Comparison of 3.0-and 1.5-tesla diffusion-weighted imaging in the visibility of breast cancer

Purpose The aim of this study was to compare diffusion-weighted imaging (DWI) at 3.0 T and 1.5 T by evaluating the apparent diffusion coefficient (ADC) value and visibility of breast cancer in the same patients. Materials and methods A total of 13 patients (16 lesions) with breast cancer underwent DWI at 3.0 T and 1.5 T. Tumors were classified into two groups based on the lesion size. The ADC values were measured, and visibility of the tumors was scored blindly. Results No significant difference was found for ADC values between 3.0 T and 1.5 T in either group (P > 0.05). All of the large lesions were visible clearly at both magnetic field strengths, and image scores were not different (P > 0.05). In contrast, small lesions were more clearly visible and had better image scores at 3.0 T than at 1.5 T (P < 0.001). Conclusion Small cancers were more clearly visible on DWI at 3.0 T than 1.5 T.     

Segmental enhancement on breast MR images: differential diagnosis and diagnostic strategy

The histopathological variations of segmental enhancement on breast magnetic resonance imaging (MRI) were investigated, with the aim of identifying imaging characteristic clues to their differential diagnosis. We reviewed 70 breast MRI examinations demonstrating segmental enhancement, classified them based on their histopathology, and assessed their MRI findings as follows: (1) confluent or not confluent, (2) late enhancement pattern, and the absence or presence of (3) clustered ring enhancements and (4) surrounding high signal intensity (SI) on T2-weighted imaging. Thirteen lesions (18.5%) were benign, eight (11.5%) were high risk, 25 (36%) were ductal carcinoma in situ (DCIS) and 24 (34%) were infiltrating mammary carcinomas (IMC). Clustered ring enhancements were demonstrated in 74% of malignancies (high risk, DCIS and IMC) but no benign lesions (P = 0.0001). The surrounding high SI on T2-weighted imaging was seen in four of five IMC with marked lymphatic involvement. Clustered ring enhancement was not demonstrated in six of seven IMC of tubular and/or lobular types. Segmental enhancement was seen in not only DCIS but also IMC, high-risk and benign lesions. Clustered ring enhancement and surrounding high SI on T2-weighted imaging were clues to their differential diagnosis and helpful to decide their diagnostic strategy.     

Mechanical stimulation improves survival in random-pattern skin flaps in rats

This was a study on the effects of 3-MHz ultrasound at 16- and 100-Hz pulse repetition frequencies on angiogenesis and viability of random-pattern skin flaps in rats. A cranially-based dorsal skin flap was raised in 60 EPM-Wistar rats, which were randomly divided into four groups: control, sham, 16-Hz and 100-Hz groups. The mean percentage of necrosis was as follows: control, 42% ± 13%; sham, 18% ± 13%; 16-Hz group, 13% ± 10%; and 100-Hz group, 15% ± 7%, with significant differences between the control and the other groups (p < 0.001). The mean vascular density was as follows: control, 5% ± 2%; sham, 7% ± 2%; 16-Hz group, 21% ± 4%; and 100-Hz group, 24% ± 10%, with significant differences between control and ultrasound groups, and between the sham and ultrasound groups (p < 0.001). Both ultrasound treatments (16- and 100-Hz PRFs) induced angiogenesis, and sham and ultrasound treatments improved viability of random-pattern skin flaps in rats.     

Origin and Molecular Evolution of the Determinant of Methicillin Resistance in Staphylococci

