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Journal articles on the topic 'Penk'

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Published: 4 June 2021
Last updated: 27 April 2022

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1

Fraser, M., SG Matthews, G. Braems, and T. Jeffray. "Developmental regulation of preproenkephalin (PENK) gene expression in the adrenal gland of the ovine fetus and newborn lamb: effects of hypoxemia and exogenous cortisol infusion." Journal of Endocrinology 155, no. 1 (October 1, 1997): 143–49. http://dx.doi.org/10.1677/joe.0.1550143.

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Development of the fetal adrenal gland is crucial not only for maturation of several fetal organ systems and the initiation of parturition, but also for the development of the fetal response to stress. The enkephalin-related peptides are present in the chromaffin cells of the fetal adrenal medulla and are secreted in response to stress and with sympathetic stimulation. However, changes in expression of preproenkephalin (PENK) with gestation and in response to stress have not been studied in detail. Therefore we examined the developmental pattern of PENK gene expression in the adrenal gland of fetal and newborn lambs, and of adult sheep. We also determined whether levels of PENK mRNA in the fetal adrenal gland changed in response to exogenous glucocorticoids in late gestation, or in response to hypoxemia. Adrenal glands were removed from fetal sheep, lambs and adult sheep at different stages of development for measurement of PENK mRNA. Cortisol was infused (5 micrograms/min) for 12, 24 or 96 h beginning on day 124-129 of gestation. Moderate hypoxemia was induced for 48 h beginning on day 126-130, or at day 134-136 of gestation, by lowering the maternal fractional inspired oxygen. At the end of the treatment periods, the ewes and fetuses were euthanized. Adrenal PENK mRNA were measured by Northern blot analysis. PENK mRNA levels in fetal adrenals were significantly higher (P < 0.05) on days 140-141 of gestation than earlier in pregnancy, and then decreased significantly with the onset of parturition (days 142-146). After cortisol infusion to the fetus for 96 h there was a significant reduction in adrenal PENK mRNA levels. Hypoxemia resulted in a significant increase in PENK mRNA levels in fetuses at day 126-130 of gestation, but not at the later time in pregnancy when endogenous plasma cortisol concentrations were higher. We conclude that there is a decrease in levels of PENK mRNA in the fetal adrenal gland before parturition at the time of the endogenous prepartum rise in plasma cortisol. Hypoxemia led to an elevation of PENK mRNA levels in fetuses at less than 130 days, but after that time, when the basal and stimulated cortisol responses had risen, there was no significant effect of hypoxemia on PENK mRNA. Cortisol infusion to the fetus at this stage of pregnancy resulted in a decrease in adrenal PENK mRNA levels. We suggest that cortisol may play an important role in the regulation of fetal adrenal PENK mRNA levels and enkephalin synthesis by the adrenal gland of the fetal sheep.
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2

Hartman, Stan J. F., Alexandra J. M. Zwiers, Nadies E. C. van de Water, Joost van Rosmalen, Joachim Struck, Janin Schulte, Oliver Hartmann, et al. "Proenkephalin as a new biomarker for pediatric acute kidney injury – reference values and performance in children under one year of age." Clinical Chemistry and Laboratory Medicine (CCLM) 58, no. 11 (October 25, 2020): 1911–19. http://dx.doi.org/10.1515/cclm-2020-0381.

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AbstractObjectivesAcute kidney injury (AKI) is common in critically ill children, but current biomarkers are suboptimal. Proenkephalin A 119–159 (PENK) is a promising new biomarker for AKI in adults, but pediatric data is lacking. We determined PENK reference intervals for healthy children, crucial for clinical implementation, and explored concentrations in critically ill infants aged under 1 year.MethodsObservational cohort study in healthy infants and critically ill children aged 0–1 years. Reference values were determined using generalized additive models. Plasma PENK concentrations between healthy children and critically ill children with and without AKI, were compared using linear mixed modelling. The performance of PENK as AKI biomarker was compared to cystatin C (CysC) and β-trace protein (BTP) using receiver-operating-characteristic (ROC) analysis.ResultsPENK concentrations in 100 healthy infants were stable during the first year of life (median 517.3 pmol/L). Median PENK concentrations in 91 critically ill children, were significantly higher in those with AKI (n=40) (KDIGO Stage 1 507.9 pmol/L, Stage 2 704.0 pmol/L, Stage 3 930.5 pmol/L) than non-AKI patients (n=51, 432.2 pmol/L) (p < 0.001). PENK appeared to relate better to AKI diagnosis than CysC and BTP (AUROC PENK 0.858, CysC 0.770 and BTP 0.711) in the first 24 h after recruitment.ConclusionsPENK reference values are much higher in young infants than adults, but clearly discriminate between children with and without AKI, with comparable or better performance than CysC and BTP. Our results illustrate the importance of establishing age-normalized reference values and indicate PENK as a promising pediatric AKI biomarker.
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Gruber, Philipp, Felix Fluri, Juliane Schweizer, Andreas Luft, Beat Müller, Mirjam Christ-Crain, and Mira Katan. "Proenkephalin A Adds No Incremental Prognostic Value After Acute Ischemic Stroke." Clinical and Applied Thrombosis/Hemostasis 26 (January 1, 2020): 107602961989531. http://dx.doi.org/10.1177/1076029619895318.

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Objective: The aim of this study was to confirm previous observations that proenkephalin A (PENK-A) may serve as prognostic marker in the setting of acute ischemic stroke in a large stroke cohort. Methods: The plasma concentration of PENK-A was measured within 72 hours of symptom onset in 320 consecutively enrolled patients with stroke. The primary outcome measures were unfavorable functional outcome (modified Rankin Scale score 0-2 vs 3-6) and mortality within 90 days. Logistic and cox proportional regression analyses were fitted to estimate odds ratios (ORs), hazard ratios (HRs) and 95% confidence intervals (CIs), respectively, for the association between PENK-A and the primary outcome measures. Results: After adjusting for demographic and vascular risk factors, PENK-A was neither independently associated with functional outcome (OR: 1.29, 95% CI: 0.16-10.35) nor mortality (HR: 1.02, 95% CI: 0.14-7.33). Conclusion: Among patients with acute stroke, PENK-A does not serve as an independent prognostic marker in this external validation cohort.
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4

Khorashadi, Mina, Remi Beunders, Peter Pickkers, and Matthieu Legrand. "Proenkephalin: A New Biomarker for Glomerular Filtration Rate and Acute Kidney Injury." Nephron 144, no. 12 (2020): 655–61. http://dx.doi.org/10.1159/000509352.

