Miracle-dz/UniFAR-FTUs huggingface dataset:
Surgical, clinical, and radiological outcomes of occipitocervical fusion using the plate–screw–rod system with allograft in craniocervical instability

Objective: We evaluated surgical, clinical, and radiological outcomes of posterior occipitocervical fusion (OCF) using plate–rod–screw construct supplemented with allograft in cases of occipitocervical instability. Study Design: This was a retrospective analysis of prospective collected data. Methods: Data of 52 patients who underwent posterior OCF using plate–screw–rod construct supplemented with allograft at a single institute from 2009 to 2014 were analyzed. Demographics, clinical parameters (Visual Analog Score [VAS], ODI, and mJOA score), functional status (McCormick scale), radiological parameters – mean atlantodens interval, posterior occipitocervical angle, occipitocervical 2 angle, and surgical parameters (operative time, blood loss, hospital stay, and fusion) with complications were evaluated. Results: The mean age of the patients was 54.56 ± 16.21 years with male: female was 28:24. The mean operative time was 142.2 min (90–185 min) and mean blood loss was 250.8 ml. The mean duration of hospital stay was 6.7 days and mean follow-up period was 65.17 ± 5.39 months. There was significant improvement in clinical parameters (modified JOA score, VAS, and Oswestry Disability Index values) postoperatively. Forty patients showed recovery in neurological status at least in Grade 1 in McCormick scale with no neurological deterioration in any patient. Furthermore, radiological parameters at cervicomedullary junction got into acceptable range. Implant-related complications noted in 1 patient and 1 patient had vertebral artery injury. We had dural tear in 3 patients and infection in 2 patients. Fusion was achieved in 46 cases with mean time for fusion was 11.039 months. Conclusion: Patients with occipitocervical instability can successfully undergo posterior OCF using plate–screw–rod construct supplemented with allograft with high fusion rate, good clinical and functional outcomes, and low complication rate.
Genome Analysis of Lactobacillus plantarum Isolated From Some Indian Fermented Foods for Bacteriocin Production and Probiotic Marker Genes

In this study, Lactobacillus plantarum strain DHCU70 isolated from dahi, a fermented milk product and L. plantarum strain DKP1 isolated from kinema, a fermented soybean food of India, respectively were evaluated for their bacteriocin production and probiotic properties. Both strains of L. plantarum (DHCU70 and DKP1) were found to have potent antimicrobial activity against Kocuria rhizophila ATCC 9341. Bacteriocin produced by L. plantarum strains DHCU70 and DKP1 did not exhibit inhibition of cell wall, DNA and fatty acids biosynthesis mechanisms as evaluated by whole cell reporter assays. We characterized the bacteriocin encoding genes in L. plantarum strains DHCU70 and DKP1 by whole genome sequence which consisted of a single and circular chromosome with genome size of 3.38 Mb (GC content of 44.3%) and 3.39 Mb, respectively and a GC content of 44.3%. L. plantarum DHCU70 has 3252 number of protein encoding genes comprising 89 number of RNA genes (69tRNA, 16rRNA, 4nc RNA) whereas L. plantarum DKP1 has total of 3277 number of protein encoding genes with 89 number. of RNA genes (69tRNA, 16S rRNA, 4nc RNA). Analysis revealed the presence of 20.5 kb long and 23 numbers of plantaricin encoding locus (pln locus) for production of antimicrobial compound. BAGEL analysis has shown that the pln locus of both the strains of L. plantarum showed maximum sequence similarity with plantaricin NC8 of L. plantarum NC8, originally isolated from grass silage. Annotated whole genome sequence of both strains DHCU70 and DKP1 was analyzed for the presence of probiotic marker genes. The probiotic properties of these strains of were also evaluated in vitro. Due to the presence of genes responsible for antimicrobial activity and probiotic properties, both strains of L. plantarum may be considered as a suitable probiotic candidate in food industry.
Handling of Ventricular Fibrillation in the Emergency Setting

