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Number of results: 7
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Abstract

Alcohol is a recognized teratogen that affects various aspects of fetal development. Tissue that is particularly susceptible to its teratogenicity is neuronal tissue. The effect of prenatal alcohol exposure (PAE) on the central nervous system has been extensively studied, yet the knowledge on the influence of PAE on the autonomic nervous system is scarce. The purpose of this article is to review the current state of knowledge about the impact of PAE on the autonomic nervous system. Studies conducted on the PAE animal model have shown that prenatal alcohol exposure is associated with significant alterations in the autonomic nervous system, but the mechanisms and consequences are not yet clearly defined. It was established that PAE causes decreased heart rate variability (HRV) in fetal cardiotocography. Several studies have revealed that later, in infancy and childhood, reduced parasympathetic activity with or without compensating sympathetic activity is observed. This may result in behavioral and attention disorders, as well as an increased predisposition to sudden infant death syndrome. Both animal and human studies indicate that the relationship between PAE and autonomic dysfunction exists, however large, well-designed, prospective studies are needed to confirm the causal relationship and characterize the nature of the observed changes.

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Authors and Affiliations

Michał Jurczyk
Katarzyna Anna Dyląg
Kamil Skowron
Krzysztof Gil
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Abstract

Colorectal cancer (CRC) is the third most common malignancy worldwide and the second most deadly cancer. Scientists have projected that by 2040, the prevalence will reach up to 3.2 million new cases annually due to population aging, disadvantageous diet transformations, and elevated exposure to risk factors. In the past decades, the five-year survival rate in colorectal cancer has significantly increased to 65% due to the development of an early endoscopic diagnosis and new chemotherapeutic approaches. Fluoropyrimidines, such as 5-fluorouracil or capecitabine, are commonly used to treat CRC. One of the most fundamental mechanisms of 5-FU is based on the inhibition of thymidylate synthase. This action is responsible for the therapeutic, but also toxic, effects of the drug. In this short review, we discuss the possible effects of vitamin D activity on colorectal cancer cells in relation to fluoropyrimidines. PubMed, Embase, and Web of Science databases were searched up to January 2022 for studies on vitamin D and 5-fluorouracil interaction mechanisms. Original studies, case reports, and review articles were included.
Vitamin D or its analogs target multiple biochemical pathways and modulate numerous pathophysiolo-gical mechanisms in the course of colon cancer, including those related to the pharmacological sites of fluoropyrimidines. However, the available data concerning vitamin D–fluoropyrimidine pharmacological interactions are limited, especially regarding patients suffering from colon cancer and being treated with fluoropyrimidines.
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Authors and Affiliations

Michał Jurczyk
1
Aleksandra Midro
1
Magdalena Król
1
Weronika Olesiak
1
Dariusz Stąpor
1
Anna Gil
1
Krzysztof Gil
1

  1. Department of Pathophysiology, Jagiellonian University Medical College, Kraków, Poland
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Abstract

B a c k g r o u n d: Stress is a major risk factor for cardiovascular (CV) disease. We hypothesized that past strong experiences might modulate acute CV autonomic responses to an unexpected acoustic stimulus.
A i m: The study’s aim was to compare acute CV autonomic responses to acoustic stress between students with and without a past strong experience associated with the acoustic stimulus.
M a t e r i a l s and M e t h o d s: Twenty five healthy young volunteers — medical and non-medical students — were included in the study. CV hemodynamic parameters, heart rate (HR), and blood pressure (BP) variability were assessed for 10 min at rest and for 10 min after two different acoustic stimuli: a standard sound signal and a specific sound signal used during a practical anatomy exam (so-called “pins”).
R e s u l t s: Both sounds stimulated the autonomic nervous system. The “pins” signal caused a stronger increase in HR in medical students (69 ± 10 vs. 73 ± 13 bpm, p = 0.004) when compared to non-medical students (69 ± 6 vs. 70 ± 10, p = 0.695). Rises in diastolic BP, observed 15 seconds after sound stressors, were more pronounced after the “pins” sound than after the standard sound signal only in medical students (3.1% and 1.4% vs. 3% and 4.4%), which was also reflected by low-frequency diastolic BP variability (medical students: 6.2 ± 1.6 vs. 4.1 ± 0.8 ms2, p = 0.04; non-medical students: 6.0 ± 4.3 vs. 4.1 ± 2.6 ms2, p = 0.06).
C o n c l u s i o n s: The “pins” sound, which medical students remembered from their anatomy practical exam, provoked greater sympathetic activity in the medical student group than in their non-medical peers. Thus, past strong experiences modulate CV autonomic responses to acute acoustic stress.
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Bibliography

