Showing 4 results for Cycle
Mohammad Reza Nikmaram,
Volume 10, Issue 4 (12-2007)
Abstract
Introduction: In resent years, neuronal type Na+ channel is one of the important currents for action potential depolarization phase in heart cells. In this study neuronal type Na+ channel is blocked by low concentration of Tetrodotoxin (TTX) to compare the effect of TTX blocker on pacemaker activity of sinoatrial node (SAN) and atrioventricular node (AVN) of mouse heart. Materials and Methods: In this experimental study the pacemaker activity of distinct intact SAN and AVN, was recorded before and during consuming 100 nM TTX, and cycle length (CL) was measured. Data was analyzed using t-test. Results: 100 nM TTX increased CL on SAN preparations by 22.2±6% and on AVN preparations by 52.5±13.5 %. These changes were significant in the two nodes. Conclusion: It is passible to conclude that the neuronal type Na+ channel was present in the two nodes, and the effect of TTX on CL of the two nodes was different.
Ahmadi, Moosavi, Hosseinpour Feizi,
Volume 13, Issue 3 (9-2010)
Abstract
Background: Recently, reports have been made of the effects of boric acid (BA) on cancer prevention and inhibition of cancer cell proliferation. This study was designed to investigate the effects of this compound on K562 cell line as a model of chronic myeloid leukemia (CML). Materials and Methods: In this experimental trial, K562 cell line was cultured in the presence of 0.75 to 12 mmol concentrations of boric acid for 24, 48, 72, and 96 hour intervals. Anti-proliferative and cytotoxic effects of BA were measured by trypan blue exclusion test and MTT assay, respectively. Flow-cytometery was utilized for evaluating the effects of BA on cell cycle. Wright-giemsa staining was used for determining the effects of BA, and latex phagocytic assay was used for evaluating the phagocytic potential of the differentiated cells. Results: BA induced growth inhibition of K562 cells in a dose and time dependent manner after 96 hours of treatment with 12 mmol BA, cell proliferation of K562 cells was inhibited to about 83% (p<0.001). In addition, BA induced G1 cell cycle arrest in a way that for instance, after 6 days of treatment with 9 mmol BA, 98% of cell populations were at G1 level. Wright-giemsa staining and latex phagocytic assay results confirmed that K562 cells differentiated toward monocyte-macrophage lineage. Conclusion: Noticing the anti-proliferative and differentiating effects of BA, and no evidence of its adverse effects, this compound can be used as alone or in combination with other drugs in CML differentiation therapy.
Shaban Ali Alizadeh, Abolfazl Fatehi, Yahya Jand, Ghasem Mosayebi, Mohammad Rafiei,
Volume 15, Issue 2 (6-2012)
Abstract
Background: Several studies have demonstrated that the levels of inflammatory markers in healthy women are under the influence of menstrual cycle changes. The aim of this study was to compare blood levels of inflammatory markers in women with appendicitis in different phases of menstrual cycle. Materials and Methods: In this case-control study, 70 female and 12 male patients with appendicitis, and 61 healthy women were enrolled based on inclusion and exclusion criteria. Inflammatory markers, such as leukocyte count, CRP, ESR, and TNF-α were measured and compared using student t-test and one-way ANOVA based on different phases of menstrual cycle. Results: There were no significant changes in the ESR, CRP, and TNF-α concentrations and the number of peripheral blood leukocytes in different phases of the menstrual cycle in women with appendicitis. The mean number of leukocytes and CRP concentrations were significantly higher in patients with appendicitis compared with the control group. Conclusion: The findings show that there are not significant differences in the inflammatory markers in women with appendicitis during the different phases of menstrual cycles. It seems that day to day variation of sexual hormones in the menstrual cycle have led to very different conclusions about the change of inflammatory markers in different phases of menstrual cycle. Therefore, studies investigating inflammatory markers in women with acute appendicitis based on day of menstrual cycle, time of sampling in the day, and severity of appendicitis are suggested.
Zahra Heidarzadeh, Roghaieh Khakpay, Seyed Mahdi Banan Khojasteh, Fatemeh Khakpai,
Volume 22, Issue 2 (6-2019)
Abstract
Background and Aim: Intra-paragigantocellularis lateralis (LPGi) injection of 17β-estradiol produces robust antinociceptive effect on the inflammatory pain in the both male and ovariectomized female rats which is possibly mediated through estrogen receptors of this nucleus. This study aimed to examine the role of estrogen receptors in the pain modulatory effect of 17β-estradiol during proestrus phase of female rats.
Materials and Methods: In this study, the female Wistar rats in the range of 200-270 gr were used. For studying the influence of intra-LPGi injection of 17β-estradiol on the acute inflammatory pain modulation, cannulation into the LPGi nucleus was performed after entrance into the proestrus cycle. After entrance in the proestrus phase once again, drugs were injected and 15 minutes later, formalin was injected into the rat's hind paw. Then, formalin-induced paw jerking behavior was recorded for 60 min.
Ethical Considerations: This study with research ethics code IR.TBZMED.VCR.REC.1397.385 has been approved by research ethics committee at Tabriz University of Medical Sciences.
Findngs: The results of this study showed that intra-LPGi injection of 17β-estradiol during proestrus phase significantly attenuated paw jerking frequency both in the first (p<0.01) and in the second (p<0.001) phases of formalin test. Pretreatment of the LPGi nucleus with estrogen receptor antagonist (ICI182,780) neutralized the 17β-estradiol-induced analgesia.
Conclusion: Our results indicated that intra-LPGi injection of 17β-estradiol induces robust analgesia on the inflammatory pain during the proestrus phase. Thus, it can be concluded that the antinociceptive effect of 17β-estradiol is probably mediated via estrogen receptors.
