Picosecond rotation of a ring-shaped optical lattice by using a chirped vortex-pulse pair.

A novel method of ultrafast rotation of a ring-shaped optical lattice in the picosecond time region was proposed and demonstrated. Our ring-lattice generator was assembled by a pair of linearly chirped pulses with a time delay, a high-order birefringent retarder, and an axially symmetric polarization element. Using a mode-locked Ti:sapphire laser oscillator as a light source, stable two-, four-, and six-petaled ring-lattice rotations were demonstrated with the rotation periods of 1.6, 3.2, and 4.8 ps, respectively. Our method has the potential to open up a new technique to resonantly excite propagating quasi-particles together with their coherent enhancement.

Preferential expression of cancer/testis genes in cancer stem-like cells: proposal of a novel sub-category, cancer/testis/stem gene.

Cancer/testis (CT) antigens encoded by CT genes are immunogenic antigens, and the expression of CT gene is strictly restricted to only the testis among mature organs. Therefore, CT antigens are promising candidates for cancer immunotherapy. In a previous study, we identified a novel CT antigen, DNAJB8. DNAJB8 was found to be preferentially expressed in cancer stem-like cells (CSCs)/cancer-initiating cells (CICs), and it is thus a novel CSC antigen. In this study, we hypothesized that CT genes are preferentially expressed in CSCs/CICs rather than in non-CSCs/-CICs and we examined the expression of CT genes in CSCs/CICs. The expression of 74 CT genes was evaluated in side population (SP) cells (=CSC) and main population (MP) cells (=non-CSC) derived from LHK2 lung adenocarcinoma cells, SW480 colon adenocarcinoma cells and MCF7 breast adenocarcinoma cells by RT-PCR and real-time PCR. Eighteen genes (MAGEA2, MAGEA3, MAGEA4, MAGEA6, MAGEA12, MAGEB2, GAGE1, GAGE8, SPANXA1, SPANXB1, SPANXC, XAGE2, SPA17, BORIS, PLU-1, SGY-1, TEX15 and CT45A1) showed higher expression levels in SP cells than in MP cells, whereas 10 genes (BAGE1, BAGE2, BAGE4, BAGE5, XAGE1, LIP1, D40, HCA661, TDRD1 and TPTE) showed similar expression levels in SP cells and MP cells. Thus, considerable numbers of CT genes showed preferential expression in CSCs/CICs. We therefore propose a novel sub-category of CT genes in this report: cancer/testis/stem (CTS) genes.

Dynamics of a paired optical vortex generated by second-harmonic generation.

We study the dynamics of a paired optical vortex (OV) generated by second-harmonic generation (SHG) using sub-picosecond pulses. By changing the position of a thin nonlinear crystal along the propagation direction, we observe a rotation of two vortices with changing separation distance. The dynamics is well explained by SHG with a beam walk-off, which introduces a contamination of zero-order Laguerre-Gaussian beam (LG(0)) together with topological charge doubling. The quantitative analysis indicates that the rotation angle of the OVs manifests the Gouy phase while the splitting provides the walk-off angle of the crystal. We also show that the subtraction of LG(0) is realized by the superposition of LG(0) with an anti-balanced phase in the pump.

Coherent transfer of orbital angular momentum to excitons by optical four-wave mixing.

We demonstrate the coherent transfer of optical orbital angular momentum (OAM) to the center of mass momentum of excitons in semiconductor GaN using a four-wave mixing (FWM) process. When we apply the optical vortex (OV) as an excitation pulse, the diffracted FWM signal exhibits phase singularities that satisfy the OAM conservation law, which remain clear within the exciton dephasing time (approximately 1ps). We also demonstrate the arbitrary control of the topological charge in the output signal by changing the OAM of the input pulse. The results provide a way of controlling the optical OAM through carriers in solids. Moreover, the time evolution of the FWM with OAM leads to the study of the closed-loop carrier coherence in materials.

A detailed deletion mapping of the short arm of chromosome 3 in sporadic renal cell carcinoma.

