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The mediodorsal thalamus (MD) and adjacent midline nuclei are important for cognition and mental illness, but their cellular composition is not well defined. Using single-nucleus and spatial transcriptomics, we identified a conserved excitatory neuron gradient, with distinct spatial mapping of individual clusters. One end of the gradient was expanded in human MD compared to mice, which may be related to the expansion of granular prefrontal cortex in hominids. Moreover, neurons preferentially mapping onto the parvocellular division MD were associated with genetic risk for schizophrenia and bipolar disorder. Midbrain-derived inhibitory interneurons were enriched in human MD and implicated in genetic risk for major depressive disorder.

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Atrial fibrillation (AF) is the most common arrhythmia in the world. Human genetics can provide strong AF therapeutic candidates, but the identification of the causal genes and their functions remains challenging. Here, we applied an AF fine-mapping strategy that leverages results from a previously published cross-ancestry genome-wide association study (GWAS), expression quantitative trait loci (eQTLs) from left atrial appendages (LAAs) obtained from two cohorts with distinct ancestry, and a paired RNA sequencing (RNA-seq) and ATAC sequencing (ATAC-seq) LAA single-nucleus assay (sn-multiome). At nine AF loci, our co-localization and fine-mapping analyses implicated 14 genes. Data integration identified several candidate causal AF variants, including rs7612445 at GNB4 and rs242557 at MAPT. Finally, we showed that the repression of the strongest AF-associated eQTL gene, LINC01629, in human embryonic stem cell-derived cardiomyocytes using CRISPR inhibition results in the dysregulation of pathways linked to genes involved in the development of atrial tissue and the cardiac conduction system.

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The BAF chromatin remodeler regulates lineage commitment including cranial neural crest cell (CNCC) specification. Variants in BAF subunits cause Coffin-Siris syndrome (CSS), a congenital disorder characterized by coarse craniofacial features and intellectual disability. Approximately 50% of individuals with CSS harbor variants in one of the mutually exclusive BAF subunits, ARID1A/ARID1B. While Arid1a deletion in mouse neural crest causes severe craniofacial phenotypes, little is known about the role of ARID1A in CNCC specification. Using CSS-patient-derived ARID1A+/- induced pluripotent stem cells to model CNCC specification, we discovered that ARID1A-haploinsufficiency impairs epithelial-to-mesenchymal transition (EMT), a process necessary for CNCC delamination and migration from the neural tube. Furthermore, wild-type ARID1A-BAF regulates enhancers associated with EMT genes. ARID1A-BAF binding at these enhancers is impaired in heterozygotes while binding at promoters is unaffected. At the sequence level, these EMT enhancers contain binding motifs for ZIC2, and ZIC2 binding at these sites is ARID1A-dependent. When excluded from EMT enhancers, ZIC2 relocates to neuronal enhancers, triggering aberrant neuronal gene activation. In mice, deletion of Zic2 impairs NCC delamination, while ZIC2 overexpression in chick embryos at post-migratory neural crest stages elicits ectopic delamination from the neural tube. These findings reveal an essential ARID1A-ZIC2 axis essential for EMT and CNCC delamination.

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A limited number of tissues can spontaneously regenerate following injury, and even fewer can regenerate to a state comparable to mature, healthy adult tissue. Mesenchymal stem cells (MSCs) were first described in the 1960s-1970s by Friedenstein et al as a small population of bone marrow cells with osteogenic potential and abilities to differentiate into chondrocytes. In 1991, Arnold Caplan coined the term "mesenchymal cells" after identifying these cells as a theoretical precursor to bone, cartilage, tendon, ligament, marrow stroma, adipocyte, dermis, muscle, and connective tissues. MSCs are derived from periosteum, fat, and muscle. Another attractive property of MSCs is their immunoregulatory and regenerative properties, which result from crosstalk with their microenvironment and components of the innate immune system. Collectively, these properties make MSCs potentially attractive for various therapeutic purposes. MSCs offer potential in sports medicine, aiding in muscle recovery, meniscal tears, and tendon and ligament injuries. In joint disease, MSCs have the potential for chondrogenesis and reversing the effects of osteoarthritis. MSCs have also demonstrated potential application to the treatment of degenerative disc disease of the cervical, thoracic, and lumbar spine.

