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PubMed1994

Surgical management of prolapse of the anterior vaginal segment: an analysis of support defects, operative morbidity, and anatomic outcome.

OBJECTIVES: The objectives of this study were to describe a group of women with prolapse of the anterior vaginal segment associated with bilateral paravaginal defects, to report the morbidity associated with the operative repair, and to analyze the results of preoperative and postoperative pelvic support defects in five vaginal sites. STUDY DESIGN: Between June 1, 1988, and Nov. 3, 1993, 62 consecutive women with prolapse of the anterior vaginal segment associated with bilateral periurethral and perivesicle support defects and other coexisting pelvic support defects were treated by paravaginal repair done via the vagina and total pelvic reconstruction. Site-specific analysis of support for the urethra, bladder, cervix or cuff, cul-de-sac, and rectum was performed preoperatively, 6 weeks postoperatively, and longitudinally to assess the anatomic outcome of surgery. Perioperative morbidity was defined as hemorrhage requiring homologous blood transfusion, pelvic nerve injury, deep venous thrombosis, visceral injury, or infection. RESULTS: One hundred percent of the study patients had preoperative evidence of bilateral paravaginal defects, and 87% had a prolapse of the anterior segment that was halfway to completely outside the hymen. Seven patients experienced perioperative morbidity none of which was unique to this procedure. Fifty-six patients have been followed up a mean of 1.6 years postoperatively. In four, anterior segment defects have developed to or through the hymen, although none is as large as the preoperative defect and none has required further surgery to date. In one patient a postoperative defect developed in the cul-de-sac extending to the hymen; she has had the defect repaired and has been followed up 1.7 years with no support defects. CONCLUSION: Paravaginal repair performed transvaginally is a safe, effective method of management of prolapse of the anterior vagina associated with paravaginal defects. Coexisting support defects that require specific identification and repair can also be managed vaginally.

Adult↗
PubMed1996

Defects of the respiratory chain in various tissues of old monkeys: a cytochemical-immunocytochemical study.

The aim of the present study was to evaluate if defects of the respiratory chain known to occur in humans, also exist in lower primates. Cytochemical-immunocytochemical studies of the respiratory chain enzymes in five monkeys (10-25 years of age) showed defects of ubiquinone cytochrome-c-oxidoreductase (complex III), of cytochrome-c-oxidase (complex IV) and of ATP-synthase (complex V) in the limb muscles, diaphragm, heart muscle and extraocular muscles of three old animals (about 25 years) and also in the heart muscle of two younger animals (10 and 15 years). Characteristically, the defects were randomly distributed and there was no loss of succinate-dehydrogenase (complex II) in the fibres. Ultracytochemistry-immunocytochemistry of complex IV disclosed that in an involved fibre segment all the mitochondria exhibited the defect. The highest number of defects was observed in the extraocular muscle (up to 340/cm2) while the lowest defect density was present in the limb muscles (2-5/cm2). Defects of complex IV occurred two to three times more often than defects of complex III and besides isolated defects of complex III and IV, combined defects of both complexes were also observed. Defects of complex V occurred exclusively in combination and were rarely seen. Using subunit specific antisera against complex IV, it could be demonstrated at light and electron microscopic level that loss of activity of cytochrome-c-oxidase was associated with a loss both of mitochondrially and nuclearly coded subunits of the enzyme. In summary, aging in lower primates and humans is characterised by a highly similar defect expression of the respiratory chain enzymes, with intercellular and interorgan differences of the aging process, underlining the universal nature of the involved pathogenetic mechanisms.

Aging↗
PubMed2005

A computer modelling study of the uptake, structure and distribution of carbonate defects in hydroxy-apatite.

