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cyclooxygenase/necrosis
Холбоосыг санах ойд хадгалдаг
Хуудас 1 -аас 4588 үр дүн
Cyclooxygenase inhibitors prevent the induction of tolerance to the toxic effects of tumor necrosis factor.
Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой
Нэвтрэх / Бүртгүүлэх
Nonsteroidal anti-inflammatory drugs, such as indomethacin (INDO), prevent acute toxicity caused by a single bolus injection of tumor necrosis factor (TNF). However, when given as a pretreatment to repetitive daily injections of TNF, INDO enhances toxicity. We investigated the effect of INDO on the
Ursolic acid enhances cyclooxygenases and tumor necrosis factor-alpha expression in mouse skin.
Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой
Нэвтрэх / Бүртгүүлэх
An anti-inflammatory triterpenoid, ursolic acid (UA), has recently been found unexpectedly to induce the release of a pro-inflammatory mediator in resting macrophages. In this study, we found that topical applications of UA to mouse skin twice a week for 2 weeks significantly enhanced mRNA
p38 Mitogen-activated protein kinase stabilizes mRNAs that contain cyclooxygenase-2 and tumor necrosis factor AU-rich elements by inhibiting deadenylation.
Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой
Нэвтрэх / Бүртгүүлэх
AU-rich elements (AREs) in 3'-untranslated regions of mRNAs confer instability. They target mRNAs for rapid deadenylation and degradation and may enhance decapping. The p38 MAPK pathway stabilizes many otherwise unstable ARE-containing mRNAs encoding proteins involved in inflammation; however, the
Tumor necrosis factor alpha and interleukin-1beta stimulate the expression of cyclooxygenase II but do not alter prostaglandin E2 receptor mRNA levels in cultured dorsal root ganglia cells.
Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой
Нэвтрэх / Бүртгүүлэх
Tumor necrosis factor alpha (TNFalpha) and interleukin 1beta (IL-1beta) are pro-inflammatory cytokines capable of altering the sensitivity of sensory neurons. Because sensitization elicited by IL-1beta and TNFalpha is blocked by inhibition of the inducible enzyme, cyclooxygenase-II (COX-2), we
Tumor necrosis factor-alpha-induced cyclooxygenase-2 expression in human tracheal smooth muscle cells: involvement of p42/p44 and p38 mitogen-activated protein kinases and nuclear factor-kappaB.
Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой
Нэвтрэх / Бүртгүүлэх
This study was to determine the mechanism of tumor necrosis factor-alpha (TNF-alpha)-enhanced cyclooxygenase (COX)-2 expression associated with prostaglandin E2 (PGE2) synthesis in human tracheal smooth muscle cells (HTSMCs). TNF-alpha markedly increased COX-2 expression and PGE2 synthesis in a
Cyclooxygenase-2 or tumor necrosis factor-α inhibitors attenuate the mechanotransductive effects of pulsed focused ultrasound to suppress mesenchymal stromal cell homing to healthy and dystrophic muscle.
Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой
Нэвтрэх / Бүртгүүлэх
Maximal homing of infused stem cells to diseased tissue is critical for regenerative medicine. Pulsed focused ultrasound (pFUS) is a clinically relevant platform to direct stem cell migration. Through mechanotransduction, pFUS establishes local gradients of cytokines, chemokines, trophic factors
Cell-cell contacts trigger programmed necrosis and induce cyclooxygenase-2 expression.
Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой
Нэвтрэх / Бүртгүүлэх
Necrosis was induced by cell-cell contacts of human dermal fibroblasts in three-dimensional culture. Dramatic induction of cyclooxygenase-2 (COX-2) expression was found throughout these necrotizing cell clusters, whereas no increase in expression of apoptosis markers was seen. The cells were rapidly
Cardiopulmonary effects of tumor necrosis factor-alpha in the piglet: influence of cyclooxygenase inhibition.
Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой
Нэвтрэх / Бүртгүүлэх
Tumor necrosis factor-alpha (TNF) is believed to play an important role in mediating many of the pathophysiologic changes accompanying bacterial sepsis. In order to characterize the cardiopulmonary responses to TNF in a young animal model and to determine to what extent these changes were secondary
Hyperplastic gastric tumors with spasmolytic polypeptide-expressing metaplasia caused by tumor necrosis factor-alpha-dependent inflammation in cyclooxygenase-2/microsomal prostaglandin E synthase-1 transgenic mice.
Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой
Нэвтрэх / Бүртгүүлэх
We showed recently that Helicobacter infection induces expression of cyclooxygenase-2 and microsomal prostaglandin E synthase-1 in the mouse stomach, and that transgenic mice expressing both cyclooxygenase-2 and microsomal prostaglandin E synthase-1 (K19-C2mE mice) develop hyperplastic gastric
Differential effects of corticosteroids on the expression of cyclooxygenase-2, tumour necrosis factor-alpha and matrix metalloproteinase-9 in an animal model of migraine.
Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой
Нэвтрэх / Бүртгүүлэх
Nitric oxide (NO) directly activates trigeminal afferents innervating the dura mater and up-regulates inflammatory mediators. We evaluated NO-mediated up-regulation of cyclooxygenase-2 (COX-2), tumour necrosis factor-alpha (TNF-alpha) and matrix metalloproteinase-9 (MMP-9), and the effect of
Tumor necrosis factor-induced mortality is reversed with cyclooxygenase inhibition.
Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой
Нэвтрэх / Бүртгүүлэх
OBJECTIVE
The authors hypothesized that TNF would induce eicosanoid synthesis, and a cyclooxygenase inhibitor would attenuate both eicosanoid synthesis and improve survival in an LD90 TNF-induced (150 ng/kg/i.v./5 min) mortality model.
BACKGROUND
Tumor necrosis factor is a cardinal mediator in
Evidence for tumor necrosis factor alpha as a mediator of the toxicity of a cyclooxygenase inhibitor in Gram-negative sepsis.
Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой
Нэвтрэх / Бүртгүүлэх
To investigate the effect of cyclooxygenase inhibition in experimental Gram-negative sepsis, indomethacin was administered to mice at different times (1 or 5 days, or 1 h) before sublethal infection with an intravenous inoculum of Pseudomonas aeruginosa Early indomethacin exposure did not alter the
Effect of 17-alpha hydroxyprogesterone caproate on the production of tumor necrosis factor-alpha and the expression of cyclooxygenase-2 in lipopolysaccharide-treated gravid human myometrial explants.
Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой
Нэвтрэх / Бүртгүүлэх
OBJECTIVE
To determine whether 17-alpha hydroxyprogesterone (17-OHPC) alters tumor necrosis factor-alpha (TNF-alpha) production and the expression of cyclooxygenase type 2 (COX-2) in myometrium exposed to lipopolysaccharide (LPS).
METHODS
Lower segment myometrial biopsies were obtained from
Expression of tumor necrosis factor-alpha and cyclooxygenase-2 mRNA in porcine split-thickness wounds treated with epidermal growth factor by quantitative real-time PCR.
Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой
Нэвтрэх / Бүртгүүлэх
Epidermal growth factor (EGF) accelerates the re-epithelialization of damaged epidermal cell layers in a wound, so it especially shortens the duration of wound healing. The effect of EGF on pro-inflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha) and cyclooxygenase-2 (COX-2), levels
Association of organochlorine pesticides with the mRNA expression of tumour necrosis factor-alpha (TNF-α) & cyclooxygenase-2 (COX-2) genes in idiopathic preterm birth.
Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой
Нэвтрэх / Бүртгүүлэх
OBJECTIVE
Preterm birth (PTB) is an important cause of prenatal death, neonatal morbidity and mortality and adult illness. Increased inflammation occurs in normal parturition, and inflammatory cytokines and oxidative stress are found to be higher in PTB cases. The present study was planned to
Шинжлэх ухаанаар баталгаажсан эмийн өвс ургамлын бүрэн мэдээллийн сан
- 55 хэл дээр ажилладаг
- Шинжлэх ухааны үндэслэсэн ургамлын гаралтай эдгэрэлт
- Ургамлыг дүрсээр таних
- Интерактив GPS газрын зураг - эмийн ургамлыг байршлаар нь тэмдэглэнэ (удахгүй)
- Хайлттай холбоотой шинжлэх ухааны нийтлэлүүдийг уншина уу
- Эмийн өвсийг үр нөлөөгөөр нь хайж олох
- Мэдээллийн судалгаа, клиник туршилт, патентыг цаг тухайд нь сонирхож, зохион байгуул
Шинж тэмдэг эсвэл өвчний талаар бичиж, тус болох ургамлын талаар уншиж, өвслөг ургамлыг бичиж, өвчний эсрэг шинж тэмдгийг үзээрэй.
* Бүх мэдээлэл нь хэвлэгдсэн эрдэм шинжилгээний судалгаанд үндэслэсэн болно
