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PubMed2001

Association of endometrial degeneration in bitches with insufficient plasma progestagen concentrations.

The relationship between changes in plasma progesterone concentrations and endometrial degeneration in bitches was determined. Mature bitches (n = 14) were ovariectomized and treated with oestradiol benzoate for 11-12 days, followed by progestagen (2 mg megestrol acetate kg-1 body weight per day) for 35-37 days. Two bitches were necropsied at this stage (progestagen group). The other bitches were treated once a day for a further 3 weeks with 0.5 mg megestrol acetate kg-1 (decreased dose group; n = 3), 2 mg megestrol acetate kg-1 (standard dose group; n = 3), or 3 (1 week), 4 (1 week) and 5 (1 week) mg megestrol acetate kg-1 (increased dose group; n = 3), or received no treatment (withdrawal dose group; n = 3). A further five bitches with intact ovaries were examined during dioestrus (n = 4) and anoestrus (n = 1; 3 weeks after plasma progesterone concentration < 0.3 nmol l-1). Marked degeneration (> 80% cells) of the luminal epithelium was observed in the withdrawal dose and decreased dose groups, and in the intact bitches with plasma progesterone concentrations of 21, 36 and 39 nmol l-1. Medium (40-60% cells) degeneration was detected in the standard dose group and in the anoestrous bitch. However, a very small proportion (< 10%) of degenerated cells was found in the increased dose and progestagen groups, and no degeneration was detected in the dioestrous bitch with a plasma progesterone concentration of 90 nmol l-1. The numbers of endometrial leucocytes were low in all groups except for the withdrawal dose group and the anoestrous bitch. These results indicate that endometrial degeneration and exfoliation in bitches reflects a reduction or insufficiency of plasma progesterone concentrations. The mechanisms involved are unclear.

Anestrus↗

PubMed1999

[Disc degeneration and cervical instability].

OBJECTIVE: To evaluate disc degeneration and segmental instability in the cervical spine by comparing the magnetic resonance imaging assessment of disc degeneration with conventional plain radiographic evaluation with cervical segmental instability. METHODS: Two hundred sixty consecutive patients with suspected cervical spine disorders were analyzed for horizontal and angular displacements on lateral flexion and extension radiographs and disc degeneration on T(2)-weighted magnetic resonance images of the cervical vertebrae. RESULTS: In all intervertebral levels, the grade of disc degeneration increased significantly (P < 0.01) with age. Cervical instability was identified in 151 segments (14.5%) and correlated with Grade 1 and Grade 2 degeneration in the intervertebral discs (P < 0.01). CONCLUSIONS: Cervical segmental instability may indicate early degeneration of intervertebral disc in the cervical vertebrae.

Adult↗

PubMed2002

[The effect of anterior cruciate ligament rupture and reconstruction on the degeneration of articular cartilage in rabbit knee].

OBJECTIVE: To investigate the effect of rupture and reconstruction of the anterior cruciate ligament (ACL) on the degeneration of rabbit knee articular cartilage. METHODS: 14 mature New Zealand white rabbits were divided into four groups. In group I, the ACL of the right knees in 7 rabbits was resected and immediately reconstructed, and the contralateral ACL was resected only in controll f group I. In group II, the ACL of the right knees in 7 rabbits was reconstructed 3 weeks after the ACL was resected and the contralateral joints in control group II, in which only a medial arthrotomy was performed. The rabbits were killed 8 weeks after the operation. The methods of ink straining, histology and SEM were used to analyze the changes in articular cartilage of the joints. RESULTS: The results of ink method and HE straining were analyzed quantitatively. The degeneration of knee articular cartilage in group I was significantly weaker than that in control group I (Hc = 5.9889, P = 0.0144). The degeneration of knee articular cartilage in group II was as serious as that in control group I (Hc = 0.7143, P = 0.785). CONCLUSIONS: Immediate reconstruction of the ACL can effectively prevent articular cartilage from degeneration. Once the articular cartilage damaged moderately, delayed reconstruction of the ACL could not effectively reduce the development of degeneration. So once the ACL is ruptured, reconstruction should be performed in the early stage to restore the stability of knee joint to prevent the articular cartilage from degeneration.

