Tissue Tensile Strength Research Articles

Resterilized Mesh in Repair of Abdominal Wall Defects in Rats

A variety of negative opinions about repeated usage of relatively expensive resterilized synthetic meshes have been considered. It had been stated that resterilized polypropylene meshes inhibits fibroblastic activity, decreases proliferative activity, and increases apoptosis in human fibroblast culture, in vitro. The purpose of this study is the in vivo evaluation of the resterilized mesh repairs of abdominal hernia defects in rat models of incisional hernia by comparing primer repair and original mesh repairs. The rats (n = 22) were separated into three groups. While the abdominal defect was repaired by primary suture in the control group (CG), the defects were repaired by original mesh (OG) or resterilized mesh (RG) in mesh-repaired groups. After 21 days, the rats were evaluated for tissue tensile strengths, tissue hydroxyproline levels, tissue inflammation, fibrosis, and apoptosis. Although the tensile strengths in OG and RG were significantly higher than those of CG (p <. 05 and p <. 05), there was no significant difference between two groups. The tissue hydroxyproline levels in OG and RG were also higher than those of CG. The difference was not significant between the two groups. The inflammation and fibrosis indexes in OG and RG were significantly higher than those of CG (p <. 0001 for both), but there was no difference between groups. While the apoptosis index in OG and RG was also higher than that of CG (p <. 0001 for both), there was no significant difference between OG and RG. The usage of resterilized mesh in abdominal wall repair did not reduce the tissue tensile strength, did not affect the tissue hydroxyproline levels, did not decrease the fibrosis, and did not increase the tissue inflammation and apoptosis. In conclusion, usage of resterilized meshes in abdominal wall defects was as safe as sterilized meshes.

Assessing Behind Armor Blunt Trauma in Accordance With the National Institute of Justice Standard for Personal Body Armor Protection Using Finite Element Modeling

To assess the possibility of injury as a result of behind armor blunt trauma (BABT), a study was undertaken to determine the conditions necessary to produce the 44-mm clay deformation as set forth in the National Institute of Justice (NIJ) Standard 0101.04. These energy levels were then applied to a three-dimensional Human Torso Finite Element Model (HTFEM) with soft armor vest. An examination will be made of tissue stresses to determine the effects of the increased kinetic energy levels on the probability of injury. A clay finite element model (CFEM) was created with a material model that required nonlinear properties for clay. To determine these properties empirically, the results from the CFEM were matched with experimental drop tests. A soft armor vest was modeled over the clay to create a vest over clay block finite element model (VCFEM) and empirical methods were again used to obtain material properties for the vest from experimental ballistic testing. Once the properties for the vest and clay had been obtained, the kinetic energy required to produce a 44-mm deformation in the VCFEM was determined through ballistic testing. The resulting kinetic energy was then used in the HTFEM to evaluate the probability of BABT. The VCFEM, with determined clay and vest material properties, was exercised with the equivalent of a 9-mm (8-gm) projectile at various impact velocities. The 44-mm clay deformation was produced with a velocity of 785 m/s. This impact condition (9-mm projectile at 785 m/s) was used in ballistic exercises of the HTFEM, which was modeled with high-strain rate human tissue properties for the organs. The impact zones were over the sternum anterior to T6 and over the liver. The principal stresses in both soft and hard tissue at both locations exceeded the tissue tensile strength. This study indicates that although NIJ standard 0101.04 may be a good guide to soft armor failure, it may not be as good a guide in BABT, especially at large projectile kinetic energies. Further studies, both numerical and experimental, are needed to assist in predicting injury using the NIJ standard.

