Portal hypertension is a common physiopathological change in liver cirrhosis. In this study, rabbits were used and the model of pre-hepatic portal hypertension (PHT) was induced by partial ligation of portal vein in two steps. We measured the diameters of portal vein and small mesenteric vein at different time-points. Then we detected the stress forces induced by blood flow in varicose veins and in portal vein; such forces included hydrostatic pressure, shear stress and circumferential stress. With the increase of the diameter of varicose small mesenteric vein, the hydrostatic pressure and circumferential stress gradually elevated and shear stress descended markedly in both the portal vein and the small mesenteric vein of PHT rabbits, between which there was a positive linear correlation. The findings in our study indicate that the complications of PHT are partially attributable to the environment of lower shear stress and higher circumferential stress in which the blood vessels of portal venous system live.
Animals ; Hemodynamics ; Hypertension, Portal ; etiology ; pathology ; physiopathology ; Mesenteric Veins ; pathology ; physiopathology ; Portal Vein ; pathology ; physiopathology ; Rabbits ; Stress, Mechanical ; Vascular Resistance ; physiology ; Venous Pressure

Bone is a load-bearing organ in human body. Fatigue damage occurs readily at the modest loads to which bone is subjected during its habitual physiological usage. Even bone fracture may occur during vigorous activity. The nature of fatigue damage is that in bone there are very fine microcracks which are smaller than typical microcracks, and may occur at the level of hydroxyapatite crystals. But bone can repair microdamage by bone remodeling. Osteocytes play an important role of signaling during bone remodeling. Some researchers attempted to describe the process of bone fatigue damage and repair by mathematic, mechanical models in order to understand it well and to apply it well in clinical practice.
Animals ; Bone Remodeling ; physiology ; Bone Resorption ; pathology ; physiopathology ; Bone and Bones ; cytology ; injuries ; physiology ; Fractures, Stress ; pathology ; physiopathology ; Humans ; Models, Biological ; Stress, Mechanical

The aim of this study is to study the damage effects of chronic hypoxia on medulla oblongata and to explore whether the damage is associated with oxidative stress and cell apoptosis. Adult male SD rats were randomly divided into two groups: control group and chronic hypoxia group. Medulla oblongata was obtained for the following methods of analyses. Nissl's staining was used to examine the Niss bodies of neurons in medullary respiratory related nuclei, biochemistry methods were utilized to examine oxidant stress damage induced by chronic hypoxia on medulla oblongata through measuring malondialdehyde (MDA) content and superoxide dismutase (SOD) activity, and RT-PCR technique was used to study the influence of apoptosis induced by chronic hypoxia on medulla oblongata through analyzing the levels of Bax mRNA and Bcl-2 mRNA. The results showed the optical densities of Nissl's staining in pre-BötC, NA, NTS, FN, and 12N were significantly decreased in chronic hypoxia group in comparison with that in control group (P < 0.05). In chronic hypoxia group, MDA level was significantly higher than that in the control group (P < 0.05), whereas SOD level had no significant difference between the two groups (P > 0.05). Bax mRNA expression had no obvious change and Bcl-2 mRNA expression significantly decreased in chronic hypoxia group in comparison with that in control group (P < 0.05). The results suggest that chronic hypoxia could bring about serious damage to medullary respiratory centers through aggravating oxidative stress and increasing cell apoptosis.
Animals ; Apoptosis ; Chronic Disease ; Hypoxia ; physiopathology ; Male ; Medulla Oblongata ; metabolism ; pathology ; physiopathology ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Respiratory Center ; metabolism ; pathology ; physiopathology ; Superoxide Dismutase ; metabolism

OBJECTIVETo explore the biomechanical mechanism of impact force-induced mandibular fractures and its finite element analysis.

