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PubMed1996

RXR alpha deficiency confers genetic susceptibility for aortic sac, conotruncal, atrioventricular cushion, and ventricular muscle defects in mice.

Retinoid-dependent pathways play a central role in regulating cardiac morphogenesis. Recently, we characterized gene-targeted RXR alpha -/- embryos, which display an atrial-like ventricular phenotype with the development of heart failure and lethality at embryonic day 14.5. To quantitate the frequency and complexity of cardiac morphogenic defects, we now use microdissection and scanning electron microscopy to examine 107 wild-type, heterozygous, and homozygous embryos at embryonic day 13.5, 14.5, and 15.5. RXR alpha -/- embryos display complex defects, including ventricular septal, atrioventricular cushion, and conotruncal ridge defects, with double outlet right ventricle, aorticopulmonary window, and persistent truncus arteriosus. In addition, heterozygous RXR alpha embryos display a predisposition for trabecular and papillary muscle defects, ventricular septal defects, conotruncal ridge defects, atrioventricular cushion defects, and pulmonic stenosis. Lastly, we show that the intermediate anatomic phenotype displayed by heterozygous embryos is mirrored in the molecular marker MLC-2a. The intermediate phenotype of RXR alpha heterozygous embryos documents a gene dosage effect for RXR alpha in maintaining normal cardiac morphogenesis. In addition, some defects in RXR alpha mutant mice are phenocopies of human congenital heart defects, thereby suggesting that a relative deficiency in RXR alpha or molecules downstream in its signaling pathway may represent congenital heart disease-susceptibility genes.

Animals↗

PubMed2004

Free scapular flap for reconstruction of upper extremity defects.

OBJECTIVE: To determine the functional outcome of free scapular flaps performed for reconstruction of complex upper extremity defects. DESIGN: Case series. PLACE AND DURATION OF STUDY: The Aga Khan University Hospital, from 1998 to 2001. SUBJECTS AND METHODS: All those patients in whom free scapular flap was done for reconstruction of upper extremity defects, were included. The important variables included demographic data, etiology of soft tissue defects, site and size of defect, complications, percentage of wound coverage by flap. Patient satisfaction, objective assessment of flap and range of motion of involved joints was determined. RESULTS: There were 9 males and 2 female patients with mean age of 31.54 +/- SD11.86 years. The causes of tissue defects were road traffic accident in eight cases, bomb blast injury in 2 and industrial injury in one case. Eight scapular flaps were performed to reconstruct the defects over the hand, wrist and forearm; two flaps for defects of arm and shoulder and one for elbow coverage. Average defect size was 18 cm long and 11 cm wide. Donor site was closed primarily in all cases. Based on cosmetic appearance, coverage of required defect, performance of activities of daily living and functional range of motion of involved joints, 7 cases were graded excellent and 4 cases were good. CONCLUSION: Scapular flap provided good robust coverage, which helped to do an early reconstruction and rehabilitation in our cases. Scapular flap can be considered workhorse for reconstruction of upper extremity defects.

Adult↗

PubMedDate not supplied

Microvascular free flap reconstructive options in patients with partial and total maxillectomy defects.

OBJECTIVE: To evaluate and discuss the free flap reconstructive options for patients with partial and total maxillectomy defects. DESIGN: Retrospective review of cases. SETTING: Two tertiary referral centers. PATIENTS: Fifty-one patients had partial or total maxillectomy defects resulting from oncologic surgical resection, and 7 had partial maxillectomy defects resulting from trauma. Inferior or partial maxillectomy defects included 10 anterior arch and hemipalate defects and 12 subtotal or total palate defects. Total maxillectomy defects with and without orbital exenteration included 36 maxilla defects with hemipalate and malar eminence. INTERVENTION: There were 11 fibula, 14 rectus abdominis, 9 scapular, 10 radial forearm, 5 latissimus dorsi, and 13 combination latissimus dorsi and scapular flaps. MAIN OUTCOME MEASURES: Separation of the oral cavity from the sinonasal cavities, diet, type of dental restoration, type of orbital restoration, speech intelligibility, and complications. RESULTS: Only 1 flap failure was reported. There was loss of bone in 2 flaps and loss of the skin paddle in 1 flap. All palatal defects were sealed by the separation of the oral and sinonasal cavities. Thirty-eight patients were able to eat a regular diet while the remaining patients maintained a soft diet. All patients conversed on the telephone without difficulty in intelligibility. Eight patients had an implant-borne dental prosthetic, and 30 patients had a conventional partial prosthetic. Orbit restoration was achieved in 2 patients with an implant-borne prosthetic, and 6 patients retained a standard orbit prosthetic. CONCLUSIONS: Free flap reconstruction of the maxilla creates reproducible permanent separation of the oral and sinonasal cavities in a single-stage procedure. In addition, there exists the potential for dental rehabilitation with restoration of masticatory and phonatory function. Free flap reconstruction also provides a good cosmetic result, which improves patients' outlook and contributes to their overall well-being. Reconstructive flaps are designed to fit specific maxillary defects and patient needs to provide optimally functional and cosmetic results.

