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Background: Individually both migraine and post-traumatic stress disorder (PTSD) prevalence estimates are higher among women. However, there is limited data on the association of migraine and PTSD in women during pregnancy. Methods: We examined the association between migraine and PTSD among women attending prenatal clinics in Peru. Migraine was characterized using the International Classification of Headache Disorders (ICHD)-III beta criteria. PTSD was assessed using the PTSD Checklist-Civilian Version (PCL-C). Multivariable logistic regression analyses were performed to estimate odds ratios (OR) and 95% confidence intervals (CI) after adjusting for confounders. Results: Of the 2922 pregnant women included, 33.5% fulfilled criteria for any migraine (migraine 12.5%; probable migraine 21.0%) and 37.4% fulfilled PTSD criteria. Even when controlling for depression, women with any migraine had almost a 2-fold increased odds of PTSD (OR: 1.97; 95% CI: 1.64–2.37) as compared to women without migraine. Specifically, women with migraine alone (i.e. excluding probable migraine) had a 2.85-fold increased odds of PTSD (95% CI: 2.18–3.74), and women with probable migraine alone had a 1.61-fold increased odds of PTSD (95% CI: 1.30–1.99) as compared to those without migraine, even after controlling for depression. In those women with both migraine and comorbid depression, the odds of PTSD in all migraine categories were even further increased as compared to those women without migraine. Conclusion: In a cohort of pregnant women, irrespective of the presence or absence of depression, the odds of PTSD is increased in those with migraine. Our findings suggest the importance of screening for PTSD, specifically in pregnant women with migraine. [ABSTRACT FROM AUTHOR]

Background: Although in the past decade occidental countries have increasingly recognized the personal and societal burden of migraine, it remains poorly understood in Africa. No study has evaluated the impact of sleep disturbances and the quality of life (QOL) in sub-Saharan Africans with migraine. Methods: This was a cross-sectional study evaluating adults, ≥ 18 years of age, attending outpatient clinics in Ethiopia. Standardized questionnaires were utilized to collect demographic, headache, sleep, lifestyle, and QOL characteristics in all participants. Migraine classification was based on International Classification of Headache Disorders (ICHD)-II criteria. The Pittsburgh Sleep Quality Index (PSQI) and the World Health Organization Quality of Life (WHOQOL-BREF) questionnaires were utilized to assess sleep quality and QOL characteristics, respectively. Multivariable logistic regression models were fit to estimate adjusted odds ratio (OR) and 95% confidence intervals (95% CI). Results: Of 1,060 participants, 145 (14%) met ICHD-II criteria for migraine. Approximately three-fifth of the study participants (60.5%) were found to have poor sleep quality. After adjustments, migraineurs had over a two-fold increased odds (OR = 2.24, 95% CI 1.49-3.38) of overall poor sleep quality (PSQI global score >5) as compared with non-migraineurs. Compared with non-migraineurs, migraineurs were also more likely to experience short sleep duration (≤7 hours) (OR = 2.07, 95% CI 1.43-3.00), long sleep latency (≥30 min) (OR = 1.97, 95% CI 1.36-2.85), daytime dysfunction due to sleepiness (OR = 1.51, 95% CI 1.12-2.02), and poor sleep efficiency (<85%) (OR = 1.93, 95% CI 1.31-2.88). Similar to occidental countries, Ethiopian migraineurs reported a reduced QOL as compared to non-migraineurs. Specifically Ethiopian migraineurs were more likely to experience poor physical (OR = 1.56, 95% CI 1.08-2.25) and psychological health (OR = 1.75, 95% CI 1.20-2.56), as well as poor social relationships (OR = 1.56, 95% CI 1.08-2.25), and living environments (OR = 1.41, 95% CI 0.97-2.05) as compared to those without migraine. Conclusion: Similar to occidental countries, migraine is highly prevalent among Ethiopians and is associated with poor sleep quality and a lower QOL. These findings support the need for physicians and policy makers to take action to improve the quality of headache care and access to treatment in Ethiopia. [ABSTRACT FROM AUTHOR]

