Assessing vaginal microbiome through Vaginal Microecology Evaluation System as a predictor for in vitro fertilization outcomes: a retrospective study.

Objective: This study aims to evaluate the effectiveness of the Vaginal Microecology Evaluation System (VMES) in assessing the dynamics of the vaginal microbiome (VM) throughout the process of in vitro fertilization and embryo transfer (IVF-ET). Furthermore, it seeks to explore the potential correlation between distinct types of VM ecology and the success rate of IVF-ET. Methods: This study employed VMES to ascertain the composition of the VM. Data were collected from infertile women who underwent their initial IVF-ET treatment for tubal factor between January 2018 and December 2021. A retrospective analysis of pregnancy outcomes resulting from their fresh embryo transfer was conducted to determine the predictive significance of the vaginal microenvironment. Results: We demonstrate that VMES is able to predict IVF-ET outcomes in patients diagnosed with Bacterial Vaginosis (BV). Notably, a discernible shift in the VM was observed in a decent subset of patients following Controlled Ovarian Stimulation (COS), though this phenomenon was not universal across all participants. Specifically, there was a noteworthy increase in the proportion of patients exhibiting BV and uncharacterized dysbiosis subsequent to COS. Furthermore, our investigation revealed a significant correlation between VM and both the live birth rate and early miscarriage rate. Employing a multivariable logistic regression model, we identified that VM status pre-COS, VM status post-COS, patient age, and the number of embryos transferred emerged as independent predictors of the live birth rate. Conclusion: Our study suggests that, during IVF-ET treatment, the VMES can effectively detect changes in the VM, which are strongly correlated with the pregnancy outcome of IVF-ET procedures.

A reference-grade genome of the xerophyte Ammopiptanthus mongolicus sheds light on its evolution history in legumes and drought-tolerance mechanisms.

Plants that grow in extreme environments represent unique sources of stress-resistance genes and mechanisms. Ammopiptanthus mongolicus (Leguminosae) is a xerophytic evergreen broadleaf shrub native to semi-arid and desert regions; however, its drought-tolerance mechanisms remain poorly understood. Here, we report the assembly of a reference-grade genome for A. mongolicus, describe its evolutionary history within the legume family, and examine its drought-tolerance mechanisms. The assembled genome is 843.07 Mb in length, with 98.7% of the sequences successfully anchored to the nine chromosomes of A. mongolicus. The genome is predicted to contain 47 611 protein-coding genes, and 70.71% of the genome is composed of repetitive sequences; these are dominated by transposable elements, particularly long-terminal-repeat retrotransposons. Evolutionary analyses revealed two whole-genome duplication (WGD) events at 130 and 58 million years ago (mya) that are shared by the genus Ammopiptanthus and other legumes, but no species-specific WGDs were found within this genus. Ancestral genome reconstruction revealed that the A. mongolicus genome has undergone fewer rearrangements than other genomes in the legume family, confirming its status as a "relict plant". Transcriptomic analyses demonstrated that genes involved in cuticular wax biosynthesis and transport are highly expressed, both under normal conditions and in response to polyethylene glycol-induced dehydration. Significant induction of genes related to ethylene biosynthesis and signaling was also observed in leaves under dehydration stress, suggesting that enhanced ethylene response and formation of thick waxy cuticles are two major mechanisms of drought tolerance in A. mongolicus. Ectopic expression of AmERF2, an ethylene response factor unique to A. mongolicus, can markedly increase the drought tolerance of transgenic Arabidopsis thaliana plants, demonstrating the potential for application of A. mongolicus genes in crop improvement.

PGF2α signaling drives fibrotic remodeling and fibroblast population dynamics in mice.

