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PubMed1981

[Algesimetry in ischemic heart disease and neurocirculatory dystonia].

Algesimetry was used to study the pain sensitivity in 143 subjects (21 healthy individuals, 20 cases with neurocirculatory dystonia, 62 with chronic ischaemic heart disease and 40 with subacute myocardial infarction). The tests were performed for the tactile threshold, pain threshold, threshold of pain endurance and the interval of pain endurance. In a part of patients indices of pain sensitivity were correlated with tolerance to physical exertion. In neurocirculatory dystonia high pain sensitivity was due to the lowering of the pain threshold. In patients with ischaemic heart disease there were three types of pain threshold (low, medium, high) and two variants as concerns the interval of pain endurance (low and high). Low interval of pain endurance corresponded to low tolerance of physical exertion, hence algesimetry can serve as an additional method of objective interpretation of the bicycle ergometry tests.

Angina Pectoris↗

PubMed2002

Interpretation of RET immunostaining in follicular lesions of the thyroid.

We applied monoclonal antibodies against RET and cytokeratin 19 (CK19) to the following tumor sections: classic papillary carcinoma (PC), 16; Hürthle-type PC (HPC), 1; sclerosing PC with nodular fasciitis-like stroma (SPC), 1; PC, follicular variant (FVPC), 12; follicular adenoma (FA), 9; Hürthle cell adenoma (HA), 4; Hürthle cell carcinoma (HC), 3; and follicular carcinoma (FC), 7. CK19+ tumors included 16 PCs, 1HPC, 1SPC, 11 FVPCs, 7 FAs, 4 FCs, and 1HC. RET+ tumors included 4 HAs, 3 HCs, 1HPC, 12 PCs, 7 FVPCs, and 2 FAs. Reverse transcriptase-polymerase chain reaction (RT-PCR) revealed a RET transcript in 6 Hürthle cell lesions. RET immunoreactivity is less sensitive and specific for PC than CK19. CK19 is useful for identifying PC, although only lesions with diffuse, intense staining should be considered positive. The detection of RET protein by immunohistochemical analysis was corroborated by the presence of the RET transcript by RT-PCR. Further study is warranted to determine whether this represents activation by gene fusion or some other mechanism in this subset of thyroid neoplasms.

Adenocarcinoma, Follicular↗

PubMed1995

[Micrographic surgery. A current methodological assessment].

Micrographic surgery is one of the most effective methods in the treatment of basal cell carcinoma. In the last 20 years this method has been further developed and modified. Three kinds of micrographic surgery are now available: the Mohs method, the margin strip method ("Tübingen torte") and the "Munich" method. All three variants have the same goal; radical tumour removal with optimal sparing of surrounding tumour-free tissue. They differ, however, in the technique of tumour excision, the preparation of the histological specimens and the interpretation of the slides. In this paper the authors take stock of the methods available and describe the differences, advantages and disadvantages.

Basal Cell Carcinoma↗

PubMed1993

Evidence that the monoclonal antibodies SMI-31 and SMI-34 recognize different phosphorylation-dependent epitopes of the murine high molecular mass neurofilament subunit.

The monoclonal antibodies SMI-31 and SMI-34 react with phosphate-dependent epitopes of the high molecular mass (200 kDa) neurofilament protein (Hphos). Determination of whether or not these monoclonals react with different epitopes would assist in interpretation of post mortem immunocytochemical analyses in neurodegenerative disorders and in normal aging. We therefore examined the relative immunoreactivity of these antibodies against Triton-insoluble (cytoskeleton-associated) and Triton-soluble Hphos variants in NB2a/d1 neuroblastoma and post-natal mouse brain in immunoblot analysis. Densitometric analysis yielded a 'reactivity ratio' (soluble Hphos/insoluble Hphos) for each antibody. This ratio was approximately 44% and 87% less for SMI-34 than for SMI-31 in neuroblastoma and brain, respectively. These findings confirm that the SMI-34 epitope is distinct from that recognized by SMI-31, and, in these systems, is preferentially associated with the cytoskeleton.

Animals↗

PubMed2025

Triazole-resistant Aspergillus fumigatus in the Netherlands between 1994 and 2022: a genomic and phenotypic study.

