Ddr 3 667: Why is my DDR3 RAM running at 667MHz?

Comparative analysis of women with different variants of the rs1107946 polymorphism of the COL1A1 gene (Table 3) showed that individuals with CA or AA genotypes, compared with carriers of the CC genotype, had higher levels of IL-4 (P = 0.006), IL- 6 (P=0.023), IL-8 (P=0.023), IL-10 (P=0.012), RANKL (P=0.022). Women with GT or TT genotypes of the rs1800012 polymorphism of the COL1A1 gene were distinguished from those with the GG genotype by reduced values ​​of IL-10 (P=0.007), OPG (P=0.013), OPG/RANKL index (P=0.042).

It should be noted that none of the above polymorphisms of the COL1A1 gene showed associations (P>0.05) with IL-1, Zh-17A, TNF-α, INF-γ. No differences were found among women depending on the polymorphisms of the LRP5 gene (Table 4) both in the concentrations of the above cytokines and a number of others (IL-4, IL-6, IL-8, OPG, RANKL). At the same time, individuals with the GA genotype of the rs4988321 polymorphism had lower IL-10 values ​​than those with the GG genotype (P=0.003). A similar decrease in the content of IL-10 in the blood serum was determined (P=0.007) in women with CT or TT genotypes of the rs3736228 polymorphism.

Discussion

Thus, the performed studies demonstrate significant changes in the status of cytokines in postmenopausal OP, which are characterized by an increase in serum concentrations of pro-inflammatory cytokines IL-1-β, IL-8, Zh-17A, TNF-α, RANKL and a decrease in the levels of anti-inflammatory cytokines IL-4, IL-10. The results obtained are consistent with modern ideas about the role of the immune system in the development of postmenopausal OP [9][10][11]. It has now been proven that a decrease in postmenopausal estrogen levels is accompanied by increased proliferation and activation of T cells, as well as inhibition of their apoptosis. As a result, the number of activated T-lymphocytes increases and their production of pro-inflammatory cytokines increases. The result of these changes is chronic stimulation of osteoclasts, leading to increased bone resorption and the development of OP. In this regard, it is believed that immune disorders play a key role in the pathogenesis of bone loss, and OP is called a chronic immune-mediated disease [9].][ten].

Analysis of cytokine levels depending on genetic markers showed that those genotypes of VDR, COL1A1 and LRP5 gene polymorphisms, which in previous studies showed an association with an increased risk of OP [5][6][7][8], for the most part found associations with increased concentrations of pro-inflammatory cytokines and decreased anti-inflammatory cytokines. And this is natural, since the above genotypes (the GG genotype of the BsmI polymorphism of the VDR gene, etc.) are more often registered among patients with OP.

Indexes level (Me ± m) among women with different genotypes of COL1A1 gene polymorphisms:

-1997 C>A (rsl 107946)

1546 (6252) G>T (Spl S>s, rsl800012)

CC

(n=126)

CA (n=46) + AA (n=8)

P

GG

(n=130)

GT (n=47) + TT (n=3)

P

IL-4 (pg/ml) (pg/ml)

1. 7±0.14

2.4±0.25

0.006

1.9±0.16

1.8±0.21

0.699

IL-6 (pg/ml) (pg/ml)

0.75±0.36

1.4±0.69

0.023

0.9±0.40

1.1 ±0.57

0.791

IL-8 (pg/ml) (pg/ml)

7.85±1.66

10.9±2.93

0.023

7.9±1.93

10.25±1.6

0.280

IL-10 (pg/ml) (pg/ml)

2.7±0.27

3.6±0.42

0.012

3.1±0.29

2.3±0.30

0.007

OPG (pg/ml) (pg/ml)

75.4±5.83

84. 5±9.53

0.281

85.5±5.88

60.1±8.99

0.013

RANKL(nrAvui) (pg/ml)

2.7±0.21

3.1 ±0.44

0.022

2.9±0.20

2.85±0.51

0.742

OPG/RANKL

24.4±10.9

26.0±7.59

0.419

28.0±10.2

9

Indicator levels (Me±m) among women with different genotypes of LRP5 gene polymorphisms:

Indexes level (Me±t) among women with different genotypes ofLRP5gene polymorphisms:

1999 G>A (Val667Met, rs4988321)

3989 C>T (Alal330Val, rs3736228)

GG (n=157)

GA (n=23) + AA (n=0)

P

CC (n=125)

CT (n=51) + TT (n=4)

P

IL-4 (pg/ml) (pg/ml)

1. 9±0.14

1.7±0.30

0.479

1.8±0.16

2.2±0.21

0.287

IL-6 (pg/ml) (pg/ml)