Ventricular fibrillation (VF) and sudden cardiac death (SCD) are predominantly caused by channelopathies and cardiomyopathies in youngsters and coronary heart disease in the elderly. Temporary factors, e.g., electrolyte imbalance, drug interactions, and substance abuses may play an additive role in arrhythmogenesis. Ectopic automaticity, triggered activity, and reentry mechanisms are known as important electrophysiological substrates for VF determining the antiarrhythmic therapies at the same time. Emergency need for electrical cardioversion is supported by the fact that every minute without defibrillation decreases survival rates by approximately 7%–10%. Thus, early defibrillation is an essential part of antiarrhythmic emergency management. Drug therapy has its relevance rather in the prevention of sudden cardiac death, where early recognition and treatment of the underlying disease has significant importance. Cardioprotective and antiarrhythmic effects of beta blockers in patients predisposed to sudden cardiac death were highlighted in numerous studies, hence nowadays these drugs are considered to be the cornerstones of the prevention and treatment of life-threatening ventricular arrhythmias. Nevertheless, other medical therapies have not been proven to be useful in the prevention of VF. Although amiodarone has shown positive results occasionally, this was not demonstrated to be consistent. Furthermore, the potential proarrhythmic effects of drugs may also limit their applicability. Based on these unfavorable observations we highlight the importance of arrhythmia prevention, where echocardiography, electrocardiography and laboratory testing play a significant role even in the emergency setting. In the following we provide a summary on the latest developments on cardiopulmonary resuscitation, and the evaluation and preventive treatment possibilities of patients with increased susceptibility to VF and SCD.
Optimization of a Method to Isolate and Culture Adult Porcine, Rats and Mice Müller Glia in Order to Study Retinal Diseases

Müller cells are the predominant glial elements in the retina, extending vertically across this structure, and they fulfill a wealth support roles that are critical for neurons. Alterations to the behavior and phenotype of Muüller glia are often seen in animal models of retinal degeneration and in retinal tissue from patients with a variety of retinal disorders. Thus, elucidating the mechanisms underlying the development of retinal diseases would help better understand the cellular processes involved in such pathological changes. Studies into Muüller cell activity in vitro have been hindered by the difficulty in obtaining pure cell populations and the tendency of these cells to rapidly differentiate in culture. Most protocols currently used to isolate Müller glia use neonatal or embryonic tissue but here, we report an optimized protocol that facilitates the reliable and straightforward isolation and culture of Müller cells from adult pigs, rats and mice. The protocol described here provides an efficient method for the rapid isolation of adult mammalian Müller cells, which represents a reliable platform to study therapeutic targets and to test the effects of drugs that might combat retinal diseases.
A Novel Prognostic Index Based on Alternative Splicing in Papillary Renal Cell Carcinoma

Background Papillary renal cell carcinoma (pRCC) is a heterogeneous multifocal or isolated tumor with an invasive phenotype. Previous studies presented that alternative splicing, as a crucial posttranscriptional regulator in gene expression, is associated with tumorigenesis. However, the association between alternative splicing and pRCC has not been clarified Methods The RNA sequencing data and clinical information were downloaded from The Cancer Genome Atlas database and mRNA splicing profiles from TCGASpliceSeq. The percent spliced in data of alternative splicing merged with survival information was firstly calculated by univariate Cox regression analysis to screen for survival‐associated alternative splicing events, and survival‐associated alternative splicing events were then analyzed by Gene Ontology categories using Kyoto Encyclopedia of Genes and Genomes. Meanwhile, the least absolute shrinkage and selection operator Cox analysis and multivariate Cox analysis were performed to calculate the prognostic index for each alternative splicing type. In addition, clinical factors were introduced to assess the performance of prognostic index. Results A total of 4,084 candidate survival-associated alternative splicing events in 2,558 genes were screened out. Patients were divided into the low-risk group and the high-risk group based on the median prognostic index value. The Kaplan-Meier survival analysis (p < 0.05) and receiver operating characteristics curves (AUC>0.9) indicated that prognostic index was effective and stable for predicting the prognosis of pRCC patients. Furthermore, a regulatory network was constructed incorporating alternative splicing events and survival-associated splicing factors. Conclusion Our study provides new insights into the mechanism of alternative splicing events in tumorigenesis and their clinical potential for pRCC.
MicroRNA-29b-3p Promotes Human Retinal Microvascular Endothelial Cell Apoptosis via Blocking SIRT1 in Diabetic Retinopathy

