SEARCH · Search PubMed

Results for “DEFECTIVES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 829 records · Page 46Linked to original sources

PubMed2004

Splitting and tuning characteristics of the point defect modes in two-dimensional phononic crystals.

Point defect modes of acoustic wave in two-dimensional square arrays of square water rods in a mercury host were studied. The defects are created by three kinds of geometry, namely, square defect, circular defect, and rectangular defect, respectively. The results show that for both square defect and circular defect, the defect modes are only related to the defect filling fraction F(d), but not with the geometry of defects (square or circular), as well as the orientations of the square defect. For the rectangular defect, the defect modes could be tuned by changing the ratio of edge width of the defect, moreover, the double degenerate one will split into two nondegenerate modes when the ratio of edge widths Lx / L(y) >9.0. Meanwhile the corresponding pressure distributions also will be changed.

Journal Article↗

PubMed1997

Effect of platelet-derived growth factor-BB on bone formation in calvarial defects: an experimental study in rabbits.

The effect of recombinant human platelet-derived growth factor-BB (rhPDGF-BB) on bone healing was examined in calvarial defects in rabbits. Bicortical circular (critical size) defects were prepared in the calvarial bone of 16 rabbits. The defects were closed on the dural side and covered externally with expanded polytetrafluoroethylene membranes to prevent interference with osteogenesis within the defect by the surrounding tissue and to keep the growth factor in place. A single dose of methylcellulose gel (4.4%) with (n = 8) or without rhPDGF-BB (50 micrograms/ml) (n = 8) was applied to the defects, and the bone formation was evaluated after 8 weeks. Healing of defects in both groups was characterized by the presence of newly formed bone along the edges of the original defect and by a central area of fibrous connective tissue. The newly formed bone in the rhPDGF-BB treated defects had a trabecular structure; in contrast, a more compact structure was found in the control defects. In the rhPDGF-BB-treated defects, the bone ingrowth was 51.8 +/- 7.1% compared to 30.5 +/- 3.3% in the control defects. Furthermore, the amount of mineralized tissue was increased 112% in the rhPDGF-BB group. The amount of bone marrow was increased 75% in the rhPDGF-BB-treated defect. The porosity of cortical lamella in the newly formed bone was 84% higher in the rhPDGF-BB-treated defects compared to the control. These results show that administration of a single dose of rhPDGF-BB stimulates bone formation in critical size calvarial defects.

Animals↗

PubMed1998

Laser scanning tomography of localised nerve fibre layer defects.

AIMS: Retinal nerve fibre layer photography is a well established method to qualitatively document early structural changes which might be induced by primary open angle glaucoma. The aim was to analyse localised retinal nerve fibre layer (RNFL) defects in a new quantitative way with respect to surface topography, defect width, and surface reflectivity by means of the technique of confocal scanning laser tomography. METHODS: 12 eyes of 12 patients with a localised RNFL defect documented in RNFL photographs and a normal appearance of the optic disc were enrolled in the study. Using confocal laser scanning tomography (Heidelberg retina tomograph, HRT) a series of 32 optical section images from different focal planes of the retina at the site of the RNFL defects were obtained. The optical section images, the reflectivity images, and the topographic images were analysed regarding the visibility of the RNFL defects. The mean surface height and the reflectance at the sites of the RNFL damage were measured and compared with the adjacent apparently normal retina. The width of the RNFL defect at 1 mm distance from the disc border was evaluated. RESULTS: RNFL defects could be detected in nine of 12 reflectivity images (75%). Single optical section images displayed the RNFL defects in 12 of 12 eyes. The defect width ranged from 0.11 to 1.0 mm. In six of 12 eyes a surface depression (34 (SD 5) microns; range 21-47 microns) was present. The reflectance ratio ranged from 0.68 to 0.94 at the site of the RNFL defect. In eyes with a glaucomatous scotoma in a 6 degrees grid visual field (VF), the defect width was at least 0.25 mm. Surface depression and low reflectance ratio were found irrespective of the presence of a scotoma in the 6 degrees grid VF. CONCLUSION: The majority of localised RNFL defects can be detected in reflectivity images from laser scanning tomograms. Localised RNFL defects may be differentiated according to surface topography into those with and those without a measurable surface depression. A small but deep RNFL defect is not necessarily associated with a scotoma in routine 6 degrees grid VF static perimetry.

Aged↗

PubMed2002

Cigarettes with defective filters marketed for 40 years: what Philip Morris never told smokers.

