The mitotic pattern of the embryonic epidermis of chick during scale morphogenesis

Development ◽  
1969 ◽  
Vol 21 (2) ◽  
pp. 235-242
Author(s):  
Takesi Yohro

The epidermis of the chick embryo has been widely used for in vitro studies of many developmental problems (Matoltsy, 1960; Billingham & Silvers, 1963). The present attempt to determine the proliferation rate of chick embryonic epidermal cells was expected to provide a base for experimental studies, but a preliminary mitotic count revealed that the number of mitoses varied greatly in different areas. This suggested accumulation of mitoses in some restricted parts of the epidermis, and so a mapping experiment was carried out to determine the distribution of mitoses in this material. The characteristic mitotic pattern which was discovered is described and discussed. About 300 White Leghorn embryos were used: 20 for study of the gross anatomy of scales, 200 for Colcemid treatment and 80 for [3H] thymidine treatment.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 5172-5172
Author(s):  
Ahmet H Elmaagacli ◽  
Michael Koldehoff ◽  
Nina K Steckel ◽  
Dietrich Beelen

Abstract Background. The protein kinase C (PKC) inhibitor PKC412 (N-benzylstaurosporine) is a derivate of the naturally occurring alkaloid staurosproine and has been shown to inhibit the conventional isoforms of PKC (alfa, beta1, beta2 and gamma). PKC412 has been shown to have an antitumor effect on non-small cell lung cancer and acute leukemia with FLT3 mutations, but little is known about its effect on multiple myeloma up to date. Methods. Since PKC is also an inhibitor of a tyrosin kinase which is associated with VEGF, and inhibits the release of Interleukin-6, TNF alfa, and that of growth factor dependent C-FOS, we postulated that PKC412 might have also strong anti-myeloma features. Here we evaluated the anti-myeloma effect of PKC412 in the multiple myeloma cell lines INA-6, OPM-2 and RPMI 8226 by measuring its effect on their proliferation rate, the apoptosis rate and the Interleukin-6 mRNA expression. Results. PKC412 showed strong anti-myeloma effects in all three celllines. 50nM of PKC412 was enough to drop the proliferation rate in all three cell lines under 10% compared to untreated cells(p<0.01). The apoptosis rate increased in INA cell line up to 2,5 times and in RPMI cell line up to 3 times (p<0.05), whereas only a moderate increase was observed in the OPM2 cell line with 500nM of PKC412. As expected, the IL-6 mRNA expression decreased after PKC412 treatment in all three cell lines more than 50%. The addition of Bevacizumab to PKC412 in RPMI and OPM-2 cell lines did not increased the apoptosis rate significantly, whereas the addition of short-interference RNA (RNAi) against VEGF increased the apoptosis rate in RPMI 8226 cells about 20% (p<0.05) and in OPM-2 cells up to 30% (p<0.01) compared to PKC412 alone, which was also associated concordantly with a further reduction of the proliferation rate in RPMI and OPM-2 cells up to 30%. Conclusions. PKC412 shows strong anti-myeloma effects and might be effective also in the treatment of patients with multiple myeloma. These in-vitro studies might encourage to initiate clinical trials with PKC412 in patients with multiple myeloma.


1980 ◽  
Vol 16 (1-3) ◽  
pp. 189-191
Author(s):  
ROBERT J. ULSHAFER ◽  
ANDRÉ CLAVERT

2006 ◽  
Vol 84 (5) ◽  
pp. 745-754 ◽  
Author(s):  
R. Badrinarayanan ◽  
S. Rengarajan ◽  
P. Nithya ◽  
K. Balasubramanian

Clinical and experimental studies, including our own observations, have shown the adverse effects of excess glucocorticoids on testicular steroid hormone production. The present study was designed to gain insight into the molecular mechanisms by which excess corticosterone impairs Leydig cell steroidogenesis. To achieve this, adult rats were administered with corticosterone-21-acetate (2 mg/100 g body weight) twice daily for 15 days. After the treatment period, rats were killed by decapitation. The testes were removed, decapsulated aseptically and used for the isolation of Leydig cells. Purified Leydig cells were used for assessing the activity of 3β- and 17β-hydroxysteroid dehydrogenases (HSDs) and total RNA isolation. For in vitro studies, purified Leydig cells (7.5 × 106 cells) of control rats were plated in culture flasks and exposed to different concentrations (50, 100, 200, 400, and 800 nmol/L) of corticosterone for 24 h. At the end of incubation, total RNA was isolated from cultured Leydig cells, and the mRNA of 3β- and 17β-HSDs was quantified by RT–PCR. A significant reduction in the activities and levels of 3β-HSD type-I and 17β-HSD type-III mRNAs in Leydig cells were observed. In vitro studies demonstrated a dose-dependent significant impairment in both the activity and mRNA expression of these enzymes. These results suggest that corticosterone might have a direct effect on the transcription of the genes of 3β- and 17β-HSD. It is inferred from the present in vivo and in vitro studies that one of the molecular mechanisms by which excess corticosterone decreases the steroidogenic potency of Leydig cells is by suppressing the mRNA expression of 3β-HSD type-I and 17β-HSD type-III enzymes.


