only stall the progression of the disease, but not reverse the disease. While stem cells or bioactive molecules therapy is promising, the limited survival and engraftment of bioactive agent due to a hostile environment is a bottleneck for MI treatment. In order to maximize the utility of stem cells and bioactive molecules for myocardial repair and regeneration, various types of biomaterials have been developed. Among them, collagen-based biomaterial is widely utilized for cardiac tissue engineering and regeneration due to its optimal physical and chemical properties. In this review, we summarize the properties of collagen-based biomaterial. Then, we discuss collagen-based biomaterial currently being applied to treat MI alone, or together with stem cells and/or bioactive molecules. Finally, the delivery system of collagen-based biomaterial will also be discussed.
Publisher: Public Library of Science (PLoS)
Date: 30-12-2009
Publisher: Wiley
Date: 28-05-2010
DOI: 10.1111/J.1463-1326.2009.01193.X
Abstract: Energy homeostasis is regulated by a complex interaction of molecules and pathways, and new antiobesity treatments are likely to require multiple pharmacological targeting of anorexigenic or orexigenic pathways to achieve effective loss of excess body weight and adiposity. Cannabinoids, acting via the cannabinoid-1 (CB1) receptor, and neuropeptide Y (NPY) are important modulators of feeding behaviour, energy metabolism and body composition. We investigated the interaction of CB1 and NPY in the regulation of energy homeostasis, hypothesizing that dual blockade of CB1 and NPY signalling will induce greater weight and/or fat loss than that induced by single blockade of either system alone. We studied the effects of the CB1 antagonist Rimonabant on food intake, body weight, body composition, energy metabolism and bone physiology in wild-type (WT) and NPY knockout (NPY(-/-)) mice. Rimonabant was administered orally at 10 mg/kg body weight twice per day for 3 weeks. Oral Rimonabant was delivered voluntarily to mice via a novel method enabling studies to be carried out in the absence of gavage-induced stress. Mice with dual blockade of CB1 and NPY signalling (Rimonabant-treated NPY(-/-) mice) exhibited greater reductions in body weight and adiposity than mice with single blockade of either system alone (Rimonabant-treated WT or vehicle-treated NPY(-/-) mice). These changes occurred without loss of lean tissue mass or bone mass. Furthermore, Rimonabant-treated NPY(-/-) mice showed a lower respiratory exchange ratio than that seen in Rimonabant-treated WT or vehicle-treated NPY(-/-) mice, suggesting that this additive effect of dual blockade of CB1 and NPY involves promotion of lipid oxidation. On the other hand, energy expenditure and physical activity were comparable amongst all treatment groups. Interestingly, Rimonabant similarly and transiently reduced spontaneous and fasting-induced food intake in WT and NPY(-/-) mice in the first hour after administration only, suggesting independent regulation of feeding by CB1 and NPY signalling. In contrast, Rimonabant increased serum corticosterone levels in WT mice, but this effect was not seen in NPY(-/-) mice, indicating that NPY signalling may be required for effects of CB1 on the hypothalamo-pituitary-adrenal axis. Dual blockade of CB1 and NPY signalling leads to additive reductions in body weight and adiposity without concomitant loss of lean body mass or bone mass. An additive increase in lipid oxidation in dual CB1 and NPY blockade may contribute to the effect on adiposity. These findings open new avenues for more effective treatment of obesity via dual pharmacological manipulations of the CB1 and NPY systems.