Background Diabetic retinopathy (DR) is a main complication of diabetes mellitus (DM). Recent studies have implicated microRNAs in human retinal microvascular endothelial cell (HRMEC) dysfunction. In this study, we aim to investigate the apoptotic promotion of miR-29b-3p by blocking SIRT1 in HRMEC for DR situation. Method Blood samples were obtained from DR patients and controls. Dual-luciferase reporter assay using HEK-293T cells was performed to show the direct interaction of miR-29b-3p and the 3′UTR of SIRT1. HRMECs were exposed to 5.5 mmol/L of glucose (normal control), 5.5 mmol/L of glucose and 24.5 mmol/L of mannitol (osmotic pressure control), 30 mmol/L of glucose [hyperglycemia (HG)], 150 μmol/L of CoCl2 (hypoxia), and 30 mmol/L of glucose plus 150 μmol/L of CoCl2 (HG-CoCl2). To identify the regulating relationship between miR-29b-3p and SIRT1, HRMECs were transfected with miR-29b-3p mimics/inhibitors or their negative controls. SRT1720 was used as a SIRT1 agonist. Cell viability was assessed with the cell counting kit-8 (CCK-8) assay, and apoptotic cells were stained by one-step terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay kit. Gene and protein expression were assayed by quantitative real-time reverse transcriptase-PCR (RT-qPCR) and western blotting separately. Result MiR-29b-3p was upregulated to 3.2-fold, and SIRT1 protein was downregulated to 65% in DR patients. Dual-luciferase reporter assay showed the direct interaction of miR-29b-3p and SIRT1. HRMECs were identified as >95% positive for CD31 and von Willebrand factor (vWF). MiR-29b-3p and Bax/Bcl-2 ratio was upregulated, whereas SIRT1 was downregulated in HRMECs in the HG-CoCl2 condition. Decreased cell viability and upregulated apoptosis were also found in HRMECs of the HG-CoCl2 condition. Upregulated miR-29b-3p decreased the expression of SIRT1 and increased the ratio of Bax/Bcl-2, whereas downregulated miR-29b-3p increased the expression of SIRT1 protein and downregulated the ratio of Bax/Bcl-2. SRT1720 rescued miR-29b-3p-induced HRMEC apoptosis via upregulating the expression of SIRT1 protein. Conclusion The dysregulation of miR-29b-3p/SIRT1 is a potential mechanism of HRMEC apoptosis in DR. MiR-29b-3p/SIRT1 may be a potential therapeutic target for DR.
Interplay Between Mitochondrial Oxidative Disorders and Proteostasis in Alzheimer’s Disease

Although the basis of Alzheimer’s disease (AD) etiology remains unknown, oxidative stress (OS) has been recognized as a prodromal factor associated to its progression. OS refers to an imbalance between oxidant and antioxidant systems, which usually consist in an overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) which overwhelms the intrinsic antioxidant defenses. Due to this increased production of ROS and RNS, several biological functions such as glucose metabolism or synaptic activity are impaired. In AD, growing evidence links the ROS-mediated damages with molecular targets including mitochondrial dynamics and function, protein quality control system, and autophagic pathways, affecting the proteostasis balance. In this scenario, OS should be considered as not only a major feature in the pathophysiology of AD but also a potential target to combat the progression of the disease. In this review, we will discuss the role of OS in mitochondrial dysfunction, protein quality control systems, and autophagy associated to AD and suggest innovative therapeutic strategies based on a better understanding of the role of OS and proteostasis.
Jasmonic Acid, Not Salicyclic Acid Restricts Endophytic Root Colonization of Rice

