27 research outputs found
Pathological changes of the skin and the oral mucosa during pregnancy : part II
The specific physiological or pathological changes of the
skin and mucous membranes can occur during pregnancy. Also
the effect of pregnancy on some skin disorders is highly variable
and are not predictable, some of the skin conditions may
improve while others are aggravated. The changes in the course
of the skin and mucous membranes disorders during pregnancy
were presented, based on data from literature.
The choice of the therapy during pregnancy is an important\ud
management option
Pathological changes of the skin and the oral mucosa during pregnancy : part I
The study describes, on the basis of the literature, various
pathological changes which appear only on the oral mucosa
as well as on the oral mucosa and the skin during pregnancy.
Diagnostic methods, clinical symptoms of the described diseases and proper local therapy (of the pathological changes in
the oral cavity) are discussed
Nesfatin-1 : a new hormone in the control of food intake and the mechanism of damage and protection of gastric mucosa
Nesfatyna 1 jest 82-aminokwasowym peptydem powsta艂ym
w wyniku potranslacyjnej hydrolizy N-ko艅cowego fragmentu
innego bia艂ka nucleobindin2 (NUCB2), b臋d膮cego prekursorem
dla nesfatyny 1 o rozpoznanej i ustalonej sekwencji aminokwas贸w, wyst臋puj膮cej powszechnie w艣r贸d ssak贸w. Interesuj膮cy jest fakt, 偶e genow膮 ekspresj臋 peptydowego uk艂adu
NUCB2/nesfatyna 1 zaobserwowano w przewodzie pokarmowym gryzoni, zw艂aszcza w b艂onie 艣luzowej szczurzego 偶o艂膮dka, szczeg贸lnie w bliskiej lokalizacji kom贸rek neuroendokrynnych cz臋艣ci trzonowej odpowiedzialnych m.in. za uwalnianie
greliny. Pierwotnie wykryto, 偶e NUCB2 i nesfatyna 1 podawane do kom贸r bocznych m贸zgu hamuj膮 przyjmowanie pokarmu w fazie nocnej u szczur贸w i 偶e efekt ten jest po艂膮czony ze
zmniejszeniem masy cia艂a tych zwierz膮t, co sugeruje, 偶e nesfatyna 1 jest peptydem anoreksygenicznym, hamuj膮cym apetyt. Dalsze badania nad fizjologicznym znaczeniem nesfatyny 1
dowodz膮, 偶e podobnie jak w przypadku innych hormon贸w
pobudzaj膮cych apetyt (np. grelina) czy hamuj膮cych apetyt (np.
leptyna), peptyd ten odznacza si臋 w艂a艣ciwo艣ciami gastroprotekcyjnymi i chroni b艂on臋 艣luzow膮 偶o艂膮dka przed uszkodzeniami indukowanymi przez czynniki korozyjne oraz mikrokrwawienia wywo艂ywane przez stres. W ten gastroprotekcyjny
mechanizm dzia艂ania nesfatyny 1 zaanga偶owane s膮 uk艂ady
endogennych prostaglandyn (PG) uwalnianych na drodze aktywacji cyklooksygenaz (COX) - COX-1 i COX-2 - oraz tlenku
azotu (NO) produkowanego przez enzymy syntaz NO, odpowiedzialne za wzrost 偶o艂膮dkowego przep艂ywu krwi, kt贸remu
towarzyszy wzrost st臋偶enia nesfatyny 1 w osoczu. Podsumowuj膮c - endogenne PG i NO s膮 mediatorami gastroprotekcji
i przekrwienia obserwowanego w b艂onie 艣luzowej 偶o艂膮dka szczur贸w pod wp艂ywem nesfatyny 1. Dlatego autorzy s膮dz膮,
偶e dalsze badania, zw艂aszcza kliniczne, maj膮ce na celu poznanie mechanizmu dzia艂ania i wyja艣nienie roli nesfatyny 1
w przewodzie pokarmowym powinny rzuci膰 nieco wi臋cej
艣wiat艂a na problem potencjalnego terapeutycznego wykorzystania tego peptydu w zapobieganiu uszkodzeniom 偶o艂膮dka,
w tym mikrokrwawieniom 偶o艂膮dkowym u ludzi.Nesfatin-1 is an 82-amino-acid peptide derived from posttranslational processing of the N-terminal fragment of nucleobindin 2 (NUCB2), a protein precursor for nesfatin-1, which is
highly conserved across mammalian species. The expression
of NUCB2/nesfatin-1 has been detected in the stomach, most
prominently within ghrelin cells of the rat gastric oxyntic