Publisher: Wiley
Date: 27-02-2019
DOI: 10.1002/JUM.14973
Abstract: To compare trunk muscle thickness of women with and without patellofemoral pain (PFP) and to assess the association of trunk muscle thickness with self-reported pain of women with PFP. Forty-four women were recruited and ided into 2 groups: a PFP group (n = 22) and a pain-free group (n = 22). The thickness of the following trunk muscles was obtained by B-mode ultrasound imaging: transversus abdominis, obliquus internus (OI), obliquus externus (OE), rectus abdominis, and multifidus. Self-reported pain was measured on a visual analog scale. The 44 participants were 18 to 35 years old. Women with PFP had lower thickness of the OI and OE than pain-free women, with moderate or large effect sizes ranging from -0.78 to -0.98, which was negatively related to self-reported pain correlations (r = -0.53 to -0.40). The contraction ratios of the OI and OE were also lower in women with PFP than in pain-free women (P < .05). No differences between groups were found for the transversus abdominis, multifidus, and rectus abdominis, with also no correlation with self-reported pain. Lower thickness of the OI and OE is present in women with PFP, which is related to self-reported pain. These findings might help in understanding the alterations in trunk biomechanics of in iduals with PFP and the mechanisms by which interventions targeting trunk muscle strength are beneficial to in iduals with PFP.
Publisher: Elsevier BV
Date: 09-2023
Publisher: Wiley
Date: 11-2011
DOI: 10.1038/OBY.2011.99
Abstract: Y2 receptors, particularly those in the brain, have been implicated in neuropeptide Y (NPY)-mediated effects on energy homeostasis and bone mass. Recent evidence also indicates a role for Y2 receptors in peripheral tissues in this process by promoting adipose tissue accretion however their effects on energy balance remain unclear. Here, we show that adult-onset conditional knockdown of Y2 receptors predominantly in peripheral tissues results in protection against diet-induced obesity accompanied by significantly reduced weight gain, marked reduction in adiposity and improvements in glucose tolerance without any adverse effect on lean mass or bone. These changes occur in association with significant increases in energy expenditure, respiratory exchange ratio, and physical activity and despite concurrent hyperphagia. On a chow diet, knockdown of peripheral Y2 receptors results in increased respiratory exchange ratio and physical activity with no effect on lean or bone mass, but decreases energy expenditure without effecting body weight or food intake. These results suggest that peripheral Y2 receptor signaling is critical in the regulation of oxidative fuel selection and physical activity and protects against the diet-induced obesity. The lack of effects on bone mass seen in this model further indicates that bone mass is primarily controlled by non-peripheral Y2 receptors. This study provides evidence that novel drugs that target peripheral rather than central Y2 receptors could provide benefits for the treatment of obesity and glucose intolerance without adverse effects on lean and bone mass, with the additional benefit of avoiding side effects often associated with pharmaceuticals that act on the central nervous system.
Publisher: BMJ
Date: 11-09-2020
DOI: 10.1136/EMERMED-2019-209294
Abstract: Low back pain, and especially non-specific low back pain, is a common cause of presentation to the emergency department (ED). Although these patients typically report relatively high pain intensity, the clinical course of their pain and disability remains unclear. Our objective was to review the literature and describe the clinical course of non-specific low back pain after an ED visit. Electronic searches were conducted using MEDLINE, CINAHL and EMBASE from inception to March 2019. We screened for cohort studies or randomised trials investigating pain or disability in patients with non-specific low back pain presenting to EDs. We excluded studies that enrolled participants with minimal pain or disability scores at baseline. Two reviewers independently screened the full texts, extracted the data and assessed risk of bias and quality of evidence. Estimates of pain and disability were converted to a common 0–100 scale. We estimated pooled means and 95% CIs of pain and disability as a function of time since ED presentation. Eight studies (nine publications) with a total of 1994 patients provided moderate overall quality evidence of the expected clinical course of low back pain after an ED visit. Seven of the eight studies were assessed to have a low risk of bias. At the time of the ED presentation, the pooled estimate of the mean pain score on a 0–100 scale was 71.0 (95% CI 64.2–77.9). This reduced to 46.1 (95% CI 37.2–55.0) after 1 day, 41.8 (95% CI 34.7 to 49.0) after 1 week and 13.5 (95% CI 5.8–21.3) after 26 weeks. The course of disability followed a similar pattern. Patients presenting to EDs with non-specific low back pain experience rapid reductions in pain intensity, but on average symptoms persisted 6 months later. This review can be used to educate patients so they can have realistic expectations of their recovery.