BACKGROUND: Aspergillus fumigatus is the main cause of invasive aspergillosis and triazole antifungals are the primary treatment option. The effectiveness of triazole therapy is hampered by the emergence of resistance, mainly caused by mutations in the cyp51A gene and a tandem repeat (TR) of 34 bases (TR34/Leu98His) and 46 bases (TR46/Tyr121Phe/Thr289Ala) in the promoter region, which correspond with signature triazole resistance phenotypes. We aimed to investigate the occurrence of triazole phenotype and genotype variation over a 29-year period in the Netherlands. METHODS: In this genomic and phenotypic study, we screened all clinical A fumigatus isolates from Dutch hospitals collected between Jan 6, 1994, and Dec 31, 2022, for resistance to triazole using agar-based methods, and characterised them by sequencing the cyp51A gene and in vitro susceptibility testing using the European Committee on Antimicrobial Susceptibility Testing reference method. Whole-genome sequencing was performed on selected isolates, including those harboring TR34 variants, high-frequency single-nucleotide polymorphisms, and wild-type strains. Clinical information such as age, underlying disease, diagnosis, therapy, and outcomes was collected for patients who had isolates cultured at the Radboud University Medical Centre, Nijmegen, Netherlands, between Jan 1, 2017, and Dec 31, 2022. FINDINGS: 1979 (15·6%) of the screened 12 679 A fumigatus isolates harboured cyp51A triazole resistance mutations, predominately TR34/Leu98His sensu stricto in 1338 (67·6%) resistant isolates and TR46/Tyr121Phe/Thr289Ala sensu stricto in 332 (16·8%) resistant isolates. Phenotype and genotype variations were observed in 325 (17·2%) triazole resistant isolates harbouring a TR-resistance mechanism, including 12 cyp51A genotype variants. Whole-genome sequencing showed that isolates with combinations of TR34-based and TR46-based polymorphisms seemed to be derived from separate populations, but there was some overlap. 59 cases of proven or probable invasive aspergillosis were identified, including 13 triazole-resistant cases, of which three were caused by genotype variants. Mixed genotype infection was observed in 11 (84·6%) of 13 triazole-resistant patients and the number of antifungal treatment switches was higher compared with triazole-susceptible disease (p<0·0001). INTERPRETATION: Our study showed variation in triazole genotypes and phenotypes in clinical A fumigatus isolates with cyp51A-mediated resistance, some of which were cultured from triazole-resistant invasive aspergillosis cases. Triazole resistance variation and mixed A fumigatus genotypes represent a major challenge in clinical management of Aspergillus diseases because current molecular diagnostic tools will increasingly fail to predict the resistance phenotype, underscoring the need for improved detection methods. FUNDING: National Key Research and Development Program of China, National Natural Science Foundation of China, and Wellcome Trust.

Aspergillus fumigatus↗

PubMed1996

Conformational changes of the yeast mitochondrial adenosine diphosphate/adenosine triphosphate carrier studied through its intrinsic fluorescence. 2. Assignment of tryptophanyl residues of the carrier to the responses to specific ligands.

Tryptophanyl substitution of the Saccharomyces cerevisiae adenine nucleotide carrier (Anc2p isoform) was not deleterious for the transport activity or the folding of the carrier [preceding paper by Le Saux et al. (1996) Biochemistry 35, 16116-16124]. Conformational changes of the isolated wild-type and Trp-substituted Anc2p variants, induced upon binding of specific substrates [adenosine triphosphate (ATP) or diphosphate (ADP)] or inhibitors [carboxyatractyloside (CATR) or bongkrekic acid (BA)], were studied by measurement of intrinsic fluorescence. Titration of CATR and BA binding sites ended in the same number of sites, namely, 6-7 nmol/mg of wild-type and variant Anc2p. Isolated Anc2p in detergent presented similar emission spectra, suggesting that all tryptophanyl residues were in environments of similar hydrophobicity. Trp87 and Trp126 contributed largely and to a similar extent to the fluorescence enhancement observed in response to ATP binding, while Trp235 contributed negatively and to a small extent to the fluorescence change. Both Trp126 and Trp235, and to a lower extent Trp87, participate in the CATR-induced fluorescence decrease of Anc2p. Responses to BA binding were observed only in the presence of ATP; they consisted of a further fluorescence increase of the Anc2p.ATP complex, which was mainly due to Trp87 and Trp126, Trp235 being much less responsive. The different fluorescence responses of the three Trp residues of Anc2 variants to ATP, CATR, and BA are in agreement with distinct binding sites for these ligands and distinct conformations of the carrier protein recognizing specifically CATR or BA. A mechanistic model is proposed to interpret the transitions between the different conformational states of Anc2p.

