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At least 37 records · Page 2Linked to original sources

PubMed1979

Comparative evaluation of skin atrophy in man induced by topical corticoids.

In this in-patient study, mild skin atrophy was observed clinically in 6 out of a total of 22 patients after fluocinolone acetonide and in one patient after flumethasone pivalate ointment applications (P less than 0,05). Investigations were discontinued prematurely on days 14 and 17 in 2 patients because they developed early atrophy due to fluocinolone acetonide applications. Histological findings indicating either moderate or marked skin atrophy were evident in 15 patients after flucinolone acetonide as against one patient after flumethasone pivalate ointment applications (P less than 0.001). In comparison with the controls the mean decrease in epidermal thickness was more marked after fluocinolone acetonide applications, namely 30.5% vs 21.3% after flumethasone pivalate applications. The ultrastructural tissue changes were less marked at the sites to which flumethasone pivalate was applied. In comparison with controls, the percentages of mean decrease in diameters of collagen fibrils measured in six volunteer patients ranged from 5.1% to 27.6% after fluocinolone acetonide and from 0% to 12.3% following flumethasone pivalate ointment applications, This difference was statistically significant (range P less than 0,01 to less than 0.001). This experimental study has demonstrated that flumethasone pivalate displays only a mild atrophogenic effect and it is clinically and histologically significantly less atrophogenic than fluocinolone acetonide. Flumethasone pivalate can therefore be reckoned as a suitable topical corticosteroid especially for the long-term treatment of corticoid-responsive dermatoses.

Administration, Topical↗

PubMed1979

Articular changes due to disuse in Sudeck's atrophy.

Two cases of Sudeck's atrophy of the foot occurring 16 months and 17 years after infected fractures of the leg were studied radiologically and pathologically. Various cartilaginous changes were observed, the nature and severity of which depended on the joint involved. They included superficial pannus, deep erosion, fibrous ankylosis and, at times, bony ankylosis. These changes are similar to those observed in nine cases studied by Rutishauser et al. Comparison of the pathological changes in human and experimental joint immobilization suggests that these changes are due mainly to decreased mobility of the joints of the foot in Sudeck's atrophy. These observations also suggest that physiotherapeutic mobilization in Sudeck's atrophy is important for the joints as well as for bone. From a more general point of view, they demonstrate that a condition which is nosologically different from the chronic rheumatic diseases can nevertheless cause lesions that are a fundamental part of the pathological changes in osteoarthritis, rheumatoid arthritis and ankylosing spondylitis.

Adult↗

PubMed2026

The miR-206-3p/Cpeb1 axis delays acetylcholine receptor degradation and preserves neuromuscular junction stability in denervation-induced muscle atrophy.

Peripheral nerve injury leads to progressive neuromuscular junction (NMJ) destabilization and acetylcholine receptor (AChR) degradation, which are critical drivers of denervation-induced muscle atrophy and impaired motor recovery. However, the post-transcriptional mechanisms regulating AChR stability during denervation remain poorly understood. Here, we investigated the role of miR-206-3p in NMJ maintenance and muscle preservation after denervation, with a focus on its interaction with the RNA-binding protein cytoplasmic polyadenylation element binding protein 1 (Cpeb1). Using C2C12 myoblasts and a sciatic nerve transection mouse model, we demonstrate that miR-206-3p promotes myogenic differentiation, enhances AChR clustering, and preserves postsynaptic AChR morphology. miR-206-3p directly targets the 3' untranslated region of Cpeb1, suppressing its expression, as confirmed by dual-luciferase reporter assays. In vivo, adeno-associated virus-mediated overexpression of miR-206-3p delayed denervation-induced AChR fragmentation, attenuated muscle atrophy, and significantly improved motor function recovery. Conversely, Cpeb1 overexpression accelerated AChR degradation and muscle wasting, whereas co-overexpression of miR-206-3p mitigated these detrimental effects, indicating that Cpeb1 is a key downstream effector of miR-206-3p. Collectively, our findings identify the miR-206-3p/Cpeb1 axis as a previously unrecognized regulator of NMJ stability and muscle integrity after denervation, providing mechanistic insight and a potential therapeutic target for preserving neuromuscular function during prolonged denervation.

Animals↗

PubMed2024

Concomitant telomere attrition is associated with spinal muscular atrophy in highly inbred region of North India: unraveling the thread in Kashmir region.

