Design of photonic-crystal surface-emitting lasers with enhanced in-plane optical feedback for high-speed operation.

Photonic-crystal surface-emitting lasers (PCSELs) use the two-dimensional (2D) resonance at the band-edge of a photonic crystal for lasing, and they feature various outstanding functionalities such as high-brightness lasing, arbitrary shaping of beam patterns and on-chip 2D beam steering. In this paper, to investigate the applicability of PCSELs for high-speed operation, we design PCSELs with enhanced in-plane optical feedback, which enable single-mode lasing inside a circular region the diameter of which is less than 10 µm. To realize a strong in-plane confinement of the lasing mode, we increase the one-dimensional coupling coefficients between counter-propagating waves through the careful design of the lattice points. We also introduce an in-plane heterostructure composed of two photonic crystals with different photonic bandgaps and utilize reflection at the boundary of the two photonic crystals in addition to the optical feedback at the band-edge of each photonic crystal. By using three-dimensional finite-difference time-domain method (3D-FDTD), we confirm that the proposed hetero-PCSELs can achieve single-mode lasing operation inside a 9-µm-diameter and possibly realize a 3-dB modulation bandwidth larger than 40 GHz.

Monitoring the build-up of hydrogen polarization for polarized hydrogen-deuteride (HD) targets with nuclear magnetic resonance (NMR) at 17 T.

We report on the frozen-spin polarized hydrogen-deuteride (HD) targets for photoproduction experiments at SPring-8/LEPS. Pure HD gas with a small amount of ortho-H2 (∼0.1%) and a very small amount of para-D2 (∼0.001%) was liquefied and solidified by liquid helium. The temperature of the produced solid HD was reduced to about 30 mK with a dilution refrigerator. A magnetic field (17 T) was applied to the HD to grow the polarization with the static method. After the aging of the HD at low temperatures in the presence of a high-magnetic field strength for three months, the polarization froze. Almost all ortho-H2 molecules were converted to para-H2 molecules. Most remaining para-D2 molecules were converted to ortho-D2 molecules. The para-H2 and ortho-D2 molecules exhibited weak spin interactions with the HD. If the concentrations of the ortho-H2 and para-D2 were reduced appropriately at the beginning of the aging process, the aging time can be shortened. We have developed a new nuclear magnetic resonance (NMR) system to measure the relaxation times (T1) of the 1H and 2H nuclei with two frequency sweeps at the respective frequencies of 726 MHz and 111 MHz and succeeded in the monitoring of the polarization build-up at decreasing temperatures from 600 mK to 30 mK at 17 T. Automatic NMR measurements with the frequency sweeps enabled us to omit the use of a manual tuning circuit and to remove magnetic field sweeps with eddy current heat. This technique enables us to optimize the concentration of the ortho-H2 and to efficiently polarize the HD target within a shortened aging time.

Antibody-like proteins that capture and neutralize SARS-CoV-2.

To combat severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) and any unknown emerging pathogens in the future, the development of a rapid and effective method to generate high-affinity antibodies or antibody-like proteins is of critical importance. We here report high-speed in vitro selection of multiple high-affinity antibody-like proteins against various targets including the SARS-CoV-2 spike protein. The sequences of monobodies against the SARS-CoV-2 spike protein were successfully procured within only 4 days. Furthermore, the obtained monobody efficiently captured SARS-CoV-2 particles from the nasal swab samples of patients and exhibited a high neutralizing activity against SARS-CoV-2 infection (half-maximal inhibitory concentration, 0.5 nanomolar). High-speed in vitro selection of antibody-like proteins is a promising method for rapid development of a detection method for, and of a neutralizing protein against, a virus responsible for an ongoing, and possibly a future, pandemic.

Influence of palatal surface shape of dentures on food perception.

The purpose of this study was to clarify the influence of the palatal surface shape of dentures on food perception. Eighteen healthy dentulous subjects (mean age, 24 years) were investigated. Four types of experimental plate were used: (i) a tailor-made plate, (ii) an average-model plate, (iii) a smooth plate, and (iv) a wrinkle plate. Test foods consisted of Bavarian cream cubes containing one to three mustard seeds and six raw carrot pieces of different shapes. Bavarian cream cubes with three seeds were used for analysis. Other foods were used as dummy foods. Subjects were required to wear experimental plates and press test foods placed on the anterior area of the tongue against the experimental plates. We measured time required to perceive number of spherical bodies, rate of correct answers, and level of perception with each type of experimental plate using a 100-mm visual analogue scale. The results showed a significant difference in response time between the average-model plate and the other experimental plates, with response time longest for the average-model plate. On the other hand, no significant differences in rate of correct answers regarding number of spherical bodies or level of perception were found among the experimental plates. When incisive papilla, palatine suture and palatal rugae based on the standard Japanese shape were replicated on the palatal surface of the plates, the time required for food perception during ingestion was prolonged in comparison to plates with other palatal surface shapes.