Methicillin-resistant Staphylococcus aureus (MRSA) is one of the most important multidrug-resistant pathogens around the world. MRSA is generated when methicillin-susceptible S. aureus (MSSA) exogenously acquires a methicillin resistance gene, mecA, carried by a mobile genetic element, staphylococcal cassette chromosome mec (SCCmec), which is speculated to be transmissible across staphylococcal species. However, the origin/reservoir of the mecA gene has remained unclear. Finding the origin/reservoir of the mecA gene is important for understanding the evolution of MRSA. Moreover, it may contribute to more effective control measures for MRSA. Here we report on one of the animal-related Staphylococcus species, S. fleurettii, as the highly probable origin of the mecA gene. The mecA gene of S. fleurettii was found on the chromosome linked with the essential genes for the growth of staphylococci and was not associated with SCCmec. The mecA locus of the S. fleurettii chromosome has a sequence practically identical to that of the mecA-containing region (∼12 kbp long) of SCCmec. Furthermore, by analyzing the corresponding gene loci (over 20 kbp in size) of S. sciuri and S. vitulinus, which evolved from a common ancestor with that of S. fleurettii, the speciation-related mecA gene homologues were identified, indicating that mecA of S. fleurettii descended from its ancestor and was not recently acquired. It is speculated that SCCmec came into form by adopting the S. fleurettii mecA gene and its surrounding chromosomal region. Our finding suggests that SCCmec was generated in Staphylococcus cells living in animals by acquiring the intrinsic mecA region of S. fleurettii, which is a commensal bacterium of animals.The first methicillin-resistant Staphylococcus aureus (MRSA) isolate was reported in England in 1961, soon after the introduction of methicillin (10). Since then, it has become an important pathogen in both health care settings and communities around the world (27). MRSA is generated when methicillin-susceptible S. aureus (MSSA) exogenously acquires a staphylococcal cassette chromosome mec (SCCmec) (9). SCCmec has been identified not only in S. aureus but also in other coagulase-positive and coagulase-negative staphylococci (8). SCCmec is speculated to be transmissible among staphylococcal species as a mobile element; however, its origin/reservoir has not been clarified yet (7). Finding the origin/reservoir of the mecA gene is important for understanding the evolution of MRSA. Moreover, it may contribute to more effective control measures for MRSA. There are various types and subtypes in SCCmec, but they are made up of the following two essential components: (i) the mec gene complex, containing the mecA gene encoding the penicillin-binding protein 2′ (PBP2′) with reduced affinity to beta-lactam antibiotics, and (ii) the ccr gene complex, encoding site-specific recombinase(s) for the movement of the element. By the action of ccr gene-encoded recombinases, SCCmec is excised from the chromosome and site-specifically integrated at the 3′ end of orfX (11), an open reading frame (ORF) of unknown function, which is located near the replication origin (oriC) on the chromosome (13). A large number of SCCmec elements have been sequenced and classified according to the combination of types of mec and ccr gene complexes (8). Although nucleotide diversity of ccr genes identified in various Staphylococcus species has been reported, mecA genes contained in SCCmec are almost identical regardless of the Staphylococcus species carrying them (8). mec gene complexes are classified into 4 classes (classes A, B, C, and D) by the presence or absence of certain insertion sequences (ISs) in the mecR1 gene, but all mec gene complexes contained IS431mec (also called IS431R) downstream of the mecA gene (Fig. ​(Fig.1)1) (8, 12). The class A mec gene complex is regarded as the prototypic structure, having the gene order IS431mec-mecA-mecR1-mecI. Class B, C, and D mec gene complexes are considered to be derived from the class A mec gene complex (8, 12). The region between the mecA gene and IS431mec is called a hypervariable region (HVR) (19), which can be used for genotyping of MRSA strains (21). The HVR contains a truncated mvaS gene encoding the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) synthase, a varied number of direct repeat units (DRUs) that is responsible for the length polymorphism of the mec gene complex (19), an intact ugpQ gene encoding glycerophosphoryl diester phosphodiesterase, and an intact maoC gene encoding the acyl dehydratase MaoC (Fig. ​(Fig.1).1). Some strains, however, lack some of the above-mentioned constituents of the HVR (16, 24).Open in a separate windowFIG. 1.Basic structure of the representative mec gene complex. The class A mec gene complex is composed of intact mecR1 and mecI, encoding the signal transducer and repressor for the mecA gene, respectively, upstream of the mecA gene without integration of an IS element. The class B and C mec gene complexes have ψIS1272 and IS431L integrated in mecR1, respectively, which results in the partial deletion of mecR1 and complete deletion of the mecI genes. Class D has no IS element, but a part of mecR1 and complete mecI genes are deleted. All mec gene complexes contained IS431mec (also called IS431R) downstream of the mecA gene.In staphylococci, previously, two mecA gene homologues with 80% and 91% nucleotide identities have been found in Staphylococcus sciuri and Staphylococcus vitulinus species, respectively (5, 22). The mecA gene homologue of S. sciuri has been considered to have a ubiquitous presence among its species and to be the evolutionary precursor of the mecA gene (5, 32). However, the mecA gene homologues found in their chromosomes were not the constituents of the mec gene complex or SCCmec. We speculated that the origin/reservoir of the mecA gene would be found in a staphylococcal species closely associated with S. sciuri and S. vitulinus. These species belong to the S. sciuri species group among the genus Staphylococcus. The group is composed of the following four species, which are resistant to novobiocin and catalase production and coagulase nonproduction: S. sciuri, S. vitulinus, Staphylococcus lentus, and Staphylococcus fleurettii (20, 25, 29, 30). They are usually isolated from a variety of animals and food products of animal origin and not frequently isolated from humans (20, 23, 25, 29, 30).We isolated staphylococcal strains of the S. sciuri species group from an animal source, tested for the presence of the mecA gene and its homologues, and determined the nucleotide sequences of the chromosome regions around the mecA gene and its homologues.     

