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Chronic shoulder pain (CSP) is a common disease causing pain and functional limitation, which is highly prevalent and has substantial negative effects on the quality of life. Acupuncture has gained popularity and has been accepted gradually by many countries because it can successfully treat patients with chronic pain, but the specific brain mechanisms under acupuncture treatment for CSP remain unclear. Therefore, in this study, we aimed to 1) compare the clinical effects between acupuncture at the contralateral and ipsilateral Tiaokou (ST 38) point in patients with unilateral shoulder pain and 2) explore how contralateral- and ipsilateral-acupuncture modulates the regional homogeneity (ReHo) of patients with CSP. This was a pilot functional magnetic resonance imaging (fMRI) trial. Twenty-four patients with CSP were recruited and randomized to the contralateral acupuncture group (contra-group) and the ipsilateral acupuncture group (ipsi-group). All patients completed resting-state functional magnetic resonance imaging (fMRI) scans before and after acupuncture treatment. Shoulder pain intensity (visual analog scale [VAS]) and shoulder joint function (Constant-Murley score [CMS]) were used to evaluate clinical efficiency of treatment. ReHo was used to assess resting-state brain activity. We found clinical improvement in decreasing pain intensity and increasing shoulder function in both groups, and the mean objective shoulder functional improvement in contra-group was better than that in ipsi-group ( = 0.010). Interestingly, the brain mechanism of contra-acupuncture at ST 38 was distinguishable from ipsi-acupuncture regarding ReHo values. Anterior cingulate cortex (ACC) may play a direct role in the regulation of brain by the contralateral acupuncture at ST 38 in patients with shoulder pain. On the contrary, the pathway of brainstem-thalamus-cortex may be likely to work in mechanism of acupuncture at ipsilateral ST 38. Our results indicate that the clinical effects and brain mechanisms are different between the stimulation given at contralateral and ipsilateral acupoints in patients with CSP and imply that the selection of either contralateral or ipsilateral acupuncture therapy to treat some chronic pain conditions is necessary.

Chronic shoulder pain (CSP) is the third most common musculoskeletal problem. For maximum treatment effectiveness, most acupuncturists usually choose acupoint in the nonpainful side, to alleviate pain or improve shoulder function. This method is named opposite needling, which means acupuncture points on the right side are selected for diseases on the left side and vice versa. However, the underlying neural mechanisms related to treatment are currently unclear. The purpose of this study was to determine whether different mechanisms were observed with contralateral and ipsilateral acupuncture at Tiaokou (ST 38) in patients with unilateral CSP. Twenty-four patients were randomized to the contralateral acupuncture group (contra-group) and the ipsilateral acupuncture group (ipsi-group). The patients received one acupuncture treatment session at ST 38 on the nonpainful or painful sides, respectively. Before and after acupuncture treatment, they underwent functional magnetic resonance scanning. The treatment-related changes in degree centrality (DC) maps were compared between the two groups. We found alleviated pain and improved shoulder function in both groups, but better shoulder functional improvement was observed in the contra-group. Increased DC in the anterior/paracingulate cortex and decreased DC in bilateral postcentral gyri were found in the contra-group, while decreased DC in the bilateral cerebellum and right thalamus was observed in the ipsi-group. Furthermore, the DC value in the bilateral anterior/paracingulate cortex was positively correlated with the treatment-related change in the Constant–Murley score. The current study reveals different changes of DC patterns after acupuncture at contralateral or ipsilateral ST 38 in patients with CSP. Our findings support the hypothesis of acupoint specificity and provide the evidence for acupuncturists to select acupoints for CSP.