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Assessment of kidney function is primarily based on urine output and Creatinine (Cr)-based methods to estimate glomerular filtration rate (GFR). The latter is confounded as Cr is not exclusively filtered by the kidney and rises relatively late after the onset of acute kidney injury (AKI). This leads to delays in recognition of reduced kidney function and diagnosis of AKI, particularly in critically ill patients where kidney function can change rapidly. The gold standard methods of GFR determination, such as inulin or iohexol clearance, are labor intensive and unfeasible in acute clinical settings. Proenkephalin A 119–159 (PENK) has been intensively studied as a novel biomarker of kidney function. PENK belongs to the enkephalin peptide family and is freely filtrated in the glomerulus. Plasma PENK concentration appears to correlate strongly with GFR. Moreover, increased plasma PENK concentrations are found to be associated with long-term kidney outcomes and mortality. In this review, we summarize the role of PENK in assessment of kidney function and its capacity to predict various clinical outcomes.
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Abu-Rumeileh, Samir, Peggy Barschke, Patrick Oeckl, Simone Baiardi, Angela Mammana, Andrea Mastrangelo, Mhd Rami Al Shweiki, et al. "Prodynorphin and Proenkephalin in Cerebrospinal Fluid of Sporadic Creutzfeldt–Jakob Disease." International Journal of Molecular Sciences 23, no. 4 (February 12, 2022): 2051. http://dx.doi.org/10.3390/ijms23042051.

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Proenkephalin (PENK) and prodynorphin (PDYN) are endogenous opioid peptides mainly produced in the striatum and, to a lesser extent, in the cerebral cortex. Dysregulated metabolism and altered cerebrospinal fluid (CSF) levels of PENK and PDYN have been described in several neurodegenerative diseases. However, no study to date investigated these peptides in the CSF of sporadic Creutzfeldt–Jakob disease (sCJD). Using liquid chromatography-multiple reaction monitoring mass spectrometry, we evaluated the CSF PDYN- and PENK-derived peptide levels in 25 controls and 63 patients with sCJD belonging to the most prevalent molecular subtypes (MM(V)1, VV2 and MV2K). One of the PENK-derived peptides was significantly decreased in each sCJD subtype compared to the controls without a difference among subtypes. Conversely, PDYN-derived peptides were selectively decreased in the CSF of sCJD MV2K, a subtype with a more widespread overall pathology compared to the sCJD MM(V)1 and the VV2 subtypes, which we confirmed by semiquantitative analysis of cortical and striatal neuronal loss and astrocytosis. In sCJD CSF PENK and PDYN were associated with CSF biomarkers of neurodegeneration but not with clinical variables and showed a poor diagnostic performance. CSF PDYN and PENK-derived peptides had no significant diagnostic and prognostic values in sCJD; however, the distinct marker levels between molecular subtypes might help to better understand the basis of phenotypic heterogeneity determined by divergent neuronal targeting.
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Mao, Hua, Yong You, Lifen Tong, Xiaohe Tang, Renbo Wei, and Xiaobo Liu. "Dielectric properties of poly(arylene ether nitrile ketone) copolymers." High Performance Polymers 31, no. 8 (November 5, 2018): 901–8. http://dx.doi.org/10.1177/0954008318808570.

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A series of poly(arylene ether nitrile ketone) (PENK) random copolymers are successfully synthesized by the nucleophilic aromatic substitution polymerization of 2,6-dichlorobenzonitrile, 4,4′-difluorobenzophenone with various bisphenol monomers (4,4′-biphenol, bisphenol A, phenolphthalein, and hydroquinone). Compared with poly(arylene ether ketone), the PENK copolymers possess better solubility in polar solvents such as N-methyl-2-pyrrolidone, N, N-dimethylacetamide, N, N-dimethylformamide, dimethylsulfoxide, and so on. Because of the different molecular structures, the PENK copolymers exhibit thermal properties with their glass transition temperature ( T g) in the range of 171–237°C and 5% weight loss temperature ( T d) ranging from 409°C to 554°C. Moreover, all polymers with an intrinsic viscosity of approximately 1 dL/g show excellent film-forming properties and outstanding mechanical strength higher than 85 MPa. The temperature dependence of the dielectric constant and dielectric loss of all derived copolymers is stable before their T g. The breakdown strength of the hydroquinone-derived PENK copolymer is as high as 253 kV/mm, resulting in an energy storage density of 1.00 J/cm3. These solvent processable PENK copolymers are potential dielectric candidates for high temperature applications.
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7

Weber, James L., and Paula E. May. "Dinucleotide repeat polymorphism at the PENK locus." Nucleic Acids Research 18, no. 8 (1990): 2200. http://dx.doi.org/10.1093/nar/18.8.2200.

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8

Comings, David E., Hezekiah Blake, George Dietz, Radhika Gade-Andavolu, Richard S. Legro, Gerard Saucier, Patrick Johnson, Ray Verde, and James P. MacMurray. "The proenkephalin gene (PENK) and opioid dependence." NeuroReport 10, no. 5 (April 1999): 1133–35. http://dx.doi.org/10.1097/00001756-199904060-00042.

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9

Wan, Yong, Casey White, Nadine Robert, Matthew B. Rogers, and Heather L. Szabo-Rogers. "Localization of Tfap2β, Casq2, Penk, Zic1, and Zic3 Expression in the Developing Retina, Muscle, and Sclera of the Embryonic Mouse Eye." Journal of Histochemistry & Cytochemistry 67, no. 12 (October 22, 2019): 863–71. http://dx.doi.org/10.1369/0022155419885112.

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Optic development involves sequential interactions between several different tissue types, including the overlying ectoderm, adjacent mesoderm, and neural crest mesenchyme and the neuroectoderm. In an ongoing expression screen, we identified that Tfap2β, Casq2, Penk, Zic1, and Zic3 are expressed in unique cell types in and around the developing eye. Tfap2β, Zic1, and Zic3 are transcription factors, Casq2 is a calcium binding protein and Penk is a neurotransmitter. Tfap2β, Zic1, and Zic3 have reported roles in brain and craniofacial development, while Casq2 and Penk have unknown roles. These five genes are expressed in the major tissue types in the eye, including the muscles, nerves, cornea, and sclera. Penk expression is found in the sclera and perichondrium. At E12.5 and E15.5, the extra-ocular muscles express Casq2, the entire neural retina expresses Zic1, and Zic3 is expressed in the optic disk and lip of the optic cup. The expression of Tfap2β expanded from corneal epithelium to the neural retina between E12.5 to E15.5. These genes are expressed in similar domains as Hedgehog ( Gli1, and Ptch1) and the Wnt ( Lef1) pathways. The expression patterns of these five genes warrant further study to determine their role in eye morphogenesis:
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10

Shime, Hiroaki, Mizuyu Odanaka, Makoto Tsuiji, Takuma Matoba, Masaki Imai, Yoshiaki Yasumizu, Ryuta Uraki, et al. "Proenkephalin+regulatory T cells expanded by ultraviolet B exposure maintain skin homeostasis with a healing function." Proceedings of the National Academy of Sciences 117, no. 34 (August 7, 2020): 20696–705. http://dx.doi.org/10.1073/pnas.2000372117.