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Common variants in the MicroRNA 137 host gene MIR137HG and its adjacent gene DPYD have been associated with schizophrenia risk and the latest Psychiatric Genomics Consortium (PGC). Genome-Wide Association Study on schizophrenia has confirmed and extended these findings. To elucidate the association of schizophrenia risk-associated SNPs in this genomic region, we examined the expression of both mature and immature transcripts of the miR-137 host gene (MIR137HG) in the dorsolateral prefrontal cortex (DLPFC) and subgenual anterior cingulate cortex (sgACC) of postmortem brain samples of donors with schizophrenia and psychiatrically-unaffected controls using qPCR and RNA-Seq approaches. No differential expression of miR-137, MIR137HG, or its transcripts was observed. Two schizophrenia risk-associated SNPs identified in the PGC study, rs11165917 (DLPFC: P = 2.0e-16; sgACC: P = 6.4e-10) and rs4274102 (DLPFC: P = 0.036; sgACC: P = 0.002), were associated with expression of the MIR137HG long non-coding RNA transcript MIR137HG-203 (ENST00000602672.2) in individuals of European ancestry. Carriers of the minor (risk) allele of rs11165917 had significantly lower expression of MIR137HG-203 compared with those carrying the major allele. However, we were unable to validate this result by short-read sequencing of RNA extracted from DLPFC or sgACC tissue. This finding suggests that immature transcripts of MIR137HG may contribute to genetic risk for schizophrenia.

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The inhibitor of κB (IκB) kinase (IKK) is a central regulator of NF-κB signaling. All IKK complexes contain hetero- or homodimers of the catalytic IKKß and/or IKKα subunits. Here, we identify a YDDΦxΦ motif, which is conserved in substrates of canonical (IκBα, IκBß) and alternative (p100) NF-κB pathways, and which mediates docking to catalytic IKK dimers. We demonstrate a quantitative correlation between docking affinity and IKK activity related to IκBα phosphorylation/degradation. Furthermore, we show that phosphorylation of the motif's conserved tyrosine, an event previously reported to promote IκBα accumulation and inhibition of NF-κB gene expression, suppresses the docking interaction. Results from integrated structural analyzes indicate that the motif binds to a groove at the IKK dimer interface. Consistently, suppression of IKK dimerization also abolishes IκBα substrate binding. Finally, we show that an optimized bivalent motif peptide inhibits NF-κB signaling. This work unveils a function for IKKα/ß dimerization in substrate motif recognition.

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BACKGROUND: Gallbladder cancer (GBC) is associated with a high mortality rate. Asian American (AsA) are among the fastest-growing populations in the United States, yet little is known about the disparity of GBC within this cohort. This study identified trends in treatment and outcomes for GBC in a disaggregated fashion, specifically for this population. METHODS: A retrospective analysis of the National Cancer Database (NCDB) between 2010 and 2019 examining all patients treated for gallbladder cancer was performed. Basic demographic factors were identified for patients of Caucasian, African American, and disaggregated Asian subpopulations. Survival curves were used to identify differences in median overall survival, and a multivariate analysis was performed to determine which factors impact overall survival. RESULTS: A total of 1317 (5%) patients were of AsA origin. Median survival for the overall AsA population is 15.1 months compared with Caucasian (11.5 months) and African Americans (11.4 months) (p < 0.0001). Within the AsA groups, the Korean subpopulation had the lowest survival at 12.6 months, whereas Filipinos had the longest survival at 19.1 months (p < 0.0001). Patients of Filipino descent had the highest rate of surgical resection but lower chemotherapy utilization. Conversely, Korean patients had the highest utilization of multimodality therapy. Multivariate analysis demonstrated that belonging to Chinese, Filipino, or Indian ethnicity was associated with decreased risk of mortality. CONCLUSIONS: There are disparate differences in survival for patients with GBC between AsA groups. Socioeconomic, genetic, and epigenetic factors may influence these differences. Further research is needed to delineate the causes of this disparity.

