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Article ; Online: The Thyroid Gland

Jacopo J. V. Branca / Alfredo Lascialfari Bruschi / Antonino Marcello Pilia / Donatello Carrino / Giulia Guarnieri / Massimo Gulisano / Alessandra Pacini / Ferdinando Paternostro

Medicina, Vol 58, Iss 137, p

A Revision Study on Its Vascularization and Surgical Implications

2022 Volume 137

Abstract: Background : The “classic” thyroid gland arterial vascularization takes into account two superior thyroid arteries (STA), two inferior thyroid arteries (ITA) and, occasionally, a thyroid ima artery (TIMA). The present review focuses on exploring the ... ...

Abstract	Background : The “classic” thyroid gland arterial vascularization takes into account two superior thyroid arteries (STA), two inferior thyroid arteries (ITA) and, occasionally, a thyroid ima artery (TIMA). The present review focuses on exploring the available data concerning thyroid gland arterial vascularization and its variations. Methods : Here, we analysed 49 articles from the last century, ranging from case reports to reviews concerning cadaver dissection classes, surgical intervention, and non-invasive techniques as well. Results : The harvested data clearly highlighted that: (i) the STA originates predominantly from the external carotid artery; (ii) the ITA is a branch of the thyrocervical trunk; and (iii) the TIMA is a very uncommon variant predominantly occurring to compensate for ITA absence. Conclusion : A systematic review of a highly vascularized organ is of great relevance during surgical intervention and, thus, the knowledge of normal anatomy and its modification is essential both for fact-finding and in surgery.
Keywords	thyroid gland ; thyroid arteries variations ; superior thyroid artery ; inferior thyroid artery ; thyroid ima artery ; Medicine (General) ; R5-920
Subject code	630
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Cadmium-Induced Cytotoxicity

Jacopo Junio Valerio Branca / Alessandra Pacini / Massimo Gulisano / Niccolò Taddei / Claudia Fiorillo / Matteo Becatti

Frontiers in Cell and Developmental Biology, Vol

Effects on Mitochondrial Electron Transport Chain

2020 Volume 8

Abstract: Cadmium (Cd) is a well-known heavy metal and environmental toxicant and pollutant worldwide, being largely present in every kind of item such as plastic (toys), battery, paints, ceramics, contaminated water, air, soil, food, fertilizers, and cigarette ... ...

Abstract	Cadmium (Cd) is a well-known heavy metal and environmental toxicant and pollutant worldwide, being largely present in every kind of item such as plastic (toys), battery, paints, ceramics, contaminated water, air, soil, food, fertilizers, and cigarette smoke. Nowadays, it represents an important research area for the scientific community mainly for its effects on public health. Due to a half-life ranging between 15 and 30 years, Cd owns the ability to accumulate in organs and tissues, exerting deleterious effects. Thus, even at low doses, a Cd prolonged exposure may cause a multiorgan toxicity. Mitochondria are key intracellular targets for Cd-induced cytotoxicity, but the underlying mechanisms are not fully elucidated. The present review is aimed to clarify the effects of Cd on mitochondria and, particularly, on the mitochondrial electron transport chain.
Keywords	cadmium ; cytotoxicity ; mitochondria ; mitochondrial electron transport chain ; mitochondrial complexes ; Biology (General) ; QH301-705.5
Subject code	500
Language	English
Publishing date	2020-11-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Retraction Note

Lorenzo Di Cesare Mannelli / Alessandra Pacini / Laura Micheli / Angelo Pietro Femia / Mario Maresca / Matteo Zanardelli / Alfredo Vannacci / Eugenia Gallo / Anna Rita Bilia / Giovanna Caderni / Fabio Firenzuoli / Alessandro Mugelli / Carla Ghelardini

Scientific Reports, Vol 13, Iss 1, Pp 1-

Astragali radix: could it be an adjuvant for oxaliplatin-induced neuropathy?