Morphological and molecular changes in denture-supporting tissues under persistent mechanical stress in rats.

The purpose of this study was to determine the effects of mechanical compression on the palatal mucosa using an experimental palatal base. The palatal base was either pressed onto (stress group) or not pressed onto (fit group) rat palatal mucosa. Blood flow was measured and the animals were sacrificed 6-72 h later for analysis. The expression of heat shock protein 70 (HSP70), vascular endothelial growth factor (VEGF) and proliferation cell nuclear antigen (PCNA) was characterized by immunohistochemical staining. For morphometric analysis, connective tissues were divided into bone side and epithelial side tissues. The ratio of PCNA-positive cells (PCNA score) was calculated, and the expressions of mRNA encoding HSP70 and VEGF was evaluated. Whereas blood flow in the stress group showed ischaemia, none was found in the fit group. Proliferation cell nuclear antigen scores on the bone side were higher than on the epithelial side in the stress group (P < 0.05). Heat shock protein 70- and VEGF-positive cells were observed under compression conditions, particularly in the periosteum. In the stress group, the expressions of mRNA encoding HSP70 and VEGF were highest at 12 h (P < 0.05). These results suggest that mechanical compression of the palatal plate induces ischaemia, and that cells in the underlying denture-supporting tissue, which includes the periosteum, synthesize HSP70 and VEGF to maintain homeostasis under these conditions.

Frequent p53 gene mutations in blast crisis of chronic myelogenous leukemia, especially in myeloid crisis harboring loss of a chromosome 17p.

We investigated chromosome alterations and mutations of the p53 gene in 118 samples from 92 patients with chronic myelogenous leukemia in various clinical phases, i.e., chronic phase, accelerated phase, and blast crisis (BC). Single-strand conformation polymorphism analysis and subsequent nucleotide sequencing disclosed no alteration of the p53 gene in chronic phase (no mutation in 80 samples), while five of 31 BC samples showed point mutations: four in myeloid and one in lymphoid crisis. One of seven accelerated phase samples also showed a p53 gene mutation. Ten of 31 BC samples showed loss of one of the short arms of chromosome 17 (17p) through the formation of isochromosome 17q, i(17q), or unbalanced translocations. Loss of heterozygosity at the p53 locus in the accelerated phase and BC was detected only in two cases with i(17q) but not in seven cases with normal chromosome 17 homologues, suggesting that loss of one p53 allele is rare without cytogenetically detectable loss of a 17p. Among those six samples with p53 gene mutations, five showed loss of a 17p cytogenetically, and only one lymphoid crisis case exhibited normal chromosome 17 homologues. Thus, mutations of the p53 gene were closely associated with myeloid crisis with loss of a 17p (four mutations in ten samples), in contrast to myeloid crisis with normal chromosome 17 homologues (zero in 13) or lymphoid crisis (one in seven). Our results also suggest that alterations of the p53 gene might occur after loss of a 17p during the course of chronic myelogenous leukemia.

Beta-catenin mutations are frequent in hepatocellular carcinomas but absent in adenomas induced by diethylnitrosamine in B6C3F1 mice.

Activating mutations in the region of the beta-catenin gene corresponding to the NH2-terminal phosphorylation sites of glycogen synthetase kinase 3beta have been causally implicated in carcinogenesis. In this study, the beta-catenin exon 3 was examined in hepatic lesions induced by diethylnitrosamine in B6C3F1 mice. PCR and DNA sequencing detected seven beta-catenin mutations in 13 samples dissected from hepatocellular carcinoma tissues, but none in 14 hepatic adenomas. All of the mutations were found in codon 41 encoding a threonine residue, one of the possible glycogen synthetase kinase-3beta phosphorylation sites. Although beta-catenin protein was immunohistochemically stained mainly on the cell membrane in preneoplastic hepatocytic foci and most adenomas, as observed in normal hepatocytes, it was detected in the cytoplasm and nuclei in addition to the cell membrane, indicating stabilization of the protein in HCCs. This shift in staining was observed not only in tumors with mutations, but also in examples lacking exon 3 mutations. Our data demonstrate that beta-catenin alterations may be important for malignant progression during multistep hepatic carcinogenesis in mice.

