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Dysmenorrheaalso known as dysmenorrhoeapainful periodsor menstrual crampsis pain during menstruation. Symptoms typically last less than three days. The pain is usually in the pelvis or lower abdomen.

Other symptoms may include back paindiarrhea, or Krampf mesh. In older women it is more often due to an underlying issues such as uterine fibroidsadenomyosisor endometriosis. It may radiate to the thighs and lower back. Symptoms of dysmenorrhea often begin immediately after ovulation and can last until the end of menstruation.

This is because dysmenorrhea is often associated with changes in hormonal levels in the body that occur with ovulation. The use of certain types of birth control pills can prevent the symptoms of dysmenorrhea because they stop ovulation from occurring. Dysmenorrhea can be classified as either Krampf mesh or secondary based on the click to see more or presence of an underlying cause. Secondary dysmenorrhea Krampf mesh dysmenorrhea which is associated with an existing condition.

Other skeletal abnormalities, such as scoliosis sometimes caused by spina bifida might be possible contributors as well. Krampf mesh a woman's menstrual cycle, the Krampf mesh thickens in preparation for potential pregnancy. After ovulationif the ovum is not fertilized and article source is no pregnancy, the built-up uterine tissue is not needed and thus shed.

Molecular compounds called prostaglandins are released during menstruation, due to the destruction of the endometrial cells, and the resultant release of their contents. These substances are thought to be a major factor in primary dysmenorrhea. These uterine contractions continue as they squeeze the old, dead endometrial tissue through the cervix and out of the body through the vagina. These contractions, and the resulting temporary oxygen deprivation to nearby tissues, are responsible for the pain or "cramps" experienced during menstruation.

Compared with other women, women with primary dysmenorrhea have increased activity of the uterine muscle with increased contractility and increased frequency of contractions. The study concluded that in dysmenorrheic patients, visible features on cycle days correlated with the degree of pain, and differed significantly from the control group. However, there is no universally accepted gold standard technique Krampf mesh quantifying the severity of menstrual pains.

Further work-up includes a specific medical history of symptoms and menstrual cycles and a pelvic exam. The intrauterine system Mirena IUD may be useful in reducing symptoms. A review found that evidence of safety is insufficient for all dietary supplements. The prevalence Krampf mesh adolescent females has been Krampf mesh to be One study indicated that in nulliparous women with primary dysmenorrhea, the severity of menstrual pain decreased significantly mit Krampfadern Fitness age From Wikipedia, the free encyclopedia.

Classification and external Lungenembolie Abstracts. Retrieved 26 June Office of Women's Health. Retrieved 25 June J Minim Invasive Gynecol. George Moore, and Joseph C. This web page of Obstetrics and Gynecology, 4th ed. The Cochrane Database of Systematic Reviews 1 : CD The Washington Manual Obstetrics and Gynecology Survival Guide.

Lippincott Williams and Wilkins, The Cochrane Database of Systematic Reviews 7 : CD Australian Medicines Handbook Adelaide: Australian Medicines Handbook; J Pediatr Adolesc Gynecol. The Cochrane Database of Krampf mesh Reviews 2 : CD Cochrane Database Syst Rev Krampf mesh : CD CS1 maint: Multiple names: authors list link.

In DeGroot, Leslie J. CS1 maint: Uses editors parameter link. In Brunton, Laurence L. J Indian Med Assoc. J Obstet Gynaecol Can. The Cochrane Database of Krampf mesh Reviews. Pain Medicine Malden, Mass. Evidence-Based Complementary and Alternative Medicine. Cochrane Database Syst Rev 2 : CD The Chiropractic Profession: Its Education, Practice, Research and Future Directions.

West Des Moines, IA: NCMIC. Cochrane Krampf mesh Syst Rev. Updated: Dec 31, Arch Pediatr Adolesc Med. J Krampf mesh Med Assoc. Ned Tijdschr Geneeskd in Dutch and Flemish. CS1 maint: Unrecognized Krampf mesh link. Female diseases of the pelvis and genitals Krampf mesh— Follicular Krampf mesh of ovary.

Hypoactive sexual desire disorder. Extended cycle combined hormonal contraceptive. Not Krampf mesh in Talk Contributions Create account Log in. Main page Contents Featured content Current events Random article Donate to Wikipedia Wikipedia store. Help About Wikipedia Community portal Recent changes Contact Krampf mesh. What links here Related changes Upload file Special pages Permanent link Page information Wikidata item Cite this page.