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Solitary fibrous tumor (SFT) is a rare fibroblastic mesenchymal neoplasm. The current classification has merged SFT and hemangiopericytoma (HPC) into the same tumor entity, while the risk stratification models have been developed to compensate for clinical prediction. Typically, slow-growing and asymptomatic, SFT can occur in various anatomical sites, most commonly in the pleura. Histologically, SFT consists of spindle to oval cells with minimal patterned growth, surrounded by stromal collagen and unique vascular patterns. Molecularly, SFT is defined by the fusion of NGFI-A-binding protein 2 (NAB2) and signal transducer and activator of transcription 6 (STAT6) genes as NAB2-STAT6. This fusion transforms NAB2 into a transcriptional activator, activating early growth response 1 (EGR1) and contributing to SFT pathogenesis and development. There are several fusion variants of NAB2-STAT6 in tumor tissues, with the most frequent ones being NAB2ex4-STAT6ex2 and NAB2ex6-STAT6ex16/ex17. Diagnostic methods play a crucial role in SFT clinical practice and basic research, including RT-PCR, next-generation sequencing (NGS), FISH, immunohistochemistry (IHC), and Western blot analysis, each with distinct capabilities and limitations. Traditional treatment strategies of SFT encompass surgical resection, radiation therapy, and chemotherapy, while emerging management regimes include antiangiogenic agents, immunotherapy, RNA-targeting technologies, and potential targeted drugs. This review provides an update on SFT's clinical and molecular aspects, diagnostic methods, and potential therapies.

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Individuals who have more ambition-a persistent striving for success, attainment, and accomplishment-are more likely to become leaders. But are these ambitious individuals also more effective in leadership roles? We hypothesize that leader ambition is related to positive self-views of leader effectiveness that remain uncorroborated by relevant third-party actors. In a multiwave, preregistered study, we find evidence for this hypothesis using a sample of executives (N = 3,830 ratings of 472 leaders) who were rated by peers, subordinates, managers, and themselves on ten leadership competencies, including their ability to motivate others, manage collaborative work, coach and develop people, and present and communicate ideas. We consider the implications of our findings for both scholars and practitioners interested in leadership selection and development.

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ABSTRACT: One-fifth of US adults experience chronic pain, which is associated with increased tobacco and cannabis use. Although bidirectional relationships between tobacco and pain have been demonstrated, pathways between pain, cannabis use, and co-use of cannabis and tobacco are understudied. We aimed to estimate the effects of (1) substance use (exclusive and co-use of cannabis and tobacco) on later pain intensity, and (2) pain intensity on later substance use. Data were from 31,983 adults in biennial surveys (2015-2021) of the US nationally representative longitudinal Population Assessment of Tobacco and Health Study (n = 71,055 pairs of consecutive surveys; T1 and T2). Past-week pain intensity was dichotomized (≤4/10 no/low pain; >4/10 moderate/severe pain). Mutually exclusive substance use categories (past 30 days) were no cannabis/tobacco use; exclusive cannabis/tobacco use; and co-use. Logistic regression assessed whether T1 substance use affected moderate/severe pain at T2. Multinomial models assessed whether pain status at T1 affected substance use at T2. Compared with no cannabis/tobacco use at T1, co-use (OR: 2.29 [95% CI: 2.09-2.51]), exclusive tobacco use (2.00 [1.86-2.14]), and exclusive cannabis use (1.35 [1.13-1.61]) were all associated with moderate/severe pain at T2. Moderate/severe pain at T1 increased odds of co-use (2.43 [2.22-2.66]), exclusive tobacco (2.12 [1.98-2.28]), and exclusive cannabis use (1.46 [1.29-1.65]) compared with no cannabis/tobacco use at T2, and increased odds of co-use at T2 compared with exclusive cannabis/tobacco use. Findings demonstrated bidirectional relationships between pain and the exclusive use and co-use of cannabis and tobacco and indicate potential synergy in the co-use of cannabis and tobacco with respect to pain.

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We hereby report the development of a novel electrochemical method to degrade perfluorooctanoic acid (C7F15COOH, PFOA). At the center of the approach are bimetallic Pd-Ru nano-catalyst materials called IMPACT: Innovative (nano)Materials and Processes for Advanced Catalytic Technologies. IMPACT uses flavonoid-sequestered Pd-Ru, allowing the development of specialized electrodes with tunable properties to sequentially degrade PFOA in wastewater samples into a sustainable byproduct via an indirect electrochemical method. Electron transfers at RuOxHy species stabilize the Pd component of the nano-catalysts, enabling the degradation process via PFOA deprotonation, chain shortening, decarboxylation, hydrolysis, fluoride elimination, and CF2 flake-off mechanism. IMPACT enabled the observation of redox peaks at -0.26 V and 0.56 V for the first time, with accompanying reduction peaks at -0.5V and 0.29 V, respectively. These redox peaks, which correlated with the concentrations of PFOA (20, 50, 100, 200, and 400. mg L-1), were verified and confirmed using electrochemical simulations. Control experiments did not show degradation of PFOA in the absence of Pd-Ru nano-catalyst. The degradation in wastewater was obtained within 3 h with an efficiency of 98.5%. The electrochemical degradation products of PFOA were identified using High-resolution desalting paper spray mass spectrometry (DPS-MS) and collision-induced dissociation (CID) analysis. The results yielded C2F5COOH, C3F7COOH, and C6F13OH with dissociation losses of CF2O or CO2. IMPACT introduces a novel nano-catalyst with high efficiency and a reliable capability that defluorinates strong C-F bonds that are components of recalcitrant organics in myriad environmental matrices.