Lymph node metastasis is associated with allelic loss on chromosome 13q12-13 in esophageal squamous cell carcinoma.

Allelotype analysis of whole chromosomes showed that loss of heterozygosity (LOH) on 13q was exclusively associated with lymph node metastasis and poor prognosis in esophageal squamous cell carcinoma (ESC). To identify a locus responsible for lymph node metastasis, we performed fine deletion mapping on 13q by analyzing 60 ESCs with 18 polymorphic markers. Allelic loss was observed with at least one marker in 34 tumors (56.7%), and lymph node metastasis was significantly correlated with LOH (P = 0.0053). We found frequent loss at D13S260 (43.7%), D13S171 (38.6%), and D13S267 (43.6%) on 13q12-13. Among these markers, LOH at D13S171 showed a significant correlation with lymph node metastasis (P = 0.0441). Because these markers flank the BRCA2 gene, we intensively examined a mutation of the gene through all coding exons and exon-intron junctions by PCR-single-strand conformational polymorphism analysis under two different assays. We found only seven nucleotide substitutions as normal polymorphic changes; tumor-specific mutations were not detected, and loss of expression was not observed, indicating that the BRCA2 gene might not be a target of allelic loss in this region. Relatively frequent LOH was also found at the RB1 locus (34.7%), but a significant correlation with lymph node metastasis was not observed (P = 0.7430). Protein expression of RB1 was examined in 31 ESC cell lines, and loss of expression was infrequent (6.5%), indicating that inactivation of the RB1 gene might not be responsible for lymph node metastasis. Taken together, allelic loss at 13q12-13 of the primary ESC was closely associated with lymph node metastasis, and unidentified tumor suppressor gene(s) in this region might be involved.

Deletion of 17p and amplification of the int-2 gene in esophageal carcinomas.

We have analyzed allelic deletion at 23 loci on 18 different chromosomes in 35 esophageal squamous cell carcinoma tissues by using restriction fragment length polymorphism markers. Loss of heterozygosity was detected on chromosomes 2, 3, 6, 7, 11-14, 16-18, 21, and 22, while no loss was detected on chromosomes 1, 4, and 8-10. Only the loss of chromosome 17p was detected with high frequency (45%), and losses on other chromosomes had frequencies of less than 22%. These losses with low frequencies might be random losses caused by chromosomal rearrangement during the course of tumor development and progression. On the contrary, the loss of 17p might play an important role in the development of esophageal squamous cell carcinoma, such as inactivation of a tumor suppressor gene. Amplification of the int-2 gene was observed in 39% of the tumors. However, no significant relationship between int-2 amplification and the deletion of any chromosome was detected.

Allelotype analysis of esophageal squamous cell carcinoma.

In previous studies, we have shown that allelic loss on chromosome 17p, on which the p53 gene is located, is very frequent, and loss-of-function mutations of the p53 gene are closely associated with the tumorigenesis of esophageal cancer. In this study, we performed allelotype analysis to investigate whether other tumor suppressor genes are also involved in esophageal cancer. Using 55 polymorphic DNA markers covering every autosomal arm except 13p, 21p, and 22p, restriction fragment length polymorphism analysis was performed on 36 esophageal squamous cell carcinomas (ESCs) and their adjacent normal tissue samples. Frequent loss of heterozygosity (LOH) of > 30% of the informative cases was observed on chromosomes 3p (41.1%), 5q (52.6%), 6p (30.4%), 8p (33.3%), 9p (35.7%), 9q (30.8%), 11p (32.4%), 13q (52.7%), 17p (55.2%), 17q (33.3%), 18q (45.7%), and 19q (30.4%). Among these, LOH on 5q, 13q, 17p, and 18q was previously reported in ESC and is considered to involve the APC, RB, p53, and DCC genes, respectively. However, our deletion analysis of chromosome 18q revealed that the region commonly lost did not include the DCC locus, suggesting that a possible tumor suppressor gene on 18q other than the DCC gene is involved in ESC. We screened 60 primary ESC tumors and 20 cultured ESC cell lines for the mutation of the APC gene within a mutation cluster region in exon 15, where the "hot spot" of somatic mutation for colorectal and pancreatic cancers is thought to be. We could not find any mutation despite the high frequency of LOH on chromosome 5q. We also analyzed the relationship between the clinicopathological data and the allelic loss and found that LOH on chromosomes 6p and 13q was associated with poor prognosis.