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Regulatory T (Treg) cells, expressing CD25 (interleukin-2 receptor α chain) and Foxp3 transcription factor, maintain immunological self-tolerance and suppress various immune responses. Here we report a feature of skin Treg cells expanded by ultraviolet B (UVB) exposure. We found that skin Treg cells possessing a healing function are expanded by UVB exposure with the expression of an endogenous opioid precursor, proenkephalin (PENK). Upon UVB exposure, skin Treg cells were expanded with a unique TCR repertoire. Also, they highly expressed a distinctive set of genes enriched in “wound healing involved in inflammatory responses” and the “neuropeptide signaling pathway,” as indicated by the high expression ofPenk.We found that not only was PENK expression at the protein level detected in the UVB-expanded skin Treg (UVB-skin Treg) cells, but that a PENK-derived neuropeptide, methionine enkephalin (Met-ENK), from Treg cells promoted the outgrowth of epidermal keratinocytes in an ex vivo skin explant assay. Notably, UVB-skin Treg cells also promoted wound healing in an in vivo wound closure assay. In addition, UVB-skin Treg cells produced amphiregulin (AREG), which plays a key role in Treg-mediated tissue repair. Identification of a unique function of PENK+UVB-skin Treg cells provides a mechanism for maintaining skin homeostasis.
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Pereira, Vanessa, Queensta Millet, Jose Aramburu, Cristina Lopez-Rodriguez, Claire Gaveriaux-Ruff, and John N. Wood. "Analgesia linked to Nav1.7 loss of function requires µ- and δ-opioid receptors." Wellcome Open Research 3 (August 16, 2018): 101. http://dx.doi.org/10.12688/wellcomeopenres.14687.1.

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Background: Functional deletion of the Scn9a (sodium voltage-gated channel alpha subunit 9) gene encoding sodium channel Nav1.7 makes humans and mice pain-free. Opioid signalling contributes to this analgesic state. We have used pharmacological and genetic approaches to identify the opioid receptors involved in this form of analgesia. We also examined the regulation of proenkephalin expression by the transcription factor Nfat5 that binds upstream of the Penk gene. Methods: We used specific µ-, δ- and κ-opioid receptor antagonists alone or in combination to examine which opioid receptors were necessary for Nav1.7 loss-associated analgesia in mouse behavioural assays of thermal pain. We also used µ- and δ-opioid receptor null mutant mice alone and in combination in behavioural assays to examine the role of these receptors in Nav1.7 knockouts pain free phenotype. Finally, we examined the levels of Penk mRNA in Nfat5-null mutant mice, as this transcription factor binds to consensus sequences upstream of the Penk gene. Results: The pharmacological block or deletion of both µ- and δ-opioid receptors was required to abolish Nav1.7-null opioid-related analgesia. κ-opioid receptor antagonists were without effect. Enkephalins encoded by the Penk gene are upregulated in Nav1.7 nulls. Deleting Nfat5, a transcription factor with binding motifs upstream of Penk, induces the same level of enkephalin mRNA expression as found in Nav1.7 nulls, but without consequent analgesia. These data confirm that a combination of events linked to Scn9a gene loss is required for analgesia. Higher levels of endogenous enkephalins, potentiated opioid receptors, diminished electrical excitability and loss of neurotransmitter release together contribute to the analgesic phenotype found in Nav1.7-null mouse and human mutants. Conclusions: These observations help explain the failure of Nav1.7 channel blockers alone to produce analgesia and suggest new routes for analgesic drug development.
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Beunders, Remi, Joachim Struck, Alan H. B. Wu, Alexander Zarbock, Salvatore Di Somma, Ravindra L. Mehta, Jay L. Koyner, et al. "Proenkephalin (PENK) as a Novel Biomarker for Kidney Function." Journal of Applied Laboratory Medicine: An AACC Publication 2, no. 3 (September 29, 2017): 400–412. http://dx.doi.org/10.1373/jalm.2017.023598.

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Saintigny, Pierre, Wenhua Lang, Jaroslav Jelinek, Curtis R. Pickering, Lei Feng, Mitchell J. Frederick, Li Zhang, et al. "New DNA methylation markers associated with oral cancer (OC) development (dvlpt)." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): 5524. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.5524.

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5524 Background: We have reported that DNA methyltransferase-3B (DNMT3B) gene expression is a strong predictor of OC dvlpt. Using high-throughput DNA methylation profiles of oral preneoplastic lesions (OPL), we identified 86 candidate genes that were hypermethylated in patients (pts) developing OC and suggested that a CpG island methylation phenotype may occur early during OC dvlpt. Our aim was to validate some of the candidate genes and to study the value of LINE1 repetitive element methylation, a surrogate of global DNA methylation, as biomarkers of risk to develop OC. Methods: Validation cohort included 40 pts with a median follow-up of 4.2 years, including 14 pts who developed OC. None of them were used in the discovery phase. Frozen OPL were collected prospectively and subject to DNA extraction. We performed a quantitative analysis of the degree of methylation of LINE1, and AGTR1, FOXI2, PENK, and HOXA9 promoters CpG sites using pyrosequencing. Results: The degree of methylation of AGTR1 (Mann-Whitney P<0.0001), FOXI2 (P=0.0002), PENK (P<0.0001), but not HOXA9 (P=0.0714) was significantly higher in pts who developed OC. On the contrary, LINE1 methylation was significantly lower in pts who developed OC (P<0.0001). The median percent of methylation was used to dichotomize the pts into high versus low methylation levels. Oral cancer-free survival (OCFS) was significantly worse in pts with high levels of AGTR1 (Log-rank P=0.0229), FOXI2 (P=0.0170), and PENK (P=0.0142) promoter methylation. No significant difference was found with HOXA9. A Methylation Index (MI) was developed by averaging the percent of methylation of AGTR1, FOXI2, and PENK promoters; pts with a high MI had a worse OCFS (P=0.0031). On the other hand, pts with low levels of LINE1 methylation had a significantly worse OCFS (P=0.0118). Finally, in 26 pts, a positive correlation was observed between DNMT3B gene expression levels and the MI (rho=0.65, P=0.0003); surprisingly, there was a negative correlation with LINE1 methylation (rho=-0.74, P<0.0001). Conclusions: AGTR1, FOXI2 and PENK promoter methylation may be associated with increased OC risk in pts with OPL and correlate with DNMT3B expression. Global DNA hypomethylation is an early event in OC dvlpt.
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Hamann, Moritz, Sabine Grill, Joachim Struck, Andreas Bergmann, Oliver Hartmann, Martin Pölcher, and Marion Kiechle. "Detection of early breast cancer beyond mammographic screening: a promising biomarker panel." Biomarkers in Medicine 13, no. 13 (September 2019): 1107–17. http://dx.doi.org/10.2217/bmm-2019-0085.

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Aim: We assessed the suitability of a biomarker panel to improve early detection and individual risk assessment in breast cancer (BC) patients. Materials & methods: PENK, pro-SP, hGH and CA15-3 of 204 BC patients and 68 healthy controls were measured. Results: PENK and human growth hormone concentrations were significantly lower and pro-SP values higher in BC patients compared with controls. C-index increased from 0.628 for CA15-3 alone to 0.754 when all three biomarkers were added to the model. Conclusion: This biomarker panel may improve early detection of BC and influence the assessment of breast imaging. It might be useful for a risk-adapted cancer surveillance or primary prevention program by a more precise determination of an individualized BC risk.
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Staszkiewicz, J., M. Skowronski, Gabriela Siawrys, T. Kaminski, B. Krazinski, K. Plonka, B. Wylot, Jadwiga Przala, and S. Okrasa. "Expression of proopiomelanocortin, proenkephalin and prodynorphin genes in porcine luteal cells." Acta Veterinaria Hungarica 55, no. 4 (December 1, 2007): 435–49. http://dx.doi.org/10.1556/avet.55.2007.4.3.

