Rejected

Chronic ethanol exposure causes neurotoxicity and long-term learning and memory impairment along with hippocampal and frontal cortical dysfunction. Flavonoids possess antioxidant and anti-inflammatory properties believed to be contributory factors in reversing cognitive decline. 6-Methoxyflavone (6-MOF), a flavonoid occurring naturally in medicinal plants, has been reported to instigate neuroprotection by reversing cisplatin-induced hyperalgesia and allodynia. Consequently, this study was designed to investigate 6-MOF activity in models of chronic ethanol-induced cognitive impairment along with neurochemical correlates.

N6-methyladenosine (mA) is the most abundant methylation modification on mRNA in mammals. Fat mass and obesity-related protein (FTO) is the main RNA mA demethylase. FTO is involved in the occurrence and maintenance of neuropathic pain (NP). NP often induces mental disorders. We found that NP downregulated the expression of FTO in the anterior cingulate cortex (ACC), inhibited the expression of matrix metalloproteinase-9 (MMP-9) in the ACC, maladjusted the brain-derived neurotrophic factor precursor (proBDNF) and mature brain-derived neurotrophic factor (mBDNF) levels in the ACC, and induced anxiety- and depression-like behaviors in mice. Blocking the downregulation of FTO in the ACC induced by peripheral nerve injury could reverse the anxiety- and depression-like behaviors of mice. Contrarily, downregulation of simulated FTO induced anxiety- and depression-like behaviors in mice. After peripheral nerve injury, the binding of FTO to MMP-9 mRNA decreased and the enrichment of mA on MMP-9 mRNA increased. In conclusion, downregulation of FTO in ACC by regulating MMP-9 mRNA methylation level contributes to the occurrence of anxiety- and depression-like behaviors in NP mice.

This work aimed to investigate the brain resting-state functional magnetic resonance imaging (fMRI) technology based on the depth autoencoders algorithm and to evaluate the clinically curative effect of pregabalin in the treatment of postherpetic neuralgia (PHN). In this study, 40 patients with PHN were selected and rolled randomly into a treatment group and a control group (20 cases in each group). Then, a depth autoencoders algorithm was constructed and applied in the brain resting-state fMRI technology. The brains of 40 patients with PHN treated with pregabalin were scanned, and the time curve extracted from MRI images was convolved by linear drift removal bandpass filtering to reduce low-frequency drift and high-frequency noise, so the low-frequency amplitude was calculated. Based on the low-frequency amplitude method, the calculated low-frequency signal energy was eventually divided by the total power of the entire frequency band to obtain the low-frequency amplitude rate value. The amplitude of low-frequency fluctuation (ALFF) and fractional ALFF (f-ALFF) before and after treatment were compared between the treatment group and the control group, and the visual analog scale (VAS) after treatment was also observed. After 4 weeks of taking the drug, the VAS scores of patients from the treatment group in the first week (6.5 ± 0.8 points), the second week (6.5 ± 0.8 points), the third week (3.1 ± 0.3 points), and the fourth week (2.3 ± 0.4 points) after treatment were lower steeply than the scores before treatment (8.3 ± 1.1 points) ( < 0.05). Resting-state fMRI images showed that the fALFF of the 4 brain areas in the treatment group was higher than that of the control group, mainly including the bilateral frontal lobes, bilateral parietal lobes, left parietal lobes, and right posterior cerebellar lobes. Besides, the f-ALFF of the 6 brain areas in the treatment group was lower than that of the control group, mainly including the right frontal lobe, right parietal lobe, right middle frontal gyrus, precuneus, left frontal lobe, and superior frontal gyrus. In conclusion, the resting-state fMRI technology based on the depth autoencoders algorithm could efficiently display the brain area characteristic changes of patients with PHN before and after treatment, thereby providing a reference for the diagnosis of the patient's condition.

Understanding gender differences in chronic pain (CP) outcome research is essential to optimal treatment delivery. This study explored the associations between gender identity, gender roles, and the number of non-life-threatening pain medication adverse effects reported as severe by people living with CP.

The median effective analgesic concentration (MEAC; EC50 = effective concentration in 50% patients) of ropivacaine in sciatic nerve block guided by ultrasound (US) required for effective postoperative analgesia following arthroscopic anterior cruciate ligament (ACL) reconstruction has not yet been found. This study aimed to determine the effectiveness of MEAC of 20 ml ropivacaine of postoperative anesthesia for patients after ACL reconstruction.