Adenosine Diphosphate↗

PubMed2002

Structural basis of cytochrome c presentation by IE(k).

The COOH-terminal peptides of pigeon and moth cytochrome c, bound to mouse IE(k), are two of the most thoroughly studied T cell antigens. We have solved the crystal structures of the moth peptide and a weak agonist-antagonist variant of the pigeon peptide bound to IE(k). The moth peptide and all other peptides whose structures have been solved bound to IE(k), have a lysine filling the p9 pocket of IE(k). However, the pigeon peptide has an alanine at p9 shifting the lysine to p10. Rather than kinking to place the lysine in the anchor pocket, the pigeon peptide takes the extended course through the binding groove, which is characteristic of all other peptides bound to major histocompatibility complex (MHC) class II. Thus, unlike MHC class I, in which peptides often kink to place optimally anchoring side chains, MHC class II imposes an extended peptide conformation even at the cost of a highly conserved anchor residue. The substitution of Ser for Thr at p8 in the variant pigeon peptide induces no detectable surface change other than the loss of the side chain methyl group, despite the dramatic change in recognition by T cells. Finally, these structures can be used to interpret the many published mutational studies of these ligands and the T cell receptors that recognize them.

Amino Acid Motifs↗

PubMed1990

Residual tRNA secondary structure in 'denaturing' 8M urea/TBE polyacrylamide gels: effects on electrophoretic mobility and dependency on prior chemical modification of the tRNA.

Fifteen individual species of tRNA were treated with the chemical modifiers diethylpyrocarbonate, 50% aqueous hydrazine or hydrazine/3 M NaCl. Following purification of the chemically modified material on polyacrylamide gels containing 8 M urea, variant minor bands, in addition to the expected main band, were observed for 12 of the 15 tRNAs. Characterization of the content of chemically altered bases in material recovered from such bands indicated that tRNAs containing modified nucleotides in base-paired stems were excluded from the main band and present, often in enhanced amounts, in the minor variant bands. The persistence of residual secondary structure on 8 M urea gels run at 45 degrees C and the ability of chemically modified bases to alter electrophoretic mobilities warrant caution in designing and interpreting experiments in which chemically modified RNA is isolated on gels prior to further analysis. tRNA(Val) (VAC) was unique in that modified bases in non base-paired regions, according to the cloverleaf model of secondary structure, caused exclusion from the main band. Consequently, we propose a secondary structure for partially denatured tRNA(Val) (VAC), in which these bases are located in double stranded regions of the molecule.

Base Sequence↗

PubMed1990

Minimal deviation melanoma (halo nevus variant).

Twenty-eight cases of minimal deviation melanoma (MDM) in the histologic setting of halo nevus formed the basis for this study. Requisites for this study included at least one of the following: a remnant of a halo nevus in a MDM; remnants of both MDM and halo nevus in a common melanoma; and a MDM of Spitz or dermal type, or MDM arising in premalignant dysplasia in which the vertical growth components manifested distinctive cytologic features and cytophilia for lymphocytes. Many of the lesions apparently represented neoplastic progressions involving a population of cells at the dermal-epidermal interface (accretive growth). Some of the lesions qualified as dermal variants and apparently represented neoplastic progressions in a dermal component (interstitial growth). Most examples of MDM in this study were borderline in size (less than 1.00 mm in vertical dimensions). The borderline MDM were interpreted as brief (and in some cases perhaps ephemeral) neoplastic interludes. For the 12 cases with follow-up, there have been no metastases or local recurrences.

Adolescent↗

PubMed2006

Genetic association of type 1 diabetes in an Azerbaijanian population: the HLA-DQ, -DRB1*04, the insulin gene, and CTLA4.