mucosa. The first biological action ascribed to NUCB2 and nesfatin-1 was the reduction of dark-phase food intake with
a concomitant reduction in body weight gain when these peptides were injected intracerebroventricularly, suggesting their
anorexigenic action in rodents. Studies on the potential physiological importance of nesfatin-1 have shown that nesfatin1, similarly as for other appetite peptides such as ghrelin and
leptin studied before, exerts protective activity against gastric
mucosal lesions induced by topical damaging agents and
seems to be also effective against those caused by stress.
This gastroprotective action of exogenous nesfatin-1 may
involve the activation of PG/COX and NO/NOS systems,
resulting in an increase in gastric blood flow accompanied by
a rise in plasma nesfatin-1 levels. Thus, it is concluded that
1) endogenous PG and NO may mediate the nesfatin-1-
induced gastroprotection in the rat stomach, and 2) clinical
studies regarding the potential benefit of nesfatin-1 observed
in animals should shed more light on the efficacy of this peptide to prevent gastric disorders including the formation of
gastric microbleeding in humans
RuvC uses dynamic probing of the Holliday junction to achieve sequence specificity and efficient resolution
Holliday junctions (HJs) are four-way DNA structures that occur in DNA repair by homologous recombination. Specialized nucleases, termed resolvases, remove (i.e., resolve) HJs. The bacterial protein RuvC is a canonical resolvase that introduces two symmetric cuts into the HJ. For complete resolution of the HJ, the two cuts need to be tightly coordinated. They are also specific for cognate DNA sequences. Using a combination of structural biology, biochemistry, and a computational approach, here we show that correct positioning of the substrate for cleavage requires conformational changes within the bound DNA. These changes involve rare high-energy states with protein-ssisted base flipping that are readily accessible for the cognate DNA sequence but not for non-cognate sequences. These conformational changes and the relief of protein-induced structural tension of the DNA facilitate coordination between the two cuts. The unique DNA cleavage mechanism of RuvC demonstrates the importance of high-energy conformational states in nucleic acid readout
SARS-CoV-2 infects an <I>in vitro</I> model of the human developing pancreas through endocytosis
Recent studies showed that SARS-CoV-2 can infect adult human pancreas and trigger pancreatic damage. Here, using human fetal pancreas samples and 3D differentiation of human pluripotent cells into pancreatic endocrine cells, we determined that SARS-CoV-2 receptors ACE2, TMPRSS2, and NRP1 are expressed in precursors of insulin-producing pancreatic 尾-cells, rendering them permissive to SARS-CoV-2 infection. We also show that SARS-CoV-2 enters and undergoes efficient replication in human multipotent pancreatic and endocrine progenitors in聽vitro. Moreover, we investigated mechanisms by which SARS-CoV-2 enters pancreatic cells, and found that ACE2 mediates the entry, while NRP1 and TMPRSS2 do not. Surprisingly, we found that in pancreatic progenitors, SARS-CoV-2 enters cells via cathepsin-dependent endocytosis, which is a different route than in respiratory tract. Therefore, pancreatic spheroids might serve as a model to study candidate drugs for endocytosis-mediated viral entry inhibition and to investigate whether SARS-CoV-2 infection may affect pancreas development, possibly causing lifelong health consequences