Insights into mechanism and modelling of dynamic moisture sorption in dual-porous insulation materials with micro- and nano-scale pores.

HYPOTHESIS: Understanding moisture sorption in porous insulation materials is challenging due to the influence of multiscale pore structures on phase behavior and transport properties. Dynamic moisture sorption in dual-porous materials is likely co-determined by interior micro- and nano-scale pores, and an accurate physical model for predicting moisture evolution can be developed by clarifying the sorption mechanisms. EXPERIMENTS: Moisture behavior during the dynamic sorption of dual-porous insulation material is measured by low-field nuclear magnetic resonance (NMR) experiments. The contributions of micro- and nano-scale pores to the adsorbed moisture are differentiated using NMR relaxometry, and the evolution of moisture morphology is quantitatively analyzed. FINDINGS: Analysis of T2 evolution reveals that the moisture in nano-scale pores alters from adsorption layers to liquid with increasing relative humidity (RH), while minimal sorption occurs in micro-scale pores. Moisture is mainly transferred as vapor molecules at low RH levels, with the dynamic sorption enhanced by molecular diffusion in micro-scale pores. Capillary flow in nano-scale pores dominates moisture transport when RH rises above a threshold, leading to a significant increase in apparent moisture diffusivity. According to the elucidated mechanism, a physical model is further developed to predict moisture sorption inside dual-porous insulation materials, and it may serve as a basis for evaluating and optimizing the performance of dual-porous systems in different environments.

Distillers' grains organic fertilizer alters soil bacterial composition and co-occurrence patterns in a tobacco-growing field.

In recent years, numerous studies have indicated that the combination of organic and inorganic fertilizers can effectively improve soil fertility and soil productivity. Distillers' grain (DG), the primary by-product of Chinese spirits production, has a high utilization value for producing organic fertilizer. We investigated the effects of distillers' grain organic fertilizer (DGOF) on soil chemical properties and microbial community composition, as well as the effects of chemical properties on the abundance of keystone species. The results indicated that the application of DGOF significantly increased tobacco yield by 14.8% and mainly affected the composition rather than the alpha diversity of the bacterial community. Ten amplicon sequence variants (ASVs) were identified as keystone species in the bacterial communities, and most of their relative abundance was influenced by the DGOF addition through affecting soil chemical properties. Our results elucidated the alterations in soil chemical properties and microbial community composition resulting from DGOF application, which is of great importance to better understand the relationship between DGOF and soil microorganisms in the flue-cured tobacco cultivation field.

TRIM21-mediated Sohlh2 ubiquitination suppresses M2 macrophage polarization and progression of triple-negative breast cancer.

Lung metastasis is the major cause of death in patients with triple-negative breast cancer (TNBC). Tumor-associated macrophages (TAMs) represent the M2-like phenotype with potent immunosuppressive activity, and play a pro-tumor role in TNBC lung metastasis. Sohlh2 belongs to the basic helix-loop-helix transcription factor family. However, its role in macrophages polarization remains unknown, especially in TNBC progression. Here we demonstrated that Sohlh2 overexpression promoted M2 macrophage polarization. Moreover, high expression of Sohlh2 in M2-like macrophage enhanced TNBC cell growth, migration and lung metastasis in vivo and in vitro. Mechanistically, we revealed that Sohlh2 functioned through up-regulating LXRα, ABCA1, ABCG1 expression and disturbing the lipid homeostasis on the membrane of macrophages. Sohlh2 could directly bind to the promoter of LXRα and promote its transcription activity. E3 ubiquitin ligase TRIM21 promoted Sohlh2 ubiquitination and degradation, and suppressed M2 macrophage polarization and TNBC progression. Collectively, our findings suggested that Sohlh2 in macrophage could be a novel therapeutic target for TNBC metastatic treatment.

The organum vasculosum of the lamina terminalis and subfornical organ: regulation of thirst.