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The NCBI web site requires JavaScript to function. When mice were treated with human FVIII, the proportion of mice that developed antibodies depended on the application route of FVIII and the activation state of the innate immune system. Interestingly, most of the 8 peptide regions contained promiscuous epitopes that bound to several different HLA-DR proteins in in vitro binding assays.

The available information on FVIII peptides presented in the context of specific human MHC class II molecules is limited. One of the peptides Krampf mesh was a promiscuous epitope that bound to several different HLA-DR proteins. In another study, James et al investigated 2 patients carrying an ArgCys mutation in the A2 domain of FVIII.

Next, we wondered whether the lack of antibody development in nonresponder mice is Krampf mesh with the specific nature of the intravenous application route. We compared intravenous application with subcutaneous application of FVIII and combined intravenous application with a concomitant activation of the innate immune system.

Our data indicate that both subcutaneous application of FVIII and a combination of intravenous FVIII together with an activation of the innate immune system result in the development of antibodies in all read more included in the study. Importantly, there was no major difference in the FVIII peptide regions Krampf mesh between intravenous and subcutaneous application of FVIII.

Most of the 8 FVIII peptide regions contained promiscuous epitopes that bound to several different HLA-DR proteins in in vitro binding assays. Mice were male and 8 to 12 weeks old at the beginning of Krampf mesh experiments. Blood samples were collected 7 Krampf mesh after the last dose of FVIII. Whole blood was added to sodium citrate at a ratio, and plasma was separated by centrifugation. Antibodies against human FVIII in plasma samples were measured using ELISAs as described.

Inhibitory antibodies were analyzed with a modified Bethesda assay Technoclone. Medikamente zur venösen Ulzera days after the last dose, spleens were obtained and spleen cells were prepared as described. After 1 hour of restimulation, 2. After incubation, cells were washed and nonspecific binding sites were blocked by a mixture of anti-CD16 and anti-CD32 antibodies Fc Block; BD Biosciences PharMingen.

Finally, cells were stained with an allophycocyanin-labeled antibody against intracellular CD clone MR1; eBioscience as described. Mice were treated with 4 to 8 weekly doses of human FVIII. Cells were then washed, fused with BW cells BW The culture medium was changed to hypoxanthine-aminopterin-thymidine Krampf mesh medium hypoxanthine-aminopterin-thymidine Krampf mesh supplement; Sigma-Aldrich after Krampf mesh hours and maintained for 2 weeks.

T-cell hybridoma clones Krampf mesh picked and screened Krampf mesh specificity to human FVIII. Culture supernatants were collected and analyzed for the release of IL-2 using either an IL-2 ELISA Kit BioLegend or an IL-2 Bio-Plex assay Bio-Rad Laboratories. Hybridoma clones with an at least 5-fold increase in IL-2 release ratio between FVIII-stimulated cultures and medium controls were considered to be FVIII-specific and were subsequently subcloned by limiting dilution 0.

Peptide specificities of individual hybridomas were identified using a cross matrix scheme Krampf mesh described by Ay et über Krampfadern in den Beinen und Fitness den. Each strip was processed into one pool Krampf mesh peptides.

Each T-cell hybridoma Krampf mesh tested against all peptide pools that were processed from the vertical and horizontal strips.

The crossing point of positive hits for the vertical and the horizontal pools revealed the peptide that was recognized by a particular T-cell hybridoma clone. In some experiments, human monocyte-derived dendritic cells were used as human antigen-presenting cells. Peptide pools with up to 33 peptides per pool were dissolved in DMSO DMSO Hybrimax; Sigma-Aldrich and further diluted in Dulbecco PBS Invitrogen.

Single peptides were synthesized using solid-phase peptide synthesis Rudolf Volkmerdissolved in DMSO and further diluted in Dulbecco PBS Invitrogen. Amino acid numbering in the human FVIII peptides is based on the full-length human FVIII protein, without the 19 amino acid signal peptide. The unpaired 2-tailed Student t test was used for comparison of means between groups. The differences in responder rates in different studies might be the result Krampf mesh the mixed background of the mice.

We treated one group Krampf mesh mice with intravenous FVIII and another group of mice with subcutaneous FVIII. Our Krampf mesh confirmed that only a fraction of mice developed antibodies after intravenous application of human FVIII Figure 2Ain contrast to conventional E17 mice that we included as a control group Figure 2A.

Based on these results, we wondered whether the proportion of link responding to treatment with intravenous FVIII would increase by concurrent activation of the innate immune system.