Animals↗

PubMed1975

Ultrastructural features of degenerated cardiac muscle cells in patients with cardiac hypertrophy.

Degenerated cardiac muscle cells were present in hypertrophied ventricular muscle obtained at operation from 12 (38%) of 32 patients with asymmetric septal hypertrophy (hypertrophic cardiomyopathy) or aortic valvular disease. Degenerated cells demonstrated a wide variety of ultrastructural alterations. Mildly altered cells were normal-sized or hypertrophied and showed focal changes, including preferential loss of thick (myosin) filaments, streaming and clumping of Z band material, and proliferation of the tubules of sarcoplasmic reticulum. Moderately and severely degenerated cells were normal-sized or atrophic and showed additional changes, including extensive myofibrillar lysis and loss of T tubules. The appearance of the most severely degenerated cells usually reflected the cytoplasmic organelle (sarcoplasmic reticulum, glycogen, or mitochondria) which underwent proliferation and filled the myofibril-free areas of these cells. Moderately and severely degenerated cells were present in areas of fibrosis, had thickened basement membranes, and had lost their intercellular connections. These observations suggest that degenerated cardiac muscle cells have poor contractile function and may be responsible for impaired cardiac performance in some patients with chronic ventricular hypertrophy.

Adolescent↗

PubMed2002

[Autopsy evaluation of the extent of degeneration of the lumbar intervertebral discs].

The aim of study was to evaluate the degree of lumbar intervertebral disc degeneration during post-mortem studies, and its relation to the age and gender of cadavers. The changes of intervertebral disc were classified according to Nachemson [13]. The study included 308 lumbar intervertebral discs taken during autopsy from 57 females (mean age 41.83) and 79 males (mean age 42.06). Two hundred and forty discs showed degenerative changes. The statistic analysis revealed that the degeneration is more pronounced with age (ANOVA p < 0.05). The study demonstrated that in males degeneration occurs a decade earlier than in females, and could be observed in the second decade of life. Similarly, the degeneration of 3rd or 4th grade could be observed a decade earlier in men than in women. The statistical analysis revealed the differences (p < 0.05) in degeneration between upper (levels L2 and L3), and lower (levels L4 and L5) lumbar spine. Analysing the discs as single levels, no statistical differences in degeneration were observed.

Adolescent↗

PubMed1991

[Nature of cloudy swelling and granular degeneration of parenchymatous organs].

There is a basis to consider a cloudy swelling of parenchymatous organs as one of manifestations of albuminous or, more correctly, albuminous-hydropic degeneration. It has characteristic macroscopic (cloudy swelling) and microscopic ("hydropic oedema", granular degeneration) signs and various patho--and morphogenetic mechanisms. Granular degeneration may be not only an expression and synonym of albuminous-hydropic degeneration but a manifestation of functional tension, i.e. adaptation, as well. Heterogeneity of the concept "cloudy swelling" is due to the peculiarities of its pathogenesis while the heterogeneity of the concept "granular degeneration" is due to double pathologic interpretation of this phenomenon, adaptation and degeneration which are divided by the time factor only which determines the break of adaptation.

Adaptation, Physiological↗

PubMedDate not supplied

Disc degeneration in the thoracolumbar junctional region. Evaluation by radiography and discography in autopsy.