2023 Volume 2

Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2023-06-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Alcohol-Induced Blood-Brain Barrier Impairment

Donatello Carrino / Jacopo Junio Valerio Branca / Matteo Becatti / Ferdinando Paternostro / Gabriele Morucci / Massimo Gulisano / Lorenzo Di Cesare Mannelli / Alessandra Pacini

International Journal of Environmental Research and Public Health, Vol 18, Iss 2683, p

An In Vitro Study

2021 Volume 2683

Abstract: In recent years, alcohol abuse has dramatically grown with deleterious consequence for people’s health and, in turn, for health care costs. It has been demonstrated, in humans and animals, that alcohol intoxication induces neuroinflammation and ... ...

Abstract	In recent years, alcohol abuse has dramatically grown with deleterious consequence for people’s health and, in turn, for health care costs. It has been demonstrated, in humans and animals, that alcohol intoxication induces neuroinflammation and neurodegeneration thus leading to brain impairments. Furthermore, it has been shown that alcohol consumption is able to impair the blood–brain barrier (BBB), but the molecular mechanisms underlining this detrimental effect have not been fully elucidated. For this reason, in this study we investigated the effects of alcohol exposure on a rat brain endothelial (RBE4) cell line, as an in vitro-validated model of brain microvascular endothelial cells. To assess whether alcohol caused a concentration-related response, the cells were treated at different times with increasing concentrations (10–1713 mM) of ethyl alcohol (EtOH). Microscopic and molecular techniques, such as cell viability assay, immunofluorescence and Western blotting, were used to examine the mechanisms involved in alcohol-induced brain endothelial cell alterations including tight junction distribution, apoptosis, and reactive oxygen species production. Our findings clearly demonstrate that alcohol causes the formation of gaps between cells by tight junction disassembly, triggered by the endoplasmic reticulum and oxidative stress, highlighted by GRP78 chaperone upregulation and increase in reactive oxygen species production, respectively. The results from this study shed light on the mechanisms underlying alcohol-induced blood–brain barrier dysfunction and a better understanding of these processes will allow us to take advantage of developing new therapeutic strategies in order to prevent the deleterious effects of alcohol.
Keywords	alcoholism ; alcohol abuse ; oxidative stress ; blood–brain barrier ; tight junction ; Medicine ; R
Subject code	616
Language	English
Publishing date	2021-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Oxaliplatin-Induced Neuropathy

Jacopo Junio Valerio Branca / Donatello Carrino / Massimo Gulisano / Carla Ghelardini / Lorenzo Di Cesare Mannelli / Alessandra Pacini

Frontiers in Molecular Biosciences, Vol

Genetic and Epigenetic Profile to Better Understand How to Ameliorate This Side Effect

2021 Volume 8

Abstract: In the most recent decades, oxaliplatin has been used as a chemotherapeutic agent for colorectal cancer and other malignancies as well. Oxaliplatin interferes with tumor growth predominantly exerting its action in DNA synthesis inhibition by the ... ...

Abstract	In the most recent decades, oxaliplatin has been used as a chemotherapeutic agent for colorectal cancer and other malignancies as well. Oxaliplatin interferes with tumor growth predominantly exerting its action in DNA synthesis inhibition by the formation of DNA-platinum adducts that, in turn, leads to cancer cell death. On the other hand, unfortunately, this interaction leads to a plethora of systemic side effects, including those affecting the peripheral and central nervous system. Oxaliplatin therapy has been associated with acute and chronic neuropathic pain that induces physicians to reduce the dose of medication or discontinue treatment. Recently, the capability of oxaliplatin to alter the genetic and epigenetic profiles of the nervous cells has been documented, and the understanding of gene expression and transcriptional changes may help to find new putative treatments for neuropathy. The present article is aimed to review the effects of oxaliplatin on genetic and epigenetic mechanisms to better understand how to ameliorate neuropathic pain in order to enhance the anti-cancer potential and improve patients’ quality of life.
Keywords	oxaliplatin ; neuropathic pain ; glial cells ; genetic mechanisms ; epigenetic mechanisms ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2021-05-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Antioxidant support to ameliorate the oxaliplatin-dependent microglial alteration

Jacopo J.V. Branca / Donatello Carrino / Ferdinando Paternostro / Massimo Gulisano / Matteo Becatti / Lorenzo Di Cesare Mannelli / Alessandra Pacini

European Journal of Histochemistry, Vol 65, Iss s

morphological and molecular study

2021 Volume 1

Abstract: Oxaliplatin is a third-generation chemotherapy drug mainly used for colorectal cancer treatment. However, it is also known to trigger neuropathy whose underlying neurobiological mechanisms are still under investigation and currently available treatments ... ...