Computer modelling techniques have been employed to qualitatively and quantitatively investigate the uptake and distribution of carbonate groups in the hydroxyapatite lattice. Two substitutional defects are considered: the type-A defect, where the carbonate group is located in the hydroxy channel, and the type-B defect, where the carbonate group is located at the position of a phosphate group. A combined type A-B defect is also considered and different charge compensations have been taken into account. The lowest energy configuration of the A-type carbonate has the O-C-O axis aligned with the channel in the c-direction of the apatite lattice and the third oxygen atom lying in the a/b plane. The orientation of the carbonate of the B-type defect is strongly affected by the composition of the apatite material, varying from a position (almost) flat in the a/b plane to being orientated with its plane in the b/c plane. However, Ca-O interactions are always maximised and charge compensating ions are located near the carbonate ion. When we make a direct comparison of the energies per substitutional carbonate group, the results of the different defect simulations show that the type-A defect where two hydroxy groups are replaced by one carbonate group is energetically preferred (DeltaH = -404 kJ mol(-1)), followed by the combined A-B defect, where both a phosphate and a hydroxy group are replaced by two carbonate groups (DeltaH = -259 kJ mol(-1)). The type-B defect, where we have replaced a phosphate group by both a carbonate group and another hydroxy group in the same location is energetically neutral (DeltaH = -1 kJ mol(-1)), but when the replacement of the phosphate group by a carbonate is charge compensated by the substitution of a sodium or potassium ion for a calcium ion, the resulting type-B defect is energetically favourable (DeltaH(Na) = -71 kJ mol(-1),DeltaH(K) = -6 kJ mol(-1)) and its formation is also promoted by A-type defects present in the lattice. Our simulations suggest that it is energetically possible for all substitutions to occur, which are calculated as ion-exchange reactions from aqueous solution. Carbonate defects are widely found in biological hydroxy-apatite and our simulations, showing that incorporation of carbonate from solution into the hydroxyapatite lattice is thermodynamically feasible, hence agree with experiment.

Bone Substitutes↗
PubMed2004

Active proliferation of mesenchymal cells prior to the chondrogenic repair response in rabbit full-thickness defects of articular cartilage.

OBJECTIVES: In full-thickness articular defects, fibroblast growth factor-2 (FGF-2) participates in the chondrogenic repair response which occurs in a defect-size dependent manner. Here we demonstrate that FGF-2 plays a critical role in the proliferation of pre-chondrogenic mesenchymal cells during chondrogenic induction. METHODS: Three-millimeter- or 5-mm-diameter cylindrical defects were created in the femoral trochlea of the rabbit knee. The defects received sterile saline or FGF-2 (50 pg/h) via an osmotic pump for the initial 2 weeks. We assessed the proliferative capacity of undifferentiated mesenchymal cells in the reparative tissue with the anti-proliferating cell nuclear antigen (PCNA) monoclonal antibody. Using a total of 180 rabbits, we performed three sets of experiments. RESULTS: In the 3-mm-diameter defects, undifferentiated mesenchymal cells spontaneously initiated chondrogenic differentiation within 2 weeks, resulting in the regeneration of surfacing articular cartilage concomitantly with the repair of subchondral bone. No evidence of chondrogenesis was seen in the 5-mm-diameter defects, whereas application of FGF-2 promoted successful regeneration of articular cartilage. In the 3-mm-diameter defects and in the FGF-2-treated 5-mm defects, PCNA immunoreactivity was widely detected in undifferentiated cells in the reparative tissue at 1 and 2 weeks after creation of the defects. In contrast, in the 5-mm-diameter defects without FGF-2 treatment, the PCNA-positive cells were found at a significantly lower incidence. CONCLUSIONS: Active expansion of undifferentiated cell population mediated by FGF-2 is required to initiate and support a chondrogenic repair response in full-thickness defects of articular cartilage. Endogenous FGF-2 could not meet the requirements of growth signaling in the center of larger sized defects.

Alkaline Phosphatase↗
PubMed1988

Nerve fiber layer and optic disc fluorescein defects in glaucoma and ocular hypertension.

Photographs of the optic discs and fluorescein angiograms of 31 patients with open-angle glaucoma and 43 patients with ocular hypertension were evaluated for nerve fiber layer (NFL) defects and absolute fluorescein filling defects. All of the glaucomatous eyes showed both defects. Of the 43 ocular hypertensive eyes, in which both NFL and absolute fluorescein filling defects were evaluated, 9% had only NFL defects, 19% had only fluorescein filling defects, 14% had both defects, and 58% had neither defect. The percent area of fluorescein defect in the optic disc increased with severity of NFL defect in glaucoma and ocular hypertension. This study confirms the relationship of fluorescein filling defects and NFL defects to glaucomatous abnormalities and thus the association between vascular damage to the optic nerve and axon loss in glaucoma. The earliest objective evidence of glaucomatous damage can be detected with a combination of NFL evaluation and optic disc fluorescein angiography.