Idiopathic pulmonary fibrosis (IPF) is a chronic parenchymal lung disease characterized by repetitive alveolar cell injury, myofibroblast proliferation, and excessive extracellular matrix deposition for which unmet need persists for effective therapeutics. The bioactive eicosanoid, prostaglandin F2α, and its cognate receptor FPr (Ptgfr) are implicated as a TGF-ß1-independent signaling hub for IPF. To assess this, we leveraged our published murine PF model (IER-SftpcI73T) expressing a disease-associated missense mutation in the surfactant protein C (Sftpc) gene. Tamoxifen-treated IER-SftpcI73T mice developed an early multiphasic alveolitis and transition to spontaneous fibrotic remodeling by 28 days. IER-SftpcI73T mice crossed to a Ptgfr-null (FPr-/-) line showed attenuated weight loss and gene dosage-dependent rescue of mortality compared with FPr+/+ cohorts. IER-SftpcI73T/FPr-/- mice also showed reductions in multiple fibrotic endpoints for which administration of nintedanib was not additive. Single-cell RNA-Seq, pseudotime analysis, and in vitro assays demonstrated Ptgfr expression predominantly within adventitial fibroblasts, which were reprogrammed to an "inflammatory/transitional" cell state in a PGF2α /FPr-dependent manner. Collectively, the findings provide evidence for a role for PGF2α signaling in IPF, mechanistically identify a susceptible fibroblast subpopulation, and establish a benchmark effect size for disruption of this pathway in mitigating fibrotic lung remodeling.

Telocyte-Derived Exosomes Provide an Important Source of Wnts That Inhibits Fibrosis and Supports Regeneration and Repair of Endometrium.

Intrauterine adhesions (IUAs) often occurred after common obstetrical and gynecological procedures or infections in women of reproductive age. It was characterized by the formation of endometrial fibrosis and prevention of endometrial regeneration, usually with devastating fertility consequences and poor treatment outcomes so far. Telocytes (TCs), as a novel interstitial cell type, present in female uterus with in vitro therapeutic potential in decidualization-defective gynecologic diseases. This study aims to further investigate the role of TC-derived Wnt ligands carried by exosomes (Exo) in reversal of fibrosis and enhancement of regeneration repair in endometrium. IUA cellular and animal models were established from endometrial stromal cells (ESCs) and mice, followed with treatment of TC-conditioned medium (TCM) or TC-derived Exo. In cellular model, fibrosis markers (collagen type 1 alpha 1 [COL1A1], fibronectin [FN], and α-smooth muscle actin [α-SMA]), angiogenesis (vascular endothelial growth factor [VEGF]), and pathway protein (ß-catenin) were determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR), Western blotting (WB), and immunofluorescence. Results showed that, TCs (either TCM or TC-derived Exo) provide a source of Wnts that inhibit cellular fibrosis, as evidenced by significantly elevated VEGF and ß-catenin with decreased fibrotic markers, whereas TCs lost salvage on fibrosis after being blocked with Wnt/ß-catenin inhibitors (XAV939 or ETC-159). Further in mouse model, regeneration repair (endometrial thickness, number of glands, and fibrosis area ratio), fibrosis markers (fibronectin [FN]), mesenchymal-epithelial transition (MET) (E-cadherin, N-cadherin), and angiogenesis (VEGF, microvessel density [MVD]) were studied by hematoxylin-eosin (HE), Masson staining, and immunohistochemistry. Results demonstrated that TC-Exo treatment effectively promotes regeneration repair of endometrium by relieving fibrosis, enhancing MET, and angiogenesis. These results confirmed new evidence for therapeutic perspective of TC-derived Exo in IUAs.

Inhibitory effect of telocyte-induced M1 macrophages on endometriosis: Targeting angiogenesis and invasion.

PURPOSE: Telocytes (TCs), a novel type of stromal cells found in tissues, induce macrophage differentiation into classically activated macrophages (M1) types and enhance their phagocytic function. The purpose of this study was to investigate the inhibitory effects of TC-induced M1 macrophages on endometriosis (EMs). METHODS: mouse uterine primary TCs and endometrial stromal cells (ESCs) were isolated and identified using double immunofluorescence staining. For the in vitro study, ESCs were treated with TC-induced M1 macrophages, and the vascular endothelial growth factor (VEGF), matrix metalloproteinase 9 (MMP9), and nuclear factor kappa B (NF-κb) genes were identified by quantitative real-time PCR (qRT-PCR) or western blotting (WB). For the in vivo study, an EMs mouse model received TC-conditioned medium (TCM) via abdominal administration, and characterized the inhibitory effects on growth (lesion weight, volume, and pathology), tissue-resident macrophages differentiation by immunostaining, angiogenic capacity (CD31 and VEGF), invasive capacity (MMP9), and NF-κb expression within EMs lesions. RESULTS: immunofluorescent staining showed that uterine TCs expressed CD34+ and vimentin+, whereas ESCs expressed vimentin+ and cytokeratin-. At the cellular level, TC-induced M1 macrophages can significantly inhibit the expression of VEGF and MMP9 in ESCs through WB or qRT-PCR, possibly by suppressing the NF-κb pathway. The in vivo study showed that macrophages switch from the alternatively activated macrophages (M2) in untreated EMs lesions to the M1 subtype after TCM exposure. Thereby, TC-induced M1 macrophages contributed to the inhibition of EMs lesions. More importantly, this effect may be achieved by suppressing the expression of NF-κb to inhibit angiogenesis (CD31 and VEGF) and invasion (MMP9) in the tissue. CONCLUSION: TC-induced M1 macrophages play a prevailing role in suppressing EMs by inhibiting angiogenic and invasive capacity through the NF-κb pathway, which provides a promising therapeutic approach for EMs.

