Biopolymer augmentation of the lag screw in the treatment of femoral neck fractures--a biomechanical in-vitro study.

The cut-out of the sliding screw is one of the most common complications in the treatment of intertrochanteric fractures. The reasons for the cut-out are: a suboptimal position of the hip-screw in the femoral head, the type of fracture and poor bone quality. The aim of this study was to reproduce the cut-out event biomechanically and to evaluate the possible prevention of this event by the use of a biopolymer augmentation of the hip screw. Concerning the density and compression force of osteoporotic femoral bone polyurethane foam according to the terms of the Association for Standard Testing Material (ASTMF 1839-97) was used as test material. The polyurethane foam Lumoltan 200 with a compression force of 3.3 Mpa and a density of 0.192 g/cm(3) was used to reproduce the osteoporotic bone of the femoral fragment (density 12 lbm/ft(3)). A cylinder of 50 mm of length and 50 mm of width was produced by a rotary splint raising procedure with planar contact. The axial load of the system was performed by a hydraulic force cylinder of a universal test machine type Zwick 1455, Ulm, Germany. The CCD-angle of the used TGN-System was preset at 130 degrees. The migration pattern of the hip screw in the polyurethane foam was measured and expressed as a curve of the distance in millimeter (mm) against the applied load in Newton (N) up to the cut-out point. During the tests the implants reached a critical changing point from stable to unstable with an increased load progression of steps of 50 Newton. This unstable point was characterized by an increased migration speed in millimeters and higher descending gradient in the migration curve. This peak of the migration curve served as an indicator for the change of the hip screw position in the simulated bone material. The applied load in the non-augmented implant showed that in this group for a density degree of 12 (0,192 g/cm(3)) the mean force at the failure point was 1431 Newton (+/- 52 Newton). In the augmented implant we found that the mean force at the failure point was 1987 Newton (+/- 84 Newton). This difference was statistically significant. In conclusion, the bone density is a significant factor for the stability of the hip screw implant. The osteosynthesis with screws in material with low density increases the chance for cut-out. A biopolymer augmented hip screw could significantly improve the stability of the fixation. The use of augmentation with a fast hardening bone replacement material containing polymer-ceramic changes the point of failure under axial load in the osteoporotic bone model and could significantly improve the failure point. Our study results indicate, that a decrease of failure in terms of cut-out can be achieved with polymer augmentation of hip screws in osteoporotic bones.

Diverticular disease is associated with an enteric neuropathy as revealed by morphometric analysis.

BACKGROUND: The pathogenesis of diverticular disease (DD) is attributed to several aetiological factors (e.g. age, diet, connective tissue disorders) but also includes distinct intestinal motor abnormalities. Although the enteric nervous system (ENS) is the key-regulator of intestinal motility, data on neuropathological alterations are limited. The study aimed to investigate the ENS by a systematic morphometric analysis. METHODS: Full-thickness sigmoid specimens obtained from patients with symptomatic DD (n = 27) and controls (n = 27) were processed for conventional histology and immunohistochemistry using anti-HuC/D as pan-neuronal marker. Enteric ganglia, nerve and glial cells were quantified separately in the myenteric, external and internal submucosal plexus compartments. KEY RESULTS: Compared to controls, patients with DD showed significantly (P < 0.05) (i) reduced neuronal density in all enteric nerve plexus, (ii) decrease of ganglionic nerve cell content in the myenteric plexus, (iii) decreased ganglionic density in the internal submucosal plexus, (iv) reduced glial cell density in the myenteric plexus, (v) decrease of ganglionic glial cell content in the myenteric plexus and increase in submucosal plexus compartments, (vi) increased glia index in all enteric nerve plexus. About 44.4% of patients with DD exhibited myenteric ganglia displaying enteric gliosis. CONCLUSIONS & INFERENCES: Patients with DD show substantial structural alterations of the ENS mainly characterized by myenteric and submucosal oligo-neuronal hypoganglionosis which may account for intestinal motor abnormalities reported in DD. The morphometric data give evidence that DD is associated with structural alterations of the ENS which may complement established pathogenetic concepts.

