bluuebunny/crossref_metadata_2025_split huggingface dataset:
Planting one thousand seeds of entrepreneurs
Authors: Queen Pamela 
Published: August 2024

Research methodology
This case is based on secondary information and data about the Goldman Sachs One Million Black Women initiative and youth entrepreneurship programs from press releases, news articles and websites. The protagonist has been disguised. This case has been classroom-tested in a core MBA course in both face-to-face and online delivery methods.

Case overview/synopsis
In March 2021, Goldman Sachs launched its One Million Black Women initiative which expanded its inclusive growth goals to support Black women entrepreneurs who were under-represented and under-resourced. This initiative is one of Goldman Sachs’s sponsored programs that aid existing entrepreneurs. This program would invest $10bn over the next decade to advance racial equity, promote entrepreneurial activity and increase and economic opportunities for these highly motivated and resilient Black women. With the buzz from this initiative, Johnnetta who was a Black female manager at a financial services competitor of Goldman Sachs conceived another approach to groom and grow future generations of women of color entrepreneurs. Her idea was to implement youth entrepreneurship programs in middle schools in states with high populations of students of color. Based on a psychological theory of entrepreneurship approach, these students would learn about entrepreneurship and gain hands-on experience with starting and operating a business. The program was called “Planting 1000 Seeds of Entrepreneurs” to develop a pipeline of savvy, well-prepared future women of color entrepreneurs. Johnnetta’s dilemma was whether to pitch this new youth entrepreneurship program as an employee at her employer as a diversity, equity and inclusion (DEI) initiative or start this program as an entrepreneur of a nonprofit in which she would have sole autonomy to administer this program. This case will enable students to develop ideas into a compelling business pitch while sparking debate about approaches to foster DEI initiatives that will have impactful economic benefits for women of color entrepreneurs.

Complexity academic level
This case is best suited for upper-level undergraduate or graduate students taking business administration courses in management, entrepreneurship, women studies or other courses that cover topics or modules related to DEI initiatives involving women in business.
Wolbachia confers protection against the entomopathogenic fungus Metarhizium pingshaense in African Aedes aegypti
Authors: Bilgo Etienne , Mancini Maria Vittoria , Gnambani Jacques E. , Dokpomiwa Houeffa Adeline Tatiana , Murdochy Shivan , Lovett Brian , St. Leger Raymond , Sinkins Steven P. , Diabate Abdoulaye 
Published: August 2024

AbstractSymbiotic and pathogenic microorganisms such as bacteria and fungi represent promising alternatives to chemical insecticides to respond to the rapid increase of insecticide resistance and vector‐borne disease outbreaks. This study investigated the interaction of two strains of Wolbachia, wAlbB and wAu, with the natural entomopathogenic fungi from Burkina Faso Metarhizium pingshaense, known to be lethal against Anopheles mosquitoes. In addition to showing the potential of Metarhizium against African Aedes aegypti wild‐type populations, our study shows that the wAlbB and wAu provide a protective advantage against entomopathogenic fungal infections. Compared to controls, fungal‐infected wAu and wAlbB‐carrying mosquitoes showed higher longevity, without any significant impact on fecundity and fertility phenotypes. This study provides new insights into the complex multipartite interaction among the mosquito host, the Wolbachia endosymbiont and the entomopathogenic fungus that might be employed to control mosquito populations. Future research should investigate the fitness costs of Wolbachia, as well as its spread and prevalence within mosquito populations. Additionally, evaluating the impact of Wolbachia on interventions involving Metarhizium pingshaense through laboratory and semi‐field population studies will provide valuable insights into the effectiveness of this combined approach.
Microtubule‐associated NAV3 regulates invasive phenotypes in glioblastoma cells
Authors: Škarková Aneta , Pelantová Markéta , Tolde Ondřej , Legátová Anna , Mateu Rosana , Bušek Petr , Garcia‐Borja Elena , Šedo Aleksi , Etienne‐Manneville Sandrine , Rösel Daniel , Brábek Jan 
Published: August 2024