An Improved Toeplitz Approximation Method for Coherent DOA Estimation in Impulsive Noise Environments.

Direction of arrival (DOA) estimation is an important research topic in array signal processing and widely applied in practical engineering. However, when signal sources are highly correlated or coherent, conventional subspace-based DOA estimation algorithms will perform poorly due to the rank deficiency in the received data covariance matrix. Moreover, conventional DOA estimation algorithms are usually developed under Gaussian-distributed background noise, which will deteriorate significantly in impulsive noise environments. In this paper, a novel method is presented to estimate the DOA of coherent signals in impulsive noise environments. A novel correntropy-based generalized covariance (CEGC) operator is defined and proof of boundedness is given to ensure the effectiveness of the proposed method in impulsive noise environments. Furthermore, an improved Toeplitz approximation method combined CEGC operator is proposed to estimate the DOA of coherent sources. Compared to other existing algorithms, the proposed method can avoid array aperture loss and perform more effectively, even in cases of intense impulsive noise and low snapshot numbers. Finally, comprehensive Monte-Carlo simulations are performed to verify the superiority of the proposed method under various impulsive noise conditions.

Disruption of Prostaglandin F2α Receptor Signaling Attenuates Fibrotic Remodeling and Alters Fibroblast Population Dynamics in A Preclinical Murine Model of Idiopathic Pulmonary Fibrosis.

Idiopathic Pulmonary Fibrosis (IPF) is a chronic parenchymal lung disease characterized by repetitive alveolar cell injury, myofibroblast proliferation, and excessive extracellular matrix deposition for which unmet need persists for effective therapeutics. The bioactive eicosanoid, prostaglandin F2α, and its cognate receptor FPr (Ptfgr) are implicated as a TGFß1 independent signaling hub for IPF. To assess this, we leveraged our published murine PF model (IER - SftpcI73T) expressing a disease-associated missense mutation in the surfactant protein C (Sftpc) gene. Tamoxifen treated IER-SftpcI73T mice develop an early multiphasic alveolitis and transition to spontaneous fibrotic remodeling by 28 days. IER-SftpcI73T mice crossed to a Ptgfr null (FPr-/-) line showed attenuated weight loss and gene dosage dependent rescue of mortality compared to FPr+/+ cohorts. IER-SftpcI73T/FPr-/- mice also showed reductions in multiple fibrotic endpoints for which administration of nintedanib was not additive. Single cell RNA sequencing, pseudotime analysis, and in vitro assays demonstrated Ptgfr expression predominantly within adventitial fibroblasts which were reprogrammed to an "inflammatory/transitional" cell state in a PGF2α/FPr dependent manner. Collectively, the findings provide evidence for a role for PGF2α signaling in IPF, mechanistically identify a susceptible fibroblast subpopulation, and establish a benchmark effect size for disruption of this pathway in mitigating fibrotic lung remodeling.

Simultaneous transfer of one good-quality and one poor-quality cleavage stage embryo does not improve pregnancy outcomes.

