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Engineering injectable vascularized tissue in the bottom-up: Character associated with in-gel extra-spheroid dermal muscle construction.
05), while the expression of hub downregulated genes was notably reduced (P less then 0.05). The proteins of CXCL1 and CXCR2 were upregulated following intestinal I/R injury (P less then 0.05) and the CXCL1/CXCR2 axis was involved with intestinal I/R injury. CONCLUSIONS The results of the present study identified IL-6, IL-10, CXCL1, CXCL2, IL-1ß, IRF7, IFIT3, IFIT1, Herc6, and Oasl2 as hub genes in intestinal I/R injury and identified the involvement of the CXCL1/CXCR2 axis in intestinal I/R injury.SLC13A5/NaCT is a sodium-coupled citrate transporter expressed in the plasma membrane of the liver, testis, and brain. In these tissues, SLC13A5 has important functions in the synthesis of fatty acids, cholesterol, and neurotransmitters. In recent years, patients homozygous for recessive mutations in SLC13A5, known as SLC13A5 deficiency [early infantile epileptic encephalopathy-25 (EIEE-25)], exhibit severe global developmental delay, early-onset intractable seizures, spasticity, and amelogenesis imperfecta affecting tooth development. Although the pathogenesis of SLC13A5 deficiency remains not clearly understood, cytoplasmic citrate deficits, decreased energy status in neurons, and citrate-zinc chelation are hypothesized to explain the neurological deficits. However, no study has examined the possibility of specific pharmacological drugs and/or lifestyle changes synergizing with heterozygosity of SLC13A5 deficiency to increase the risk of EIEE-25 clinical phenotype. Here, we report on a heterozygous SLC13A5-deficient patient who demonstrated evidence of pharmaco-synergistic heterozygosity upon administration of metformin, valproic acid, and starvation. The report illustrates the importance of careful consideration of the potential adverse effects of specific pharmacological treatments in patients with heterozygosity for disease-causing recessive mutations in SLC13A5.
Bipolar disorder (BD) is a chronic, disabling disease characterised by alternate mood episodes, switching through depressive and manic/hypomanic phases. Mood stabilizers, in particular lithium salts, constitute the cornerstone of the treatment in the acute phase as well as for the prevention of recurrences. The pathophysiology of BD and the mechanisms of action of mood stabilizers remain largely unknown but several pieces of evidence point to gene x environment interactions. Epigenetics, defined as the regulation of gene expression without genetic changes, could be the molecular substrate of these interactions. In this literature review, we summarize the main epigenetic findings associated with BD and response to mood stabilizers.

We searched PubMed, and Embase databases and classified the articles depending on the epigenetic mechanisms (DNA methylation, histone modifications and non-coding RNAs).

We present the different epigenetic modifications associated with BD or with mood-stabilizers. The major reported mechanisms were DNA methylation, histone methylation and acetylation, and non-coding RNAs. Overall, the assessments are poorly harmonized and the results are more limited than in other psychiatric disorders (e.g. schizophrenia). However, the nature of BD and its treatment offer excellent opportunities for epigenetic research clear impact of environmental factors, clinical variation between manic or depressive episodes resulting in possible identification of state and traits biomarkers, documented impact of mood-stabilizers on the epigenome.

Epigenetic is a growing and promising field in BD that may shed light on its pathophysiology or be useful as biomarkers of response to mood-stabilizer.
Epigenetic is a growing and promising field in BD that may shed light on its pathophysiology or be useful as biomarkers of response to mood-stabilizer.
Genome-wide association studies (GWAS) of alcohol dependence syndrome (ADS) offer a platform to detect genetic risk loci. However, the majority of the ADS GWAS undertaken, to date, have utilized a case-control design and have failed to identify consistently replicable loci with the exception of protective variants within the alcohol metabolizing genes, notably ADH1B. The ADS phenotype shows considerable variability which means that the use of quantitative variables as a proxy for the severity of ADS has the potential to facilitate identification of risk loci by increasing statistical power. The current study aims to examine the influences of using binary and adjusted quantitative measures of ADS on GWAS outcomes and on calculated polygenic risk scores (PRS).

A GWAS was performed in 1251 healthy controls with no history of excess alcohol use and 739 patients with ADS classified using binary DMS-IV criteria. Two additional GWAS were undertaken using a quantitative score based on DSM-IV criteria, which were applied assuming both normal and non-normal distributions of the phenotypic variables. PRS analyses were performed utilizing the data from the binary and the quantitative trait analyses.

No associations were identified at genome-wide significance in any of the individual GWAS; results were comparable in all three. The top associated single nucleotide polymorphism was located on the alcohol dehydrogenase gene cluster on chromosome 4, consistent with previous ADS GWAS. The quantitative trait analysis adjusted for the distribution of the criterion score and the associated PRS had the smallest standard errors and thus the greatest precision.

Further exploitation of the use of qualitative trait analysis in GWAS in ADS is warranted.
Further exploitation of the use of qualitative trait analysis in GWAS in ADS is warranted.
Retrospective Cohort Study OBJECTIVE. To determine that rates of preoperative opioid use in patients undergoing single-level ACDF without myelopathy and determine the association with reoperations over 5 years SUMMARY OF BACKGROUND DATA. Preoperative opioid use before cervical spine surgery has been linked to worse postoperative outcomes. However, no studies have determined the association of duration and type of opioid used with reoperations after anterior discectomy and fusion (ACDF).

