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Biomedical subjects

J D Regan

Publications and source records attributed to J D Regan.

At least 19 recordsLinked to original sources
PubMed1999

Response of periradicular tissues to growth factors introduced into the surgical site in the root-end filling material.

AIM: The objective of this study was to evaluate the healing of the periradicular tissues when exogenous growth factors were delivered to the respected root-end. The healing response was compared with that when Diaket was used as a control. METHODOLOGY: Non-surgical root canal treatment was performed on mandibular teeth in mongrel dogs. Surgical treatment followed and included root-end resection and root-end cavity preparation. Insulin-like growth factor in combination with platelet-derived growth factor, or fibroblast growth factor alone, were then placed in the root-end preparations on a polylactic acid carrier (Atrisorb) with or without the incorporation of the carrier tetracalcium phosphate. The healing was evaluated at 60 days with regard to presence of inflammatory response, bone regeneration, periodontal ligament formation and cementum formation. RESULTS: Osseous regeneration in the excisional would and periodontal formation were significantly greater when Diaket was used as the root-end filling material. Likewise, cementum deposition occurred significantly more frequently in the Diaket group (P < 0.05). The polylactic carrier Atrisorb remained in the surgical sites for the duration of the study. CONCLUSIONS: The use of specific growth factors, FGF and a combination of IGF/PDGF, delivered to the prepared root end in a collagen carrier did not initiate the desired periradicular tissue response of regeneration. Diaket, as used in this study, did stimulate a periradicular tissue response compatible with regeneration.

Analysis of Variance↗
PubMed1999

Rapid thrombectomy of superior sagittal sinus and transverse sinus thrombosis with a rheolytic catheter device.

Thrombosis of the dural venous sinuses is a potentially lethal condition that remains a diagnostic dilemma. Clinical outcome is typically dependent on the timeliness of diagnosis and definitive treatment. We report a case of successful rapid thrombectomy of extensive thrombus within the superior sagittal and transverse sinuses using a rheolytic catheter device. This appears to be a promising treatment option, particularly in those patients who do not respond to other, more established, forms of therapy.

Acute Disease↗
PubMed1998

Infected renal artery pseudoaneurysm and mycotic aortic aneurysm after percutaneous transluminal renal artery angioplasty and stent placement in a patient with a solitary kidney.

Endovascular infections after percutaneous transluminal renal angioplasty with stenting (PTRAS) are rarely reported. Because strict longitudinal follow-up of patients undergoing PTRAS is lacking, the true incidence of such complications remains obscure. We report the first case of a patient with an infected renal artery pseudoaneurysm and de novo mycotic aortic aneurysm after PTRAS. This case serves to illustrate several important points, including (1) the retrieval of renal function in patients with renal artery occlusion, (2) the pathogenesis of infection after PTRAS, (3) the diagnosis and management of endovascular infection after percutaneous vascular intervention, and (4) recommendations for periprocedural antibiotic prophylaxis during PTRAS.

Aged↗
PubMed1998

Primary stenting of the extracranial internal carotid artery in a patient with multiple cervical dissections: technical case report.

OBJECTIVE AND IMPORTANCE: Spontaneous dissection of the extracranial internal carotid artery (ICA) and vertebral artery (VA) is a well-documented cause of stroke in young, previously healthy patients. The majority of patients with spontaneous dissection are successfully treated with antiplatelet or anticoagulation therapy, but a significant proportion of patients progress to suffer devastating morbidity and mortality. Surgical intervention has primarily consisted of proximal ligation, extracranial-intracranial bypass, or endarterectomy. Generally, these procedures are technically demanding and yield disappointing clinical results. CLINICAL PRESENTATION/INTERVENTION: A 36-year-old man without a significant medical history initially presented with a several-day history of episodic right upper extremity weakness and numbness and visual obscurations. Cerebral angiography revealed bilateral ICA long segment narrowing (95%), distal left VA high-grade (95%) stenosis compatible with dissections, and right VA proximal occlusion. While therapeutically anticoagulated on heparin, the patient continued to experience crescendo episodes of right upper extremity paresis and paresthesias as well as aphasia. The patient underwent primary stenting of the left ICA, using a series of six overlapping stents (three Gianturco-Roubin coronary stents and three Palmaz-Schatz coronary stents). The patient remained symptom-free without neurological complications, and subsequent angiography performed at the 9-month follow-up examination confirmed continued patency of the stented left ICA as well as recanalization of the right ICA and VA. CONCLUSION: Neurovascular stents offer a minimally invasive and potentially efficacious treatment for the prevention of cerebral ischemia in patients with spontaneous extracranial dissection who remain symptomatic despite therapeutic anticoagulation.