BACKGROUND: Little is known on the genetic susceptibility to type 1 diabetes mellitus (T1DM) in the nations of the former Soviet part of south-west Asia. OBJECTIVE: The aim of the study was to characterize the genetic association of T1DM in the Azeri, the majority population of Azerbaijan. SUBJECTS AND METHODS: One hundred and sixty patients with childhood-onset T1DM, and 271 healthy unrelated controls were compared in a case-control study. All declared themselves as Azeri. The human leukocyte antigen (HLA)-DQB1, -DQA1 alelles, of DRB1*04 subtypes, and of insulin gene and cytotoxic T-lymphocyte-associated protein 4 (CTLA4) single nucleotide polymorphisms were determined using polymerase chain reaction (PCR) techniques, the association was tested from cross-tabulations, and quantified using odds ratios (OR). In the non-HLA factors, analyses were also stratified according to the HLA-conferred risk. RESULTS: Risk for T1DM was associated with presence of the HLA-DQB1*02-DQA1*05, OR = 6.6 [95% confidence interval (CI) 4.3-10], the HLA-DQB1*0302-DQA1*03, OR = 3.9 (95% CI 2.6-6.0), and an unexpectedly high risk was observed for DQB1*0304, OR = 10.9, but the very wide CI (CI 95% 2.4-49) prompts careful interpretation. A negative association with diabetes was observed for the DQB1*0602, 0503, 0301, and 0601 alleles, as well as the DRB1*0403 subtype. A strong protection was also associated with the less frequent variant of the insulin gene (OR of the phenotypic positivity was 0.28, CI 95% 0.17-0.46), while the CTLA4 +49 A/G transition was not associated with T1DM. CONCLUSIONS: We bring the first report on both HLA, and non-HLA association of T1DM from the majority Azeri population of Azerbaijan.

Age of Onset↗

PubMed2026

Exome sequencing and large-scale analysis of electronic medical record-linked biobank data identify candidate deafness genes.

INTRODUCTION: Rapid advances in whole-exome sequencing (WES) have enabled large-scale detection of pathogenic variants. Although hundreds of genes are implicated in hearing loss, up to half of inherited cases remain unsolved, limiting eligibility for gene therapy trials that require genetic diagnosis. Biobanks and electronic medical records (EMRs) offer opportunities to integrate genomic and clinical data at scale and expand the spectrum of hearing loss genes. Despite clinical value, EMRs often lack key information such as inheritance patterns, posing challenges for accurate interpretation. METHODS: WES was performed on DNA samples from 1038 hearing-impaired patients enrolled in the Maccabi Research and Innovation Center Tipa Biobank. Clinical data were extracted from EMRs. Audiograms were available for all cases, although data on age of onset, family history and mode of inheritance were mostly unavailable. We applied a scalable bioinformatics analysis strategy for high-throughput annotation, filtering and prioritisation of WES variants across more than 1000 patients, designed to accommodate incomplete and heterogeneous clinical records. RESULTS: Using this approach, 15% of cases were solved or potentially solved through known or novel variants in established deafness genes. Homozygous variants in novel candidate genes were identified in 3% of cases. Functional characterisation was performed for promising candidate genes to validate their role in the ear. CONCLUSION: These findings demonstrate that WES can determine disease aetiology in large, genetically heterogeneous populations, even in the context of incomplete clinical data. This approach supports large-scale genetic screening and provides a framework for identifying patients who may benefit from emerging gene-based therapies.

Genetic Testing↗

PubMed1995

A Golgi and horseradish peroxidase study of the sonic motor nucleus of the oyster toadfish.

The sonic motor nucleus (SMN) of the oyster toadfish Opsanus tau, a single midline structure in the occipital spinal cord and caudal medulla, contains large electrically-coupled motoneurons. Although interpretation is complicated by multiyear growth in soma size, neurons in males may be either large (L) or small (S), whereas females have exclusively S neurons. Golgi stains have allowed separation of five neuron variants (rostral, dorsal, stellate, ventral and caudal) which differ in location, soma shape and size, and direction and pattern of dendritic branching. All variants are present in L and S males and in females, and retrograde transport of horseradish peroxidase indicates that all variants are motoneurons. The SMN is organized into three horizontal layers with rostral and dorsal neurons forming a rostrocaudally arrayed network across the dorsal-dorsolateral surface. Stellate cells are found in the middle layer, and ventral cells with laterally directed dendrites that exit the SMN line the inferior surface. Caudal neurons with caudally directed exiting dendrites are arranged in parallel rows in the caudal fifth of the SMN. We suggest that variant differences in dendritic orientation relate to different patterns of innervation by multiple afferents to the SMN and function to maximize contacts between neurons as a means of facilitating synchronization within the nucleus. Sexual dimorphism has been demonstrated to a minor degree: all variants have larger somas in L fish than S fish, but no difference has been found in primary dendrite diameter. Larger somas would potentially support the greater amount of sound production by nesting males who produce a mating boatwhistle call. Equivalent dendrite diameter in females, who are just as likely as males to grunt, an agonistic call, suggests that female Opsanus have a well developed sonic circuitry compared to Porichthys, another toadfish in which females are typically silent.