Patients undergoing single-level ACDF without myelopathy between 2007 and 2016 with at least 5 year follow up were identified in one private insurance administrative database. Preoperative opiate use was divided into acute (within 3 months), subacute (acute use and use between 3-6 months), and chronic (subacute use and use prior to 6 months) and by the opiate medication prescribed (tramadol, oxycodone, and hydrocodone). Postoperative rates of additional cervical spine surgery were determined at 5-years and multivariate logpathic patients. This information is critical when counseling patients preoperatively and developing preoperative opioid cessation programs.

3.
3.
Observational study.

The aim of this study was to evaluate whether inflammatory and/or muscle regeneration markers in paraspinal tissues (multifidus muscle/fat) during microdiscectomy surgery in patients with lumbar disc herniation (LDH) with radiculopathy, differ between individuals with good or poor outcome.

Structural back muscle changes, including fat infiltration, muscle atrophy, and fiber changes, are ubiquitous with LBP and are thought to be regulated by inflammatory and regeneration processes. Muscle changes might be relevant for recovery after microdiscectomy, but a link between expression of inflammatory and muscle regeneration genes in paraspinal tissues and clinical outcome has not been tested.

Paraspinal tissues from deep multifidus muscles and fat (intramuscular, sub-cutaneous, epidural) were harvested from twenty-one patients with LDH undergoing microdiscectomy surgery. Quantitative polymerase chain reaction (qPCR) measured expression of 10 genes. Outcome was defined as good (visual anacal outcome.Level of Evidence 4.
Case-control study.

The aim of the study was to compare growth-friendly systems traditional growing rod, guided growth systems (GGS), and vertical expandable prosthetic titanium rib in the context of titanium release.

The problem of scoliosis affects even up to 3% of the population, and ca. 0.1% of patients need surgical treatment. Surgical treatment carries the risk of a long-term presence of implants in the organism, which may result in release of metal ions into the tissues and bloodstream.

Seventy-one patients (13.5 ± 3.54 years' old) were treated for spinal deformity using various surgical systems and the samples of paraspinal tissue, blood, nails, and hair were collected before and after treatment. The quantification of titanium was performed using inductively coupled plasma optical emission spectrometry.

The metallic particles were released into the peri-implant tissue, and the greatest amounts of titanium were detected in patients with GGS. The concentration of soluble titanium forms in subclevel of titanium with GGS system is probably associated with the friction between implant components, whereas the components in the other systems are immobile relative to each other.Level of Evidence 3.
Retrospective comparative study.

The aim of this study was to compare cervical sagittal alignment after posterior fusion surgery with lateral mass screw (LMS) and cervical pedicle screw (CPS) fixation.

LMS fixation in the subaxial cervical spine has become the preferred method of posterior cervical fusion. Although CPS has biomechanical benefits, it also has neurovascular risks. Few studies to date have compared sagittal alignment changes after posterior cervical fusion using CPS and LMS fixation.

From 2006 to 2017, 71 consecutive patients underwent posterior cervical fusion using CPS (n = 51) or LMS (n = 20) fixation. Patients who underwent fusion with both types of screws and those who planned to undergo additional anterior fusion surgery were excluded. The minimum follow-up period was 12 months. C2-C7 Cobb angle for cervical lordosis (CL), fusion segmental angle (SA), C2-C7 sagittal vertical axis (SVA), and T1 slope (T1S) were measured.

Immediate postoperative SA and SVA differed significantly in patients who underwent CPS and LMS fixation. SA changes were more substantial after CPS fixation, with a significant difference maintained until final follow-up. Over time, CL, SVA, and T1S tended to return to their preoperative states regardless of screw type. B022 Two patients who underwent LMS fixation, but none who underwent CPS fixation, required unplanned or additional anterior fusion surgery for revision.

The present study is the first radiologic comparison of LMS and CPS fixation after posterior-only fusion surgery. CPS resulted in more reliable and well-preserved SA correction, whereas CL and SVA did not differ between the two groups over time due to loss of correction.Level of Evidence 4.
The present study is the first radiologic comparison of LMS and CPS fixation after posterior-only fusion surgery. CPS resulted in more reliable and well-preserved SA correction, whereas CL and SVA did not differ between the two groups over time due to loss of correction.Level of Evidence 4.
International, multicenter, prospective, longitudinal observational cohort.

To assess how new motor deficits affect patient reported quality of life scores after adult deformity surgery.

Adult spinal deformity surgery is associated with high morbidity, including risk of new postoperative motor deficit. It is unclear what effect new motor deficit has on Health-related Quality of Life scores (HRQOL) scores.

Adult spinal deformity patients were enrolled prospectively at 15 sites worldwide. Other inclusion criteria included major Cobb more than 80°, C7-L2 curve apex, and any patient undergoing three column osteotomy. American Spinal Injury Association (ASIA) scores and standard HRQOL scores were recorded pre-op, 6 weeks, 6 months, and 2 years.

Two hundred seventy two complex adult spinal deformity (ASD) patients enrolled. HRQOL scores were worse for patients with lower extremity motor score (LEMS). Mean HRQOL changes at 6 weeks and 2 years compared with pre-op for patients with motor worsening were ODI (+12.
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