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This final analysis from the phase 4 BYOND trial reports outcomes with bosutinib in patients with previously treated chronic myeloid leukemia (CML); 163 patients with CML resistant/intolerant to previous tyrosine kinase inhibitors received bosutinib (starting dose: 500 mg QD). At study completion (median follow-up, 47.8 months), 48.1% (n = 75/156) of patients with Philadelphia chromosome-positive chronic phase CML were still receiving treatment. Among evaluable patients, 71.8% (95% CI, 63.9-78.9) and 59.7% (95% CI, 51.4-67.7) attained or maintained major molecular response (MMR) and molecular response (MR)4, respectively, at any time on treatment. The majority of patients achieved a deeper molecular response relative to baseline while on bosutinib. Kaplan-Meier probabilities (95% CI) of maintaining MMR and MR4 at 36 months were 87.2% (78.0-92.7) and 80.7% (69.4-88.1), respectively. At 48 months, the Kaplan-Meier overall survival rate was 88.3% (95% CI, 81.8-92.6); there were 17 deaths, including 2 that were considered CML related. Long-term adverse events (AEs) were consistent with the known safety profile of bosutinib, and no new safety issues were identified. The management of AEs through dose reduction maintained efficacy while improving tolerability. These results support the use of bosutinib in patients with previously treated CML.ClinicalTrials.gov, NCT02228382.

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The cotranslational misfolding of the cystic fibrosis transmembrane conductance regulator chloride channel (CFTR) plays a central role in the molecular basis of cystic fibrosis (CF). The misfolding of the most common CF variant (ΔF508) remodels both the translational regulation and quality control of CFTR. Nevertheless, it is unclear how the misassembly of the nascent polypeptide may directly influence the activity of the translation machinery. In this work, we identify a structural motif within the CFTR transcript that stimulates efficient -1 ribosomal frameshifting and triggers the premature termination of translation. Though this motif does not appear to impact the interactome of wild-type CFTR, silent mutations that disrupt this RNA structure alter the association of nascent ΔF508 CFTR with numerous translation and quality control proteins. Moreover, disrupting this RNA structure enhances the functional gating of the ΔF508 CFTR channel at the plasma membrane and its pharmacological rescue by the CFTR modulators contained in the CF drug Trikafta. The effects of the RNA structure on ΔF508 CFTR appear to be attenuated in the absence of the ER membrane protein complex (EMC), which was previously found to modulate ribosome collisions during "preemptive quality control" of a misfolded CFTR homolog. Together, our results reveal that ribosomal frameshifting selectively modulates the assembly, function, and pharmacological rescue of a misfolded CFTR variant. These findings suggest interactions between the nascent chain, quality control machinery, and ribosome may dynamically modulate ribosomal frameshifting in order to tune the processivity of translation in response to cotranslational misfolding.

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Mood disorders affect over ten percent of humans, but studies dissecting the brain anatomical and molecular neurobiological mechanisms underlying mood (dys)functions have not consistently identified the patterns of pathological changes in relevant brain regions. Recent studies have identified pathological changes in the anterior insula (Ant-Ins) and subgenual anterior cingulate (sgACC) brain network in mood disorders, in line with this network's role in regulating mood/affective feeling states. Here, we applied whole-tissue RNA-sequencing measures of differentially expressed genes (DEGs) in mood disorders versus (vs.) psychiatrically unaffected controls (controls) to identify postmortem molecular pathological markers for mood disorder phenotypes. Using data-driven factor analysis of the postmortem phenotypic variables to determine relevant sources of population variances, we identified DEGs associated with mood disorder-related diagnostic phenotypes by combining gene co-expression, differential gene expression, and pathway-enrichment analyses. We found downregulation/under expression of inflammatory, and protein synthesis-related genes associated with psychiatric morbidity (i.e., all co-occurring mental disorders and suicide outcomes/death by suicide) in Ant-Ins, in contrasts to upregulation of synaptic membrane and ion channel-related genes with increased psychiatric morbidity in sgACC. Our results identified a preponderance of downregulated metabolic, protein synthesis, inflammatory, and synaptic membrane DEGs associated with suicide outcomes in relation to a factor representing longevity in the Ant-Ins and sgACC (AIAC) network. Our study revealed a critical brain network molecular repertoire for mood disorder phenotypes, including suicide outcomes and longevity, and provides a framework for defining dosage-sensitive (i.e., downregulated vs. upregulated) molecular signatures for mood disorder phenotypic complexity and pathological outcomes.

