Plejotropowe działanie melatoniny

2018 ◽  
Vol 21 (1) ◽  
Author(s):  
Zofia Dzierżewicz ◽  
Radosław Balwierz ◽  
Dominik Marciniak ◽  
Beata Sarecka-Hujar ◽  
Marcin Delijewski ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
Nervous System ◽  
Hydroxyl Radicals ◽  
Basic Function ◽  
Oxygen Radical ◽  
Over The Counter ◽  
Seasonal Rhythms ◽  
Over The Counter Medicines ◽  
Nerve Cell Death

Melatonin is a hormone synthesized mainly by the pineal gland. Its precursor is the exogenous amino acid L-tryptophan. The basic function of this hormone is the regulation of circadian and seasonal rhythms. As an amphiphilic molecule, melatonin can easily cross biological barriers, which is why its effects can be exerted through a variety of mechanisms. Both in experimental and clinical studies, the cardioprotective effect of melatonin has been demonstrated. Melatonin also plays a role in the regulation of the immune response. In addition, it is particularly effective in inactivating hydroxyl radicals, including the most reactive oxygen radical. Melatonin can inhibit the division of tumor cells by affecting the release of other hormones and substances involved in the process of carcinogenesis. It also limits the process of nerve cell death and adverse changes in the nervous system associated with the etiopathogenesis of Alzheimer’s disease. Melatonin is on the list of OTC preparations (over the counter), medicines available at the pharmacy without a prescription. This paper presents the biosynthesis of melatonin and its metabolism and discusses its physiological and clinical significance in the human body.

Legal Regulation of Treatment for Depression

2017 ◽  
Author(s):  
Hugh Series
Keyword(s):  
Legal Regulation ◽  
Mental Capacity ◽  
Medicinal Products ◽  
Over The Counter ◽  
Controlled Drugs ◽  
Treatment Of Depression ◽  
Mental Capacity Act 2005 ◽  
Incapacitated Patients ◽  
Mental Capacity Act ◽  
Over The Counter Medicines

This chapter reviews the legal regulation of treatment of depression as it exists in England and Wales, where medicinal products are regulated largely by the Medicines Act 1988 and the Misuse of Drugs Act 1971. The Medicines Act divides medicinal products into pharmacy only medicines, which can only be purchased under the supervision of a pharmacist, over-the-counter medicines, and prescription only medicines. The Misuse of Drugs Act is concerned with controlled drugs. These are divided into three classes according to their perceived degree of harmfulness. This chapter considers treatment with valid consent and two pieces of legislation that govern people who are sufficiently ill and need to be admitted to hospital: the Mental Health Act 1983 (MHA) and the Mental Capacity Act 2005 (MCA). It also discusses treatment of mentally incapacitated patients and the issue of liberty regarding the admission of a compliant but incapacitated patient to hospital. Finally, it looks at three types of non-medical prescribing in England, issued by independent prescribers, supplementary prescribers, and community practitioners.

scholarly journals ZBP1 promotes LPS-induced cell death and IL-1β release via RHIM-mediated interactions with RIPK1

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Hayley I. Muendlein ◽  
Wilson M. Connolly ◽  
Zoie Magri ◽  
Irina Smirnova ◽  
Vladimir Ilyukha ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
Complex Formation ◽  
Complex I ◽  
Yersinia Pseudotuberculosis ◽  
Caspase 8 ◽  
Inflammasome Activation ◽  
Inflammatory Signaling ◽  
Complex Ii ◽  
Dependent Model

AbstractInflammation and cell death are closely linked arms of the host immune response to infection, which when carefully balanced ensure host survival. One example of this balance is the tightly regulated transition from TNFR1-associated pro-inflammatory complex I to pro-death complex II. By contrast, here we show that a TRIF-dependent complex containing FADD, RIPK1 and caspase-8 (that we have termed the TRIFosome) mediates cell death in response to Yersinia pseudotuberculosis and LPS. Furthermore, we show that constitutive binding between ZBP1 and RIPK1 is essential for the initiation of TRIFosome interactions, caspase-8-mediated cell death and inflammasome activation, thus positioning ZBP1 as an effector of cell death in the context of bacterial blockade of pro-inflammatory signaling. Additionally, our findings offer an alternative to the TNFR1-dependent model of complex II assembly, by demonstrating pro-death complex formation reliant on TRIF signaling.