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Authors and Affiliations

Michał Jurczyk
1
Andrzej Boryczko
1
Agata Furgała
1
Adrian Poniatowski
1
Andrzej Surdacki
2
Krzysztof Gil
1

  1. Department of Pathophysiology, Jagiellonian University Medical College, Kraków, Poland
  2. Second Department of Cardiology, Institute of Cardiology, Jagiellonian University Medical College, Kraków, Poland
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Abstract

Increasing numbers of implanted cardiovascular electronic devices, results in a need for lead extractions, which has increased to an annual volume of over 10,000 worldwide. We present a cadaveric dissection body with a single chamber pacemaker implanted 5y before death.

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Authors and Affiliations

Marcin Kuniewicz
Jerzy Andrzej Walocha
Kinga Budnicka
Małgorzata Mazur
Ewa Walocha
Michał Jurczyk
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Abstract

5-fluorouracil (5-FU), which is a commonly used chemotherapy agent exerts undesired cardiac toxicity. Mitochondrial dysfunction is thought to be one of potentially important mechanisms of 5-FU- induced cardiotoxicity. α-ketoglutarate dehydrogenase (α-KGDHC) is the key regulatory enzyme of TCA cycle. The complex consists of multiple copies of three catalytic subunits: α-ketoglutarate dehydrogenase (E1), dihydrolipoamide succinyltransferase (E2) and dihydrolipoamide dehydrogenase (E3). α-KGDHC together with branched chain α-ketoacid dehydrogenase (BCKDHC) and pyruvate dehydrogenase (PDHC), are the members of 2-oxoacid dehydrogenases family that share some structural and functional similarities. Recently, it has been found that 5-FU stimulates BCKDHC in rat’s cardiac muscle. Therefore, we hypothesize that 5-FU modifies α-KGDHC activity and affects cardiac muscle metabolism. The aim of this study was to determine the effect of 5-FU on α-KGDHC activity and protein levels of E1 and E2 subunits of the complex in rat’s cardiac muscle. Wistar male rats were administered with 4 doses of 5-FU, 150 mg/kg b.wt. each (study group) or 0.3% methylcellulose (control group). α-KGDHC activity was assayed spectrophotometrically. The E1 and E2 proteins levels were quantified by Western blot. 5-FU administration resulted in stimulation of myocardial α-KGDHC activity in rats. In addition, E2 protein level increased in response to 5-FU treatment, while the E1 protein level remained unchanged. Up- regulation of α-KGDHC appears to result from change in E2 subunit protein level. However, the effect of 5-FU on factors modifying α-KGDHC activity at post-translational level cannot be excluded.
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Authors and Affiliations

Małgorzata Knapik-Czajka
1
Anna Gawędzka
1
Michał Jurczyk
2
Jagoda Drąg
1
Małgorzata Belczyk
1
Veronika Aleksandrovych
2
Anna Gil
3
Krzysztof Gil
1

  1. Department of Biochemical Analytics, Jagiellonian University Medical College, Kraków, Poland
  2. Department of Pathophysiology, Jagiellonian University Medical College, Kraków, Poland
  3. Department of Anatomy, Jagiellonian University Medical College, Kraków, Poland
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Abstract

