Browse by Audience
Hospitalizations related to opioid use disorder (OUD) are rising. Addiction consultation services (ACS) increasingly provide OUD treatment to hospitalized patients, but barriers to initiating and continuing medications for OUD remain. We examined facilitators and barriers to hospital-based OUD treatment initiation and continuation from the perspective of patients and healthcare workers in the context of an ACS.
Learn More >Background and purpose – Total hip arthroplasty (THA) is an effective and common procedure. However, persistent pain and analgesic requirement up to 2 years after THA surgery are common. We examined the trends in the utilization of analgesics before and after THA, overall, and in relation to socioeconomic status (SES) in a populationbased cohort. Patients and methods – We used the Danish Hip Arthroplasty Register to identify 103,209 patients who underwent THA between 1996 and 2018. Data on prescriptions and SES markers was obtained from Danish medical databases. Prevalence rates of redeemed prescriptions for analgesics with 95% confidence intervals were calculated for 4 quarters before and 4 quarters after THA for the entire THA population, and by 3 SES markers (education, cohabiting status, and wealth). Results – Overall, the prevalence of analgesic use prior to surgery was 42% at 9-12 months and 59% at 0-3 months before the THA. The prevalence of analgesics reached its highest at 64% 0-3 months after THA but declined to 27% at 9-12 months after THA. Low education, living alone, and having low wealth (low SES) were associated with higher prevalence of analgesics use both before and after THA. Interpretation – 59% of patients used analgesics 0-3 months before surgery, which could indicate that THA might not be considered the last option for treatment and that surgery criteria might depend more on factors such as patient preferences or hip function. Moreover, health professionals should prioritize the use of a detailed plan when phasing out analgesics after THA to counteract unnecessary use, especially when treating patients with low SES.
Learn More >Microglial activation and inflammatory response play a critical role in spinal cord ischemia-reperfusion injury (SCIRI). This study aimed to investigate whether lidocaine relieves SCIRI via modulating MIAT-mediated Notch1 downregulation. Mouse SCIRI was induced by the obstruction of the aortic arch. Lidocaine was injected after reperfusion. Microglial activation and inflammatory response were assessed by Iba1, interleukin 1 beta (IL-1β), and tumor necrosis factor alpha (TNF-α) levels. The interaction between MIAT and Notch1 was assessed by RNA pull-down and RNA immunoprecipitation assays. Lidocaine treatment relieved SCIRI by reducing Iba1 and serum TNF-α and IL-1β levels. After lidocaine treatment, MIAT expression was elevated in lipopolysaccharide- (LPS-) induced BV2 cells. The interference of MIAT and the overexpression of MIAT and Notch1 restored TNF-α and IL-1β levels in supernatants. Notch1 protein was existent in MIAT-pull-down compounds, and the expression of MIAT was markedly elevated in Notch1-immunoprecipitants. The overexpression of MIAT markedly promoted the degradation of Notch1 and increased the level of ubiquitin-bound Notch1 complex. The therapeutic effect of lidocaine on SCIRI mice could be reversed by adeno-associated virus-mediated MIAT knockdown. In conclusion, lidocaine treatment relieved SCIRI via inhibiting microglial activation and reducing the inflammatory response. The molecular mechanism was partly through MIAT-mediated Notch1 downregulation.
Learn More >Patients with chronic kidney disease (CKD) frequently experience unpleasant symptoms. These can be gastrointestinal (constipation, nausea, vomiting and diarrhoea), psychological (anxiety and sadness), neurological (lightheadedness, headache and numbness), cardiopulmonary (shortness of breath and oedema), dermatological (pruritus and dry skin), painful (muscle cramps, chest pain and abdominal pain) or involve sexual dysfunction, sleep disorders and fatigue. These symptoms often occur in clusters, with one of them as the lead symptom and others as secondary symptoms. Uraemic toxins (also called uremic toxins) are often considered to be the main cause of CKD-associated symptom burden, but treatment of uraemia by dialysis often fails to resolve them and can engender additional symptoms. Indeed, symptoms can be exacerbated by comorbid conditions, pharmacotherapies, lifestyle and dietary regimens, kidney replacement therapy and ageing. Patients with kidney disease, including those who depend on dialysis or transplantation, should feel actively supported in their symptom management through the identification and targeting of unpleasant symptoms via a tailored palliative care approach. Such an approach may help minimize the burden and consequences of kidney disease, and lead to improved patient outcomes including health-related quality of life and better life participation.
Learn More >It is well known that acute exposure to physical stress produces a transient antinociceptive effect (called stress-induced analgesia [SIA]). One proposed mechanism for SIA involves noradrenaline (NA) in the central nervous system. NA has been reported to activate inhibitory neurons in the spinal dorsal horn (SDH), but its in vivo role in SIA remains unknown. In this study, we found that an antinociceptive effect on noxious heat after acute exposure to restraint stress was impaired in mice with a conditional knockout of α-adrenaline receptors (α-ARs) in inhibitory neurons (Vgat-Cre;Adra1a mice). A similar reduction was also observed in mice treated with N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine, a selective neurotoxin for NAergic neurons in the locus coeruleus (LC). Furthermore, whole-cell patch-clamp recordings using spinal cord slices revealed that NA-induced increase in the frequency of spontaneous inhibitory postsynaptic currents in the substantia gelatinosa neurons was suppressed by silodosin, an α-AR antagonist, and by conditional knockout of α-ARs in inhibitory neurons. Moreover, under unstressed conditions, the antinociceptive effects of intrathecal NA and phenylephrine on noxious heat were lost in Vgat-Cre;Adra1a mice. Our findings suggest that activation of α-ARs in SDH inhibitory neurons, presumably via LC-NAergic neurons, is necessary for SIA to noxious heat.
Learn More >Chronic pain and the accompanying level of disability is a healthcare crisis that reaches epidemic proportions and is now considered a world level crisis. Chronic non-specific low back pain (CNLBP) contributes a significant proportion to the chronic pain population. CNLBP occurs with overlapping psychosocial factors. This study was design to investigate specific psychosocial factors and their influence on reported disability in a population with CNLBP.
Learn More >Chronic migraine places a disabling burden on patients, which is extensively modeled by the nitroglycerin (NTG)-treated animal model. Although the NF-κB pathway is involved in an increase in CGRP levels and activation of the trigeminal system in the NTG model, the relationship between NTG and neuroinflammation remains unclear. This study aimed to optimize a chronic NTG rat model with hyperalgesia and the ethological capacity for estimating migraine therapies and to further explore the underlying mechanism of NTG-induced migraine.
Learn More >Neurological symptoms are frequent among patients with COVID-19. Little is known regarding the repercussions of neurological symptoms for patients and how these symptoms are related to one another.
Learn More >