This experiment was designed to explore the correlation between the mechanism of immobilization-induced skeletal muscle atrophy and the apoptosis of muscular cells. The models of skeletal muscle atrophy induced by immobilization for different length of time were established according to Sievanen II methods. 24 rabbits, each of them having one hind leg fixed by the tubal plaster and the other one free as control, were randomly divided into four groups depending on time of fixation (3, 7, 14, and 28 days respectively). The animals were sacrificed by the end of fixation. TdT-mediated d-UTP nick end labeling (TUNEL) was used to investigate the apoptotic muscle cells in the animal's bone. By comparing the apoptotic muscle cells with the morphology of the skeletal muscle, the correlation between cell apoptosis and skeletal muscle atrophy were analyzed. Apoptotic muscle cells did appear after immobilization in the atrophied skeletal muscle. In various groups, some cells with false positive stained TUNEL were found in the atrophic muscle, which could be distinguished from apoptotic cells by their characteristics. In conclusion, cell apoptosis participates in the process of skeletal muscle atrophy induced by immobilization; the amount of apoptotic cells is strongly associated with the time of immobilization, its peak appears on the 14th day of immobilization; the distribution of apoptotic skeletal muscle cell varies with the time of fixation. The severity of skeletal muscle atrophy is associated with the degree of the muscle cell apoptosis.
Animals ; Apoptosis ; physiology ; Immobilization ; In Situ Nick-End Labeling ; Muscle, Skeletal ; pathology ; Muscular Atrophy ; etiology ; Rabbits

Occurance of atrophic nonunion is a complex process. Previous studies suggested that atrophic nonunion was mainly due to lack of blood supply of fracture fragments, but recent studies found that blood supply was not deficiency in middle and late stages, indicating that decreased osteogenic factors and blood supply in early stages might play an important role in morbidity. Current effective treatment measures for atrophic nonunion mainly include bone graft and fixation,physical therapy, local injection therapy. All-round preventive could reduce incidence of atrophic nonunion. Atrophic nonunion is still a troublesome complication of fractures in orthopaedics, and more attention should be paid for its effective prevention and treatment. The paper summarized recent original articles about atrophic nonunion and reviewed the occurrence mechanisms, diagnosis, prevention and treatment measures of this disease.
Atrophy ; diagnosis ; etiology ; prevention & control ; therapy ; Fracture Healing ; drug effects ; Fractures, Bone ; pathology ; Humans

Angiotensin II ; metabolism ; Animals ; Male ; Muscle, Skeletal ; Muscular Atrophy ; etiology ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley

Bilateral suprascapular nerve entrapment syndrome is very rare. It presents with shoulder pain, weakness and atrophy of the supraspinatus and infraspinatus muscles. We present a twenty-year old man having a history of bilateral shoulder pain associated with weakness. Electromyographic studies revealed signs of a lesion that caused a neupraxic state of the left suprascapular nerve, moderate axonal loss of the right suprascapular nerve and denervation of the right suprascapular muscle. The patient was treated with physical and medical therapy. Due to worsening of the symptoms, a surgical operation was performed by the excision of the transverse scapular ligaments bilaterally. His pain, weakness and atrophy had diminished on examination six weeks later. Suprascapular nerve entrapment should be considered in patients with shoulder pain, particularly those with weakness and atrophy of the supraspinatus and infraspinatus muscles.
Adult ; *Back ; Human ; Magnetic Resonance Imaging ; Male ; Muscle Weakness/etiology/*pathology ; Muscular Atrophy/etiology/*pathology ; Nerve Compression Syndromes/complications/*pathology ; Pain/etiology/pathology ; *Shoulder

A study on the pathologic findings after recession and resection of extraocular muscles in rabbits was performed. Fibrosis of the extraocular muscles increased with time, which showed no difference between the recessed and resected muscles. Inflammation and foreign body reaction decreased with time, which showed no difference between the recessed and resected muscles. Adhesions of extraocular muscles to the sclera were observed from one month after the operation. The resected muscles showed milder adhesion to the sclera than the recessed ones. The operated extraocular muscles showed atrophies at one month, which showed no difference between the recessed and resected muscles. According to our results, when reoperation is needed, fibrosis of the extraocular muscles after recession and resection should be considered when making a decision on the amount of muscle to be recessed and resected.
Animals ; Atrophy/etiology ; Fibrosis/etiology ; Foreign-Body Reaction/pathology ; Inflammation/etiology/pathology ; Oculomotor Muscles/pathology/*surgery ; Postoperative Complications/*pathology ; Rabbits ; Reoperation