Adolescent↗

PubMed2002

Comparison of glaucomatous visual field defects using standard full threshold and Swedish interactive threshold algorithms.

OBJECTIVES: To compare the severity, size, and depth of glaucomatous visual field defects using standard full threshold (FT), Swedish interactive threshold algorithm (SITA) standard (SS), and SITA fast (SF) algorithms of the Humphrey perimeter. METHODS: A prospective observational case series of 77 patients with glaucoma performed FT, SS, and SF 30-2 white-on-white testing programs on the same day on 2 occasions for 1 month. The severity of defects was compared using the mean deviation, pattern standard deviation, Advanced Glaucoma Intervention Study, and Hodapp-Anderson-Parrish severity scores. The sizes of defects were compared using the total number of abnormal points on the pattern deviation plot that fit standard criteria for glaucomatous visual field defects. The depths of the defects were compared using the sum of the threshold values for points identified in the pattern deviation plot as fitting criteria for glaucomatous defects. RESULTS: The mean deviations were slightly better using the SS (-9.6 +/- 7.1 dB) or the SF (-9.1 +/- 6.7 dB) algorithm compared with the FT algorithm (-10.3 +/- 7.1 dB) (P<.005). There were no significant differences in pattern standard deviations between SS (8.6 +/- 4.0, P =.08) and SF (8.1 +/- 3.6, P =.19) compared with FT (8.3 +/- 3.3), although the pattern standard deviation was higher in SS fields compared with SF fields (P<.001). Advanced Glaucoma Intervention Study scores were slightly better when the SS (7.5 +/- 5.6) or SF (7.2 +/- 5.4) algorithm was used compared with the FT algorithm (8.6 +/- 5.4) (P<.001). The sizes of glaucomatous defects were slightly larger using the SS (20.9 +/- 10.7) algorithm compared with the FT algorithm (19.2 +/- 10.9) (P =.004) but not the SF algorithm (20.0 +/- 10.6) (P =.11). The depth of defects measured by the SS (220.4 +/- 108.0 dB) and SF (219.8 +/- 101.3 dB) algorithms was significantly shallower compared with that measured by the FT algorithm (152.3 +/- 79.1 dB) (P<.001). There were no significant differences in Hodapp-Anderson-Parrish severity scores among algorithms (P =.12). CONCLUSIONS: Glaucomatous defects are measured significantly shallower using the new SITA algorithms but are approximately the same size and severity compared with FT measurements. Care should be taken when using threshold values to compare glaucomatous defects in a patient when converting from FT to SITA algorithms.

Adult↗

PubMedDate not supplied

Exploratory spatial analysis of birth defect rates in an urban population.