Undisturbed branched-chain amino acids (BCAA) catabolism is necessary for normal heart function. The key enzyme in BCAA catabolism is a multienzyme branched-chain α-keto acid dehydro-genase complex (BCKDH). BCKDH activity is regulated mainly by reversible dephosphorylation (activa-tion)/phosphorylation (inactivation) cycle catalyzed by regulatory enzymes, a specific phosphatase (PPM1K) and kinase (BDK). 5-fluorouracil (5-FU) is widely used in the treatment of different types of cancer. 5-FU has the potential to cause a wide spectrum of cardiotoxicity, ranging from asymptomatic electrocardiographic changes to cardiomyopathy and subsequent cardiac failure. We hypothesize that 5-FU modifies BCKDH activity and affects cardiac muscle metabolism. The current study was aimed at the investigation of the in vivo effect of 5-FU on BCKDH activity and mRNA levels for E1, PPM1K and BDK. Wistar male rats were administered with 4 doses of 5-FU, 150 mg/kg b.wt. each (study group) or 0.3% methylcellulose (control group). BCKDH activity was assayed spectrophotometrically. The mRNA levels were quantified by real-time PCR. 5-FU treatment caused an increase in BCKDH activity that appears to result mainly from increased dephosphorylation of the complex and is associated with an increase of PPM1K mRNA level and reduction of BDK and E1 mRNA levels. It is conceivable that 5-FU stimulation of BCKDH is an adaptive reaction with the purpose of enhancing the BCAA catabolism and protecting from toxic effect caused by excessive accumulation of these amino acids in heart.
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Authors and Affiliations

Małgorzata Knapik-Czajka
1
Michał Jurczyk
2
Justyna Bieleń
1
Veronika Aleksandrovych
2
Anna Gawędzka
1
Paulina Stach
2
Jagoda Drąg
1
Krzysztof Gil
3

  1. Department of Biochemical Analytics, Jagiellonian University Medical College, Kraków, Poland
  2. Department of Pathophysiology, Jagiellonian University Medical College, Kraków, Poland
  3. 2Department of Pathophysiology, Jagiellonian University Medical College, Kraków, Poland
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Abstract

Anorexia nervosa (AN) is an eating disorder characterized by distinct etiopathogenetic concepts that are gradually being linked together to unravel the dominant pathophysiological pathways underlying the disease. Excessive food restrictions, often accompanied by over-exercise and undertaken to lose weight, lead to the development of numerous complications. The biological concept of neurohormonal dysfunc-tion in AN seems incomplete without demonstrating or excluding the role of the enteric nervous system (ENS). Using an animal model of activity-based anorexia (ABA), we conducted the preliminary assess-ment of the ENS structure. Here we show, in preparations stained by immunohistochemistry with anti- ChAT, anti-NOS, anti-PGP 9.5, anti-c-fos, and anti-TH antibodies, a lower density of cholinergic and nitrergic nerve fibers as well as reduced neuronal activity in myenteric plexus. Such structural and functional damage to the ENS may be responsible for a number of gastrointestinal symptoms that worsen the course of the disease. In addition, we expanded the study to address the unresolved issue of mechanical and thermal pain sensitivity in AN. The Von Frey and hot plate tests revealed, that in ABA animals, the pain threshold for mechanical stimulus decreases while for thermal increases. In this way, we have sig-nificantly supplemented the background of AN with potentially observable nervous system changes which may influence the evolution of the therapeutic approach in the future.
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Authors and Affiliations

Kamil Skowron
1
Paulina Stach
1
Magdalena Kurnik-Łucka
1
Katarzyna Chwaleba
1
Mateusz Giełczyński
1
Wiktoria Suchy
1
Veronika Aleksandrovych
1
Michał Jurczyk
1
Beata Kuśnierz-Cabala
2
Krzysztof Gil
1

  1. Department of Pathophysiology, Faculty of Medicine, Jagiellonian University Medical College, Kraków, Poland
  2. Chair of Clinical Biochemistry, Department of Diagnostics, Faculty of Medicine, Jagiellonian University Medical College, Kraków, Poland

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