Low-grade appendiceal mucinous neoplasm with puffer ball-like appearance: A case report.

We report a case of ruptured low-grade appendiceal mucinous neoplasm with an impressive toy puffer ball-like appearance on magnetic resonance imaging. A 79-year-old woman with lower abdominal pain underwent computed tomography scanning, revealing a 6-cm mass in the right lower abdomen. T2-weighted images showed a radial low-signal structure in the central area of the mass, which was presumed to be fibrotic. Pathology confirmed ruptured low-grade appendiceal mucinous neoplasm. The rupture point was at the tip of the appendix, coinciding with the center of radial fibrosis. The unique morphology of the puffer ball-like appearance in this case may be a characteristic of low-grade appendiceal mucinous neoplasms.

[Two cases of unresectable advanced gastric cancer treated with S-1, CDDP and trastuzumab].

We report two cases of unresectable advanced gastric cancer treated with S-1, CDDP and trastuzumab. A significant reduction of tumors was observed in these cases. A 77-year-old man was diagnosed as unresectable gastric cancer. The pathological diagnosis was tub2 and human epidermal growth factor receptor 2(HER2)positive(3+IHC method). We started chemotherapy(S-1+CDDP+trastuzumab). After 2 courses of S-1+CDDP, the findings of upper gastrointestinal endoscopy and CT were much improved to PR. But after 6 courses of S-1+CDDP, they worsened to PD. The regimen of chemotherapy was changed to weekly paclitaxel. The other patient, a 68-year-old woman, was diagnosed as far advanced gastric cancer. The pathological diagnosis was tub2=por2 and HER2 positive(3+IHC method). We started chemotherapy(S- 1+CDDP+trastuzumab). After 3 courses of S-1+CDDP, the tumor reduced significantly to PR. We continued this regimen. From the result of the ToGA trial, addition of trastuzumab to chemotherapy(capecitabine+CDDP or fluorouracil+CDDP) has been recommended as a new standard first-line regimen for HER2-positive advanced gastric cancer. But there is no evidence that trastuzumab added to the other regimen improved survival in patients with advanced gastric cancer. It is necessary to conduct a clinical trial to evaluate the treatment effect of this chemotherapy.

The herpes simplex virus type 1 BgKL variant, unlike the BgOL variant, shows a higher association with orolabial infection than with infections at other sites, supporting the variant-dispersion-replacement hypothesis.

The identification and geographic distribution of the herpes simplex virus type 1 (HSV-1) BglII restriction fragment length polymorphism (RFLP) variants named BgK(L) and BgO(L) in clinical isolates from orolabial and cutaneous sites were described in our previous reports, in which the dispersion and replacement of HSV-1 variants were proposed. The base substitution sites deduced from the BgK(L) multiple RFLP variations were mapped to the U(L)12 (DNase), R(L)2 (alpha0 transactivator), and latency-associated transcript genes in the present study. The results show that the relative frequencies (RFs) of BgK(L) are significantly higher in orolabial and cutaneous HSV-1 infections than in ocular infections. For the BgO(L) variant, the opposite was found; i.e., the RF of BgO(L) was significantly lower in orolabial and cutaneous infections than in ocular infections. No significant differences in the RFs of non-BgK(L):non-BgO(L) isolates were observed. The ratio of the BgK(L) RF to the BgO(L) RF was much higher for the orolabial and cutaneous infection groups than for the ocular infection group, whereas the BgK(L) RF-to-non-BgK(L):non-BgO(L) RF ratios for the former groups were slightly higher than those for the latter group. The higher efficiency of orolabial and cutaneous infections caused by BgK(L) compared to the efficiency of infections caused by BgO(L) allows BgK(L) to spread more efficiently in human populations and to displace BgO(L), because the mouth and lips are the most common HSV-1 infection sites in children. The present study supports our HSV-1 dispersion-and-replacement hypothesis and suggests that HSV-1, the latency-reactivation of which allows variants to accumulate in human populations, has evolved under competitive conditions, providing a new perspective on the polymorphism or variation of HSV-1.

Genome types of adenovirus type 7 isolated in Hiroshima City.

One hundred thirty-two strains of adenovirus type 7 were isolated in Hiroshima City during the period 1995-1999. About 80% of the viruses were isolated from patients with respiratory illness, and about 70% were isolated from children younger than 6 years old. DNA restriction analysis was performed on 58 of the 132 isolates. Two genome types corresponding to adenovirus 7d and adenovirus 7h were recognized using BamHI. By using an additional 10 restriction endonucleases (BclI, BglI, BglII, BstEII, HindIII, HpaI, SmaI, PstI, PvuII, and SacI), the 58 isolates were classified finally into five genome types according to Wadell and coworkers' nomenclature system: adenovirus 7d2 (54 isolates), adenovirus 7d3 (one isolate), adenovirus 7d4 (one isolate), adenovirus 7d5 (one isolate), and adenovirus 7h (one isolate), among which adenovirus 7d3, 7d4, and 7d5 were new genome types. Our results indicate that the predominant genome type of adenovirus 7 that circulated in Hiroshima City during the period May 1995-November 1999 was adenovirus 7d2.

Molecular and epidemiological analyses of human adenovirus type 7 strains isolated from the 1995 nationwide outbreak in Japan.

The adenovirus type 7 (Ad7) isolates from the 1995 nationwide outbreak in Japan were genetically and seroepidemiologically analyzed in comparison with Japanese Ad7 strains isolated before 1995 to determine their genome type and to speculate on their origin and causative factors of the outbreak. Twenty-six Ad7 isolates from the outbreak were identified by restriction enzyme analysis as the Ad7d2 genome type, while 22 Ad7 strains sporadically isolated in Japan before 1995 were identified as Ad7d. Partial nucleotide sequencing of the E3 region of Ad7d2 revealed a nucleotide substitution of G to A at position 265, resulting in the absence of the BstEII site and making Ad7d2 distinct from Ad7d. In Hiroshima City, Japan, no Ad7 was isolated from 1982 to 1994, but 43 and 50 Ad7 strains were isolated in 1995 and 1996, respectively. A seroepidemiological study of 251 serum samples collected in 1989 in Hiroshima City showed that only 2.8% of the samples were positive for Ad7. These results indicate that the 1995 outbreak of Ad7 in Japan was caused by the Ad7d2 genome type, which might have been introduced from outside Japan. The results also suggest that the low mass immunity in Japan was critical for the outbreak and that the mutation in the E3 region in Ad7d2 may have influenced transmission.