Thirst and water intake are regulated by the organum vasculosum of the lamina terminalis (OVLT) and subfornical organ (SFO), located around the anteroventral third ventricle, which plays a critical role in sensing dynamic changes in sodium and water balance in body fluids. Meanwhile, neural circuits involved in thirst regulation and intracellular mechanisms underlying the osmosensitive function of OVLT and SFO are reviewed. Having specific Nax channels in the glial cells and other channels (such as TRPV1 and TRPV4), the OVLT and SFO detect the increased Na+ concentration or hyperosmolality to orchestrate osmotic stimuli to the insular and cingulate cortex to evoke thirst. Meanwhile, the osmotic stimuli are relayed to the supraoptic nucleus (SON) and paraventricular nucleus of the hypothalamus (PVN) via direct neural projections or the median preoptic nucleus (MnPO) to promote the secretion of vasopressin which plays a vital role in the regulation of body fluid homeostasis. Importantly, the vital role of OVLT in sleep-arousal regulation is discussed, where vasopressin is proposed as the mediator in the regulation when OVLT senses osmotic stimuli.

Activation of Kv7 channels normalizes hyperactivity of the VTA-NAcLat circuit and attenuates methamphetamine-induced conditioned place preference and sensitization in mice.

The brain circuit projecting from the ventral tegmental area (VTA) to the nucleus accumbens lateral shell (NAcLat) has a key role in methamphetamine (MA) addiction. As different dopamine (DA) neuron subpopulations in the VTA participate in different neuronal circuits, it is a challenge to isolate these DA neuron subtypes. Using retrograde tracing and Patch-seq, we isolated DA neurons in the VTA-NAcLat circuit in MA-treated mice and performed gene expression profiling. Among the differentially expressed genes, KCNQ genes were dramatically downregulated. KCNQ genes encode Kv7 channel proteins, which modulate neuronal excitability. Injection of both the Kv7.2/3 agonist ICA069673 and the Kv7.4 agonist fasudil into the VTA attenuated MA-induced conditioned place preference and locomotor sensitization and decreased neuronal excitability. Increasing Kv7.2/3 activity decreased neural oscillations, synaptic plasticity and DA release in the VTA-NacLat circuit in MA-treated mice. Furthermore, overexpression of only Kv7.3 channels in the VTA-NacLat circuit was sufficient to attenuate MA-induced reward behavior and decrease VTA neuron excitability. Activation of Kv7 channels in the VTA may become a novel treatment strategy for MA abuse.

Dopamine D1 receptor in orbitofrontal cortex to dorsal striatum pathway modulates methamphetamine addiction.

The orbitofrontal cortex (OFC)-dorsal striatum (DS) is an important neural circuit that contributes to addictive behavior, including compulsive reinforcement, yet the specific types of neurons that play a major role still need to be further elucidated. Here, we used a place conditioning paradigm to measure the conditioned responses to methamphetamine (MA). The results demonstrated that MA increases the expression of c-Fos, synaptic plasticity in OFC and DS. Patch-clamp recording showed that MA activated projection neurons from the OFC to the DS, and chemogenetic manipulation of neuronal activity in OFC-DS projection neurons affects conditioned place preference (CPP) scores. And the combined patch-electrochemical technique was used to detect the DA release in OFC, the data indicated that the DA release was increased in MA group. Additionally, SCH23390, a D1R antagonist, was used to verify the function of D1R projection neurons, showing that SCH23390 reversed MA addiction-like behavior. Collectively, these findings provide evidence for the D1R neuron is sufficient to regulate MA addiction in the OFC-DS pathway, and the study provides new insight into the underlying mechanism of pathological changes in MA addiction.

Temporal transcriptome analysis reveals several key pathways involve in cadmium stress response in Nicotiana tabacum L.