A role for decorin in cutaneous wound healing and angiogenesis

Decorin is known to influence tissue tensile strength and cellular phenotype. Therefore, decorin is likely to have an impact on tissue repair, including cutaneous wound healing. In this study, cutaneous healing of both excisional and incisional full-thickness dermal wounds was studied in decorin-deficient (Dcn(-/-)) animals. A statistically significant delay in excisional wound healing in the Dcn(-/-) mice occurred at 4 and 10 days postwounding and, in incisional wounds at 4, 10, and 18 days when compared with wild-type (Dcn(-/-)) controls. Fibrovascular invasion into polyvinylalcohol sponges was significantly increased by day 18 in Dcn(-/-) mice relative to Dcn(+/+) mice. The 18-day sponge implants in the Dcn(-/-) mice showed a marked accumulation of biglycan when compared with the corresponding implants in Dcn(+/+) mice. Thus, regulated production of decorin may serve as an excellent therapeutic approach for modifying impaired wound healing and harmful foreign body reactions.

Impact of collagen subtype proportions in peritoneal tissues on inguinal hernia formation in adults and infants

Impaired collagen subtype proportions in the matrices results in the alteration of tissue tensile strength, and is an underlying cause of adult inguinal hernia formation; however, it remains unclear if this alteration is also responsible for infantile inguinal hernia formation. We correlated the ratios of collagen type I to type III between adults and infants with and those without an inguinal hernia, in an attempt to clarify the pathogenesis of this disorder. We extracted collagen from the hernial sacs of patients with an inguinal hernia, and from the normal peritoneum of patients without an inguinal hernia. After separation by electrophoresis, the collagen bands were quantified and we compared the ratios of collagen type I to type III between the patients with and those without an inguinal hernia. The ratio of collagen type I to type III was significantly lower in the adults with an inguinal hernia (n=8, 6.17+/-2.69) than in those without an inguinal hernia (n=8, 9.38+/-2.99, P=0.041), whereas the ratios were similar in infants with (n=10, 5.72+/-2.66) and those without an inguinal hernia (n=6, 5.60+/-1.88, P=0.925). Our results showed that tissue weakness was not involved in the pathogenesis of infantile inguinal hernia formation, confirming that simple herniotomy is adequate treatment.

Targeted Modification of Atrial Electrophysiology by Homogeneous Transmural Atrial Gene Transfer

Safe and effective myocardial gene transfer remains elusive. Heterogeneous ventricular gene delivery has been achieved in small mammals but generally with methods not readily transferable to the clinic. Atrium-specific gene transfer has not yet been reported. We hypothesized that homogeneous atrial gene transfer could be achieved by direct application of adenoviral vectors to the epicardial surface, use of poloxamer gel to increase virus contact time, and mild trypsinization to increase virus penetration. We "painted" recombinant adenovirus encoding the reporter gene Escherichia coli beta-galactosidase directly onto porcine atria. Investigational variables included poloxamer use, trypsin concentration, and safety. Using the painting method, we modified the atrial phenotype with an adenovirus expressing HERG-G628S, a long-QT-syndrome mutant. Our results showed that application of virus with poloxamer alone resulted in diffuse epicardial gene transfer with negligible penetration into the myocardium. Dilute trypsin concentrations allowed complete transmural gene transfer. After trypsin exposure, echocardiographic left atrial diameter did not change. Left atrial function decreased on postoperative day 3 but returned to baseline by day 7. Tissue tensile strength was affected only in the 1% trypsin group. HERG-G628S gene transfer prolonged atrial action potential duration and refractory period without affecting ventricular electrophysiology. We show complete transmural atrial gene transfer by this novel painting method. Adaptation of the method could allow application to other tissue targets. Use with functional proteins in the atria could cure or even prevent diseases such as atrial fibrillation or sinus node dysfunction.

Influence of Terminalia chebula on dermal wound healing in rats.