Adult↗
PubMed1997

Update on interventional uroradiology.

From its humble beginnings as a method of expediently decompressing the obstructed kidney, the field of interventional uroradiology has evolved in the hands of urologists and interventional radiologists to a means of addressing myriad problems in the urinary tract and has changed the day-to-day practice of urology. The foundation of interventional uroradiology is the creation of an appropriate entry into the urinary system. After a review of this basic procedure, extensions of the technique and new applications of emerging technology are reviewed.

Cystoscopy↗
PubMed1997

UVB DNA dosimeters analyzed by polymerase chain reactions.

Purified bacteriophage lambda DNA was dried on a UV-transparent polymer film and served as a UVB dosimeter for personal and ecological applications. Bacteriophage lambda DNA was chosen because it is commercially available and inexpensive, and its entire sequence is known. Each dosimeter contained two sets of DNA sandwiched between UV-transparent polymer films, one exposed to solar radiation (experimental) and another protected from UV radiation by black paper (control). The DNA dosimeter was then analyzed by a polymerase chain reaction (PCR) that amplifies a 500 base pair specific region of lambda DNA. Photoinduced damage in DNA blocks polymerase from synthesizing a new strand; therefore, the amount of amplified product in UV-exposed DNA was reduced from that found in control DNA. The average lesion frequency per 500 base pair per strand at 16 PCR cycles was approximately 1.22, 1.00, 0.70 and 0.50 for 30 ng, 50 ng, 100 ng and 150 ng of dried DNA, respectively, after a total dose of 60 kJ m(-2) delivered with a solar UVB simulator. Although the average lesion frequency increases linearly with increasing doses for four different amounts of template DNA, the lesion frequency seems to be averaged by the amplified products from the protected lambda DNA molecules below the top few layers. The average daily dose, equivalent to the UV dose applied with the solar UVB simulator was 10.2 +/- 0.4 kJ m(-2) with the 50 ng containing DNA dosimeter in September 1995 in Melbourne, FL. Both 50 ng and 150 ng containing DNA dosimeters produced the same average daily dose within experimental error in January 1996, which was 5.2 +/- 0.3 kJ m(-2) at the same location. The dried lambda DNA dosimeter is compact, robust, safe and transportable, stable over long storage times and provides the total UVB dose integrated over the exposure time.

Australia↗
PubMed1997

Solar UVB dosimetry by amplification of short and long segments in phage lambda DNA.

DNA UVB dosimeters, consisting of minidots of dried bacteriophage DNA placed on a UV-transparent polymer film, were analyzed by polymerase chain reactions (PCR). Ultraviolet-B dosimetry obtained with amplification of phage lambda DNA of segments of 1.08 kilobase pairs (kbp) and 2.24 kbp was compared with that obtained with amplification of a 0.5 kbp segment (H. Yoshida and J. D. Regan, 66, 82-88, Photochem. Photobiol. 1997). The number of lesions in each segment induced by UV radiation is proportional to the size of the amplified segments; thus, the average lesion frequency per unit dose was greatest in the 2.24 kbp and least in the 0.5 kbp segment. The average lesion frequency per unit dose was approximately 3.5 x 10(-2) and approximately 11.9 x 10(-2) m2 kJ-1 for 1.08 kbp and 2.24 kbp, respectively, compared to that for 0.5 kbp of approximately 1.7 x 10(-2) m2 kJ-1 at 50 ng DNA. Dependability of DNA dosimeters, containing 50 ng and 100 ng, was tested by placing the DNA dosimeters for a time period of either 1 or 2 days outdoors on 8-12 January at Melbourne, FL. The daily dose was obtained directly with amplification of the 2.24 kbp segment and the 2 day continuous dose was obtained with amplification of the 1.08 kbp segment. Although the average lesion frequencies were different, both 50 ng and 100 ng DNA dosimeters provided about the same UVB dose, equivalent to the dose applied with a solar UVB simulator. The total UVB dose for 4 days obtained by amplification of the 1.08 and 2.24 kbp segments was 19.4-20.8 kJ m-2, which is within experimental error with the 4 day continuous dose obtained with 0.5 kbp segments. The average daily dose obtained by 0.5 kbp and 1.08 kbp agreed with the average daily dose directly obtained with 2.24 kbp.