Tobacco has a strong cadmium (Cd) enrichment capacity, meaning that it can absorb large quantities from the environment, but too much Cd will cause damage to the plant. It is not yet clear how the plant can dynamically respond to Cd stress. Here, we performed a temporal transcriptome analysis of tobacco roots under Cd treatment from 0 to 48 h. The number of differentially expressed genes (DEGs) was found to change significantly at 3 h of Cd treatment, which we used to define the early and middle stages of the Cd stress response. The gene ontology (GO) term analysis indicates that genes related to photosynthesis and fatty acid synthesis were enriched during the early phases of the stress response, and in the middle phase biological process related to metal ion transport, DNA damage repair, and metabolism were enriched. It was also found that plants use precursor mRNA (pre-mRNA) processes to first resist Cd stress, and with the increasing of Cd treatment time, the overlapped genes number of DEGs and DAS increased, suggesting the transcriptional levels and post-transcriptional level might influence each other. This study allowed us to better understand how plants dynamically respond to cadmium stress at the transcriptional and post-transcriptional levels and provided a reference for the screening of Cd-tolerant genes in the future.

Systematic pan-cancer analysis identifies transmembrane protein 158 as a potential therapeutic, prognostic and immunological biomarker.

The purpose of this study was to investigate the expression significance, predictive value, immunologic function, and biological role of transmembrane protein 158 (TMEM158) in the development of pan-cancer. To achieve this, we utilized data from multiple databases, including TCGA, GTEx, GEPIA, and TIMER, to collect gene transcriptome, patient prognosis, and tumor immune data. We evaluated the association of TMEM158 with patient prognosis, tumor mutational burden (TMB), and microsatellite instability (MSI) in pan-cancer samples. We performed immune checkpoint gene co-expression analysis and gene set enrichment analysis (GSEA) to better understand the immunologic function of TMEM158. Our findings revealed that TMEM158 was significantly differentially expressed between most types of cancer tissues and their adjacent normal tissues and was associated with prognosis. Moreover, TMEM158 was significantly correlated with TMB, MSI, and tumor immune cell infiltration in multiple cancers. Co-expression analysis of immune checkpoint genes showed that TMEM158 was related to the expression of several common immune checkpoint genes, especially CTLA4 and LAG3. Gene enrichment analysis further revealed that TMEM158 was involved in multiple immune-related biological pathways in pan-cancer. Overall, this systematic pan-cancer analysis suggests that TMEM158 is generally highly expressed in various cancer tissues and is closely related to patient prognosis and survival across multiple cancer types. TMEM158 may serve as a significant predictor of cancer prognosis and modulate immune responses to various types of cancer.

Exploring the role and mechanism of gut microbiota in methamphetamine addiction using antibiotic treatment followed by fecal microbiota transplantation.

Recently, the role of the gut microbiota in the context of drug addiction has attracted the attention of researchers; however, the specific effects and underlying mechanisms require further exploration. To accomplish this, C57BL/6 mice were firstly treated with methamphetamine (MA). Conditioned place preference (CPP) behavior changes, gut permeability and function, microglial activation, and inflammatory cytokine expression were systematically analyzed in antibiotics-treated mice with microbiota depletion and in fecal microbiota transplantation mice with microbiota reconstitution. MA treatment altered microbiota composition and caused gut dysbiosis. Depletion of gut microbiota with antibiotics inhibited MA-induced CPP formation, and fecal microbiota transplantation reversed this inhibition. Mechanistic analyses indicated that antibiotic treatment decreased gut permeability and neuroinflammation, while fecal microbiota transplantation offset the impact of antibiotic treatment. Additionally, MA-induced microglial activation was suppressed by antibiotics but restored by microbiota transplantation, and this correlated well with the CPP score. Compared to antibiotic treatment, microbiota transplantation significantly increased 5-HT4 receptor expression in both the nucleus accumbens and the hippocampus. Furthermore, when fecal microbiota from healthy mice was transplanted into MA-treated mice, the CPP scores decreased. Our results provide a novel avenue for understanding MA addiction and suggest a potential future intervention strategy.

Systematic analysis of the pectin methylesterase gene family in Nicotiana tabacum and reveal their multiple roles in plant development and abiotic stresses.