Spinal muscular atrophy (SMA) is a rare genetic disorder that unequivocally results in the degeneration of motor neurons, leading to muscle weakness and atrophy. This condition is caused by a mutation in the survival motor neuron 1 (SMN1) gene, which inevitably results in a deficiency of the SMN protein. In present study, we investigated the potential role of telomere attrition in SMA patients. Relative telomere length in peripheral blood lymphocytes was measured by Monochrome Multiplex Quantitative Polymerase Chain Reaction (MMQPCR) in 98 subjects and we conclusively found that SMA cases exhibit telomere attrition compared to healthy controls (P = 4 × 10- 2). Moreover, significant attrition was also observed in severe form of SMA, i.e. SMA type 0 (P = 0.04) as well.Although, the exact mechanism through which telomere shortening contributes to the pathogenesis of SMA is not fully understood and is yet to be delineated. However, one possibility is that telomere shortening leads to genomic instability and DNA damage, which can contribute to motor neuron degeneration. Another possibility is that telomere shortening leads to cellular senescence, which can impair the ability of motor neurons to regenerate and repair themselves. Recent studies have suggested that telomere shortening may be a potential therapeutic target in SMA. Thus, understanding the role of SMN1 gene in disease pathogenesis & its effect on telomere length will aid in estimating the risk & prognosis of SMA in genetically less explored & highly inbred region of Kashmir, Northern India.

Humans↗

PubMed1975

Lipid disturbances associated with spiral muscular atrophy. Clinical, electromyographic, histochemical, and lipid studies.

Twelve patients with juvenile- and adult-onset spinal muscular atrophy have been studied. Eleven of the twelve patients had either type II, type IV, or borderline abnormal phenotypes, suggesting a possible relationship between serum lipid abnormalities and neuronal degeneration in the spinal muscular atrophies. Muscle enzyme histochemical studies provided valuable diagnostic information. Extensor toe signs and talipes cavus were common clinical observations.

Adenosine Triphosphatases↗

PubMed1976

Genetic investigations on chronic forms of infantile and juvenile spinal muscular atrophy.

A material of 247 cases selected from 260 cases of spinal muscular atrophy in the Warsaw Department of Neurology in 1960-1974 was analyzed. The size of sibships was established and calculations were made of the mean distribution of the age at onset, also according to sex, for the different clinical forms, genetical proportions by the method of siblings and of probands, and coefficient of sib-sib correlation for the material as a whole and separately for males, females and male-female pairs. The analysis shows the course of the disease to differ between the sexes and to be mild in males more often than in females, as is particularly noticeable in the higher age groups. Cases of Kugelberg-Welander's disease are predominantly male. The hypothesis is advanced that a proportion of male patients have a sex-linked modifying gene of a fairly high frequency (possibly of the range of 1 in 5 males, and 1 in 25, in the homozygous state, in females). Although it would not disprove conclusively the nosological distinctness of different forms of infantile and juvenile spinal muscular atrophy, the existence of the modifying gene, if proved, would tend rather to add to the likelihood of their constituting a single recessive autosomal disease.

Adolescent↗

PubMed1975

Sensory system involvement in infantile spinal muscular atrophy.

Nine cases of infantile spinal muscular atrophy were studied post-mortem. Their ages at death ranged from 5 months to 10 years. In all cases severe loss of anterior horn cells in the spinal cord and neurogenic muscular atrophy were characteristic of this disease. In 6 cases there was also loss of myelin in the posterior columns particularly affecting the lumbar contribution. Sensory ganglia, especially from the lumbar region, contained nodules of Nageotte, indicating sensory neuron degeneration. These sensory abnormalities were more severe in the longer surviving cases. It seems possible that sensory neuron degeneration occurs more commonly in Werdnig-Hoffmann disease than has previously been supposed but that it is less severe and develops more slowly than motor neuron degeneration.

Anterior Horn Cells↗

PubMed1976

[Multiple systemic atrophies, mental retardation, neurogenic amyotrophy and congenital bone fragility. A new neuro-generative disorder].

Five cases of a congenital neurological disorder are reported. Four patients, born after a breech delivery, belong to one sibship while the fifth patient is the only child in another family. The clinical features include quadriplegia, amyotrophy, a peripheral neuropathy, severe mental retardation and a subluxation of the hips. X-rays reveal diffuse osteoporosis and multiple spontaneous fractures. Autopsies in 3 patients showed multiple system atrophies involving the spinal cord and the cerebellum, coarse cerebral gyri and a marked reduction in volume of the white matter. These various pathological features are compared with the lesions found in a few other cases reported in the literature, none of which can be considered to be identical to the ones described. It is therefore felt that the condition under discussion represents a new syndrome to be classified, at least temporarily, within the group of multiple system atrophies.

Atrophy↗

PubMed1979

Sulphur and phosphorus content in relation to fibre composition and atrophy of skeletal muscle in patients with Parkinson's disease.