scholarly journals A novel gene signature based on five immune checkpoint genes predicts the survival of glioma

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Wei Zhang ◽  
You Zhai ◽  
Guanzhang Li ◽  
Tao Jiang
Keyword(s):  
Gene Expression ◽  
Central Nervous System ◽  
Immune Response ◽  
Nervous System ◽  
Cox Regression ◽  
Gene Signature ◽  
Immune Checkpoints ◽  
The Novel ◽  
The Central Nervous System ◽  
Checkpoint Genes

Abstract Background Glioma is the most common and fatal type of nerve neoplasm in the central nervous system. Several biomarkers have been considered for prognosis prediction, which is not accurate enough. We aimed to carry out a gene signature related to the expression of immune checkpoints which was enough for its performance in prediction. Methods Gene expression of immune checkpoints in TGGA database was filtrated. The 5 selected genes underwent verification by COX and Lasso-COX regression. Next, the selected genes were included to build a novel signature for further analysis. Results Patients were sub-grouped into high and low risk according to the novel signature. Immune response, clinicopathologic characters, and survival showed significant differences between those 2 groups. Terms including “naive,” “effector,” and “IL-4” were screened out by GSEA. The results showed strong relevance between the signature and immune response. Conclusions We constructed a gene signature with 5 immune checkpoints. The signature predicted survival effectively. The novel signature performed more functional than previous biomarkers.

scholarly journals Importance of the PD-1/PD-L1 Axis for Malignant Transformation and Risk Assessment of Oral Leukoplakia

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 194
Author(s):  
Jutta Ries ◽  
Abbas Agaimy ◽  
Falk Wehrhan ◽  
Christoph Baran ◽  
Stella Bolze ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Malignant Transformation ◽  
Immune Escape ◽  
Checkpoint Inhibitors ◽  
Precancerous Lesions ◽  
Death Receptor ◽  
Oral Leukoplakia ◽  
Significant Difference

Background: The programmed cell death ligand 1/programmed cell death receptor 1 (PD-L1/PD-1) Immune Checkpoint is an important modulator of the immune response. Overexpression of the receptor and its ligands is involved in immunosuppression and the failure of an immune response against tumor cells. PD-1/PD-L1 overexpression in oral squamous cell carcinoma (OSCC) compared to healthy oral mucosa (NOM) has already been demonstrated. However, little is known about its expression in oral precancerous lesions like oral leukoplakia (OLP). The aim of the study was to investigate whether an increased expression of PD-1/PD-L1 already exists in OLP and whether it is associated with malignant transformation. Material and Methods: PD-1 and PD-L1 expression was immunohistologically analyzed separately in the epithelium (E) and the subepithelium (S) of OLP that had undergone malignant transformation within 5 years (T-OLP), in OLP without malignant transformation (N-OLP), in corresponding OSCC and in NOM. Additionally, RT-qPCR analysis for PD-L1 expression was done in the entire tissues. Additionally, the association between overexpression and malignant transformation, dysplasia and inflammation were examined. Results: Compared to N-OLP, there were increased levels of PD-1 protein in the epithelial and subepithelial layers of T-OLP (pE = 0.001; pS = 0.005). There was no significant difference in PD-L1 mRNA expression between T-OLP and N-OLP (p = 0.128), but the fold-change increase between these groups was significant (Relative Quantification (RQ) = 3.1). In contrast to N-OLP, the PD-L1 protein levels were significantly increased in the epithelial layers of T-OLP (p = 0.007), but not in its subepithelial layers (p = 0.25). Importantly, increased PD-L1 levels were significantly associated to malignant transformation within 5 years. Conclusion: Increased levels of PD-1 and PD-L1 are related to malignant transformation in OLP and may represent a promising prognostic indicator to determine the risk of malignant progression of OLP. Increased PD-L1 levels might establish an immunosuppressive microenvironment, which could favor immune escape and thereby contribute to malignant transformation. Hence, checkpoint inhibitors could counteract tumor development in OLP and may serve as efficient therapeutic strategy in patients with high-risk precancerous lesions.

Sign in / Sign up

Export Citation Format

Share Document