Are birth defect rates unusually high in particular urban localities? The answer requires that the birth defect rate for which 'significance' is claimed be adjusted for the variable population sizes of each area for which the rate is computed and for the spatial dependence of rates based on shared observations between neighboring areas. By address-matching birth and birth defect records to a digital road map, we are able to compute local birth defect rates at regular grid locations by dividing the number of birth defects that occurred in the geographical vicinity of a grid location by the total number of births in the same vicinity. We test for significance, at regular spatial intervals, against the null hypothesis that the observed rate at any locality could reasonably have arisen by chance alone, given the underlying geographical variation in births. Significance is determined by using Monte Carlo simulations, where each birth location has an identical probability of being a defect. From 1000 simulations, a statistical distribution of the birth defect rate for each grid location is determined. The proportion of the simulated birth defect rates that are less than the observed rate at any grid location is the probability that the observed rate is significant. These probabilities, portrayed as isarithmic maps, show areas that have significantly high birth defect rates. Our results show birth defect rates for the period 1983 to 1990 in Des Moines, Iowa, U.S.A.

Cluster Analysis↗

PubMed1987

Limb-body wall complex: II. Limb and spine defects.

Limb defects from 25 fetuses with limb-body wall (LBW) complex were evaluated to determine the mechanism of limb damage. The limb defects could be divided into 3 pathogenetic groups: (1) secondary to disruption of embryonic vessels and surrounding tissue (84%), (2) secondary to amniotic bands or adhesions (16%), and (3) deformation versus hemorrhage (44% with club feet), with some fetuses having more than one pathogenetic mechanism causing limb defects. The hypothesis that the majority of limb defects resulted from disruption of embryonic vessels was supported by the following findings: 96% of the LBW complex fetuses had limb defects; the lower limbs were at greater risk of damage than the upper limbs (28% rt arm, 52% lt arm, 60% rt leg, 72% lt leg); there was a distal to proximal progression of limb damage in 92% of the fetuses; statistical analysis of comparing the location of the most severe limb defect and the body wall defect did not find concordance between the side (p = 1.0) and the region (p = 0.18) of the body wall defect; and limb defects found in the human specimens were similar to those produced in experimental animals following disruption of embryonic vessels at a corresponding gestation. In the specimens with amniotic band related limb defects (16%), the most likely pathogenesis is mechanical rupture through the amnion in the presence of a persistent extraembryonic coelom or from adhesion of the amnion to necrotic embryonic tissue after the initial disruptive event. Club feet were present in 44% and may be due either to disruption of embryonic vessels or to deformation. Further studies are needed to resolve this question.

Abdominal Muscles↗

PubMed2003

Increased risk of birth defects among children from multiple births.

BACKGROUND: Multiple births are increasing, and may be associated with birth defects. METHODS: To explore this relationship, data from the Virginia birth defects registry (VaCARES) was analyzed. RESULTS: During 1989-1998, a total of 44505 children from singleton births and 2258 children from multiple births were born with birth defects in Virginia. The risk of birth defects was significantly increased in children from multiple births as compared to singleton births (birth defect rate per 10000 live births: singleton 482.3, twin 922.0, triplet 1300.0, and quadruplet or higher 2222.2). Increased risk was observed for 39 of 86 diagnoses. The five diagnoses with the highest risk ratio per 10000 live births (RR) were: neurofibromatosis (RR, 12.80), retrolental fibroplasia (RR, 9.96), microphthalmos (RR, 5.24), pulmonary valve anomalies (RR, 5.00), and patent ductus arteriosus (RR, 4.68). A significantly reduced risk ratio for congenital hip dislocation was found in these children (RR, 0.54). In most multiple births, only one child was born with birth defects (81% in twin births, 71% in triplet births, and 56% in quadruplet and higher births). The diagnosis of birth defects might be concordant or discordant for children in which all siblings had birth defects. The children from multiple births who had birth defects were generally preterm and had significantly lower birth weight. A higher fatality and mortality rate and longer hospital stay were also observed. CONCLUSIONS: Overall, children from multiple births have an increased risk of birth defects.

Congenital Abnormalities↗

PubMed2004

Bone-defect healing with calcium-sulfate particles and cement: an experimental study in rabbit.