Abstract	Oxaliplatin is a third-generation chemotherapy drug mainly used for colorectal cancer treatment. However, it is also known to trigger neuropathy whose underlying neurobiological mechanisms are still under investigation and currently available treatments show limited efficacy. It is now established that neurons are not the only cell type involved in chronic pain and that glial cells, mainly astrocytes and microglia, are involved in the initiation and maintenance of neuropathy. Among all the pathogenetic factors involved in neuropathic pain, an oxaliplatin-dependent oxidative stress plays a predominant role. In our study, the antioxidant properties of magnesium (Mg), manganese (Mn) and zinc (Zn) salts were evaluated in order to counteract microglial activation induced by oxaliplatin. The antioxidant efficacy of these metals was evaluated by the means of molecular and morphological assays on the BV-2 microglial cell line. Our data clearly show that Mg, Mn and Zn are able to prevent oxaliplatin-dependent microglial alterations by reducing both oxidative and endoplasmic reticulum stress.
Keywords	neuropathic pain ; oxaliplatin ; magnesium ; manganese ; zinc ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2021-11-01T00:00:00Z
Publisher	PAGEPress Publications
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Inhibitors of Mitochondrial Human Carbonic Anhydrases VA and VB as a Therapeutic Strategy against Paclitaxel-Induced Neuropathic Pain in Mice

Laura Micheli / Lara Testai / Andrea Angeli / Donatello Carrino / Alessandra Pacini / Francesco Margiotta / Lorenzo Flori / Claudiu T. Supuran / Vincenzo Calderone / Carla Ghelardini / Lorenzo Di Cesare Mannelli

International Journal of Molecular Sciences, Vol 23, Iss 6229, p

2022 Volume 6229

Abstract: Neuropathy development is a major dose-limiting side effect of anticancer treatments that significantly reduces patient’s quality of life. The inadequate pharmacological approaches for neuropathic pain management warrant the identification of novel ... ...

Abstract	Neuropathy development is a major dose-limiting side effect of anticancer treatments that significantly reduces patient’s quality of life. The inadequate pharmacological approaches for neuropathic pain management warrant the identification of novel therapeutic targets. Mitochondrial dysfunctions that lead to reactive oxygen species (ROS) increase, cytosolic Ca 2+ imbalance, and lactate acidosis are implicated in neuropathic pain pathogenesis. It has been observed that in these deregulations, a pivotal role is played by the mitochondrial carbonic anhydrases (CA) VA and VB isoforms. Hence, preclinical studies should be conducted to assess the efficacy of two novel selenides bearing benzenesulfonamide moieties, named 5b and 5d , and able to inhibit CA VA and VB against paclitaxel-induced neurotoxicity in mice. Acute treatment with 5b and 5d (30–100 mg/kg, per os – p.o.) determined a dose-dependent and long-lasting anti-hyperalgesic effect in the Cold plate test. Further, repeated daily treatment for 15 days with 100 mg/kg of both compounds (starting the first day of paclitaxel injection) significantly prevented neuropathic pain development without the onset of tolerance to the anti-hyperalgesic effect. In both experiments, acetazolamide (AAZ, 100 mg/kg, p.o.) used as the reference drug was partially active. Moreover, ex vivo analysis demonstrated the efficacy of 5b and 5d repeated treatments in reducing the maladaptive plasticity that occurs to glia cells in the lumbar portion of the spinal cord and in improving mitochondrial functions in the brain and spinal cord that were strongly impaired by paclitaxel-repeated treatment. In this regard, 5b and 5d ameliorated the metabolic activity, as observed by the increase in citrate synthase activity, and preserved an optimal mitochondrial membrane potential (ΔΨ) value, which appeared depolarized in brains from paclitaxel-treated animals. In conclusion, 5b and 5d have therapeutic and protective effects against paclitaxel-induced neuropathy without tolerance development. ...
Keywords	neuropathic pain ; Taxus brevifolia ; carbonic anhydrase ; CA VA and VB ; mitochondria ; glial cells ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The Protection of Zinc against Acute Cadmium Exposure