The effects of topical administration of an alcohol extract of the leaves of an evergreen plant, Terminalia chebula, on the healing of rat dermal wounds, in vivo, was assessed. T. chebula treated wounds healed much faster as indicated by improved rates of contraction and a decreased period of epithelialization. Biochemical studies revealed a significant increase in total protein, DNA and collagen contents in the granulation tissues of treated wounds. The levels of hexosamine and uronic acid in these tissues, also increased upto day 8 post-wounding. Reduced lipid peroxide levels in treated wounds, as well as ESR measurement of antioxidant activity by DPPH radical quenching, suggested that T. chebula possessed antioxidant activities. The tensile strength of tissues from extract-treated incision wounds increased by about 40%. In addition, T. chebula possessed antimicrobial activity and was active largely against Staphylococcus aureus and Klebsiella. These results strongly document the beneficial effects of T. chebula in the acceleration of the healing process.

Increased Amount of Type III pN-collagen in AAA when Compared with AOD

Objective: the extent of the processing of type III procollagen to type III collagen was determined in nine human abdominal aortic aneurysms (AAA), and compared with ten samples of aortoiliac occlusive disease (AOD).Methods : the aminoterminal propeptide (PIIINP) and telopeptide (IIINTP) of type III procollagen and collagen, respectively, were immunologically measured in the soluble and insoluble fractions of the extracellular matrix. The assay for PIIINP in the insoluble matrix was further validated. Results: the insoluble matrices of AAAs contained at least 12 times more incompletely processed type III pN-collagen than AOD specimens (0.74% and 0.061%, respectively). Also, the soluble extracts of AAAs tended to contain more non-processed type III pN-collagen than free, properly cleaved aminoterminal propeptide. Conclusions: the larger amount of type III pN-collagen suggests an alteration in the metabolism of type III collagen in AAAs. This may partially explain the decreased tensile strength of the aortic tissue.

Activation of matrix metalloproteinase dilates and decreases cardiac tensile strength

Previous studies demonstrated that transition from compensatory pressure overload hypertrophy to decompensatory volume overload heart failure is associated with decreased cardiac tensile strength and activation of matrix metalloproteinase (MMP) in spontaneously hypertensive rat (SHR). To test the hypothesis that in the absence of nitric oxide activation of MMP during cardiac failure causes disruption in the organization of extracellular matrix (ECM) and leads to decrease systolic and diastolic cardiac tensile strength, we employed SHR of 24–32 weeks, which demonstrates significant cardiac hypertrophy and fibrosis. The normotensive Wistar rats (NWR) were used as control. To determine whether cardiac hypertrophy is associated with increased elastinolytic matrix metalloproteinase-2 (MMP-2) activity; quantitative elastin-zymography was performed on cardiac tissue homogenates. The MMP-2 activity was normalized by the levels of actin. The MMP-2/actin ratio was 2.0±0.5 in left ventricle (LV) and 1.5±0.25 in right ventricle (RV) of SHR 32wks; and 0.5±0.25 in LV and 0.25±0.12 in RV of NWR 32wks ( P<0.02 when SHR compared with NWR). To measure passive diastolic cardiac function, rings from LV as well as RV through transmyocardial wall from male SHR and NWR of 6–8 weeks and 24–36 weeks were prepared. The LV wall thickness from endocardium to epicardium was 3.75±0.25 mm in SHR 32wks as compared to 2.25±0.50 mm in NWR 32wks ( P<0.01). The ring was placed in tissue myobath and length–tension relationships were assessed. The pressure–length relationship was shifted to left in SHR as compared to NWR. The amounts of cardiac elastin and collagen were determined spectrophotometrically by measuring desmosine–isodesmosine and hydroxyproline contents, respectively. A negative correlation between elastic tensile strength and elastin/collagen ratio was elucidated. To create situation analogous to heart failure and MMP activation, we treated cardiac rings with active MMP-2 and length–tension relation was measured. The relationship was shifted to right in both SHR and NWR when compared to their respective untreated groups. The results suggested that activation of MMP led to decreased cardiac tissue tensile strength and may cause systolic and diastolic dysfunction.