Chronic shoulder pain (CSP) is a common health problem associated with shoulder dysfunction and persistent pain for many different reasons. However, the studies of pain-related functional brain regions in CSP have been poorly investigated. The main purpose of our study was to observe whether there are abnormal functional changes in brain regions in patients with CSP by using functional magnetic resonance imaging (fMRI). We compared the differences of brain regions between 37 patients with CSP and 24 healthy controls (HC) using regional homogeneity (ReHo) method. The patients with chronic shoulder pain and healthy controls were matched for age and gender. Brain regions which had abnormal ReHo values were defined as seed region of interests. The approach of seed-based functional connectivity (FC) was further performed to analyze the connectivity between the seeds and whole brain regions. The relationship between abnormal regions and current clinical pain was also evaluated. Compared to healthy controls, the patients with CSP showed increased ReHo values in the left middle temporal gyrus and decreased ReHo values in right orbitofrontal cortex (OFC). The seed-based analyses demonstrated decreased connectivity between the right OFC and right rectus, superior frontal gyrus in patients with chronic shoulder pain. However, a correlation between ReHo values and clinical characteristics in CSP patients was not found. The observed results indicate that there are abnormal ReHo values in brain regions of patients with CSP, especially in the OFC and middle temporal gyrus. Our findings demonstrate that the experience of CSP patients may be mainly associated with cognitive-affective pain processing, rather than nociception.

Although deqi, the phenomenon whereby excitation of Qi in the meridians occurs with needling, is critical to the practice of acupuncture and its efficacy, it is poorly understood. So we investigate the influence of the deqi sensation on the analgesic effects of acupuncture in patients who were enrolled in a randomised controlled trial for the treatment of patients with primary dysmenorrhea, a painful and common condition, and cold and dampness stagnation. Two groups were assessed: a deqi group (undergoing deep needling with thick needles and manipulation, n=17) and a non-deqi group (undergoing shallow needling with thin needles and no manipulation, n=51). The Sanyinjiao (SP6) was needled for 30 min in both groups. Pain scores at baseline, upon needle removal, and at 10, 20, and 30 min after needle removal were evaluated by the Visual Analogue Scale for pain. The deqi sensation was evaluated by the Acupuncture Deqi Clinical Assessment Scale. Patients who experienced a genuine deqi sensation (n=39) were selected for further analysis. Compared with patients in the non-deqi group who experienced deqi (n=25), patients who self-reported deqi in the deqi group (n=14) felt a stronger deqi sensation, experienced soreness and fullness more frequently, felt a greater intensity of soreness, fullness, electric sensation, spreading, and radiating, and experienced larger spreading distances. In those who experienced the deqi sensation in the deqi group, the intensity of the sensation, as well as their degree of soreness and fullness, was negatively correlated with pain reduction. In patients who experienced the deqi sensation in the non-deqi group, deqi intensity was positively correlated with pain reduction, while soreness was negatively correlated with pain reduction. The distance of spreading was not correlated with pain reduction in either group. We found, in SP6 needling of patients with primary dysmenorrhea with cold and dampness stagnation, that a moderate deqi response predicted a prolonged analgesic effect better than a strong deqi response.

IntroductionSubjective cognitive decline (SCD) refers to individuals’ perceived decline in memory and/or other cognitive abilities relative to their previous level of performance, while objective neuropsychological deficits are not observed. SCD may represent a preclinical phase of Alzheimer’s disease. At this very early stage of decline, intervention could slow the rate of incipient decline to prolong and preserve cognitive and functional abilities. However, there is no effective treatment recommended for individuals with SCD. Acupuncture, as a non-pharmacological intervention, has been widely employed for patients with cognitive disorders.Methods and analysisThe proposed study is a randomised, assessor-blinded and placebo-controlled study that investigates the efficacy and mechanism of acupuncture in SCD. Sixty patients with SCD will be randomly allocated either into an acupuncture group or a sham acupuncture group. They will receive 24 sessions of real acupuncture treatment or identical treatment sessions using a placebo needle. Global cognitive changes based on a multidomain neuropsychological test battery will be evaluated to detect the clinical efficacy of acupuncture treatment at baseline and end of treatment. MRI scans will be used to explore acupuncture-related neuroplasticity changes. Correlation analyses will be performed to investigate the relationships between the changes in brain function and symptom improvement.Ethics and disseminationThe trial was approved by the research ethics committee. The results of the study will be published in a peer-reviewed academic journal and will also be disseminated electronically through conference presentations.Trial registration numberNCT03444896.