Publisher: Springer Science and Business Media LLC
Date: 03-07-2018
DOI: 10.1007/S00586-018-5673-2
Abstract: The aim of this study was to provide an overview of the recommendations regarding the diagnosis and treatment contained in current clinical practice guidelines for patients with non-specific low back pain in primary care. We also aimed to examine how recommendations have changed since our last overview in 2010. The searches for clinical practice guidelines were performed for the period from 2008 to 2017 in electronic databases. Guidelines including information regarding either the diagnosis or treatment of non-specific low back pain, and targeted at a multidisciplinary audience in the primary care setting, were considered eligible. We extracted data regarding recommendations for diagnosis and treatment, and methods for development of guidelines. We identified 15 clinical practice guidelines for the management of low back pain in primary care. For diagnosis of patients with non-specific low back pain, the clinical practice guidelines recommend history taking and physical examination to identify red flags, neurological testing to identify radicular syndrome, use of imaging if serious pathology is suspected (but discourage routine use), and assessment of psychosocial factors. For treatment of patients with acute low back pain, the guidelines recommend reassurance on the favourable prognosis and advice on returning to normal activities, avoiding bed rest, the use of nonsteroidal anti-inflammatory drugs (NSAIDs) and weak opioids for short periods. For treatment of patients with chronic low back pain, the guidelines recommend the use of NSAIDs and antidepressants, exercise therapy, and psychosocial interventions. In addition, referral to a specialist is recommended in case of suspicion of specific pathologies or radiculopathy or if there is no improvement after 4 weeks. While there were a few discrepancies across the current clinical practice guidelines, a substantial proportion of recommendations was consistently endorsed. In the current review, we identified some differences compared to the previous overview regarding the recommendations for assessment of psychosocial factors, the use of some medications (e.g., paracetamol) as well as an increasing amount of information regarding the types of exercise, mode of delivery, acupuncture, herbal medicines, and invasive treatments. These slides can be retrieved under Electronic Supplementary Material.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 07-2017
Publisher: Public Library of Science (PLoS)
Date: 22-12-2009
Publisher: Springer Science and Business Media LLC
Date: 17-11-2010
DOI: 10.1038/IJO.2009.232
Abstract: Neuropeptide Y and its Y receptors are important players in the regulation of energy homeostasis. However, while their functions in feeding regulation are well recognized, functions in other critical aspects of energy homeostasis are largely unknown. To investigate the function of Y1 receptors in the regulation of energy homeostasis, we examined energy expenditure, physical activity, body composition, oxidative fuel selection and mitochondrial oxidative capacity in germline Y1(-/-) mice as well as in a conditional Y1-receptor-knockdown model in which Y1 receptors were knocked down in peripheral tissues of adult mice. Germline Y1(-/-) mice of both genders not only exhibit a decreased respiratory exchange ratio, indicative of increased lipid oxidation, but interestingly also develop late-onset obesity. However, the increased lipid oxidation is a primary effect of Y1 deletion rather than secondary to increased adiposity, as young Y1(-/-) mice are lean and show the same effect. The mechanism behind this is likely because of increased liver and muscle protein levels of carnitine palmitoyltransferase-1 (CPT-1) and maximal activity of key enzymes involved in beta-oxidation beta-hydroxyacyl CoA dehydrogenase (betaHAD) and medium-chain acyl-CoA dehydrogenase (MCAD), leading to increased mitochondrial capacity for fatty acid transport and oxidation. These effects are controlled by peripheral Y1-receptor signalling, as adult-onset conditional Y1 knockdown in peripheral tissues also leads to increased lipid oxidation, liver CPT-1 levels and betaHAD activity. Importantly, these mice are resistant to diet-induced obesity. This work shows the primary function of peripheral Y1 receptors in the regulation of oxidative fuel selection and adiposity, opening up new avenues for anti-obesity treatments by targeting energy utilization in peripheral tissues rather than suppressing appetite by central effects.