Childhood obesity and headache are both significant health concerns that often have a marked impact both personally and socially, that if not addressed can carry over into adulthood. For many individuals, these effects may be magnified when obesity and headache are seen in conjunction. It is this overlap between obesity and headache in children, as well as similarities in the known mechanism of action for feeding and headache, which led to a suspected association between the two. Unfortunately, although recent studies have supported this association, only a limited number have been conducted to directly address this. Furthermore, despite rising rates of childhood obesity and headache, the associated medical comorbidities, and the significant financial cost for these conditions, there is a relative void in studies investigating treatment options that address both underlying conditions of obesity and headache in children. [ABSTRACT FROM AUTHOR]

Migraine is a common and often disabling neurovascular disorder. It has been linked with several psychiatric disorders, such as depression and anxiety, and to stress-related disorders, such as abuse and posttraumatic stress disorder (PTSD). Epidemiological data have consistently shown a higher prevalence of migraine, depression, anxiety, abuse, and PTSD in women as compared with men. The increased vulnerability of women to migraine and psychiatric disorders often occurs during periods of marked hormonal fluctuations of ovarian hormones. One consequence of these associations is the hypothesis that estrogens have a role in the pathophysiology of both disorders. This article offers an in-depth review of several studies linking psychiatric disorders and stress-related disorders with migraine. We also discuss the role of estrogen in the pathophysiologic overlap between these disorders. Finally, we briefly touch on where future research may be headed, in light of these data. [ABSTRACT FROM AUTHOR]

There is evidence that the prevalence of migraine in children and adolescents may be increasing. Current theories of migraine pathophysiology in adults suggest activation of central cortical and brainstem pathways in conjunction with the peripheral trigeminovascular system, which ultimately results in release of neuropeptides, facilitation of central pain pathways, neurogenic inflammation surrounding peripheral vessels, and vasodilatation. Although several risk factors for frequent episodic, chronic, and refractory migraine have been identified, the causes of migraine progression are not known. Migraine pathophysiology has not been fully evaluated in children. In this review, we will first discuss the evidence that early therapeutic interventions in the child or adolescent new onset migraineur, may halt or limit progression and disability. We will then review the evidence suggesting that many adults with chronic or refractory migraine developed their migraine as children or adolescents and may not have been treated adequately with migraine-specific therapy. Finally, we will show that early, appropriate and optimal treatment of migraine during childhood and adolescence may result in disease modification and prevent progression of this disease. [ABSTRACT FROM AUTHOR]

Technology has revolutionized the ability of both patients and physicians to find and retrieve medical information. In particular, the Internet has become an increasingly important source of information for patients and physicians in all medical fields, including headache. Although these resources may be readily available, it is not certain that those who would benefit most from these websites are aware of their existence or how to differentiate if the website is reputable. This article briefly reviews how patients and physicians can differentiate which sites provide legitimate and reputable information and then focuses on where to find online information on cluster headache. [ABSTRACT FROM AUTHOR]

Genomes of all mammals encode apobec3 genes, which are thought to have a function in intrinsic cellular immunity to several viruses including human immunodeficiency virus type 1 (HIV-1). APOBEC3 (A3) proteins are packaged into virions and inhibit retroviral replication in newly infected cells, at least in part by deaminating cytidines on the negative strand DNA intermediates. However, the role of A3 in innate resistance to mouse retroviruses is not understood. Here we show that A3 functions during retroviral infection in vivo and provides partial protection to mice against infection with mouse mammary tumour virus (MMTV). Both mouse A3 and human A3G proteins interacted with the MMTV nucleocapsid in an RNA-dependent fashion and were packaged into virions. In addition, mouse A3-containing and human A3G-containing virions showed a marked decrease in titre. Last, A3-/- mice were more susceptible to MMTV infection, because virus spread was more rapid and extensive than in their wild-type littermates. [ABSTRACT FROM AUTHOR]

The HER-2/Neu oncogene has been implicated in human and mouse breast cancer. Indeed, transgenic MMTV-neu mice expressing this oncogene from the mammary tumor virus long terminal repeat develop spontaneous mammary tumors and die within 1 year of life. We have expressed the class II transactivator (CIITA) and/or the costimulatory molecule CD80 (B7.1) in a mammary carcinoma cell line (MCNeuA) derived from these mice. Class II transactivator directs the expression of MHC class II and the machinery for antigen processing and presentation by this pathway. When injected into MMTV-neu mice, tumor cells expressing CD80 or CD80 and CIITA, were rejected completely. In addition, following the rejection of dual expressing cells, 75% of the mice were protected against the development of subsequent spontaneous tumors. Cells expressing only CD80 or CIITA were not as effective as antitumor vaccines in preventing the development of spontaneous tumors. Thus, converting cancer cells into antigen presenting cells could represent an effective immunotherapy for breast cancer.Cancer Gene Therapy (2006) 13, 1002–1010. doi:10.1038/sj.cgt.7700974; published online 7 July 2006 [ABSTRACT FROM AUTHOR]