Embryo quality and quantity are key factors that determine the success of IVF-ET. Yet it is still unclear if, for those patients with only one good-quality embryo in an IVF cycle, the inclusion of a poor-quality embryo increases the procedure's success rate. This is a common question for both clinicians and patients in determining their course of treatment. The purpose of this work was to answer this intriguing question in the context of prognosis of patients undergoing fresh cycles with only one good-quality and more than one poor-quality cleavage-stage embryos. To control for confounding effects, we only included patients at similar age, body mass index (BMI), level of basal follicle stimulating hormone (FSH) and endometrial thickness from January 2015 to June 2021. A propensity score-matched analysis was performed to extract the matched pairs. Then we evaluated pregnancy outcome, including the rate of clinical pregnancy, live birth, embryo implantation, early miscarriage, and ectopic pregnancy. We found that the clinical pregnancy rate (34.8 vs. 38.0%, p = 0.553), live birth rate (27.1 vs. 29.9%, p = 0.598), early miscarriage rate (18.1 vs. 9.5%, p = 0.171) and ectopic pregnancy rate (1.3 vs. 1.2%, p = 1.000) did not significantly differ between those two groups, notwithstanding significant difference of the implantation rate (34.8 vs. 21.3%, p <0.001). Our work indicates that, for prognosis patients at approximately 34 years old with only one good-quality embryo, having additional poor-quality embryos does not seem to help to improve ART success rates per intended embryo transfer. In conclusion, we found that simultaneous transfer of one good-quality and one poor-quality cleavage stage embryo does not improve pregnancy outcomes.

Germplasm resources of three wood plant species enriched with nervonic acid.

Nervonic acid (NA) is a very-long-chain monounsaturated fatty acid with pharmaceutical and nutraceutical functions that plays an important role in treating several neurological disorders. One major source of NA is plant seed oil. Here we report fatty acid profiles of seeds and germplasm diversity of six plant species, including three woody plants with high amounts of NA-enriched seed oil, Malania oleifera, Macaranga adenantha, and M. indica. M. oleifera had the largest seed (average 7.40 g single seed), highest oil content (58.71%), and highest NA level (42.22%). The germplasm diversity of M. oleifera is associated with its habitat but not elevation. Seeds of M. adenantha contained higher NA levels (28.41%) than M. indica (21.77%), but M. indica contained a significantly higher oil content (29.22%) and seed yield. M. adenantha germplasm varied among populations, with one population having seeds with high oil content (22.63%) and NA level (37.78%).Although M. indica grow naturally at a range of elevations, no significant differences were detected between M. indica populations. These results suggest that M. indica and M. oleifera have greater potential as a source of NA, which will contribute to constructing a germplasm resource nursery and establishing a selection and breeding program to improve the development of NA-enriched plants.

Telocytes in Fibrosis Diseases: From Current Findings to Future Clinical Perspectives.

Telocytes (TCs), a distinct type of interstitial (stromal) cells, have been discovered in many organs of human and mammal animals. TCs, which have unique morphological characteristics and abundant paracrine substance, construct a three-dimensional (3D) interstitial network within the stromal compartment by homocellular and heterocellular communications which are important for tissue homeostasis and normal development. Fibrosis-related diseases remain a common but challenging problem in the field of medicine with unclear pathogenesis and limited therapeutic options. Recently, increasing evidences suggest that where TCs are morphologically or numerically destructed, many diseases continuously develop, finally lead to irreversible interstitial fibrosis. It is not difficult to find that TCs are associated with chronic inflammation and fibrosis. This review mainly discusses relationship between TCs and the occurrence of fibrosis in various diseases. We analyzed in detail the potential roles and speculated mechanisms of TCs in onset and progression of systemic fibrosis diseases, as well as providing the most up-to-date research on the current therapeutic roles of TCs and involved related pathways. Only through continuous research and exploration in the future can we uncover its magic veil and provide strategies for treatment of fibrosis-related disease.

Identification of an arthropod molecular target for plant-derived natural repellents.

Arthropods maintain ecosystem balance while also contributing to the spread of disease. Plant-derived natural repellents represent an ecological method of pest control, but their direct molecular targets in arthropods remain to be further elucidated. Occupying a critical phylogenetic niche in arthropod evolution, scorpions retain an ancestral genetic profile. Here, using a behavior-guided screening of the Mesobuthus martensii genome, we identified a scorpion transient receptor potential (sTRP1) channel that senses Cymbopogon-derived natural repellents, while remaining insensitive to the synthetic chemical pesticide DEET. Scrutinizing orthologs of sTRP1 in Drosophila melanogaster, we further demonstrated dTRPγ ion channel as a chemosensory receptor of natural repellents to mediate avoidance behavior. This study sheds light on arthropod molecular targets of natural repellents, exemplifying the arthropod­plant adaptation. It should also help the rational design of insect control strategy and in conserving biodiversity.

