T. Milten. Westminster Theological Seminary in California.
Nocardia accounts infammation generic coumadin 5 mg without a prescription blood pressure medication ed, meningitis cheap coumadin 1mg otc prehypertension, and spinal cord lesions generic coumadin 2 mg with mastercard 5 hypertension, have for 2% of all brain abscesses and are 2 discount coumadin 1 mg heart attack 6 days collections. A 60-year-old woman with amyloidosis who was immunocompromised afer heart transplantation. A 60-year-old woman with amyloidosis who was Afer the patient had received efective antibiotic therapy, the immunocompromised afer heart transplantation. T1-weighted image afer contrast administration tients showing pronounced disruption of conscious- 6. Typhoid Fever Typhoid fever is caused by Salmonella typhii associ- ated with enteric disease, with worldwide distribution. During epidemics approximately 535% of all patients have Neisseria meningitidis is a strictly human bacterium. Neurological The human nasopharynx is the only known natural res- sequelae are rare. A history of re- brain abscess, transient Parkinsonism, motor neuron cent upper respiratory tract infection is common. Fulminant meningococcal sepsis, the most encephalopathy is not totally understood. Salmonella devastating form of sepsis with a mortality rate varying meningitis mainly afects infants and children and rarely from 20 to 30%, is characterized by circulatory collapse, causes purulent meningitis. Spinal intrath- cord, and arachnoiditis associated with meningococcal ecal actinomycosis is extremely rare. Extremely rare young age is associated with a greater risk of developing is the primary cerebral location of the disease. This disease is commonly seen in fve clinical the most frequently isolated species from clinical speci- syndromes: ulceroglandular; oculoglandular; oropha- mens. Fusobac- Tularemic meningitis is a rare complication with terium species can form aggregates with other bacteria only about 15 cases reported in the literature to date. Devitalized tissue may provide one case report tularemia meningitis was presented that a suitable environment for the growth of these organ- was complicated by the formation of multiple cerebral isms. The production of proteolytic enzymes by Fusobacterium Actinomycosis, derived endogenously and not spread organisms may allow for invasion of regional veins. Disseminated by cavernous sinus thrombosis, carotid artery stenosis, infection has been reported. Septic throm- usually occur both in immunocompetent persons and bophlebitis of the orbit and cavernous sinus was seen in in persons with impaired host defenses. Multiple brain abscesses caused by Fusobacteri- demonstrate strong peripheral ring enhancement in multiple um nucleatum in a 51-year-old immunocompromised woman lesions. Rev Infect Dis 9:855865 sans P, Becq-Giraudon B (2003) Characteristics of brain Van Buiren M, Uhl M (2003) Images in clinical medicine. Scand J In- lateral striatal necrosis associated with Mycoplasma pneu- fect Dis 35:318321 moniae infection. Herpes viruses encephalitis is an epidemiological problem in Asia, and multiply mainly in neuronal and glial cells of the limbic is the most important cause of epidemic viral encepha- system. The ten involve meningeal and ependymal cells, but rarely most important causative agents of virus encephalitis are nerve cells. Certain encephalitic Common fndings are focal or difuse brain oedema in viral infections resemble each other with regard to their the acute phase and focal atrophy in the chronic stage; pathological features: Macroscopically, in the early stage therefore, neuroradiological imaging techniques, such the brain parenchyma is normal. Microscopically, perivascular infltrations, of the most common causes of meningoencephalitis gliosis, destroyed nerve cells and viral inclusion bodies in immunocompetent adult persons. Half of the pa- fammatory reaction may be absent at the beginning de- tients are younger than 50 years. Molecular nocompromised persons the neuronal damage results analyses of paired oral/labial and brain sites have indi- more or less only from direct toxic efects of the virus. The most reliable and rapid method for the con- nerves into the anterior or middle cranial fossa. The pro- from 70% in untreated adults to 20% in treated adults, dromal stage of the herpes encephalitis lasts 14 days and in children from 80 to 50%. Typically, the putamen 615% of the cases with herpes encephalitis in adults are is spared. Afer the course of the acute infammatory are parenchymal petechial haemorrhages at the corti- stage, a cysticgliotic residual defect zone remains lead- comedullary junction with initially high signal on T1- ing to focal or difuse brain atrophy. Both during primary infection