Seventeen patients with Parkinson's disease have been compared with 8 normal individuals by biopsy of either the biceps brachii or quadriceps femoris muscles. All biopsies were investigated by enzyme histochemistry. With 13 patients, as well as all controls, scanning electron microscopy with X-ray microanalysis was employed on cryo-sections adjacent to those prepared for light microscopy. Thus, the elemental composition of single muscle fibres was obtained and could be related to histochemical fibre types. Fibre type analysis on the diseased material, based on differential stainability for alkali- and acid-stable ATPase, showed a normal type I and type IIA fibre frequency. A mild type IIB dominance at the expense of type IIA fibres was regarded as a significant deviation from normal. A slight to moderate muscle atrophy affected type IIB fibres almost exclusively. Normal content of sulphur and phosphorus was detected in type I and type IIA Fibres but a lowered sulphur content was obvious in type IIB fibres, especially in the atrophic ones, which also exhibited an increase in phosphorus content. The shift in fibre composition from IIA to IIB, the type IIB fibre atrophy and the change in sulphur and phosphorus content of type IIB fibres are interpreted as signs of a disuse which preferentially affects fast twitch type IIB motor units. These presumably have the highest threshold for activation under pathological conditions characterized by increased muscular tone and difficulties in the performance of rapid and strong voluntary movements.

Adenosine Triphosphatases↗

PubMed2026

C9orf72-associated poly-GR in skeletal muscle leads to neuromuscular junction deficits and muscle atrophy.

Hexanucleotide repeat expansions in C9orf72 produce dipeptide repeat (DPR) proteins that are widely expressed, including in the nervous system and skeletal muscle. Among these DPRs, arginine-containing proteins, poly-GR and poly-PR, are toxic in the nervous system, but whether DPRs in skeletal muscle contribute to amyotrophic lateral sclerosis (ALS) pathogenesis is unclear. Here, we show that muscle-restricted expression of poly-GR drives motor deficits in mice, including muscle atrophy and neuromuscular junction (NMJ) deficits. Poly-GR in muscle interacted with the NMJ key organizer MuSK and promoted MuSK degradation, disrupting postsynaptic structure and impairing neuromuscular transmission. Importantly, a MuSK agonist antibody (X-17) stabilized NMJs and rescued neuromuscular transmission. Moreover, poly-GR in muscle activated the integrated stress response (ISR), elevating eIF2α phosphorylation and broadly suppressing protein translation. ISR inhibition with ISRIB restored translation and MuSK protein levels and ameliorated both muscle atrophy and NMJ deficits. These findings demonstrate that skeletal muscle actively contributes to C9orf72-ALS pathology. Targeting muscle with ISRIB offers a therapeutic strategy to preserve motor function in C9orf72-ALS.

Animals↗

PubMed1978

Lactic acidosis associated with cerebellar vermal atrophy and cardiomyopathy.

The association of fluctuating neurological signs and congestive cardiomyopathy with chronic lactic acidosis is described in a 5 1/2 year-old-boy who ultimately succumbed to congestive heart failure. The autopsy findings included severe atrophy of the anterior cerebellar vermis and a hypertrophied heart with left sided endocardial fibroelastosis. Skeletal and cardial muscle calcification was prominent and probably due to the effect of intracellular metabolic alterations associated with lactic acidosis. A review of the literature shows that the combination of cardiomyopathy, isolated atrophy of cerebellar vermis and muscle fiber calcification have not been reported in association with idiopathic lactic acidosis previously.

Acidosis↗

PubMed1975

A family with apparently sex-linked optic atrophy.

A family is described in which a probable new form of sex-linked optic atrophy was found in eight individuals. Some additional neurological abnormalities were noted. Results of studies of the Xg blood group excluded close linkage between the optic atrophy and Xg genes. As a probable coincidence, Huntington's chorea was found in a side branch of the family.

Adolescent↗

PubMed1976

Mechanism of local skin atrophy caused by intradermally injected corticosteroids.

Different hydrocortisone microcrystal suspensions applied intradermally in rabbits caused skin atrophy. This could be ascribed to secondary tissue degeneration as was ascertained histologically. The degree of degeneration was related to the concentration of the suspension, size of the microcrystals and frequency of the intervals between the injections. The ground substance of the connective tissue changes and is characterized by a basophilic granular mass, homogenized collagen fibers and degeneration of the elastic fibers. The pathomechanism of local skin atrophy not only differs from connective tissue degeneration caused by systemic corticosteroid treatment but also from the degeneration caused by topical treatment.

Animals↗

PubMed1978

Bicaudate index in computerized tomography of Huntington disease and cerebral atrophy.