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The objective of the study was to examine the expression of the genes coding for proopiomelanocortin (POMC), proenkephalin (PENK) and prodynorphin (PDYN) in porcine luteal cells isolated from corpora lutea (CL) collected on days 3–6, 8–10 and 13–16 of the oestrous cycle. Total RNA was purified from non-incubated cells and from cells incubated for 48 h in the absence or presence of luteinising hormone (LH). The semi-quantitative RT-PCR technique, involving coamplification of the target and control cDNA (β-actin or 18S rRNA), was used to examine gene expression. It was found that the genes coding for opioid precursors are expressed in both non-incubated and incubated porcine luteal cells representing the early, mid- and late luteal phase. In non-incubated cells, only POMC mRNA content changed during CL development, whereas the expression of PENK and PDYN genes remained relatively constant. Additionally, the treatment of cells with LH markedly affected the expression of POMC and PENK, but no influence on PDYN expression was observed. The present study indicates that porcine luteal cells may produce opioid peptides and that gene expression of their precursors (except for PDYN) may be modulated in these cells by LH. Moreover, the present results support the involvement of opioid peptides in local regulation within the CL of the pig.
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Würfel, Marleen, Jana Breitfeld, Claudia Gebhard, Markus Scholz, Ronny Baber, Steffi G. Riedel-Heller, Matthias Blüher, Michael Stumvoll, Peter Kovacs, and Anke Tönjes. "Interplay between adipose tissue secreted proteins, eating behavior and obesity." European Journal of Nutrition 61, no. 2 (October 12, 2021): 885–99. http://dx.doi.org/10.1007/s00394-021-02687-w.

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Abstract Purpose Adipokines may play an important role in the complex etiology of human obesity and its metabolic complications. Here, we analyzed the relationship between 15 adipokines, eating behavior and body-mass index (BMI). Methods The study included 557 participants of the Sorbs (62.1% women, 37.9% men) and 3101 participants of the population-based LIFE-Adult cohorts (53.4% women, 46.4% men) who completed the German version of the Three-Factor-Eating Questionnaire to assess the eating behavior types cognitive restraint, disinhibition and hunger. Serum levels of 15 adipokines, including adiponectin, adipocyte fatty acid-binding protein (AFABP), angiopoietin-related growth factor (AGF), chemerin, fibroblast growth factor (FGF)-19, FGF-21, FGF-23, insulin-like growth factor (IGF)-1, interleukin (IL) 10, irisin, progranulin, vaspin, pro-neurotensin (pro-NT), pro-enkephalin (PENK) and leptin were measured. Based on significant correlations between several adipokines with different eating behavior items and BMI, we conducted mediation analyses, considering the eating behavior items as potential mediation variable towards BMI. Results Here, we found that the positive association between chemerin, AFABP or leptin and BMI in Sorbian women was mediated by higher restraint or disinhibited eating, respectively. Additionally, in Sorbian women, the negative relation between IGF-1 and BMI was mediated by higher disinhibition and the positive link between AGF and BMI by lower disinhibition. In Sorbian men, the negative relationship between PENK and BMI was mediated by lower disinhibition and hunger, whereas the negative relation between IGF-1 and BMI was mediated by higher hunger. In the LIFE-Adult women´s cohort, associations between chemerin and BMI were mediated by decreased hunger or disinhibition, respectively, whereas relations between PENK and BMI were fully mediated by decreased disinhibition. Conclusion Our study suggests that adipokines such as PENK, IGF-1, chemerin, AGF, AFABP and leptin might affect the development of obesity by directly modifying individual eating behavior. Given the observational nature of the study, future experimental or mechanistic work is warranted.
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Racz, I., A. Bilkei-Gorzo, K. Michel, and A. Zimmer. "STRESS-INDUCED ETHANOL DRINKING IN CB1???/???, POMC AND PENK KNOCKOUT MICE." Alcoholism: Clinical & Experimental Research 28, Supplement (August 2004): 74A. http://dx.doi.org/10.1097/00000374-200408002-00407.

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Gaiddon, C., D. Monnier, AL Boutillier, and JP Loeffler. "Oncogenic Gαs proteins stimulate proopiiomelanocortin (POMC) and proenkephalin (PEnk) gene transcription." Regulatory Peptides 54, no. 1 (November 1994): 101–2. http://dx.doi.org/10.1016/0167-0115(94)90409-x.

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Poirel, Laurent, José-Manuel Rodriguez-Martinez, Patrick Plésiat, and Patrice Nordmann. "Naturally Occurring Class A ß-Lactamases from the Burkholderia cepacia Complex." Antimicrobial Agents and Chemotherapy 53, no. 3 (December 15, 2008): 876–82. http://dx.doi.org/10.1128/aac.00946-08.

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ABSTRACT Chromosomally encoded ß-lactamases from the Burkholderia cepacia complex species (formerly Pseudomonas cepacia) were characterized. Cloning and sequencing identified an Ambler class A ß-lactamase (PenB) from B. cenocepacia. It shares 82% amino acid identity with the PenA ß-lactamases previously identified from B. multivorans 249. Its expression was dependent upon a LysR-type regulatory protein. Its narrow-spectrum hydrolysis activity mostly included penicillins but also included expanded-spectrum cephalosporins and aztreonam at lower levels. In that study, Pen-like ß-lactamases (PenC, PenD, PenE, PenF) that shared 63 to 92% identity with PenB from B. cenocepacia were identified from other Burkholderia species. The corresponding ß-lactamase genes might be used as genetic tools for accurate Burkholderia species identification.
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van der Werff, Frederique, and Hilko de Wolf. "PEEK-PEKK en de PEAK-familie." Tandartspraktijk 37, no. 6 (August 2016): 32–36. http://dx.doi.org/10.1007/s12496-016-0078-z.

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Monnier, D., C. Gaiddon, AL Boutillier, F. Barthel, and JP Loeffler. "PACAP 27 and 38 stimulate proopiomelanocortin (POMC) and proenkephalin (PENK) gene transcription." Regulatory Peptides 54, no. 1 (November 1994): 199–200. http://dx.doi.org/10.1016/0167-0115(94)90459-6.

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Litt, M., and A. Buder. "A frequent RFLP identified by a human proenkephalin genomic clone [HGM9 symbol PENK]." Nucleic Acids Research 17, no. 1 (1989): 465. http://dx.doi.org/10.1093/nar/17.1.465.

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Bojnik, Engin, Patrycja Kleczkowska, Ezequiel Marron Fernandez de Velasco, Maïthé Corbani, Fruzsina Babos, Andrzej W. Lipkowski, Anna Magyar, and Sandor Benyhe. "Bioactivity studies on atypical natural opioid hexapeptides processed from proenkephalin (PENK) precursor polypeptides." Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology 174 (August 2014): 29–35. http://dx.doi.org/10.1016/j.cbpb.2014.06.002.