Calcium sulfate (CaS) has been shown to be a reasonable alternative to autogenous bone graft for treating bone lesions in dentistry. The aim of this work was an histological study of the bone healing of defects treated with calcium sulfate in the form of cement or beads, in animal. Eight New Zealand rabbits, weighing about 2.5 Kg were used in this study. In each rabbit, four 6 mm bone defects were created in the tibial metaphysis. The 2 defects in the right tibia were filled with calcium sulfate as cement, while the 2 defects in the left one were filled with calcium sulfate as beads. Four rabbits were killed after respectively 2 and 4 weeks, with an intravenous injection of Tanax, and the block sections, containing the bone defects, were retrieved. A total of 16 defects filled by cement and a total of 16 defects filled by beads were retrieved. The specimens were processed to obtain thin ground sections with the Precise 1 Automated System. In the first phases of healing it was possible to observe an intense osteoblastic activity, and in some areas osteoid matrix was present. After two weeks the calcium sulfate (both cement and beads) was still present, and biological fluids and cells were present inside the material. Newly formed bone surrounded the calcium sulfate and filled about 10% of the defect. After four weeks the calcium sulfate was almost completely resorbed and substituted by new bone. Approximately 34% of the defects were filled by newly formed bone. BEI and XRM evaluations showed the structural components of the filled defects. In none of the specimens were inflammatory cells present. No significant differences were found using both calcium sulfate as cement and beads, and they both have shown a high biocompatibility, appearing to promote newly bone formation in the rabbit model, and they did not induce any untoward effect on the bone regeneration processes.

Absorptiometry, Photon↗

PubMed1991

Effects of osteochondral defect size on cartilage contact stress.

Contact stress distributions were studied in vitro for 13 dog knees, with full-thickness osteochondral defects drilled in the weight-bearing area of both femoral condyles. Diameters of the circular defects were concentrically enlarged from 1 to 7 mm. Digitally-imaged Fuji film was used to record cartilage contact stress distribution on femoral condyles for each increment of defect diameter. All specimens showed at least some tendency for contact stress concentration at the rim of the defects. However, detailed distributions had large interspecimen variability and, within a given specimen, contact stress distributions became progressively more nonuniform around the defect rim as the diameter was enlarged. Averaged over the full series of 26 condyles, circumferential mean cartilage contact stress around the defect rim was only moderately higher (by 10-30%) than intact surface's peak local contact stress [series average = 6.2 mega pascals (MPa)]. Maximal rim stress concentration occurred for 2 mm defects, there being a consistent trend toward mild rim stress decrease with further defect enlargement. Such modest contact stress elevations, per se, are probably insufficient to inhibit defect repair or to cause degeneration of surrounding cartilage. However, near the defect rim (for all diameters), the radial component of the gradient of contact stress (i.e., radial-direction variation of contact stress) was consistently elevated by an order of magnitude above that for intact, condyle articular cartilage.

Animals↗

PubMed1994

Chondrocyte-fibrin matrix transplants for resurfacing extensive articular cartilage defects.

Cartilage resurfacing by chondrocyte implantation, with fibrin used as a vehicle, was examined in large (12 mm) full-thickness articular cartilage defects in horses. Articular chondrocytes, isolated from a 9-day-old foal, were mixed with fibrinogen and injected with thrombin, in a 1:1 mixture, into 12 mm circular defects on the lateral trochlea of the distal femur of eight normal horses. The contralateral femoropatellar (knee) joint served as a control in which the defect was left empty. Synovial fluid from the femoropatellar joints was sampled on days 0, 4, 7, 30, 120, and 240 postoperatively. Groups of four horses were killed at 4 or 8 months postoperatively, and the repair tissue was evaluated by gross and histologic examination with use of hematoxylin and eosin and safranin O staining and by autoradiography. Biochemical analyses included quantitation of proteoglycan, total collagen, and type-II collagen in the repair tissue. Grossly, grafted defects had improved filling of the cartilage lesions; histologically, these areas consisted of differentiated chondrocytes in the deep and middle zones. The cellular arrangement in these zones resembled that of hyaline cartilage. The control defects contained poorly attached fibrous tissue throughout. Grafted tissue at 8 months had increased proteoglycan synthesis evident by both safranin O staining and autoradiography. Glycosaminoglycan quantitation by dye-binding assay confirmed a significantly elevated glycosaminoglycan content in grafted defects (58.8 micrograms/mg of dry weight) compared with control defects (27.4 micrograms/mg; p < 0.05). Similarly, the levels of chondroitin sulfate/dermatan sulfate was significantly elevated in the grafted defects, and this was the predominant glycosaminoglycan epitope present. There was a statistically significant (p < 0.05) increase in type-II collagen in the grafted tissue at 8 months (61.2% grafted; 25.1% control). This resurfacing attempt with use of allograft chondrocytes, secured in large full-thickness articular defects with polymerized fibrin, resulted in an improved cartilage surface in comparison with the control defects, a significantly greater aggrecan level, and a significantly higher proportion of type-II collagen.