Aged↗
PubMed2003

Effects of a cultured autologous chondrocyte-seeded type II collagen scaffold on the healing of a chondral defect in a canine model.

Using a previously established canine model for repair of articular cartilage defects, this study evaluated the 15-week healing of chondral defects (i.e., to the tidemark) implanted with an autologous articular chondrocyte-seeded type II collagen scaffold that had been cultured in vitro for four weeks prior to implantation. The amount and composition of the reparative tissue were compared to results from our prior studies using the same animal model in which the following groups were analyzed: defects implanted with autologous chondrocyte-seeded collagen scaffolds that had been cultured in vitro for approximately 12 h prior to implantation, defects implanted with autologous chondrocytes alone, and untreated defects. Chondrocytes, isolated from articular cartilage harvested from the left knee joint of six adult canines, were expanded in number in monolayer for three weeks, seeded into porous type II collagen scaffolds, cultured for an additional four weeks in vitro and then implanted into chondral defects in the trochlear groove of the right knee joints. The percentages of specific tissue types filling the defects were evaluated histomorphometrically and certain mechanical properties of the repair tissue were determined. The reparative tissue filled 88+/-6% (mean+/-SEM; range 70-100%) of the cross-sectional area of the original defect, with hyaline cartilage accounting for 42+/-10% (range 7-67%) of defect area. These values were greater than those reported previously for untreated defects and defects implanted with a type II collagen scaffold seeded with autologous chondrocytes within 12 h prior to implantation. Most striking, was the decreased amount of fibrous tissue filling the defects in the current study, 5+/-5% (range 0-26%) as compared to previous treatments. Despite this improvement, indentation testing of the repair tissue formed in this study revealed that the compressive stiffness of the repair tissue was well below (20-fold lower stiffness) that of native articular cartilage.

Animals↗
PubMedDate not supplied

Guided bone regeneration of cranial defects, using biodegradable barriers: an experimental pilot study in the rabbit.

The aim of this study was to test if a biodegradable barrier could be used to achieve proper bone healing of full-thickness trephine skull defects, applying the biological principle of guided tissue regeneration (GTR). Two New Zealand white rabbits were used. In each animal, 2 circular through-and-through bone defects with a diameter of 8 mm were created in the midline of the frontal and parietal bones of the calvarium. One defect was covered with the mucoperiosteal flaps without placement of an intervening membrane barrier (control). One test defect (test 1) was covered by a biodegradable, non-porous polylactic acid membrane on the outer (supra-calvarial) side of the defect, and 2 test defects (tests 2 and 3) were covered by similar membranes on both the outer and the inner aspects of the defects, prior to flap closure. 6 weeks postsurgically, the animals were sacrificed and the defect areas including surrounding tissues were harvested for histological preparation. The control defect was essentially occupied by supra-calvarial soft tissue, located in direct contact with the dural tissue. In the test cavities, there was a continuous bridge of regenerated bone extending from one edge of the defect to the other, although in test 1 not attaining the same thickness as the bone bordering the defect. In the 2 other test defects, the regenerated bone had reached a thickness almost corresponding to that of the surrounding bone. The bone regeneration was achieved without recourse to adjunctive bone graft materials.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Birth defects in children with newborn encephalopathy.

This study was designed to investigate birth defects found in association with newborn encephalopathy. All possible birth defects were ascertained in a population-based study of 276 term infants with moderate or severe encephalopathy and 564 unmatched term control infants. A strong association between birth defects and newborn encephalopathy was found with defects affecting 27.5% of children with encephalopathy and 4.3% of control children (odds ratio 8.55; 95% confidence interval 5.25 to 13.91;p<0.001). In 11.8% of infants with a birth defect the defect was not diagnosed until after the newborn period, illustrating one of the difficulties in attempting to exclude infants with birth defects from studies of newborn encephalopathy. The majority of defects (89%) were not specific anomalies of the CNS. In 36.8% of children with encephalopthy who had a birth defect, the defect was considered to be the probable cause of the encephalopathy. Infants with birth defects who had encephalopathy had a poorer prognosis than those without: they were twice as likely to die by the age of 2 years and three times more likely to have cerebral palsy. This study catalogues the spectrum of birth defects associated with newborn encephalopathy and illustrates the importance of their inclusion when investigating both the aetiology and outcome of this condition.