and during virus reactivation encephalitis or In immunocompromised adults, for instance, in patients Guillain-Barr syndrome may arise. Hyperintensity in the basal ganglia on T2-weighted im- Later the children become apparent with deafness, epi- ages are typical. Extended Varicella-Zoster-Virus Encephalitis periventricular tissue necrosis is evident. The lesions are fectious encephalomyelitis or cerebellitis subsequent to ofen blurred and slightly space occupying. Clinically, the disease is char- enpox is about 30%, that of cerebellitis only 05%. In acterized by slowly progressive demential reduction, adults the prognosis is good. Distur- oligodendrocytes, ependymal cells and endothelial cells bance of the motor coordination, such as tremor and are preferentially infected. Subsequently, secondary ischaemic brain behavioural disturbances and motor defcits. By the use of antiretro- sides directly viral-induced tissue damage, also second- viral drugs the course of the disease can be infuenced ary immunomediated mechanisms are potential causes positively, at best. Intrauterine infection may infammatory parenchymal reaction with the formation lead to a severe necrotizing encephalomyelitis. This phenomenon can be used as a di- reveal irregularities of the cerebral arteries. Brain atrophy and confuent hyper- the hyperintense lesions spare the subcortical U-fbres slowly progressive over months. This variant is characterized by signal changes defcits, defects of the visual feld or ataxia. Sometimes predominately in the deep frontal cerebral white matter hemipareses may develop. Particular cases with spontaneous cessa- tion of the disease have been described; therefore, with 7. Hyperintensity in the lef cerebellar hemisphere (a) and in the lef occipital lobe (a). In progressed cases confu- ent and enlarging white matter lesions with high signal 7. Involvement of the brain stem Measle infection may result in three forms of encepha- and the cerebellum may also ofen occur. The hyperintensity in the cerebellar hemisphere (a), in the lef occipital lobe (a,b) and in the right central region (c) have markedly increased. Now, extensive hyperintensity also in the right temporal lobe c is present (a,b) encephalitis develops in 10/100,000 children below diseased with measles before the second year of life. It begins shortly afer the mea- The typical age of manifestation is before the thirti- sle exanthema or as acute progressive encephalitis eth year of life, the average being the age of 7 years. The possibility to become diseased The causative agent is a mutational variant of the from an encephalitis afer immunization accounts measle virus. A subacute measle encephalitis, which typically postinfectious encephalitis is characterized by re- manifests 110 months afer measle infection in im- currence of fever, reduced consciousness, epilepsy munocompromised persons. The resistance of epilepsy to therapy is typical fects mostly children and adolescents who had been for the subacute measle encephalitis. The lesions have c further markedly increased symptom of this type of encephalitis.
As a single modality purchase 2 mg coumadin with visa pulse pressure variation critical care, it has a higher sensitivity than other imaging modalities for identifying solitary adenomas generic coumadin 5mg online arteria dorsalis scapulae. However buy 1 mg coumadin amex blood pressure charts readings by age, false-positives may be due to thyroid nodules generic 5mg coumadin with visa blood pressure medication dosages, lymph nodes, and brown adipose. Patients with negative sestamibi scan results are more likely to have lower operative cure rates (92%) than those whose scans showed a distinct adenoma (99%). Patients who are taking a calcium channel blocker are more likely to have a negative sestamibi scan result. Radiotracer retention is necessary in order for the sestamibi scan result to be positive; therefore, patients with high levels of P-glycoprotein (a multidrug resistance protein) are likely to have a negative result. The thyroid is imaged as well, looking for nodules or intrathyroidal parathyroids. Doppler is added to image the vascular structures and to visualize vessels supplying adenomas. Thyroid nodules, especially those posteriorly located, can also be difficult to differentiate from parathyroids. However, it can help predict four-gland hyperplasia (necessitating bilateral neck exploration) more frequently than other imaging modalities. It has also been shown to pick up some parathyroid adenomas previously missed on ultrasound scans. It is helpful in patients who have had a negative result on localization imaging studies or who need a reoperation. Adjuncts in parathyroid surgery As minimally invasive procedures become more popular, the