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排序方式: 共有1048条查询结果,搜索用时 15 毫秒
1.
Leonidas JC; Berdon WE; Valderrama E; Neveling U; Schuval S; Weiss SJ; Hilfer C; Godine L 《Radiology》1996,198(2):377
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Kaufmann SJ; Sharif K; Sharma V; McVerry BA 《Human reproduction (Oxford, England)》1998,13(2):498-499
The patient was diagnosed in childhood as having severe congenital
neutropenia and had recurrent admissions with severe infections. In 1987,
prior to getting married, she was sterilized. She continued to require i.v.
antibiotics when she contracted a severe infection. On one occasion, she
was treated with growth colony stimulating factor (G- CSF). Her increased
neutrophil count was sustained following this treatment. In June 1993, she
wished to start a family and underwent in- vitro fertilization (IVF)
treatment. G-CSF was given prior to oocyte retrieval. She conceived on her
first cycle and an ultrasound scan revealed a singleton pregnancy.
Throughout the course of the pregnancy, her white cell count was monitored
closely and remained at <1.0x10(9)/l. The pregnancy progressed
uneventfully and at 37 weeks gestation she was admitted for G-CSF
injections. At 38 weeks she was delivered of a boy weighing 3350 g, by
elective Caesarean section. His white cell count was normal. This is the
first case of G-CSF being used before conception and during pregnancy in a
patient with congenital neutropenia. It shows that advances in cytokine
therapy and close interdisciplinary liaison can lead to a successful
outcome and help patients, who would otherwise remain childless, to achieve
a family.
相似文献
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Silber SJ; Nagy Z; Devroey P; Tournaye H; Van Steirteghem AC 《Human reproduction (Oxford, England)》1997,12(11):2422-2428
The aim of the study was to determine whether a prior diagnostic testicle
biopsy can predict success or failure of testicular sperm extraction (TESE)
with intracytoplasmic sperm injection (ICSI) in patients with
non-obstructive azoospermia caused by testicular failure, and what is the
minimum threshold of sperm production in the testis which must be surpassed
for spermatozoa to reach the ejaculate. Forty- five patients with
non-obstructive azoospermia caused by testicular failure underwent
diagnostic testicle biopsy prior to a planned future TESE-ICSI procedure.
The diagnostic testicle biopsy was analysed quantitatively, and correlated
with the quantitative findings of spermatogenesis in patients with normal
spermatogenesis, as well as with the results of subsequent attempts at
TESE-ICSI. Men with non- obstructive azoospermia caused by germinal failure
had a mean of 0-6 mature spermatids/seminiferous tubule seen on a
diagnostic testicle biopsy, compared to 17-35 mature spermatids/tubule in
men with normal spermatogenesis and obstructive azoospermia. These findings
were the same for all types of testicular failure whether Sertoli cell
only, maturation arrest, cryptorchidism, or post-chemotherapy azoospermia.
Twenty-two of 26 men with mature spermatids found in the prior testis
biopsy had successful retrieval of spermatozoa for ICSI, 12 of their
partners became pregnant, and are either ongoing or delivered. The study
suggests that 4-6 mature spermatids/tubule must be present in the testis
biopsy for any spermatozoa to reach the ejaculate. More than half of
azoospermic patients with germinal failure have minute foci of
spermatogenesis which are insufficient to produce spermatozoa in the
ejaculate. Prior diagnostic testicle biopsy analysed quantitatively (for
the presence of mature spermatids) can predict subsequent success or
failure with TESE-ICSI. Incomplete testicular failure may involve a sparse
multi-focal distribution of spermatogenesis throughout the entire testicle,
rather than a regional distribution. Therefore, it is possible that massive
testicular sampling from many different regions of the testes may not be
necessary for successful TESE-ICSI.
相似文献
6.
β-Lactoglobulin was isolated from infant formulae that were ultra high temperature (UHT) -treated, sterilized or spray-dried. The effect of the isolated β-lactoglobulin on SfaII-fimbriae-mediated adhesion of Escherichia coli to human ileostomy glycoproteins was studied in vitro. β-Lactoglobulin isolated from sterilized formulae was found to perform significantly less well than preparations from spray-dried formulae (p = 0:05). Great heterogeneity was observed in the adhesion inhibitory capacity of β-lactoglobulin isolated from UHT-treated formulae. Therefore, no significant difference was observed between UHT-treated and sterilized formulae or spray-dried formulae (p < 0:10). It can be hypothesized that β-lactoglobulin from spray-dried and some UHT-treated infant formulae may affect the colonization of mucous membranes by E. coli strains causing neonatal septicaemia and meningitis. 相似文献
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Exposure to certain organophosphorus compounds results in a neurological condition known as organophosphorus-induced delayed neurotoxicity (OPIDN). OPIDN is characterized clinically by an initial post-exposure delay period of 8-14 days after which signs of progressively developing ataxia and paralysis of the hindlimbs are observed. Although several studies have reported the presence of degeneration induced by organophosphorus delayed neurotoxins in specific central nervous system (CNS) structures, none have systematically examined CNS changes seen in the most frequently studied animal model for OPIDN--the domestic fowl. In the present study, we assessed the location and extent of anterograde degeneration in the chicken CNS following exposure to tri-o-tolyl phosphate (TOTP). All birds were dosed with 500 mg TOTP/kg body weight and killed after post-exposure periods of 1, 2, 3, or 4 weeks. The brains and spinal cords were processed with Fink-Heimer and Nissl stains. In the spinal cord, axon degeneration was noted in the fasciculus gracilis at cervical levels two weeks after exposure to TOTP. At 3 weeks, degeneration was also present in the cervical part of the dorsal spinocerebellar tract, in the lumbar part of the medial pontine-spinal tract, and in lamina VII in the lumbar ventral horn. In the medulla, moderate amounts of terminal and preterminal degeneration appeared at two weeks in the lateral vestibular, gracile, external cuneate, and lateral cervical nuclei. Lesser amounts of degeneration were noted in the solitary, inferior olivary, and raphae nuclei, in the medial, descending and lateral vestibular nuclei, and in the lateral paragigantocellular, gigantocellular, and lateral reticular nuclei. Fiber degeneration was also present in the medullary portions of the dorsal and ventral spinocerebellar tracts and spinal lemniscus. In the cerebellum, moderate amounts of terminal degeneration appeared in the deep cerebellar nuclei at one week while moderate mossy fiber degeneration was first noted in the granular layers of cerebellar folia I-V at 3 weeks. These results indicate (1) that, in the CNS, axonal and terminal degeneration resulting from TOTP intoxication appears to be confined to the spinal cord, medulla and cerebellum, (2) that the time of onset of degeneration in different fiber tracts and nuclei ranges from one to three weeks post-exposure, and (3) that the delay in the appearance of clinical signs of OPIDN is consistent with the delayed onset of degeneration in many of the affected CNS fiber systems. 相似文献
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