A detailed analysis of loss of heterozygosity in 40 sporadic renal cell carcinomas was performed by using 30 restriction fragment length polymorphism markers which were mapped on the short arm of chromosome 3. A total of 30 of 38 informative cases (79%) showed loss of heterozygosity at one or more loci. Two commonly deleted regions have been identified at 3p13-14.3 and 3p21.3. One of them (at 3p13-14.3) spans the breakpoint of the (3;8) translocation in hereditary renal cell carcinoma previously reported (A. J. Cohen et al., N. Engl. J. Med., 301:592-595, 1979). The second common region of deletion at chromosome 3p21.3 encompasses D3F15S2, at which a high incidence of loss of heterzygosity in renal cell carcinoma has been reported. In addition to the gene at 3p25 being responsible for the hereditary type of renal cell carcinoma in patients with von Hippel-Lindau disease, our results suggest that at least two tumor suppressor genes for sporadic renal cell carcinoma exist on the short arm of chromosome 3.

Allelotype of renal cell carcinoma.

Several recent studies based on restriction fragment length polymorphism analysis have supported the concept that the accumulation of multiple genetic alterations converts a normal cell to a malignant cell. Activation of oncogenes and/or inactivation of tumor suppressor genes have been observed during tumor progression in colorectal cancer, lung cancer, and breast cancer. To investigate the possibility that multiple genes are altered during the progression of renal cell carcinoma, we have used restriction fragment length polymorphism markers throughout the genome to test for loss of heterozygosity in 38 renal cell carcinomas. Nearly 64% of the tumors had lost heterozygosity on the short arm of chromosome 3. We also observed loss of heterozygosity averaging about 30% at informative loci on six other chromosomal arms (chromosomes 5q, 6q, 10q, 11q, 17p, and 19p). These results lead us to suspect the existence of several tumor suppressor genes associated with carcinogenesis of renal cell carcinoma.

Common regions of deletion on chromosomes 5q, 6q, and 10q in renal cell carcinoma.

Relatively frequent losses of heterozygosity on chromosomes 5q, 6q, and 10q, in addition to loss of heterozygosity on the short arm of chromosome 3, have been observed in renal cell carcinomas. As the first step toward isolation of tumor suppressor genes on these three chromosomal arms, we used six restriction fragment length polymorphism markers for 5q, nine for 6q, and eight for 10q to identify regions commonly deleted in a panel of 64 renal cell carcinomas. Allelic losses were common at chromosome 5q21, the region where the MCC (mutated in colorectal cancer) gene was recently identified; at chromosome 6q27; and at chromosome 10q21-23. Furthermore, as association was observed between accumulation of allelic losses on these three chromosomal arms and progression of tumors. Loss of heterozygosity on chromosome 5 showed a correlation with the histopathological grade of a given tumor and the incidence of distant metastasis.

Allelotype of human ovarian cancer.

In order to determine which chromosome(s) carries a tumor suppressor gene(s) for human ovarian cancer, we examined loss of heterozygosity in 37 tumors with a set of polymorphic DNA markers which cover each autosomal chromosome arm partially. Frequent losses were observed in chromosomes 4p (42%), 6p (50%), 7p (43%), 8q (31%), 12p (38%), 12q (33%), 16p (33%), 16q (38%), 17p (46%), 17q (39%), and 19p (34%). In addition to these chromosomes, frequent losses of alleles on chromosomes 6q, 13q, and 19q were observed uniquely in serous and serous papillary cystadenocarcinomas; loss of heterozygosity was detected only rarely on these chromosomal arms in nonserous types of tumors. The average (0.12) of fractional allelic loss seen in mucinous cystadenocarcinoma, which usually has a better prognosis than other types, was much lower than that of other tumor phenotypes including serous cystadenocarcinoma (0.31) and clear cell carcinoma (0.20). These results suggested that (a) a large number of tumor suppressor genes might play a role in ovarian cancer, (b) losses of alleles in different chromosomal regions could account for differences in histopathological features and/or prognoses among patients, and (c) this kind of analysis can contribute to an improved understanding of tumor development and/or progression in human ovarian cancer.

Minimally Invasive Laminate Veneers: Clinical Aspects in Treatment Planning and Cementation Procedures.

When a definitive aesthetic treatment is determined, it is crucial to grant the patient's wish with the necessary dental treatment. Thus, conservative treatments that are the solution to aesthetic problems involving morphologic modifications and provide the result that the patient expects should always be the first therapeutic option. In this context, ceramic laminate veneers, also known as "contact lens," are capable of providing an extremely faithful reproduction of the natural teeth with great color stability and periodontal biocompatibility. Minimal or no preparation veneers are heavily advertised as the answer to our patients' cosmetic needs, which they can be if they are used correctly in the appropriate case. This report is about ultraconservative restorations to achieve functional and aesthetic rehabilitation through treatment planning. Thus, clinicians should be aware that the preparation for laminate veneers remains within enamel, to ensure the bond strength and avoid or minimize the occurrence of postoperative sensitivity.

p16INK4a inactivation is not frequent in uncultured sporadic primary cutaneous melanoma.