0.9±0.32

1.3±1.39

0.594

0.8±0.37

1.0±0.66

0.497

IL-8 (pg/ml) (pg/ml)

8.2±1.62

10.0±3.04

0.419

8.2±1.93

8.9±1.92

0.981

IL-10 (pg/ml) (pg/ml)

3.1±0.24

1.7±0.70

0.003

3.1±0.27

2.2±0.43

0.007

OPG (pg/ml) (pg/ml)

80.3±5.54

76.2±9. 42

0.530

82.1±6.29

76.2±7.96

0.959

RANKL (pg/ml) (pg/ml)

2.8±0.22

3.1±0.40

0.689

2.8±0.25

3.0±0.34

0.589

OPG/ RANKL

25.4±9.05

21.0±7.78

0.589

27.4±10.81

23.6±8.70

0.650

At the same time, it is necessary to note the peculiarities of the cytokine status of women with some polymorphic variants of the studied genes. For example, the rs3736228 and rs4988321 polymorphisms of the LRP5 gene were associated with changes in the levels of only one cytokine (IL-10), while the rs1800012 polymorphism of the COL1A1 gene was associated with only two cytokines (IL-10 and OPG). It is important to note that significant associations of OPG serum concentrations were characteristic only with the genotypes of the rs1800012 polymorphism of the COL1A1 gene. At the same time, there were no changes in OPG levels depending on other studied polymorphisms, as well as on the state of the skeletal system of women.

To date, possible mechanisms that could explain the association of genotypes of COL1A1 and LRP5 gene polymorphisms with changes in immune parameters remain unknown. It is possible that the role of these polymorphisms in the development of OP is not even due to their direct effect on the production of cytokines. And the revealed links with the levels of cytokines are mediated by other reasons, due to complex interactions in the «gene-gene», «gene-external factors» systems. After all, OP is a polygenic disease. Its etiopathogenesis involves many genes that mutually influence each other, the phenotypic manifestations of which are realized under the influence of a wide range of external factors (the presence and severity of estrogen, vitamin D and calcium deficiency, physical inactivity, smoking, racial differences, etc. ). This is confirmed by the opinion that mutations in the COL1A1 gene involved in the formation of collagen cause structural and functional changes in the main component of the connective tissue and thus contribute to the development of OP. In particular, one of these mutations is the rs1800012 polymorphism in the COL1A1 gene, which leads to an increase in the ratio of α-1 and α-2 collagen chains and, ultimately, to a deterioration in bone microarchitecture and an increase in the risk of fractures [12][13].

Mutations in the LRP5 gene are known to have a direct effect on bone cell function, bone formation and bone tissue resorption. The protein associated with the type 5 low density lipoprotein receptor, which is encoded by the LRP5 gene, is an important factor in signaling via the canonical Wnt signaling pathway [14]. The canonical (β-catenin-dependent) Wnt signaling pathway is one of the most important molecular signaling pathways that regulates embryonic development and differentiation of cells, including cells of the skeletal system. Disturbances in Wnt signaling, which may be caused by mutations in the LRP5 gene, are accompanied by an increase in the intensity of bone formation in the direction of increase, and in the direction of decrease, by a decrease in bone mass and skeletal disorders [15]. At the same time, it is necessary to point out the important role of the canonical Wnt signaling pathway in the regulation of not only bone cells, but also cells of the immune system [16]. Based on this, it can be assumed that the effect of LRP5 gene polymorphisms on the risk of developing AP may be indirect and through the impact on the function of dendritic cells and lymphocytes. Among other things, it has been shown that a decrease in LRP5/6-mediated signaling in dendritic cells leads to an increase in the differentiation of effector T cells, an increase in the production of pro-inflammatory cytokines, and a decrease in the production of IL-10 [17][18][19]. This is consistent with our results demonstrating an association between the GA genotype of the 1999 G>A polymorphism (Val667Met, rs4988321) and the CT or TT genotypes of the 3989 C>T polymorphism (Ala1330Val, rs3736228) of the LRP5 gene with a decrease in serum levels of IL-10.