Abnormalities, Multiple↗
PubMedDate not supplied

The effect of monopolar radiofrequency energy on partial-thickness defects of articular cartilage.

PURPOSE: To evaluate the effect of monopolar radiofrequency (RF) energy on partial-thickness defects of articular cartilage, comparing the outcome of partial-thickness defects treated with monopolar RF energy with that of treatment by conversion of partial-thickness defects to full-thickness defects by curettage and microfracture. TYPE OF STUDY: Randomized trial using adult female sheep. MATERIALS AND METHODS: Thirty-six sheep were used in this study. Both stifles in each animal were randomly assigned to 1 of the following 3 procedures: (1) partial-thickness defect without any treatment to serve as a sham-operated control, (2) partial-thickness defect with RF energy treatment, and (3) partial-thickness defect treated by conversion of the defect to a full-thickness defect by curettage and microfracture. Nine sheep were euthanized at 0, 2, 12, and 24 weeks after surgery (n = 6 per group). After euthanasia, cartilage samples were harvested from the defect sites, and chondrocyte viability was analyzed by confocal laser microscopy using a triple-labeling technique. Cartilage samples also were decalcified and stained with hematoxylin and eosin and safranin-O for histologic analysis. Surface properties of cartilage samples were analyzed using scanning electron microscopy. RESULTS: The analysis of chondrocyte viability showed that RF treatment caused death of almost all chondrocytes in the defect. Histologic analysis showed that RF treatment caused detrimental effects to chondrocytes and proteoglycan concentration that progressed over time, and that full-thickness defects were repaired by fibrocartilage by 24 weeks after surgery. Scanning electron microscopy analysis indicated that RF-treated groups were significantly smoother and less irregular than control groups at 2, 12, and 24 weeks after surgery. CONCLUSIONS: This study showed that monopolar RF energy caused long-term damage to cartilage in this sheep model and did not appear to have the beneficial effects reported in a previous study that evaluated application of this technique using a bipolar RF probe.

Animals↗
PubMed1982

[Topography of early glaucomatous visual field defects in computerized perimetry].

A total of 301 visual fields of 215 glaucoma patients exhibiting early glaucomatous field loss up to Stage II according to Aulhorn were investigated to determine the frequency distribution of absolute and relative defects at the 73 test points of Program 31 of the Octopus computer perimeter. The following results were obtained: (1) The frequency of absolute and relative defects was higher in the upper half of the visual field; (2) The frequency of both absolute and relative defects increased from 6 to 30 degrees eccentricity in the upper visual field, predominantly in the upper nasal quadrant, whereas in the temporal lower quadrant there were less absolute defects but equally frequent relative defects; (3) Defects in the nasal quadrant and above the horizontal meridian are most frequent (between 18 and 30 degrees absolute, between 12 and 30 degrees relative), while temporally of the blind spot and below the horizontal meridian they are quite rare; (4) In the upper half of the field, defects are closer to the fixation point and blind spot; the area between blind spot and macula largely free of defects. --In 71 eyes of 69 patients a similar frequency distribution was found with the Competer computer perimeter (test field 15-20 degrees eccentricity) giving good correlation with the Octopus results. --In 301 eyes of 215 patients with early glaucomatous defects the four test points in the region of the blind spot were evaluated and compared with the results of 121 eyes of 71 patients with ocular hypertension and no field changes. It appears highly probable that an increase in the size of the blind spot is associated with the incidence of field defects. --The distribution of early glaucomatous field defects in 214 eyes revealed a combination of paracentral scotomata with peripheral defects in 75.2%, exclusively peripheral scotomata in 19.6% and exclusively paracentral scotomata in 5.1%. The significance of the results with regard to the pathophysiology of glaucomatous visual field loss is discussed.

Computers↗
PubMed1993

Representative and misrepresentative associations of birth defects in livebirths. Conditions under which relative risks greater than unity in livebirths necessarily imply relative risks greater than unity in all conceptuses.