Disc dimensions and lengths of spondylophytes in the thoracolumbar junctional region (T 10-L 1) of 37 male cadaveric spines were measured from conventional radiographs. The disc degeneration was assessed by discography. The surface areas of the spondylophytes at vertebral body margins were recorded directly from the bones of 24 of the spines. Disc degeneration and the largest spondylophytes at corresponding levels measured from radiographs were related at T10-11 and at T11-12 (r = 0.41 and r = 0.43; p less than 0.01), but not at T12-L1 (r = 0.14). In the individual discs, however, only large spondylophytes in radiographs (actual length over 4 mm) were related to signs of disc degeneration. In addition, 'traction spurs' and Scheuermann's changes were more often associated with severe disc degeneration than 'claw-type' spondylophytes. The intervertebral disc space height correlated poorly with disc degeneration except, to some extent, at T11-12. Thus, the assessment of disc degeneration from conventional radiographs seems unreliable at this region of the spine.

Adult↗

PubMed1988

Visual system degeneration in the glaucomatous albino quail.

The peripheral (eye, retina, optic nerve) and central (primary optic tracti and centers, centrifugal visual tractus and nucleus) visual system of an imperfect albino quail mutant with a sex linked recessive gene was examined in 32 specimens ages 1 week - 16 months-hatch using various histological techniques. During the first weeks the visual system was normal and comparable in its overall organization to that found in the pigmented quail. However, the ipsilateral retinal projections were observed to be weaker in the young mutant, then completely disappeared two months after birth. Initial signs of the bupthalmos, a form of spontaneous glaucoma, appeared between the 3rd and 5th months. This was characterized by a distention of the eye linked to an increase in intraocular pressure. The pathological process was progressive and at 16 months the eye was very prominent, the anterior chamber deep and a large and globular cornea was noted. The glaucoma progressively induced different histopathological changes in the visual system including: cupping of the optic disc, degeneration of optic axons and their parent ganglion and centrifugal cells and cavernous degeneration. All of these phenomena were identifiable at about the 10th post-natal month and progressed in a relatively constant and orderly manner. The retinal projections to the nucleus ectomamillaris, ventral and lateral optic tectum and ventral pretectum were the first to degenerate. The degeneration of optic fibers attaining the dorsal pretectum and dorsal thalamus occurred later. Furthermore the retrograde degeneration in the centrifugal isthmo-optic nucleus progressed from the external to the internal pole. The mechanisms involved in the selective degeneration of centrifugal and centripetal optic fibers is discussed.

Age Factors↗

PubMed1979

[Dynamics of axonal degeneration in the neuronally isolated cerebral cortex].

The brains of 11 cats were studied after unilateral isolation of the cortex after M. M. Khananashvily (1961) by means of resection of the projection fibres connecting the cortex with subcortical formations. The character and peculiarities of axonal degeneration in the large hemisphere cortex, were investigated after Nauta and Fink--Heimer. It was found that distribution of degenerating terminals in every layer depended on the time when the material was taken for investigation. Maximal concentration of the degenerating fibres was observed 3--5--10 days after the operation, then a gradual decrease in density of degeneration in every cortical layer was observed. By the 9th month after the operation, the processes of axonal degeneration completely came to their end. The problem of retrograde and anterograde nature of the axonal degeneration in the cortex of the large hemispheres was discussed in the article and it was demonstrated that in the field 4 of the neuronally isolated cortex it is of mixed nature.

Animals↗

PubMed1997

[Subacute combined degeneration of the spinal cord: manifestations of esophageal epidermoid carcinoma].