BACKGROUND: More than 90% of the cigarettes sold worldwide have a filter. Nearly all filters consist of a rod of numerous ( > 12 000) plastic-like cellulose acetate fibres. During high speed cigarette manufacturing procedures, fragments of cellulose acetate that form the mouthpiece of a filter rod become separated from the filter at the end face. The cut surface of the filter of nearly all cigarettes has these fragments. In smoking a cigarette in the usual manner, some of these fragments are released during puffing. In addition to the cellulose acetate fragments, carbon particles are released also from some cigarette brands that have a charcoal filter. Cigarettes with filters that release cellulose acetate or carbon particles during normal smoking conditions are defective. OBJECTIVE: Specific goals were to review systematically the writings of tobacco companies to: (a) identify papers that would document the existence of defective filters; (b) characterise the extent of the defect; (c) establish when the defect became known; (d) determine whether the defect exists on cigarettes marketed currently; (e) assess the prevalence of the defect on cigarettes manufactured by different companies; (f) define whether the knowledge of the defect had been withheld by the tobacco company as confidential and not disclosed publicly; and (g) ascertain the feasibility of correcting or preventing the defect. METHODS: Document searches utilised databases of the scientific literature, medical journals, chemical abstracts, US Patents, Tobacco Abstracts, papers presented at tobacco meetings and court documents. RESULTS: Sixty one documents of Philip Morris, Inc were selected for study because they disclosed specifically the "fall-out" of cellulose acetate filter fibres and, for cigarettes with charcoal filters, carbon particles from cigarette filters. The term "fall-out" was defined in 1985 laboratory protocols of Philip Morris, Inc. as "loose fibers (or particles) that are drawn out of the filter during puffing of the cigarette". As early as 1957, the health concern of inhaling cellulose acetate fibres released from cigarette filters was addressed by Philip Morris, Inc. A 1962 document reported the results of laboratory tests conducted by Phillip Morris, Inc that compared the "fall-out" of cellulose acetate fibres from the filters of their cigarettes (Marlboro) and cigarettes of their competitor (Liggett & Meyers). A 1997 overview by Phillip Morris of documents addressing the "fallout of carbon particles and cellulose acetate fibers from filters" stated that they were "essentially routine reports" of cigarette filter assays, and referenced a "Filter Fallout" memo written in 1961-more than 40 years ago. Most likely these tests are being conducted presently as illustrated by a 1999 report that details the revisions of the "fall-out" protocol of Phillip Morris, Inc and reports the results of tests that measured the discharge of cellulose acetate fibres and silica gel from beta cigarettes with a new type of filter. Our analysis of the "fall-out" tests results presented in the 61 "fall-out" documents showed that filter fibres and carbon particles were discharged from the filters of all types of cigarettes tested. These cigarette types (n = 130) included both coded cigarettes and popular brand name cigarettes. No publications were found in the scientific literature of the "fall-out" studies. Thus, the results of the "fall-out" studies are thought to have been withheld as confidential to Philip Morris, Inc. We have identified also other companies that have tested recently cigarettes for defective filters. In addition, our searches have shown that simple, expedient, and inexpensive technologies for decontaminating cigarette filters of loose cellulose acetate fibres and particles from the cut surface of the filter have been developed and described in 1997 and 1998 US patents. What is more important is that these patents also define methods for preventing or reducing the broken plastic-like fibres that arise during cigarette making. Many US patents (n = 607; 1957 to 2001) have been awarded for cigarette filters. Some of these inventions describe novel materials and unique filtration schemes that would eliminate or minimise the discharge of filter materials into mainstream smoke. CONCLUSIONS: We have shown that: (a) the filter of today's cigarette is defective; (b) Philip Morris, Inc has known of this filter defect for more than 40 years; (c) the existence of this filter defect has been confirmed by others in independent studies; (d) many methods exist to prevent and correct the filter defect, but have not been implemented; and (e) results of investigations substantiating defective filters have been concealed from the smoker and the health community. The tobacco industry has been negligent in not performing toxicological examinations and other studies to assess the human health risks associated with regularly ingesting and inhaling non-degradable, toxin coated cellulose acetate fragments and carbon microparticles and possibly other components that are released from conventional cigarette filters during normal smoking. The rationale for harm assessment is supported by the results of consumer surveys that have shown that the ingestion or inhalation of cigarette filter fibres are a health concern to nearly all smokers.

Carbon Dioxide↗

PubMed1992

Regional thallium uptake in irreversible defects. Magnitude of change in thallium activity after reinjection distinguishes viable from nonviable myocardium.