The mechanisms by which VDR gene mutations, including the BsmI polymorphism, are involved in the development of osteoporotic changes are still debatable. It is assumed that risk alleles cause a decrease in the expression of this receptor [15], which is accompanied by a decrease in the regulatory effects of vitamin D on the cell. There is a picture of vitamin D deficiency even with its sufficient amount. The result of this is the inhibition of the genomic effects of the vitamin on calcium absorption in the intestinal epithelium. Deficiency of the direct mechanisms of vitamin action on the cells of the skeletal system, including osteoblasts, also develops [20]. All of these may be important links in the pathogenesis of OP. In addition, the regulating effect of vitamin D on immune cells also suffers. To date, its important function in providing an immune response, including the suppression of excessive production of pro-inflammatory cytokines and an increase in the formation of IL-10, has been established [21]. Apparently, the presence of the GG genotype of the 283 A>G polymorphism (BsmI, rs1544410) is combined with a decrease in the effects of vitamin D on cells of the immune system, which may be accompanied by the changes in the cytokine balance that were identified in our work, namely, an increase in the levels of IL- 1-β, RANKL, OPG/RANKL index and a decrease in IL-10.

Conclusion

Thus, it was found that women with postmenopausal osteoporosis are characterized by a significant (P<0.05) increase in serum concentrations of IL-1-β, IL-8, IL-17A, TNF-α, RANKL and a decrease levels IL-4, IL-10. Polymorphic variants of the VDR, COL1A1 and LRP5 genes, which were associated with the development of postmenopausal osteoporosis, in most cases had a similar association with changes in the levels of the above cytokines. At the same time, features of the cytokine status in women depending on genetic polymorphisms were also found. The data obtained reflect important pathogenetic aspects of postmenopausal osteoporosis, including those depending on genetic factors, and can be used to develop individualized schemes for treatment and prevention.

1. Boudin E., Van Hul W. Mechanisms in endocrinology: Genetics of human bone formation. // Eur J Endocrinol. — 2017. — V.177(2). – P.69-83. doi: 10.1530/EJE-16-0990.

2. Khusainova R.I., Khusnutdinova E.K. Molecular genetic basis of osteoporosis. // Biomics. — 2014. — T. 6. — No. 1. – P. 24–51.

3. Rocha-Braz M.G., Ferraz-de-Souza B. Genetics of osteoporosis: searching for candidate genes for bone fragility. // Arch Endocrinol Metab. – 2016. – V. 60(4). – P.391-401. doi: 10.1590/2359-3997000000178.

4. Urano T., Inoue S. Genetics of osteoporosis. // Biochem. Biophys. Res. commun. — 2014. — V.452(2). – P.287-293. doi: 10.1016/j.bbrc.2014.07.141

5. Maylyan E.A. Influence of polymorphism 283 A>G (BSMI) of the vitamin D receptor gene on the development of osteoporosis in postmenopausal women. // Medical Bulletin of the South of Russia. — 2016. — No. 4. — S. 32-38. doi: 10.21886/2219-80752016-4-32-38

6. Maylyan E.A. The role of polymorphism -1997 C>A of the COL1A1 gene in the development of osteoporosis of various parts of the skeleton in postmenopausal women // Bulletin of the Smolensk State Medical Academy. — 2017. — T. 16. — No. 1. — S. 105-110.

7. Maylyan E.A. Sp1 polymorphism of the COL1A1 gene and the risk of osteoporosis in postmenopausal women. Kuban Scientific Medical Bulletin. — 2017. — No. 1. — S. 90-94. doi: 10.25207/1608-6228-2017-1-90-94.

8. Maylyan E.A. Associations of individual LRP5 and IL-6 gene polymorphisms with postmenopausal osteoporosis. Siberian Medical Review. — 2017. — No. 6. – P. 98103. doi: 10.20333/2500136-2017-6-98-103.

9. Ginaldi L., De Martinis M. Osteoimmunology and Beyond. // Curr Med Chem. – 2016. – V.23(33). — P. 3754-3774.

10. Liu H., Luo T., Tan J., Li M., Guo J. Osteoimmunology’ Offers New Perspectives for the Treatment of Pathological Bone Loss. // Curr Pharm Des. – 2017. – V.23(41). – P.6272-6278. doi: 10.2174/1381612823666170511124459

11. Povoroznyuk V.V., Reznichenko N.A., Maylyan E.A. The role of immune factors in the pathogenesis of postmenopausal osteoporosis // Problems of osteology. — 2013. — T. 16. — No. 3. — P. 3-7.