Animals↗

PubMed2002

A cautionary tale on ancient migration detection: mitochondrial DNA variation in Santa Cruz Islands, Solomon Islands.

Over the past decade, the origin of the first Malayo-Polynesian settlers of the island Pacific has become a contentious issue in molecular anthropology as well as in archaeology and historical linguistics. Whether the descendants of the ancestral Malayo-Polynesian speakers moved rapidly through Indonesia and Island Melanesia in a few hundred years, or whether they were the product of considerable intermingling within the more westerly part of the latter region, it is widely accepted that they were the first humans to colonize the distant Pacific islands beyond the central Solomon Islands approximately 3,000 years ago. The Santa Cruz Islands in the Eastern Solomons would have most likely been the first in Remote Oceania to be colonized by them. Archaeologically, the first Oceanic Austronesian settlement of this region appears to have been overlain by various later influences from groups farther west in a complex manner. Molecular anthropologists have tended to equate the spread of various Austronesian-speaking groups with a particular mitochondrial variant (a 9-base-pair [bp] deletion with specific D-loop variants). We have shown before that this is an oversimplified picture, and assumed that the Santa Cruz situation, with its series of intrusions, would be informative as to the power of mitochondrial DNA haplotype interpretations. In the Santa Cruz Islands, the 9-bp deletion is associated with a small number of very closely related hypervariable D-loop haplotypes resulting in a star-shaped Bandelt median network, suggesting a recent population expansion. This network is similar to Polynesian median networks. In a pairwise mismatch comparison, the Santa Cruz haplotypes have a bimodal distribution, with the first cluster being composed almost entirely of the 9-bp-deleted haplotypes-again attesting to their recent origins. Conversely, the nondeleted haplogroups bear signatures of more ancient origins within the general region. Therefore, while the profiles of the two sets of haplotypes indicate very distinctive origins in different populations with divergent expansion histories, the sequence of their introduction into the Santa Cruz Islands clearly does not follow simply.

DNA, Mitochondrial↗

PubMed2006

Cerulean, Venus, and VenusY67C FRET reference standards.

Förster's resonance energy transfer (FRET) can be used to study protein-protein interactions in living cells. Numerous methods to measure FRET have been devised and implemented; however, the accuracy of these methods is unknown, which makes interpretation of FRET efficiency values difficult if not impossible. This problem exists due to the lack of standards with known FRET efficiencies that can be used to validate FRET measurements. The advent of spectral variants of green fluorescent protein and easy access to cell transfection technology suggests a simple solution to this problem: the development of genetic constructs with known FRET efficiencies that can be replicated with high fidelity and freely distributed. In this study, fluorescent protein constructs with progressively larger separation distances between donors and acceptors were generated and FRET efficiencies were measured using fluorescence lifetime spectroscopy, sensitized acceptor emission, and spectral imaging. Since the results from each method were in good agreement, the FRET efficiency value of each construct could be determined with high accuracy and precision, thereby justifying their use as standards.

Cell Line↗

PubMed2006

Common laboratory methods in pharmacogenomics studies.

PURPOSE: Common laboratory methods used in pharmacogenomics studies are described. SUMMARY: The reliable and accurate determination of a person's genetic makeup at a particular locus in the DNA molecule, or genotype, is fundamental to pharmacogenomics. Whole blood cells and buccal cells are commonly collected to obtain a DNA sample. Once DNA is collected, the genomic DNA must be isolated from other cellular material. Next, a specific region of interest must be identified and amplified, performed via polymerase chain reaction (PCR). Gel electrophoresis is often performed after PCR to verify that PCR was successful and that the amplified target sequence is the correct size. Numerous methods are available to determine a person's genotype and differ based on allele discrimination and detection. PCR coupled with restriction fragment length polymorphism (RFLP) analysis, a conventional genotyping method, does not rely on automated technology and is practical for laboratories that genotype a limited number of samples. Pyrosequencing is an automated genotyping method in which the principal allele discrimination method is a primer extension reaction coupled with a luciferase-based enzyme reaction. TaqMan relies on the use of fluorescencelabeled probes, in addition to PCR primers, in the reaction mixture, enabling PCR amplification and allele discrimination in the same step. Mass spectrometry differentiates DNA molecules using a defined mass. Denaturing high-performance liquid chromatography (DHPLC) uses a reverse-phase ion-pair column to discriminate between variant and nonvariant alleles. CONCLUSION: An understanding of the common genotyping methods used in pharmacogenomics studies, including PCR-RFLP analysis, pyrosequencing, TaqMan, mass spectrometry, and DHPLC, will aid pharmacy practitioners and students when interpreting the methods sections of such studies.