Research on the interaction between the non-nodule-forming bacterial endophytes and their host plants is still in its infancy. Especially the understanding of plant control mechanisms which govern endophytic colonization is very limited. The current study sets out to determine which hormonal signaling pathway controls endophytic colonization in rice, and whether the mechanisms deviate for a pathogen. The endophyte Azoarcus olearius BH72—rice model was used to investigate root responses to endophytes in comparison to the recently established pathosystem of rice blight Xanthomonas oryzae pv. oryzae PXO99 (Xoo) in flooded roots. In the rice root transcriptome, 523 or 664 genes were found to be differentially expressed in response to Azoarcus or Xoo colonization, respectively; however, the response was drastically different, with only 6% of the differentially expressed genes (DEGs) overlapping. Overall, Xoo infection induced a much stronger defense reaction than Azoarcus colonization, with the latter leading to down-regulation of many defense related DEGs. Endophyte-induced DEGs encoded several enzymes involved in phytoalexin biosynthesis, ROS (reactive oxygen species) production, or pathogenesis-related (PR) proteins. Among putative plant markers related to signal transduction pathways modulated exclusively during Azoarcus colonization, none overlapped with previously published DEGs identified for another rice endophyte, Azospirillum sp. B510. This suggests a large variation in responses of individual genotypic combinations. Interestingly, the DEGs related to jasmonate (JA) signaling pathway were found to be consistently activated by both beneficial endophytes. In contrast, the salicylate (SA) pathway was activated only in roots infected by the pathogen. To determine the impact of SA and JA production on root colonization by the endophyte and the pathogen, rice mutants with altered hormonal responses were employed: mutant cpm2 deficient in jasmonate synthesis, and RNA interference (RNAi) knockdown lines of NPR1 decreased in salicylic acid-mediated defense responses (NPR1-kd). Only in cpm2, endophytic colonization of Azoarcus was significantly increased, while Xoo colonization was not affected. Surprisingly, NPR1-kd lines showed slightly decreased colonization by Xoo, contrary to published results for leaves. These outcomes suggest that JA but not SA signaling is involved in controlling the Azoarcus endophyte density in roots and can restrict internal root colonization, thereby shaping the beneficial root microbiome.
Essential Role of Sperm-Specific PLC-Zeta in Egg Activation and Male Factor Infertility: An Update

Sperm-specific phospholipase C zeta (PLCζ) is widely considered to be the physiological stimulus responsible for generating calcium (Ca2+) oscillations that induce egg activation and early embryonic development during mammalian fertilization. In the mammalian testis, PLCζ expression is detected at spermiogenesis following elongated spermatid differentiation. Sperm-delivered PLCζ induces Ca2+ release via the inositol 1,4,5-trisphosphate (InsP3) signaling pathway. PLCζ is the smallest known mammalian PLC isoform identified to date, with the simplest domain organization. However, the distinctive biochemical properties of PLCζ compared with other PLC isoforms contribute to its unique potency in stimulating cytosolic Ca2+ oscillations within mammalian eggs. Moreover, studies describing PLCζ “knockout” mouse phenotypes confirm the supreme importance of PLCζ at egg activation and monospermic fertilization in mice. Importantly, a number of clinical reports have highlighted the crucial importance of PLCζ in human fertilization by associating PLCζ deficiencies with certain forms of male factor infertility. Herein, we give an update on recent advances that have refined our understanding of how sperm PLCζ triggers Ca2 + oscillations and egg activation in mammals, while also discussing the nature of a potential “alternative” sperm factor. We summarise PLCζ localization in mammalian sperm, and the direct links observed between defective PLCζ protein in sperm and documented cases of male infertility. Finally, we postulate how this sperm protein can be used as a potential diagnostic marker, and also as a powerful therapeutic agent for treatment of certain types of male infertility due to egg activation failure or even in more general cases of male subfertility.
Fluorination of Organic Spacer Impacts on the Structural and Optical Response of 2D Perovskites

Low-dimensional hybrid perovskites have triggered significant research interest due to their intrinsically tunable optoelectronic properties and technologically relevant material stability. In particular, the role of the organic spacer on the inherent structural and optical features in two-dimensional (2D) perovskites is paramount for material optimization. To obtain a deeper understanding of the relationship between spacers and the corresponding 2D perovskite film properties, we explore the influence of the partial substitution of hydrogen atoms by fluorine in an alkylammonium organic cation, resulting in (Lc)2PbI4 and (Lf)2PbI4 2D perovskites, respectively. Consequently, optical analysis reveals a clear 0.2 eV blue-shift in the excitonic position at room temperature. This result can be mainly attributed to a band gap opening, with negligible effects on the exciton binding energy. According to Density Functional Theory (DFT) calculations, the band gap increases due to a larger distortion of the structure that decreases the atomic overlap of the wavefunctions and correspondingly bandwidth of the valence and conduction bands. In addition, fluorination impacts the structural rigidity of the 2D perovskite, resulting in a stable structure at room temperature and the absence of phase transitions at a low temperature, in contrast to the widely reported polymorphism in some non-fluorinated materials that exhibit such a phase transition. This indicates that a small perturbation in the material structure can strongly influence the overall structural stability and related phase transition of 2D perovskites, making them more robust to any phase change. This work provides key information on how the fluorine content in organic spacer influence the structural distortion of 2D perovskites and their optical properties which possess remarkable importance for future optoelectronic applications, for instance in the field of light-emitting devices or sensors.
Enalapril Influence on Arterial Stiffness in Rheumatoid Arthritis Women: A Randomized Clinical Trial