A New Species of Vetubrachypsectra from Mid-Cretaceous Amber of Northern Myanmar (Coleoptera: Brachypsectridae).

A new species, Vetubrachypsectra huchengi Li, Kundrata & Cai sp. nov., is described from mid-Cretaceous Burmese amber on the basis of a single adult female. The species is assigned to genus Vetubrachypsectra Qu & Cai based on its serrate antennae, long maxillary palps, presence of tibial spurs, and elytra without clear striae. Vetubrachypsectra huchengi differs distinctly from V. burmitica Qu & Cai, the only other species in the genus, in having the pedicel apically attached to the scape. Some other differences between the female of V. huchengi and the male of V. burmitica include less serrate antennae, a broader pronotal disc, a broader scutellar shield and smaller tibial spurs. However, at least some of these characters can be considered sexually dimorphic.

The industrial solvent 1,4-dioxane causes hyperalgesia by targeting capsaicin receptor TRPV1.

BACKGROUND: The synthetic chemical 1,4-dioxane is used as industrial solvent, food, and care product additive. 1,4-Dioxane has been noted to influence the nervous system in long-term animal experiments and in humans, but the molecular mechanisms underlying its effects on animals were not previously known. RESULTS: Here, we report that 1,4-dioxane potentiates the capsaicin-sensitive transient receptor potential (TRP) channel TRPV1, thereby causing hyperalgesia in mouse model. This effect was abolished by CRISPR/Cas9-mediated genetic deletion of TRPV1 in sensory neurons, but enhanced under inflammatory conditions. 1,4-Dioxane lowered the temperature threshold for TRPV1 thermal activation and potentiated the channel sensitivity to agonistic stimuli. 1,3-dioxane and tetrahydrofuran which are structurally related to 1,4-dioxane also potentiated TRPV1 activation. The residue M572 in the S4-S5 linker region of TRPV1 was found to be crucial for direct activation of the channel by 1,4-dioxane and its analogs. A single residue mutation M572V abrogated the 1,4-dioxane-evoked currents while largely preserving the capsaicin responses. Our results further demonstrate that this residue exerts a gating effect through hydrophobic interactions and support the existence of discrete domains for multimodal gating of TRPV1 channel. CONCLUSIONS: Our results suggest TRPV1 is a co-receptor for 1,4-dioxane and that this accounts for its ability to dysregulate body nociceptive sensation.

A Pan-Cancer Analysis of Clinical Prognosis and Immune Infiltration of CKS1B in Human Tumors.

Although more and more evidence supports CDC28 protein kinase subunit 1B (CKS1B) is involved significantly in the development of human cancers, most of the researches have focused on a single disease, and pan-cancer studies conducted from a holistic perspective of different tumor sources have not been reported yet. Here, for the first time, we investigated the potential oncogenic and prognostic role of CKS1B across 33 tumors based on public databases and further verified it in a small scale by RNA sequencing or quantitative real-time PCR. CKS1B was generally highly expressed in a majority of tumors and had a notable correlation with the prognosis of patients, but its prognostic significance in different tumors was not exactly the same. In addition, CKS1B expression was also closely related to the infiltration of cancer-associated fibroblasts in tumors such as breast invasive carcinoma, kidney chromophobe, lung adenocarcinoma, and tumor-infiltrating lymphocytes in tumors such as glioblastoma multiforme, bladder urothelial carcinoma, and brain lower grade glioma. Moreover, reduced CKS1B methylation was observed in certain tumors, for example, adrenocortical carcinoma. Cell cycle and kinase activity regulation and PI3K-Akt signaling pathway were found to be involved in the functional mechanism of CKS1B. In conclusion, our first pan-cancer analysis of CKS1B contributes to a better overall understanding of CKS1B and may provide a new target for future cancer therapy.

Discovery of a new class of integrin antibodies for fibrosis.