The pectin methylesterases (PMEs) play multiple roles in regulating plant development and responses to various stresses. In our study, a total of 121 PME genes were identified in the tobacco genome, which were clustered into two groups based on phylogenetic analysis together with Arabidopsis members. The investigations of gene structure and conserved motif indicated that exon/intron and motif organizations were relatively conserved in each group. Additionally, several stress-related elements were identified in the promoter region of these genes. The survey of duplication events revealed that segmental duplications were critical to the expansion of the PME gene family in tobacco. The expression profiles analysis revealed that these genes were expressed in various tissues and could be induced by diverse abiotic stresses. Notably, NtPME029 and NtPME043, were identified as homologues with AtPME3 and AtPME31, respectively. Furthermore, NtPME029 was highly expressed in roots and the over-expression of the NtPME029 gene could promote the development of roots. While NtPME043 could be induced by salt and ABA treatments, and the over-expression of the NtPME043 gene could significantly enhance the salt-stress tolerance in tobacco. Overall, these findings may shed light on the biological and functional characterization of NtPME genes in tobacco.

Astrocyte-derived lactate/NADH alters methamphetamine-induced memory consolidation and retrieval by regulating neuronal synaptic plasticity in the dorsal hippocampus.

Drug memory is associated with drug-taking experience and environmental cues, which mainly contribute to addiction. Recent studies report that glycogenolysis-derived lactate from astrocyte transport to neurons is necessary for long-term potentiation and memory formation instead of its function as an energy substrate. However, the role of astrocyte-neuron lactate transfer in neuronal plasticity and methamphetamine (METH)-induced addiction memory consolidation and retrieval, especially the underlying mechanisms, are not clear. C57BL/6 J mice trained for METH-induced conditioned place preference (CPP) were stereotaxically injected with the glycogen phosphorylase inhibitor 1,4-dideoxy-1,4-imino-D-arabinitol (DAB) into the dorsal hippocampus (dHPC) 15 min before training. The CPP score was recorded, and neuronal synaptic plasticity was detected with Golgi staining. The neuronal Ca2+ levels were examined using AAV-GCaMP6 injection. Moreover, monocarboxylate transporters (MCT1, MCT2, MCT4) were inhibited with oligodeoxynucleotides in the dHPC to further prove the METH appetitive memory changes. The data showed that inhibiting lactate transport by microinjection with DAB or monocarboxylate transporter oligodeoxynucleotides in the dHPC completely destroyed METH-induced CPP, reduced Npas4 and other plasticity-associated gene expression and decreased neuronal Ca2+ levels and neuronal arborization and spine density, all of which were fully rescued by L-lactate coadministration except for MCT2-ODN administration. Furthermore, the downstream signaling molecule NADH could mimic lactate's effects and trigger METH CPP by influencing the redox state of neurons and regulating NMDA receptor activity. Collectively, these findings indicate that astrocyte-neuron lactate transfer is crucial for METH-induced memory consolidation and retrieval.

Celastrol attenuates 6-hydroxydopamine-induced neurotoxicity by regulating the miR-146a/PI3K/Akt/mTOR signaling pathways in differentiated rat pheochromocytoma cells.

BACKGROUND: Parkinson's disease (PD) is a neurological disorder. Recently, celastrol (Cel) has been reported to have neuroprotective properties. We investigated the protective effects of Cel on PD in a cell model with 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in PC12 cells and further addressed the underlying protective mechanisms of Cel. METHODS: PC12 cells were treated with 6-OHDA, and Cel was added to the medium at various concentrations. The CCK-8 assay, Hoechst/PI staining, and flow cytometry analysis were performed to detect cellular viability and apoptosis. Mitochondrial membrane potential (MMP) was examined by JC-1 staining. ROS level was quantified by ROS staining. The effects of Cel on the expression of miR-146a and PI3K/Akt/mTOR pathway were then clarified using real-time PCR and Western blotting. Moreover, a miR-146a mimic was synthesized and transfected into PC12 cells to further determine the mechanisms of Cel's neuronal protection against 6-OHDA-induced neurotoxicity. RESULTS: Cel greatly improved cell viability and lessened apoptosis. Flow cytometry showed that Cel especially inhibited early apoptosis. Cel also obviously restored the MMP and decreased ROS level destroyed by 6-OHDA. Moreover, 6-OHDA increased the expression of miR-146a and decreased pAkt/mTOR protein levels, whereas Cel reversed these changes. In particular, miR-146a targeted and inhibited the expression of PI3K, an upstream molecule of Akt/mTOR. Transfection of 6-OHDA-treated neurons with miR-146a mimic notably attenuated Cel's protective effects. LIMITATIONS: There were no animal experiments in our study. CONCLUSIONS: Cel exerts neuroprotective activity against 6-OHDA-caused neurotoxicity by regulating miR-146a/PI3K/Akt/mTOR pathway, which provides a potential application of Cel for treating neurodegenerative diseases.