Our results show that all mice responded with antibodies to FVIII when treated intravenously with a mixture of FVIII and Krampf mesh, a well-known Krampf mesh of the innate immune system 35 Figure 2C. Previously, we demonstrated a correlation between binding antibodies as detected in ELISA assays and neutralizing antibodies as detected in Bethesda assays when mice were treated with intravenous FVIII. We used a peptide library of human FVIII that contained mer peptides shifted by 3 amino acids to characterize the peptide specificity of each individual T-cell hybridoma clone.

In total, we analyzed 63 hybridoma clones obtained from mice treated with intravenous FVIII and hybridoma clones obtained from mice treated with subcutaneous FVIII. We identified 8 FVIII peptide regions containing T-cell epitopes Figure 3A ; supplemental Table 1. Five of these 8 Krampf mesh regions were identical, including the 3 dominant peptide regions, after intravenous and subcutaneous application of FVIII Figure 3A.

Three minor peptide regions were only found for 1 of the Krampf mesh application routes. However, these minor differences might disappear when analyzing a larger number of hybridoma clones. For comparison, we identified FVIII peptide regions containing T-cell epitopes involved in the immune response to intravenous FVIII in conventional hemophilic E17 mice. The C2 domain of human FVIII is generally considered read article be very immunogenic.

However, this assumption is mainly based on epitope data for antibodies against FVIII. Therefore, Krampf mesh were wondering whether these mice would still develop antibodies against the C2 domain.

We treated mice either intravenously or subcutaneously Krampf mesh FVIII and analyzed antibodies against full-length human FVIII and Krampf mesh the C2 domain of human FVIII. Our data indicate that all mice that developed antibodies against full-length Kürbis Thrombophlebitis also developed antibodies against the C2 domain of human FVIII Figure 4.

All negative controls showed negative results that were indistinguishable from the medium controls Figure 5C. Based on these data, we conclude that FVIII-specific Krampf mesh cells that recognize Volksmittel Kampf gegen Krampfadern epitopes as identified by hybridoma technology are detectable in the spleen of mice treated with FVIII.

Vidovic et al demonstrated that MHC class II-matched human antigen-presenting cells can stimulate T-cell hybridomas generated from human MHC class II transgenic mice if they present the correct peptide.

Similar to Krampf mesh, antibodies against FVIII Krampf mesh neutralizing activity. We used ng FVIII per dose, which was required to induce antibodies after 8 weekly intravenous doses.

Patients develop neutralizing antibodies against FVIII Krampf mesh an average of 10 to 50 exposure days. However, a couple of questions arose that needed to be addressed to evaluate the quality just click for source this new model. First, we had to demonstrate that the lack of antibody development in a proportion of mice after Krampf mesh FVIII treatment is associated with the intravenous application route and Krampf mesh not reflect the inability of these mice to respond to FVIII.

Several reports have indicated that the intravenous application route for proteins is associated with a less immunogenic response than the subcutaneous or intramuscular application routes. Our data confirmed this assumption. All mice developed antibodies after subcutaneous application of FVIII. The increased incidence of antibody development after intravenous FVIII application in the presence of a concomitant activation of the innate immune system further supports the conclusion that all mice are able to respond to FVIII.

We speculate that intravenous application of FVIII induces peripheral immune tolerance in nonresponder mice and that the activation of the innate immune system by LPS creates pro-inflammatory conditions Krampf mesh counter the potential tolerogenic immune response after wenn Schwangerschaft Varizen gefährliche FVIII.

We are currently testing this hypothesis in follow-up studies. Several studies indicate that the induction of antibody responses against Krampf mesh in hemophilia A is T-cell dependent. Currently, we are in the process of identifying the Krampfadern der zu unteren FVIII peptide sequences required to stimulate FVIII-specific T-cell hybridomas that we generated.

These studies will reveal the exact FVIII sequences that constitute the actual Krampf mesh epitopes. So far we Krampf mesh used only mer and mer peptides. One of Krampf mesh FVIII peptide regions that we identified is located in the B domain. Aledort recently indicated that B domain-deleted FVIII and full-length FVIIII might express different immunogenicities. Our results indicate that this is indeed the case, which supports the potential relevance for humans of the FVIII peptide regions identified in humanized mice.

However, the on-rates and off-rates of peptide binding were different for the different HLA-DR click. Future studies will show how Krampf mesh binding kinetics result in potential functional differences.

Reding et al described T-cell epitopes in the C2 domain please click for source FVIII but did not specify the MHC class II haplotype of their study participants. However, it is to be expected that T-cell epitopes and B-cell epitopes of FVIII Krampf mesh not necessarily overlap.

B-cell epitopes are often conformational epitopes composed of amino acids from different parts of a polypeptide chain, which are brought Krampf mesh close proximity by the 3-dimensional structure of the mature protein. However, other hemophilic mouse models expressing Krampf mesh MHC class II molecules could complement this model in the future.

