Filial Cannibalism by Male Fish as an Infanticide to Restart Courtship by Self-Regulating Androgen Levels.

Parental care is costly for animal parents [1-3], who often desert, abort, or kill their offspring and sometimes even eat them-so-called filial cannibalism [1, 4]. A primary adaptive hypothesis for filial cannibalism centers on the expected nutritional benefits from eating offspring (the energy-based [EB] hypothesis [5-7]). However, many empirical studies are inconsistent with the EB hypothesis [8, 9]. One notable case is total filial cannibalism observed in some fishes. The caregiving males of these species eat all eggs and restart reproduction when tending a small number of eggs, as predicted by the EB hypothesis; but, this is puzzling because they can potentially court females even while tending eggs and increase the eggs by additional matings. Here we show that brood termination known as total filial cannibalism in blenniid fish Rhabdoblennius nitidus males is an endocrinological necessity to restart courtship behavior for subsequent mating. Males exhibit androgen-dependent brood cycling, and they are normally incapable of exhibiting courtships during the parental phase [10]. Egg manipulation experiments demonstrated that egg presence in the nest is a key stimulus regulating male androgen levels; they cannot restart courtship until removing all eggs. Furthermore, surprisingly, eggs were sometimes spit out without being consumed, and the occurrence of cannibalization and removal of all eggs was not associated with male condition. These results strongly suggest that the egg cannibalistic and removal behaviors that have been regarded as total filial cannibalism in this species are infanticide or embryocide rather than cannibalism, which serve to increase the males' androgen levels.

A case of combined Morgagni and esophageal hiatal hernias successfully repaired by endoscopy and laparoscopy.

An 87-year-old woman with a 4-month history of postprandial gastrointestinal obstruction was admitted to our facility after suddenly vomiting black matter. Computed tomography and esophagogastroduodenoscopy revealed gastric prolapse and prolapse of the duodenum and transverse colon. Morgagni hernia combined with esophageal hiatal hernia was diagnosed. Gastric and duodenal obstructions were successfully repaired by endoscopy, followed by laparoscopic repair. Endoscopic repair helped the patient avoid fasting before surgery. The patient had a history of several chest bruises, which were detected by chest X-rays and suspected to be the cause of the hernias over time.

Small nonfunctioning islet cell tumor in the body of the pancreas: report of a case.

Islet cell tumors of the pancreas are uncommon, and nonfunctioning tumors are even rarer than functioning ones. We report the case of a 67-year-old woman with a small nonfunctioning islet cell tumor, 6 x 5 mm in diameter, which was detected incidentally by ultrasonography, and subsequently confirmed by double-helical computed tomography. Diagnosis was established by histopathological examination after 80% distal pancreatectomy with splenectomy, and by various laboratory tests. Histologically, the islet cell tumor showed highly cellular spindle or epithelioid cells, which were positive for Grimelius stain. Immunohistochemical examination revealed that the tumor cells were positive for chromogranin A, but negative for somatostatin, insulin, glucagon, and gastrin. Its small size, location, and benignity make this a very rare type of nonfunctioning islet cell tumor.

Expression of heat shock protein (Hsp) 70 and Hsp 40 in gastric cancer.

Heat shock proteins (Hsp) 70 and Hsp 40 are stress proteins that cooperate as chaperones in mammalian cells. We determined the expression of Hsp 70 and Hsp 40 in 81 gastric cancers. Immunoreactivities to Hsp 70 and Hsp 40 were detected in 67.9 and 22.2% of tumors, respectively. Immunohistochemical analysis showed enhanced Hsp 70 and Hsp 40 expression in gastric tumor tissue, relative to the surrounding normal tissue. Overexpression of Hsp 70 and Hsp 40 was also confirmed by immunoblotting. Among various clinicopathological parameters, low histopathological differentiation was associated with reduced expression of both proteins.

Chromosome 8 numerical aberrations in stage II invasive ductal carcinoma: correlation with patient outcome and poor prognosis.