Migraine is a common chronic disorder that presents with recurrent attacks of headache and associated symptoms. Various somatic and psychiatric conditions have been reported as comorbid conditions with migraine. Among the psychiatric disorders that have been reported as comorbid with migraine are major depression, anxiety, panic disorder, and bipolar disorder. Recent studies discussing the comorbidity of headache and psychiatric disorders are reviewed here. [ABSTRACT FROM AUTHOR]

c-Myc promotes cellular proliferation, sensitizes cells to apoptosis and prevents differentiation. It binds cyclin T1 structurally and functionally from the positive transcription elongation factor b (P-TEFb). The cyclin-dependent kinase 9 (Cdk9) in P-TEFb then phosporylates the C-terminal domain of RNA polymerase II, which is required for the transition from initiation to elongation of eukaryotic transcription. Inhibiting P-TEFb blocks the transcription of its target genes as well as cellular proliferation and apoptosis induced by c-Myc.Oncogene (2003) 22, 5707-5711. doi:10.1038/sj.onc.1206800 [ABSTRACT FROM AUTHOR]

In the mouse, replication of human immunodeficiency virus type 1 (HIV) is blocked at the levels of entry, transcription and assembly. For the latter effect, the amounts of unspliced viral genomic RNA could have an important function. Indeed, in murine cells, HIV transcripts are spliced excessively, a process that is not inhibited by the murine splicing inhibitor p32 (mp32). In marked contrast, its human counterpart, hp32, not only blocks this splicing but promotes the accumulation of viral genomic transcripts and structural proteins, resulting in the assembly and release of infectious virions. A single substitution in hp32 of Gly 35 to Asp 35, which is found in mp32, abrogates this activity. Thus, hp32 overcomes an important post-transcriptional block to HIV replication in murine cells. [ABSTRACT FROM AUTHOR]

Viruses that induce chronic infections can evade immune responses. HIV is a prototype of this class of pathogen. Not only does it mutate rapidly and make its surface components difficult to access by neutralizing antibodies, but it also creates cellular hideouts, establishes proviral latency, removes cell-surface receptors and destroys immune effectors to escape eradication. A better understanding of these strategies might lead to new approaches in the fight against AIDS. [ABSTRACT FROM AUTHOR]

Bare lymphocyte syndrome (BLS) is an autosomal recessive severe-combined immunodeficiency that can result from mutations in four different transcription factors that regulate the expression of major histocompatibility complex (MHC) class II genes. We have identified here the defective gene that is responsible for the phenotype of the putative fifth BLS complementation group. The mutation was found in the regulatory factor that binds X-box 5 (RFX5) and was mapped to one of the arginines in a DNA-binding surface of this protein. Its wild-type counterpart restored binding of the RFX complex to DNA, transcription of all MHC class II genes and the appearance of these determinants on the surface of BLS cells. [ABSTRACT FROM AUTHOR]

Adequate control of HIV requires impairing the infection, replication and spread of the virus, no small task given the extraordinary capacity of HIV to exploit the cell's molecular machinery in the course of infection. Understanding the dynamic interplay of host cell and virus is essential to the effort to eradicate HIV. [ABSTRACT FROM AUTHOR]

We investigated the function of the evolutionary conserved X2 box in the promoter of the HLA-DRA gene from the human major histocompatibility complex (MHC) in resting and activated B cells. NF-X2, which contains members of the AP-1/ATF/CREB families of transcription factors, interacts with the X2 box (5′-TGCGTCA-3′) from positions –97 to –91 in the DRA promoter. In resting Raji cells, little to no binding to the X2 box was observed. In sharp contrast, in B cells treated with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA), strong interactions between the X2 box and NF-X2 containing c-Fos were observed. As determined by transient expression and RNA analyses, the activation of protein kinase C (PKC) also increased rates of transcription from the wild-type DRA promoter but not from a DRA promoter bearing clustered point mutations in the X2 box. Since the co-expression with a dominant negative c-Fos abolished the responsiveness to TPA, we conclude that activated transcription of the DRA gene depends on interactions between the X2 box and NF-X2, which contains c-Fos. [ABSTRACT FROM AUTHOR]