Role and mutational heterogeneity of the p53 gene in hepatocellular carcinoma.

The mutational spectrum of the p53 gene was analyzed in 53 hepatocellular carcinomas. Somatic mutations of the p53 gene were detected in 17 cases (32%). Among these 17 mutations, 9 were missense mutations; the mutations in the other 8 cases were nonsense mutations, deletions, or mutations at the intron-exon junctions. These mutations were found in a wide region stretching from exon 4 to exon 10 without any single mutational hot spot. G:C to T:A transversions were predominant, suggesting the involvement of environmental mutagens in the mutagenesis of the p53 gene in a subset of the hepatocellular carcinoma cases. Mutations of the p53 gene occurred frequently in advanced tumors, although several tumors in the early stages also showed mutations. A deletion map of chromosome 17 was constructed by using 10 polymorphic probes and was compared with the p53 gene mutation in each case. Loss of heterozygosity (LOH) on chromosome 17p was observed in 49% of the cases (24 of 49), and two commonly deleted regions were detected (around the p53 locus and at 17p13.3 to the telomere). Sixteen of the 17 cases with p53 gene mutations showed LOH around the p53 locus, and mutations were rare in hepatocellular carcinomas without LOH. However, no mutations were detected in 8 cases with LOH on 17p, suggesting the possibility that an unidentified tumor suppressor gene(s) located on 17p may have also been involved in hepatocarcinogenesis.

Chromosomal reorganization for the expression of recessive mutation of retinoblastoma susceptibility gene in the development of osteosarcoma.

Recent evidence indicates that the mutation of retinoblastoma susceptibility (RB) gene is also involved in the development of osteosarcoma. We studied 30 cases of osteosarcoma for the structural anomalies of the RB gene by Southern hybridization analysis with cDNA probes of the RB gene. Thirteen cases (43%) showed structural anomalies of the RB gene. They included the total or partial deletion, or rearrangement of the RB gene; seven with homozygous deletions and six with hemizygous deletions or rearrangements. By the use of restriction fragment length polymorphism fragments as chromosome markers, those seven tumors having homozygous deletions and four of six tumors having hemizygous anomalies showed the loss of heterozygosity at other loci on chromosome 13. Among those tumors with no apparent structural changes of the RB gene, seven cases showed the loss of heterozygosity on chromosome 13, and altogether the loss of heterozygosity by either homozygosity or hemizygosity was found in 18 (64%) of 28 informative cases. The loss of heterozygosity was also found for nine of 10 other chromosomes, of which chromosome 17 showed the highest frequency (77%). The tumors with loss of chromosome 13 alleles also showed additional losses of alleles on other chromosomes, while tumors retaining heterozygosity of chromosome 13 also retained heterozygosity at the informative loci on other chromosomes. Southern hybridization and karyotype analysis in some selected cases suggest that the concerted loss of heterozygosity at multiple loci may be a consequence of the polyploidization-segregation process.

Methylation of the 5' CpG island of the FHIT gene is closely associated with transcriptional inactivation in esophageal squamous cell carcinomas.

Previous studies suggested that the FHIT (fragile histidine triad) gene on 3p14.2 might be involved in the development of esophageal squamous cell carcinomas, but the mechanisms for inactivating the gene have not been fully revealed. In the present study, we examined aberrations of the FHIT gene in 23 esophageal squamous cell carcinoma cell lines and 35 primary tumors. We detected aberrant expression in seven cell lines (30%), including a shorter transcript in two cell lines and loss of apparent transcript in five cell lines. Genomic PCR or cDNA sequencing analysis revealed a single exon deletion in two cell lines with a shorter transcript and one cell line without expression, but no structural alterations were found in the other 20 cell lines, including transcriptionally repressed four cell lines. Next we examined methylation of the 5' CpG island of the FHIT gene by bisulfite genomic sequencing. Hypermethylation of the 5' CpG island of the FHIT gene was observed in three of four structurally unaltered but transcriptionally repressed cell lines. The remaining cell line harbored a point mutation upstream of exon 1. All methylated cell lines exhibit re-expression of the FHIT gene and demethylation in the CpG island after treatment with demethylating agent 5-aza-2'-deoxycytidine. Hypermethylation was also found in 5 of 35 (14%) primary tumors, whereas corresponding normal tissue shows no methylation. These findings suggest that methylation of the 5' CpG island of the FHIT gene is closely associated with transcriptional inactivation and might be involved in tumor development of the esophagus.