BACKGROUND: Thallium reinjection immediately after stress-redistribution imaging identifies ischemic but viable myocardium in as many as 50% of the regions characterized by conventional redistribution imaging as irreversibly injured. However, we have previously shown that some regions in which irreversible defects persist despite reinjection are metabolically active, and hence viable, by positron emission tomography. In the current study, we determined whether the severity of reduction in thallium activity within irreversible defects on redistribution images and the magnitude of change in regional thallium activity after reinjection can further discriminate viable from nonviable myocardium in such defects. METHODS AND RESULTS: We studied 150 patients with coronary artery disease by exercise thallium tomography using the rest-reinjection protocol. The three sets of images (stress, redistribution, and reinjection) were then analyzed quantitatively. The increase in regional thallium activity from redistribution to reinjection was computed, normalized to the increase observed in a normal region, and termed "differential uptake." Of the 175 myocardial regions designated to have irreversible thallium defects on conventional 3-4 hour redistribution images, 132 had only mild-to-moderate reduction in thallium activity (51-85% of normal activity), and 43 had severe reduction in thallium activity (less than or equal to 50% of normal activity). Thallium reinjection resulted in enhanced relative activity in 60 of 132 (45%) of the mild-to-moderate irreversible defects and 22 of 43 (51%) of the severe irreversible defects, leaving roughly half of these defects remaining irreversible after reinjection. However, in regions that appeared to remain irreversible despite reinjection, the magnitude of differential uptake differed between mild-to-moderate (74 +/- 14%) and severe (35 +/- 16%) irreversible defects (p less than 0.001). All regions with mild-to-moderate defects demonstrated greater than 50% differential uptake after reinjection. In contrast, all except two of the regions with severe irreversible defects demonstrated differential uptake of less than 50%. Fifteen patients also underwent positron emission tomography at rest with 18F-fluorodeoxyglucose (FDG) and 15O-water. FDG uptake was present in 91% of regions with mild-to-moderate reduction in thallium activity, and the results of differential uptake and FDG data were concordant in 81% of these regions. CONCLUSIONS: These data indicate that the magnitude of thallium uptake after reinjection differs between mild-to-moderate and severe irreversible defects on standard 3-4 hour redistribution images. The substantial differential uptake of thallium (greater than 50%) after reinjection in mild-to-moderate defects, even when relative thallium activity does not increase appreciably (and the defect appears to remain irreversible), coupled with preserved metabolic activity by positron emission tomography, supports the concept that such mild-to-moderate irreversible defects represent viable myocardium.

Adult↗

PubMed2000

Recurrent miscarriage syndrome due to blood coagulation protein/platelet defects: prevalence, treatment and outcome results. DRW Metroplex Recurrent Miscarriage Syndrome Cooperative Group.

Although first-time miscarriages are usually caused by chromosomal defects, about 55% of recurrent miscarriages are caused by procoagulant defects that induce thrombosis and infarction of placental vessels. Of recurrent miscarriages, about 7% are caused by chromosome defects, 15% to hormonal defects, and 10% to 15% to anatomical defects. Recurrent miscarriage involves more than 500,000 women in the United States each year. During the past 4 years, 179 patients, prescreened for chromosomal, hormonal, and anatomical defects, and found to harbor none, underwent hemostasis defect evaluation. A total of 160 of these have been analyzed. A hemostasis defect was found in 150 of 160 women (n = 94% of screened women). The mean age was 33 years; the mean number of miscarriages before referral was three. All women with a procoagulant defect (149) were treated with preconception ASA at 81 mg/d, and unfractionated porcine heparin at 5000 U every 12 hours was added immediately postconception; both agents were used to term delivery. Only two of 149 patients failed therapy. The defects found were as follows: antiphospholipid syndrome, 67%; sticky platelet syndrome, 21%; tissue plasminogen activator (TPA) deficiency, 9%; factor V Leiden, 7%; high PAI-1, 6%; protein S, 5%; high LP(a), 3%; AT, 2%; protein C, 1%. Thirty-eight patients had more than one defect. In the group with antiphospholipid syndrome, 24% only had a subgroup antibody (antiphosphatidyl-serine, -inositol, -ethanolamine, -choline, -glycerol) or antiphosphatidic acid antibody, in the absence of anticardiolipin antibody or lupus anticoagulant. This finding is similar to that recently reported in early age ischemic stroke patients (<50 years old). In summary, about 55% of patients with recurrent miscarriage harbor a procoagulant defect to account for placental vascular occlusion. More than 98% will have a normal term delivery with preconception aspirin (ASA) and addition of postconception heparin to term. Patients should be screened by an obstetrician or by reproductive specialists for hormonal and anatomic defects before initiating a procoagulant evaluation; if such prescreening is done, the yield of a defect is high and appropriate therapy leads to an excellent outcome.