METHODSThree mandibular impact fracture models were prepared using intact human mandibular specimens and simulated maxillary models according to the Hanau principle of articulator and a MTS-858 biological material testing machine. Mandibular impact was delivered in the direction of the chin level at the mandibular postural position (MPP) on MTS. The computerized mandibular model was then established from 3-dimensional laser scanning images for finite element analysis using ANSYS7.0.

RESULTSThe 3 mandibular specimens were fractured at the chin, where the maximum force was 2151.10-/+ 125.18 N with response time of 17.3-/+2.3 ms. Impact simulation with ANSYS mimicking stress changes in the internal jaw suggested the chin as place where maximum stress occurred. According to the stress curve, the maximum stress of 3201.35 kPa occurred at the point 1.92 cm from the upper edge of the chin.

CONCLUSIONThe combination of mandibular impact experiments and finite element analysis allows quantification of several parameters of the jaw and provides clues for understanding the biomechanical mechanism of mandibular impact fractures.

Biomechanical Phenomena ; Finite Element Analysis ; Humans ; Mandible ; pathology ; physiopathology ; Mandibular Fractures ; physiopathology ; Models, Anatomic ; Stress, Mechanical ; Tensile Strength

Animals ; Antidepressive Agents ; pharmacology ; Brain-Derived Neurotrophic Factor ; metabolism ; Cyclic AMP Response Element-Binding Protein ; metabolism ; Depression ; metabolism ; pathology ; physiopathology ; Hippocampus ; metabolism ; pathology ; physiopathology ; Humans ; Nerve Degeneration ; physiopathology ; Nerve Regeneration ; drug effects ; Neurons ; pathology ; Stress, Psychological ; metabolism ; pathology ; physiopathology

OBJECTIVETo investigate the characteristics of work needed to release adhesion in the early stage of flexor tendon healing.

METHODSEighty-four profoundus flexor tendons of the 3rd toe of Sanhuang chicken were severed and repaired by either Modified Kessler technique or Tsuge technique randomly. At 0, 1, 4, 7, 10, 14, 21 d after the operation, 6 tendons from each repair technique group were harvested and tested by biomechanical test machine. An elongation force-elongation distance curve was obtained and work of adhesion release was calculated in this curve. Whether adhesion band had been released or not was confirmed by gross inspection immediately after the test.

RESULTSWork of adhesion release: this work significantly increased at the 7th day in Modified Kessler group and at the 10th day in Tsuge group. Modified Kessler group was significantly higher than Tsuge group at the 7th day. At the 21st day after operation, adhesion could not be effectively released by full range excursion of flexor tendon profoundus.

CONCLUSIONWork of adhesion release begins to increase significantly since the 7th approximately 10th day postoperatively. At the 21st day after the operation, adhesion could not be fully released by full range of flexor tendon profoundus flexion.

Animals ; Chickens ; Male ; Stress, Mechanical ; Suture Techniques ; Tendon Injuries ; physiopathology ; surgery ; Tendons ; pathology ; physiopathology ; Tensile Strength ; Time Factors ; Tissue Adhesions ; physiopathology ; Wound Healing

OBJECTIVETo establish a mouse model of abdominal aorta stenosis and analyze the alterations in the arterial wall response to high and low shear stress.

METHODSTwenty mouse were randomized equally into 4 groups, including 3 test groups (1, 7 and 14 day groups) with surgically induced stenosis of the abdominal aorta, and a sham-operated group without stenosis. The hemodynamics and the internal diameter of the blood vessel were measured by color Doppler flow imaging. The wall shear stress was calculated by Poiseiulle hydrodynamics formula (τ(m)=η×4×V(m)/D). Pathological examination and immunohistochemistry were performed to observe the arterial morphological changes and the endothelial vascular cell adhesion molecule-1 (VCAM-1) expression. The intimal-media thickness of the aorta was measured and endothelial VCAM-1 expression analyzed quantitatively.

RESULTSRegions of low and high flow shear stress were created upstream from the stenosis and within the stenosis, respectively. Compared with the sham-operated group, the mice with aorta stenosis showed gradually increased vascular intimal-media thickness and VCAM-1 expression intensity in the upstream aorta, but not within the regions of the stenosis.