Animals↗

PubMed1992

Absence of limbs and gross body wall defects: an epidemiological study of related rare malformation conditions.

The study is based on almost 10 million births and reports on 215 infants with two unusual malformations: amelia and gross body wall defect. Amelia without body wall defect was present in 116 cases, 67 had body wall defects without amelia, and 32 had both. The total rate was 2.2 per 100,000 births. The infants were divided into five mutually exclusive groups. There were 40 infants (0.4 per 100,000) with agenesis of the body stalk, 18 with amelia and other types of gross body wall defects (0.2 per 100,000), 56 with amelia and malformations other than gross body wall defects (0.6 per 100,000), 41 with amelia (with or without other limb reduction defects) but no nonlimb malformations (0.4 per 100,000), and 60 infants with gross body wall defects of a type other than agenesis of body stalk and without amelia (0.6 per 100,000). A weak trend of decreasing prevalence of these malformations was found during the observation period. Infants with agenesis of the body stalk and infants with amelia combined with other types of gross body wall defects occurred at an increased rate in infants of young women. This maternal age effect is also found with gastroschisis, but not with omphalocele, and may indicate etiological or pathogenetic similarities between gastroschisis and the two former groups of defect. In infants with amelia, additional limb reduction defects could be of any type: transverse, longitudinal, or intercalary. Therefore, amelia may be the end result of different types of disturbances of limb morphogenesis. There was an increased rate of twinning. The relationship with amniotic band syndrome is discussed.

Abdominal Muscles↗

PubMed1994

On the use of affected controls to address recall bias in case-control studies of birth defects.

Inferences regarding causes of birth defects in humans are often based on results of case-control studies conducted after birth. To address bias in these studies caused by potential differential recall of past exposures between case and control mothers, many investigators have advocated the use of affected controls (babies with birth defects other than the one of interest). To evaluate whether the use of affected controls is warranted for a wide range of scenarios, we analyzed data from a population-based case-control study of birth defects in Atlanta, in which there were 4,918 babies with serious defects ascertained in the first year of life and 3,029 babies without defects. We compared the magnitude of the odds ratios for 10 specific defects--risk factor associations between normal and affected controls. These associations included demographic factors (e.g., advanced maternal age and Down syndrome), chronic maternal illnesses (e.g., diabetes and cardiac defects), chronic exposures (e.g., multivitamins and neural tube defects), and acute exposures (e.g., flu and neural tube defects). In all instances, the use of affected controls did not change etiologic inferences derived from using normal controls and there were only moderate changes in odds ratios. On the basis of theoretical considerations, we show that recall bias can lead to spurious inferences only under extreme conditions. We conclude that concerns about recall bias are overrated in birth defects studies and that the use of normal controls is acceptable unless evidence of substantial recall bias exists.

Case-Control Studies↗

PubMed1976

Defective prophages of bacteriophage Mu.

A method is described for the isolation of thermoinducible defective Mu lysogens. Four of these defective lysogens were studied more extensively. By marker-rescue experiments it was shown that the strain harbouring the smallest defective prophage contains the immunity gene cts and the genes A and B; the strain with the largest defective prophage still contains all the known essential genes of Mu, A to S (see Fig. 1). After induction at 43 degrees C all the defective lysogens are killed, whereas no lysis occurs. Although in all the thermoinducible defective lysogens the A and B gene products could be demonstrated by complementation, these gene products are not responsible for the killing of the host, suggesting the presence of another unknown early gene product of Mu. The level of complementation of a mutation in gene A is reduced by the presence in the cell of another defective Mu prophage containing the "G" beta part of Mu. This effect on A gene complementation is markedly enhanced when the defective prophage, containing the "G" beta part, is located on an episome instead of on the chromosome. Complementation of late genes by a defective prophage located on the chromosome, is extremely low or undetectable. A stimulation of complementation by a factor of 10 to 40 was found when the same defective prophage was situated on a F' factor. A possible explanation for this "episome" effect will be discussed.