INTRODUCTION: Subacute combined degeneration of the spinal cord associated with vitamin B12 deficit is well known. However a paraneoplastic induced cyanocobalamin malabsorption responsible for either subacute combined degeneration of the spinal cord, has not been reported. Moreover, the possibility of either subacute combined degeneration of the spinal cord may be manifestation of a cancer, it's unknown. CLINICAL CASE: We present the case of a 73-year-old woman with cutaneous paleness and clinical manifestations of a subacute combined degeneration of the spinal cord. Laboratory analysis showed a megaloblastic anemia and Schilling test showed cyanocobalamin malabsorption corrected by intrinsic factor. Anti-intrinsic factor antibodies were positive. Chronic atrophic gastritis and immunological diseases associated with pernicious anemia or with anti-intrinsic factor positive, were excluded. A hidden esophageal squamous cell carcinoma was discovered. Necropsy confirmed both, subacute combined degeneration of the spinal cord and esophageal carcinoma in the absence of chronic atrophic gastritis. CONCLUSIONS: Anti-intrinsic factor antibodies were the only found factor which could explain cyanocobalamin malabsorption. A esophageal squamous cel carcinoma was discovered. In our case, vitamin B12 malabsorption had a paraneoplastic origin mediated by anti-intrinsic factor antibodies. Subacute combined degeneration of the spinal cord may be the manifestation of a hidden esophageal squamous cell carcinoma.

Aged↗

PubMed1998

Menadione-induced cell degeneration is related to lipid peroxidation in human cancer cells.

The role of lipid peroxidation, intracellular glutathione and Ca2+ concentration in menadione-mediated toxicity was investigated in human hepatoma cell lines, Hep G2 and Hep 3B, and in human leukemia cell lines, CCRF-CEM and MOLT-3. Incubation of these cells with 80 microM menadione at 37 degrees C resulted in depletion of intracellular glutathione, increased intracellular Ca2+, and increased lipid peroxidation, events leading to cell degeneration. The sensitivity of these cells to menadione, in order, was: Hep G2 cells > Hep 3B cells > CCRF-CEM cells and MOLT-3 cells. The extent of menadione-induced lipid peroxidation in different cell types followed the same order as did their susceptibility to menadione-induced cell degeneration. The menadione-induced depletion in glutathione level was in the following sequence: Hep G2 cells > MOLT-3 and CCRF-CEM cells > Hep 3B cells. The extent of the menadione-induced increase in the intracellular Ca2+ concentration was: Hep G2 cells > Molt-3 cells > CCRF-CEM cells and Hep 3B cells. Pre-treatment of Hep G2 cells with 20 mM deferoxamine mesylate, an iron chelator, reduced both the menadione-induced cell degeneration and lipid peroxidation; however, it did not prevent the menadione-induced increase in intracellular Ca2+ nor the depletion of glutathione. These data suggest that menadione-induced cell degeneration is directly linked to lipid peroxidation, and that it is less related to the rise in intracellular Ca2+ and the depletion in glutathione content. Dicumarol (an inhibitor of DT diaphorase) enhanced the capacity of menadione to induce Hep 3B cell degeneration from 71.3% to 86.2% after 120 min of menadione treatment at 37 degrees C, but did not have this effect in Hep G2, CCRF-CEM or MOLT-3 cells. The activities of DT diaphorase were 52.4, 39.6, 1.5 and 1.8 nmol cytochrome c reduced/min/mg protein in Hep G2, Hep 3B, CCRF-CEM and MOLT-3 cells, respectively. The activity of DT diaphorase was much higher in Hep G2 cells than in the other cells. It seems that DT diaphorase may not, as suggested by others, protect against cell degeneration by quinones, such as menadione.

Calcium↗

PubMed1998

[Mutation of the concept of degeneration in French-speaking Switzerland 1870-1920].

Between 1870 and 1920 the concept of degeneration changed radically. Away from an organization principle of mental diseases, degeneration became progressively a disease entity capable of affecting the human species as a whole. In the French-speaking part of Switzerland, fear of a "degeneration of the race" reached considerable dimensions in the years around 1910. The study of the introduction and then diffusion of the degeneration concept reveals clearly the social commitment of the medical profession. Although the French-speaking Swiss psychiatrists showed no tendency to give clinical value to this concept, they are, however, at the origin, through this social discourse, of the success that the idea of degeneration had. Hygienist, anti-alcoholic and political environments took over the job to perpetuate this discourse and finally managed to empty the concept of degeneration of its substance.