Abortion, Spontaneous↗

PubMed1985

Hydroxylapatite as an alloplastic graft in the treatment of human periodontal osseous defects.

Twelve patients, 32 to 60 years of age, received a polycrystalline ceramic form of pure dense hydroxylapatite as an alloplastic bone implant material in intrabony defects following reflection of full mucoperiosteal flaps, root planing and defect-curettement. The defects were measured from an acrylic stent, using an endodontic silver point which was placed to the base of the defect. Similarly, debrided and curetted defects in the same patients were not implanted and served as controls. Recalls for documentation and plaque control were at 1, 2, and 4 weeks, and at 3, 6 and 9 months. Measurements relating to changes in defect-depth were made upon reentry at 9 months. The twelve defects, serving as controls, showed very little difference between the pretherapy and 9-month measurements. The initial mean measurement from the base of the defect to the highest alveolar crest was 4.27 mm and the 9-month mean measurement after curettage only was 3.36 mm. In terms of resolution of the original defect this amounted to 19.49% reduction, but a 0.46-mm mean loss in height of the alveolar crest provided an actual percentage fill of the original defect of 9.91%. Of sixteen experimental defects, the same initial mean measurement from the base of the defect to the highest alveolar crest was 5.18 mm and the 9-month mean measurement after grafting was 2.43 mm. In terms of resolution of the original defect, this amounted to a 53.57% reduction, but in contradistinction to the curettage sites, a mean increase in height of the highest alveolar crest of 0.61 mm gave a true percentage fill of the original defect of 66.89%. At the 9-month reentry, the implanted mass seemed to be partially "calcified" and was resistant to penetration with a probe or removal with a curette. The data and clinical impression strongly suggest that hydroxylapatite has a potential as an alloplastic implant with clinically apparent acceptance by the soft and hard tissues.

Adult↗

PubMed2004

Periodontal repair in surgically created intrabony defects in dogs: influence of the number of bone walls on healing response.

BACKGROUND: The objective of this study was to histologically evaluate periodontal healing following flap surgery in intrabony periodontal defects to determine the influence of the number of bone walls on periodontal regeneration. METHODS: One-, 2-, and 3-wall intrabony periodontal defects were surgically produced at the proximal aspect of mandibular premolars in either right or left jaw quadrants in six beagle dogs. Mucoperiosteal flaps were positioned and sutured to their presurgery position following defect preparation. The animals were euthanized at 8 weeks post-surgery, and block sections of the defect sites were collected for histologic and histometric analysis. RESULTS: Bone and cementum regeneration was positively correlated to the number of bone walls limiting the intrabony periodontal defects. The junctional epithelium averaged (+/- SD) 1.5 +/- 0.2, 1.2 +/- 0.3, and 0.9 +/- 0.2 mm for the 1-, 2-, and 3-wall defects, respectively, with the 3-wall defects being significantly different from the 1-wall defects (P <0.05). Cementum regeneration averaged 1.2 +/- 0.6, 2.0 +/- 0.6, and 2.8 +/- 0.5 mm for the 1-, 2-, and 3-wall defects, respectively; all groups were significantly different from each other (P <0.05). Bone regeneration averaged 1.5 +/- 0.5, 1.7 +/- 0.6, and 2.3 +/- 0.5 mm for the 1-, 2-, and 3-wall defects, respectively, with the 3-wall defects being significantly different from the 1-wall defects (P <0.05). CONCLUSIONS: The results suggest that the number of bone walls is a critical factor determining treatment outcomes in intrabony periodontal defects. One- and 3-wall intrabony defects appear to be reproducible models to evaluate candidate technologies for periodontal regeneration.

Alveolar Bone Loss↗

PubMed2004

Clinical evaluation of calcium sulfate in combination with demineralized freeze-dried bone allograft for the treatment of human intraosseous defects.