Cold Temperature↗

PubMedDate not supplied

Effects of altered left ventricular geometry on quantitative technetium 99m sestamibi defect size in humans: perfusion imaging during coronary angioplasty.

BACKGROUND: Serial myocardial perfusion imaging is used to assess exercise-induced myocardial ischemia and myocardial risk area, salvage, and viability in patients with myocardial infarction. In an experimental animal model it has been shown that abnormal regional wall motion and altered left ventricular geometry can produce apparent perfusion defects independent of changes in blood flow. The effects of regional alteration in ventricular geometry on perfusion images in humans are not defined. The purpose of our investigation was to evaluate quantitatively the effect of altered left ventricular geometry on myocardial perfusion imaging with technetium 99m sestamibi during coronary angioplasty. METHODS AND RESULTS: Nine patients with normal baseline left ventricular function referred for angioplasty of the left anterior descending coronary artery were studied. 99mTc sestamibi was administered intravenously before angioplasty. Baseline planar electrocardiographic-gated imaging was performed. Imaging was repeated in the catheterization laboratory during angioplasty vessel occlusion when altered left ventricular geometry was produced and again later after angioplasty. Summed static, end-systolic, and end-diastolic images were generated from the electrocardiographic-gated acquisitions. Circumferential count profiles of images obtained during percutaneous transluminal coronary angioplasty (PTCA) were compared with those of a normal 99mTc sestamibi database and their own baseline images. Defect integral (the area below the reference profile) and nadir (maximum percent decrease in activity) were derived. Compared with a normal database, new quantitative defects appeared on PTCA-summed images in only two patients. The defects were small to moderate in size. However, compared with their own baseline profile, six patients had quantitative defects during PTCA (mean defect integral 3 +/- 2; mean defect nadir 12% +/- 7%). Defect nadir was larger on end-diastolic images compared with summed images (22% +/- 7% and 12% +/- 7%, respectively; p < 0.05). CONCLUSIONS: Altered left ventricular geometry may create apparent, albeit small, planar myocardial perfusion defects in humans. Changes in defect size on serial images may be only partially caused by changes in regional wall motion or geometry.

Adult↗

PubMed2003

Filling defect artefacts in magnetic resonance urography.

The aim of this study was to determine the prevalence of filling defect artefacts (FDA) in magnetic resonance urography (MRU). Retrospectively, we assessed MRU examinations of 45 patients with neurogenic bladder dysfunction (21 men, 24 women; mean age 35 years, age range 18-71 years). The MRU was performed 30 min after intramuscular injection of 20 mg frusemide using heavily T2-weighted fast-spin-echo techniques [axial, thick coronal slab, coronal maximum intensity projection (MIP) images] with fat saturation. The images were reviewed by two observers to determine the presence of filling defects and dilatation of pelvicalyceal system and ureters. The filling defects were classified into central, eccentric and complete. Clinical course and plain films were reviewed to determine significance of the detected filling defects. True filling defects were observed in 5 patients (11%) and all due to stones seen on the plain radiograph of the abdomen. Filling defects artefacts (FDAs) were seen in 23 patients (51%; 17 pelvicalyceal system, 17 upper third of ureters, 7 mid ureters and 1 distal ureter). No stones were seen on the plain radiograph of these patients and they had a favourable clinical course for over 24 months. The true filling defects were large in size, eccentric in position and seen in more than one sequence of the MRU examination (axial, n=5; slab, n=5; and MIP, n=4). Four (80%) of the patients with true defects and 21 (91%) of those with FDAs had dilatation of the pelvicalyceal system and ureters. The FDAs were small in size, centrally placed (74%) and always seen in axial images, rarely in slab images (2 cases) and not seen in MIP images. Artefactual filling defects can be seen in MRU examinations. The cause of the FDAs is not fully explained and could be secondary to turbulent and fast flow of the urine. Some of the FDAs seen in the calyces could be due to the tips of the papillae. Awareness of such defects obviates misinterpretation and prevents unnecessary further investigations or interventions.