need becomes greater to provide minimally invasive parathyroidectomies. With a minimally invasive parathyroidectomy, as previously mentioned, preoperative imaging is necessary in order to determine which gland needs to be removed. Additionally, intraoperative adjuncts (described below) are frequently used in order to decrease operative time and increase operative success. The most common reason for a failed initial operation is missed multigland disease. Additional intervals are also measured if deemed necessary by the operating surgeon. It is also beneficial in reoperative parathyroidectomies, when it is necessary to find the source of disease. After the surgical field is exposed, the radioactivity of the parathyroid adenoma, thyroid, and surrounding area are all re- measured. An adenoma is defined as an ex-vivo parathyroid with at least 20% of the background radioactivity. The empty parathyroid bed is also checked for radioactivity, and any remaining tissue should only have up to 3% of the radioactivity of the adenoma. It allows re-checking not only of the operative field for radioactivity after removal of the presumed source but also of the removed tissue, in order to be certain that the hyperactive adenoma has been removed. It is also helpful for reoperations, because scar tissue makes finding the adenoma of interest much more difficult. Despite advances in preoperative imaging studies, their accuracy remains limited; sampling parathyroids intraoperatively, before excision, may be necessary to look for hypercellularity. During the freezing process, the tissue can be damaged and distorted, leading to a delay in diagnosis (while awaiting final pathology results) or to an error in diagnosis. In small glands, the sample may not be large enough for an adequate diagnosis (although this is not an issue with enlarged, abnormal glands). It can be very difficult to differentiate thyroid nodules from intrathyroidal parathyroids. Scrape cytology requires few instruments and little equipment, which makes it a more economical test. Its main drawback is that, in very small glands, obtaining an adequate sample may be more difficult. This method is more cost-effective than frozen section analysis because it allows for intraoperative identification without the need for pathologic evaluation. Some have raised the concern that this method can damage normal parathyroids, yet no evidence of this effect exists. Its sensitivity for identifying parathyroid tissue is 99%, using 1,000 pg/mL as the cutoff. Percutaneous aspiration can be performed safely with minimal associated complications. Although this method allows for accurate identification of parathyroid tissue, the false-negative rate is 13% (likely depending on the needle aspiration technique). Most clinicians agree that candidates for a minimally invasive parathyroidectomy need to have two concordant preoperative imaging studies (typically, sestamibi and ultrasound scans). Most patients have single-gland disease, so a minimally invasive approach seems preferable. All patients undergoing a focused parathyroidectomy were thought to possibly have single-gland disease, per preoperative imaging. A 2-cm transverse incision is made over the site of the suspected adenoma, at the medial border of the ipsilateral sternocleidomastoid muscle. The sternocleidomastoid muscle and carotid artery are retracted laterally, and the thyroid is retracted anteromedially. If the adenoma is not identified, the ipsilateral neck should be explored; conversion to a traditional bilateral exploration may be necessary. Although focused parathyroidectomy allows for a smaller cosmetic incision, the downside is that conversion to a bilateral neck exploration may require a second incision. The skin and subcutaneous layers are divided down through the platysma, and the subplatysmal flaps are raised. The median raphe of the strap muscles is divided; the ipsilateral strap muscles are retracted laterally; and the thyroid lobe is rotated anteromedially. Both parathyroids on the ipsilateral side should be visualized: one normal and one abnormal gland should be visualized. However, if both those glands appear normal, or if an abnormal adenoma is not localized, the contralateral side must be explored. Frequently, this operation is coupled with intraoperative adjuncts to help guide the extent of resection. The Michigan group reported no incidence of recurrent disease after unilateral neck explorations and a follow-up of 4 years. They use a 2-cm suprasternal incision for a 5-mm trocar, and then place 2 to 3 needle trocars and one more 5-mm trocar on the medial aspect of the ipsilateral sternocleidomastoid muscle. Endoscopic scissors and dissectors are used to dissect out the borders of the thyroid and trachea. The specimen is retrieved through an incision of 2 to 3 cm at the maxillary angle. Single adenomas as well as multigland disease can be effectively treated with this method. Then a 5-mm trocar is placed near the lower edge of the sternocleidomastoid muscle, 2 cm above the incision on the opposite side of the lesion. Endoscopic scissors are used to create a plane between the sternocleidomastoid and the strap muscles. The carotid sheath and thyroid lobe are exposed, and the fascia of the thyroid is incised, to mobilize the thyroid anteromedially after dividing the middle thyroid vein.