Bacteriophage lambda↗
PubMed1996

The T cell receptor gene usage by simian immunodeficiency virus gag-specific cytotoxic T lymphocytes in rhesus monkeys.

MHC class I-restricted CTL play an important role in limiting the spread of HIV-1 in the infected individual. Elucidating the molecular interactions of CTL with the virus is, therefore, of central importance for characterizing the immune control of this infection. In exploring this CTL response, we have defined the TCR usage by SIVmac Gag-specific CTL in rhesus monkeys. Thirty-nine CTL clones were generated from PBL of three SIVmac-infected monkeys expressing the MHC class I Mamu-A*01 gene product, all of which were shown to recognize a single SIVmac Gag peptide in association with Mamu-A*01. Sixty-six percent of CTL clones derived from two monkeys early after infection expressed TCR genes of the V beta 13 family; 70% of these V beta 13+ CTL clones expressed a TCR heterodimer composed of V alpha 1 and V beta 13 gene products. In addition, there appeared to be a selection of a single conserved amino acid and restricted CDR3 lengths in junctional regions of TCR beta-chains expressed by the V beta 13+ CTL clones. These findings indicate significant structural constraints on the CTL-TCR interaction with the AIDS virus. Interestingly, 55% of the CTL clones derived from the third animal at a later time following infection employed genes of the V beta 6 family in their TCR. Despite the preferential use of TCR V family genes by the CTL clones, the SIVmac Gag-specific CTL response was clearly polyclonal; TCR expressed by these CTL clones displayed varied sequences in their CDR3 regions. Other V gene families, including V beta 23, V alpha 8, and V alpha 20, were used in TCR expressed by SIVmac Gag-specific CTL clones. These studies, therefore, indicate that the TCR repertoire of SIVmac Gag-specific CTL that share a peptide and MHC class I recognition specificity can be diverse. Such a broad CTL-TCR repertoire may be advantageous for the host in containing an AIDS virus infection.

Amino Acid Sequence↗
PubMed1995

DNA UVB dosimeters.

DNA can be used to establish and monitor solar UVB dose. Since the principal molecular site of UVB damage in living organisms is DNA, it is logical to quantitate biologically effective solar UVB in DNA dosimeters. In addition to their particular sensitivity to UVB, DNA dosimeters have the advantage of a 2 pi geometry for collecting diffuse UVB radiation from all vectors, low cost, small size and portability, and no moving parts. Both molecular (cyclobutane pyrimidine dimers) and biological (bacteriophage plaques) dosimeters can be quantitated as endpoints to yield the total dose. DNA dosimeters integrate the absorbed energy of all UVB wavelengths (290-320 nm), are highly sensitive to the differential biological effectiveness of these wavelengths, and also integrate over time in hours, days or weeks of exposure. Our experiments have focused on the demonstration of DNA solar dosimeters in the ocean at various depths, the application of the dosimeters to the terrestrial monitoring of solar UVB under various conditions, and the development of a mini-dosimeter which uses nanograms of DNA and is assayed by polymerase chain reaction.

Animals↗
PubMed1994

An acutely lethal simian immunodeficiency virus stimulates expansion of V beta 7- and V beta 14-expressing T lymphocytes.

SIVsmmPBj14, a variant simian immunodeficiency virus isolated from a pig-tailed macaque, stimulates the proliferation of macaque T lymphocytes in vitro and induces an acutely lethal disease in macaques characterized, in part, by lymphadenopathy and splenomegaly. To determine whether SIVsmmPBj14 exhibits superantigen-like activity, in vitro and in vivo studies of T-cell receptor V beta repertoire were undertaken using PCR-based quantitative methods. Whereas in vitro phytohemagglutinin stimulation of macaque peripheral blood lymphocytes did not cause a perturbation of T-cell receptor V beta repertoire, SIVsmmPBj14 stimulated the expansion of both CD4+ and CD8+ T-lymphocyte subpopulations expressing the V beta 7 and V beta 14 gene families. Such V beta 7 and V beta 14 expansions could be confirmed by a multiple RNase protection assay. Furthermore, the expansion of the same lymphocyte subpopulations was also detected in peripheral blood lymphocytes and lymph node cells of virus-infected macaques. These observations suggest that SIVsmmPBj14-mediated V beta expansion may contribute to the induction of an acutely lethal disease in macaques.