Gut microbiota dysbiosis: The potential mechanisms by which alcohol disrupts gut and brain functions.

Alcohol use disorder (AUD) is a high-risk psychiatric disorder and a key cause of death and disability in individuals. In the development of AUD, there is a connection known as the microbiota-gut-brain axis, where alcohol use disrupts the gut barrier, resulting in changes in intestinal permeability as well as the gut microbiota composition, which in turn impairs brain function and worsens the patient's mental status and gut activity. Potential mechanisms are explored by which alcohol alters gut and brain function through the effects of the gut microbiota and their metabolites on immune and inflammatory pathways. Alcohol and microbiota dysregulation regulating neurotransmitter release, including DA, 5-HT, and GABA, are also discussed. Thus, based on the above discussion, it is possible to speculate on the gut microbiota as an underlying target for the treatment of diseases associated with alcohol addiction. This review will focus more on how alcohol and gut microbiota affect the structure and function of the gut and brain, specific changes in the composition of the gut microbiota, and some measures to mitigate the changes caused by alcohol exposure. This leads to a potential intervention for alcohol addiction through fecal microbiota transplantation, which could normalize the disruption of gut microbiota after AUD.

Paliperidone alleviates MK-801-induced damage to prefrontal cortical neurons via the PP2A/PTEN pathway.

BACKGROUND: The putative mechanisms underlying the efficacy of the US Food and Drug Administration-approved antipsychotic drug paliperidone for the treatment of schizophrenia deserve additional investigation, which is the aim of the present animal study. METHODS: The behavioral activities of mice were recorded in the open field test and light-dark box test. The effects of paliperidone on MK-801-induced neuronal damage in the prefrontal cortex were tested by flow cytometry, TUNEL staining assays, and ROS staining assays. The neuroprotective effects of paliperidone on neural dendrites and synapses were evaluated using Golgi staining and Sholl analysis. An adenovirus vector containing a Ca2+ indicator was used to monitor the calcium ion concentration in the prefrontal cortex. The expression levels of protein phosphatase 2A (PP2A) and phosphatase and tensin homolog (PTEN) were investigated using Western blotting. RESULTS: The data showed that MK-801 caused stereotyped behavior in mice and induced synaptic damage and dendritic spine impairment compared with the control, whereas paliperidone ameliorated these changes. Moreover, paliperidone reversed MK-801-induced decreases in PP2A and PTEN levels in prefrontal cortical neurons. Furthermore, in primary cultured cortical neurons and HT-22 cells, paliperidone inhibited cell apoptosis caused by MK-801. In particular, pretreatment with the PP2A inhibitor LB-100 significantly restrained the protective effects of paliperidone on MK-801-treated neurons and on locomotor activity and stereotypical behavior of mice. LIMITATIONS: Whether other proteins are involved in this pathway and how the pathway works have not been revealed. CONCLUSION: Our data show that paliperidone alleviates neuronal damage induced by MK-801 via the PP2A/PTEN pathway.

Inactivation of the Lateral Hypothalamus Attenuates Methamphetamine-Induced Conditioned Place Preference through Regulation of Kcnq3 Expression.

Repeated administration of methylamphetamine (MA) induces MA addiction, which is featured by awfully unpleasant physical and emotional experiences after drug use is terminated. Neurophysiological studies show that the lateral hypothalamus (LH) is involved in reward development and addictive behaviors. Here, we show that repeated administration of MA activates the expression of c-Fos in LH neurons responding to conditioned place preference (CPP). Chemogenetic inhibition of the LH can disrupt the addiction behavior, demonstrating that the LH plays an important role in MA-induced reward processing. Critically, MA remodels the neurons of LH synaptic plasticity, increases intracellular calcium level, and enhances spontaneous current and evoked potentials of neurons compared to the saline group. Furthermore, overexpression of the potassium voltage-gated channel subfamily Q member 3 (Kcnq3) expression can reverse the CPP score and alleviate the occurrence of addictive behaviors. Together, these results unravel a new neurobiological mechanism underlying the MA-induced addiction in the lateral hypothalamus, which could pave the way toward new and effective interventions for this addiction disease.