BACKGROUND: Medical-grade calcium sulfate (CS) is a biocompatible, bioabsorbable, and clinically versatile ceramic for use in bone repair. This study compared the clinical efficacy of a combination of calcium sulfate dihydrate, as a binder and barrier, and demineralized freeze-dried bone allograft (DFDBA) to polytetrafluoroethylene (ePTFE) and DFDBA for the treatment of human periodontal defects. METHODS: Two intrabony defects were compared in each of 19 patients with chronic periodontitis. After initial preparation, full-thickness mucoperiosteal flaps were elevated, osseous defects debrided, and the roots prepared (ultrasonic, hand curets, and tetracycline conditioning). Defects were randomly treated with either a combination graft of DFDBA with CS (4:1) covered by a CS barrier or with DFDBA and fitted with an ePTFE barrier. Flaps were coronally positioned to obtain primary closure. Clinical soft tissue measurements were recorded at 6 months, and all study sites were surgically reentered for evaluation. RESULTS: The mean presurgical measurements for defects randomized to the CS and ePTFE treatments, respectively, were similar for attachment level (AL; 6.2 +/- 1.8 mm and 6.1 +/- 1.7 mm), probing depth (PD; 6.3 +/- 1.1 mm and 6.2 +/- 1.1 mm), and gingival recession (0.1 +/- 1.9 mm and 0.2 +/- 1.4 mm). Defects treated with CS or ePTFE demonstrated statistically significant (P < or = 0.0001) reductions in mean PD (2.7 +/- 1.4 mm and 3.4 +/- 1.3 mm, respectively) and gains in mean AL (1.8 +/- 1.5 mm and 1.7 +/- 1.4 mm, respectively). Recession increased by 0.8 +/- 1.4 mm at CS sites and 1.6 +/- 1.7 mm at ePTFE-treated sites (P < or = 0.05). Pretreatment mean defect depths were 4.1 +/- 1.0 mm and 3.7 +/- 1.0 mm for CS and ePTFE sites, respectively. Reentry evaluations revealed a mean defect fill of 2.7 +/- 1.5 mm and 2.5 +/- 0.9 mm for the CS and ePTFE sites, respectively, with a corresponding mean defect resolution of 80.3 +/- 18.7% and 76.7 +/- 18.5%. The CS and ePTFE sites did not differ significantly in mean defect fill or defect resolution. CONCLUSIONS: The results of this study indicate that calcium sulfate, when used as a binder and barrier in combination with DFDBA, supports significant clinical improvement in intrabony defects, as evidenced by reductions in probing depth, gains in clinical attachment level, and defect fill and resolution. Calcium sulfate represents an important alternative to non-resorbable ePTFE barriers in combination with DFDBA for the treatment of intrabony defects.

Adult↗

PubMed1996

Repair of partial-thickness defects in articular cartilage: cell recruitment from the synovial membrane.

Partial-thickness defects evolving in mature articular cartilage do not heal spontaneously. This type of defect was created in the articular cartilage of adult rabbits and Yucatan minipigs, and the effects of chondroitinase ABC or trypsin, fibrin clots, and mitogenic growth factors on the healing process were examined histologically at intervals ranging from one to forty-eight weeks. The effect of chondroitinase ABC or trypsin was examined initially. Articular cartilage contains macromolecules, including proteoglycans, which render the surfaces of this tissue, and of partial-thickness defects within it, antiadhesive. Chondroitinase ABC digests the glycosaminoglycan chains of cartilage proteoglycans, and trypsin degrades their core proteins. To test the hypothesis that mesenchymal cells may be prevented from adhering to and migrating over the surfaces of partial-thickness defects by proteoglycans, we removed a superficial layer of these macromolecules from the surface of the defect with use of one of these enzymes. The treatment evoked an increase in the coverage of the defect surface with mesenchymal cells; when combined with the local application of a mitogenic growth factor (basic fibroblast growth factor, transforming growth factor-beta 1, epidermal growth factor, insulin-like growth factor-1, or growth hormone), the coverage was more extensive but mesenchymal cells did not extend into and completely fill the volume of the defect. When the surface of the defect was treated with chondroitinase ABC and the cavity of the defect was filled with a fibrin clot to furnish a matrix or scaffolding for the migration of cells therein, there was migration and proliferation of cells throughout the volume of the defect but at a low population density. Mesenchymal cells remodeled the deposited fibrin matrix, which was replaced by a loose fibrous connective tissue. When defects that had been treated with chondroitinase ABC were filled with a fibrin clot containing a mitogenic growth factor, mesenchymal cells filled the entire cavity of the defect, and the density of the cells was greatly increased, particularly when transforming growth factor-beta 1 was used. Histological studies revealed a continuous layer of mesenchymal cells extending from the synovial membrane across the superficial tangential zone of normal articular cartilage into the defect, indicating that the cells that were recruited for the repair process were of synovial origin. At forty-eight weeks, the entire cavity of the defect remained filled with a fibrous connective tissue.