Increased amount of type III pN-collagen in human abdominal aortic aneurysms: Evidence for impaired type III collagen fibrillogenesis

Purpose: This study aimed to characterize the distribution of structural domains of type I and III collagens in the wall of abdominal aortic aneurysms (AAAs), by the use of undilated atherosclerotic aortas (aortoiliac occlusive disease [AOD]) and healthy abdominal aortas as controls. Methods: Immunohistochemical staining was applied with antibodies for the aminoterminal propeptides of type I (PINP) and type III (PIIINP) procollagens, which represent newly synthesized type I and III pN-collagens. In addition, an antibody against the aminoterminal telopeptide of type III collagen (IIINTP) was used as a means of detecting maturely cross-linked type III collagen fibrils. Results: The newly synthesized type III procollagen detected by means of PIIINP staining was concentrated in the media in aneurysmal aortas, whereas type I pN-collagen was localized in the intima in both AAAs and AODs. The healthy aortas showed no immunoreactivity for either PIIINP or PINP. The cross-linked type III collagen, detected by means of IIINTP staining, stained transmurally in all study groups, but appeared more abundant in the media in AAAs. Conclusion: Our results strongly suggest that the metabolism of type III collagen is enhanced in AAAs. Intensive type III pN-collagen staining was present mainly in the media layer in AAAs, suggesting a role of type III collagen in aneurysm formation, whereas type I pN-collagen was present in the intima in both AAAs and AODs, suggesting that type I collagen synthesis is a fibroproliferative response related to the atherosclerotic process. The increased type III pN-collagen in AAAs may result in impaired fibril formation and, thus, in decreased tensile strength of aneurysmal tissue. (J Vasc Surg 2000;32:1201-7.)

Regulation of Human COL2A1 Gene Expression in Chondrocytes: IDENTIFICATION OF C-Krox-RESPONSIVE ELEMENTS AND MODULATION BY PHENOTYPE ALTERATION

Regulation of Human COL2A1 Gene Expression in Chondrocytes: IDENTIFICATION OF C-Krox-RESPONSIVE ELEMENTS AND MODULATION BY PHENOTYPE ALTERATION

Proteinase Imbalance versus Biomechanical Stress in Pulmonary Emphysema

Emphysema is a slowly progressive degenerative lung disease involving fragmentation and depletion of elastic fibers, loss of lung elastance, and architectural destruction with ectasia, tortuosity, and loss of bronchioles irrespective of localization or morphological type. Occurring under physiological conditions, predominantly in geriatrics, matrix laxity and destructive parenchymal lesions are indicative of a pathological loss of tissue tensile strength attributable to bioengineering or structural fatigue in repetitively stressed tissues. The occurrence of severe premature emphysema in inherited connective tissue diseases and under some experimental and iatrogenic conditions is supportive evidence. Experiments advocating unrestrained proteolysis as a cause or pathogenic factor are invalid, being based on a false premise and assumed causality.

Injury threshold: Whiplash-associated disorders

Objectives: To review current knowledge and recent concepts of the causes of injuries after minor impact automobile collisions and to acquaint those who treat these types of injuries with possible injury thresholds and mechanisms that may contribute to symptoms. Data Sources: A review of literature involving mechanisms of injury, tissue tensile threshold, and neurologic considerations was undertaken. A hand-search of relevant engineering, medical/chiropractic, and computer Index Medicus sources in disciplines that cover the variety of symptoms was gathered. Results: Soft-tissue injuries are difficult to diagnose or quantify. There is not one specific injury mechanism or threshold of injury. With physical variations of tissue tensile strength, anatomic differences, and neurophysiologic considerations, such threshold designation is not possible. Conclusions: To make a competent assessment of injury, it is important to evaluate each patient individually. The same collision may cause injury to some individuals and leave others unaffected. With the variability of human postures, tensile strength of the ligaments between individuals, body positions in the vehicle, collagen fibers in the same specimen segment, the amount of muscle activation and inhibition of muscles, the size of the spinal canals, and the excitability of the nervous system, one specific threshold is not possible. How individuals react to a stimulus varies widely, and it is evident peripheral stimulation has effects on the central nervous system. It is also clear that the somatosensory system of the neck, in addition to signaling nociception, may influence the control of neck, eyes, limbs, respiratory muscles, and some preganglionic sympathetic nerves. (J Manipulative Physiol Ther 2000;23:420–7)