Improved 3-D-echocardiographic endocardial border delineation using the contrast agent FS069 (Optison) transesophageal studies in a porcine model.

3-D echocardiography has the potential for quantitative assessment of regional wall motion. However, the 3-D procedures used to date do not provide the same spatial and temporal resolution as 2-D echocardiography, which results in problems with border delineation of the endocardium. There are, as yet, few studies testing if the use of contrast agent can improve endocardial definition in the 3-D data set. FS069 (Optison) was used for the first time for this purpose in the present study. A total of 12 mechanically-ventilated pigs were examined by transesophageal 3-D echocardiography, 1. using fundamental imaging and 2. following left-atrial injection of FS069 (Optison). The left ventricle was analyzed using an 18-segment model. Score with the value 0 (not visible), 1 (moderately visible) and 2 (well defined) were used to rate endocardial definition. All segments were assessed both end-diastolic and end-systolic. Various LV regions were examined by grouping segments (anterior/lateral/inferior and basal/mid-ventricular/apical). Using the contrast agent, the proportion of nonvisible segments fell diastolic from 40 (18.5%) to 15 (6.9%), and systolic from 26 (12.0%) to 11 (5.1%). The proportion of well defined segments increased diastolic from 62 (28.7%) to 108 (50%) and systolic from 73 (33.8%) to 123 (56.9%). The mean visibility score increased diastolic from 1.10 +/- 0.68 to 1.43 +/- 0.62 (p < 0.001), systolic from 1.22 +/- 0.64 to 1.52 +/- 0.59 (p < 0.001). The benefit was greatest in regions where the visibility score was lowest without contrast: in the area of the lateral wall and systolic near the apex. In conclusion, the use of FS069 (Optison) results in significantly better endocardial delineation in the 3-D data set. This could be important in future for the 3-D echocardiographic assessment of regional wall motion.

[E rosette inhibition in alcoholic liver disease]. / Inhibición de rosetas E en la enfermedad hepática alcohólica.

Various studies performed in chronic alcoholic patients have demonstrated immunologic alterations, which have been described more often in patients with alcoholic hepatitis or liver cirrhosis. We have observed that the serum of some patients with alcoholic liver cirrhosis produces the inhibition of E rosette formation by T lymphocytes. This observation induced us to study E rosette formation and its probable inhibition by the serum of chronic alcoholic patients. Subjects were split into three groups: Group 1: n = 21. Normal individuals. Group 2: n = 15. Chronic alcoholic patients without cirrhosis. Group 3: n = 26. Chronic alcoholic patients with histologically demonstrated liver cirrhosis. E rosette and E rosette inhibition (TIRE) sera tests were performed utilizing subject's sera tested against lymphocytes of normal individuals not related to group 1. The results found are listed in detail in Table 1 (mean = -SD) and Figure 1 (median), for each of the test groups. We applied unifactorial variance analysis and observed highly significant differences between the groups studied in all tests performed. It was found that tests that utilized I.E. discriminate most efficiently among the three groups of patients and that those which utilize unabsorbed assay serum (S/A) yield the best differentiation. Using this last assay it was observed that 20/21 control individuals showed less than 15% inhibition. On this basis, we decided to separate the results into 15% regular intervals (Table 3). Inhibition above 30% was found only in cirrhotic patients with the exception of one individual of the control group and one non-cirrhotic alcoholic patient with no alcoholic liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibición de rosetas E en la enfermedad hepática alcohólica. / [E rosette inhibition in alcoholic liver disease]