12. Dytfeld J., Marcinkowska M., Drwęska-Matelska N., Michalak M., Horst-Sikorska W., Słomski R. Association analysis of the COL1A1 polymorphism with bone mineral density and prevalent fractures in Polish postmenopausal women with osteoporosis . // Arch Med Sci. – 2016. – V.12(2). – P.288-294. doi: 10.5114/aoms.2016.59253

13. Kurt-Sirin O., Yilmaz-Aydogan H., Uyar M., Seyhan M.F., Isbir T., Can A. Combined eff ects of collagen type I alpha1 (COL1A1) Sp1 polymorphism and osteoporosis risk factors on bone mineral density in Turkish postmenopausal women. // Gene. — 2014. — V.540(2). – P.226-231. doi: 10.1016/j. gene.2014.02.028

14. Lerner U.H., Ohlsson C. Th e WNT system: background and its role in bone. // J Intern Med. — 2015. — V.277(6). – P.630649. doi:10.1111/joim.12368

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16. Pai S.G., Carneiro B.A., Mota J.M., Costa R., Leite C.A., Barroso-Sousa R. et al. Wnt/beta-catenin pathway: modulating anticancer immune response. // J Hematol Oncol. – 2017. – V.10(1). – P.101. doi: 10.1186/s13045-017-0471-6

17. Fu C., Liang X., Cui W., Ober-Blobaum J.L., Vazzana J., Shrikant P.A. et al. Beta-Catenin in dendritic cells exerts opposite functions in cross-priming and maintenance of CD8+ T cells through regulation of IL-10. // Proc Natl Acad Sci USA. — 2015. — V.112. – P.2823-2828. doi: 10.1073/pnas.1414167112

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19. Suryawanshi A., Manoharan I., Hong Y., Swaff ord D., Majumdar T., Taketo M.M. et al. Canonical WNT signaling in dendritic cells regulates Th 1/Th 17 responses and suppresses autoimmune neuroinfl ammation. // J Immunol. – 2015. – V.194. — P.3295-3304. doi: 10.4049/jimmunol.1402691

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Characteristics of reproductive function in women suffering from recurrent depressive disorder » Obstetrics and Gynecology

DOI

https://dx.doi.org/10.18565/aig.2019.3.92-97

First Moscow State Medical University. I.M. Sechenov” of the Ministry of Health of Russia (Sechenov University), Russia, Moscow

Purpose of the study. The study of the ratio of reproductive function (FR) and recurrent depressive disorder (RDD) in women.
Material and methods. 120 women with RDD and 120 mentally healthy women, 18–65 years old, were examined.
Results. Quantitative characteristics of RF in women with RDR and healthy women are presented. With depression, there is a later onset and irregularity of menstruation, earlier recovery of menstrual function after childbirth, the occurrence of PMS and premenopause, which leads to a decrease in the number of pregnancies, childbirth, and children. Depression negatively affects social and family adaptation. The most malignant in terms of the effect on FR are depressions that debuted in puberty, the least — with a debut in postmenopause.
Conclusion. Depressive disorders are associated with periods of hormonal adjustment. Depressive symptoms in PMS predict future depression or indicate incomplete remission. In women with RDR, menstrual and reproductive function is disturbed.