Influence of Ripening and Turgor on the Tensile Properties of Pears: A Microscopic Study of Cellular and Tissue Changes

The tensile properties of european pear (Pyrus communis L. `Beurre Bosc') and asian pear (Pyrus pyrifolia Nakai `Choguro') were examined using a microscope-mounted apparatus that allowed direct observation and recording of cell and tissue changes during testing. To manipulate turgor potential, tissue slices from fruit of different firmness (ripeness) were incubated in sucrose solutions of differing water potential. Solution water potentials were adjusted for individual fruit, and varied between -2.5 and 1 MPa from the water potential of the expressed juice. Fruit firmness declined from 100 to 20 N and from 60 to 25 N during ripening of european and asian pears, respectively. For both european and asian pears the relationship between fruit firmness and tensile strength of tissue soaked in isotonic solutions was sigmoidal, with the major mechanism of tissue failure being cell wall failure and cell fracture at high firmness and intercellular debonding at low firmness. In the intermediate zone, where fruit firmness and tissue tensile strength decreased simultaneously, a mixture of cell wall rupture and intercellular debonding could be observed. Tissue and cell extension at maximum force both declined similarly as fruit softened. Tensile strength of tissue from firm pears (&gt;50 N firmness, &gt;0.8 N tensile strength) decreased by as much as 0.6 N during incubation in solutions that were more concentrated than the cell sap (hypertonic solutions). When similar tissue slices were incubated in solutions that were less concentrated than the cell sap (hypotonic solutions), the tensile strength increased by up to 0.4 N. This is interpreted as stress-hardening of the cell wall in response to an increase in cell turgor. Tensile strength of tissue from soft pears was not affected by osmotic changes, as the mechanism of tissue failure is cell-to-cell debonding rather than cell wall failure.

Tissue properties and propensity for damage in carrot (Daucus carota L.) storage roots

SummaryCarrot roots from a range of environments, developmental stages and cultivars showed variation in splitting susceptibility from 3.8% to 72.5%. Estimates of tissue tensile strength, fracture toughness and residual strain for roots from these sources were not related to estimates for damage. The measurement of release of intrinsic stress from whole-root sections showed some relationship with damage in that the most susceptible cultivars also displayed greater release of stress. These same varieties had larger storage cells in their outer parenchyma. Developmental variation in tissue strength induced by different sowing dates and years was inconsistent between years. Increases in strength of root tissue with advancing date during the autumn observed in field experiments, were not related to temperature changes imposed in controlled environment. Variation in water and solute potentials was generally greater than variation in turgor potential, which remained well conserved in all experiments. Fracture toughness, which is dependent on tissue water status, was not well related to turgor in these experiments.

Images in cardiovascular medicine. Connective tissue skeleton of the human heart: a demonstration by cell-maceration scanning electron microscope method.

The stroma of the heart maintains the structure of the myocardium, determining tissue tensile strength and stiffness.1 In addition, it contributes to ventricular function through the transmission of myocyte-generated force to the atrial and ventricular chambers and to the relengthening of myocytes in diastole.2 The three-dimensional configuration of cardiac collagen has been determined by scanning electron microscopy3 4 5 : the epimysium envelops the entire cardiac muscle; the perimysium, which is an extension of the epimysium, serves to enwrap groups of myocytes; and the endomysium, as final arborization of the perimysium, supports and connects individual cells. The endomysial weave envelops each individual myocyte and is …