In an attempt to examine whether the inactivation of p16INK4a is an important early event in the development of sporadic melanoma in vivo, we have systematically analysed 46 uncultured primary cutaneous melanomas. Loss of heterozygosity (LOH) of chromosome region 9p21-22 (where the p16INK4a resides) was detected in 11 tumours (24%) by PCR-based LOH analyses. Direct sequencing of all three exons of the p16INK4a gene in these 11 tumours revealed no somatic mutation although germline mutations which have not been reported previously as common polymorphisms were detected in two patients. Further sequencing analyses of the p16INK4a gene exon 2 in 19 additional tumours with no evidence of LOH on 9p21-22 identified only one heterozygous C- >T mutation at codon 81 altering a proline to a leucine. A sensitive methylation-specific PCR assay did not reveal de novo methylation of the 5'CpG island in exon 1 of the p16INK4a gene in any of the tumours showing 9p21-22 allelic loss or a heterozygous p16INK4a mutation. Complete loss of p16INK4a protein, most likely due to homozygous deletion of the p16INK4a gene, was observed in 6 (15%) out of 39 evaluable cases by immunohistochemical analyses on frozen sections using two different anti-p16INK4a antibodies. The results show that inactivation of p16INK4a is not as frequent in primary melanoma as has been reported in cell lines, and warrant further search for another tumour suppressor on 9p21-22. This study also emphasizes the importance of examining uncultured primary tumours rather than cell lines to define early events in tumorigenesis.

A complete deletion mutant of the Escherichia coli dnaKdnaJ operon.

Southern hydridization analyses of genomic DNAs from various dnaJ mutants of Escherichia coli showed that mutant K7052, which has well characterized dnaK706 and dnaJ705 double mutantions, is a deletion mutant. The deletion is about 8.0 kb long and encompasses the whole of the dnaKdnaJ operon.

Relations of preoperative hemodynamics and coronary blood flow to improved left ventricular function after valve replacement for aortic regurgitation.

In this study of the limits of reversibility of left ventricular function after aortic valve replacement for aortic regurgitation, measurements were made of pre- and postoperative coronary blood flow and left ventricular volumes. Eighteen patients who had undergone aortic valve replacement for pure aortic regurgitation using the Björk-Shiley valve or the Bicerval valve were restudied an average of 8 +/- 3 months after surgery. Postoperative left ventricular end-systolic and end-diastolic volumes returned to near normal values. The slight left ventricular wall thickening apparent before surgery remained unchanged after surgery and, consequently, left ventricular mass, though somewhat reduced, remained abnormally high. Ejection fraction, which was low preoperatively, returned to normal postoperatively. Total coronary sinus blood flow decreased after surgery, but coronary sinus blood flow per 100 g of left ventricular mass increased. This recovery of coronary flow per unit mass was believed to cause the improvement in left ventricular function. A significant correlation was found between postoperative systolic function and preoperative left ventricular end-systolic and end-diastolic volumes, wall thickness and, especially, left ventricular mass, the latter indicating that, if preoperative left ventricular mass is less than 350 g/m2, postoperative improvement of systolic function is attainable. Another significant correlation was indicated by measurements of coronary sinus blood flow per 100 g of left ventricular mass. If this is greater than 35 ml/min before surgery, a postoperative improvement in systolic function to within the normal range may be expected.

Clinical results and in vivo valve function after implantation of a Bicer valve prosthesis in the aortic position.

