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"Xin-Yue, Wang"
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The strengthening of Amazonian precipitation during the wet season driven by tropical sea surface temperature forcing
Amazonian rainfall plays a critical role in the global climate system and the hydrological cycle. It is thus important to quantify changes in the Amazonian rainfall and clarify its mechanism. Previous studies indicate that the interannual variability of Amazonian precipitation could be largely attributed to variabilities in the South American monsoon system and the El Niño Southern Oscillation. However, the trend of the wet season tropical Amazonian precipitation during recent decades is not very well investigated. In this study, by combining both satellite and in situ observations, it is revealed that tropical Amazonian precipitation has significantly increased by ∼180 to 600 mm (in different datasets) in the wet season during the satellite era from 1979 to 2015. We then use a state-of-the-art atmospheric model to simulate the impact of the tropical sea surface temperatures (SSTs) on the precipitation changes. Results show that the multidecadal warming of the tropical Atlantic has contributed more than half of this precipitation change over the past three decades, while the east Pacific cooling plays a secondary role. We finally combine the simulation results and the reanalysis data to investigate the mechanisms of this process, i.e. the SST variability dramatically increases the convergence of the moisture transport over the Amazon region. The precipitation changes over the Amazon region largely impact on the local hydrological cycle and the ecosystem, and have important impacts on the global climate system by mediating the teleconnection between the Pacific and the Atlantic oceans. Our results show that the long-term change in the wet season Amazonian precipitation is important and deserves further investigation and discussion.
Journal Article
A glutamatergic DRN–VTA pathway modulates neuropathic pain and comorbid anhedonia-like behavior in mice
Chronic pain causes both physical suffering and comorbid mental symptoms such as anhedonia. However, the neural circuits and molecular mechanisms underlying these maladaptive behaviors remain elusive. Here using a mouse model, we report a pathway from vesicular glutamate transporter 3 neurons in the dorsal raphe nucleus to dopamine neurons in the ventral tegmental area (VGluT3
DRN
→
DA
VTA
) wherein population-level activity in response to innocuous mechanical stimuli and sucrose consumption is inhibited by chronic neuropathic pain. Mechanistically, neuropathic pain dampens VGluT3
DRN
→ DA
VTA
glutamatergic transmission and DA
VTA
neural excitability. VGluT3
DRN
→ DA
VTA
activation alleviates neuropathic pain and comorbid anhedonia-like behavior (CAB) by releasing glutamate, which subsequently promotes DA release in the nucleus accumbens medial shell (NAcMed) and produces analgesic and anti-anhedonia effects via D2 and D1 receptors, respectively. In addition, VGluT3
DRN
→ DA
VTA
inhibition produces pain-like reflexive hypersensitivity and anhedonia-like behavior in intact mice. These findings reveal a crucial role for VGluT3
DRN
→ DA
VTA
→ D2/D1
NAcMed
pathway in establishing and modulating chronic pain and CAB.
The neural circuit mechanisms underlying chronic pain and comorbid anhedonia remain poorly understood. Here, the authors show the critical role of the DRN–VTA–NAcMed pathway in establishing and modulating chronic neuropathic pain and comorbid anhedonia.
Journal Article
Advances in nitrogen-containing helicenes: synthesis, chiroptical properties, and optoelectronic applications
Helicenes, a class of non-planar polycyclic aromatic hydrocarbons composed of ortho -fused aromatic rings forming helical architectures, have attracted considerable attention due to their intrinsic chirality and tunable optoelectronic properties. Among them, nitrogen-doped helicenes (azahelicenes) and their heteroatom-co-doped counterparts – such as B/N-, O/N-, S/N-, and Se/N-doped helicenes – have emerged as highly versatile scaffolds for chiral optoelectronic applications. The incorporation of nitrogen enables precise modulation of electronic structures, redox characteristics, and intermolecular interactions, thereby enhancing performance in circularly polarized luminescence (CPL), thermally activated delayed fluorescence (TADF), and chiral sensing. Notably, recent developments have yielded π-extended, structurally robust, and stimuli-responsive azahelicenes exhibiting record-high dissymmetry factors (| g abs | and | g lum |), elevated CPL brightness ( B CPL ), and efficient integration into CPL-OLEDs and redox-switchable emitters. Boron–nitrogen co-doping strategies, in particular, have facilitated the development of materials with ultra-narrowband emissions, near-unity photoluminescence quantum yields, and electroluminescence dissymmetry factors (| g EL |) exceeding 10 −3 . Likewise, heteroatom co-doping with oxygen, sulfur, or selenium enables spectral tuning across the visible to near-infrared range, improved photostability, and dual-state emissive behavior. In parallel, significant progress in synthetic methodologies – including enantioselective catalysis, electrochemical cyclizations, and multicomponent reaction systems – has granted access to increasingly complex helicene frameworks with well-defined chirality. This review systematically summarizes recent advancements in the synthesis, structural engineering, and chiroptical performance of nitrogen-doped helicenes and their heteroatom-doped derivatives, emphasizing their potential as next-generation chiral optoelectronic materials and outlining future directions toward multifunctional integration and quantum technological applications.