Mutation spectrum of the retinoblastoma gene in osteosarcomas.

We have performed an intensive mutation survey of the Rb gene in 63 osteosarcomas. Loss of heterozygosity (LOH) at the Rb locus was analyzed by using polymerase chain reaction at four intronic polymorphic sites, and 62.9% (39 of 62) of tumors showed LOH. Mutation analysis of the Rb gene was performed by Southern blot for structural anomalies, polymerase chain reaction-single strand conformation polymorphism analysis followed by direct genomic sequencing for subtle mutations, and immunohistochemistry for protein expression. The frequencies of each type of abnormalities were: structural anomalies, 28.6% (18 of 63); subtle mutations, 6.0% (3 of 50); negative protein expression, 53.6% (30 of 56); 54.5% (18 of 33) of tumors with LOH at the Rb locus were proved to show negative Rb expression, while 50.0% (11 of 22) of tumors without LOH also showed negative Rb, indicating that LOH at the Rb locus in osteosarcoma will not necessarily correlate with the actual inactivation of the Rb gene at the protein level. Findings in primary tumors were correlated with clinical outcome, and the presence of LOH and DNA alterations of the Rb gene were proved to indicate poor prognosis.

Influence of cigarette smoking and schistosomiasis on p53 gene mutation in urothelial cancer.

The mutation patterns of the p53 tumor suppressor gene have been shown to reflect the specific carcinogen(s) involved, or the epidemiological background in some cancers. To elucidate the impact of cigarette smoking or bilharzial infection on the p53 gene mutation pattern, 61 cases of urothelial cancer from Japan and 7 cases of bladder cancer with schistosomiasis from Egypt were examined for mutations of the p53 gene. In total, p53 gene mutations were detected in 20 Japanese cases (33%) and 6 Egyptian cases (86%). Although the incidence of p53 gene mutation was not significantly influenced by habitual smoking, a different mutation pattern was observed as follows: 4 of 10 mutations in smokers in Japan were A:T to G:C transitions, whereas such mutations were not detected in any of 10 mutations in nonsmokers, or in any of 6 mutations associated with schistosomiasis. Although no specific mutation pattern was detected for the squamous cell carcinomas with schistosomiasis, all 8 base substitutions observed in tumors with squamous cell carcinomas occurred at G:C sites, whereas base substitutions at A:T sites were observed in 33% (6 of 18) of mutations in transitional cell carcinomas. Our results suggest that cigarette smoking may have a significant impact on the mutations of the p53 gene in urothelial cancers. Furthermore, the distinct spectrum of the p53 gene mutation found in tumors with squamous cell carcinomas may reflect their unique etiological backgrounds.

Allelotype analysis in osteosarcomas: frequent allele loss on 3q, 13q, 17p, and 18q.

We have investigated the involvement of tumor suppressor genes in the genesis of osteosarcoma by analyzing allele losses at polymorphic loci in tumor tissues. Genotypes of DNA from primary osteosarcoma tissue and corresponding normal cells from 37 patients were analyzed at 58 polymorphic loci representing each autosomal chromosome arm except 5p and 20q. Allele losses were found at polymorphic loci on 36 of 37 chromosome arms analyzed. In particular, four of them showed frequencies of allele loss higher than 60%: 3q (75%); 13q (68%); 17p (72%); and 18q (64%). This result suggests that, in addition to the RB (retinoblastoma) gene on 13q and the p53 gene on 17p, at least two more tumor suppressor genes located on 3q and 18q are frequently involved in the development of osteosarcoma. The extent of allele losses as defined by fractional allelic loss among 36 tumors was diverse, from 0 to 0.64. The median fractional allelic loss value of 0.32 was much higher than those previously reported in colorectal carcinoma and breast carcinoma. Although no definite association of fractional allelic loss value to clinical prognosis of each case was found in osteosarcoma, tumors with 17p loss were more prone to the early onset of lung metastasis than tumors without 17p loss, indicating that allele loss on chromosome 17p can be a useful measure of prognosis.