Colorectal cancer (CRC) is the third most diagnosed cancer worldwide. Progesterone is associated with a decreased risk of CRC and leads to a favourable prognosis. However, the specific mechanism by which progesterone suppresses malignant progression remains to be elucidated. In the present study, the level of progesterone was first analysed in 77 patients with CRC, and immunohistochemistry was performed to detect the expression of progesterone receptor (PGR) in the paired specimens. The correlations between progesterone, PGR and CRC prognosis were assessed. A Cell Counting Kit-8 assay was then used to detect proliferation of the CRC cells. Flow cytometry was performed to estimate apoptosis and to evaluate the cycle of the CRC cells. A xenograft tumour model was established in nude mice to assess the role of progesterone in tumour growth. Finally, a PCR microarray was used to screen differentially expressed genes to further interpret the mechanism by which progesterone inhibits the malignant progression of CRC. It was found that low expression of progesterone and PGR were significantly associated with poor prognosis of CRC. In addition, progesterone suppressed CRC cell proliferation by arresting the cell cycle and inducing apoptosis in vitro. Moreover, the inhibitory role of progesterone in tumour growth was verified in vivo. Further investigation showed that the level of growth arrest and DNA damage-inducible protein α (GADD45α) was up-regulated by progesterone, and this was followed by the activation of the JNK pathway. Progesterone increased the activity of the JNK pathway via GADD45α to inhibit proliferation by arresting the cell cycle and inducing apoptosis, thereby suppressing the malignant progression of CRC. Therefore, it can be concluded that progesterone and PGR might act as inhibiting factors for poor prognosis of CRC.

Color serves as a crucial visual signal for attracting pollinating insects and directly affects the fruit set rate in woody crops. This study investigated the molecular mechanisms underlying flower color formation in macadamia. The results demonstrated that darker flower colors were associated with higher fruit set rates: the rates for purple, pink, pinkish-white, and white flowers were 2.78, 1.99, 1.35, and 1.31, respectively. High-throughput sequencing identified 1359 differentially accumulated metabolites, including benzoic acid, 4-hydroxybenzaldehyde, and isorhamnetin. Transcriptional regulators such as ERF, MYB, and WRKY were significantly up-regulated in darker flowers. KEGG analysis revealed two key metabolic pathways, in which genes including HCT (shikimate hydroxycinnamoyl transferase) and F3GalTase (flavonol 3-O-galactosyltransferase), as well as related metabolites such as p-coumaric acid, chlorogenic acid, and myricetin, showed higher expression levels in darker flowers. Anthocyanin content was highest in pink and pinkish-purple varieties (462.79 and 446.35 μg/g, respectively), and lower in white and light pink varieties (140.52 and 167.97 μg/g). In conclusion, flower color intensity is positively correlated with both fruit set rate and anthocyanin content. Genes involved in the flavonoid and phenylpropanoid pathways, along with transcription factors such as WRKY and MYB, collectively regulate flower color formation. This study provides a theoretical basis for macadamia flower color breeding.

Chronic stress exposure is a potent risk factor for anxiety, disrupting adaptive responses and increasing vulnerability. Astrocytes, as essential regulators of synaptic function and neuroimmune homeostasis, are implicated in mood regulation and neuropsychiatric pathogenesis. However, the precise molecular mechanisms of astrocytes involved in stress-induced anxiety remain poorly understood. In this study, we reveal a pivotal role of astrocytic brain-derived neurotrophic factor (BDNF) in modulating anxiety sensitivity through coordinated regulation with hippocampal CA1 neurons. Chronic restraint stress induces anxiety-like behaviors and disrupts presynaptic glutamatergic transmission in hippocampal CA1 neurons, with astrocytes potentially playing a central regulatory role in a Ca2+-dependent manner. Pharmacological manipulation confirms the involvement of BDNF/TrkB signaling, while knockdown of astrocytic BDNF further impairs synaptic function and exacerbates stress-induced anxiety. Transcriptomic analysis suggests interferon-related signaling pathways as potential downstream effectors, amplifying anxiety sensitivity through altered astrocytic activation and neuroimmune dynamics. Our study provides critical mechanistic insights into astrocytic regulation of anxiety sensitivity and highlights astrocytic BDNF as a promising therapeutic target for stress-related anxiety disorders.