AbstractGlioblastomas are aggressive brain tumors for which effective therapy is still lacking, resulting in dismal survival rates. These tumors display significant phenotypic plasticity, harboring diverse cell populations ranging from tumor core cells to dispersed, highly invasive cells. Neuron navigator 3 (NAV3), a microtubule‐associated protein affecting microtubule growth and dynamics, is downregulated in various cancers, including glioblastoma, and has thus been considered a tumor suppressor. In this study, we challenge this designation and unveil distinct expression patterns of NAV3 across different invasion phenotypes. Using glioblastoma cell lines and patient‐derived glioma stem‐like cell cultures, we disclose an upregulation of NAV3 in invading glioblastoma cells, contrasting with its lower expression in cells residing in tumor spheroid cores. Furthermore, we establish an association between low and high NAV3 expression and the amoeboid and mesenchymal invasive phenotype, respectively, and demonstrate that overexpression of NAV3 directly stimulates glioblastoma invasive behavior in both 2D and 3D environments. Consistently, we observed increased NAV3 expression in cells migrating along blood vessels in mouse xenografts. Overall, our results shed light on the role of NAV3 in glioblastoma invasion, providing insights into this lethal aspect of glioblastoma behavior.
Reproduce to validate: A comprehensive study on the reproducibility of economics research
Authors: Herbert Sylvérie , Kingi Hautahi , Stanchi Flavio , Vilhuber Lars 
Published: August 2024

AbstractJournals have pushed for transparency of research through data availability policies. Such data policies improve availability of data and code, but what is the impact on reproducibility? We present results from a large reproduction exercise for articles published in the American Economic Journal: Applied Economics, which has had a data availability policy since its inception in 2009. Out of 363 published articles, we assessed 274 articles. All articles provided some materials. We excluded 122 articles that required confidential or proprietary data or that required the replicator to otherwise obtain the data (44.5% of assessed articles). We attempted to reproduce 152 articles and were able to fully reproduce the results of 68 (44.7% of attempted reproductions). A further 66 (43.4% of attempted reproductions) were partially reproduced. Many articles required complex code changes even when at least partially reproduced. We collect bibliometric characteristics of authors, but find no evidence for author characteristics as determinants of reproducibility. There does not appear to be a citation bonus for reproducibility. The data availability policy of this journal was effective to ensure availability of materials, but is insufficient to ensure reproduction without additional work by replicators.
Deciphering the neuroprotective mechanisms of RACK1 in cerebral ischemia‐reperfusion injury: Pioneering insights into mitochondrial autophagy and the PINK1/Parkin axis
Authors: Zhao Lanqing , Chen Yu , Li Hongxi , Ding Xiaoxu , Li Jinwei 
Published: August 2024

AbstractIntroductionCerebral ischemia‐reperfusion injury (CIRI) is a common and debilitating complication of cerebrovascular diseases such as stroke, characterized by mitochondrial dysfunction and cell apoptosis. Unraveling the molecular mechanisms behind these processes is essential for developing effective CIRI treatments. This study investigates the role of RACK1 (receptor for activated C kinase 1) in CIRI and its impact on mitochondrial autophagy.MethodsWe utilized high‐throughput transcriptome sequencing and weighted gene co‐expression network analysis (WGCNA) to identify core genes associated with CIRI. In vitro experiments used human neuroblastoma SK‐N‐SH cells subjected to oxygen and glucose deprivation (OGD) to simulate ischemia, followed by reperfusion (OGD/R). RACK1 knockout cells were created using CRISPR/Cas9 technology, and cell viability, apoptosis, and mitochondrial function were assessed. In vivo experiments involved middle cerebral artery occlusion/reperfusion (MCAO/R) surgery in rats, evaluating neurological function and cell apoptosis.ResultsOur findings revealed that RACK1 expression increases during CIRI and is protective by regulating mitochondrial autophagy through the PINK1/Parkin pathway. In vitro, RACK1 knockout exacerbated cell apoptosis, while overexpression of RACK1 reversed this process, enhancing mitochondrial function. In vivo, RACK1 overexpression reduced cerebral infarct volume and improved neurological deficits. The regulatory role of RACK1 depended on the PINK1/Parkin pathway, with RACK1 knockout inhibiting PINK1 and Parkin expression, while RACK1 overexpression restored them.ConclusionThis study demonstrates that RACK1 safeguards against neural damage in CIRI by promoting mitochondrial autophagy through the PINK1/Parkin pathway. These findings offer crucial insights into the regulation of mitochondrial autophagy and cell apoptosis by RACK1, providing a promising foundation for future CIRI treatments.
Effects of batroxobin on the antithrombotic system in patients with cerebral venous thrombosis: Clues to mechanisms
Authors: Lan Duo , Jiao Baolian , Song Siying , Wang Mengqi , Zhang Xiaoming , Huang Xiangqian , Guo Yibing , Ding Yuchuan , Ji Xunming , Meng Ran 
Published: August 2024