Ventricular sizes on computerized tomographic (CT) scans were compared in seven patients with Huntington disease, 20 patients with cerebral atrophy, and 20 normal controls. The bicaudate index--the ratio of the width of both lateral ventricles at the level of the heads of the caudate nuclei to the distance between the outer tables of the skull at the same level--significantly discriminated among the three groups. The bicaudate indices were: Huntington disease 0.209 +/- 0.007, cerebral atrophy 0.121 +/- 0.006, and controls 0.092 +/- 0.003.

Adult↗

PubMed1976

[Huntington's chorea and cerebellar atrophy. Apropos of amanatomo-clinical case].

The authors report the clinical and pathological findings in a 46 years old woman with Huntington's chorea and cerebello-olivar atrophy. Eight previously reported cerebellar atrophies in Huntington's chorea with pathological examination are reviewed. The primary or secondary nature of the cerebellar lesions is discussed.

Adult↗

PubMed1975

Lymphoid cell necrosis, thymic atrophy, and growth retardation in newborn mice inoculated with murine cytomegalovirus.

During studies on the effect of murine cytomegalovirus on the developing retina, virus was inoculated into the eyes of newborn Swiss mice, and the animals were sacrificed at various times thereafter. Controls consisted of mice inoculated with ultraviolet-inactivated murine cytomegalovirus and uninjected mice. Marked lymphoid cell necrosis, thymic atrophy, pronounced growth retardation, bacteremia, and death occurred in the animals inoculated with live virus. this virus-induced injury resulted in a marked depletion of lymphocytes in the subcapsular and cortical areas of the thymus as well as in the spleen, lymph nodes, and Peyer's patches. Areas of necrosis with viral inclusions were present at the site of inoculation and in various other organs including the spleen and bone marrow. Since growth retardation has been associated with thymic atrophy due to other causes, the observed abnormal physical development in the present study was interpreted as a sequel to the thymic injury. An implication of this study is that some human infants with concomitant immune deficiency and viral infection may have a primary viral disease with resultant secondary lymphoid tissue alterations, rather than a thymic disorder with a subsequent viral infection.

Animals↗

PubMed1979

Agenesis or atrophy of the testis and vas deferens.

In this study the author examines the relationship between agenesis or atrophy of the testis and of the vas deferens. From a prospective study of 237 cases of unilateral and bilateral undescended testis, 12 cases of agenesis of a testis were seen; 9 of the 12 cases were associated with agenesis of the vas deferens and in 3 of these unilateral renal agenesis was also present, not necessarily ipsilaterally. Three other cases of testicular agenesis and four cases of extreme testicular atrophy were seen. In all seven, the vas deferens was present in part or in its entirety and roentgenography disclosed a normal upper urinary tract. Agenesis of the vas deferens was seen only in patients with monorchism. No patient was anorchid. It is concluded that an important link exists between agenesis of the vas deferens and agenesis of the testis.

Abnormalities, Multiple↗

PubMed2025

Marek's disease virus-1 unique gene LORF1 is involved in viral replication and MDV-1/Md5-induced atrophy of the bursa of Fabricius.

Marek's disease virus (MDV), an alphaherpesvirus, causes severe immunosuppression and T cell lymphomas in chickens, known as Marek's disease (MD), an economically important poultry disease primarily controlled by vaccination. Importantly, it also serves as a comparative model for studying herpesvirus-induced tumor formation in humans. MDV encodes more than 100 genes, most of which have unknown functions. MDV LORF1 is unique to serotype I MDV (MDV-1), lacking homologs in other herpesviruses, and has not been explored yet. To this end, an infectious bacterial artificial chromosome (BAC) harboring the complete genome of the MDV-1 very virulent strain Md5 was generated, and the rescued rMd5 maintained biological properties similar to the parental virus both in vitro and in vivo. Subsequently, rMd5ΔLORF1, a recombinant Md5 virus deficient in pLORF1 expression, was generated by a frameshift mutation in the LORF1 gene. Chickens infected with rMd5ΔLORF1 exhibited a lower mortality rate and delayed bursal atrophy than those infected with the parental rMd5 and the revertant virus (rMd5-reLORF1). Consistently, viral loads of rMd5ΔLORF1 were obviously lower than those of rMd5 or rMd5-reLORF1 in the bursa, but not in the spleen. Importantly, we found that pLORF1 deficiency impairs viral replication in bursal B cells. Furthermore, we showed that pLORF1 associated with the cellular membrane, interacted with MDV structural proteins, and exhibited punctate colocalization with tegument or capsid proteins in the cytoplasm. Taken together, this study demonstrates for the first time that the MDV-1 unique gene LORF1 is involved in MDV-induced bursal atrophy but not in tumor formation.

Animals↗