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Lindberg, Julia, Peter Saetre, Seiji Nishino, Emmanuel Mignot, and Elena Jazin. "Reduced expression of TAC1, PENK and SOCS2 in Hcrtr-2 mutated narcoleptic dog brain." BMC Neuroscience 8, no. 1 (2007): 34. http://dx.doi.org/10.1186/1471-2202-8-34.

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Wong, Y. F., T. H. Cheung, W. K. Lo, S. F. Yim, Y. M. Wong, and T. K. H. Chung. "389 POSTER Hypermethylation induced SPARC, TIMP-3 and PENK down-regulation in endometrial cancer." European Journal of Cancer Supplements 4, no. 12 (November 2006): 120. http://dx.doi.org/10.1016/s1359-6349(06)70394-9.

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Jabbari, Kosar, Garrett Winkelmaier, Cody Andersen, Paul Yaswen, David Quilici, Saori Furuta, Qingsu Cheng, and Bahram Parvin. "Protein Ligands in the Secretome of CD36+ Fibroblasts Induce Growth Suppression in a Subset of Breast Cancer Cell Lines." Cancers 13, no. 18 (September 8, 2021): 4521. http://dx.doi.org/10.3390/cancers13184521.

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Reprogramming the tumor stroma is an emerging approach to circumventing the challenges of conventional cancer therapies. This strategy, however, is hampered by the lack of a specific molecular target. We previously reported that stromal fibroblasts (FBs) with high expression of CD36 could be utilized for this purpose. These studies are now expanded to identify the secreted factors responsible for tumor suppression. Methodologies included 3D colonies, fluorescent microscopy coupled with quantitative techniques, proteomics profiling, and bioinformatics analysis. The results indicated that the conditioned medium (CM) of the CD36+ FBs caused growth suppression via apoptosis in the triple-negative cell lines of MDA-MB-231, BT549, and Hs578T, but not in the ERBB2+ SKBR3. Following the proteomics and bioinformatic analysis of the CM of CD36+ versus CD36− FBs, we determined KLF10 as one of the transcription factors responsible for growth suppression. We also identified FBLN1, SLIT3, and PENK as active ligands, where their minimum effective concentrations were determined. Finally, in MDA-MB-231, we showed that a mixture of FBLN1, SLIT3, and PENK could induce an amount of growth suppression similar to the CM of CD36+ FBs. In conclusion, our findings suggest that these ligands, secreted by CD36+ FBs, can be targeted for breast cancer treatment.
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Alda, Martin, Gustavo Turecki, Paul Grof, Patrizia Cavazzoni, Anne Duffy, Eva Grof, Bernd Ahrens, et al. "Association and linkage studies of CRH and PENK genes in bipolar disorder: A collaborative IGSLI study." American Journal of Medical Genetics 96, no. 2 (April 3, 2000): 178–81. http://dx.doi.org/10.1002/(sici)1096-8628(20000403)96:2<178::aid-ajmg11>3.0.co;2-c.

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Vucetic, Zivjena, Jessica Kimmel, Kathy Totoki, Emily Hollenbeck, and Teresa M. Reyes. "Maternal High-Fat Diet Alters Methylation and Gene Expression of Dopamine and Opioid-Related Genes." Endocrinology 151, no. 10 (August 4, 2010): 4756–64. http://dx.doi.org/10.1210/en.2010-0505.

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Maternal obesity during pregnancy increases the risk of obesity in the offspring. Obesity, arising from an imbalance of energy intake and expenditure, can be driven by the ingestion of palatable [high fat (HF), high sugar], energy-dense foods. Dopamine and opioid circuitry are neural substrates associated with reward that can affect animals’ preference for palatable foods. Using a mouse model, the long-term effect of maternal consumption of a HF diet on dopamine and opioid gene expression within the mesocorticolimbic reward circuitry and hypothalamus of the offspring was investigated. Mice from dams fed a HF diet during pregnancy and lactation showed an increased preference for sucrose and fat. Gene expression, measured using quantitative real-time PCR, revealed a significant approximately 3- to 10-fold up-regulation of dopamine reuptake transporter (DAT) in the ventral tegmental area, nucleus accumbens, and prefrontal cortex and a down-regulation of DAT in the hypothalamus. Additionally, expression of both μ-opioid receptor (MOR) and preproenkephalin (PENK) was increased in nucleus accumbens, prefrontal cortex, and hypothalamus of mice from dams that consumed the HF diet. Epigenetic mechanisms have been associated with long-term programming of gene expression after various in utero insults. We observed global and gene-specific (DAT, MOR, and PENK) promoter DNA hypomethylation in the brains of offspring from dams that consumed the HF diet. These data demonstrate that maternal consumption of a HF diet can change the offsprings’ epigenetic marks (DNA hypomethylation) in association with long-term alterations in gene expression (dopamine and opioids) and behavior (preference for palatable foods).
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Sobhani, Iradj, Emma Bergsten, Séverine Couffin, Aurélien Amiot, Biba Nebbad, Caroline Barau, Nicola de’Angelis, et al. "Colorectal cancer-associated microbiota contributes to oncogenic epigenetic signatures." Proceedings of the National Academy of Sciences 116, no. 48 (November 11, 2019): 24285–95. http://dx.doi.org/10.1073/pnas.1912129116.

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Sporadic colorectal cancer (CRC) is a result of complex interactions between the host and its environment. Environmental stressors act by causing host cell DNA alterations implicated in the onset of cancer. Here we investigate the stressor ability of CRC-associated gut dysbiosis as causal agent of host DNA alterations. The epigenetic nature of these alterations was investigated in humans and in mice. Germ-free mice receiving fecal samples from subjects with normal colonoscopy or from CRC patients were monitored for 7 or 14 wk. Aberrant crypt foci, luminal microbiota, and DNA alterations (colonic exome sequencing and methylation patterns) were monitored following human feces transfer. CRC-associated microbiota induced higher numbers of hypermethylated genes in murine colonic mucosa (vs. healthy controls’ microbiota recipients). Several gene promoters including SFRP1,2,3, PENK, NPY, ALX4, SEPT9, and WIF1 promoters were found hypermethylated in CRC but not in normal tissues or effluents from fecal donors. In a pilot study (n = 266), the blood methylation levels of 3 genes (Wif1, PENK, and NPY) were shown closely associated with CRC dysbiosis. In a validation study (n = 1,000), the cumulative methylation index (CMI) of these genes was significantly higher in CRCs than in controls. Further, CMI appeared as an independent risk factor for CRC diagnosis as shown by multivariate analysis that included fecal immunochemical blood test. Consequently, fecal bacterial species in individuals with higher CMI in blood were identified by whole metagenomic analysis. Thus, CRC-related dysbiosis induces methylation of host genes, and corresponding CMIs together with associated bacteria are potential biomarkers for CRC.
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Niren, Ann Glazer. "Leonard Bernstein and His Young People's Concerts. By Alicia Kopfstein-Penk . Lanham, MD: Rowman and Littlefield, 2015." Journal of the Society for American Music 12, no. 1 (January 25, 2018): 107–10. http://dx.doi.org/10.1017/s1752196317000566.