Development ◽  
1978 ◽  
Vol 46 (1) ◽  
pp. 187-205
Author(s):  
E. J. Sanders ◽  
Ruth Bellairs ◽  
P. A. Portch

An unusual example of the invasion of one tissue by another occurs during gastrulation in the chick embryo when the definitive endoblast becomes inserted into the hypoblast. The two tissues were examined morphologically by SEM and TEM. They resemble each other in being of an epithelial type, though neither possesses a basal lamina. The definitive endoblast cells are flatter than the hypoblast cells and more closely attached to one another. When they were explanted in hanging drop cultures, the two tissues were found to exhibit differences in their behaviour. In comparison with the definitive endoblast, the hypoblast cells attached more readily to the glass, produced larger ruffle membranes, moved more rapidly, showed poorer contact-inhibition of locomotion and showed a greater tendency to break away from the main explant. When a hypoblast explant was confronted with a definitive endoblast explant, the hypoblast cells became displaced by the definitive endoblast. The hypoblast explant tended to fragment into smaller groups of cells, many of which migrated around the definitive endoblast, thus mimicking the situation in vivo. Control experiments comprised confronting hypoblast with hypoblast, hypoblast with somites, definitive endoblast with definitive doblast, and definitive endoblast with somites. The hypoblast explants behaved in a consistent manner, always fragmenting when coming into contact with cells from a confronting xplant. The definitive endoblast explants showed more contact inhibition of locomotion when confronted with definitive endoblast or with somites than when confronted with hypoblast. It is suggested therefore that the ability of the hypoblast cells to separate from one another may play an important role in the penetration of the hypoblast by the definitive endoblast both in vitro and in vivo.


PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e10303
Author(s):  
Olav K. Straum

Background In the last decades, several in vitro studies have tested the effect of plate-rich plasma (PRP) on the proliferation of human cells in search of a wizard for the use of PRP in a clinical setting. However, the literature displays striking differences regarding this question despite the relatively similar experimental design. The aim of this review is twofold: describe and explain this diversity and suggest basic principles for further in vitro studies in the field. The optimal platelet concentration in vivo will also be discussed. Methods A search in mainly EMBASE and PubMed was performed to identify in vitro studies that investigate the effect of different PRP concentrations on human cell proliferation. The assessment of bias was based on the principles of “Good Cell Culture Practice” and adapted. Results In total, 965 in vitro studies were detected. After the initial screening, 31 studies remained for full-text screening. A total of 16 studies met the criteria of final inclusion and appeared relatively sound. In general, the studies state consistently that PRP stimulates the proliferation of the human cell. Two main types of experimental techniques were detected: 1. The Fixed PRP Concentration Group using a fixed PRP concentration throughout the experiment, which leads to a substantial decrease in nutrition available at higher concentrations. 2. The Fixed PRP Volume Group using a fixed PRP-to-media ratio (Vol/Vol) throughout the experiment. A general tendency was observed in both groups: when the PRP to media ratio increased (Vol/Vol), the proliferation rate decreased. Further, The Low Leukocyte group observed a substantial higher optimal PRP concentration than The High leukocyte group. No prominent tendencies was seen regarding anticoagulants, activation methods, and blood donor (age or sex). Discussion Two major biases regarding optimal proliferation in vitro is pointed out: 1. Too high PRP volume. It is speculated that the techniques used by some studies led to an adverse growth condition and even cell starvation at higher concentrations. 2. High leukocyte levels. Reduced proliferation rate due to proinflammatory substances released during degranulation of leukocytes. Conclusions The two main biases may explain the bell-shaped effect of PRP and the detrimental effects at higher platelet concentrations observed in several studies. These biases may also explain the low optimal PRP concentration observed in some studies. Even if one universal optimal PRP concentration does not exist, the review indicates that PRP concentrations in the upper parts of the scale is optimal or at least beneficial. Finally, following basic experimental principles are suggested. 1: The PRP/media ratio (Vol/Vol) should be kept as constant. 2: The PRP/media ratio should provide a sufficient nutrition supply, that is, PRP ≤ 10% (Vol/Vol). 3: The cell density per well (cells/mL) should be defined. 4: Leukocyte level should be kept low, preferable depleted (< 0.1 PLT/µL).


2018 ◽  
Vol 47 (4) ◽  
pp. 1422-1431 ◽  
Author(s):  
Junyu Zhao ◽  
Chunmei Xu ◽  
Jinming Yao ◽  
Changzhen Yu ◽  
Lin Liao ◽  
...  

Background/Aims: Experimental studies have reported the antineoplastic effects of statins in thyroid carcinoma; however, observational studies suggested that statins might increase the risk of thyroid carcinoma. Therefore, this study evaluated the antineoplastic effects of statins in both in vitro studies and animal models, as well as the epidemiological evidence. Methods: Databases—PubMed, Cochrane Library, SinoMed, CNKI, Wanfang, and clinical trial registries— were searched. A meta-analysis was performed with sufficiently homogeneous studies. Eighteen articles were involved. Results: In in vitro studies, statins showed a concentration-dependent inhibition of cell line growth (weighted mean difference –34.68, 95% confidence interval –36.53 to –32.83). A significant efficacy of statin-induced apoptosis was observed (weighted mean difference [95% confidence interval]: 24 h, 57.50 [55.98–59.03]; 48 h, 23.43 [22.19–24.66]; 72 h, 51.29 [47.52–55.07]). Early apoptosis was increased in a dose- and time-dependent manner. In in vivo antitumor studies, lovastatin inhibited tumor growth, as shown by a reduction in tumor volume. However, two clinical studies showed discordant results from the experimental studies. Conclusion: Experimental studies revealed the antineoplastic efficacy of statins but statins were associated with thyroid carcinoma in clinical studies. This discrepancy may be due to the different concentrations of statins used and the effects of hyperlipidemia interventions, and thus further study is required.


2010 ◽  
Vol 30 (2) ◽  
pp. 107
Author(s):  
Hannah Galantino-Homer ◽  
Susan Megee ◽  
Makoto Senoo

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