Aberrations in chromosome 8 are common in breast cancer. However, the relationship between numerical aberrations of chromosome 8 and clinical behavior (especially prognosis) in breast cancer is not well understood. In this study, a total of 40 specimens of stage II invasive ductal carcinomas (IDCs) was analyzed by fluorescence in situ hybridization (FISH) with a chromosome 8 centromere-specific probe and DNA flow cytometry (stage IIA: 20 cases; stage IIB: 20 cases). All cases were followed for at least 5.7 yr (mean: 7.5 yr; median: 7.7 yr) after surgery or until death. Single (loss), double, and triple or more signals (gain) of chromosome 8 were found in 7.6 +/- 3.5% (range: 2-16%; median: 7%), 53.7 +/- 13.2% (range: 25-81%, median: 53%), and 38.7 +/- 13.2% (range: 17-65%, median: 38%), respectively, of tumors. The frequencies of chromosome 8 gain and disomy correlated with patient outcome (respectively p < 0.05 and p < 0.01). When median ratios of chromosome 8 loss, disomy, and gain were used as the cutoff values, the survival curves revealed that patients in the low-frequency group survived significantly longer than those in the high-frequency group for chromosome 8 gain (p < 0.05), and patients in the high-frequency group survived significantly longer than those in the low-frequency group for chromosome 8 disomy (p < 0.05). Poor prognosis was not associated with age, tumor size, lymph node metastasis, histologic type, TNM stage, estrogen-receptor status, progesterone- receptor status, or DNA ploidy. Our results suggest that the frequencies of chromosome 8 gain and disomy is a potentially useful parameter for predicting prognosis of stage II IDCs.

Anorectal melanoma: successful treatment by surgical excision and combination chemoimmunotherapy.

Anorectal melanoma is an extremely rare malignancy, and has a poor prognosis mainly due to delays in diagnosis and lack of effective systemic therapy. We report the case of a 63-year-old female patient with anorectal melanoma. Diagnosis was established after surgery by histology and immunohistochemistry. Surgical management consisted of abdominoperineal resection of the rectum. Postoperatively, the patient received combination therapy of dacarbazine, nimustine hydrochloride, vincristine sulfate, and interferon-beta for 3 cycles. Ten months later, a solitary brain metastatic tumor was noted in the left occipital region, which was resected surgically followed by the above combination therapy for 2 cycles. The last metastatic work-up was normal, and no evidence of recurrence was observed at 2-year follow-up. In our case, abdominoperineal resection of the rectum appears to have some effect in preventing regional and lymph node recurrence. Furthermore, our case suggests that prolongation of survival may depend on extensive block resection and combination therapy of DAV and interferon-beta.

Clinical significance of nm23 expression and chromosome 17 numerical aberrations in primary gastric cancer.

The metastasis suppressor gene nm23 located on chromosome 17 might be one of the targets in deletions of chromosome 17. In this study, we analyzed the expression of nm23 and chromosome 17 aberrations in gastric cancer and assessed their clinicopathological and prognostic significance. In 103 gastric cancer patients, we examined nm23 expression by immunohistochemistry and detected chromosome 17 aberrations by fluorescence in situ hybridization. There was a significant difference in the expression of nm23 among differentiated histologic types (well > moderately > poorly) (p < 0.01). Negative expression of nm23 correlated with depth of invasion (p < 0.01), lymph node metastasis (p < 0.05), lymphatic invasion (p < 0.05), venous invasion (p < 0.05), poor prognosis (p < 0.05), and chromosome 17 loss (p < 0.05). Chromosome 17 aberrations broadly correlated with clinicopathological variables and were associated with poor prognosis (p < 0.05). Univariate analyses identified nm23 (p < 0.05), chromosome 17 aberrations (p < 0.05), tumor size (p < 0.01), depth of invasion (p < 0.0001), lymph node metastasis (P < 0.001), hepatic metastasis (p < 0.01), peritoneal dissemination (p < 0.01), and lymphatic invasion (p < 0.01) as significant prognostic factors. Multivariate analysis showed that expression of nm23 and chromosome 17 aberrations were not independent prognostic indicators. Our results indicate that negative expression of nm23 and chromosome 17 numerical aberrations correlate with tumor progression and poor prognosis but are not independent prognostic indicators.