Various studies performed in chronic alcoholic patients have demonstrated immunologic alterations, which have been described more often in patients with alcoholic hepatitis or liver cirrhosis. We have observed that the serum of some patients with alcoholic liver cirrhosis produces the inhibition of E rosette formation by T lymphocytes. This observation induced us to study E rosette formation and its probable inhibition by the serum of chronic alcoholic patients. Subjects were split into three groups: Group 1: n = 21. Normal individuals. Group 2: n = 15. Chronic alcoholic patients without cirrhosis. Group 3: n = 26. Chronic alcoholic patients with histologically demonstrated liver cirrhosis. E rosette and E rosette inhibition (TIRE) sera tests were performed utilizing subjects sera tested against lymphocytes of normal individuals not related to group 1. The results found are listed in detail in Table 1 (mean = -SD) and Figure 1 (median), for each of the test groups. We applied unifactorial variance analysis and observed highly significant differences between the groups studied in all tests performed. It was found that tests that utilized I.E. discriminate most efficiently among the three groups of patients and that those which utilize unabsorbed assay serum (S/A) yield the best differentiation. Using this last assay it was observed that 20/21 control individuals showed less than 15

inhibition. On this basis, we decided to separate the results into 15

regular intervals (Table 3). Inhibition above 30

was found only in cirrhotic patients with the exception of one individual of the control group and one non-cirrhotic alcoholic patient with no alcoholic liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Fibrosis hepatica y progesterona

Con el fin de estudiar la acción de la Prog sobre la fibrosis hepática, fue inducida esta alteración por medio de la ingesta de C14C y etanol, en 55 conejos, entre 1 y 2 años, raza New Zealand; desarrolando la fibrosis en 6 meses. El grupo de animales tratados con Prog, ya sea desde el comienzo o después de 180 días de recibir el tóxico, presentaba disminución o menos fibrosis; así como protección del hepatocito, que se evidenciaba por la nobalonización o vacuolización de las células, no infiltrado inflamatorio, ni tampoco metamorfosis grasa. Si algunas de estas alterraciones habían aparecido, al iniciar el tratamiento con Prog disminuían gradualmente hasta desaparecer. Los datos de laboratorio tuvieron una diferencia altamente significativa a los 60 y 180 días entre los grupos que recibían el tóxico y los que revibían Prog, ya sea desde el comienzo o diferida. La Prog, como se ha visto en cultivos de fibroblastos fetales y en el tratamiento de tumores desmoides o adhesiones quirúrgicas, destruye los fibroblastos y por consiguiente disminuye el tamaño de estos tumores y la cohesión de las adherencias. La razón de no haberse hallado una resolución total de la cirrosis (aunque si una disminución manifiesta de la fibrosis) puede deberse a la actividad de miofibroblastos que provocan la retracción del tejido hepático dañado

Fibrosis hepatica y progesterona

Con el fin de estudiar la acción de la Prog sobre la fibrosis hepática, fue inducida esta alteración por medio de la ingesta de C14C y etanol, en 55 conejos, entre 1 y 2 años, raza New Zealand; desarrolando la fibrosis en 6 meses. El grupo de animales tratados con Prog, ya sea desde el comienzo o después de 180 días de recibir el tóxico, presentaba disminución o menos fibrosis; así como protección del hepatocito, que se evidenciaba por la nobalonización o vacuolización de las células, no infiltrado inflamatorio, ni tampoco metamorfosis grasa. Si algunas de estas alterraciones habían aparecido, al iniciar el tratamiento con Prog disminuían gradualmente hasta desaparecer. Los datos de laboratorio tuvieron una diferencia altamente significativa a los 60 y 180 días entre los grupos que recibían el tóxico y los que revibían Prog, ya sea desde el comienzo o diferida. La Prog, como se ha visto en cultivos de fibroblastos fetales y en el tratamiento de tumores desmoides o adhesiones quirúrgicas, destruye los fibroblastos y por consiguiente disminuye el tamaño de estos tumores y la cohesión de las adherencias. La razón de no haberse hallado una resolución total de la cirrosis (aunque si una disminución manifiesta de la fibrosis) puede deberse a la actividad de miofibroblastos que provocan la retracción del tejido hepático dañado (AU)

[Hepatic fibrosis and progesterone]. / Fibrosis hepática y progesterona.