AbstractBackground and PurposeMore evidence supports the benefits of batroxobin combined with anticoagulation in correcting acute cerebral venous thrombosis (CVT). The dynamic fluctuations of peripheral blood platelets, fibrinolysis, and coagulation biomarkers during this therapy were analyzed.MethodsWe investigated batroxobin's effects on the antithrombotic system under two regimens. The pretreatment group included patients on anticoagulants for at least 1 week before starting batroxobin. The simultaneous treatment group began both treatments upon admission. The control group received only anticoagulation. Batroxobin was given on alternate days at doses of 10BU, 5BU, and 5BU, totaling three doses. Anticoagulation was continuous. Baseline data were T0; the next day after each batroxobin dose was T1, T2, and T3. Data from these four time points was analyzed.ResultsThe time‐point paired sample T‐test results of the pretreatment group [n = 60; mean age (SD), 43.3(16.5); 38 (63.35%) women] showed that batroxobin significantly inhibited ADP‐induced platelet aggregation rate (T1–T0: p = 0.015; T2–T0: p = 0.025; T3–T0: p = 0.013), decreased fibrinogen level (T1–T0: p < 0.001; T2–T0: p < 0.001; T3–T0: p < 0.001), and increased D‐dimer (T1–T0:p < 0.001; T2–T0: p < 0.001; T3–T0: p < 0.001), TT (T1–T0:p = 0.046; T2–T0: p = 0.003; T3–T0: p < 0.001), and APTT (T1–T0:p = 0.021; T2–T0: p = 0.012; T3–T0: p = 0.026). Compared to the control group, the simultaneous treatment group showed significantly higher TT (T2: p = 0.002; T3: p = 0.004) and D‐dimer (T1: p < 0.001; T2: p < 0.001; T3: p < 0.001) values, while fibrinogen (T2: p < 0.001; T3: p < 0.001) levels were significantly lower. Using batroxobin can alleviate the amplitude of changes in coagulation indicators other than TT caused by anticoagulants. The above conclusions are consistent with the results of repeated measurement data analysis.ConclusionsBatroxobin can significantly inhibit ADP‐induced platelet aggregation rate, increase D‐dimer, decrease fibrinogen, and prolong TT and APTT in the presence of anticoagulant agents. Using batroxobin can reduce the amplitude of changes in coagulation indicators caused by anticoagulants. These results reveal the potential mechanism of batroxobin combined with anticoagulation in the safe and effective treatment of CVT.
Nesfatin‐1 inhibits cerebral aneurysms by activating Nrf2 and inhibiting NF‐κB signaling
Authors: Yu Huimin , Liu Qingyuan , Xie Minghong , Fan Junquan , Luo Jiajia , Huang Junping , Chen Lei 
Published: August 2024

AbstractAimsCerebral aneurysm (CA) has been considered one of the most common cerebrovascular diseases, affecting millions of people worldwide. A therapeutic agent is currently missing for the treatment of CA. Nesfatin‐1 (Nes‐1) is an 82‐amino acid adipokine which possesses a wide range of biological functions. However, the physiological function of Nes‐1 in CA is still unknown. Here, we aimed to assess the preventive effects of Nes‐1 in the pathological development of CA and elucidate the mechanisms behind this.MethodsWe used an elastase‐induced CA model, accompanied by a high‐salt diet to induce hypertension. Additionally, diverse experimental techniques, including Verhoeff‐Van Gieson staining, real time PCR, enzyme‐linked immuno sorbent assay (ELISA), and immunofluorescence staining, were employed to assess CA formation, gene and protein expression, as well as the macrophage infiltration.ResultsOur results indicate that administration of Nes‐1 significantly decreased the aneurysm size. Additionally, Nes‐1 prevented inflammatory response by inhibiting the expression of interleukin‐6 (IL‐6), tumor necrosis factor‐α (TNF‐α), and monocyte chemoattractant protein 1 (MCP‐1) at both the mRNA and protein levels in the Circle of Willis (COW) region. Also, the increased levels of matrix metalloproteinase‐2 (MMP‐2) and matrix metalloproteinase‐9 (MMP‐9) in the COW region were reduced by Nes‐1. We found that Nes‐1 administration suppressed the invasion of macrophages. Mechanistically, Nes‐1 activated Nrf‐2 by promoting its nuclear translocation but prevented the activation of the IκBα/NF‐κB signaling pathway.ConclusionThese findings suggest that Nes‐1 might be used as a promising agent for the prevention of CA.
Treating activated regulatory T cells with pramipexole protects human dopaminergic neurons from 6‐OHDA‐induced degeneration
Authors: Guevara‐Salinas Adrián , Netzahualcoyotzi Citlalli , Álvarez‐Luquín Diana Denisse , Pérez‐Figueroa Erandi , Sevilla‐Reyes Edgar E. , Castellanos‐Barba Carlos , Vega‐Ángeles Vera Teresa , Terán‐Dávila Edgar , Estudillo Enrique , Velasco Iván , Adalid‐Peralta Laura 
Published: August 2024