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Watson, Charles G., Teresa Kucala, and Victor Manifold. "A cross-validation of the keane and penk MMPI scales as measures of post-traumatic stress disorder." Journal of Clinical Psychology 42, no. 5 (September 1986): 727–32. http://dx.doi.org/10.1002/1097-4679(198609)42:5<727::aid-jclp2270420508>3.0.co;2-4.

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Xu, Jian, Mingqiang Sun, Yuanyuan Wang, Anmu Xie, and Jian Gao. "Identification of Hub Genes of Mesio Temporal Lobe Epilepsy and Prognostic Biomarkers of Brain Low-grade Gliomas Based on Bioinformatics Analysis." Cell Transplantation 29 (January 1, 2020): 096368972097872. http://dx.doi.org/10.1177/0963689720978722.

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Mesio temporal lobe epilepsy (MTLE) syndrome is the most common form of intractable epilepsies. Meanwhile, seizures are common in patients with cancer as a consequence of brain tumors, including brain low-grade gliomas (LGG). However, the underlying molecular mechanisms of MTLE remain poorly understood. Also, the relationship between MTLE and LGG needs our attention. In this study, we aimed to investigate the hub genes and potential mechanism in MTLE, and the relationship between MTLE and LGG, the gene expression profiles (GSE88992) were downloaded from the Gene Expression Omnibus (GEO) database. Difference analysis for MTLE versus control groups under the three time points was conducted to select the differentially expressed genes (DEGs). Time series clustering analysis was used to select the trend genes. Then a series of bioinformatics analyses including functional enrichment analysis, protein–protein interaction (PPI) network and module analyses, and transcription factor (TF) and miRNA prediction were performed. Also, the overall survival analysis and expression of hub genes in LGG were performed using UALCAN from TCGA database. At 6 h, there were 351 upregulated and 80 downregulated DEGs. At 12 h, there were 499 upregulated and 231 downregulated DEGs. Additionally, 532 upregulated and 402 downregulated DEGs were obtained at 24 h. After time series clustering analysis of the DEGs, we obtained 323 uptrend and 248 downtrend genes. We identified 10 key genes with higher degrees, including C3, TIMP1, PENK, CKAP4, etc. Five PPI modules were identified by MCODE. TF analysis predicted four TFs: JUN, STAT3, NR4A2, and Myc. A total of 26,834 miRNA–mRNA pairs were predicted. Moreover, survival analysis of UALCAN suggested that C3, TIMP1, PENK, GNG2, CKAP4, TNC, JUN, STAT3, NR4A2, and Myc can be potential biomarkers for the prognosis of LGG. In summary, DEGs and hub genes were identified in the present study, which provides novel insight into the development of MTLE.
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Navarro, Sandra, Lucia Soletto, Sara Puchol, Josep Rotllant, Jose Luis Soengas, and Jose Miguel Cerdá-Reverter. "60 YEARS OF POMC: POMC: an evolutionary perspective." Journal of Molecular Endocrinology 56, no. 4 (May 2016): T113—T118. http://dx.doi.org/10.1530/jme-15-0288.

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Proopiomelanocortin (POMC) is a complex precursor that comprises several peptidic hormones, including melanocyte-stimulating hormones (MSHs), adrenocorticotropic hormone (ACTH), and β-endorphin. POMC belongs to the opioid/orphanin gene family, whose precursors include either opioid (YGGF) or the orphanin/nociceptin core sequences (FGGF). This gene family diversified during early tetraploidizations of the vertebrate genome to generate four different precursors: proenkephalin (PENK), prodynorphin (PDYN), and nociceptin/proorphanin (PNOC) as well as POMC, although both PNOC and POMC seem to have arisen due to a local duplication event. POMC underwent complex evolutionary processes, including internal tandem duplications and putative coevolutionary events. Controversial and conflicting hypotheses have emerged concerning the sequenced genomes. In this article, we summarize the different evolutionary hypotheses proposed for POMC evolution.
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34

Goo, Young Ah, and Alvin Y. Liu. "1429: Proenkephalin (PENK): A Candidate Stromal Mesenchyme Cell Gene in Epithelial Differentiation whose Expression is Down-Regulated in Cancer." Journal of Urology 173, no. 4S (April 2005): 387–88. http://dx.doi.org/10.1016/s0022-5347(18)35563-0.

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Garcia-Garcia, Luis, Vivian Llewellyn-Jones, I. Fernandez Fernandez, José A. Fuentes, and Jorge Manzanares. "Acute and repeated ECS treatment increases CRF, POMC and PENK gene expression in selected regions of the rat hypothalamus." NeuroReport 9, no. 1 (January 1998): 73–77. http://dx.doi.org/10.1097/00001756-199801050-00015.

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36

Koch, Hugh. "Book Review Treating PTSD in Military Personnel Bret A Moore, Walter E Penk Guildford, 2011, 382pp, ISBN: 9781609186357, £30.50." British Journal of Mental Health Nursing 1, no. 1 (March 20, 2012): 64. http://dx.doi.org/10.12968/bjmh.2012.1.1.64a.

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37

Seitz, S., F. Barvencik, M. Gebauer, J. Albers, J. Schulze, T. Streichert, M. Amling, and T. Schinke. "Preproenkephalin (Penk) is Expressed in Differentiated Osteoblasts, and its Deletion in Hyp Mice Partially Rescues Their Bone Mineralization Defect." Calcified Tissue International 86, no. 4 (March 4, 2010): 282–93. http://dx.doi.org/10.1007/s00223-010-9344-5.

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38

Milwid, Jack M., Jessica S. Elman, Matthew Li, Keyue Shen, Arjun Manrai, Aaron Gabow, Joshua Yarmush, et al. "Enriched Protein Screening of Human Bone Marrow Mesenchymal Stromal Cell Secretions Reveals MFAP5 and PENK as Novel IL-10 Modulators." Molecular Therapy 22, no. 5 (May 2014): 999–1007. http://dx.doi.org/10.1038/mt.2014.17.

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39

Sobhani, Iradj, Roberto Incitti, and Jean-Pierre Roperch. "A new noninvasive blood-test for the early detection of colorectal cancer." Journal of Clinical Oncology 31, no. 4_suppl (February 1, 2013): 348. http://dx.doi.org/10.1200/jco.2013.31.4_suppl.348.