The authors thank Elisabeth Hopfner, Thomas Prenninger, Markus Pasztorek, Ginta Pordes, Lydia Suely, Nidha Abrar, and Monika Grewal for technical assistance and Elise Langdon-Neuner for editing the manuscript. The remaining author declares no competing financial interests. National Library of Medicine. NCBI Skip to main. US National Library of Medicine. National Institutes of Health Search database PMC All Databases Assembly Biocollections BioProject BioSample BioSystems Books ClinVar Clone Conserved Domains dbGaP dbVar EST Gene Genome Krampf mesh DataSets GEO Profiles GSS GTR HomoloGene MedGen MeSH NCBI Web Site NLM Catalog Nucleotide OMIM PMC PopSet Probe Protein Protein Clusters PubChem BioAssay PubChem Compound PubChem Substance PubMed PubMed Health SNP Sparcle SRA Structure Taxonomy ToolKit ToolKitAll ToolKitBook ToolKitBookgh UniGene Search term.

Journal List Europe PMC Author Manuscripts PMC Author manuscript; available in PMC Apr PMCID: PMC EMSID: EMS Katharina N. Steinitz1 Pauline M. WraithKrampf mesh Sabine Unterthurner1 Corinna Hermann1 Maria Schuster1 Rafi U. Ahmad1 Markus Weiller1 Christian Lubich1 Maurus de la Rosa1 Hans Peter Schwarz1 and Birgit M. Reipert 1 1 Baxter BioScience, Vienna, Austria Correspondence: Birgit M. Reipert, Baxter BioScience, Industriestrasse 72, A Vienna, Austria; moc.

Detection of antibodies against human FVIII and against the C2 domain of human FVIII Blood samples were collected 7 days after Krampf mesh last dose of FVIII. Generation of Click here T-cell hybridoma clones and assessment of peptide specificity Mice were treated with 4 to 8 weekly doses of human FVIII. Human dendritic cells In some experiments, human monocyte-derived dendritic cells were used as human antigen-presenting cells.

Statistical analysis The unpaired 2-tailed Student t test was used for comparison of means between groups. Supplementary Material Supplementary methods and tables Click here to view. This work was supported by Baxter BioScience. Hoyer LW, Aledort LM, Lisher JM, Reisner HM, White GC. The incidence of read article VIII inhibitors in patients with severe hemophilia A.

In: Aledort LM, Hoyer LW, Lusher JM, Reisner HM, White GC, editors. Inhibitors to Coagulation Factors. Plenum; New Krampf mesh, NY: Oldenburg J, Pavlova A. Genetic risk factors for inhibitors to factors VIII and IX. Gouw SC, van der Bom JG, van den Berg H. Treatment-related risk factors of inhibitor development in previously untreated patients with hemophilia A: the CANAL cohort study.

Clonal selection and learning in the antibody system. Vinuesa CG, Tangye SG, Moser B, Mackay CR. Follicular B helper T cells in antibody responses and Krampf mesh. Ragni MV, Bontempo FA, Lewis JH. Disappearance of inhibitor to factor VIII in HIV-infected hemophiliacs with Krampf mesh to AIDS or severe ARC.

Sasgary M, Krampf mesh RU, Schwarz HP, Turecek PL, Reipert BM. Single cell analysis of factor VIII-specific T cells in hemophilic mice after treatment with human factor VIII. Sinigaglia F, Hammer J. Defining rules for the peptide-MHC class II interaction. Suri A, Lovitch SB, Unanue ER. The wide Krampf mesh and complexity of peptides bound to class II MHC molecules. Banchereau J, Steinman RM. Dendritic cells and the control of immunity.

Pratt KP, Thompson AR. B-cell and T-cell epitopes in anti-factor VIII immune responses. Clin Rev Allergy Immunol. Hu GL, Okita DK, Conti-Fine BM.

T cell recognition of the A2 domain of coagulation factor VIII in hemophilia patients and healthy subjects. Reding MT, Okita DK, Diethelm-Okita BM, Anderson TA, Conti-Fine BM. Jacquemin M, Vantomme V, Buhot C, et al. James EA, Kwok WW, Ettinger RA, Thompson AR, Pratt KP. T-cell responses over time in a mild hemophilia A Krampf mesh subject: epitope identification and transient immunogenicity of the corresponding self-peptide.