Jacopo J. V. Branca / Donatello Carrino / Ferdinando Paternostro / Gabriele Morucci / Claudia Fiorillo / Claudio Nicoletti / Massimo Gulisano / Carla Ghelardini / Lorenzo Di Cesare Mannelli / Matteo Becatti / Alessandra Pacini

Cells, Vol 11, Iss 1646, p

A Morphological and Molecular Study on a BBB In Vitro Model

2022 Volume 1646

Abstract: Cadmium (Cd) is a well-known occupational and environmental pollutant worldwide, and its toxicity is widely recognised. Cd is reported to increase the permeability of the blood–brain barrier (BBB) and to penetrate and accumulate in the brain. Although ... ...

Abstract	Cadmium (Cd) is a well-known occupational and environmental pollutant worldwide, and its toxicity is widely recognised. Cd is reported to increase the permeability of the blood–brain barrier (BBB) and to penetrate and accumulate in the brain. Although many lines of evidence show that Cd toxicity is induced by different mechanisms, one of the best known is the Cd-dependent production of reactive oxygen species (ROS). Zinc is a trace element known as coenzyme and cofactor for many antioxidant proteins, such as metallothioneins and superoxide dismutase enzymes. To date, very little is known about the role of Zn in preventing Cd-induced blood–brain barrier (BBB) alterations. The goal of this study was to test the Zn antioxidant capacity against Cd-dependent alterations in a rat brain endothelial cell line (RBE4), as an in vitro model for BBB. In order to mimic acute Cd poisoning, RBE4 cells were treated with CdCl 2 30 µM for 24 h. The protective role of ZnCl 2 (50 µM) was revealed by evaluating the cell viability, reactive oxygen species (ROS) quantification, cytochrome C distribution, and the superoxide dismutase (SOD) protein activity. Additionally, the effectiveness of Zn in counteracting the Cd-induced damage was investigated by evaluating the expression levels of proteins already known to be involved in the Cd signalling pathway, such as GRP78 (an endoplasmic reticulum (ER) stress protein), caspase3 pro- and cleaved forms, and BAX. Finally, we evaluated if Zn was able to attenuate the alterations of zonula occludens-1 (ZO-1), one of the tight-junction (TJ) proteins involved in the formation of the BBB. Our data clearly demonstrate that Zn, by protecting from the SOD activity impairment induced by Cd, is able to prevent the triggering of the Cd-dependent signalling pathway that leads to ZO-1 dislocation and downregulation, and BBB damage.
Keywords	antioxidant ; zinc ; cadmium ; blood–brain barrier ; RBE4 ; oxidative stress ; Biology (General) ; QH301-705.5
Subject code	500
Language	English
Publishing date	2022-05-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Effect of Vitis vinifera hydroalcoholic extract against oxaliplatin neurotoxicity

Laura Micheli / Luisa Mattoli / Anna Maidecchi / Alessandra Pacini / Carla Ghelardini / Lorenzo Di Cesare Mannelli

Scientific Reports, Vol 8, Iss 1, Pp 1-

in vitro and in vivo evidence

2018 Volume 14

Abstract: Abstract Oxaliplatin treatment is associated with the development of a dose-limiting painful neuropathy impairing patient’s quality of life. Since oxidative unbalance is a relevant mechanism of oxaliplatin neurotoxicity, we assessed the potential ... ...

