Synchronous bilateral neuroendocrine ductal carcinoma in situ.

Neuroendocrine ductal carcinoma in situ (NE-DCIS) is a breast malignancy that has characteristic clinicopathological features and can, therefore, be regarded as a distinct variant of DCIS. The patient was a 54-year-old premenopausal woman with hemorrhagic nipple discharge in her left breast. Magnetic resonance imaging and ultrasound (US) images of the left breast showed mass-like lesions, while concurrent images of the right breast showed non-mass-like lesions. These findings suggested the presence of both benign and malignant tumors. Pathological findings from US-guided core-needle biopsy of the left mass were highly suspicious of a malignant tumor. Excisional biopsy of both breasts was performed. We could define the diagnosis of breast cancer by the second opinion on pathological diagnosis. The tumor cells showed histological characteristics of NE-DCIS. Bilateral breast lesions had histopathological similarities and were composed of predominantly solid growth of carcinoma cells, frequently with well-developed vascular structures, in mammary ducts and ductules. Carcinoma cells were polygonal or occasionally spindle shaped and had fine-granular, relatively eosinophilic cytoplasm. The nuclei of these cells showed round to ovoid in shape and fine-granular chromatin pattern. There was not any invasive component, as confirmed by careful histological examination. Thus, additional immunohistochemical stainings for NE markers (chromogranin A and synaptophysin) were performed. Staining statuses of these markers were positive in almost all tumor cells from both breasts. Both tumors were therefore diagnosed as NE-DCIS. To our knowledge, this case is the first report of NE-DCIS diagnosed synchronously in both breasts.

Validity of the six stages of change for exercise.

We examined the validity of 'Transtheoretical Model of Behavior Change' six stages in exercise domain. A paper-pencil survey was completed by 457 workers. Self-efficacy tended to increase from Precontemplation to Action, did not change from Action to Maintenance, and then increase from Maintenance to Termination. Pros tended to increase and cons decrease only from Precontemplation to Action. A follow-up survey was completed by 331 workers. More preparers (25.4%) moved to Action compared to precontemplator (3.8%) and contemplators (6.5%). Relapse rates were lower among those in Termination (17.0%) than those in Action (43.8%) and Maintenance (38.1%). These results partially supported the validity.

Bilateral stenosis of carotid siphon in Hutchinson-Gilford progeria syndrome.

Hutchinson-Gilford progeria syndrome (HGPS) is a rare premature aging disease, caused by a de novo mutation of lamin-A gene, LMNA G608G. Accumulation of abnormal lamin-A (progerin) compromises nuclear membrane integrity and results in the accelerated senescence. Affected patients show a typical feature of birdlike face, alopecia, sclerotic skin, loss of subcutaneous fat, and short stature with advancing years. Neonatal scleroderma is the first presentation, although early diagnosis is challenging. The leading cause of death is cardio-/cerebro-vascular accidents associated with atherosclerosis. However, not all findings may recapitulate the aging process. We herein report a 9-year-old Japanese male with HGPS who developed cerebral infarction. The genetic study of peripheral blood-derived DNA determined a heterozygous c.1824C>T mutation, p.G608G. Telomere length of lymphocytes was normal. Bilateral stenosis of carotid siphons was prominent, while systemic arteriosclerosis was unremarkable assessed by the ankle-brachial index, carotid ultrasound imaging and funduscopic study. HGPS patients have marked loss and functional defects in vascular smooth muscle cells, leading to the vulnerability to circulatory stress. Symmetrical stenosis of siphons might occur as a distinctive cerebral vasculopathy of HGPS, rather than simple vascular senescence. Peripheral blood study on LMNA G608G and telomere length could screen progerias in infancy for early therapeutic intervention.

Three cases of granulocyte colony-stimulating factor-producing urinary upper tract carcinomas.

This report presents three cases of urinary upper tract carcinomas producing granulocyte colony-stimulating factor (G-CSF), with high blood leukocyte counts and poor prognoses. Case 1 was a 73-year-old man who underwent nephroureterectomy for left renal pelvic carcinoma. Pathologically, urothelial carcinoma (UC), high-grade, was observed, and immunohistochemical analysis showed positive staining for G-CSF. Progressive disease (PD) was observed despite administration of systemic chemotherapy for disease relapse, and the patient died 4.5 months after the operation. Case 2 was a 74-year-old man who had left renal pelvic carcinoma with para-aortic lymph-node metastases. The serum G-CSF was elevated (169 pg/ml). The patient refused any aggressive treatment, and died 2.3 months after his first visit to the hospital. Case 3 was a 75-year-old woman who had left renal pelvic carcinoma with adrenal metastasis. Biopsy confirmed the diagnosis as UC with squamous differentiation, and the serum G-CSF was elevated (138 pg/ml). Systemic chemotherapy was administered. However, the patient showed PD, and died 6.9 months after her first visit to the hospital. Effective treatment strategies are warranted for carcinomas producing G-CSF. Elucidation of the actions of G-CSF on both the carcinoma cells and the tumor microenvironment may contribute to the development of useful strategies.

Emergence of vancomycin resistance during therapy against methicillin-resistant Staphylococcus aureus in a burn patient--importance of low-level resistance to vancomycin.

OBJECTIVES: Staphylococcus aureus with low-level resistance to vancomycin (VLSA) which could develop into vancomycin-resistant S. aureus (VRSA) is most important. However, VLSA is difficult to detect by standard laboratory methods. We describe here improved methods to detect VLSA. METHODS: Three methicillin-resistant S. aureus (MRSA) strains, designated Fu6, Fu10, and Fu18, were sequentially isolated from the burn wound site of a patient, during vancomycin therapy. The properties of these strains were compared with those of reference strains Mu3 and Mu50 (previous resistant isolates from other patients). RESULTS: The isolated strains, Fu10 and Fu18, had identical phenotypes and genotypes. The vancomycin resistance of Fu10 was equivalent to that of strain Mu3, whereas Fu18 had much higher vancomycin resistance than Fu10 and Mu3, although reaching the level of Mu50. Fu18 showed similar growth to Mu50 on gradient gels and on Mu3 medium. CONCLUSIONS: Our data indicate that the VLSA developed vancomycin resistance during exposure to vancomycin in vivo. The population analysis of tested VLSA and vancomycin intermediately resistant S. aureus (VISA) indicates that a penem at relatively low concentrations induced a significant increase in the number of vancomycin-resistant subpopulations. Furthermore, we confirmed that gradient gel analysis and Mu3 medium are simple and useful methods for the detection of VLSA judged as VSSA by its conventional MIC alone.