Animals↗

PubMed1993

Lack of correlation between site of wrist pain and location of noncommunicating defects shown by three-compartment wrist arthrography.

OBJECTIVE: Communicating defects shown by wrist arthrography often correlate poorly with the location of the patient's symptom(s). No study of wrist arthrography in which noncommunicating defects have been isolated, described, and correlated with the site of patients' symptoms has been reported. The aim of this study was to correlate the site(s) of patients' pain and the location(s) of noncommunicating defects shown by wrist arthrography. MATERIALS AND METHODS: One hundred noncommunicating capsular defects and incomplete defects of the interosseous ligaments and triangular fibrocartilage in 82 patients were identified from 462 three-compartment wrist arthrograms. Correlation between the sites of pain and sites of the noncommunicating defect was described as: (1) exact correlation, (2) ulnar/radial side correlation, (3) ambiguous correlation, or (4) no correlation. Statistical analysis was performed for each type of defect separately, in aggregate for patients who had more than one defect, and by separate analysis using patients' age (less than or greater than 30 years old). RESULTS: Capsular defects were detected in 65 patients, incomplete perforations of the triangular fibrocartilage in 28 patients, and incomplete defects of the scapholunate and lunotriquetral ligament in three patients each. No statistically significant correlation was found between individual defects and symptoms or between the site(s) of symptoms and patterns of multiple noncommunicating defects. Further, age did not influence the degree of correlations (chi 2 = 0.000-0.476, p values = 0.49-1.00). CONCLUSION: Attribution of patient's symptoms to noncommunicating defects shown by wrist arthrography is not reliable. Cases in which site-specific arthrographic defects directly correlate may be fortuitous. Additional studies will be necessary to determine the future role of wrist arthrography in the evaluation of the painful wrist.

Adult↗

PubMed2004

Gated (99m)Tc-tetrofosmin SPECT for discriminating infarct from artifact in fixed myocardial perfusion defects.

UNLABELLED: Soft-tissue attenuation artifacts generally appear as fixed perfusion-scan defects. Gated (99m)Tc-tetrofosmin SPECT may help differentiate myocardial infarction (MI) from artifacts, as fixed defects with decreased function (wall motion and thickening) probably represent MI, whereas attenuation artifacts represent preserved function. METHODS: Ungated stress and gated rest (99m)Tc-tetrofosmin SPECT was performed on 153 consecutive patients referred for evaluation of coronary artery disease. From stress and summed gated rest images, 107 patients (70%) were identified with isolated fixed defects. The function of the defects was assessed semiquantitatively from gated stress images. The findings were correlated with clinical (history or electrocardiographic Q waves) evidence of MI. RESULTS: Of 62 patients with fixed defects and clinical MI, 60 (97%) had an abnormal defect function. Of 45 patients with no clinical MI, 16 (36%) had decreased function of the defect, possibly indicating silent MI. In 29 of the 45 patients (64%) with no clinical MI, defect function was normal. Because most (90%) fixed defects with normal systolic function occurred in men with inferior fixed defects (87%) or women with anterior fixed defects (3%), these were most likely attenuation artifacts. By reclassifying the condition of patients with fixed defects and normal function as normal, patients with unexplained fixed defects (no clinical MI) decreased from 29% to 10%. CONCLUSION: Gating adds considerable value to (99m)Tc-tetrofosmin SPECT myocardial perfusion imaging in characterizing fixed defects and potentially improves test specificity.

Adenosine↗

PubMed2006

[Infant mortality due to birth defects in the Czech Republic in 1994-2004].