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348 Background: Colorectal cancer (CRC) remains a major medical problem in the world. Its early detection impacts the prognosis and the cost of treatment. Fecal occult blood test is a current noninvasive screening method for CRC detection in asymptomatic average risk individuals. It detects less than 50% of cancers and yields a high number of “normal” colonoscopies. The dysregulation of DNA methylation has been recognized as playing a crucial role during CRC development. The aim of the study was to develop a CRC-specific methylated DNA test in serum. Methods: First, the GoldenGate Methylation microarray containing 1,505 CpG loci within 807 cancer-related genes was used to study methylation patterns in CRC patients. We performed such assays on 9 tissues (4 CRC, 4 normal autologous tissues, 1 polyp), 17 blood and urine pooled samples (7 CRC, 6 polyps, 4 normal) and 20 stool samples (7 CRC, 3 polyps, 10 normal). The clinical status of each sample was assessed by colonoscopy and/or pathology findings. Among methylated genes detected in tumour tissue, stools, and blood, NPY, PENK and WIF1 genes were selected taking into account their high degree of methylation. We then carried out a clinical validation by quantitative multiplex methylation-specific PCR (QM-MSP) in two phases: firstly on 30 tissues (15 CRC, 15 homologous normal tissues) and secondly on 193 serum samples (32 CRC, 161 normal). Results: For to obtain the best accuracy of QM-MSP test, we defined for both biological sources a cumulative methylation index (CMI) by adding of the methylation percentage of each gene. At the CMI of 20.0% on tissues, our QM-MSP test allows to diagnose the CRC with the highest accuracy (100% of specificity and 100% of sensitivity). From sera, the CMI has been standardized at 2.0% giving a sensitivity and specificity for detecting CRC of 94.4% and 59.4% respectively (NPV of 92.1% and PPV of 67.8%). Conclusions: We developed a QM-MSP-based analysis of NPY, PENK, and WIF1 methylated genes in serum. This test classified correctly and with a high accuracy the healthy individuals and colon cancer patients. We propose here new sensitive serum-based epigenetic biomarkers as an effective and simple new noninvasive test for CRC screening in the average and high risk populations.
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Sul, C., D. Koo, K. Kim, J. Shin, Y. Na, H. Kim, J. Lim, et al. "MP-2.10: Identification of Aberrant Promoter Methylation of TBX5, PENK and T in Detection of Urothelial Carcinoma in Exfoliated Urine Cells." Urology 72, no. 5 (November 2008): S69—S70. http://dx.doi.org/10.1016/j.urology.2008.08.177.

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Liu, Xin‐Li, Wen‐Jing Liu, Qiang Chen, Jie Liu, Chang‐Qing Yang, Ge Zhang, Shi‐Long Zhang, et al. "miR‐506‐loaded gelatin nanospheres target PENK and inactivate the ERK/Fos signaling pathway to suppress triple‐negative breast cancer aggressiveness." Molecular Carcinogenesis 60, no. 8 (June 2021): 538–55. http://dx.doi.org/10.1002/mc.23310.

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Gieryk, Agnieszka, Barbara Ziolkowska, Wojciech Solecki, Jakub Kubik, and Ryszard Przewlocki. "Forebrain PENK and PDYN gene expression levels in three inbred strains of mice and their relationship to genotype-dependent morphine reward sensitivity." Psychopharmacology 208, no. 2 (December 9, 2009): 291–300. http://dx.doi.org/10.1007/s00213-009-1730-1.

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43

Lopatin, D. V., V. P. Chichagov, T. M. Skovitina, and A. A. Shchetnikov. "THEORETICAL FOUNDATION OF STRUCTURAL GEOMORPHOLOGY (TO THE 110TH BIRTHDAY ANNIVERSARY OF N.A. FLORENSOV)." Geodynamics & Tectonophysics 10, no. 1 (March 23, 2019): 181–88. http://dx.doi.org/10.5800/gt-2019-10-1-0410.

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Nikolai Aleksandrovich Florensov is a Russian scientist who is famous for his contribution to the theoretical foundations of structural geomorphology.He formulated the law of the circulation of material in the Earth's crust, which is manifested by a periodically arisinglithodynamicflow, in the development cycle of which two main phases are distinguished as ascending and descending geodynamics. In our opinion, there is also the third phase, stabilization.This process is reflected in the morphological types of mountains. Considering the conditions of intracontinental orogeny, N.A.Florensovdistinguished two main types: constructive and destructive.Developing this concept, he solved a number of theoretical and philosophical problems concerning the inextricable relationship between the relief and the structure of the geological substratum, its geodynamics and, as a consequence, proposed to consider their relationship as changes in geomorphological formations in time and space. The scientific creativity of NA. Florensov, as a whole, is comparable in importance with that of other most prominent geomorphologists of the late 19th and 20th centuries, including V.M. Davis, W. Penk, S.S. Shults, I.P. Gerasimov, and L. King.
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Loite, Ulvi, Liisi Raam, Ene Reimann, Paula Reemann, Ele Prans, Tanel Traks, Eero Vasar, Helgi Silm, Külli Kingo, and Sulev Kõks. "The Expression Pattern of Genes Related to Melanogenesis and Endogenous Opioids in Psoriasis." International Journal of Molecular Sciences 22, no. 23 (December 2, 2021): 13056. http://dx.doi.org/10.3390/ijms222313056.

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The melanocortin system is a major regulator of stress responses in the skin and is responsible for the induction of melanin synthesis through activation of melanogenesis enzymes. The expression of both melanocortin system genes and melanogenesis enzyme genes is altered in psoriasis, and the focus here was on twelve genes related to the signal transduction between them. Additionally, five endogenous opioid system genes that are involved in cutaneous inflammation were examined. Quantitative real-time-PCR was utilized to measure mRNA expression in punch biopsies from lesional and non-lesional skin of psoriasis patients and from the skin of healthy control subjects. Most of the genes related to melanogenesis were down-regulated in patients (CREB1, MITF, LEF1, USF1, MAPK14, ICAM1, PIK3CB, RPS6KB1, KIT, and ATRN). Conversely, an up-regulation occurred in the case of opioids (PENK, PDYN, and PNOC). The suppression of genes related to melanogenesis is in agreement with the reported reduction in pigmentation signaling in psoriatic skin and potentially results from the pro-inflammatory environment. The increase in endogenous opioids can be associated with their involvement in inflammatory dysregulation in psoriasis.
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45

Chan, Rebecca J., Andrew W. McBride, Holly R. Thomasson, Abi Ykenney, and David W. Crabb. "Allele Frequencies of the Preproenkephalin A (PENK) Gene CA Repeat in Asians, African-Americans, and Caucasians: Lack of Evidence for Different Allele Frequencies in Alcoholics." Alcoholism: Clinical and Experimental Research 18, no. 3 (June 1994): 533–35. http://dx.doi.org/10.1111/j.1530-0277.1994.tb00905.x.

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46

Pulverer, Walter, Kristi Kruusmaa, Silvia Schönthaler, Jasmin Huber, Marko Bitenc, Thomas Bachleitner-Hofmann, Jagdeep Singh Bhangu, Rudolf Oehler, Gerda Egger, and Andreas Weinhäusel. "Multiplexed DNA Methylation Analysis in Colorectal Cancer Using Liquid Biopsy and Its Diagnostic and Predictive Value." Current Issues in Molecular Biology 43, no. 3 (October 3, 2021): 1419–35. http://dx.doi.org/10.3390/cimb43030100.