History, 19th Century↗

PubMed2005

Cone cGMP-gated channel mutations and clinical findings in patients with achromatopsia, macular degeneration, and other hereditary cone diseases.

Unrelated patients with achromatopsia, macular degeneration with onset under age 50 years, cone degeneration or dysfunction, cone-rod degeneration, or macular malfunction were screened for mutations in the three genes known to be associated with achromatopsia: the GNAT2 gene encoding the alpha subunit of cone transducin and the CNGA3 and CNGB3 genes encoding the alpha and beta subunits of the cone cGMP-gated cation channel. We found no examples of patients with GNAT2 mutations. Out of 36 achromats, 12 (33%) had mutations in CNGA3 (13 different mutations including five novel mutations) and 12 (33%) had mutations in CNGB3 (six different mutations including four novel mutations). All achromats with CNG mutations had residual, presumably cone function as determined by computer-averaged 30-Hz electroretinograms (ERGs). There was considerable variability in acuity and color vision, with most patients having acuities of 20/200-20/400 and complete absence of color perception, and others having acuities of 20/25-20/40 and some color vision. Two pseudodominant achromatopsia cases were uncovered, both with CNGA3 mutations, including one family in which some compound heterozygotes with achromatopsia mutations were clinically unaffected. We found two novel CNGB3 changes in three patients with juvenile macular degeneration, a phenotype not previously associated with mutations in the cone channel subunits. These patients had subnormal acuity (20/30-20/60), normal to subnormal color vision, and normal to subnormal full-field cone ERG amplitudes. Our results indicate that some patients with channel protein mutations retain residual foveal cone function. Based on our findings, CNGB3 should be considered as a candidate gene to be evaluated in patients with forms of cone dysfunction, including macular degeneration.

Adult↗

PubMed1989

Wallerian degeneration in the peripheral nervous system: participation of both Schwann cells and macrophages in myelin degradation.

This study examined the role of Schwann cells and hematogenous macrophages in myelin degradation and Ia antigen expression during Wallerian degeneration of rodent sciatic nerve. To identify and distinguish between macrophages and Schwann cells we used, in addition to electron microscopy, immunocytochemical staining of teased nerve fibres and 1 microns thick cryosections. Before the appearance of adherent macrophages the myelin sheath fragmented into ovoids, small whorls of myelin debris appeared within Schwann cell cytoplasm and the Schwann cell displayed numerous lipid droplets. However, at least in large fibres most myelin degradation and removal was accomplished or assisted by macrophages, identified by their expression of the ED1 marker. These cells began entering the nerve from blood vessels by day 2, migrated to degenerating nerve fibres and adhered to nerve fibres in the regions of the ovoids. There they penetrated the Schwann cell basal lamina to occupy an intratubal position and phagocytose myelin. During Wallerian degeneration a subpopulation of ED1-positive monocytes/macrophages expressed Ia antigen; Schwann cells were Ia-negative. Ia expression by monocytes/macrophages appeared to be a transient event and was not seen in post-phagocytic macrophages, as indicated by the fact that ED1-positive phagocytes with large vacuoles were Ia-negative. Our data show that both Schwann cells and macrophages play important roles in degrading and removing myelin during Wallerian degeneration. The expression of Ia antigen during Wallerian degeneration indicates that Ia expression need not necessarily reflect specific immune events but in some instances can represent a nonspecific response to PNS damage.

Acrylamide↗

PubMed1975

Transganglionic degeneration in trigeminal primary sensory neurons.

