Does a cervical pessary reduce the rate of preterm birth in women with a short cervix?

OBJECTIVES: To evaluate neonatal outcomes after the use of a cervical pessary in Japanese women with short cervical length (CL) less than 25 mm. METHODS: This multicenter study involved women with singleton pregnancies between 20 and 29+6 gestational weeks and a CL of less than 25 mm. The primary outcome was preterm birth (PTB) before 34 weeks of gestation. This study was registered in the Japan Registry of Clinical Trials (JRCT: jRCTs042180102). RESULTS: Two hundred pregnant women were enrolled; 114 in the pessary group and 86 in the expectant management group as controls. In the pessary group, all 114 neonates were investigated for perinatal outcomes, and 112 pregnant women were investigated for primary, and secondary outcomes. In the control group, 86 pregnant women were investigated for primary and secondary outcomes and 86 neonates were investigated for neonatal outcomes. There were no significant differences in PTB in ≤34, ≤37, and ≤28 weeks of gestation or in preterm rupture of membranes (PROM) ≤34 weeks between the groups. The gestational weeks at birth and birth weight were significantly higher in the pessary group. Regression analysis demonstrated that the CL decreased without a pessary, whereas the shortening rate was suppressed during the intervention. No significant differences were observed in adverse neonatal outcomes, chorioamnionitis, or preterm PROM. CONCLUSIONS: The cervical pessary effectively reduced CL shortening during pregnancy resulting in an average increased gestational age, however, did not reduced the rates of preterm birth.

Alteration of developmental program in Paramecium by treatment with trichostatin a: a possible involvement of histone modification.

In the ciliate Paramecium caudatum, the somatic macronucleus for the next generation differentiates from a zygotic germinal micronucleus during conjugation. Subsequently, progeny are programmed to enter a sexually "immature" period, during which cells do not mate. This programming occurs at a critical period during the fifth cell cycle after conjugation. Here, we show that treatment with trichostatin A, a histone deacetylase inhibitor, leads to a partial recovery of mating reactivity in immature cells, suggesting that histone acetylation can affect the developmental program. In addition, immunostaining demonstrated that Lys 4 methylation of histone H3 was absent from or present at an undetectable level in the nascent macronucleus during the first cell cycle after conjugation. The methylation level gradually increased in proportion to de novo DNA synthesis, until the new macronucleus reached the maximum level of methylation, concomitant with its full maturation. A link between gene expression and Lys 4 methylation is indirectly supported by the observation that a transcriptionally active gene was enriched by chromatin immunoprecipitation with an antibody directed against methyl-Lys 4 H3, whereas a silent gene was not. These results provide evidence that histone modification plays a key role in the regulation of gene expression and the developmental programming that determine sexual immaturity after conjugation.

Pathological evaluation of massive left atrial calcification 35 years after mitral-aortic valve replacement.

Massive calcification of the left atrium is an uncommon complication of long-standing rheumatic valve disease, and is frequently revealed in patients with a previous operation on the mitral valve. An 84-year-old woman, who had a history of rheumatic valvulopathy and mitral-aortic valve replacement surgery 35 years previously, was admitted to our hospital due to congestive heart failure. Chest X-ray showed severe cardiomegaly with rim of calcification outlining the enlarged left atrium. Computed tomographic scan of the thorax clearly illustrated dense and partially thick plate-like calcification of left atrial free wall and interatrial septum. She died due to congestive heart failure 14 days after hospitalization and an autopsy was performed. Enlargement of left atrium with massive calcification was evident by gross pathology. Thick plate-like calcification with both erosion and mural hemorrhage was clearly shown by a cross-section of atrial wall. Organized and fresh fibrin thrombi were identified at the surface of left atrium. Calcified tissue penetrated into the wall of the left atrium and lack of myocardium underneath the massive calcified lesion was evident. Although rheumatic calcification of left atrium revealed by medical images was previously described, this is the first case report that demonstrates histopathological evaluation of massive atrial calcification. .

Primary extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue type with malakoplakia in the urinary bladder: a case report.