Miscellaneous Item

CardioOascular Research introduced a Cardiovascular w x Mystery Series several years ago 1 . Included amongst its Ž . objectives: a an exploration of less well known aspects of Ž . cardiovascular disease; b an integration of basic and Ž . clinical sciences and c an intention to be provocative. A clinical vignette, in the form of a mystery story, sets the stage for an invited mini-review on a topic that addresses these objectives. As Series Editor, I was delighted when Professor of Pathology, William E. Stehbens, found the w x vignette ‘Vascular aneurysms: a side-splitting affair’ 2 and its patients M. and F. sufficiently provocative to bring forward his views in a Letter to the Editor entitled ‘The pathogenesis of arterial aneurysms and associated lesions’. Drawing on traditional concepts, Stehbens has emphasized the importance of ‘hemodynamic biomechanical stress’ in promoting such iterations in vascular architecture. He indicates ‘‘...aneurysms develop when intravascular pressure is greater than the wall can withstand...’’ and ‘‘...aneurysms indicate mural weakness’’. I completely concur with the latter—an intrinsic defect in the tensile strength of the vessel wall is responsible for its aneurysmal dilatation—and would add that such loss of vascular integrity is not based on prevailing andror repetitive surges in intraluminal pressure. Hypertension is not a prerequisite; it does predispose to aneurysmal dilatation in a weakened vessel. Aneurysms complicate many different diseases and clearly do not have a single pathogenic origin. Potential causes include abnormal structural protein phenotype and proteinase-mediated degradation of such proteins as collagen and elastin. One would not confuse the pathogenesis of aneurysmal dilatation seen in inherited connective tissue Ž . disorders e.g., Marfan’s syndrome with that associated with acquired atherosclerotic disease. In the mini-review w x that follows the vignette 3 , Herron provides a compelling argument for the involvement of matrix metalloproteinases in the formation of abdominal aortic aneurysm. Stehbens goes on to discuss patient M. with adult dominant polycystic kidney disease and correctly indicates that it is unknown whether proteinase activity is increased in the aneurysms of the cerebral circulation that appear in this entity. This is also true for abdominal aortic aneurysm, dissecting aneurysm of the thoracic aorta, mitral valve prolapse and intestinal diverticula associated with this inherited disorder. There likewise is no documented evidence for abnormal structural protein phenotype in this entity. However, does it not seem likely that either scenario would explain this unusual predisposition to ‘weakness’ in these diverse tissues whose fibrillar type I collaw x gen should have the tensile strength of steel 4 ? Weightlifters experience sudden and marked increments in arterial pressure during isometric exercise, but they experience neither mitral valve prolapse nor arterial aneurysm. Aneurysmal formation appears subsequent to emboli of myxomatous tissue as was the case in patient F. In contrast to septic or bland emboli, such tumor emboli contain pluripotent cells, such as the myofibroblast phenotype w x 5,6 . These cells can express proteinases that account for their ability to invade vascular tissue with destruction of w x elastic lamina and media 7,8 . These emboli resemble the metastatic behavior of neoplastic tissue, where proteinase w x activation is an integral feature 9 . Even after removal of the tumor embolus, the continued presence of such cells within the invaded vessel leads to its destruction with w x subsequent aneurysmal formation 10 . In closing, a localized defect in tissue tensile strength leads to its distention. This is expressed as aneurysmal dilatation in the case of blood vessels, diverticula of the intestine and prolapse of valve leaflets. To implicate hypertension, a hemodynamic condition present throughout the arterial vasculature and left ventricular chamber, as the predominant causal mechanism for localized tissue weakness is no longer tenable and unwarranted, in my opinion. We are what we know and we see what we want according

An Experimental Study on the Effects of Elastase, Bleomycin and Infection on the Growth and Tensile Strength of Elastic Tissue in Rabbit Fetal Membranes