NtNAC053, A Novel NAC Transcription Factor, Confers Drought and Salt Tolerances in Tobacco.

The NAC (NAM, ATAF1/2, and CUC2) family acts as one of the largest families of the transcription factor in the plant kingdom and was revealed to function as the important regulators in various environmental stresses. However, a few studies were reported about the biofunctions of the NAC transcription factor in tobacco. In the current study, we characterized a novel NAC transcription factor encoding the gene NtNAC053 in tobacco, which was significantly up-regulated when exposed to salt and drought treatments. The results of cis-acting elements analysis suggested that the promoter region of NtNAC053 gene possesses a number of stress-responsive elements, and this gene could be induced by exogenous abscisic acid (ABA) treatment. Moreover, the NtNAC053-GFP fusion protein was localized in the cell nucleus and possessed a transactivation domain in its C-terminal, implying that NtNAC053 may undertake as a transcriptional activator in tobacco. Notably, the overexpression of NtNAC053 in tobacco resulted in hypersensitivity to ABA treatment. Furthermore, these overexpression lines showed significantly enhanced tolerances to drought and salt stresses. Under salt and drought stresses, these overexpression lines possessed higher superoxide dismutase (SOD), catalase (CAT), and peroxidase (POD) activities. Interestingly, the expressions of putative stress-related genes, including NtCOR15A, NtRAB18, NtDREB1A, NtERF5, NtKAT2, and NtERD11, were up-regulated in these overexpression lines when subjected to salt and drought stresses. The clues provided in our study suggested that the NtNAC053 gene encodes a novel NAC transcription factor and could confer the drought and salt stress tolerances by inspiring the downstream stress-responsive genes and antioxidant system in tobacco.

Diagnostic Value of Model-Based Iterative Algorithm in Tuberculous Pleural Effusion.

Although there are several diagnostic modalities for tuberculous pleurisy, there is still a lack of easy, cost-effective, and rapid methods for confirming the diagnosis. In order to facilitate clinicians to diagnose patients with tuberculous pleurisy at an early stage, help patients to obtain treatment early, and reduce lung damage, it is hoped that new techniques will be available in the future to help diagnose tuberculous pleurisy rapidly in the clinic. To this end, this paper investigates the problem of bidirectional consistency based on event-triggered iterative learning. Firstly, a dynamic linearized data model of TB pleurisy intelligent system is established using compact-form dynamic linearization method, and a parameter estimation algorithm of TB pleurisy data model is proposed; then, based on this data model, an output observer and a dead zone controller are designed, and an event-triggered distributed model-free iterative learning bidirectional consistency control strategy is constructed by combining with signal graph theory. In this paper, 112 patients with pleural effusion were collected, including 76 patients with confirmed or clinically diagnosed tuberculous pleural effusion and 36 patients with nontuberculous pleural effusion. Pleural effusion T-SPOT.TB, blood T-SPOT.TB, pleural effusion Xpert MTB/RIF, and pleural effusion adenosine deaminase (ADA) tests were performed before treatment in the included patients. The sensitivity of pleural effusion T-SPOT.TB was higher than that of peripheral blood T-SPOT.TB (76.32%, 58/76), pleural effusion Xpert MTB/RIF (65.79%, 50/76), and pleural effusion ADA (28.95%, 22/76); the differences were statistically significant (x 2 = 14.74, 25.22, and 76.45, P < 0.01). The specificity of the Xpert MTB/RIF test for pleural effusion (100%, 36/36) was higher than that for pleural effusion T-SPOT.TB (77.78%, 28/36), peripheral blood T-SPOT.TB, and pleural effusion T-SPOT.TB. The sensitivity of the combined Xpert MTB/RIF test (64.47%, 49/76) was lower than that of the pleural effusion T-SPOT.TB alone (97.37%, 74/76).

