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An electrophoretic transfer technique was used to investigate qualitatively the production of antibodies to Strongyloides stercoralis larvae in 56 patients with strongyloidiasis. SDS-PAGE analysis of the larval extract revealed the presence of at least 33-39 polypeptide bands under either reducing or non-reducing condition. In the immunoblot analysis, almost all patients showed positive reactivity to the polypeptide bands. The reactivity, however, revealed significant variation among the patients, ranging in number of bands from only one to more than 18. Among the bands, 4 with molecular sizes of 97, 66, 41 and 26 kDa were frequently recognized by the patients' sera, indicating that these antigenic components may form an available antigen for immunological testing for strongyloidiasis. On the other hand, the reactivities were very faint in cases of overwhelming strongyloidiasis.

Objective:To evaluate the TRUCLEAR™ system (Smith and Nephew Inc., London, UK), a hysteroscopic system that morcellates and aspirates masses, in terms of the operating time, surgeon's convenience, and effect on patients compared with conventional electrosurgical resection.Methods:Patients undergoing hysteroscopic resection of endometrial polyps were randomly allocated to undergo hysteroscopic morcellation or electrosurgical resection (UMIN-CTR identifier: UMIN000019649). The primary outcome was the operating time. Secondary outcomes were the removal success, fluid deficit, convenience with the technique, insertion time, number of insertions during the operation, visibility of the operative field, recurrence of the patient's chief complaint, and adverse events.Results:Sixty-seven women were randomly allocated to the morcellation arm (n = 34) or electrosurgical resection arm (n = 33) from November 2015 to November 2016. The polyps were completely removed, and no adverse events were observed in all 67 patients. The average operating time (8.3 min vs. 12.0 min, P = 0.014), insertion time (5.0 min vs. 9.0 min, P < 0.001), and number of insertions (1.0 vs. 8.2, P < 0.001) were significantly lower in the morcellation arm than in the electrosurgical resection arm. Surgeons' subjective evaluation measured on a 10-cm visual analog scale was higher in the morcellation arm than in the electrosurgical resection arm in terms of easiness of removal (8.4 vs. 6.5, P < 0.001) and visibility of the operative field (7.8 vs. 6.4, P < 0.001).Conclusion:Surgeons gave the hysteroscopic morcellator system a better evaluation compared than electrosurgical resection, and the system shortened the operating time.

Estrogen-related receptor ␣ (ERR␣) is a member of the nuclear receptor superfamily and regulates many physiological functions, including mitochondrial biogenesis and lipid metabolism. ERR␣ enhances the transactivation function without endogenous ligand by associating with coactivators such as peroxisome proliferator-activated receptor ␥ coactivator 1 ␣ and ␤ (PGC-1␣ and -␤) and members of the steroid receptor coactivator family. However, the molecular mechanism by which the transactivation function of ERR␣ is converted from a repressive state to an active state is poorly understood. Here we used biochemical purification techniques to identify ERR␣-associated proteins in HeLa cells stably expressing ERR␣. Interestingly, we found that double PHD fingers protein DPF2/BAF45d suppressed PGC-1␣-dependent transactivation of ERR␣ by recognizing acetylated histone H3 and associating with HDAC1. DPF2 directly bound to ERR␣ and suppressed the transactivation function of nuclear receptors such as androgen receptor. DPF2 was recruited to ERR target gene promoters in myoblast cells, and knockdown of DPF2 derepressed the level of mRNA expressed by target genes of ERR␣. These results show that DPF2 acts as a nuclear receptor-selective co-repressor for ERR␣ by associating with both acetylated histone H3 and HDAC1.Nuclear receptors (NRs) 3 play pivotal roles during the development of vertebrates and in diverse physiological events in adults (1, 2). NRs constitute a gene superfamily and act as transcription factors. For most members of the NR superfamily, the transcriptional function is dependent on binding of lipophilic ligands such as steroid hormones and fat-soluble vitamins. The other subset of NRs is considered an orphan receptor, as physiologically relevant ligands remain to be identified. Orphan receptors are constitutively active or repressive transcription factors; however, their potency in transcriptional regulation appears to be dependent on cell types and the promoter context (3).For ligand-dependent transcriptional controls by nuclear steroid/vitamin receptors, several distinct classes of transcriptional co-regulators-co-regulator complexes are indispensable in addition to basic transcription machinery to reorganize chromatin state (4). Transcriptional co-regulators for NRs can be divided into two classes in terms of chromatin reorganization (5-7). One class consists of histone-modifying enzymes that reversibly modify the N-terminal tails of histone proteins (8, 9). For example, acetylation and methylation at histone H3K4 and H3K36 are chromatin-activating modifications and support transcriptional activation by NRs (8, 10, 11). In contrast, transcriptional repression by NRs is coupled with inactivating modifications like deacetylation and methylation at histone H3K9 and H3K27. Accordingly, cognate histone modifying enzymes serve as NR co-regulators.The other class of transcriptional co-regulators are chromatin remodeling factors that directly reorganize nucleosomal arrays through ATP hydrolysis (11). Chromatin remod...

Unlike previously reported cases with total protein 4.2 deficiency due to mutations in the EPB42 gene, we describe a total deficiency in protein 4.2 with normal EPB42 alleles. Hereditary spherocytosis (HS) was observed in a Japanese woman (unsplenectomized) and her daughter (splenectomized). The mother showed a partial deficiency in band 3 and a proportional reduction in protein 4.2. She was heterozygous for a novel allele of the EPB3 gene, allele Okinawa, which contains the two mutations that define the Memphis II polymorphism (K56E, AAG → GAG, and P854L, CCG → CTG) and, additionally, the mutation: G714R, GGG → AGG, located in a highly conserved position of transmembrane segment 9. The latter change was responsible for HS. In trans to allele Okinawa, the daughter displayed allele Fukuoka: G130R, GGA → AGA, an allele known to alter the binding of protein 4.2 to band 3. The daughter presented with a more pronounced decrease of band 3, and lacked protein 4.2, resulting in aggravated haemolytic features. Although the father was not available for study, heterozygosity for allele Fukuoka has been documented in another individual who showed no clinical or haematological signs, and a normal content of band 3. We suggest that band 3 Okinawa binds virtually all the protein 4.2 in red cell precursors, band 3 Fukuoka being unable to do so, and that the impossibility of band 3 Okinawa incorporation into the membrane leads to degradation of the band 3 Okinawa protein 4.2 complex. In contrast, band 3 Fukuoka, free of bound protein 4.2, could then incorporate normally into the bilayer. Thus, protein 4.2 would not appear in the daughter's red cell membrane.