Do prune-belly syndrome and neural tube defects change testicular growth? A study on human fetuses.

BACKGROUND: There are no reports comparing testicular volume between normal fetuses, fetuses with prune-belly syndrome (PBS), and fetuses with anencephaly. The study hypothesis was that PBS and especially anencephaly alter the testicular volume during the human fetal period. AIM: The objective of the study was to compare the testicular growth in fetuses with anencephaly, with PBS, and without anomalies. STUDY DESIGN: This is a morphometric study of human fetuses. Seventy testes from fetuses without anomalies aged 11-22 weeks post-conception (WPC), 30 testes from fetuses with anencephaly aged 13-19 WPC, and eight testes from fetuses with PBS aged 13-16 WPC were studied. Testicular length, width, and thickness were evaluated with the aid of computer programs (Image Pro and ImageJ) (Figure). The fetal testicular volume was calculated using the ellipsoid formula: Testicular volume (TV) = [length × thickness × width] × 0.523. The Shapiro-Wilk test was used to ascertain the normality of the data and to compare quantitative data between normal fetuses vs. fetuses with anencephaly, while the Kruskal-Wallis test was used to assess gender and laterality differences. Simple linear correlations (LCs) were calculated for testicular volume according to fetal age, weight, and crown-rump length. RESULTS: All 108 testes studied were abdominal. The right (p = 0.0310) and left (0.0470) testicular volumes were significantly smaller in fetuses with anencephaly than those in the control group. The linear regression analysis indicated that the right and the left testis volume in the control group (right: r2 = 0.6665; left: r2 = 0.6707) and PBS group (right: r2 = 0.9937; left: r2 = 0.9757) increased with fetal age (p < 0.0001). This analysis also indicated that the testicular volume in fetuses with anencephaly did not increase with fetal age (right: r2 = 009816; left: r2 = 0.07643). DISCUSSION: This article is the first to report testicular volume correlations with fetal parameters in fetuses with anencephalic and fetuses with PBS. Significant alterations were observed in testicular growth in the anencephalic group compared with the control group, and it was also observed that the bilateral cryptorchidism in PBS does not alter the testicular development and growth during the fetal period. The unequal WPC distribution between fetuses with PBS, fetuses with anencephaly, and controls and the small sample size are limitations of this study. Further studies should be performed to confirm this study's findings. CONCLUSIONS: Testicular growth is slower and does not show significant correlations with fetal parameters in fetuses with anencephalic. Significant differences in testicular development in fetuses with PBS was not observed.

TGIF2 interacts with histone deacetylase 1 and represses transcription.

TG-interacting factor (TGIF) is a transcriptional repressor, which represses transcription by binding directly to DNA or interacts with transforming growth factor beta (TGF beta)-activated Smads, thereby repressing TGF beta-responsive gene expression. Mutation of TGIF in humans causes holoprosencephaly, a severe genetic disorder affecting craniofacial development. Searching human expressed sequence tag data bases revealed the presence of clones encoding a TGIF-related protein (TGIF2), which contains two regions of high sequence identity with TGIF. Here we show that, like TGIF, TGIF2 recruits histone deacetylase, but in contrast to TGIF, is unable to interact with the corepressor CtBP. TGIF2 and TGIF have very similar DNA-binding homeodomains, and TGIF2 represses transcription when bound to DNA via a TGIF binding site. TGIF2 interacts with TGF beta-activated Smads and represses TGF beta-responsive transcription. TGIF2 appears to be a context-independent transcriptional repressor, which can perform similar functions to TGIF and may play a role in processes, which, when disrupted by mutations in TGIF, cause holoprosencephaly.

New approaches for the preparation of hydrophobic heparin derivatives.

A heparin derivative sufficiently lipophilic to be bound to plastics, forming blood-compatible supports, or to be used as an anticoagulant by transdermal or oral routes would be of great pharmaceutical interest. For such applications, the functional groups within heparin's antithrombin III binding site, responsible for its anticoagulant activity, cannot be modified. Chemistry is described in which lipophilic substituents were attached to the reducing termini of heparin chains. Substituents introduced at this position had a minimal effect on the antithrombin III binding sites found in heparin's interior. These derivatives, with enhanced hydrophobicities, were prepared using two distinctly different approaches. First, octyl isocyanate and octadecyl isocyanate were coupled to the core peptide of peptidoglycan heparin to form octyl- and octadecyl-peptidoglycan heparin. These octyl- and octadecyl-peptidoglycan heparins were then purified by hydrophobic interaction chromatography on phenyl-Sepharose CL-4B, demonstrating their enhanced hydrophobicities. Second, the lipophilic acyl hydrazides of various long chain fatty acids were coupled to heparin's reducing end. Caprylic (C8), capric (C10), lauric (C12), and stearic (C18) hydrazide derivatives of heparin were prepared using this approach. Only the stearyl hydrazide derivative of heparin showed a measurable increase in lipophilicity. This result demonstrated that a single small linear C8, C10, or C12 aliphatic chain was ineffective in enhancing the hydrophobicity of the highly negative, polyanionic heparin molecule. Two lipophilic chains, lauryl (C12) and stearyl (C18), were then coupled to a single heparin chain, resulting in a heparin derivative having enhanced hydrophobicity. All the heparin derivatives prepared in this study maintained some of their anticoagulant activity.

Anestesia balanceada com nalbufina/enflurano para cirurgia de revascularizaçäo do miocardio / Balanced anesthesia with nalbuphine and enflurane for myocardial revascularization

A nalbufina é um narcótico agonista/antagonista com potência analgésica similar à da morfina. Em doses equi-analgésicas, assemelha-se à nalorfina no que diz respeito à elevada relaçäo antagonista/atividade analgésica. Neste trabalho, foi estudada uma técnica da anestesia balanceada com nalbufina e enflurano em 16 pacientes submetidos à cirurgia de revascularizaçäo do miocárdio. A idade média dos pacientes foi 57,1 + ou - 16,3 anos e o peso médio foi 66,2 + ou - 14,5 kg. A medicaçäo pré-anestésica constou de diazepam 10 mg IM uma hora antes da induçäo. Esta foi obtida com nalbufina 0,25 mg.kg-1 e diazepam 0,4 mg.kg-1 por via venosa, seguindo-se pancurônio e intubaçäo orotraqueal. A anestesia foi mantida com nalbufina em doses intermitentes e enflurano administrado através de vaporizador calibrado, em oxigênio puro. Ventilaçäo controlada mecânica, sistema sem reinalaçäo, mistura gasosa ar/oxigênio com FiO2 = 50%. Monitorizaçäo de PAM, PVC, produto FC x PAS, ECG e gases sangüíneos. A dose total média de nalbufina foi 62,1 + ou - 15,5 mg e o consumo horário médio de 0,34 + ou - 0.13 mg.kg-1. h-1. A concentraçäo inspirada de enflurano oscilou entre 1,0 e 2,0, exceto por ocasiäo da intubaçäo traqueal e de incisäo torácica, quando foi necessário elevá-la para 2,5-3,0% a fim de manter PAM e produto FC x PAS próximoa aos valores de controle. Os resultados indicaram que a combinaçäo de nalbufina e enflurano é segura e eficaz em técnica de anestesia balanceada para pacientes submetidos à cirurgia de revascularizaçäo do miocárdio. Os pacientes foram extubados em média 6,8 + ou - após o término da cirurgia, completamente acordados e com necessidades mínimas de analgésicos para controle da dor pós-operatória. Näo se observou depressäo respiratória após a extubaçäo