AbstractBackgroundParkinson's disease (PD) is a chronic neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra, which promotes a sustained inflammatory environment in the central nervous system. Regulatory T cells (Tregs) play an important role in the control of inflammation and might play a neuroprotective role. Indeed, a decrease in Treg number and function has been reported in PD. In this context, pramipexole, a dopaminergic receptor agonist used to treat PD symptoms, has been shown to increase peripheral levels of Treg cells and improve their suppressive function. The aim of this work was to determine the effect of pramipexole on immunoregulatory Treg cells and its possible neuroprotective effect on human dopaminergic neurons differentiated from human embryonic stem cells.MethodsTreg cells were sorted from white blood cells of healthy human donors. Assays were performed with CD3/CD28‐activated and non‐activated Treg cells treated with pramipexole at concentrations of 2 or 200 ng/mL. These regulatory cells were co‐cultured with in vitro‐differentiated human dopaminergic neurons in a cytotoxicity assay with 6‐hydroxydopamine (6‐OHDA). The role of interleukin‐10 (IL‐10) was investigated by co‐culturing activated IL‐10‐producing Treg cells with neurons. To further investigate the effect of treatment on Tregs, gene expression in pramipexole‐treated, CD3/CD28‐activated Treg cells was determined by Fluidigm analysis.ResultsPramipexole‐treated CD3/CD28‐activated Treg cells showed significant protective effects on dopaminergic neurons when challenged with 6‐OHDA. Pramipexole‐treated activated Treg cells showed neuroprotective capacity through mechanisms involving IL‐10 release and the activation of genes associated with regulation and neuroprotection.ConclusionAnti‐CD3/CD28‐activated Treg cells protect dopaminergic neurons against 6‐OHDA‐induced damage. In addition, activated, IL‐10‐producing, pramipexole‐treated Tregs also induced a neuroprotective effect, and the supernatants of these co‐cultures promoted axonal growth. Pramipexole‐treated, activated Tregs altered their gene expression in a concentration‐dependent manner, and enhanced TGFβ‐related dopamine receptor regulation and immune‐related pathways. These findings open new perspectives for the development of immunomodulatory therapies for the treatment of PD.
Determining the role of statins in Parkinson's disease risk reduction and disease modification: A comprehensive meta‐analysis of 4 million participants' data
Authors: Mady Abdelrahman , Nabil Yehia , Daoud Asma , Alnajjar Asmaa Zakria , Alsalloum Taleb , Marwan Menna , Abdelmeseh Maickel , Elsayed Moaz , Krayim Abdulrahman , Alaa Mohamed , Masoud Mahmoud , Bushara Nagham , Faisal Roaa , Ahmed Hayat , Saad Mohamed , Belabaci Zineddine , Barrett Matthew J. , Berman Brian , Negida Ahmed 
Published: August 2024