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Multidisciplinary tumor boards (MTBs) facilitate decision-making among subspecialists in the care of oncology patients, but the mechanisms by which they enhance outcomes remain incompletely understood. Our aim was to measure the agreement between sarcoma MTBs and radiology reports' disease assessment and management recommendations. This single-center IRB-approved retrospective study evaluated cases presented at a weekly sarcoma MTB from 1 August 2020 to 31 July 2021. Cases without clinical notes, imaging studies, or radiology reports were excluded. The data collected included the patient's clinical status at the time of the MTB, the treatment response assessment by the MTB and radiologists (stable disease; partial response; complete response; progressive disease/recurrence), and the recommendations of the radiology reports and of the MTB. The agreement between the initial radiologist review and MTB on disease assessment and recommendations was analyzed using kappa statistics. In total, 283 cases met the inclusion criteria. Radiology reports provided recommendations in 34.3% of cases, which were adhered to by the ordering providers in 73.2% of cases. The agreement between MTBs and radiology reports was moderate in disease assessment (86.2% agreement; κ = 0.78; p < 0.0001) and negligible in recommendations (36% agreement; κ = 0.18; p < 0.0001). Radiologists were more likely to assign progressive disease/recurrence than MTBs (54.4% vs. 44.4%; p < 0.001) and to recommend short-term imaging follow-up more commonly than MTBs (46.4% vs. 21.7%; p < 0.001). At a tertiary care center, radiologists' isolated interpretations of imaging findings and management recommendations frequently differ from the MTB's consensus, reflecting the value of multidisciplinary discussions incorporating the patient's clinical status and the available treatment options into the final radiographic assessment.

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Osteosarcoma (OS) is a bone malignant tumor affecting children, adolescents and young adults. Currently, osteosarcoma is treated with chemotherapy regimens established over 40 years ago. The investigation of novel therapeutic strategies for the treatment of osteosarcoma remains an important clinical need. Cyclin-dependent kinases (CDKs) have been considered promising molecular targets in cancer therapy. Among these, CDK12 has been shown to play a crucial role in the pathogenesis of malignancies, but its clinical significance and biological mechanisms in osteosarcoma remain unclear. In the present study, we aim to determine the expression and function of CDK12, and evaluate its prognostic and therapeutic value in metastatic osteosarcoma. We found that overexpression of CDK12 was associated with high tumor grade, tumor progression and reduced patient survival. Underlying mechanism revealed that knockdown of CDK12 expression with siRNA or functional inhibition with the CDK12-targeting agent THZ531 effectively exhibited time- and dose-dependent cytotoxicity. Downregulation of CDK12 paused transcription by reducing RNAP II phosphorylation, interfered with DNA damage repair with increased γH2AX, and decreased cell proliferation through the PI3K-AKT pathway. This was accompanied by the promotion of apoptosis, as evidenced by enhanced Bax expression and reduced Bcl-xL expression. Furthermore, the CDK12 selective inhibitor THZ531 also hindered ex vivo 3D spheroid formation, growth of in vitro 2D cell colony, and prevented cell mobility. Our findings highlight the clinical importance of CDK12 as a potentially valuable prognostic biomarker and therapeutic target in metastatic osteosarcoma.