Lung fibrosis, or the scarring of the lung, is a devastating disease with huge unmet medical need. There are limited treatment options and its prognosis is worse than most types of cancer. We previously discovered that MK-0429 is an equipotent pan-inhibitor of αv integrins that reduces proteinuria and kidney fibrosis in a preclinical model. In the present study, we further demonstrated that MK-0429 significantly inhibits fibrosis progression in a bleomycin-induced lung injury model. In search of newer integrin inhibitors for fibrosis, we characterized monoclonal antibodies discovered using Adimab's yeast display platform. We identified several potent neutralizing integrin antibodies with unique human and mouse cross-reactivity. Among these, Ab-31 blocked the binding of multiple αv integrins to their ligands with IC50s comparable to those of MK-0429. Furthermore, both MK-0429 and Ab-31 suppressed integrin-mediated cell adhesion and latent TGFß activation. In IPF patient lung fibroblasts, TGFß treatment induced profound αSMA expression in phenotypic imaging assays and Ab-31 demonstrated potent in vitro activity at inhibiting αSMA expression, suggesting that the integrin antibody is able to modulate TGFß action though mechanisms beyond the inhibition of latent TGFß activation. Together, our results highlight the potential to develop newer integrin therapeutics for the treatment of fibrotic lung diseases.

A Mitochondrial DNA Variant Elevates the Risk of Gallstone Disease by Altering Mitochondrial Function.

BACKGROUND AND AIMS: Gallstone disease (cholelithiasis) is a cholesterol-related metabolic disorders with strong familial predisposition. Mitochondrial DNA (mtDNA) variants accumulated during human evolution are associated with some metabolic disorders related to modified mitochondrial function. The mechanistic links between mtDNA variants and gallstone formation need further exploration. METHODS: In this study, we explored the possible associations of mtDNA variants with gallstone disease by comparing 104 probands and 300 controls in a Chinese population. We constructed corresponding cybrids using trans-mitochondrial technology to investigate the underlying mechanisms of these associations. Mitochondrial respiratory chain complex activity and function and cholesterol metabolism were assessed in the trans-mitochondrial cell models. RESULTS: Here, we found a significant association of mtDNA 827A>G with an increased risk of familial gallstone disease in a Chinese population (odds ratio [OR]: 4.5, 95% confidence interval [CI]: 2.1-9.4, P=1.2×10-4). Compared with 827A cybrids (haplogroups B4a and B4c), 827G cybrids (haplogroups B4b and B4d) had impaired mitochondrial respiratory chain complex activity and function and activated JNK and AMPK signaling pathways. Additionally, the 827G cybrids showed disturbances in cholesterol transport and accelerated development of gallstones. Specifically, cholesterol transport through the transporter ABCG5/8 was increased via activation of the AMPK signaling pathway in 827G cybrids. CONCLUSIONS: Our findings reveal that mtDNA 827A>G induces aberrant mitochondrial function and abnormal cholesterol transport, resulting in increased occurrence of gallstones. The results provide an important biological basis for the clinical diagnosis and prevention of gallstone disease in the future.

Molecular Profiling Reveals a Common Metabolic Signature of Tissue Fibrosis.

Fibrosis, or the accumulation of extracellular matrix, is a common feature of many chronic diseases. To interrogate core molecular pathways underlying fibrosis, we cross-examine human primary cells from various tissues treated with TGF-ß, as well as kidney and liver fibrosis models. Transcriptome analyses reveal that genes involved in fatty acid oxidation are significantly perturbed. Furthermore, mitochondrial dysfunction and acylcarnitine accumulation are found in fibrotic tissues. Substantial downregulation of the PGC1α gene is evident in both in vitro and in vivo fibrosis models, suggesting a common node of metabolic signature for tissue fibrosis. In order to identify suppressors of fibrosis, we carry out a compound library phenotypic screen and identify AMPK and PPAR as highly enriched targets. We further show that pharmacological treatment of MK-8722 (AMPK activator) and MK-4074 (ACC inhibitor) reduce fibrosis in vivo. Altogether, our work demonstrate that metabolic defect is integral to TGF-ß signaling and fibrosis.

Iliac Bone Harvesting Techniques for Bone Reconstruction. Comparative Study Between Tricortical Bone Harvesting vs Trapdoor Technique.