UNLABELLED: AIM AND TYPE OF STUDY: A retrospective data study with an analysis of pre- and postnatal occurrence of selected types of birth defects in the Czech Republic during 1994 to 2004 period. An analysis of infant mortality rate in children with selected types of birth defects during their first year of life is described. METHODOLOGY: Data on prenatal diagnostics were obtained from particular departments of medical genetics. Data on birth defects incidences were obtained from National Health registers - Institute of Health Information and Statistics (National Register of Congenital Anomalies and National Newborns Register) from the 1996-2004 period were used. A case analysis of incidences of 14 types of pre- and postnatally diagnosed birth defects was performed for the period 1994-2004. In postnatally diagnosed cases, an analysis of survival and extinction of particular types of defects during the first year of life was also performed. RESULTS: During 1994-2004, there were 1 030 069 children born in the Czech Republic. Including prenatally diagnosed cases, we registered 305 cases of anencephaly, 454 spina bifida, 156 encephalocele, 528 cases of congenital hydrocephalus, 304 omphalocele and 302 cases of gastroschisis, 241 oesophageal defects, 302 anorectal malformations, 312 cases of diaphragmatic hernia, 518 renal agenesis/hypoplasia cases, 529 cases of cystic kidneys and 1764 Down syndrome cases. Secondary prevention rate was high in neural tube defects (61-100%), abdominal wall defects (60-79%) and Down syndrome (63%). In operable defects, a first-year survival was lowest in congenital hydrocephalus (63%) and neural tube defects -excluding anencephaly - (82%). In abdominal wall defects, diaphragmatic hernia, oesophageal and anorectal malformations, the survival rate was, however, 76-91% of children. CONCLUSIONS: Birth defects present a major contribution to infant mortality and morbidity. Prematurity in a combination with a birth defect prolongs inpatient days and increases a need of a total parenteral feeding in a newborn and it also makes a worse prognosis for the infants with birth defects. An improvement of prenatal diagnostics with an early detection of the most severe types along with the associate ones could decrease incidences of such cases. A progress in surgical techniques and a special neonatal and infant intensive health care would also contribute an improvement of survival.

Congenital Abnormalities↗

PubMed1995

Using gated technetium-99m-sestamibi SPECT to characterize fixed myocardial defects as infarct or artifact.

UNLABELLED: Perfusion-scan fixed defects may result from soft tissue attenuation, decreasing test specificity for coronary disease and myocardial infarction (MI). Gated 99mTc-sestamibi SPECT may help differentiate MI from artifact since fixed defects with decreased function (wall motion and thickening) probably represent MI, whereas attenuation artifacts either have normal function or at least do not demonstrate markedly reduced function. METHODS: Ungated resting and gated stress 99mTc-sestamibi SPECT was performed in 551 consecutive patients referred for evaluation of coronary disease. From resting and summed gated stress images, 180 patients (33%) were identified with isolated fixed defects. Function of the defects was assessed subjectively from gated stress images and results were correlated with clinical (history and/or ECG Q-waves) evidence of MI. RESULTS: Of 102 patients with fixed defects and clinical MI, 98 (96%) had abnormal defect function. Of 78 patients with no clinical MI, 18 (23%) had decreased function of the defect, possibly indicating silent MI. In 60 of the 78 patients (77%) with no clinical MI, defect function was normal. Because most (91%) of fixed defects with normal systolic function occurred in women with anterior fixed defects (48%) or men with inferior fixed defects (43%), these were most likely attenuation artifacts. By reclassifying patients with fixed defects and normal function as normal, patients with unexplained fixed defects (no clinical MI) decreased from 14% to 3%. CONCLUSION: Gating provides a valuable adjunct to 99mTc-sestamibi SPECT in characterizing fixed defects and potentially improving test specificity.

Artifacts↗

PubMed1994

Long-term fate and effects of exercise on sternal cartilage autografts used for repair of large osteochondral defects in horses.

Bilateral osteochondral defects (10 mm2 x 3 mm deep) were created on the distal articular surface of the radial carpal bone of ten, 2- to 3-year-old horses. One defect of each horse was repaired, using a sternal cartilage autograft (treated), and the other was left untreated (control). The horses were exercised on a high-speed treadmill at incrementally increased speed and duration over the course of 12 months. Horses were evaluated arthroscopically at 6 to 7 weeks, and clinical examinations were conducted weekly at exercise. Twelve months after surgery, carpuses of each horse were radiographed and clinically examined prior to euthanasia. A gross pathologic evaluation of each joint was conducted, and samples were collected for histologic, histochemical, histomorphometric, and biochemical evaluation. Radiographically, the grafted joints had more extensive evidence of arthropathy, and clinically, 8 of the 10 horses were more lame in the grafted limb. On the basis of histomorphometry, the repair tissue of the grafted defects contained a greater median percentage of hyaline cartilage (45%) than that of control defects (4.5%), and the control defects contained a greater percentage of fibrocartilage (82%) than did grafted defects (28.5%). A greater median percentage of repair tissue stained with safranin-O in the grafted defects (24.5%) than in the control defects (3.5%). On gross pathologic and histologic evaluation, repair tissue of the control defects had better continuity and was more firmly attached to the subchondral bone than was repair tissue of the grafted defects. Repair tissue of the grafted defects had extensive fissure and flap formation. Histologically, subchondral bone reactivity and fibroplasia was extensive in grafted joints. Repair tissue of grafted defects had a greater percentage of type II collagen (mean +/- SEM, 83.5 +/- 2.95%) than did controls (mean, 79.4 +/- 3.87%) that was not statistically significant. Hexosamine content was significantly higher (P < 0.05) in repair tissue of the grafted defect (mean, 28.9 +/- 3.00 mg/g of dry weight) vs control (mean, 20.6 +/- 1.85 mg/g of dry weight). On the basis of this experimental model, sternal cartilage autografts cannot be recommended at this time for repair of osteochondral defects in athletic horses.