recurrent depressive disorder

female depression

menstrual function

reproductive function

puberty

postpartum period

menopause

premenstrual syndrome

The full text of article
is available in the Doctor’s Library

1. Tyuvina N. A. Depression in women. M.: Publishing house «Servier»; 2006.
2. Nolen-Hoekesma S. Gender differences in depression. Curr. Direct. Psychol. sci. 2001; 10(5): 173-6.
3. Zhilyaeva T.V. Premenstrual mood disorders: etiology, pathogenesis, diagnosis and treatment (literature review). reproduction problems. 2015; 21(4): 76-85.
4. Smetnik V.P., Kulakov V.I. Guide to menopause. M.: MIA; 2001.
5. Smetnik V.P., Tkachenko N.M., Glezer G.A., Moskalenko N.P. Climacteric syndrome. M.; 1988.
6. Yureneva S.V., Kamenetskaya T.Ya. Depressive disorders in peri- and postmenopausal women. Gynecology. 2007; 9(2): 40-3.
7. Bennett H.A., Einarson A., Taddio A., Koren G., Einarson T.R. Prevalence of depression during pregnancy: a systematic review. obstet. Gynecol. 2004; 103(4): 698-709.
8. Bromberger J.T., Kravitz H.M., Chang Y.F., Cyranowski J.M., Brown C., Matthews K.A. Major depression during and after the menopausal transition: Study of Women’s Health Across the Nation (SWAN). Psychol. Med. 2011; 41(9): 1879-88.
9. Bromberger J.T., Matthews K.A., Schott L.L., Brockwell S., Avis N.E., Kravitz H.M. et al. Depressive symptoms during the menopausal transition: the Study of Women’s Health Across the Nation (SWAN). affect. Discord. 2007; 103(1-3): 267-72.
10. Epperson C.N., Steiner M., Hartlage S.A., Eriksson E., Schmidt P.J., Jones I., Yonkers K.A. Premenstrual dysphoric disorder: evidence for a new category for DSM-5. Am. J. Psychiatry. 2012; 169(5): 465-75.
11. Ross L., Steiner M. A biopsychosocial approach to premenstrual dysphoric disorder. Psychiatr. Clin. North Am. 2003; 26(3): 529-46.
12. Tyuvina N.A., Balabanova V.V., Voronina E.O. Gender characteristics of depressive disorders in women. Neurology, neuropsychiatry, psychosomatics. 2015; 7(2): 75-8.
13. Romans S.E., Kreindler D., Asllani E., Einstein G., Laredo S., Levitt A. et al. Mood and the menstrual cycle. Psychother. Psychosom. 2013; 82(1): 53-60.
14. Woods N. F., Smith-Dijulio K., Percival D.B., Tao E.Y., Taylor H.J., Mitchell E.S. Symptoms during the menopausal transition and and early postmenopause and their relation to endocrine levels over time: observations from the Seattle Midlife Women’s Health Study. J. Women’s Health (Larchmt). 2007; 16(5): 667-77.
15. Viviand-Taylor J., Hickey M. Menopause and depression: is there a link? Maturitas. 2014; 79(2): 142-6.
16. Romans S., Clarkson R., Einstein G., Petrovic M., Stewart D. Mood and the menstrual cycle: a review of prospective data studies. Gend. Med. 2012; 9(5): 361-84.
17. Rubinow D.R., Schmidt P.J. Gonadal steroid regulation of mood: the lessons of premenstrual syndrome. front. Neuroendocrinol. 2006; 27(2): 210-6.
18. Lokuge S., Frey B.N., Foster J.A., Soares C.N., Steiner M. Depression in women: windows of vulnerability and new insights into the link between estrogen and serotonin. J.Clin. Psychiatry. 2011; 72(11): 1563-9.
19. Weiss E.L., Longhurst J. G., Mazure C.M. Childhood sexual abuse as a risk factor for depression in women: Psychosocial and neurobiological correlates. Am. J. Psychiatry. 1999; 156(6): 816-28.
20. Young E., Korszun A. Women, stress, and depression: Sex differences in hypothalamic-pituitary-adrenal axis regulation. J. Gend. specif. Med. 1998; 1(1): 21-7.
21. Tyuvina N.A. Clinical features of premenstrual syndrome in major mental illnesses: diss. … cand. honey. Sciences. M.; 1983.

Received 06/15/2018

Accepted for publication 06/22/2018

Ivanets Nikolai Nikolaevich, Doctor of Medical Sciences, Professor, Corresponding Member. RAS; Honored Worker of Science of the Russian Federation; Honorary Head. Department of Psychiatry and Narcology
Federal State Autonomous Educational Institution of Higher Education “First Moscow State Medical University named after I.I. THEM. Sechenov” of the Ministry of Health of Russia (Sechenov University).
Address: 119021, Russia, Moscow, st. Rossolimo, 11, building 9. Phone: +79859998294. ORCID: http://orcid.org/0000-0002-0013-5031
Tyuvina Nina Arkadievna, Doctor of Medical Sciences, Professor of the Department of Psychiatry and Narcology, First Moscow State Medical University
them. THEM. Sechenov” of the Ministry of Health of Russia (Sechenov University).
Address: 119021, Russia, Moscow, st. Rossolimo, 11, building 9. Phone: +7

30020. E-mail: [email protected]. ORCID: https://orcid.org/0000-0002-5202-1407
Voronina Ekaterina Olegovna, Candidate of Medical Sciences, Assistant of the Department of Psychiatry and Narcology, First Moscow State Medical University. I.M. Sechenov” of the Ministry of Health of Russia (Sechenov University).
Address: 119021, Russia, Moscow, st. Rossolimo, 11, building 9. Phone: +79660656900. E-mail: [email protected]. ORCID https://orcid.org/0000-0001-5751-0579
Balabanova Vera Vladimirovna, Candidate of Medical Sciences, Associate Professor at the Department of Psychiatry and Medical Psychology; Associate Professor of the Department of Psychiatry and Narcology, Federal State Autonomous Educational Institution of Higher Education
«First Moscow State Medical University named after I. I. THEM. Sechenov” of the Ministry of Health of Russia (Sechenov University).
Address: 119021, Russia, Moscow, st. Rossolimo, 11, building 9. Phone: +7

41257. E-mail: [email protected]. ORCID: https://orcid.org/0000-0001-7420-9585

For citation: Ivanets N.N., Tyuvina N.A., Voronina E.O., Balabanova V.V. Characteristics of reproductive function in women suffering from recurrent depressive disorder. Obstetrics and gynecology. 2019; 3:92-7.
https://dx.doi.org/10.18565/aig.2019.3.92-97

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