OBJECTIVE: To investigate the effects of trapdoor-procedure-based bone harvesting and tricortical iliac bone harvesting on the iliac bone-graft donor site pain experienced by patients and their clinical effects. METHODS: A retrospective analysis was performed using the clinical data of 65 patients with tibial plateau fractures who received autologous iliac bone-supporting grafts in two hospitals between January 2014 and January 2019. The patients who received trapdoor-procedure-based bone harvesting (34 cases) were in the experimental group, and those who received tricortical iliac bone harvesting (31 cases) were in the control group. This study compared differences in iliac bone-graft donor site incision length, intraoperative blood loss, amount of bones harvested, operation time, and postoperative complications between the two bone-harvesting methods. Subsequently, it evaluated the pain experienced by the two patient groups in their iliac bone-graft donor sites and their clinical effects. RESULTS: One week after surgery, the differences between the iliac bone-graft donor site pain score (measured using SF-MPQ-2) of the experimental group and the control group were not statistically different. However, 3 weeks, 5 weeks, and 3 months after surgery, the iliac bone-graft donor site pain scores of the experimental group were significantly lower than those of the control group. The iliac bone-graft donor site incision length and operation time of the experimental group were not significantly different from those of the control group. However, the iliac bone-graft donor site intraoperative blood loss, amount of bones harvested and the incidence of complications of the experimental group were significantly lower than those of the control group. CONCLUSION: Trapdoor-procedure-based bone harvesting has lower donor site pain, intraoperative blood loss, and postoperative complications. However, for bone grafting in regions with significant bone loss, tricortical iliac bone harvesting remains the optimal option.

Site- and species-specific climatic responses of two co-occurring shrubs in the temperate Alxa Desert Plateau, northwest China.

In the context of global precipitation anomalies and climate warming, the evolution of fragile desert ecosystems, which account for one-third of the world's land area, will become more complex. Studies of regional climate change and ecosystem response are important components of global climate change research, especially in arid desert regions. Zygophyllum xanthoxylum and Ammopiptanthus mongolicus are two dominant but endangered shrub species in the Alxa Desert in the arid region of central Asia. Using dendrochronological methods, we studied the response of radial growth of those two species to climate factors, and the adaptability of the two shrub populations under a regional warming trend. We found that radial growth of both shrubs was mainly affected by precipitation during the growing season. In additionally, along with the decrease of precipitation and the increase of temperature from east to west of Alxa desert Plateau, the limiting effect of drought during the growing season on radial growth increased. The climate response characteristics and changes between dry and wet periods exhibited spatial and temporal heterogeneity due to micro-level geomorphological factors. Under a regional climate warming trend, individual growth and population development of the two endangered shrubs will be adversely affected. In areas where these species are naturally distributed, populations will gradually become concentrated in micro-geomorphic regions with better soil moisture conditions, such as low-lying areas in the gullies that develop in alluvial fans. This finding has important scientific significance for understanding the development of the region's dominant shrub populations and protection of these and other endangered plants in arid desert areas.

Recovery from tachyphylaxis of TRPV1 coincides with recycling to the surface membrane.

The transient receptor potential vanilloid-1 (TRPV1) ion channel is essential for sensation of thermal and chemical pain. TRPV1 activation is accompanied by Ca2+-dependent desensitization; acute desensitization reflects rapid reduction in channel activity during stimulation, whereas tachyphylaxis denotes the diminution in TRPV1 responses to repetitive stimulation. Acute desensitization has been attributed to conformational changes of the TRPV1 channel; however, the mechanisms underlying the establishment of tachyphylaxis remain to be defined. Here, we report that the degree of whole-cell TRPV1 tachyphylaxis is regulated by the strength of inducing stimulation. Using light-sheet microscopy and pH-sensitive sensor pHluorin to follow TRPV1 endocytosis and exocytosis trafficking, we provide real-time information that tachyphylaxis of different degrees concurs with TRPV1 recycling to the plasma membrane in a proportional manner. This process controls TRPV1 surface expression level thereby the whole-cell nociceptive response. We further show that activity-gated TRPV1 trafficking associates with intracellular Ca2+ signals of distinct kinetics, and recruits recycling routes mediated by synaptotagmin 1 and 7, respectively. These results suggest that activity-dependent TRPV1 recycling contributes to the establishment of tachyphylaxis.