Abstract	Abstract Oxaliplatin treatment is associated with the development of a dose-limiting painful neuropathy impairing patient’s quality of life. Since oxidative unbalance is a relevant mechanism of oxaliplatin neurotoxicity, we assessed the potential antioxidant properties of Vitis vinifera extract in reducing oxaliplatin-induced neuropathy as a valuable therapeutic opportunity. A hydroalcoholic extract of Vitis vinifera red leaf was characterized and tested in primary rat astrocyte cells treated with oxaliplatin (100 μM). Oxaliplatin lethality in the human adenocarcinoma cell line HT-29 was evaluated in the absence and presence of the extract. In vivo, pain hypersensitivity was measured in a rat model of neuropathy induced by oxaliplatin and ex vivo molecular targets of redox balance were studied. Vitis vinifera extract (50 μg mL−1, 4 h incubation) significantly reduced the oxaliplatin-dependent superoxide anion increase and lipid peroxidation in rat astrocytes but did not interfere with the mortality elicited by oxaliplatin in HT-29 cancer cells. In oxaliplatin-treated rats, a repeated daily administration of the Vitis vinifera extract (300 mg kg−1, p.o.) significantly prevented mechanical and thermal hypersensitivity to noxious and non noxious stimuli. mRNA and protein levels of Nrf2 were normalized in spinal cord and DRGs. Moreover, in the spinal cord, the extract significantly decreased the activation of astrocytes. Vitis vinifera reduced oxidative damages and relieved pain without influencing oxaliplatin anti-cancer activity.
Keywords	Medicine ; R ; Science ; Q
Subject code	500
Language	English
Publishing date	2018-09-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Carbonic Anhydrase IV Selective Inhibitors Counteract the Development of Colitis-Associated Visceral Pain in Rats

Elena Lucarini / Alessio Nocentini / Alessandro Bonardi / Niccolò Chiaramonte / Carmen Parisio / Laura Micheli / Alessandra Toti / Valentina Ferrara / Donatello Carrino / Alessandra Pacini / Maria Novella Romanelli / Claudiu T. Supuran / Carla Ghelardini / Lorenzo Di Cesare Mannelli

Cells, Vol 10, Iss 2540, p

2021 Volume 2540

Abstract: Persistent pain affecting patients with inflammatory bowel diseases (IBDs) is still very difficult to treat. Carbonic anhydrase (CA) represents an intriguing pharmacological target considering the anti-hyperalgesic efficacy displayed by CA inhibitors in ... ...

Abstract	Persistent pain affecting patients with inflammatory bowel diseases (IBDs) is still very difficult to treat. Carbonic anhydrase (CA) represents an intriguing pharmacological target considering the anti-hyperalgesic efficacy displayed by CA inhibitors in both inflammatory and neuropathic pain models. The aim of this work was to evaluate the effect of inhibiting CA IV, particularly when expressed in the gut, on visceral pain associated with colitis induced by 2,4-di-nitrobenzene sulfonic acid (DNBS) in rats. Visceral sensitivity was assessed by measuring animals’ abdominal responses to colorectal distension. Repeated treatment with the selective CA IV inhibitors AB-118 and NIK-67 effectively counteracted the development of visceral pain induced by DNBS. In addition to pain relief, AB-118 showed a protective effect against colon damage. By contrast, the anti-hyperalgesic activity of NIK-67 was independent of colon healing, suggesting a direct protective effect of NIK-67 on visceral sensitivity. The enzymatic activity and the expression of CA IV resulted significantly increased after DNBS injection. NIK-67 normalised CA IV activity in DNBS animals, while AB-118 was partially effective. None of these compounds influenced CA IV expression through the colon. Although further investigations are needed to study the underlying mechanisms, CA IV inhibitors are promising candidates in the search for therapies to relieve visceral pain in IBDs.
Keywords	IBDs ; visceral hypersensitivity ; carbonic anhydrase IV ; colon ; inflammation ; Biology (General) ; QH301-705.5
Subject code	616
Language	English
Publishing date	2021-09-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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