Genetic: in the genetic (or developmental) theories generic coumadin 5mg visa arteria descendens genus, aging is considered as a programmed and genetically controlled process of maturation coumadin 2mg without prescription blood pressure 120 0, successive to the development of the organism or cell order coumadin 2mg with amex heart attack burger. These theories are supported by the elevated species-specicity of the maximum lifespan but are in contrast with the variable control and manifestation of aging in different individuals of the same species cheap coumadin 5 mg with mastercard blood pressure chart emt. Longevity genes: there are several evidences about the existence of genetic elements able to regulate senescence, in particular responsible for the regulation of the maximum lifespan. Studies regarding the role of genes involved in the increment of lifespan were primarily performed on simple eukaryotes like yeast and C. Recently, different transgenic mouse models 522 showing aging phenotypes similar to those observed in humans were also settled . Neuroendocrine theory: this is based on the importance of the hormones secreted in the brain (hypothalamic, pituitary, and adrenal hormones) in the regulation of organismic aging and on the decrement in brain neurons . Immunologic theory: this is based on the decreased T-cell response and increased autoimmune reactions during aging . As for the neuroendocrine theory, the weak point is that complex immune and neuronal systems are not present in simple eukaryotes although theyshow characteristics of aging comparable to higher organisms. Cellular senescence: cellular cultures were used as a model for the comprehension of senescence processes due to their usefulness in studying the basic molecular mechanisms, unlike the whole organisms. Data on the genetic effectors responsible for the regulation of cell senescence sustain the hypothesis that organismic aging reects the senescence of single cell lines or tissues. Cellular senescence is often indicated as replicative senescence, since the genes involved in this phenomenon are mainly genes related to the replication machinery and since the cellular senescence becomes evident through decline in growth rate and proliferative activity and alterations in the signal transduction and adaptive response pathways. All these alterations characterize a senescent cell growth status, which is quite different from the young cells . The rst event characterized as a potential cellular clock was the mechanism of telomere shortening . Another two genes of the replicative machinery, retinoblastoma and p53, are well known to be involved in cell senescence; their activity is generally increased in senescent cells . These data are consistent with the hypothesis that cellular senescence has evolved as a mechanism of tumor suppression . Cell death: strictly linked to the mechanisms of cellular replication and senescence, the mechanism of apoptosis is considered as a cause of aging since it consists of a process of active, gene-dependent and injury-independent cell death . More recently, evidence that epigenetic mechanisms could have a role in cellular degeneration and aging has been supported by technical advances allowing a detailed study of the epige- nome and of the epigenetic mechanisms and by the discovery of a complex, non-Mendelian, nature of many age-associated disorders. In yeast and mice, signicant changes in gene expression during cellular degeneration are related to signicant and net loss of heterochromatin, with consequent overexpression of heterochromatin-associated silenced genes . For this reason, it has been proposed that loss of repressive chromatin domains (heterochromatin) may contribute to cellular degeneration and aging processes. Other CpG islands in promoter regions of several genes exhibit age- related hypermethylation in colon mucosa [29,34]. Most of the CpG islands found hyper- methylated in primary colon tumors were hypermethylated to a lesser extent in the aging colon, but a minor number of islands were hypermethylated only in subsets of colon cancers. These ndings stress the hypothesis that two kinds of methylation exist: (1) one age-related methylation, presents in the normal mucosa as a function of the age and (2) a cancer-related methylation, not observed in normal colon. More recently, thanks to the power of the genome-wide studies comparing younger to older subjects, it was possible to conrm on a large-scale basis that methylation changes (both in the direction of hyper- and hypo-methylation) are associated with aging, both in humans [36e38] and in animal models . Even after these recent results, the idea that the methylation status of a larger part of the examined genes and sequences seem unchanged during aging  is, so far, still preserved. This is not at all, of course, a negative or controversial result for the disciples of the epigenetic theory of aging, but it just points out the idea that the age-associated epigenetic drift targets specic genes involved in aging processes. Aberrant methylation of CpG islands in the promoter region may contribute to the progressive inactivation of growth-inhibitory genes during aging, resulting in the clonal selection of cells with growth advantage towards cancer development. All the above-reported data evidence that the methylation pattern established during the development is not stable or denitive in adult life and, in particular, during aging. In our laboratory, we obtained earlier indirect indications that rapid demethyl- ation, not compatible with the time necessary for cellular replication, occurred at a specic CpG site of myogenin gene promoter during myogenic differentiation in vitro . Using a transgenic mouse model of Alzheimers disease we showed that the inhibition of the metabolic pathway that generates the methyl donor S-adenosylmethionine resulted in the impairment of the methylase activities and the improvement of the demethylase activity in mice brain d a tissue known for its scarce cellular proliferation. We can therefore conclude that the methylation pattern of specic genes is not xed in adults and non- proliferating tissues but undergoes dynamic regulation under appropriate stimuli. Neurodegenerative disorders represent the main class of age-associated diseases and, among these, Alzheimers disease represents the most prevalent form of neurodegenerative disease. Moreover, many of these disorders have been recently associated with epigenetic events. For this reasons, it seems of particular relevance in the discussion of the epigenetic changes occurring in the brain and observed in adulthood and aging; an excellent and comprehensive review of these mechanisms was recently published by J. The paper by Murgatroyd and colleagues  has to be considered as a milestone in this area. In their work, they demonstrated that early life stress in mice was associated with behavioral changes in adult life via a mechanism involving epigenetic modications of hypothalamic neurons. Early exposure of mice to environmental stress during the rst 10 days of life resulted in impaired avoidance learning, sustained hyperactivity of the hypothalamicepituitaryeadrenal axis, and corticosterone and pituitary adrenocorticotropin prohormone hypersecretion. Experi- mental models taking advantage of early-life stresses represent promising approaches to study the modication of adult stress response, cognition and behavior, induced by epigenetic modications [58,59]. A different approach was used to study the age-dependent decrease of caspase-3 in rat brain, associated with alterations of the methylation pattern of specic CpG sites in the promoter of 527 the gene . The promoter sequence interested by methylation alteration lies in a region of the promoter necessary for its activity. Since these two factors seem not to be altered during aging, it is possible to appreciate the relevance of methylation status, mediating transcription factors binding and activity. Dynamic changes of methylation patterns even showed cyclical regulation associated with cyclical activation/inactivation of transcription [45,57]. As a matter of fact, specic brain regions such as cortex and hippocampus appear more prone to be interested by these aging-related changes [86e88]. This region-specicity could be also observed when alterations of gene transcription are analyzed. A role for epigenetic mechanisms, which are responsible for regulating gene expression, is now clearly claimed in these aging-related changes [91e93]. As previously stated for Alzheimers disease, aging is the most evident risk factor associated with aging-related diseases . Epigenetic modica- tions, being involved in aging-associated changes in different experimental models and organisms, could represent a link between normal and pathological aging . Besides this general loss of methylation, specic hypomethylation of both coding and non- coding regions