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Early diagnosis of colorectal cancer (CRC) is of high importance as prognosis depends on tumour stage at the time of diagnosis. Detection of tumour-specific DNA methylation marks in cfDNA has several advantages over other approaches and has great potential for solving diagnostic needs. We report here the identification of DNA methylation biomarkers for CRC and give insights in our methylation-sensitive restriction enzyme coupled qPCR (MSRE-qPCR) system. Targeted microarrays were used to investigate the DNA methylation status of 360 cancer-associated genes. Validation was done by qPCR-based approaches. A focus was on investigating marker performance in cfDNA from 88 patients (44 CRC, 44 controls). Finally, the workflow was scaled-up to perform 180plex analysis on 110 cfDNA samples, to identify a DNA methylation signature for advanced colonic adenomas (AA). A DNA methylation signature (n = 44) was deduced from microarray experiments and confirmed by quantitative methylation-specific PCR (qMSP) and by MSRE-qPCR, providing for six genes’ single areas under the curve (AUC) values of >0.85 (WT1, PENK, SPARC, GDNF, TMEFF2, DCC). A subset of the signatures can be used for patient stratification and therapy monitoring for progressed CRC with liver metastasis using cfDNA. Furthermore, we identified a 35-plex classifier for the identification of AAs with an AUC of 0.80.
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Godbole, Surekha Dubey, Aditi Vinay Chandak, and Tanvi Rajesh Balwani. "Poly Ether Ether Ketone (PEEK) Applications in Prosthodontics – A Review “Peek into PEEK at Peak”." Journal of Evolution of Medical and Dental Sciences 9, no. 43 (October 26, 2020): 3242–46. http://dx.doi.org/10.14260/jemds/2020/711.

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48

Bettin, Alfonso, Ismael Reyes, and Niradiz Reyes. "Gene Expression Profiling of Prostate Cancer–Associated Genes Identifies Fibromodulin as Potential Novel Biomarker for Prostate Cancer." International Journal of Biological Markers 31, no. 2 (April 2016): 153–62. http://dx.doi.org/10.5301/jbm.5000184.

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Background The aim of this study was to evaluate the gene expression profiles of a set of prostate cancer–associated genes in prostate cancer cell lines, to determine their association with different cancer phenotypes and identify potential novel biomarkers for this disease. Methods Quantitative real-time PCR was used to determine the expression profiles of 21 prostate cancer–associated genes in the human prostate cancer cell lines PC-3 and LNCaP, using the nontumorigenic cell line PWR-1E as control cell line. Genes evaluated were ESM-1, SERPINE2, CLU, BGN, A2M, PENK, FMOD, CD81, DCN, TSPAN8, KBTBD10, F2RL1, TMSB4X, SNCG, CXXC5, FOXQ1, PDPN, SPN, CAV1, CD24 and KLK3. A potential biomarker from this set of genes, the FMOD gene, encoding the small leucine-rich proteoglycan fibromodulin, was selected for further evaluation in clinical samples from patients diagnosed with benign or malignant prostatic disease. Results Several of the evaluated genes showed significantly altered expression in the prostate cancer cell lines, compared with nontumorigenic PWR-1E cells. Further evaluation of FMOD transcript in prostate clinical samples from patients diagnosed with benign or malignant prostatic disease identified a significant difference in the expression levels of this proteoglycan between benign and malignant tissue (p<0.05). Conclusions A number of gene transcripts were differentially expressed by the cell lines assayed. Among them, FMOD was further evaluated in clinical samples and was found to be differentially expressed between benign and prostate cancer tissue. Further validation of FMOD transcript in a larger population is required to ascertain its usefulness as biomarker for prostate cancer.
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Ladd, Thatcher B., James A. Johnson, Christen L. Mumaw, Hendrik J. Greve, Xiaoling Xuei, Ed Simpson, Mark A. Barnes, et al. "Aspergillus versicolor Inhalation Triggers Neuroimmune, Glial, and Neuropeptide Transcriptional Changes." ASN Neuro 13 (January 2021): 175909142110198. http://dx.doi.org/10.1177/17590914211019886.

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Increasing evidence associates indoor fungal exposure with deleterious central nervous system (CNS) health, such as cognitive and emotional deficits in children and adults, but the specific mechanisms by which it might impact the brain are poorly understood. Mice were exposed to filtered air, heat-inactivated Aspergillus versicolor (3 × 105 spores), or viable A. versicolor (3 × 105 spores) via nose-only inhalation exposure 2 times per week for 1, 2, or 4 weeks. Analysis of cortex, midbrain, olfactory bulb, and cerebellum tissue from mice exposed to viable A. versicolor spores for 1, 2, and 4 weeks revealed significantly elevated pro-inflammatory ( Tnf and Il1b) and glial activity ( Gdnf and Cxc3r1) gene expression in several brain regions when compared to filtered air control, with the most consistent and pronounced neuroimmune response 48H following the 4-week exposure in the midbrain and frontal lobe. Bulk RNA-seq analysis of the midbrain tissue confirmed that 4 weeks of A. versicolor exposure resulted in significant transcriptional enrichment of several biological pathways compared to the filtered air control, including neuroinflammation, glial cell activation, and regulation of postsynaptic organization. Upregulation of Drd1, Penk, and Pdyn mRNA expression was confirmed in the 4-week A. versicolor exposed midbrain tissue, highlighting that gene expression important for neurotransmission was affected by repeated A. versicolor inhalation exposure. Taken together, these findings indicate that the brain can detect and respond to A. versicolor inhalation exposure with changes in neuroimmune and neurotransmission gene expression, providing much needed insight into how inhaled fungal exposures can affect CNS responses and regulate neuroimmune homeostasis.
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Thulin, Sara, Per Olcén, Hans Fredlund, and Magnus Unemo. "Total Variation in the penA Gene of Neisseria meningitidis: Correlation between Susceptibility to β-Lactam Antibiotics and penA Gene Heterogeneity." Antimicrobial Agents and Chemotherapy 50, no. 10 (October 2006): 3317–24. http://dx.doi.org/10.1128/aac.00353-06.

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ABSTRACT In recent decades, the prevalence of Neisseria meningitidis isolates with reduced susceptibility to penicillins has increased. The intermediate resistance to penicillin (Peni) for most strains is due mainly to mosaic structures in the penA gene, encoding penicillin-binding protein 2. In this study, susceptibility to β-lactam antibiotics was determined for 60 Swedish clinical N. meningitidis isolates and 19 reference strains. The penA gene was sequenced and compared to 237 penA sequences from GenBank in order to explore the total identified variation of penA. The divergent mosaic alleles differed by 3% to 24% compared to those of the designated wild-type penA gene. By studying the final 1,143 to 1,149 bp of penA in a sequence alignment, 130 sequence variants were identified. In a 402-bp alignment of the most variable regions, 84 variants were recognized. Good correlation between elevated MICs and the presence of penA mosaic structures was found especially for penicillin G and ampicillin. The Peni isolates comprised an MIC of >0.094 μg/ml for penicillin G and an MIC of >0.064 μg/ml for ampicillin. Ampicillin was the best antibiotic for precise categorization as Pens or Peni. In comparison with the wild-type penA sequence, two specific Peni sites were altered in all except two mosaic penA sequences, which were published in GenBank and no MICs of the corresponding isolates were described. In conclusion, monitoring the relationship between penA sequences and MICs to penicillins is crucial for developing fast and objective methods for susceptibility determination. By studying the penA gene, genotypical determination of susceptibility in culture-negative cases can also be accomplished.
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