Type II restriction modification system in Ureaplasma parvum OMC-P162 strain.

Ureaplasma parvum serovar 3 strain, OMC-P162, was isolated from the human placenta of a preterm delivery at 26 weeks' gestation. In this study, we sequenced the complete genome of OMC-P162 and compared it with other serovar 3 strains isolated from patients with different clinical conditions. Ten unique genes in OMC-P162, five of which encoded for hypothetical proteins, were identified. Of these, genes UPV_229 and UPV_230 formed an operon whose open reading frames were predicted to code for a DNA methyltransferase and a hypothetical protein, respectively. DNA modification analysis of the OMC-P162 genome identified N4-methylcytosine (m4C) and N6-methyladenine (m6A), but not 5-methylocytosine (m5C). UPV230 recombinant protein displayed endonuclease activity and recognized the CATG sequence, resulting in a blunt cut between A and T. This restriction enzyme activity was identical to that of the cultivated OMC-P162 strain, suggesting that this restriction enzyme was naturally expressed in OMC-P162. We designated this enzyme as UpaP162. Treatment of pT7Blue plasmid with recombinant protein UPV229 completely blocked UpaP162 restriction enzyme activity. These results suggest that the UPV_229 and UPV_230 genes act as a type II restriction-modification system in Ureaplasma OMC-P162

Direct observation of ESR spectra of bicyclic nine-membered enediynes at ambient temperature

The ESR spectra for synthetic bicyclo[7.3.0]epoxydodecadienediynes in solution at room temperature are steady. These spectra originate from the Masamune-Bergman cyclization of bicyclo[7.3.0]epoxydodecadienediynes to p-benzyne biradicals and the equilibrium between the two forms. Comparison of the ESR spectra of the unlabeled and 13C-labeled nine-membered enediynes indicated that the spectra are not directly due to the p-benzyne biradicals but rather to more stable secondary radical intermediates

Prenatal features of congenital peribronchial myofibroblastic tumor

Here, we report a case of a congenital peribronchial myofibroblastic tumor (CPMT). A 34-year-old primigravida was referred to our hospital at 31 gestation weeks because of suspected congenital pulmonary airway malformation (CPAM). Fetal ultrasonography showed a mass measuring 4.6 × 4.0 × 3.9 cm with mixed high and low echogenicity in the left lung, which was associated with microvascular blood flow in the tumor. Fetal magnetic resonance imaging (MRI) revealed a low-intensity left lobe lung lesion on a T2-weighted image. These findings suggested that the mass was a CPAM with atypical hypointense findings on MRI T2-weighted images or a rare primary pulmonary tumor, such as a CPMT. Unfortunately, the fetus died in utero at 34 gestation weeks due to cardiovascular failure, which could have resulted from direct encasement of the great vessels or cardiac compression due to rapid tumor growth. The autopsy findings confirmed the diagnosis of CPMT. Primary pulmonary tumors, such as CPMT, are extremely rare lung diseases that develop in utero. These tumors often rapidly grow during pregnancy, resulting in intrauterine fetal death. However, if the patient survives surgical mass resection, the prognosis is good. Given the adverse outcomes observed in our case, careful fetal monitoring is required in case of suspected CPMT during the third trimester of pregnancy. Moreover, in case the well-being of the fetus cannot be assured, immediate delivery should be considered, even in the preterm period, followed by surgery