was observed during aging. Examples of gene-specic hypermethylation related to aging were also evidenced, together with the silencing of the associated genes. Once again, it is the brain that offers a clear example of this complexity, since it was demonstrated that methylation patterns are region-specic . Finally, a further degree of complexity is added by the possibility that many of the above- discussed changes in the epigenome of the aging brain could have an unsuspected early (even developmental) origin. This hypothesis is supported by the strong association between age-related low methylation status and cognitive decits or neurological and neurodegenerative pathologies [4,26,27]. However, it is still not completely clear whether epigenetic changes actually represent a cause or a consequence of the disease. This gap is due to the high complexity of the epigenetic mechanisms and of their regulation Epigenetics in Human Disease during aging; moreover it is possible that epigenetic studies on pathological aging could be biased by the involvement of subjects in an advanced stage of disease or, in any case, subjects in which the epigenetic changes started even many years before the comparison of the rst symptoms. An active role for epigenetics in normal and pathological aging must meet two conditions: specic epigenetic changes must occur during aging and they must be functionally associated with the aged and/or the diseased phenotype. Assuming that specic epigenetic modications can have a direct functional outcome in aging or age-related diseases, it is also essential to establish whether they depend on genetic, environmental, or stochastic factors . Few objections could be moved to the statement that the two cited conditions (the specicity of the epigenetic changes and the functional association to a phenotype) are demonstrated in the relationship between aging and cancer. As a matter of fact, epigenetic modications play a major role in cancer, inuencing tumor outcome by interfering with key senescence pathways .
Reduced expression of progesterone receptor-B in the endometrium of women with endometriosis and in cocultures of endometrial cells exposed to 2 order coumadin 2mg blood pressure medication causing dizziness,3 discount 1mg coumadin blood pressure 60100,7 best coumadin 5mg blood pressure xls,8-tetrachlorodibenzo-p-dioxin generic coumadin 5mg on-line blood pressure index chart. Changes in gene expression during the early to mid-luteal (receptive phase) transition in human endometrium detected by high-density microarray screening. Expression proling of endometrium from women with endometriosis reveals candidate genes for disease-based implantation failure and infertility. Gene expression analysis of endo- metrium reveals progesterone resistance and candidate susceptibility genes in women with endometriosis. Whole genome deoxyribonucleic acid microarray analysis of gene expression in ectopic versus eutopic endometrium. Molecular proling of experimental endometriosis identied gene expression patterns in common with human disease. Human endometriosis is associated with plasma cells and overexpression of B lymphocyte stimulator. Global gene analysis of late secretory phase, eutopic endometrium does not provide the basis for a minimally invasive test of endome- triosis. Aberrant gene expression prole in a mouse model of endometriosis mirrors that observed in women. Microarray analysis provides insight into the early steps of pathophysiology of mouse endometriosis model induced by autotransplantation of endo- metrium. Sonographically guided therapeutic aspiration of benign-appearing ovarian cysts and endometriomas. Deoxyribonucleic acid methyltransferases and methyl-CpG-binding domain proteins in human endometrium and endometriosis. Transcriptional activation of steroidogenic factor-1 by hypomethylation of the 5 CpG island in endometriosis. Promoter methylation regulates estrogen receptor 2 in human endometrium and endometriosis. An epigenetic disorder may cause aberrant expression of aromatase gene in endometriotic stromal cells. Demethylation of a nonpromoter cytosine-phosphate-guanine island in the aromatase gene may cause the aberrant up-regulation in endo- metriotic tissues. In search of pathogenic mechanisms in endo- metriosis: the challenge for molecular cell biology. Trichostatin A, a histone deacetylase inhibitor, attenuates invasiveness and reactivates E-cadherin expression in immortalized endometriotic cells. A system-wide analysis of differentially expressed genes in ectopic and eutopic endometrium. Research resource: genome-wide proling of methylated promoters in endometriosis reveals a subtelomeric location of hypermethylation. Application of the histone deacetylase inhibitors for the