To study the progesterone (Prog.) action on the hepatic fibrosis, we produced fibrosis on 55 New Zealand male rabbits, by oral ingestion of carbon tetrachloride (Cl4C) and ethanol. They developed it in six months. All the animals received the toxic. A group of these animals also received the Prog since the onset (0.66 mg/3 times a week, IM) and the rest received it 180 days after the beginning of the experiment. We could see in the biopsies of the animals who received Prog since the beginning or after 180 days: protection of the hepatocytes, no vacuolization of the cell, no inflammatory infiltrate, no fat metamorphosis, very thin fibrous hands. If one of these alterations had appeared with the toxic, the Prog action would have diminished it gradually until its disappearance. Between the groups who received only toxic and the groups that received th Prog (at the beginning or deferred), the laboratory results showed a high significative difference (p less than o.01) especially in the transferases (ASAT-ALAT) in the 60-180 days period. The Prog in the fibroblasts culture and in the treatment of desmoid tumours, on operative adhesions, destroy the fibroblasts and for this action diminished the volume of the tumour and the adhesions. Perhaps the incomplete resolution of the cirrhosis (though the hands of fibrosis diminished considerably) could be explained by the activity of another kind of fibroblast (the myofibroblast), which provokes the retraction of cirrhotic hepatic tissue.

Fibrosis hepática y progesterona. / [Hepatic fibrosis and progesterone]

To study the progesterone (Prog.) action on the hepatic fibrosis, we produced fibrosis on 55 New Zealand male rabbits, by oral ingestion of carbon tetrachloride (Cl4C) and ethanol. They developed it in six months. All the animals received the toxic. A group of these animals also received the Prog since the onset (0.66 mg/3 times a week, IM) and the rest received it 180 days after the beginning of the experiment. We could see in the biopsies of the animals who received Prog since the beginning or after 180 days: protection of the hepatocytes, no vacuolization of the cell, no inflammatory infiltrate, no fat metamorphosis, very thin fibrous hands. If one of these alterations had appeared with the toxic, the Prog action would have diminished it gradually until its disappearance. Between the groups who received only toxic and the groups that received th Prog (at the beginning or deferred), the laboratory results showed a high significative difference (p less than o.01) especially in the transferases (ASAT-ALAT) in the 60-180 days period. The Prog in the fibroblasts culture and in the treatment of desmoid tumours, on operative adhesions, destroy the fibroblasts and for this action diminished the volume of the tumour and the adhesions. Perhaps the incomplete resolution of the cirrhosis (though the hands of fibrosis diminished considerably) could be explained by the activity of another kind of fibroblast (the myofibroblast), which provokes the retraction of cirrhotic hepatic tissue.

[Use of medroxyprogesterone in human hepatic cirrhosis]. / Utilización de medroxiprogesterona en cirrosis hepática humana.

The effect of medroxyprogesterone in 14 patients with hepatic cirrhosis demonstrated with histological technics was studied. Eight of the 14 patients were controlled over a period of one year and three months. Six of this eight patients presented subjective clinical improvement and the ascitis disappeared in 5/7 cases, so that the doses of lactona could be diminished. Three of the male patients recovered their sexual potency although all were in alcoholic abstinence for more than one year. Histologically 5/6 patients presented a diminishing fibrosis in the control biopsy and the 3 patients controlled with hemodynamic studies presented lower portal pression. We didn't found secondary effects, except obesity in 3 cases. We concluded that it would be important to continue this experience with a greater number of patients and adding appropriate biochemical controls.

Utilización de medroxiprogesterona en cirrosis hepática humana. / [Use of medroxyprogesterone in human hepatic cirrhosis]

The effect of medroxyprogesterone in 14 patients with hepatic cirrhosis demonstrated with histological technics was studied. Eight of the 14 patients were controlled over a period of one year and three months. Six of this eight patients presented subjective clinical improvement and the ascitis disappeared in 5/7 cases, so that the doses of lactona could be diminished. Three of the male patients recovered their sexual potency although all were in alcoholic abstinence for more than one year. Histologically 5/6 patients presented a diminishing fibrosis in the control biopsy and the 3 patients controlled with hemodynamic studies presented lower portal pression. We didnt found secondary effects, except obesity in 3 cases. We concluded that it would be important to continue this experience with a greater number of patients and adding appropriate biochemical controls.