James EA, van Haren SD, Ettinger RA, et al. T-cell responses in two unrelated hemophilia A inhibitor subjects include an epitope at the Krampf mesh VIII RC missense site. HLA-DR-presented peptide-repertoires derived from human monocyte-derived dendritic cells pulsed with blood coagulation factor VIII. Reipert BM, Steinitz KN, van Helden LFK Ziel Krampf, et al.

Opportunities and limitations of mouse models humanized for HLA class II antigens. Hay CR, Ollier W, Pepper L, et al. HLA Krampf mesh II profile: a weak determinant of factor VIII inhibitor development in severe haemophilia A: UKHCDO Inhibitor Working Party. Oldenburg Krampf mesh, Picard JK, Schwaab R, Brackmann HH, Tuddenham EG, Simpson E. HLA genotype of patients with severe haemophilia A due to intron 22 inversion with and without inhibitors of factor VIII.

Pavlova A, Delev D, Lacroix-Desmazes S, et al. Impact of polymorphisms of the major histocom-patibility complex Krampf mesh II, interleukin, tumor necrosis factor-alpha and cytotoxic T-lymphocyte antigen-4 genes on inhibitor development in severe hemophilia A.

Woods A, Chen HY, Trumbauer ME, Sirotina A, Cummings R, Zaller DM. Human major histocom-patibility complex class II-restricted T cell responses in transgenic mice. Bi L, Lawler AM, Antonarakis SE, High KA, Gearhart JD, Kazazian HH. Targeted disruption of the mouse factor VIII gene produces a model of haemophilia A. Muchitsch EM, Turecek PL, Zimmermann K, et al. Phenotypic expression of murine hemophilia. Hausl C, Maier E, Krampf mesh HP, et al. Long-term persistence of anti-factor VIII antibody-secreting cells in hemophilic mice after treatment with human factor VIII.

Frentsch M, Arbach O, Kirchhoff D, et al. Hausl C, Ahmad RU, Schwarz HP, et al. Preventing restimulation of memory B cells in hemophilia A: a potential new strategy for the treatment of antibody-dependent immune disorders. Production of mouse T cell hybridomas. Ay B, Streitz M, Boisguerin P, et Krampf mesh. Sorting and pooling strategy: a novel tool to Krampf mesh a virus proteome for CD8 T-cell epitopes.

Pickl WF, Majdic O, Kohl P, et al. Pasqual N, Krampf mesh M, Aude-Garcia C, et al. Quantitative and qualitative changes in V-J alpha rearrangements during mouse thymocytes differentiation: Krampf mesh for a limited T cell receptor alpha chain repertoire.

Klein L, Hinterberger M, Wirnsberger G, Kyewski B. Antigen presentation in the thymus for positive selection and central tolerance induction. Selection of the T-cell repertoire: receptor-controlled checkpoints in T-cell development. Kumar H, Kawai T, Akira S. Toll-like receptors and innate immunity. Biochem Krampf mesh Res Commun.

Vidovic D, Graddis TJ, Stepan LP, Krampf mesh DM, Laus R. Specific learn more here of MHC-transgenic mouse T-cell hybridomas with xenogeneic APC.

MHC-dependent antigen processing and peptide presentation: providing ligands for T lymphocyte activation. Houston EG, Jr, Fink PJ. MHC drives Krampf mesh repertoire shaping, but not maturation, in recent thymic emigrants. Wight J, Paisley S. The epidemiology of inhibitors in haemophilia A: a systematic review.

Peng A, Gaitonde P, Kosloski MP, Code Krampfadern der unteren RD, See more P, Balu-Iyer SV. Effect of route of administration of human recombinant factor VIII on its immunogenicity in hemophilia A mice. Factors influencing the immuno-genicity of therapeutic proteins. Aledort LM, Navickis RJ, Wilkes MM.

Can B-domain deletion alter the immunogenicity of recombinant factor VIII? A meta-analysis of prospective clinical studies.

Gregersen JW, Holmes S, Fugger L. Humanized animal models for autoimmune diseases. Das P, Abraham R, David C. HLA transgenic mice as models of human autoimmune diseases. Forsthuber TG, Shive CL, Wienhold W, et al. Hammer J, Valsasnini P, Tolba K, et al. Promiscuous and allele-specific anchors in HLA-DR-binding peptides.

Reding MT, Wu H, Krampf M, et al. Mariuzza RA, Phillips SE, Poljak RJ. The structural basis of antigen-antibody recognition. Annu Rev Biophys Biophys Chem. Germain RN, Margulies DH. The biochemistry and cell biology of antigen processing and presentation.

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Dysmenorrhea, also known as dysmenorrhoea, painful periods, or menstrual cramps, is pain during menstruation. It usually begins around the time that menstruation begins.
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