Adolescent↗

PubMed2004

Bone defect repair in rat tibia by TGF-beta1 and IGF-1 released from hydrogel scaffold.

Bone repair is one of the major challenges facing reconstructive surgery. Bone regeneration is needed for the repair of large defects and fractures. The ability of TGF-beta1 and IGF-1 incorporated into hydrogel scaffold to induce bone regeneration was evaluated in a rat tibia segmental defect model. External fixation was performed prior to the induction of the segmental bone defect in order to stabilize the defect site. Hydrogel scaffold containing either TGF-beta, IGF-1, TGF-beta + IGF-1, hydrogel containing saline or saline, were inserted in the defect. Calcified material was observed in the defects treated with TGF-beta 2 weeks following the start of treatment. Bone defects treated with TGF-beta, IGF-1 or TGF-beta + IGF-1 revealed significant bone formation after 4 and 6 weeks when compared to the control specimens. X-ray images showed that solid bone was present at the defect site after 6 weeks of treatment with TGF-beta or TGF-beta + IGF-1. A less pronounced bone induction was observed in the control specimens and bones treated with IGF-1. Percent closure ratio of bone defects after 6 weeks were 40, 80, 89, and 97% for saline, hydrogel, IGF-1, TGF-beta and IGF-1 + TGF-beta groups, respectively. It is concluded that hydrogel scaffold can serve as a good osteoconductive matrix for growth factors, and that it provides a site for bone regeneration and enhances bone defect healing and could be used as alternative graft material.

Animals↗

PubMed1991

The effect of defect size on the stress concentration and fracture characteristics for a tubular torsional model with a transverse hole.

The maximum stress location and crack resistance of a tubular torsional model with varying transverse circular defects were determined by the use of experimental and global-local finite element modeling techniques. The experimental results showed that the reduction in torsional strength was inversely proportional to defect size. In addition, the maximum stress location around the defect was closely related to the normalized defect diameter. By measuring the shifted angle associated with each defect ratio, a linear relationship, delta theta = -6.28 + 0.55*(d/D), was determined. Finite element results indicated that the stress concentration factor, Kg, for a single-cortex defect is similar to that of a double-cortex defect of identical dimension. Application of the strain energy density (SED) theory proposed by Sih and Oliveira Faria (Fracture Mechanics Methodology, Martinus Nijhoff, The Hague, 1984), indicated that the fracture toughness, KIC, for large defects was greater than that for small defects. This implies that tubular structures with large defects have a greater resistance to crack initiation and growth.

Animals↗

PubMed1994

Mesenteric defects as a cause of intestinal volvulus without malrotation and as the possible primary etiology of intestinal atresia.

Mesenteric defects can lead to intestinal volvulus even when the midgut is normally rotated. There are two types of mesenteric defects: basilar, in which the entire base of the mesentery is involved, and segmental, in which only an isolated portion of the mesentery is affected. These defects can present at any age, and the clinical symptoms depend on the extent of the disease and the amount of intestine involved in the volvulus. In the newborn, the basilar defects have clinical signs and symptoms similar to those of midgut volvulus secondary to malrotation. Similar to midgut volvulus secondary to malrotation, this is a surgical emergency. In older patients, basilar defects can be misdiagnosed because of the normal placement of the ligament of Treitz and because of failure to consider mesenteric defects as a possible cause. The treatment for basilar mesenteric defects is intestinal fixation. Intestinal volvulus secondary to segmental defects always presents as intestinal obstruction. In the newborn, these lesions may be indistinguishable from intestinal atresia. Older children present with intestinal obstruction of an unknown cause. Resection of the affected intestine is the treatment for segmental mesenteric defects. Intestinal mesenteric abnormalities as a cause of intestinal atresia unifies under one etiology all the lesions observed in intestinal atresia. Although this theory does not rule out other causes of intestinal atresia, intestinal mesenteric defects may be the primary condition under which intestinal atresia occurs.

Child↗