Fetal goitrous hypothyroidism due to maternal thyroid stimulation-blocking antibody: a case report

Most fetal goitrous hypothyroidisms are reportedly caused by the maternal use of an antithyroid drug or fetal dyshormonogenesis. However, fetal goitrous hypothyroidism due to the transplacental passage of maternal thyroid stimulation-blocking antibody (TSBAb) is extremely rare. A woman at 28 weeks of gestation was found to have a fetal goiter by ultrasonography. Because the maternal serum showed hypothyroidism with an elevated titer of TSBAb, levothyroxine sodium was administered. The patient delivered a male infant, 3,412 g, with a goiter at term. Umbilical blood revealed primary hypothyroidism with increased TSBAb, and the infant was given levothyroxine sodium. After a month, neonatal thyroid function and TSBAb levels became normal. Attention should be paid to possible fetal hypothyroidism when a fetal goiter is observed to avoid impaired mental development of the neonate.     

E‐selectin targeting to visualize tumorsin vivo

Generally angiogenic factors induce the expression of E‐selectin in vascular endothelial cells in the tumors. In this study, we employed an anti‐E‐selectin monoclonal antibody to target tumors in vivo and evaluated an optical imaging reagent to visualize tumor regions. The anti‐E‐selectin antibody was conjugated on the surface of liposomes, which encapsulated the near‐infrared fluorescent substances Cy3 or Cy5.5. The liposomes efficiently recognized human umbilical vein endothelial cells only when E‐selectin was induced by angiogenic factors such as TNF‐α in vitro. Cy5.5 encapsulated into liposomes that were conjugated with an anti‐E‐selectin antibody successfully visualized Ehrlich ascites tumor cells when transplanted into mice. Thus, E‐selectin targeting with liposomes containing a near‐infrared fluorescent dye was found effective in visualizing tumors in vivo. This strategy should be extremely useful as a method to identify sentinel lymphatic nodes and angiogenic tumors as well as use for drug delivery to tumor cells. Copyright © 2010 John Wiley & Sons, Ltd.     

Pulmonary artery calcification in contact with a left coronary artery bypass graft: An X-ray computed tomographic study

Calcification in the pulmonary artery (PA) occurs in rare cases. There have been no studies of calcification in the PA at the site of its contact with a left coronary artery bypass graft (CABG). In the present study, X-ray computed tomography (CT) was employed for examination of such calcification. The subjects were 53 patients (49 male and 4 female, mean age of 56.7 years) who underwent 74 left CABGs (69 saphenous veins and five internal thoracic arteries). Following surgery, non-contrasted CT was performed from the lower level of the aortic arch to the lower boundary of the left ventricle at 5-mm horizontal intervals, and contrasted CT was performed at the level of the PA; this procedure was repeated at approximately six-month intervals after the operation. In addition, aortography and selective graft angiography were carried out at 7.6 months post-operatively. The inner diameter of the grafts and the levels of serum cholesterol were also examined. Calcification in the PA was detected in 24 cases (all of them saphenous vein grafts), but graft angiography found no stenosis in those sites. Calcification size varied from 1 mm to 14 mm, with 10 of the cases at or exceeding 10 mm and showing high density. Only three of the cases enlarged with time. Calcification appeared at 2.9 to 54.3 months postoperatively and the mean time of onset was 10.0 ± 15.7 months. The mean age of the patients with PA calcification was 58.7 ± 5.9 years while that of the patients without calcification was 57.3 ± 10.0 years. Graft diameter was 5.9 ± 1.9 mm in the former group and 5.6 ± 1.7 mm in the latter. Serum cholesterol level was 235 ± 32 mg/dl in the former group and 243 ± 42 mg/dl in the latter. There were three cases of occlusion in the calcification group, and four in the other. There were no significant intergroup differences in these four parameters. The incidence of CT-detected calcification in the PA was found to be high at its point of contact with saphenous vein grafts.A working version of this report was presented in part at the 41st Annual World Congress of the International College of Angiology, Sapporo, Japan, July 1999.     