One may express the relative risk of defect in all conceptuses, r(def), as a function of the relative risk of defect in livebirths, r(def,lb), and in embryonic and fetal deaths, r(def,efd), as r(def) = C(lb)r(def,lb) + C(efd)r(def,efd), where C(lb) and C(efd) are coefficients defined in terms of conceptus and defect viability and lethality. If the relative risk of birth defect in livebirths, r(def,lb), is greater than unity, but the relative risk of defect in all conceptuses, r(def), is equal to or less than unity (or the reverse pattern holds), then the relative risk of defects in livebirths may be said to be "distorting" or "misrepresentative" because it does not reflect the nature of the association in all conceptuses. The authors define and present an explicit expression for a boundary upon the relative risk of defect in livebirths. If the relative risk of defect in livebirths is (validly) greater than this boundary value, then the relative risk in all conceptuses must be greater than unity and the observed relative risk of defect in births is "representative" and not distorting. The authors show that the boundary value is equal to 1/C(lb), where C(lb) is a simple function of the lethality of all unexposed conceptuses, the lethality of unexposed conceptuses with defect, and the relative risk of any embryonic and fetal death. Tables of the boundary relative risk for various values of these variables are presented. Over a very wide range of reference variables, a (valid) relative risk of defect in livebirths of 3.5 or greater implies a positive association with defect in all (recognized) conceptuses in the population studied.

Congenital Abnormalities↗
PubMed2005

Factors affecting progression of knee cartilage defects in normal subjects over 2 years.

OBJECTIVES: Cartilage defects are present in subjects with knee osteoarthritis (OA). Although they are often present in healthy subjects, there is little data on the natural history of cartilage defects. The aim of this study was to examine the change in cartilage defects over 2 yr and to identify factors associated with this change. METHODS: One hundred and twenty-four healthy subjects underwent magnetic resonance imaging of their dominant knee at baseline and follow-up. Cartilage defects were scored (0-4) at five sites. Bone size was determined at medial and lateral tibial plateau and patella. Height, weight, body mass index and physical activity were measured by standard protocols. RESULTS: Eighty-six subjects completed the study. The mean cartilage defect score of each tibiofemoral compartment increased over time. However, medial and lateral tibiofemoral defect score decreased in 5% of the subjects. Cartilage defects were more likely to progress in males than females in each individual compartment (P<0.001 for medial tibiofemoral, P=0.005 for lateral tibiofemoral and P=0.01 for patellar cartilage). Baseline cartilage defect score was negatively associated with the progression of cartilage defects in each compartment (all P<0.001). CONCLUSION: Although knee cartilage defects progressed over time in the majority of normal subjects, those of the highest severity tended to regress. Male gender and baseline cartilage defect score were the main factors associated with the progression of cartilage defects. Larger studies will be required to identify factors associated with the progression and regression of lesions.

Body Mass Index↗
PubMed2000

Reconstruction of large sacral defects following total sacrectomy.

Total sacrectomies for cancer ablation often result in extensive defects that are challenging to reconstruct. In an effort to elucidate the criteria to select the most effective reconstructive options, we reviewed our experience with the management of large sacral wound defects. All patients who had a sacral defect reconstruction after a total sacrectomy at our institution between January of 1993 and August of 1998 were reviewed. The size of the defect, the type of reconstruction, postoperative complications, and functional outcome in each patient were assessed. A total of 27 flaps were performed in 25 patients for sacral defect reconstruction after a total sacrectomy. Diagnoses consisted of chordoma (n = 13), giant cell carcinoma (n = 2), sarcoma (n = 5), rectal adenocarcinoma (n = 4), and radiation induced necrosis (n = 1). The size of sacral defects ranged from 18 to 450 cm2 (mean, 189.8 cm2). Ten patients, including five who had preoperative radiation therapy, underwent transpelvic vertical rectus abdominis myocutaneous (VRAM) flap reconstruction for sacral defects with a mean size of 203.3 cm2. Of these, five patients (50 percent) had complications (four minor wound dehiscences and one seroma). Eight patients, including one who had preoperative radiation therapy, underwent bilateral gluteal advancement flap reconstruction for sacral defects with a mean size of 198.0 cm2. They had no complications. Two patients, both of whom had preoperative radiation therapy, underwent gluteal rotation flap reconstruction for sacral defects of 120 cm2 and 144 cm2. Both patients had complications (one partial flap loss and one nonhealing wound requiring a free flap). Three patients, including one who had preoperative radiation therapy, underwent reconstruction with combined gluteal and posterior thigh flaps for sacral defects with a mean size of 246 cm2; two of these patients had partial necrosis of the posterior thigh flaps. Three patients, all of whom had preoperative radiation therapy, underwent free flap reconstruction for sacral defects with a mean size of 144.3 cm2. They had no complications. Our experience suggests that there are three reliable options for the reconstruction of large sacral wound defects: bilateral gluteal advancement flaps, transpelvic rectus myocutaneous flaps, and free flaps. In patients with no preoperative radiation therapy and intact gluteal vessels, the use of bilateral gluteal advancement flaps should be considered. In patients with a history of radiation to the sacral area and in patients whose gluteal vessels have been damaged, the use of the transpelvic VRAM flap should be considered. If the transpelvic VRAM flap cannot be used because of previous abdominal surgery, a free flap should be considered as a last option.