Acute Disease↗
PubMed1992

DNA as a solar dosimeter in the ocean.

Stratospheric ozone depletion may result in increased solar UV-B radiation to the ocean's upper layers and may cause deleterious effects on marine organisms. The primary UV-B damage induced in biological systems is to DNA. While physical measurements of solar UV-B penetration into the sea have been made, the effective depth and magnitude of actual DNA damage have not been determined. In the experiments reported here, UV-B-induced photoproducts (cyclobutane pyrimidine dimers) have been quantified in DNA molecules exposed to solar UV at the surface and at various depths in clear, tropical marine waters off Lee Stocking Island (23 degrees 45' N, 76 degrees 0.7' W), Exuma Cays, Bahamas. (14C)thymidine-labeled DNA or unlabeled bacteriophage phi X174 DNA was placed in specially designed quartz tubes at various depths for up to five days. Following exposure, DNA samples were removed to the laboratory where UV-B-induced pyrimidine dimers were quantified using a radiochromatographic assay, and bacteriophage DNA inactivation by solar UV-B was assayed by plaque formation in spheroplasts of Escherichia coli. Pyrimidine dimer induction was linear with time but the accumulation of dimers in DNA with time varied greatly with depth. Attenuation of dimer formation with depth of water was exponential. DNA at 3 m depth had only 17% of the pyrimidine dimers found at the surface. Bacteriophage phi X174 DNA, while reduced 96% in plaque-forming ability by a one day exposure to solar UV at the surface of the water, showed no effect on plaque formation after a similar exposure at 3 m. The data collected at the water's surface showed a "surface-enhanced dose" in that DNA damages at the real surface were greater than at the imaginary surface, which was obtained by extrapolating the data at depth to the surface. These results show the sensitivity of both the biochemical (dimers) and biological (phage plaques) DNA dosimeters. DNA dosimeters offer a sensitive, convenient and relatively inexpensive monitoring system, having both biochemical and biological endpoints for monitoring the biologically effective UV-B flux in the marine environment. Unlike physical dosimeters, DNA dosimeters do not have to be adjusted for biological effectiveness since they are sensitive only to DNA-mediated biologically effective UV-B radiation. Results of pyrimidine dimer induction in DNA by solar UV accurately predicted UV doses to the phage DNA.

Bacteriophage phi X 174↗
PubMed1990

Cyclobutane-pyrimidine dimer excision in UV-sensitive CHO mutants and the effect of the human ERCC2 repair gene.

Using a radiochromatographic assay, we have examined cis-syn cyclobutane-pyrimidine dimer removal after ultraviolet irradiation in cell lines representative of the first 6 complementation groups of Chinese hamster ovary DNA nucleotide excision repair mutants. AA8, the CHO cell line from which these mutants were derived, consistently showed normal dimer excision for a rodent cell. The mutants uniformly exhibited no significant dimer excision within the limits of determination. Additionally, V-H1, a mutant belonging to complementation group 2 and derived from V79 hamster cells, exhibited no dimer excision. Two UV5 derived transformants that carry the complementing human ERCC2 repair gene showed a capacity for dimer excision comparable to the AA8 wild-type cells.

Animals↗
PubMed1989

CHO mutant UV61 removes (6-4) photoproducts but not cyclobutane dimers.