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In many animal species, the oocyte meiotic spindle, which is required for chromosome segregation, forms without centrosomes. In some systems, Ran-GEF on chromatin initiates spindle assembly. We found that in Caenorhabditis elegans oocytes, endogenously-tagged Ran-GEF dissociates from chromatin during spindle assembly but re-associates during meiotic anaphase. Meiotic spindle assembly occurred after auxin-induced degradation of Ran-GEF, but anaphase I was faster than controls and extrusion of the first polar body frequently failed. In search of a possible alternative pathway for spindle assembly, we found that soluble tubulin concentrates in the nuclear volume during germinal vesicle breakdown. We found that the concentration of soluble tubulin in the metaphase spindle region is enclosed by ER sheets which exclude cytoplasmic organelles including mitochondria and yolk granules. Measurement of the volume occupied by yolk granules and mitochondria indicated that volume exclusion would be sufficient to explain the concentration of tubulin in the spindle volume. We suggest that this concentration of soluble tubulin may be a redundant mechanism promoting spindle assembly near chromosomes.

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Human plasminogen (PLG), the zymogen of the fibrinolytic protease, plasmin, is a polymorphic protein with two widely distributed codominant alleles, PLG/Asp453 and PLG/Asn453. About 15 other missense or non-synonymous single nucleotide polymorphisms (nsSNPs) of PLG show major, yet different, relative abundances in world populations. Although the existence of these relatively abundant allelic variants is generally acknowledged, they are often overlooked or assumed to be non-pathogenic. In fact, at least half of those major variants are classified as having conflicting pathogenicity, and it is unclear if they contribute to different molecular phenotypes. From those, PLG/K19E and PLG/A601T are examples of two relatively abundant PLG variants that have been associated with PLG deficiencies (PD), but their pathogenic mechanisms are unclear. On the other hand, approximately 50 rare and ultra-rare PLG missense variants have been reported to cause PD as homozygous or compound heterozygous variants, often leading to a debilitating disease known as ligneous conjunctivitis. The true abundance of PD-associated nsSNPs is unknown since they can remain undetected in heterozygous carriers. However, PD variants may also contribute to other diseases. Recently, the ultra-rare autosomal dominant PLG/K311E has been found to be causative of hereditary angioedema (HAE) with normal C1 inhibitor. Two other rare pathogenic PLG missense variants, PLG/R153G and PLG/V709E, appear to affect platelet function and lead to HAE, respectively. Herein, PLG missense variants that are abundant and/or clinically relevant due to association with disease are examined along with their world distribution. Proposed molecular mechanisms are discussed when known or can be reasonably assumed.

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Recurrent pregnancy loss devastates parents and frustrates doctors, especially when the pregnancy progresses to the second trimester. Cervical insufficiency is the most common cause of second-trimester pregnancy loss. Abdominal cerclage is the treatment option for women with failed vaginally applied cervical cerclage. We report a 33-year-old para 0 with a history of nine second-trimester pregnancy losses. She had six failed transvaginal cerclages using McDonald's procedure. A vaginal double cervical cerclage was placed in her index pregnancy. Two mersilene tape purse-string sutures were placed in the submucosal layer of the cervix; the first 1cm below and the second at the level of the internal os. Both sutures were knotted at the 12 O'Clock position on the cervix. She carried her pregnancy to almost term and delivered a healthy baby girl weighing 2.5kg. We recommend a transvaginal double cervical cerclage with mersilene tape using a modified McDonald's technique as a viable alternative to abdominal cervical cerclage. (Afr J Reprod Health 2024; 28 [6]: 117-125).

Les fausses couches récurrentes sont dévastatrices pour les parents et frustrent les médecins, surtout lorsque la grossesse progresse jusqu'au deuxième trimestre. L'insuffisance cervicale est la cause la plus fréquente de fausse couche au deuxième trimestre. Le cerclage abdominal est l'option de traitement pour les femmes dont le cerclage cervical appliqué par voie vaginale a échoué. Nous rapportons une para 0 de 33 ans avec des antécédents de neuf fausses couches au deuxième trimestre. Elle a eu six cerclages transvaginaux selon la procédure McDonald's qui ont échoué. Un double cerclage vaginal vaginal a été placé lors de sa grossesse index. Deux fils de suture en bourse en ruban de mersilène ont été placés dans la couche sous-muqueuse du col de l'utérus ; le premier 1cm en dessous et le second au niveau de l'os interne. Les deux sutures ont été nouées à la position 12 heures sur le col. Elle a mené sa grossesse presque à terme et a donné naissance à une petite fille en bonne santé pesant 2,5 kg. Nous recommandons un double cerclage cervical transvaginal avec du ruban de mersilène en utilisant une technique McDonald's modifiée comme alternative viable au cerclage cervical abdominal. (Afr J Reprod Health 2024; 28 [6]: 117-125).

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