Adult↗
PubMed2006

Fetal fatty acid oxidation defects and maternal liver disease in pregnancy.

OBJECTIVE: The objective was to evaluate the relationships between all types of fetal fatty acid oxidation defects and maternal liver disease, including acute fatty liver of pregnancy and hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome. METHODS: This was a case-control study comparing fetal fatty acid oxidation defects to the outcome of maternal liver disease. Fifty case infants with fatty acid oxidation defects were identified, with 25 matched controls collected per case. This generated a total of 50 case infants and 1,250 control infants. Pregnancies were evaluated for the presence of maternal liver disease (comprised of acute fatty liver of pregnancy, HELLP syndrome, and preeclampsia evolving into HELLP syndrome) using a conditional logistic regression model. Subgroup analysis compared long chain to short and medium chain fatty acid defects. RESULTS: Maternal liver disease was noted in 16.00% of all fatty acid oxidation defect pregnancies compared with 0.88% in the general population (odds ratio 20.4, 95% confidence interval 7.82-53.2). These pregnancies demonstrated an 18.1-fold increase in maternal liver disease when compared with our matched population controls with unaffected fetuses. All classifications of fatty acid oxidation defects were at high risk of developing maternal liver disease. Long chain defects were 50 times more likely than controls to develop maternal liver disease and short and medium chain defects were 12 times more likely to develop maternal liver disease. CONCLUSION: Maternal liver disease is significantly higher across the entire spectrum of fatty acid oxidation defects pregnancies compared with the matched control population. Notably, there is significant risk to the pregnancies with fetuses affected with short and medium chain defects, not just those with fetal long chain fatty acid oxidation defects as previously reported. Future studies should examine the pathophysiology of all infant fatty acid oxidation defects and its implications for maternal liver disease for improved future health outcomes. LEVEL OF EVIDENCE: II-2.

Case-Control Studies↗
PubMed2003

Induction of bone ingrowth from acetabular defects to a porous surface with OP-1.

Reliable ingrowth of bone into porous-coated cementless total hip components can be expected in primary surgery. In the revision scenario, however, bone deficiency frequently is encountered and the remaining bone may have less ingrowth potential. Allograft bone and bone graft substitutes may be successful in healing bone defects, but have virtually no capacity to induce bone growth from the defect into the porous surface. To evaluate the role osteoinductive bone proteins may play in enhancing bone ingrowth, six canines had bilateral total hip arthroplasties with a cementless press-fit porous-coated acetabular component. A defect 8 mm in diameter and 5 mm in depth was created in the superior weightbearing area of each acetabulum. One defect in each animal was filled with recombinant human osteogenic protein-1. Each contralateral defect was filled with allograft bone, left empty (defect healing control), or no defect was created (intact) to serve as a control for ideal conditions for bone ingrowth. The osteogenic protein-treated defects healed more completely than allograft bone-treated or empty defects and achieved a bone density equivalent to the intact acetabulum. Bone ingrowth also occurred to a significantly higher degree in the osteogenic protein group compared with the allograft or empty defects achieving a degree of ingrowth equivalent to the intact acetabulum controls. The osteogenic bone protein was successful in achieving complete defect healing and inducing extensive ingrowth from the defect into the adjacent porous coating.

Acetabulum↗
PubMed2006

Prediction of visual field defects on standard automated perimetry by screening C-20-1 frequency doubling technology perimetry.