Assignment of common allele loss in osteosarcoma to the subregion 17p13.

Human osteosarcomas frequently show loss of alleles on chromosome 17 as well as those on chromosome 13 that harbors the retinoblastoma gene, indicating concerted operation of another tumor-suppressing gene on chromosome 17. To assign the affected gene to a defined region of chromosome 17, we performed mitotic recombination/deletion mapping by the use of 10 polymorphic loci on chromosome 17. Of 37 tumors studied, 28 (75.7%) showed loss of heterozygosity on chromosome 17. The affected regions varied among tumors, ranging in extent from a whole chromosome to a distal segment of the short arm. However, allele loss in one region, notably in 17p13 between D17S1 and D17S30, was common to all 28 tumors, suggesting the presence of a tumor-suppressing gene in this defined region.

Loss of 17p, mutation of the p53 gene, and overexpression of p53 protein in esophageal squamous cell carcinomas.

We analyzed mutations of the p53 gene by single-strand conformation polymorphism analysis of polymerase chain reaction products and direct sequencing through all coding exons and exon-intron junctions in 32 cases with esophageal squamous cell carcinoma. Mutations were detected in 15 of 32 (47%) tumor samples, in which G:C to T:A transversions were rather frequent (33%). Previously, we reported deletion of chromosome 17p where the p53 gene is located in 45% of Japanese esophageal squamous cell carcinoma, and here the relationship between mutation of the p53 gene and loss of 17p was analyzed. Mutations were observed in 12 of 16 patients with loss of 17p, whereas only 2 of 11 without loss were positive for mutations, suggesting that mutations of the p53 gene were closely associated with a 17p deletion. Furthermore, we immunohistochemically analyzed the expression of p53 protein in esophageal squamous cell carcinoma tumor tissues using a monoclonal antibody. Five of 6 tumors with missense mutations of the p53 gene were positively stained, while in tumors with nonsense mutations or without mutations of the p53 gene staining was very weak or negative. These results suggest a good correlation between mutations and abnormal expression of the p53 gene.

Frequency and structure of p53 rearrangements in human osteosarcoma.

Osteosarcoma is the most frequent childhood bone cancer (Tebbi, C. K., and Gaeta, J. Pediatr. Ann., 17:285-300, 1988). Using Southern blot mapping, we found that 11 of 60 (18%) osteosarcomas had altered restriction patterns of the p53 gene and that six of these had loss of the other p53 allele. In contrast, no alteration of the p53 gene was detected in 50 samples from other types of sarcomas. Fifty % of osteosarcoma cell lines (4 of 8) also had gross rearrangements of one p53 allele with loss of the second allele, and these had no detectable p53 mRNA. Osteosarcoma cell lines with no detectable alteration of the p53 gene contained abundant p53 transcripts. Taken together, data show that human osteosarcomas can have rearrangements of the p53 gene; these rearrangements may cause loss of normal constraints on cellular growth.

Molecular cloning of guinea pig CYP1A1: complete primary structure and fast mobility of expressed protein on electrophoresis.

Guinea pig CYP1A1 cDNA was isolated from a liver cDNA library of guinea pig treated with 3-methylcholanthrene. The cDNA, named GPc1, was 2674 bp long and contained an entire coding region for 516 amino acids. The amino acid sequence of guinea pig CYP1A1 shared 74-78% identity with those of the other mammalian CYP1A1s. RNA blot and immunoblot analyses revealed that CYP1A1 was constitutively expressed and was induced by 3-methylcholanthrene in guinea pig liver. On sodium dodecyl sulfate-polyacrylamide gel electrophoresis, guinea pig CYP1A1 expressed in yeast had a significantly smaller apparent molecular mass than expressed mouse CYP1A1. An alignment of the amino acid sequences of mammalian CYP1A1s demonstrated that guinea pig CYP1A1 was several residues shorter than the counterparts in the N-terminal region. Thus, to clarify the contribution of the N-terminal sequence of guinea pig CYP1A1 to the fast mobility on the electrophoresis, mouse-guinea pig chimeric CYP1A1 was prepared through cDNA-directed expression in yeast. The chimeric CYP1A1 protein had an intermediate molecular mass between mouse and guinea pig CYP1A1s indicating that the anomalous mobility of guinea pig CYP1A1 is in part due to the shortened N-terminal amino acid sequence of the protein.