CONCLUSIONVascular remodeling may occur shortly after exposure to low shear stress, which plays a significant role in initiation and progression of the pathological process of atherosclerosis mediated by VCAM-1, whereas high shear stress may exert an anti-atherosclerotic effect.

Animals ; Aorta, Abdominal ; metabolism ; pathology ; physiopathology ; Aortic Valve Stenosis ; physiopathology ; Atherosclerosis ; physiopathology ; Constriction ; Hemodynamics ; Male ; Mice ; Shear Strength ; physiology ; Stress, Mechanical ; Vascular Cell Adhesion Molecule-1 ; metabolism

Adolescent ; Child ; Female ; Fractures, Stress ; diagnostic imaging ; pathology ; physiopathology ; Humans ; Male ; Tibial Fractures ; diagnostic imaging ; pathology ; physiopathology ; Tomography, X-Ray Computed ; Young Adult

BACKGROUNDWall shear stress is an important factor in the destabilization of atherosclerotic plaques. The purpose of this study was to assess the distribution of wall shear stress in advanced carotid plaques using high resolution magnetic resonance imaging and computational fluid dynamics.

METHODSEight diseased internal carotid arteries in seven patients were evaluated. High resolution magnetic resonance imaging was used to visualize the plaque structures, and the mechanic stress in the plaque was obtained by combining vascular imaging post-processing with computational fluid dynamics.

RESULTSWall shear stresses in the plaques in all cases were higher than those in control group. Maximal shear stresses in the plaques were observed at the top of plaque hills, as well as the shoulders of the plaques. Among them, the maximal shear stress in the ruptured plaque was observed in the rupture location in three cases and at the shoulder of fibrous cap in two cases. The maximal shear stress was also seen at the region of calcification, in thrombus region and in the thickest region of plaque in the other three cases, respectively.

CONCLUSIONDetermination of maximal shear stress at the plaque may be useful for predicting the rupture location of the plaque and may play an important role in assessing plaque vulnerability.

Aged ; Carotid Arteries ; pathology ; physiopathology ; Carotid Artery Diseases ; pathology ; physiopathology ; Computer Simulation ; Female ; Humans ; Magnetic Resonance Imaging ; methods ; Male ; Middle Aged ; Stress, Mechanical

The hemodynamic characteristics of abdominal arterial bifurcation, such as blood flowing velocity vector, the shear stress at the vessel wall were calculated, studied and compared using the newly-induced boundary element method in this study. It was analysed why the atherosclerosis is asymmetrical at the bifurcation of abdominal arterial. The hemodynamic causes of production and development of the atherosclerotic were reasonabley explained by the shear stress calculation results of left and right common iliac branch vessel walls before and after the lesions. It is shown that the distribution of blood flowing velocity vector, the shear stress at the vessel wall are asymmetrical because of the asymmetrical geometry at the bifurcation of abdominal arterial, so that the shear stress of inner wall is higher than outside. The inner wall shear stress of right common iliac is higher than left. Blood velocity and shear stress increase at the atherosclerotic lesion because the blood vessel becomes narrower, and the blood velocity and shear stress decrease at the downstream of the lesion. It was also shown that the hemodynamic characteristics played a great important role in the occurrence and development of the atherosclerosis diseases at the bifurcation of abdominal arterial. Because of the increase of the shear stress, the atherosclerotic plaque surface will be damaged, leading to tissue hyperplasia. It will be lead to blood cell coacervation that the blood velocity and shear stress decrease at the atherosclerotic plaque downstream.
Aorta, Abdominal ; pathology ; physiopathology ; Atherosclerosis ; pathology ; physiopathology ; Blood Flow Velocity ; physiology ; Finite Element Analysis ; Hemodynamics ; Humans ; Shear Strength ; physiology ; Stress, Mechanical