PURPOSE: To determine if perimetric defects, initially seen with C-20-1 frequency doubling technology (FDT) in eyes with normal standard automated perimetry (SAP), will subsequently develop on standard automated perimetry. METHODS: Review of patients considered high-risk glaucoma suspects (GS) or with ocular hypertension (OHT), who underwent one C-20-1 FDT in 1997 or 1998. An abnormal frequency doubling technology was defined in two ways, as having either at least one, or at least two abnormal locations. An abnormal standard automated perimetry was defined as fulfilling two of three modified Anderson criteria for abnormality on two consecutive tests and at final standard automated perimetry. RESULTS: Of 63 eyes (50 patients), 18 (28.6%) had >or=1 FDT defects, and 12 (19.0%) had >or=2 defects. After follow-up of 62 +/- 26 months, an abnormal standard automated perimetry developed in 5 eyes (28%) with frequency doubling technology defects at 22 +/- 13 months (28% of eyes with >or=1 defect and 42% of eyes with >or=2 FDT defects), and in 4 of 45 eyes (9%) with normal frequency doubling technology at 32 +/- 30 months. Kaplan-Meier survival analysis revealed the risk of an abnormal standard automated perimetry at 5 years with or=1 defects, and >or=2 defects, was 10.3%, 11.8%, 30.6%, and 46.4% respectively (P = 0.060 for >or=1 defects compared with no defects; P = 0.002 for >or=2 defects compared with <or=1 defect). CONCLUSIONS: Abnormal results on C-20-1 frequency doubling technology perimetry predicted glaucomatous visual field loss on standard automated perimetry in some patients in this patient population, though a relatively high false positive rate was noted. Abnormality on C-20-1 frequency doubling technology warrants close observation, and further prospective evaluation is warranted.

Aged↗
PubMed2006

Defect solitons in photonic lattices.

Nonlinear defect modes (defect solitons) and their stability in one-dimensional photonic lattices with focusing saturable nonlinearity are investigated. It is shown that defect solitons bifurcate out from every infinitesimal linear defect mode. Low-power defect solitons are linearly stable in lower bandgaps but unstable in higher bandgaps. At higher powers, defect solitons become unstable in attractive defects, but can remain stable in repulsive defects. Furthermore, for high-power solitons in attractive defects, we found a type of Vakhitov-Kolokolov (VK) instability which is different from the usual VK instability based on the sign of the slope in the power curve. Lastly, we demonstrate that in each bandgap, in addition to defect solitons which bifurcate from linear defect modes, there is also an infinite family of other defect solitons which can be stable in certain parameter regimes.

Journal Article↗
PubMed2005

Influence of prenatal diagnosis and pregnancy termination of fetuses with birth defects on the perinatal mortality rate in Victoria, Australia.

Historical data show that in Victoria birth defects have accounted for approximately 25% of all perinatal deaths. Terminations of pregnancies (TOPs) for birth defects occurring at > or =20 weeks gestation are included in the population-based perinatal data collection. These are classified as stillbirths or neonatal deaths. Some would have survived the perinatal period if no termination had taken place, and as a result they have the effect of increasing the perinatal mortality rate (PMR). Conversely, TOPs <20 weeks gestation, of fetuses with lethal birth defects that would have resulted in a perinatal death, are not included in the statistics and therefore reduce the PMR. The aim of this study was to examine the effect on the PMR of TOPs following the prenatal detection of birth defects, taking into account the severity or 'lethality' of the birth defects. Data on live births, stillbirths, neonatal deaths and TOPs carried out because of a birth defect were collected from the Victorian Birth Defects Register (BDR) for 1989-2000. Birth defects were categorised into three groups, according to the estimated likelihood of a baby with that condition dying in the perinatal period: a 'lethal' birth defect was one where there was >50% likelihood of death, 'possibly lethal' 15-50% and 'non-lethal' less than 15%. Based on these 'lethality' groups and associated assumptions about average survival rates beyond the neonatal period, the PMR was recalculated. TOPs for 'non-lethal' birth defects at > or =20 weeks gestation increased the PMR by 3.8%. TOPs for 'lethal' birth defects <20 weeks decreased the PMR by 14.4%. The net effect on the overall PMR from TOPs for birth defects was a 10.6% decrease.

Abortion, Induced↗