Journal Article
Association between CD4+ T cell counts and gut microbiota and serum cytokines levels in HIV-infected immunological non-responders
Background
CD4
+
T cell counts in certain human immunodeficiency virus (HIV)-infected patients called immunological non-responders (INRs) could not return to a normal level even with sustained antiretroviral therapy (ART) because of persistent immune activation, which is associated with pro-inflammatory cytokines production and an altered intestinal microbiome profile. Changes in gut bacterial composition have been linked to low CD4
+
T cell counts in HIV-infected individuals. However, the association between CD4
+
T cell counts and gut microbiota community composition and cytokines levels in INRs (CD4
+
T cell counts < 500 cells/μL) from Yunnan Province, China, has not been previously investigated.
Methods
To address this issue, we carried out a cross-sectional study of 34 HIV-infected INRs. The patients were divided into CD4 count > 200 cells/μL group and CD4 count < 200 cells/μL group. The gut microbiota composition of each subject was analyzed by
16S
rRNA gene sequencing. We also compared CD8
+
T cell counts, pro-inflammatory cytokines levels, and nutritional status between the two groups.
Results
Compared to INRs with CD4 count > 200 cells/μL, those with CD4 count < 200 cells/μL had a lower CD4/CD8 ratio, lower nutritional status and higher serum levels of tumor necrosis factor (TNF)-α, interferon-γ-inducible protein (IP)-10 and interleukin (IL)-1α.
Ruminococcaceae
was less abundant in the CD4 count < 200 cells/μL group than in the CD4 count > 200 cells/μL group, and difference in alpha diversity was observed between the two groups. Moreover, CD4
+
T cell counts were negatively associated with TNF-α and IL-1α levels and positively associated with the relative abundance of
Ruminococcaceae
.
Conclusions
Our study demonstrated that lower CD4
+
T cell counts in INRs are associated with a reduced abundance of
Ruminococcaceae
in the gut and elevated serum pro-inflammatory cytokines levels. Thus, interventions targeting gut microbiota to increase CD4
+
T cell counts are a potential strategy for promoting immune reconstitution in HIV-infected INRs.
Journal Article
Semi-analytical solution of cohesive zone model for cement-based materials
The low tensile strength characteristics of cement-based materials are the biggest defect restricting their use. Understanding the mechanisms behind tensile cracking shows great significance in guiding the design of cement-based materials and their structures. Hence, a semi-analytical solution of the cohesive zone model (CZM) was developed to describe the failure mode of cement-based materials. This study used the boundary collocation method to obtain the linear elastic solution of stress function that satisfies the boundary conditions, on the basis of the Williams stress function. Subsequently, the semi-analytic solution of CZM was proposed through the weighted integral method by combining CZM and the bonding zone (CZ), and crack opening displacement (COD) obtained from wedge-splitting tests. Finally, the distribution of cohesion and COD were obtained. The results indicated that the COD obtained from CZM showed great agreement with the COD obtained from the tests, with a maximal error of 15.5%. Meanwhile, the cohesion at the CZ tip in CZM has an error of 2.1% compared to the tensile strength of cement-based materials obtained from experiments. These results indicate the high accuracy of proposed CZM in describing the failure of cement-based materials. A new method is proposed to determine the analytical solution of cohesive zone model based on the stress function of fracture specimen and the measurable fracture test data.
Journal Article
A corticothalamic circuit modulates pain sensitivity and mediates innate fear-induced analgesia in male mice
Fear and pain are two frequently co-occurring states that mammals need to orchestrate to ensure survival. Nevertheless, how the brain dynamically prioritizes between them remains poorly understood. Here, we demonstrate that innate fear suppresses both acute and chronic pain, whereas pain does not reciprocally modulate fear responses in male mice. Using fiber photometry, virus tracing, and electrophysiological approaches, we show that exposure to a fear-inducing odor activates GABAergic neurons in the anterior piriform cortex (APC), which subsequently attenuates pain-associated hyperactivity in the downstream mediodorsal thalamus (MD). Crucially, inhibiting either APC
GABA
neurons or the APC
GABA
-MD circuit enhances pain sensitivity and abolishes fear-induced analgesia. Conversely, activation of APC
GABA
neurons or the APC
GABA
-MD circuit induces freezing responses and relieves pain, mimicking fear-induced analgesia. These findings unveil a corticothalamic circuit that bidirectionally regulates pain processing and underlies fear-provoked analgesia, offering potential therapeutic avenues for pain management.
Survival requires prioritizing threats over pain. The authors identify a brain circuit in male mice, where fear signals from the cortex block pain-associated activation in the thalamus, revealing how fear suppresses pain and offering a potential target for therapies.