The effects of bleomycin, elastase and infection on the tensile strength of rabbit fetal membranes and the structure of the elastic tissue of rabbit amnion were studied. The experimental subjects were rabbits to which bleomycin (total dose, 20 mg) or elastase (total dose, 60 mg) was administered from 18 days of pregnancy. In addition to the fetal membranes from these treated animals, fetal membranes with amniotic infection induced by injection of Escherichia coli into the amniotic fluid (AF) of rabbits at 22 or 23 days of pregnancy were examined, and those from rabbits administered physiological saline solution were used as controls. The results obtained were as follows. Determination of tensile strength of the fetal membranes revealed that the infected membranes had minimum rupture pressure (18.67 +/- 6.30 mm Hg), followed by the elastase administration group (46.67 +/- 3.51 mm Hg). The value in the bleomycin administration group (99.67 +/- 12.89 mm Hg) was significantly higher than that in the control group (61.80 +/- 6.30 mm Hg). Histological changes in the fibroblast layer of these fetal membranes included elastic fibrosis due to excessive collagen production, which was mostly manifested as fibrosis densa, in the bleomycin administration group. In the elastase administration group, the elastic fibers were eliminated or became minute, as in the infection groups. The above results showed the adverse effects of elastase and bleomycin and the destructive effect of infection on the growth and properties of elastic tissue in the amnion, suggesting their pathophysiological importance.

End-to-side and end-to-end vascular anastomoses with a carbon dioxide laser

This study was designed to compare anastomoses performed with a carbon dioxide laser and conventional anastomoses performed with 7-0 polypropylene suture. In each of 80 rabbits, the divided left carotid artery was anastomosed by a continuous suture technique and the right carotid was anastomosed with a carbon dioxide laser. In each of 40 additional rabbits, both end-to-end and end-to-side laser anastomoses were performed on the same carotid artery. The laser technique involved the placement of three stay sutures (end-to-end technique) or four stay sutures (end-to-side technique) of 7-0 polypropylene and an everting laser seal at a power level of 65 mW. The 1-year overall patency rate was 98% (78/80) in laser anastomoses, 79% (63/80) in suture anastomoses, and 95% (38/40) in combined end-to-end and end-to-side laser anastomoses. Microscopic findings in laser anastomoses demonstrated degeneration of collagen and protein in the adventitia and media, but much less intimal injury than in suture anastomoses, with reendothelialization beginning earlier (within 7 days after anastomosis as compared with 2 to 4 weeks). The tissue tensile strength at 1 hour was less in laser anastomoses than in suture anastomoses, but the laser anastomoses still withstood an intraluminal pressure load of 380 mm Hg. Laser anastomosis improved the microscopic and histologic appearance of the intimal layer, allowing for rapid early reendothelialization and resulting in excellent patency rates.

The Marfan syndrome: a deficiency in chemically stable collagen cross-links.

THE reduced tensile strength of tissues supporting the ocular lenses, cardiac valves, and aorta in heritable connective-tissue diseases is probably due to a defective organization of collagen. Sinc...

Normal pressure hydrocephalus and hypertensive cerebrovascular disease.

Neither the diagnostic criteria nor the pathogenesis of the normal pressure hydrocephalus (NPH) syndrome has been fully clarified. In two cases fulfilling currently accepted clinical and radiologic criteria, autopsy showed extensive hypertensive cerebrovascular disease with multiple small infarcts of the deep cerebral and cerebellar gray and white matter but normal leptomeninges and arachnoid villi. Therefore, hypertensive vascular disease with multiple deep cerebral infarctions may be the initial pathologic process in some cases of NPH. Such infarctions could reduce periventricular tissue tensile strength and elastic properties permitting the ventricles to enlarge under the stress of the intraventricular pulse pressure. Some patients with so-called arteriosclerotic parkinsonism and arteriosclerotic dementia clinically resemble patients with NPH. Some of these cases could represent NPH due to multiple small infarctions and, as in one of the cases reported here, might improve following ventricular shunting.