AbstractBackgroundMany observational studies have examined the association between statins and the incidence of Parkinson's disease (PD) in high‐risk populations. On the other hand, clinical trials as well as other observational studies investigated the safety and efficacy of statins in slowing disease progression in PD patients. However, the evidence has been inconclusive in both questions. To that end, we conducted this systematic review and meta‐analysis to synthesize evidence on the role of statins in decreasing the risk of PD among high‐risk populations and as a possible disease‐modifying agent for patients with PD.MethodsA comprehensive literature search of electronic databases including PubMed, Scopus, Cochrane, and Web of Science has been performed. Relevant studies were chosen and data were extracted and analyzed using RevMan software version 5.4.1.ResultsTwenty‐five studies (14 cohort, 9 case–control, and 2 randomized controlled trials) have been included in the present systematic review. Of them, 21 studies reported the association between statins and PD risk. Statins were found to significantly reduce the risk of developing PD (pooled RR 0.86, 95% CI [0.77–0.95], p < 0.005). Four studies investigated statins as a disease‐modifying agent. The pooled mean difference (MD) in the UPDRS‐III from baseline to endpoint did not differ significantly between the statin and control groups (MD −1.34 points, 95% CI [−3.81 to 1.14], p = 0.29).ConclusionAlthough epidemiological observational studies showed that statin use was associated with a reduced risk of PD, current evidence is insufficient to support the role of statins in slowing the progression of PD. These findings are limited by the fact that most of the included studies are observational studies which carry a high risk of confounding bias which highlights the need for future well‐designed RCTs.
Serotonin (5‐HT)2A/2C receptor agonist 2,5‐dimethoxy‐4‐iodophenyl‐2‐aminopropane hydrochloride improves detrusor sphincter dyssynergia by inhibiting L‐type voltage‐gated calcium channels in spinal cord injured rats
Authors: Lv Rong , Li Mingzhuo , Chen Xun , Li Shengtian , Cao Nailong , Gu Baojun 
Published: August 2024

AbstractAimsTo explore the role of voltage‐gated calcium channels (VGCC) in 5‐HT2A/2C receptor agonist 2,5‐dimethoxy‐4‐iodophenyl‐2‐aminopropane hydrochloride's improvement of spinal cord injury (SCI) induced detrusor sphincter dyssynergia and the expressions of the 5‐hydroxy tryptamine (5‐HT) 2A receptors and VGCCs in lumbosacral cord after SCI.MethodsFemale Sprague–Dawley rats were randomized into normal control group and SCI group (N = 15 each). Cystometrogram (CMG), simultaneous CMG, and external urethral sphincter electromyography (EUS‐EMG) were conducted in all groups under urethane anesthesia. Drugs were administered intrathecally during CMG and EUS‐EMG. Rats were euthanized and L6‐S1 spinal cord were acquired for immunofluorescence.ResultsIn SCI rats, intrathecal administration of 2,5‐dimethoxy‐4‐iodophenyl‐2‐aminopropane hydrochloride or L‐type VGCC blocker, nifedipine, could significantly increase voiding volume, voiding efficiency, and the number of high‐frequency oscillations. They could also prolong EUS bursting activity duration on EUS‐EMG. Moreover, the effect of 2,5‐dimethoxy‐4‐iodophenyl‐2‐aminopropane hydrochloride can be eliminated with the combined administration of L‐type VGCC agonist, (±)‐Bay K 8644. No significant differences were observed in CMG after intrathecal administration of T‐type VGCC blocker TTA‐P2. Additionally, immunofluorescence of the lumbosacral cord in control and SCI rats showed that the 5‐HT2A receptor and Cav1.2 immunolabeling‐positive neurons in the anterior horn of the lumbosacral cord were increased in SCI rats.ConclusionsOur study demonstrated that 5‐HT2A/2C agonist 2,5‐dimethoxy‐4‐iodophenyl‐2‐aminopropane hydrochloride may improve SCI‐induced DSD by inhibiting the L‐type voltage‐gated calcium channel in lumbosacral cord motoneurons.
Progress and recognition of idiopathic intracranial hypertension: A narrative review
Authors: Zhou Chenxia , Zhou Yifan , Liu Lu , Jiang Huimin , Wei Huimin , Zhou Chen , Ji Xunming 
Published: August 2024

AbstractBackgroundIdiopathic intracranial hypertension (IIH) mainly affects obese young women, causing elevated intracranial pressure, headaches, and papilledema, risking vision loss and severe headaches. Despite weight loss as the primary treatment, the underlying mechanisms remain unclear. Recent research explores novel therapeutic targets.AimsThis review aimed to provide a comprehensive understanding of IIH's pathophysiology and clinical features to inform pathogenesis and improve treatment strategies.MethodsRecent publications on IIH were searched and summarized using PubMed, Web of Science, and MEDLINE.ResultsThe review highlights potential pathomechanisms and therapeutic advances in IIH.ConclusionIIH incidence is rising, with growing evidence linking it to metabolic and hormonal disturbances. Early diagnosis and treatment remain challenging.