Rheumatoid arthritis is a chronic inflammatory autoimmune disease that can lead to synovial damage, persistent joint pain, and functional disability. Our objective was to evaluate baseline synovial transcriptome from early inflammatory arthritis patients (EIA) and identify pretreatment biomarkers that could potentially provide insights into long-term functional outcomes of rheumatoid arthritis (RA).

Auditory hallucination is usually associated with psychiatric diseases and organic brain illness. It was rarely found as adverse events of antidepressants. Amitriptyline is considered as one of the first line medications for the psychopharmacotherapy of chronic pain including atypical odontalgia (AO) which shows chronic tooth pain without corresponding abnormalities. Anticholinergic adverse events induced by amitriptyline are usually bearable and not critical since the prescription dose is very low for the patients with AO. This is a first case report about the AO patients who showed auditory hallucination by the low dose of amitriptyline. A 43-years-old female, housewife, complained chronic toothache following dental procedures and was diagnosed as AO. Amitriptyline was initially prescribed 25 mg and gradually increased up to 60 mg with the improvement of AO symptoms in 7 months. Although the temporary recurrence was observed following to the retreatment of prosthodontic dental procedures, it improved in a few weeks. Therefore, the dose of amitriptyline was decreased, and the continuation dose was set 30 mg. In 24 months, the AO symptoms were very much improved; however, she reported that she had been heard the voices at midnight for a year. The voices were neighborhoods' and talking about the noise troubles she had claimed before. She had not realized that the voices were auditory hallucination since they were heard only at midnight infrequent and not bothering her daily life. At the time she reported auditory hallucination, she worried whether organic brain diseases are hiding because the frequency of voices was increased and sometimes occurred in daytime. The adverse event of amitriptyline was suspected since she had never had psychotic symptoms before. Amitriptyline was decreased and continued with the dose of 25 mg. Magnetic resonance imaging and psychiatric consultation revealed no abnormality of brain and in psychiatric aspects. After final prosthodontic treatment, the amitriptyline was discontinued in 30 months. Two months after the discontinuation, auditory hallucination was almost disappeared with no recurrence of AO. The present case report suggests that amitriptyline has possibility to induce auditory hallucination even in conventional dose throughout the treatment of chronic pain including AO.

Inflammatory pain is the most common type of pain encountered in clinical practice; however, the currently available treatments are limited by insufficient efficacy and side effects. Therefore, new methods to relieve inflammatory pain targeting new mechanisms are urgently needed. Preclinical investigations have shown that CR (calorie restriction) exerts analgesic effects in neuropathic and cancer pain; however, the effect of CR on chronic inflammatory pain remains unknown. During calorie restriction, autophagy, a lysosome-dependent degradation process, can be activated to support cell survival. In the present study, we investigated the analgesic effects of CR on complete Freund's adjuvant (CFA)-induced inflammatory pain. The accumulation of LC3-II and p62 showed impaired autophagic flux in the ipsilateral spinal cord of mice with CFA-induced inflammatory pain. CR alleviated mechanical allodynia and thermal hyperalgesia and reduced paw edema and pro-inflammatory factors following CFA administration. CR exerted an analgesic effect by restoring autophagic flux in the spinal cord. Regarding the mechanisms underlying the analgesic effects of CR, β-hydroxybutyric acid (BHB) was studied. CR increased BHB levels in the ipsilateral spinal cord. Furthermore, exogenous BHB administration exerted an analgesic effect by restoring autophagic flux in the spinal cords of CFA-induced inflammatory pain mice. Taken together, these results illustrated that CR relieved inflammatory pain by restoring autophagic flux in the spinal cord, while BHB controlled the benefits of CR, suggesting that CR or BHB might be a promising treatment for inflammatory pain.

Reducing postoperative pain immediately after surgery is crucial because severe postoperative pain reduces quality of life and increases the likelihood that patients develop chronic pain. Even though postoperative pain has been widely studied and there are national guidelines for pain management, the postoperative course is differently from one patient to the next. Different postoperative courses could be explained by factors related to the treatment context and the patients. Preoperative emotional states and treatment expectations are significant predictors of postoperative pain. However, the interaction between emotional states and preoperative treatment expectations and their effect on postoperative pain have not yet been studied. The aim of our study was to identify the interaction between emotional states, treatment expectation and early postsurgical acute pain.