Animals↗

PubMed2001

Clinical analysis of families with heart, midline, and laterality defects.

Disturbances of the normal asymmetric placement of organs, such as polysplenia or situs inversus, have been defined traditionally as laterality defects. However, there is compelling evidence from vertebrate models and human birth defects to hypothesize that defects of the midline, isolated congenital heart defects, and laterality defects are etiologically related. We present the clinical characteristics of three families that exhibit a variety of midline defects and isolated heart defects in addition to laterality defects. These observations suggest that the phenotypic consequences of mutations causing laterality defects include defects of the midline as well as isolated heart defects. To further explore the relationship between midline, heart, and laterality defects, it is imperative that detailed phenotyping of individuals and families with laterality defects be done and a classification system created to facilitate identification of genes causing human laterality disorders.

Blood Vessels↗

PubMed1990

Diagnosis, therapy, and outcome of ventricular septal defects in the 1st year of life: a two-dimensional colour-Doppler echocardiography study.

Between January 1987 and July 1989 a ventricular septal defect (VSD) as a single cardiac lesion was detected in 269 small infants aged less than 1 year. The diagnosis was achieved by two-dimensional echocardiography and Doppler colour flow mapping using subcostal, parasternal, apical, and suprasternal views. VSDs were divided into perimembraneous, muscular, malalignment, and subpulmonary defects. Septal defects in complex lesions and atrioventricular defects were excluded. In group 1 (174 infants up to 4 weeks of age, mean 10 days) 125 muscular (71.8%), 35 (20.1%) perimembraneous, 12 (6.9%) malalignment, and 2 (1.1%) subpulmonary defects were diagnosed. One baby had a combined perimembraneous and muscular defect. In another baby a malalignment defect was associated with an av-canal. In group 2 (95 infants aged 4 weeks to 1 year, mean 4.0 months), 57 (60%) muscular, 32 (33.6%) perimembraneous and 6 (6.3%) malalignment defects were found. Within the maximum observation period of 13 months, spontaneous closure occurred in 72 (42.6%) of 169 infants who had a sufficient follow up. Sixty-four had a muscular (88.9%) and 8 (11.1%) a perimembraneous defect. Surgical intervention was required in 11 patients: five perimembraneous defects were closed, one was palliated. Five infants with a malalignment defect were palliated. The malalignment defect frequently needed surgical intervention even in newborns; it never closed spontaneously. About 10% of patients with perimembraneous septal defect required surgery. Spontaneous closure rarely occurred in early infancy. Muscular VSDs were most frequent but virtually never required therapy. Spontaneous closure rate was about 50% during the 1st year of life.

Echocardiography, Doppler↗

PubMed2003

The epidemiology of cardiovascular defects, part I: a study based on data from three large registries of congenital malformations.

To analyze complex and noncomplex cardiac malformations regarding prevalence and in relation to demographic variables, we pooled data on infants (age 1 year or younger) with congenital cardiovascular defects from three large birth defect registries in California, Sweden, and France. Altogether, 12,932 infants had one or more congenital heart defects out of 4.4 million live births and stillbirths. The registries in Sweden and France obtained data through reporting from various sources; in California, medical records were reviewed. As expected, definitions and ascertained conditions differed among each of the registries. The total rates for severe defects were similar (1.43 per 1,000), but differed for specific defects. Clear differences in epidemiological characteristics existed for specific defects; for example, severe cardiac defects sex ratios were significantly high for hypoplastic left heart syndrome, d-transposition of great vessels, double outlet right ventricle, total anoralous pulmonary venous return, tetralogy of Fallot, and significantly low for pulmonary atresia without ventricular septal defect and endocardial cushion defect. Few defects were similar for several epidemiological characteristics, but, for example, the combination of ventricular and atrial septal defects appeared equivalent with endocardial cushion defect under some circumstances, yet behaved differently with regard to associated noncardiovascular defects.

Age Factors↗