The octamer binding site, which is located immediately upstream of the poorly conserved DRA TATA sequence, is important fof high levels of expression of this human major histocompatibility class II gene in B cells. In this study, we demonstrate that the substitution of the DRA TATA sequence with the TATA box from the adenovirus E1b promoter revomes the requirements for the octamer binding site for high levels of expression from DRA promoter. Since only the TATA box from the E1b but bot the DRA promoters binds the TATA binding protein, we conclude that the octamer binding site helps to recruit TBP to the DRA promoter. [ABSTRACT FROM AUTHOR]

The relationship between DNA methylation and HLA-DR gene expression was investigated in six mononuclear cell lines. RPMI-4265 (B cell) and HUT-78 (T cell) constitutively express HLA-DR. HL-60 (myelomonocyte) and U-937 (monocyte) can be induced to express HLA-DR. Jurkat and Molt-4 (T cells) do not and cannot be induced to express HLA-DR. Based on the known nucleotide sequence of the HLA-DR gene, methylation-sensitive restriction endonucleases Msp I, Hpa II, Hha I, Ava I, Hae II, and Sma I were used to detect the CpG methylation in three regions of the HLA-DR gene: (1) the 5′flanking region, (2) the exon 1 region, and (3) the coding region containing exons 2, 3, 4, and 5. This precise mapping of CpG methylation yielded no correlation between DNA hypomethylation and HLA-DR gene expression. In all cell lines, exon 1 region is hypomethylated, whereas 5′ and coding regions are hypermethylated. Whereas hypermethylation of the coding region does not block transcription, hypomethylation of the exon 1 region may be essential but is clearly not sufficient for HLA-DR gene transcription. This exon 1 region demethylation may result in an open (deoxyribonuclease I hypersensitive) chromatin conformation around the promoter where trans-acting regulatory factors presumably bind and initiate HLA-DR transcription. In the course of this study, a novel Msp I polymorphism in the intron 1 of the HLA-DR, gene was found. [ABSTRACT FROM AUTHOR]

The article reports on the functions of lenvtiviral Nef protein in the evasion of host immune defenses. Nef is a small protein that is myristylated at the N terminus and is anchored to cellular membranes which is essential for its function. It also facilitates the infection of T cells, in part through virological synapses between cells and in part through the secretion of cytokines and lymphokines from infected macrophages that render T cells more susceptible to infection.

We evaluated the correlation between clinical signs, electrophysiological data and molecular genetics findings in patients with HMSN 1. We found a duplication in the PMP-22 gene in 60% of HMSN 1 families. We compared clinical and electrophysiological data between 23 patients with duplication and 18 patients without duplication. No statistically significant differences in age of onset of symptoms, clinical signs and electrophysiological parameters were found. [ABSTRACT FROM AUTHOR]

In our study we searched for an association between the insertion/deletion (I/D) polymorphism at the ACE locus as well as apo A-I promoter polymorphism and coronary artery disease (CAD) in patients with familial hypercholesterolemia (FH). 34 FH patients over 40 years were ascertained; 16 patients with CAD were compared with 18 patients without CAD. There was an excess of DD or ID genotype in FH patients with CAD (OR=4.9, CI = 1.17-22.17; Fisher exact p=0.012), however, no association between G to A substitution in the promoter region of the apo A-I gene and CAD was found. Our results suggest that the DD/ID genotype at the ACE gene locus might be an important genetic risk factor for CAD in FH patients. [ABSTRACT FROM AUTHOR]

The mutation responsible for DM has been identified as the amplification of a polymorphic (CTG)n repeat in the 3′ untranslated region. of the myotonin proteinase gene. To examine somatic instability of the repeat, we studied tissue variability of the CTG expansion of three mesodermally derived tissues: lymphocytes, cultured fibroblasts and muscle cells. In six patients with adult onset DM, the repeat region was larger in skeletal muscles and fibrolasts as compared to lymphocytes. Our findings indicate that somatic CTG instability between examined tissues might take place postnatally by a selection mechanism in lymphocytes. [ABSTRACT FROM AUTHOR]