Journal Article
KLF5 promotes cervical cancer proliferation, migration and invasion in a manner partly dependent on TNFRSF11a expression
Although the transcription factor Krüppel-like factor 5 (KLF5) plays important roles in both inflammation and cancer, the mechanism by which this factor promotes cervical carcinogenesis remains unclear. In this study, we demonstrated a potential role for tumour necrosis factor receptor superfamily member 11a (TNFRSF11a), the corresponding gene of which is a direct binding target of KLF5, in tumour cell proliferation and invasiveness. Coexpression of KLF5 and TNFRSF11a correlated significantly with tumorigenesis in cervical tissues (
P
< 0.05) and manipulation of KLF5 expression positively affected TNFRSF11a mRNA and protein expression. Functionally, KLF5 promoted cancer cell proliferation, migration and invasiveness in a manner dependent partly on TNFRSF11a expression. Moreover,
in vivo
functional TNFRSF11a-knockdown mouse studies revealed suppression of tumorigenicity and liver metastatic potential. Notably, tumour necrosis factor (TNF)-α induced KLF5 expression by activating the p38 signalling pathway and high KLF5 and TNFRSF11a expression increased the risk of death in patients with cervical squamous cell carcinoma. Our results demonstrate that KLF5 and TNFRSF11a promote cervical cancer cell proliferation, migration and invasiveness.
Journal Article
ARHGAP15 promotes metastatic colonization in gastric cancer by suppressing RAC1-ROS pathway
The molecular mechanism of tumor metastasis, especially how metastatic tumor cells colonize in a distant site, remains poorly understood. Here we reported that ARHGAP15, a Rho GTPase activating protein, enhanced gastric cancer (GC) metastatic colonization, which was quite different from its reported role as a tumor suppressor gene in other cancers. It was upregulated in metastatic lymph nodes and significantly associated with a poor prognosis. Ectopic expression of ARHGAP15 promoted metastatic colonization of gastric cancer cells in murine lungs and lymph nodes in vivo or protected cells from oxidative-related death in vitro . However, genetic downregulation of ARHGAP15 had the opposite effect. Mechanistically, ARHGAP15 inactivated RAC1 and then decreased intracellular accumulation of reactive oxygen species (ROS), thus enhancing the antioxidant capacity of colonizing tumor cells under oxidative stress. This phenotype could be phenocopied by inhibition of RAC1 or rescued by the introduction of constitutively active RAC1 into cells. Taken together, these findings suggested a novel role of ARHGAP15 in promoting gastric cancer metastasis by quenching ROS through inhibiting RAC1 and its potential value for prognosis estimation and targeted therapy.
Journal Article
Tachykinin receptor 3 in the lateral habenula alleviates pain and anxiety comorbidity in mice
The coexistence of chronic pain and anxiety is a common clinical phenomenon. Here, the role of tachykinin receptor 3 (NK3R) in the lateral habenula (LHb) in trigeminal neuralgia and in pain-associated anxiety was systematically investigated. First, electrophysiological recording showed that bilateral LHb neurons are hyperactive in a mouse model of trigeminal neuralgia made by partial transection of the infraorbital nerve (pT-ION). Chemicogenetic activation of bilateral LHb glutamatergic neurons in naive mice induced orofacial allodynia and anxiety-like behaviors, and pharmacological activation of NK3R in the LHb attenuated allodynia and anxiety-like behaviors induced by pT-ION. Electrophysiological recording showed that pharmacological activation of NK3R suppressed the abnormal excitation of LHb neurons. In parallel, pharmacological inhibition of NK3R induced orofacial allodynia and anxiety-like behavior in naive mice. The electrophysiological recording showed that pharmacological inhibition of NK3R activates LHb neurons. Neurokinin B (NKB) is an endogenous high-affinity ligand of NK3R, which binds NK3R and activates it to perform physiological functions, and further neuron projection tracing showed that the front section of the periaqueductal gray (fPAG) projects NKB-positive nerve fibers to the LHb. Optogenetics combined with electrophysiology recordings characterize the functional connections in this fPAG NKB → LHb pathway. In addition, electrophysiological recording showed that NKB-positive neurons in the fPAG were more active than NKB-negative neurons in pT-ION mice. Finally, inhibition of NKB release from the fPAG reversed the analgesic and anxiolytic effects of LHb Tacr3 overexpression in pT-ION mice, indicating that fPAG NKB → LHb regulates orofacial allodynia and pain-induced anxious behaviors. These findings for NK3R suggest the cellular mechanism behind pT-ION in the LHb and suggest that the fPAG NKB → LHb circuit is involved in pain and anxiety comorbidity. This previously unrecognized pathway might provide a potential approach for relieving the pain and anxiety associated with trigeminal neuralgia by targeting NK3R.
Journal Article