Between December 1981 and June 1987, 71 patients underwent aortic valve replacement with a Bicer monostrut tilting disc prosthesis. Clinical results and in vivo function of the artificial valve were assessed. The average age of the 71 patients at the time of operation was 51.3 +/- 11.5 years. The hospital mortality rate was 2.8% (two patients) and there were no further deaths during a mean (+/- SD) follow-up period of 2.4 +/- 1.6 years (range 1 month to 5.5 years) after surgery. There was also no occurrence of thromboembolism or valve dysfunction. Function of the Bicer valve prosthesis was assessed in 17 patients: 5 with a 21 mm valve, 7 with a 23 mm valve and 5 with a 25 mm valve. Examination was performed on average 10.3 +/- 8.1 months after surgery. Valve function was examined at rest and during exercise performed with a bicycle ergometer. Pressure gradients at rest were low: 21 mm valve = 8 mm Hg, 23 mm valve = 3 mm Hg and 25 mm valve = 2 mm Hg; the gradients during exercise were 11, 8 and 8 mm Hg, respectively. The valves had the following effective orifice area at rest: 21 mm valve = 1.54 cm2, 23 mm valve = 4.20 cm2 and 25 mm valve = 3.76 cm2; during exercise, the respective areas were 1.57, 3.48 and 3.01 cm2. These valves are deemed to be sufficiently wide for effective valve function. Aortographic observation indicated mild regurgitation that was within reasonable limits and posed no problem.(ABSTRACT TRUNCATED AT 250 WORDS)

[Bronchial artery embolization for treatment of mediastinal hemorrhage after pulmonary resection: report of a case].

We report a rare case of mediastinal hemorrhage after pulmonary resection. A 64-year-old woman with hypersensitivity pneumonitis was diagnosed as adenocarcinoma of the lung by bronchoscopical examination. Left lower lobectomy and mediastinal lymph node dissection were performed. Sudden chest pain and dry cough developed 14 days after the operation. Her diastolic pressure rose transiently but electrocardiogram remained normal. Chest X-ray showed widening of the mediastinum and enhanced chest computed tomography (CT) showed extravasation of the contrast media just under the bifurcation of the trachea. Multi projection volume reconstruction revealed mediastinal hemorrhage from the bronchial artery. The chest pain disappeared after a successful bronchial artery embolization and the patient discharged 21 days later. Hemorrhage after pulmonary resection is a common complication, but no previous report has described mediastinal hemorrhage occurring 2 weeks after the operation. In a similar case, bronchial artery embolization is a reliable and minimally invasive therapy for mediastinal hemorrhage.

Association of increased intracellular free Ca2+ by platelet-derived growth factor with mitogenesis but not with proteoglycan synthesis in chondrocytes--effect of suramin.

The effects of platelet-derived growth factor (PDGF) on the intracellular free Ca2+ concentration [( Ca2+]i) in chondrocytes were studied with a fluorescent Ca2+ indicator, fura 2, and compared with the effects of PDGF on mitogenesis and proteoglycan synthesis. PDGF evoked phasic and then tonic increase in [Ca2+]i dose-dependently in quiescent cultures of chondrocytes, and it also stimulated both DNA and proteoglycan syntheses dose-dependently similar to somatomedins. Suramin, which inhibits the interaction of PDGF with its receptors, caused dose-dependent inhibition of both the PDGF-evoked increase in [Ca2+]i and stimulation of DNA synthesis by PDGF. However, suramin rather enhanced the proteoglycan synthesis induced by PDGF without affecting the basal level of proteoglycan synthesis directly. These results suggest that [Ca2+]i may be an important signal for the action of PDGF on cell proliferation in chondrocytes, and that the initial signal for proteoglycan synthesis is different from that for DNA synthesis induced by PDGF after the activation of PDGF receptor.

Comparison of genetic profiles between primary melanomas and their metastases reveals genetic alterations and clonal evolution during progression.

To examine for the genetic basis of metastatic progression in cutaneous melanoma, we have compared loss of heterozygosity (LOH) of several selected chromosome regions that are implicated in the initiation and progression of melanoma, and alterations of the p16INK4a gene in 14 pairs of primary tumor and synchronous or asynchronous metastasis excised from the same patients. The most frequent genetic alteration during metastatic progression detected was the loss of p16INK4a protein expression (four of 14 cases), whereas no somatic p16INK4a gene mutations were found in any primary or metastatic tumors. LOH analyses showed that most of the chromosome losses including 6q, 8p, 9p, 9q, and 18q were shared between primary tumors and their metastases. Nevertheless, LOH of 6q and 11q and LOH of 7q not detected in primary tumors were, respectively, observed in two lymph node metastases. These results suggest that loss of p16INK4a protein expression (but not p16INK4a gene mutation) and the losses of chromosome arms 6q, 7q, and 11q play an important role in the acquisition of metastatic potential in sporadic melanoma. Furthermore, comparison of genetic profiles between the primary tumor and its metastasis revealed in several cases that heterogenous tumor cell populations might already exist at the early stage of tumorigenesis and evolve independently in the primary tumor and its metastasis, strongly suggesting that metastatic progression of sporadic melanoma is not accounted for by a linear progression model.

