Analysis of optical damage mechanisms in hollow-core waveguides delivering nanosecond pulses from a Q-switched Nd:YAG laser.

Hollow-core waveguides consisting of a glass capillary tube with an internal reflective coating are capable of delivering pulse energies of tens of millijoules with improved focusability compared to step index fibers of similar core diameter. We demonstrate the capability of these fibers to deliver high-power Q-switched pulses at the fundamental (1064 nm), second (532 nm), and third (355 nm) harmonics of a Nd:YAG laser, both in terms of peak power and beam quality delivered. In terms of peak power delivery, the primary limitation is the occurrence of bend-induced optical damage to the reflective coating. The damage mechanism and the influential factors are analyzed, in particular, the dependence upon the number of guided modes, core diameter, coating thicknesses, and input polarization alignment.

Kaposi's sarcoma associated herpesvirus deoxyribonucleic acid sequences: lack of detection in prostatic tissue of human immunodeficiency virus-negative immunocompetent adults.

PURPOSE: A recent study argued that Kaposi's sarcoma associated herpesvirus is ubiquitous, as reflected by the frequent detection of its deoxyribonucleic acid (DNA) sequences in the prostatic tissue of healthy Italian men. Because these findings are discordant with serological data, our objective was to reassess the prevalence of this virus in prostate tissue from immunocompetent men. MATERIALS AND METHODS: Normal tissue samples from 45 human immunodeficiency virus-negative men undergoing radical prostatectomy for prostate carcinoma were snap frozen. DNA was extracted from normal noncancerous tissue. DNA was confirmed to be polymerase chain reaction amplifiable. Then, using multiple primer sets, extracted prostatic DNA was blinded, polymerase chain reaction amplified and screened for Kaposi's sarcoma herpesvirus by Southern blot. RESULTS: Kaposi's sarcoma herpesvirus DNA sequences were not detected in either the 45 prostatic DNA or in blinded internal negative controls, but they were consistently identified in all positive internal controls. CONCLUSIONS: Since Kaposi's sarcoma herpesvirus was undetectable in any of the prostatic samples despite high assay sensitivity, it is unlikely that the prostate serves as a reservoir for this virus in immunocompetent North American men. These findings also suggest that Kaposi's sarcoma herpesvirus is not ubiquitous.

Nucleotide sequence of the Kaposi sarcoma-associated herpesvirus (HHV8).

The genome of the Kaposi sarcoma-associated herpesvirus (KSHV or HHV8) was mapped with cosmid and phage genomic libraries from the BC-1 cell line. Its nucleotide sequence was determined except for a 3-kb region at the right end of the genome that was refractory to cloning. The BC-1 KSHV genome consists of a 140.5-kb-long unique coding region flanked by multiple G + C-rich 801-bp terminal repeat sequences. A genomic duplication that apparently arose in the parental tumor is present in this cell culture-derived strain. At least 81 ORFs, including 66 with homology to herpesvirus saimiri ORFs, and 5 internal repeat regions are present in the long unique region. The virus encodes homologs to complement-binding proteins, three cytokines (two macrophage inflammatory proteins and interleukin 6), dihydrofolate reductase, bcl-2, interferon regulatory factors, interleukin 8 receptor, neural cell adhesion molecule-like adhesin, and a D-type cyclin, as well as viral structural and metabolic proteins. Terminal repeat analysis of virus DNA from a KS lesion suggests a monoclonal expansion of KSHV in the KS tumor.

Kaposi's sarcoma-associated herpesvirus infection prior to onset of Kaposi's sarcoma.

OBJECTIVES: Kaposi's sarcoma-associated herpesvirus (KSHV), a newly discovered human gammaherpesvirus, is found in the majority of KS lesions from patients with and without AIDS. Peripheral blood mononuclear cells (PBMC) were examined for KSHV DNA to determine whether viral infection precedes onset of this neoplasm. DESIGN: Randomized and blinded case-control study of prospectively collected PBMC samples from ongoing cohort studies. METHODS: Paired PBMC drawn before and after KS onset from 21 AIDS-KS patients were compared to paired PBMC from 23 high-risk HIV-infected homo-/bisexual patients who did not develop KS and to a single PBMC sample from 19 low-risk, HIV-infected hemophiliac patients. Extracted DNA samples were amplified by polymerase chain reaction (PCR) using two non-overlapping nested primer sets to control for potential PCR contamination. RESULTS: In all comparisons, patients who went on to develop KS were significantly more likely to show evidence of KSHV infection prior to onset of KS than either control group. Of PBMC samples from AIDS-KS patients drawn prior to KS, 52% were positive for KSHV DNA whereas both high- and low-risk control groups had lower rates of PBMC infection (9-13%). KSHV infection can precede KS onset by up to 21 months among AIDS-KS patients. CONCLUSIONS: AIDS-KS patients are significantly more likely to show evidence of KSHV infection in PBMC prior to KS onset than control HIV-infected patients. Because identical PBMC samples from cases and controls were examined blindly, these results are not caused by a bias in tissue sampling. Homo-/bisexual and hemophiliac AIDS patients who do not develop KS appear to have a low prevalence of infection. These findings indicate that KSHV infection is specifically associated with the subsequent development of KS in AIDS patients.