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Zusammenfassung Hiluszellwucherungen im Ovar bei angeborenem adrenogenitalem Syndrom (AGS) werden als Gegenstück zu dem Vorkommen von Leydigzellproliferationen des Hodens bei AGS angesehen, wie sie von Landing (1951) und Odunjo (1962) beschrieben worden sind. Eine eigene Beobachtung bei einem neugeborenen Mädchen bestätigt die Annahme einer Homologie von Hilus- und Zwischenzellen.Unter den pathogenetischen Mechanismen kommt eine gemeinsam gesteigerte corticound gonadotrope Stimulation der adrenalen und ovariellen Zellwucherungen ebenso in Frage wie die Möglichkeit einer Angleichung der gewucherten Hiluszellen an die Funktion der Zellen der Nebennierenrinde und ihre Abhängigkeit von der ACTH-Stimulation.
Nodular hilar cell proliferation of the ovary in connatal adrenogenital syndrome
Summary The occurrence of nodular hilar cell proliferations of the ovary in adrenogenital syndrome (AGS), as observed in a newborn girl, should be interpreted as the female counterpart to occasional testicular Leydig cell hyperplasia described in AGS by Landing (1951) and Odunjo (1962). This observation favours the assumption of homology of ovarian hilar cells and testicular interstitial cells.—The mechanisms involved in the development of hilar cell hyperplasia may be a pituitary hypersecretion not only of corticotropic but concomitantly also of gonadotropic hormones. On the other hand, it is possible that the hyperplastic hilar cells adjust to the function of the cells of the adrenal cortex and their dependence on ACTH stimulation.
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In rats, 3 days treatment with paracetamol (1 oral dose of 1 g/kg daily) produced a complete protection against the hepatotoxic actions of a further dose of paracetamol as documented by determination of serum enzyme activities (glutamic-oxaloacetic transaminase, (GOT), glutamic-pyruvic transaminase (GPT), sorbitol dehydrogenase (SDH), bromsulphthalein retention and histological investigations. Subacute paracetamol treatment decreased liver glutathione levels by 46%, liver microsomal cytochrome P-450 content by 23%, hepatic hydroxylation of aniline by 29% and hepatic demethylation of aminopyrine by 46%. It afforded also some protection against the hepatotoxic actions of carbon tetrachloride, bromobenzene and thioacetamide, but did not influence the antiphlogistic activity of paracetamol (carrageenan paw edema test). Plasma and liver concentrations of free paracetamol after oral administration of 1 g/kg paracetamol were somewhat higher in the subacutely paracetamol-pretreated rats than in the non-pretreated control animals whereas no differences in the concentrations of conjugated paracetamol were found between the 2 groups. Pretreatment with paracetamol did not influence the urinary excretion of free paracetamol but caused some shift in the urinary excretion of paracetamol conjugates: pretreated rats excreted 23% less of the paracetamol glucuronide and sulfate and 33% more of the paracetamol mercapturate than the control animals. A depression of the microsomal mixed-function oxidase activity is presumed to be the main cause of the paracetamol-induced protection against paracetamol hepatotoxicity.  相似文献   
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Four cases of rarely occurring meningiomas of the lateral ventricles are reported. These tumors are said to originate from meningeal cell clusters that have been mislocated during embryonal development. Patients of clinical history, diagnostic and surgical findings, and the postoperative course are described, with special emphasis on tumor growth aspects.  相似文献   
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In spite of extensive, conservative methods for treating spondylitis, more or less distinct kyphotic deformities are common. Pain usually plays a minor role as an indication for surgery either as local instability or as impairment of the large hip or knee joints. Much more common are the loss of social contact and the lack of visual contact with the surroundings, both of which the patients find unacceptable. The monosegmental, lumbar correction method as used at an early stage implicated a high rate of complications. The implant supported methods, and in particular those that allow the potential for dorsal transpediculated fixation, allowed, in the early 1980s, dorsal lordotic measures in the form of a multilocus method and, in the mid-1980s, a modified monosegmentary method as well. Both of these methods are widely accepted because of their good long-term results. The possible complications no longer include the disturbance of the spinal cord but are rather to be found in the poor general condition of the patient. The restoration of a largely normal equilibrium of the backbone relieves the musculature and is therefore a definitive pain therapy for muscle tension problems. Straightening the backbone also relieves the hip joints and therefore it is possible in many cases to delay the implantation of a hip prosthesis.  相似文献   
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Second central nervous system (CNS) relapses represent about 7.3% of subsequent recurrences of childhood acute lymphoblastic leukemia (ALL). In most children these subsequent CNS relapses occur during the first 18 months after diagnosis of the first relapse (mean 1.42 +/- 0.73 years). We present a patient who suffered a second ALL relapse in the CNS more than seven years after diagnosis of his first relapse. The leukemic clone was completely stable over more than ten years as shown by minimal residual disease techniques. Possible reasons for the recurrence of the leukemic clone after this very long period of dormancy (e.g. role of the disease site, immune system dysfunction) are discussed.  相似文献   
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The hepatotoxic effects of eight compounds as determined by serum activities of glutamic-oxaloacetic transaminase (GOT), glutamic-pyruvic transaminase (GPT), and sorbitol dehydrogenase (SDH) were investigated in normally fed mice on the one hand and 24-hr-fasted mice on the other. Fasting strongly enhanced serum-enzyme elevations induced by carbon tetrachloride, paracetamol, thioacetamide, and bromobenzene. The hepatotoxic effects of phalloidin and allyl alcohol were only moderately increased by fasting and those of α-amanitin and praseodymium not at all. The fasting-induced aggravation of CCl4 hepatotoxicity (evidenced also by histological findings) appeared already after 12 hr and was maximal after 24 hr of food deprivation. Fasting for 24 hr decreased the liver weight by 29%, hepatic glycogen by 93%, and hepatic glutathione (GSH) by 50% but increased liver triglycerides by 162%. Aniline hydroxylase and aminopyrine N-demethylase activities were higher in the liver homogenate supernatants from fasted than from fed mice but microsomal protein content as well as microsomal NADPH-cytochrome c-reductase activity remained unchanged and microsomal cytochrome P-450 content even decreased upon fasting. Fasting did not influence the in vitro irreversible binding of 14CCl4 and [3H]paracetamol to hepatic microsomal proteins nor the in vivo binding to hepatic proteins of [3H]paracetamol. It enhanced, however, the total concentration of 14CCl4 in the liver by 30% and produced a trend toward higher values in the extent of 14CCl4 bound in vivo to hepatic protein. Spontaneous and CCl4-induced lipid peroxidation were the same in hepatic microsomes from fed and fasted mice. No unique explanation can be made for the increased susceptibility of mouse liver to toxic injury induced by fasting. Several factors must be considered: depletion of both hepatic glycogen and glutathione as well as hepatic lipid accumulation. Overnight fasting of mice (and of other small animals presumably too) may change the results of toxicological experiments to an unpredictable degree and should thus be avoided.  相似文献   
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