Adenylate cyclase activation and competitive binding with renal tissue using synthetic eel calcitonin analog and its fragments.

The structure-function relationship of calcitonin (CT) was investigated using a synthetic eel CT (E-CT) analog and its fragments. Adenylate cyclase activation and competitive binding to rat renal receptors were used as parameters of function. [Asu1,7]E-CT analog, synthesized by replacing the S-S bond of Cys1-Cys7 in the natural hormone with ethylene linkage of 1-amino suberic acid (Asu), and E-CT fragment 11-32 had about 1/5th and 1/50th the potencies of synthetic E-CT, respectively, in both adenylate cyclase activation and competitive inhibition of 125I-labeled [Asu1,7]iodo-E-CT binding on rat renal plasma membranes. The minimal chain length required to activate adenylate cyclase in rat renal plasma membranes was between 12-18 amino acids, and the minimal chain length required to affect the CT receptor binding was between 6-12 amino acids, near the C-terminus. Fragments, including the C-terminus, show a disproportionate and potent inhibition of the binding compared with the potency required for adenylate cyclase activation. Thus, the amino acid sequence near the C-terminus probably plays an important role in the binding of CT to the receptor. (Endocrinology 108: 698, 1981.)

Circulating 1,25-dihydroxyvitamin D concentrations in patients with renal cell carcinoma-associated hypercalcemia are rarely suppressed.

We measured serum 1,25-dihydroxyvitamin D concentrations in 18 patients with renal cell carcinoma-associated hypercalcemia. Only 2 patients (11%) had low serum 1,25-dihydroxyvitamin D (less than 15 pg/ml) levels, and the mean 1,25-dihydroxyvitamin D level in the 18 patients was 44 +/- 30 (+/- SD) pg/ml, not different from the value of 42 +/- 22 pg/ml in 75 age-matched normocalcemic patients with various malignancies. Eighty-seven percent (26 of 30) of the hypercalcemic patients with extensive skeletal metastases due to other malignancies or with hematological malignancies had suppressed serum 1,25-dihydroxyvitamin D levels (less than 15 pg/ml). In hypercalcemic patients with other malignancies and no skeletal metastases, only 54% (21 of 39) had low serum 1,25-dihydroxyvitamin D levels. The mean serum 1,25-dihydroxyvitamin D level in the latter group was 21 +/- 26 pg/ml, significantly lower than that in normocalcemic patients. In renal cell carcinoma-associated hypercalcemia, suppression of circulating 1,25-dihydroxyvitamin D concentrations is uncommon.

Converting enzyme inhibitor improves forearm reactive hyperemia in essential hypertension.

Endothelial function is known to be impaired in essential hypertensive patients. In this study, we examined whether antihypertensive drugs improve forearm vasodilatory response to reactive hyperemia in 26 patients with essential hypertension (62 +/- 2 years) without diabetes mellitus, hyperlipidemia, coronary heart disease, or cerebrovascular disease. Antihypertensive drugs were never given or were discontinued for at least 4 weeks before the study. Patients were treated with monotherapy of either temocapril (2 or 4 mg, n = 15) or amlodipine (2.5 or 5 mg, n = 11) for 6 months. Forearm blood flow was measured by strain-gauge plethysmography. Vasodilator response to the release of upper arm compression at 300 mm Hg for 5 minutes and to sublingual administration of nitroglycerin (0.3 mg) were assessed. Changes of forearm blood flow response to reactive hyperemia were significantly less in hypertensive patients (99 +/- 18%) than in age-matched normotensive control subjects (150 +/- 22%, P < .01, n = 39). Blood pressure (mm Hg) was similarly decreased by the treatment with temocapril (160 +/- 4/94 +/- 2 to 139 +/- 3/83 +/- 3, P < .001) or amlodipine (165 +/- 5/94 +/- 3 to 141 +/- 4/82 +/- 3, P < .001). Response to nitroglycerin was not changed by either drug. Forearm vasodilatory response to reactive hyperemia was improved by temocapril (102 +/- 20% to 168 +/- 25%, P < .01) but not by amlodipine (97 +/- 16% to 114 +/- 14%, NS). These results indicate that the treatment with the angiotensin-converting enzyme inhibitor temocapril improved forearm vasodilatory response to reactive hyperemia, suggesting its beneficial effect on endothelial function.