1.Distribution of intracellular and extracellular expression of transforming growth factor-beta1 (TGF-beta1) in human testis and their association with spermatogenesis.
Masaki DOBASHI ; Masato FUJISAWA ; Takafumi YAMAZAKI ; Hiroshi OKADA ; Sadao KAMIDONO
Asian Journal of Andrology 2002;4(2):105-109
AIMSpermatogenic dysfunction may result from thickening of seminiferous tubular basement membrane (BM) with tubular sclerosis. Transforming growth factor beta1 (TGF-beta1) plays an important role in fibrogenesis. The intracellular and extracellular expression of TGF-beta1 in the testis were immunohistochemically determined, using LC antibody (LC) for intracellular TGF-beta1 and CC antibody (CC) for extracellular TGF-beta1.
METHODSTwenty-three testicular biopsy specimens were obtained from varicocele and five from Sertoli-cell-only (SCO) patients, and five from normal volunteers. The relative area involved by the expression of TGF-beta1 for CC or LC (TGF-beta1 index for CC or LC) was examined, and semen parameters and serum hormonal levels and TGF-beta1 were analyzed. The Johnson score (JS), the BM thickness, and the tubular diameter were also determined.
RESULTSImmunoreactivity for CC was hardly detected. That for LC was detected in the Sertoli and germ cells. The TGF-beta1 index for LC was significantly higher in the varicoceles than in the normal testes. Interestingly, that for LC was significantly higher in the varicoceles than in the SCO. The level of serum TGF-beta1 was significantly higher in varicoceles than in the normal testes.
CONCLUSIONThe distribution of the intracellular and extracellular expression of TGF-beta1 in human testis was demonstrated. It suggests that TGF-beta1 is related to fibrosis of seminiferous tubules and may lead to spermatogenic disruption.
Adult ; Biopsy ; Estrogens ; blood ; Follicle Stimulating Hormone ; blood ; Humans ; Luteinizing Hormone ; blood ; Male ; Prolactin ; blood ; Reference Values ; Sertoli Cells ; physiology ; Spermatogenesis ; physiology ; Testis ; cytology ; pathology ; physiology ; Testosterone ; blood ; Transforming Growth Factor beta ; blood ; metabolism ; Varicocele ; blood ; physiopathology
2.Rapid Changes in Serum Lipid Profiles during Combination Therapy with Daclatasvir and Asunaprevir in Patients Infected with Hepatitis C Virus Genotype 1b.
Takeshi CHIDA ; Kazuhito KAWATA ; Kazuyoshi OHTA ; Erika MATSUNAGA ; Jun ITO ; Shin SHIMOYAMA ; Satoru YAMAZAKI ; Hidenao NORITAKE ; Tetsuro SUZUKI ; Takafumi SUDA ; Yoshimasa KOBAYASHI
Gut and Liver 2018;12(2):201-207
BACKGROUND/AIMS: Changes in lipid profiles in patients infected with hepatitis C virus (HCV) during direct-acting antiviral therapy have been reported in recent years. However, the clinical aspects of disturbed lipid metabolism in chronic HCV infection have not been fully elucidated. METHODS: Dynamic changes in serum total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol and apolipoprotein levels in patients infected with HCV genotype 1b were examined during combination therapy with daclatasvir (DCV) and asunaprevir (ASV). RESULTS: Total, LDL−, and HDL-cholesterol levels increased rapidly and persistently after week 4. Apolipoprotein (apo) A-I, apo B, apo C-II, and apo C-III levels were significantly higher at week 4 than at week 0. In contrast, apo A-II and apo E levels were significantly lower. The differences in LDL− and HDL-cholesterol levels were positively correlated with those of apo B and apo A-I, respectively. Interestingly, in patients with non-sustained virological response, these cholesterol levels decreased rapidly after viral breakthrough or viral relapse. Furthermore, similar changes were observed for apo A-I, apo B and apo C-III levels. CONCLUSIONS: Clearance of HCV using combination therapy with DCV and ASV results in rapid changes in serum lipid profiles, suggesting an influence of HCV infection on disturbed lipid metabolism.
Apolipoprotein A-I
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Apolipoprotein A-II
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Apolipoprotein C-II
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Apolipoprotein C-III
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Apolipoproteins
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Apolipoproteins B
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Apolipoproteins E
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Cholesterol
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Genotype
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Hepacivirus*
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Hepatitis C*
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Hepatitis*
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Humans
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Lipid Metabolism
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Lipoproteins
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Recurrence