Clinical Laboratory Techniques↗

PubMed2005

An intact phosphocholine binding site is necessary for transgenic rabbit C-reactive protein to protect mice against challenge with platelet-activating factor.

C-reactive protein (CRP), an acute phase protein in humans and rabbits, is part of the innate immune system. The role of CRP in host defense has been thought to be largely due to its ability to bind phosphocholine, activate complement, and interact with IgGRs (FcgammaRs). We have shown previously that transgenic rabbit CRP (rbCRP) protects mice from lethal challenges with platelet-activating factor (PAF). To investigate the mechanism of this protection, we created additional lines of transgenic mice that express either wild-type rbCRP, a variant of rbCRP with altered complement activation activity (Y175A), or a variant of rbCRP unable to bind phosphocholine (F66Y/E81K). In the current study, these lines were challenged with a single injection of PAF and their survival monitored. Mice expressing wild-type and Y175A rbCRP were protected against challenge by PAF whereas mice expressing F66Y/E81K rbCRP were not. Treatment with cobra venom factor did not affect survival, confirming the results with the Y175A rbCRP variant and indicating that complement activation was not required to mediate protection. Both wild-type rbCRP and Y175A rbCRP were capable of binding PAF in vitro whereas F66Y/E81K rbCRP was not. Although other interpretations are possible, our results suggest that the protective effect of rbCRP against PAF is due to sequestration of PAF.

Animals↗

PubMed2004

G20210A prothrombin gene variant and clinical outcome in patients with a first acute coronary syndrome.

BACKGROUND AND OBJECTIVES: The prognostic value of the G20210A prothrombin gene polymorphism in patients with a first acute coronary syndrome has not been previously assessed. We conducted a prospective study to investigate this issue. DESIGN AND METHODS: Genotyping at the 20210 prothrombin gene locus was performed in 162 patients with a first episode of myocardial infarction (MI) or unstable angina (UA) occurring before 65 years of age. Patients were stratified according to cardiovascular risk factors and to treatment strategy. The subsequent two-year relative risk (RR) of adverse events (death, MI and UA) was adjusted for possible confounders and analyzed according to genotype, risk factor category, and treatment allocation. RESULTS: In the entire study population, the prothrombin variant did not significantly increase the two-year risk of events: the adjusted RR for GA vs GG carriers was 1.82 (95% CI 0.68-4.89). However, in the absence of traditional cardiovascular risk factors the risk of events was consistently higher: among the 46 patients without hypertension, diabetes and hypercholesterolemia, GA vs GG carriership was associated with an adjusted RR at two years of 5.64 (95% CI 1.07-29.84). The gene variant also enhanced the risk of events among the 98 patients who did not undergo myocardial revascularization procedures (RR for GA vs GG: 2.89, 95% CI 1.04-8.00), but not among those who did. INTERPRETATION AND CONCLUSIONS: The present prospective study suggests that heterozygosity for the G20210A prothrombin polymorphism adversely affects prognosis after a first acute coronary syndrome in the subgroup of patients without metabolic risk factors and in those not treated by revascularization procedures.

3' Untranslated Regions↗

PubMed1986

The effect of high dose long-wave ultraviolet radiation (UVA) on epidermal melanocytes in human skin: a transmission electron microscopic study.

Five healthy subjects with skin type III and IPD (immediate pigment darkening reaction) were irradiated with a glass-filtered UVA-sun 2000 lamp and exposed to 50, 100 and 150 J cm-2 of UVA. Transmission electron microscopy showed a statistically significant increase in the number of epidermal melanocytes with enlarged Golgi apparatus with associated vesicles, predominantly of the coated variant, swollen mitochondria with ruptured cristae, and extensive endo/exocytotic activity. Cells with 2 nuclei were also observed. It is concluded that UVA alone, in doses producing erythema, can give rise to these ultrastructural changes, interpreted as an increased secretory activity in a portion of the epidermal melanocytes.

Adult↗