ÁOK Gyógyszertudomány Doktori Iskola
http://pea.lib.pte.hu/handle/pea/74
2024-02-16T08:34:06ZThe tachykinin hemokinin-1 as a mediator in neuronal- and immune functions in mouse models of pain, arthritis, and dermatitis
http://pea.lib.pte.hu/handle/pea/34580
The tachykinin hemokinin-1 as a mediator in neuronal- and immune functions in mouse models of pain, arthritis, and dermatitis
Pain is one of the most common complaints for people seeking medical help(1). While in most
cases the underlying problem can be resolved, about 10-20% of pain becomes chronic(2). The
currently used main groups of analgesic drugs (nonsteroidal anti-inflammatory drugs: NSAIDs,
opioids and adjuvant analgesics) are not effective in every case, and long-term administration
can lead to a variety of side-effects(3). Many forms of chronic pain begin with (autoimmune)
inflammation; and damage to the nervous system potentially resulting in chronic pain can lead
to local inflammation as well(4, 5). Nociceptors transmit the pain stimulus from the periphery to
the spinal dorsal horn, where descending pathways from the brain modulate the sensation.
Sensitization of nociceptors in pathological conditions can occur through both peripheral and
central mechanisms. A subtype of the nociceptors is the capsaicin sensitive nerve ending which
expresses the Transient Receptor Potential Vanilloid-1 (TRPV1) ion channel on its surface(6).
These have a local efferent function called neurogenic inflammation when inflammatory
neuropeptides are released from the nerve endings(7). Crosstalk between the nervous- and
immune systems is substantial, as nociceptors release neuropeptides that regulate immune
cells(8); microglia as well as other immune cells influence the developing brain(9), and lymphatic
vessels have been discovered in the meninges(10, 11). Exploring these interactions and the
molecules playing a role in them could advance treatment of painful pathological conditions.
2021-07-20T00:00:00ZA hólyagfájdalom szindrómában szenvedő betegek innovatív terápiás lehetőségei
http://pea.lib.pte.hu/handle/pea/34539
A hólyagfájdalom szindrómában szenvedő betegek innovatív terápiás lehetőségei
2023-04-25T00:00:00ZIllóolajok antibakteriális hatásának vizsgálata in vitro módszerekkel
http://pea.lib.pte.hu/handle/pea/34537
Illóolajok antibakteriális hatásának vizsgálata in vitro módszerekkel
2023-02-21T00:00:00ZEffect of experimental hyperglycemia on oxidative transformations of endogenous and exogenous compounds in the rat
http://pea.lib.pte.hu/handle/pea/34529
Effect of experimental hyperglycemia on oxidative transformations of endogenous and exogenous compounds in the rat
Diabetes mellitus (DM) is a common disease with a complex
metabolic and endocrine system influencing a large proportion of the
global population. DM is described by its high blood glucose level
because of insufficient action and secretion of insulin from beta-cells
of the pancreas. Hyperglycemia is considered a source of the
development of diabetic complications via altering a variety of
signaling pathways, leading to the induction of reactive oxygen
species, oxidative stress, and cell death. A high rate of reactive oxygen
species (ROS) generated from the inducted oxidative stress is
considered to contribute to the pathogenesis of diabetic patients.
In addition, besides their insulin injection and/or
consumption of diabetic medications, patients are supposed to use a
variety of other medicines. However, how and to what degree diabetes
affects the metabolism of drugs has not been well studied.
Pathophysiological changes during diabetes can affect various drugs'
absorption, distribution, metabolism, and excretion. However,
previous studies have provided inconsistent data for multiple drugs,
possibly due to variations in patient characteristics or control of
patients’ diabetes at the time of data collection.
2023-02-21T00:00:00Z