asphyxia/protease

Kiungo kimehifadhiwa kwenye clipboard

Chagua aina ya aina

Ukurasa 1 kutoka 27 matokeo

Propofol administration to the maternal-fetal unit improved fetal EEG and influenced cerebral apoptotic pathway in preterm lambs suffering from severe asphyxia.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

BACKGROUND Term and near-term infants are at high risk of developing brain injury and life-long disability if they have suffered from severe perinatal asphyxia. We hypothesized that propofol administration to the maternal-fetal unit can diminish cerebral injury in term and near-term infant fetuses

[Ultrastructural features of heart insufficiency and its correction during the post-asphyxia period].

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

The ultrastructure of myocardium was studied in the experiments on rats during 24 hours after 6-min mechanical asphyxia with following clinical death. It has been established that the contractile cardiac apparatus of myocytes lesions on the intracellular edema background is the main while energy

[Effect of leptin on expression of calpain-1 and Bcl-2 and apoptosis in myocardial tissue of neonatal rats after asphyxia].

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

OBJECTIVE To study the effect of leptin on the expression of calcium-activated neutral protease 1 (calpain-1) and B cell lymphoma-2 (Bcl-2) and apoptosis in the myocardial tissue of neonatal rats after asphyxia. METHODS A total of 48 neonatal rats were randomly and equally divided into normal

Nitrotyrosine in brain tissue of neonates after perinatal asphyxia.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

OBJECTIVE Nitrotyrosine, a reaction product of peroxynitrite and proteins, could be demonstrated in the postmortem examination of brain tissue of full-term neonates who had severe perinatal asphyxia. METHODS The brain tissue of 22 full-term neonates who died after severe perinatal asphyxia was

Cellular alterations associated with perinatal asphyxia.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

Asphyxia triggers a cascade of cellular biochemical events that lead to temporary alterations in cellular function and/or cell death. Tissue hypoxia and ischemia lead to depolarization of neuronal membranes, alteration in cellular ion homeostasis and changes in energy metabolism. The changes are

Microglia/macrophage-derived inflammatory mediators galectin-3 and quinolinic acid are elevated in cerebrospinal fluid from newborn infants after birth asphyxia.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

Activation of microglia/macrophages is important in neonatal hypoxic-ischemic (HI) brain injury. Based on experimental studies, we identified macrophage/microglia-derived mediators with potential neurotoxic effects after neonatal HI and examined them in cerebrospinal fluid (CSF) from newborn infants

Inhibition of PAR-2 Attenuates Neuroinflammation and Improves Short-Term Neurocognitive Functions via ERK1/2 Signaling Following Asphyxia-Induced Cardiac Arrest in Rats.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

Global cerebral ischemia induced neuroinflammation causes neurofunctional impairment following cardiac arrest. Previous studies have demonstrated that the activation of protease activated receptor-2 (PAR-2) contributes to neuroinflammation. In the present study, we aimed to determine

Erythropoiesis suppression is associated with anthrax lethal toxin-mediated pathogenic progression.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

Anthrax is a disease caused by the bacterium Bacillus anthracis, which results in high mortality in animals and humans. Although some of the mechanisms are already known such as asphyxia, extensive knowledge of molecular pathogenesis of this disease is deficient and remains to be further

C1 inhibitor: molecular and clinical aspects.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

C1 inhibitor (C1-INH) is a serine protease inhibitor (serpins) that inactivates several different proteases in the complement, contact, coagulation, and fibrinolytic systems. By its C-terminal part (serpin domain), characterized by three beta-sheets and an exposed mobile reactive loop, C1-INH binds,

Brazilian guidelines for the diagnosis and treatment of hereditary angioedema.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

Hereditary angioedema is an autosomal dominant disease characterized by edema attacks with multiple organ involvement. It is caused by a quantitative or functional deficiency of the C1 inhibitor, which is a member of the serine protease inhibitor family. Hereditary angioedema is unknown to many

Effect of blood deposition phenomenon on flesh quality of yellowtail (Seriola quinqueradiata) during storage.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

We examined the influence of blood deposition on flesh quality of ordinary muscle in yellowtail. This study compared the flesh quality changes in upper and under-sides of yellowtails killed by two different methods: spinal-cord destruction (SCD) with blood removal and suffocation in air without

Pathophysiology of perinatal brain damage.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

Perinatal brain damage in the mature fetus is usually brought about by severe intrauterine asphyxia following an acute reduction of the uterine or umbilical circulation. The areas most heavily affected are the parasagittal region of the cerebral cortex and the basal ganglia. The fetus reacts to a

[Effects of Ucf-101 on expression of Omi/HtrA2 in kidneys of postasphyxial neonatal rats].

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

OBJECTIVE To investigate the expression of serine protease Omi/HtrA2 in kidneys of postasphyxial neonatal rats, and to study the effects of Ucf-101 on apoptosis and the expression of Omi/HtrA2 in these rats. METHODS Seventy-two neonatal Wistar rats of 7-10 days old were randomly divided into 3

New therapies for hereditary angioedema: disease outlook changes dramatically.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

Hereditary angioedema (HAE) is an autosomal dominant disease associated with episodic attacks of nonpitting edema that may affect any external or mucosal body surface. Attacks most often affect the extremities, causing local swelling, the GI tract, leading to severe abdominal pain, and the mouth and

Managing hereditary angioedema patients undergoing otolaryngeal procedures.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

BACKGROUND Hereditary angioedema (HAE), a rare autosomal dominant disorder, is characterized by repeated attacks of swelling of the skin, gastrointestinal tract, face, larynx, and other organs. In most cases it is caused by low levels of functional C1 esterase inhibitor (C1-INH), a serine protease

Iliyotangulia
1
2
Ifuatayo

Jiunge na ukurasa
wetu wa facebook

Herbal & Natural Medicine

Hifadhidata kamili ya mimea ya dawa inayoungwa mkono na sayansi

Inafanya kazi katika lugha 55
Uponyaji wa mitishamba unaungwa mkono na sayansi
Kutambua mimea kwa picha
Ramani ya GPS inayoshirikiana
Soma machapisho ya kisayansi yanayohusiana na utafutaji wako
Tafuta mimea ya dawa na athari zao
Panga maslahi yako na fanya tarehe ya utafiti wa habari, majaribio ya kliniki na ruhusu

Andika dalili au ugonjwa na usome juu ya mimea ambayo inaweza kusaidia, chapa mimea na uone magonjwa na dalili ambazo hutumiwa dhidi yake.
* Habari zote zinategemea utafiti wa kisayansi uliochapishwa