The CHO mutant UV61 was previously assigned to complementation group 6 of UV-sensitive rodent cell mutants. UV61 is less sensitive to killing by UV radiation than mutants such as UV5, which is highly defective in the incision process that acts on UV-induced lesions. The D37 for cell survival is approximately 4 J/m2 for UV61, compared with 10 J/m2 for the parental AA8 line and approximately 2 J/m2 for UV5. Similarly, mutation induction at the hprt and aprt loci shows an intermediate response to UV61. In a post-replication recovery assay, the kinetics of maturation of pulse-labelled nascent DNA were normal after UV irradiation in UV61. Data from alkaline elution and alkaline unwinding assays showed that the rates of break accumulation and resealing, measured 0-120 min after irradiation, were also normal in the mutant. This repair incision correlated with the rapid, normal removal of pyrimidine(6-4)pyrimidone photoproducts in UV61 measured using a radioimmunoassay that is specific for this class of damage. In contrast, after exposure to 10 or 15 J/m2, no detectable removal of cyclobutane dimers from DNA was found in UV61 while AA8 cells removed 32% by 24 h. We suggest that the mutation in UV61 specifically lowers the affinity of a repair protein for cyclobutane dimers, which are also inefficiently removed from the bulk DNA of normal CHO cells. The resistance of UV61 to killing by the direct acting chemical 7-bromomethylbenz[a]anthracene was only slightly greater than that of UV5, indicating defective repair of bulky chemical adducts in addition to cyclobutane dimers.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Detection and repair of a UV-induced photosensitive lesion in the DNA of human cells.

Irradiation with UV light results in damage to the DNA of human cells. The most numerous lesions are pyrimidine dimers; however, other lesions are known to occur and may contribute to the overall deleterious effect of UV irradiation. We have observed evidence of a UV-induced lesion other than pyrimidine dimers in the DNA of human cells by measuring DNA strand breaks induced by irradiating with 313-nm light following UV (254-nm) irradiation. These breaks, measured by alkaline sucrose sedimentation, increased linearly with the dose of UV light over the range tested (10-40 J/m2). The breaks cannot be photolytically induced 5 h after a UV dose of 20 J/m2 in normal cells; however, in xeroderma pigmentosum variant cells, the breaks are inducible for up to 24 h after UV irradiation. Xeroderma pigmentosum group A cells in the same 5-h period show an increase in the number of strand breaks seen with 313-nm light photolysis from about 2 to 4 breaks/10(9) dalton DNA. These breaks can then be induced for up to 24 h. These data suggest that, in normal cells, the lesion responsible for this effect is rapidly repaired or altered; whereas, in xeroderma pigmentosum variant cells it seems to remain unchanged. Some change apparently occurs in the DNA of xeroderma pigmentosum group A cells which results in an increase in photolability. These data indicate a deficiency in DNA repair of xeroderma pigmentosum variant cells as well as in xeroderma pigmentosum group A cells.

DNA↗
PubMed1986

Quantitation of carcinogen-induced DNA damage and repair in human cells with the UVR ABC excision nuclease from Escherichia coli.

Recent studies by others have shown that the endonuclease complex coded for by the uvrA, uvrB and uvrC genes of Escherichia coli (UVR ABC excision nuclease) can incise DNA containing a variety of 'bulk-type' lesions, such as those resulting from u.v. light, (+/-)-7 alpha,8 beta-dihydroxy-9 alpha,10 alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (anti-BPDE), and N-acetoxy-2-acetylaminofluorene. Using partially purified UVR ABC excision nuclease, we have quantitated the number of endonuclease sensitive sites (ESS) in purified DNA isolated from human fibroblasts treated with u.v. light or BPDE. The number of ESS/10(8) daltons of DNA were calculated from the number average mol. wt. of the DNA as determined by sedimentation in alkaline sucrose gradients. The number of endonuclease sites increased linearly with increasing doses of either u.v. light or BPDE. The UVR ABC excision nuclease was able to incise a majority of the BPDE-DNA adducts. Xeroderma pigmentosum fibroblasts, complementation group A (XP12BE) had 20-25% more ESS at each dose than the BPDE-treated normal (HSBP) cells. Cells treated with 4 microM BPDE and allowed 12 h of incubation to perform excision repair showed removal of 60% of the initial number of ESS from HSBP DNA and 40% of the ESS from XP-A DNA. Beyond 12 h XP12BE cells lost no additional ESS while HSBP cells continued to lose ESS, although at a slower rate, until at 48 h only 22% of the initial ESS remained. In cells treated with 10 J/m2 of u.v. light, the UVR ABC excision nuclease detected 60% of the sites recognized by the pyridimine dimer specific Micrococcus luteus glycosylase/apyrimidinic endonuclease. These results demonstrate the potential use of the UVR ABC excision nuclease in a quantitative assay for determining the number of carcinogen-induced lesions in human DNA.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