Melatonin for premenstrual syndrome: A potential remedy but not ready.

Premenstrual syndrome (PMS), a recurrent and moderate disorder that occurs during the luteal phase of the menstrual cycle and quickly resolves after menstruation, is characterized by somatic and emotional discomfort that can be severe enough to impair daily activities. Current therapeutic drugs for PMS such as selective serotonin reuptake inhibitors are not very satisfying. As a critical pineal hormone, melatonin has increasingly been suggested to modulate PMS symptoms. In this review, we update the latest progress on PMS-induced sleep disturbance, mood changes, and cognitive impairment and provide possible pathways by which melatonin attenuates these symptoms. Moreover, we focus on the role of melatonin in PMS molecular mechanisms. Herein, we show that melatonin can regulate ovarian estrogen and progesterone, of which cyclic fluctuations contribute to PMS pathogenesis. Melatonin also modulates gamma-aminobutyric acid and the brain-derived neurotrophic factor system in PMS. Interpreting the role of melatonin in PMS is not only informative to clarify PMS etiology but also instructive to melatonin and its receptor agonist application to promote female health. As a safe interaction, melatonin treatment can be effective in alleviating symptoms of PMS. However, symptoms such as sleep disturbance, depressive mood, cognitive impairment are not specific and can be easily misdiagnosed. Connections between melatonin receptor, ovarian steroid dysfunction, and PMS are not consistent among past studies. Before final conclusions are drawn, more well-organized and rigorous studies are recommended.

Acupuncture therapy for Alzheimer's disease: The effectiveness and potential mechanisms.

Alzheimer's disease (AD) is a common neurodegenerative disease that accounts for approximately 70% of dementia. Following the global escalation of the aging process, the morbidity of AD is increasing rapidly. The current treatment for AD is mainly limited to medications, such as acetylcholinesterase inhibitors. However, the efficacy of acetylcholinesterase inhibitors in improving memory and cognitive functions is not satisfactory. It is a challenge to find an effective alternative therapy for ameliorating AD symptoms. As an important therapeutic technique in traditional Chinese medicine, acupuncture has been proved effective in treating many neurologic diseases including AD. The efficacy of acupuncture is also acknowledged by the National Institutes of Health of the United States. Here, we summarized the effectiveness of acupuncture for treating AD. Especially, the role of acupuncture at certain acupuncture points in modulating the brain function through meridians activity based on Chinese meridian theory is discussed. How acupuncture at a certain acupoint can improve AD symptoms is also described. Furthermore, the possible molecular mechanisms of acupuncture for AD are reviewed, and the role of acupuncture in modulating signaling molecules in neural protection and homeostasis is highlighted. This study may help to understand the theoretical basis and potential molecular mechanisms of acupuncture therapy for AD.

MUD1, a RING-v E3 ubiquitin ligase, has an important role in the regulation of pectin methylesterification in Arabidopsis seed coat mucilage.

Pectin is one of the major components of plant primary cell wall polysaccharides. The degree of pectin methylesterification (DM) plays an important role in the process of plant growth. However, little is known about the underlying regulatory mechanisms during the process of pectin demethylesterification. Here, we characterized mucilage defect 1 (mud1), a novel Arabidopsis thaliana mutant, which displays increased mucilage adherence resulting from increased activities of pectin methylesterases (PMEs) and decreased degree of pectin methylesterification (DM). MUD1 encodes a nuclear protein with a Really Interesting New Gene (RING)-v domain and is highly expressed in developing seed coat when seed coat mucilage starts to accumulate. We have demonstrated that MUD1 has E3 ubiquitin ligase activity in vitro. The expression of PME-related genes, including MYB52, LUH, SBT1.7, PMEI6, and PMEI14 decreased considerably in mud1. We propose that MUD1 acts as an ubiquitin ligase potentially regulating the DM of pectin by post-transcriptionally removing proteins that normally negatively regulate the level or activity of PMEs in the seed coat mucilage.