Publisher: SAGE Publications
Date: 21-12-2021
DOI: 10.1177/02692155211065974
Abstract: To investigate what format for providing patient information (i.e. written summary, infographic or video animation) is most effective for promoting correct beliefs about imaging and inevitable consequences of low back pain (LBP). Randomised controlled trial. One hundred and fifty-nine patients with non-specific LBP were recruited from outpatient physiotherapy clinics. Participants were randomised to receive patient information in one of three formats: video animation, infographic or written summary. Patients were allowed to read or watch the materials for up to 20 min. Outcome were assessed before and immediately after the intervention. The primary outcome was the Back Beliefs Questionnaire. The secondary outcome was beliefs about imaging for LBP assessed by two questions. All 159 patients completed the study. Our findings revealed no difference between groups for the Back Beliefs Questionnaire. Correct beliefs about imaging were more likely with the infographic than the video animation (Question 1- Odds Ratio [OR] = 3.9, 95% confidence interval [CI]: 1.7, 8.7 Question 2- OR = 6.8, 95%CI: 2.7, 17.2) and more likely with the written summary than the video animation (Question 1- OR = 3.3, 95%CI: 1.5, 7.4 Question 2- OR = 3.7, 95%CI: 1.6, 8.5). No difference between infographic and written summary formats were reported for the questions assessing LBP imaging beliefs. The three materials were equally effective in improving patient's general beliefs about LBP care. However, the traditional written summary or infographic formats were more effective than the video animation format for improving beliefs about imaging for LBP.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 09-2020
Publisher: Springer Science and Business Media LLC
Date: 11-2007
DOI: 10.1038/NM1677
Abstract: Anorexia and weight loss are part of the wasting syndrome of late-stage cancer, are a major cause of morbidity and mortality in cancer, and are thought to be cytokine mediated. Macrophage inhibitory cytokine-1 (MIC-1) is produced by many cancers. Examination of sera from in iduals with advanced prostate cancer showed a direct relationship between MIC-1 abundance and cancer-associated weight loss. In mice with xenografted prostate tumors, elevated MIC-1 levels were also associated with marked weight, fat and lean tissue loss that was mediated by decreased food intake and was reversed by administration of antibody to MIC-1. Additionally, normal mice given systemic MIC-1 and transgenic mice overexpressing MIC-1 showed hypophagia and reduced body weight. MIC-1 mediates its effects by central mechanisms that implicate the hypothalamic transforming growth factor-beta receptor II, extracellular signal-regulated kinases 1 and 2, signal transducer and activator of transcription-3, neuropeptide Y and pro-opiomelanocortin. Thus, MIC-1 is a newly defined central regulator of appetite and a potential target for the treatment of both cancer anorexia and weight loss, as well as of obesity.
Publisher: American Diabetes Association
Date: 15-11-2012
DOI: 10.2337/DB12-0156
Abstract: Recruitment of activated immune cells into white adipose tissue (WAT) is linked to the development of insulin resistance and obesity, but the mechanism behind this is unclear. Here, we demonstrate that Y1 receptor signaling in immune cells controls inflammation and insulin resistance in obesity. Selective deletion of Y1 receptors in the hematopoietic compartment of mice leads to insulin resistance and inflammation in WAT under high fat–fed conditions. This is accompanied by decreased mRNA expression of the anti-inflammatory marker adiponectin in WAT and an increase of the proinflammatory monocyte chemoattractant protein-1 (MCP-1). In vitro, activated Y1-deficient intraperitoneal macrophages display an increased inflammatory response, with exacerbated secretion of MCP-1 and tumor necrosis factor, whereas addition of neuropeptide Y to wild-type macrophages attenuates the release of these cytokines, this effect being blocked by Y1 but not Y2 receptor antagonism. Importantly, treatment of adipocytes with the supernatant of activated Y1-deficient macrophages causes insulin resistance, as demonstrated by decreased insulin-induced phosphorylation of the insulin receptor and Akt as well as decreased expression of insulin receptor substrate 1. Thus, Y1 signaling in hematopoietic-derived cells such as macrophages is critical for the control of inflammation and insulin resistance in obesity.
Publisher: Elsevier BV
Date: 05-2018
Publisher: Public Library of Science (PLoS)
Date: 29-06-2012
No related grants have been discovered for Crystian Bitencourt Soares de Oliveira.