treatment of endometriosis: histone modications as pathogenesis and novel therapeutic target. Expression patterns of the steroid receptor coactivator family in human ovarian endometriosis. Romidepsin reduces histone deacetylase activity, induces acetylation of histones, inhibits proliferation, and activates apoptosis in immortalized epithelial endometriotic cells. Levo-tetrahydropalmatine retards the growth of ectopic endometrial implants and alleviates generalized hyperalgesia in experimentally induced endometriosis in rats. Regulation of chromatin structure by 465 site-specic histone H3 methyltransferases. Maternal care associated with methyl- ation of the estrogen receptor-alpha1b promoter and estrogen receptor-alpha expression in the medial preoptic area of female offspring. Developmental exposure to diethylstilbestrol elicits demethylation of estrogen-responsive lactoferrin gene in mouse uterus. Persistent hypo- methylation in the promoter of nucleosomal binding protein 1 (Nsbp1) correlates with overexpression of Nsbp1 in mouse uteri neonatally exposed to diethylstilbestrol or genistein. Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse. Early nutrition, epigenetic changes at transposons and imprinted genes, and enhanced susceptibility to adult chronic diseases. Histone deacetylase inhibitors trichostatin A and valproic acid induce cell cycle arrest and p21 expression in immortalized human endometrial stromal cells. Constitutive and tumor necrosis factor-alpha-stimulated activation of nuclear factor-kappaB in immortalized endometriotic cells and their suppression by trichostatin A. Distribution of cyclooxygenase-2 in eutopic and ectopic endometrium in endometriosis and adenomyosis. Cyclooxygenase-2 expression in deep endometriosis and matched eutopic endometrium. Cyclooxygenase-2 overexpression in ovarian endometriomas is asso- ciated with higher risk of recurrence. Peroxisome proliferator-activated receptor-gamma and retinoid X receptor agonists syner- gistically suppress proliferation of immortalized endometrial stromal cells. Peroxisome proliferator-activated receptor-gamma ligand reduced tumor necrosis factor-alpha-induced interleukin-8 production and growth in endometriotic stromal cells. Peroxisome proliferator-activated receptor-gamma agonist rosiglitazone reduces the size of experimental endometriosis in the rat model. Peroxisome proliferator-activated receptor-gamma induces regression of endometrial explants in a rat model of endometriosis. Involvement of the nuclear factor-kappaB pathway in the pathogenesis of endometriosis. Inhibition of transcription, expression, and secretion of the vascular epithelial growth factor in human epithelial endometriotic cells by romidepsin. Induction of tumor angiogenesis by Slit-Robo signaling and inhibition of cancer growth by blocking Robo activity. Histone deacetylase inhibitors and a functional potent inhibitory effect on human uterine contractility. The patterns of uterine contractility in normal menstruating women: from physiology to pathology. Progesterone, but not 17-alpha- hydroxyprogesterone caproate, inhibits human myometrial contractions. Trichostatin A, a histone deacetylase inhibitor, reduces lesion growth and hyperalgesia in experimentally induced endometriosis in mice. Valproic acid and progestin inhibit lesion growth and reduce hyperalgesia in experimentally induced endometriosis in rats. Valproic acid alleviates generalized hyperalgesia in mice with induced adenomyosis. The Retardation of Myometrial Inltration, Reduction of Uterine Contractility, and Alleviation of Generalized Hyperalgesia in Mice With Induced Adenomyosis by Levo- Tetrahydropalmatine (l-thp) and Andrographolide. The induction and maintenance of central sensitization is dependent on N-methyl- D-aspartic acid receptor activation; implications for the treatment of post-injury pain hypersensitivity states. Central sensitization: a generator of pain hypersensitivity by central neural plas- ticity. Effects of levetiracetam and valproate on repro- ductive endocrine function studied in human ovarian follicular cells. The effect of valproate and levetiracetam on steroidogenesis in forskolin-stimulated H295R cells. Histone deacetylase inhibitors exert time-dependent effects on nuclear factor-kappaB but consistently suppress the expression of proinammatory genes in human myometrial cells. The immunoconjugate icon targets aberrantly expressed endothelial tissue factor causing regression of endometriosis. Synergy of demethylation and histone deacetylase inhibition in the re-expression of genes silenced in cancer. A genomic screen for genes upregulated by demethylation and histone deacetylase inhibition in human colorectal cancer.
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