In 16 kittens either the frontal or the inferior alveolar nerve was transected and in 17 adult rats either the supraorbital, the infraorbital or the mental nerve was divided. The postoperative survival periods were kept at 3-28 days for the kittens and 15-26 days for the rats. Sections from the caudal brain stem and the upper part of the cervical cord were impregnated according to the Fink-Heimer method, procedure II. In the kittens degeneration was found after the 8th postoperative day ipsilaterally in both the spinal and main sensory trigeminal nuclei and the spinal trigeminal tract. In the rats degeneration was found in all cases in the same ipsilateral structures as in the kittens. The amount of degeneration was relatively great in the rats, whereas it was very modest in the kittens. A somatotopical pattern was found for the degeneration both within the spinal and the main sensory nuclei. It was in agreement with what has been found in earlier studies, where other techniques have been used. By a comparison with the results of a previous study on the trigeminal nerve in the rat, where partial lesions of the ganglia had been made, it was found that the degeneration in the present study did not cover the whole area receiving primary trigeminal afferents. Possible explanations for this are discussed.

Age Factors↗

PubMed1988

The rate of Wallerian degeneration in the absence of immunoglobulins. A study in chick and mouse peripheral nerve.

Sciatic nerves undergoing Wallerian degeneration are subject to massive invasion by monocytes bearing Fc receptors. The present experiments were done to explore the potential role of the Fc receptors. The effect of suppressed immunoglobulin levels on the rate of Wallerian degeneration was studied in the n. medioulnaris of the chick and in murine sciatic nerve. In the avian model, total immunoglobulin production was eliminated by bursectomy. The mice were injected after birth with antibodies against IgM, causing a selective reduction of immunoglobulin M levels. Myelin degeneration was measured in both groups by computer-assisted line sampling and corrected for intrafascicular edema. In both models, there were only minor differences with the controls. Immunoglobulins, accordingly, do not seem to play a significant role in the efficiency of myelin phagocytosis by monocytes during Wallerian degeneration. The study also includes data on the degree and the distribution of edema in nerves undergoing Wallerian degeneration.

Animals↗

PubMed1988

Patterns of change in endoneurial capillary permeability and vascular space during Wallerian degeneration.

In degenerating frog sciatic nerves an in situ perfusion technique was used to measure the permeability coefficient-surface area product (PA) of endoneurial capillaries to [14C]sucrose, and the endoneurial vascular space (V). Both PA and V started to increase after the 3rd day of degeneration. The increase in PA peaked around the 14th day of degeneration and then declined to reach near normal levels at 6 weeks post-transection. V increased until about the end of the 3rd week of degeneration and then declined to near normal levels at 6 weeks after transection. The delayed increase in capillary permeability may reflect an adaptive reorganization of endoneurial capillary structure and function in response to altered conditions of the endoneurial microenvironment, and it is suggested that this permeability increase is induced by breakdown products of axons or chemical signals from Schwann cells enveloping transected axons. Fluid extravasation from these leaking capillaries is probably responsible for the endoneurial oedema observed in Wallerian degeneration. The recovery of endoneurial capillary tone to near-normal levels at 6 weeks after transection leads to the intriguing conclusion that healthy nerve fibers are not essential for the maintenance of normal endoneurial capillary permeability.

Animals↗

PubMed2000

Depletion of macrophages reduces axonal degeneration and hyperalgesia following nerve injury.

Inflammatory mechanisms are believed to play an important role in hyperalgesia resulting from nerve injury. Hyperalgesia following nerve injury is temporally linked with Wallerian degeneration and macrophage recruitment, and is reduced in WLD mice, in which Wallerian degeneration is delayed. We sought more direct evidence that macrophages contribute to hyperalgesia and Wallerian degeneration by depleting macrophages with liposomes loaded with dichloromethylene diphosphonate (clodronate, Cl(2)MDP). Rats were subjected to partial ligation of the sciatic nerve. Intravenous injection of liposome-encapsulated clodronate reduced the number of macrophages in the injured nerve, alleviated thermal hyperalgesia and protected both myelinated and unmyelinated fibres against degeneration. The results confirm the role of circulating monocytes/macrophages in the development of neuropathic hyperalgesia and Wallerian degeneration due to partial nerve injury. Macrophage depletion immediately after nerve injury could have some clinical potential in prevention of neuropathic pain.

Analgesics, Non-Narcotic↗