An epidemiological study regarding the hearing acuity of residents in the area with high level of aircraft noise: results of hearing tests conducted in the vicinity of Kadena Air Base]

Hearing tests, primary and secondary, were conducted in two communities vicinal to Kadena US Air Base in Okinawa from May 1996 to July 1998. The noise exposure expressed in WECPNL as designated by the Defense Facilities Administration Agency ranged from 85 to 95 and above. A total of 2035 subjects aged between 25 and 69 years inclusive were considered eligible for inclusion in this study and among them 137 males and 206 females underwent the primary test. Before the test, subjects were asked about hearing difficulty, tinnitus, otological anamnesis and past experience of noise exposure at work and/or hobbies. The primary test was a pure tone audiometry using the ascending method of limits with 5 dB step at 7 test frequencies of 0.5 to 8 kHz. Forty individuals who were judged to have possible noise induced hearing loss were sent to Okinawa Chubu Hospital as subjects for the secondary test. The secondary test consisted of pure tone audiometry with 1 dB step at 9 test frequencies with the addition of 3 kHz and 6 kHz to the primary test frequencies, a Short Increment Sensitivity Index (SISI), test, tympanometry and audioscan audiometry. Based on test findings 12 subjects were considered to have noise induced hearing loss. The examiners interviewed the 12 subjects again to confirm that they had not experienced habitual or repeated intense noise exposure other than aircraft noise exposure around their homes. The geographical distribution of the subject's residences showed their proximity to the airfield, which strongly suggests that the cause of hearing loss may be exposure to aircraft noise from Kadena Air Base.     

Nonbacterial thrombotic endocarditis complicated with stage Ia ovarian cancer

Nonbacterial thrombotic endocarditis (NBTE) commonly occurs in advanced malignancies associated with a cancer-related hypercoagulable state, but the prevalence of NBTE in patients with less advanced malignancies is unknown. A 46-year-old woman had multiple thromboembolic events and disseminated intravascular coagulation on admission. Transthoracic echocardiography showed several growths on the mitral valve. Pelvic magnetic resonance imaging revealed a rapidly enlarging large tumor. In spite of anticoagulation therapy, she died 1.5 months after admission. At autopsy, NBTE with stage Ia ovarian cancer was diagnosed. In cases of higher-growth rate tumors with abundant necrosis, NBTE may occur in early-stage (even in stage Ia) ovarian cancer. In the majority of stage Ia ovarian cancers, curative surgical resection can be done. Prognostic improvement may be gained by such positive intervention, although this depends on the patient’s general condition when NBTE occurs. With tumor resection, there is a possibility that the patient will recover from the hypercoagulable state and a poor outcome will be avoided.     

Primary osteosarcoma of ovary

Primary osteosarcoma originating from the ovary is an exceedingly rare, highly malignant tumor. Only a few cases have been reported in the past few decades. We describe a 50-year-old postmenopausal woman who presented with a large abdominal mass. The clinical diagnosis was malignant ovarian cancer. Her disease was aggressive; she had no response to systemic chemotherapy and died within 1 month of presentation. A definitive diagnosis of primary ovarian osteosarcoma was made by histopathological examination of autopsy specimens. Although rare, primary ovarian osteosarcoma should be considered in the differential diagnosis of a large, rapidly progressing pelvic mass in a postmenopausal woman. Early diagnosis provides hope of a complete surgical resection, which is currently the only promising treatment.