Prolonged administration of anterior hypophyseal, adrenocortical, or thyroid hormones is known to cause degeneration, degranulation and necrosis of the beta-cells in the Langerhans islets of the pancreas. However, the effects of extirpation of these endocrine glands upon the Langerhans islets has not been reported, a1though it is known that removal of any of these glands bring about hypoglycemia, decreased tissue uptake of glucose, and increased tissue sensitivity to insulin. The present investigation is studies of the morphologic alterations of the beta-cells in the Langerhans islets following hypophysectomy, adrenalectomy, or thyroidectomy in rats. Hypophysectomy, adrenalectomy, and thyroidectomy, all induce similar morphologic alterations in the beta-cells of the islets. These consist of increased beta-cell population, the accumlnation of beta-granules, and atrophy of the individual betacell. Therefore, these changes are considered to be not specific following the withdrawal of specific hormones but a common effect of the hypoglycemia due to removal of the hypophysis, adrenals, or thyroid glands. A similar common degeneration of the beta-cells due to hyperglycemia occurs when hormones of these endocrine glands are given excessively.
Adrenal Cortex Hormones/physiology ; Adrenalectomy* ; Animal ; Atrophy/etiology ; Blood Glucose ; Diabetes Mellitus/etiology ; Glycogen/metabolism ; Hyperglycemia/etiology ; Hypoglycemia/etiology ; Hypophysectomy* ; Insulin/secretion ; Islets of Langerhans/pathology* ; Liver Glycogen/metabolism ; Muscles/metabolism ; Myocardium/metabolism ; Necrosis/etiology ; Rats ; Staining and Labeling ; Thyroidectomy* ; Thyroxine/physiology

Spinal and bulbar muscular atrophy (SBMA) is a rare X-linked motor neuron disease with significant phenotypic viability. Here, we present a genetically identified SBMA family without bulbar paralysis or androgen insensitivity. All four male patients presented with progressive lower motor neuron paralysis in all limbs, with distal extremities more dominant. None of them had bulbar palsy or androgen insensitivity. A consistently mild elevated blood creatine phosphokinase (CPK) levels were detected in all patients and the EMG showed a chronic neurogenic damage. Muscle biopsy of propositus indicated a typical neurogenic amyotrophy. Genetic testing for SMA of mutation in SMN1 was negative, while for SBMA of androgen receptor showed the increased CAG repeat in exon 1, suggesting that although bulbar symptoms and androgen insensitivity are characteristic symptoms of SBMA, they are not obligatory for the diagnosis. In adult males with a chronic motor neuron syndrome without upper motor neuron signs, even in absence of the classical features of androgen insensitivity or bulbar findings, genetic testing for SBMA should be strongly considered.
Adult ; Bulbo-Spinal Atrophy, X-Linked ; complications ; diagnosis ; genetics ; Creatine Kinase ; blood ; Genetic Testing ; Humans ; Male ; Motor Neurons ; pathology ; Muscular Atrophy ; etiology ; Mutation ; genetics ; Paralysis ; diagnosis ; etiology ; Pedigree ; Receptors, Androgen ; genetics

Papillary cystadenoma of the epididymis is a rare benign tumor, accounting for only 4 per cent of all epididymal tumors. Histologically, it can be confused with metastatic renal cell carcinoma. This extremely rare lesion may occur sporadically or as a manifestation of von Hippel-Lindau(VHL) disease. The present paper reported a case of papillary cystadenoma accompanied by testicular atrophy with no signs of VHL syndrome or infertility. To date, no similar case was reported in the literature. The tumor measured 5.0 cm x 4.0 cm x 4.0 cm and was located in the right epididymis. Histopathologic examination of a surgically removed specimen indicated a primary papillary cystadenoma. Histomorphologically, these tumors are characterized by cysts with colloid-like contents and papillary formations of light epithelium. Since metastatic renal cell carcinoma may be histologically similar to papillary cystadenoma, the importance of long-term urologic follow-up for possible presentation of renal cell carcinoma is discussed.
Adult ; Atrophy ; etiology ; Cystadenoma, Papillary ; complications ; pathology ; Epididymis ; Genital Neoplasms, Male ; complications ; pathology ; Humans ; Male ; Testis ; pathology

Atrophy ; diagnosis ; Brain Diseases ; diagnosis ; pathology ; Child ; Humans ; Magnetic Resonance Imaging ; Male ; Nervous System Malformations ; diagnosis ; pathology ; Seizures ; etiology ; Syndrome

A 32-year-old man with blurred vision in the right eye and headache presented with anterior uveitis, an intraocular pressure (IOP) of 60 mmHg, an open angle, no visual field defects, and normal optic nerve. He had a history of five previous similar attacks. In each of the previous instances, his anterior uveitis and high IOP were controlled with antiglaucoma medications and topical steroids. However, at the fifth attack, his optic disc was pale and a superior paracentral visual field defect was shown. Brain magnetic resonance image studies were normal. This case represents that a recurrent Posner-Schlossman syndrome (PSS)-induced optic disc atrophy likely due to ocular ischemia caused by a recurrent, high IOP. Although PSS is a self-limiting syndrome, we should manage high IOP and prevent ischemia of the optic nerve head by treating with ocular antihypertensive medications.
Atrophy/diagnosis/etiology ; Diagnosis, Differential ; Glaucoma, Open-Angle/*complications/diagnosis/physiopathology ; Humans ; *Intraocular Pressure ; Male ; Optic Disk/*pathology ; Optic Nerve Diseases/diagnosis/*etiology/physiopathology ; Syndrome ; Young Adult