Primary malignant lymphoma of the urinary bladder is a rare disease constituting less than 1% of neoplasms of the urinary bladder. The most prevalent histological subtype is extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue type (MALT lymphoma). It is frequently associated with chronic cystitis and predominantly occurs in females. On the other hand, malakoplakia is thought to be a reactive granulomatous lesion occurring most prevalently in the genitourinary tracts. It is frequently found in females and often associated with bacterial infection in immunosuppressive status. Here we report a rare case of concurrent primary MALT lymphoma and malakoplakia in the urinary bladder in a 78-year-old Japanese female. Presumably, both lymphoma and malakoplakia are considered to be involved in the antecedent cystitis and might contribute to the development of the urinary bladder tumor of the patient, leading to the occlusion of the right ureter with subsequent hydronephrosis.

A proximal conserved repeat in the Xist gene is essential as a genomic element for X-inactivation in mouse.

X-inactivation in female mammals is triggered by the association of non-coding Xist RNA in cis with the X chromosome. Although it has been suggested that the A-repeat located in the proximal part of the Xist RNA is required for chromosomal silencing in ES cells, its role in mouse has not yet been addressed. Here, we deleted the A-repeat in mouse and studied its effects on X-inactivation during embryogenesis. The deletion, when paternally transmitted, caused a failure of imprinted X-inactivation in the extraembryonic tissues, demonstrating the essential role of the A-repeat in X-inactivation in the mouse embryo. Unexpectedly, the failure of X-inactivation was caused by a lack of Xist RNA rather than by a defect in the silencing function of the mutated RNA, which we expected to be expressed from the mutated X. Interestingly, the normally silent paternal copy of Tsix, which is an antisense negative regulator of Xist, was ectopically activated in the preimplantation embryo. Furthermore, CpG sites in the promoter region of paternal Xist, which are essentially unmethylated in the extraembryonic tissues of the wild-type female embryo, acquire a significant level of methylation on the mutated paternal X. These findings demonstrate that the DNA sequence deleted on the mutated X, most probably the A-repeat, is essential as a genomic element for the appropriate transcriptional regulation of the Xist/Tsix loci and subsequent X-inactivation in the mouse embryo.

Interactions between newly developed macronuclei and maternal macronuclei in sexually immature multinucleate exconjugants of Paramecium caudatum.

The macronucleus of Paramecium caudatum controls most cellular activities, including sexual immaturity after conjugation. Exconjugant cells have two macronuclear forms: (1) fragments of the maternal macronucleus, and (2) the new macronuclei that develop from the division products of a fertilization micronucleus. The fragments are distributed into daughter cells without nuclear division and persist for at least eight cell cycles after conjugation. Conjugation between heterokaryons revealed that the fragmented maternal macronuclei continued to express genetic information for up to eight cell cycles. When the newly developed macronucleus was removed artificially within four cell cycles after conjugation, the clones regenerated the macronuclear fragments (macronuclear regeneration; MR) and showed mating reactivity, because they were sexually mature. However, when the new macronucleus was removed during later stages, many MR clones did not show mating reactivity. In some extreme cases, immaturity continued for more than 50 fissions after conjugation, as seen with normal clones that had new macronuclei derived from a fertilization micronucleus. These results indicate that the immaturity determined by the new macronucleus is not annulled by the regenerated maternal macronucleus. Mature macronuclear fragments may be "reprogrammed" in the presence of the new macronucleus, resulting in their expression of "immaturity."

Delayed degradation of parental macronuclear DNA in programmed nuclear death of Paramecium caudatum.

In the ciliated protozoan Paramecium caudatum, a parental macronucleus that is fragmented into some 40-50 pieces during conjugation does not degenerate immediately, but persists until the eighth cell cycle after conjugation. Here we demonstrate that the initiation of the parental macronuclear degeneration occurs at about the fifth cell cycle. The size of parental macronuclear fragments continued to increase between the first and fourth cell cycle, but gradually decreased thereafter. By contrast, a new macronucleus grew and reached a maximum size by the fourth cell cycle, suggesting that the new macronucleus matured by that stage. Southern blot analysis revealed that parental macronuclear DNA was degraded at about the fifth cell cycle. The degradation was supported by acridine orange staining, indicating degeneration of the macronuclear fragments. Prior to the degradation, the fragments once attached to the new macronucleus were subsequently liberated from it. These observations lead us to conclude that once a new macronucleus has been fully formed by the fourth cell cycle, the parental macronuclear fragments are destined to degenerate, probably through direction by new macronucleus. Considering the long persistence of the parental macronucleus during the early cell cycles after conjugation, the macronuclear fragments might function in the maturation of the imperfect new macronucleus. Two possible functions, a gene dosage compensation and adjustment of ploidy level, are discussed.