Introduction: Cardiovascular parameters disruption can be found in patients at early stages of rheumatoid arthritis (RA). The primary endpoint of this study was the reduction of arterial stiffness in RA patients without traditional cardiovascular risk factors or previous comorbidities, measured by cardio-ankle vascular index (CAVI) through the enalapril intervention. The secondary endpoints were the enalapril influence on carotid femoral pulse wave velocity (cfPWV), carotid intima media thickness (cIMT), carotid artery distensibility (cDistensibility), Young's incremental elastic modulus (Einc)]. Materials and Methods: Fifty-three patients were enrolled in a clinical, randomized, closed-label trial. The subjects were randomly assigned into two groups: One receiving 5 mg of enalapril (27) or placebo (26), both twice a day. The drug was acquired at Victory Enterprises®. The placebo was kindly provided by the Universidad de Guadalajara (UdeG), as well as the blinding into two groups: A and B. Enalapril and placebo were packed into bottles without labeling. Clinical assessment included a structured questionnaire to gather demographic and clinical variables as well as determination of CAVI, cfPWV, cIMT, carotid artery distensibility and Einc. The whole set of evaluations were analyzed at the baseline and at the end of 12 weeks of intervention. Results: The CAVI measurement at baseline was 7.1 ± 1.4 and increased up to 7.5 ± 1.2 at the end of 12 weeks. Meanwhile, the enalapril group was as follows: 7.4 ± 1.2 and at the of intervention, reduced to 7.1 ± 0.9. A reduction in delta CAVI of 0.21 in the enalapril intervention group was found. In contrast, an increase of 0.39 was observed in the placebo group. The delta CAVI reduction was not influenced by age or peripheral systolic blood pressure (pSBP). Discussion: Enalapril seems to be effective in CAVI reduction in RA patients. The effect of enalapril intervention on arterial stiffness translated to the clinical context might be interpreted as a reduction of 6.4 years of arterial aging. Trial Registration: The protocol was approved by the Institutional Review Board with the register CI-0117 from UdeG, and 0211/18 from Hospital Civil “Dr. Juan I. Menchaca”, Secretaría de Salud Jalisco: DGSP/DDI/D.INV. 28/18 and retrospectively registered at ClinicalTrials.gov Protocol Registration and Results System: NCT03667131.
Urbanization without isolation: the absence of genetic structure among cities and forests in the tiny acorn ant Temnothorax nylanderi

Urban alteration of neutral and adaptive evolutionary processes is still underexplored. Using a genome-wide SNP dataset, we investigated (i) urban-induced modifications of population demography, genetic diversity and population structure and (ii) signature of divergent selection between urban and forest populations in the ant species, Temnothorax nylanderi. Our results did not reveal an impact of urbanization on neutral processes since we observed: (i) analogous genetic diversity among paired urban/forest sites and two control populations; (ii) weak population genetic structure explained neither by habitat (urban versus forest) nor by geography; (iii) a remarkably similar demographic history across populations with an ancestral growth followed by a recent decline, regardless of their current habitat or geographical location. The micro-geographical home range of ants may explain their resilience to urbanization. Finally, we detected 19 candidate loci discriminating urban/forest populations and associated with core cellular components, molecular function or biological process. Two of these loci were associated with a gene ontology term that was previously found to belong to a module of co-expressed genes related to caste phenotype. These results call for transcriptomics analyses to identify genes associated with ant social traits and to infer their potential role in urban adaptation.