Background The deafness-associated gene mutation profile varies greatly among regions and races. Due to the multi-ethnic coalition of over one thousand years, non-syndromic deafness (NSD) patients of Uyghur ethnicity may exhibit a unique deafness-associated gene mutation spectrum as compared to Han Chinese deaf population. Methods In order to characterize nine loci of four deafness-associated genes of Uyghur NSD patients in comparison with Chinese Han deaf population, NSD patients (n = 350) were enrolled, including Uyghur (n = 199) and Han Chinese (n = 151). Following the history taking, blood samples were collected for DNA extraction. DNA microarray was performed on nine loci of four deafness-associated genes, including 35delG, 176-191del16, 235delC, 299-300delAT, 538C > T, 1555A > G, 1494C > T, 2168A > G, and IVS7-2A > G. The samples that showed the absence of both wild and mutant probe signals were tested for further DNA sequencing analysis. Results The mutations in the nine loci of prevalent deafness-associated genes were detected in 13.06% of Uyghur NSD patients and 32.45% of Han Chinese patients ( P < 0.05), respectively. GJB2 mutation was detected in 9.05% of Uyghur patients and 16.56% of Han Chinese patients ( P > 0.05), respectively. 235delC was the hotspot mutation region in NSD patients of the two ethnicities, whereas 35delG was the mutation hotspot in Uyghur patients. 187delG mutation was detected for the first time in Uyghur NSD patients and considered as an unreported pathological variant of GJB2. SLC26A4 mutation was found in 2.01% of Uyghur patients and 14.57% of Han Chinese patients ( P < 0.05), respectively. The frequencies of mtDNA 12S rRNA mutation in Uyghur and Han Chinese patients were 2.01% and 2.65% ( P > 0.05), respectively. The NSD patients exhibited a low frequency of GJB3 mutation regardless of ethnicity. Conclusion Prevalent deafness-associated gene mutations in the nine loci studied were less frequently detected in Uyghur NSD patients than in Han Chinese patients. GJB2 was the most common mutant gene in the two ethnicities, whilst the two ethnicities differed substantially in hotspot mutations. A low-frequency SLC26A4 mutation was detected in Uyghur NSD patients. Uyghur NSD patients differed significantly from Han Chinese patients in gene mutation profile.

Colorectal cancer (CRC) is the third most diagnosed cancer worldwide. Progesterone is associated with a decreased risk of CRC and leads to a favourable prognosis. However, the specific mechanism by which progesterone suppresses malignant progression remains to be elucidated. In the present study, the level of progesterone was first analysed in 77 patients with CRC, and immunohistochemistry was performed to detect the expression of progesterone receptor (PGR) in the paired specimens. The correlations between progesterone, PGR and CRC prognosis were assessed. A Cell Counting Kit-8 assay was then used to detect proliferation of the CRC cells. Flow cytometry was performed to estimate apoptosis and to evaluate the cycle of the CRC cells. A xenograft tumour model was established in nude mice to assess the role of progesterone in tumour growth. Finally, a PCR microarray was used to screen differentially expressed genes to further interpret the mechanism by which progesterone inhibits the malignant progression of CRC. It was found that low expression of progesterone and PGR were significantly associated with poor prognosis of CRC. In addition, progesterone suppressed CRC cell proliferation by arresting the cell cycle and inducing apoptosis in vitro. Moreover, the inhibitory role of progesterone in tumour growth was verified in vivo. Further investigation showed that the level of growth arrest and DNA damage-inducible protein [alpha] (GADD45[alpha]) was up-regulated by progesterone, and this was followed by the activation of the JNK pathway. Progesterone increased the activity of the JNK pathway via GADD45[alpha] to inhibit proliferation by arresting the cell cycle and inducing apoptosis, thereby suppressing the malignant progression of CRC. Therefore, it can be concluded that progesterone and PGR might act as inhibiting factors for poor prognosis of CRC. Key words: progesterone, colorectal carcinoma, proliferation, c-Jun N-terminal kinases, GADD45[alpha]