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Biomedical subjects

J Borg

Publications and source records attributed to J Borg.

At least 19 recordsLinked to original sources
PubMed2006

Symptoms and disability until 3 months after mild TBI.

OBJECTIVE: Examine frequency, character and course of symptoms until 3 months after MTBI and the relation between symptoms and disability. METHODS: Prospective cohort study of 122 consecutive patients with MTBI. Symptom assessment after 1, 7 and 14 days and 3 months post-injury by use of Rivermead Post-concussional Questionnaire. Disability assessment by use of Rivermead Head Injury Follow-up Questionnaire. RESULTS: Patients reporting one or more symptoms declined from 86% on day 1 to 49% 3 months post-injury, when 25% also reported change in one or more domains of everyday activities. Poor memory, sleep disturbance and fatigue were most commonly reported. Symptom and disability scores were correlated (tau = 0.60; p < 0.001). Early symptom load correlated with late symptom load (tau = 0.38; p < 0.01). CONCLUSIONS: Symptoms gradually decline post-injury. Symptoms correlate with disability at 3 months. Patients with early high symptom load are at risk for developing persisting complaints.

Activities of Daily Living↗
PubMed2004

Diagnostic assessment of the developmental potential of human cryopreserved ovarian tissue from multiple patients using xenografting.

BACKGROUND: Although ovarian tissue cryopreservation for women at risk of losing ovarian function is offered by many clinics, there is a lack of evidence relating to the developmental potential of the stored tissue and, therefore, its clinical potential. This study was designed to use xenografting of cryopreserved tissue from multiple patients to assess the reproducibility of preservating developmental potential, the variation in developing follicle profile and the relationship between pre-freeze histology and post-thaw development. METHODS: Using previously published methods, cryopreserved ovarian cortex from nine patients was thawed and grafted under the kidney capsules of immunodeficient mice. Development of follicles was assessed after 26 weeks and compared to histology prior to freezing. RESULTS: Multiple growing follicles including antral stages were observed in multiple grafts of tissue from all patients. Metaphase II oocytes (n=9) were observed in follicles in grafts from five patients. There was no relationship between pre-freeze histology and developing follicle profile in xenografts. CONCLUSIONS: The propanediol freezing method used in this study is capable of reproducibly preserving the developmental potential of human ovarian follicles. The developing follicle profile after cryopreservation cannot be accurately predicted from pre-freeze histology. Xenografting provides a powerful tool for assessing the potential of human cryopreserved ovarian tissue.

Adolescent↗
PubMed2003

Oocyte maturation, follicle rupture and luteinization in human cryopreserved ovarian tissue following xenografting.

BACKGROUND: Previous studies have demonstrated development of antral follicles in cryopreserved human ovarian tissue after autografting and xenografting, thus indicating successful preservation of follicular function. The study aim was to assess whether these follicles could also undergo periovulatory changes in response to hCG. METHODS: Ovarian tissue from three patients were dehydrated in propanediol (PROH)/sucrose and cryopreserved using the slow cooling/rapid thaw procedure. Thawed tissue was placed under the kidney capsule in immunodeficient mice. Following growth (>20 weeks) in the presence of gonadotrophin, hCG was administered and ovarian tissue examined histologically. RESULTS: Thirty-two antral follicles (diameter range 0.6 to 5 mm) were examined. Histological evidence of a response to hCG was evident in all follicles. Disruption of the concentric layers of mural granulosa and theca cells was apparent in all antral cavities. In 17 (53%) follicles the exterior follicular wall had reduced to a few cells thick, and in eight (25%) the wall had ruptured. Mucified oocyte-cumulus cell complexes were present in 32 follicles, 17 of which had begun to detach from the pedicle. Resumption of meiosis had occurred in over half the oocytes (five metaphase II and seven metaphase I oocytes, eight germinal vesicle breakdown). Two corpora lutea were also detected. CONCLUSIONS: Follicles cryopreserved within human ovarian tissue using the PROH procedure, can develop to the antral stage and undergo periovulatory changes following xenografting and exposure to a luteinizing stimulus.

Adolescent↗
PubMed2001

Hydrogen bonds in polymer folding.

We studied the thermodynamics of a homopolymeric chain with both van der Waals and directed hydrogen bond interaction. The effect of hydrogen bonds is to reduce dramatically the entropy of low-lying states and to give rise to long-range order and to conformations displaying secondary structures. For compact polymers a transition is found between helix-rich states and low-entropy sheet-dominated states. The consequences of this transition for protein folding and, in particular, for the problem of prions are discussed.

Hydrogen Bonding↗
PubMed2001

Selective changes in mitochondria respiratory properties in oxidative or glycolytic muscle fibers isolated from G93AhumanSOD1 transgenic mice.

Cases of familial amyotrophic lateral sclerosis (FALS) are associated with mutations in cytosolic copper, zinc superoxide dismutase (SOD1). Total SOD activity and functional mitochondrial properties were studied in muscles and nervous tissues of control and transgenic mice mimicking the disease. It was found that total SOD activity was lower in nervous tissues than in muscles in both transgenic and control mice. In addition SOD activity increased during progression of disease in muscle but not in nervous tissue of transgenic mice. Maximal oxygen consumption and apparent Km for ADP were decreased in mitochondria from transgenic soleus (an oxidative muscle). However there was no difference between control and transgenic mice in respiratory parameters of mitochondria in the EDL muscle (a glycolytic muscle). These findings indicate that oxidative stress due to SOD1 mutations could alter energy metabolism in FALS mice, thereby affecting primarily oxidative muscle of the limbs, independently of motoneuron loss.

Adenosine Diphosphate↗
PubMed2001

Primary brain tumors following traumatic brain injury--a population-based cohort study in Sweden.

OBJECTIVES: The aim of this study was to explore the association between traumatic brain injury and brain tumor development. METHODS: A cohort of patients hospitalized for traumatic brain injury during 1965-1994 was compiled using the Swedish Inpatient Register. Complete follow-up through 1995 was attained through record linkage with the Swedish Cancer Register, the Cause of Death Register, and the Emigration Register. Standardized incidence ratios (SIRs), defined as the ratios of the observed to the expected numbers of brain tumors, were used as the measure of relative risk. The expected number of brain tumors was calculated by multiplying the observed person-time by age-, gender- and calendar year-specific incidence-rates derived from the general Swedish population. RESULTS: The cohort included 311,006 patients contributing 3,225,317 person-years. A total of 281 cases of brain tumors were diagnosed during follow-up. No associations were found between traumatic brain injury and the risk of primary brain tumors, neither overall (SIR: 1.0; 95% confidence interval (CI): 0.9-1.2), nor in analyses broken down by main groups of brain tumors. Stratified analyses according to age at entry into the cohort, year of follow-up, and severity of the brain injury all showed essentially the same null results. CONCLUSION: No association between traumatic head injury and primary brain tumors has been found.

Adolescent↗
PubMed2000

Muscle biopsy, macro EMG, and clinical characteristics in patients with schizophrenia.

BACKGROUND: In a previous study of motor unit properties in patients with schizophrenia, muscle fiber histologic and electrophysiologic abnormalities were observed. The present study was designed to compare patients with schizophrenia with healthy control subjects with regard to muscle fiber histology and motor unit function. A second objective was to relate these variables to clinical characteristics. METHODS: Twelve patients with first-episode schizophrenia and fifteen patients with chronic schizophrenia (DSM-III-R) and 27 matched control subjects were included in the study. Muscle biopsies were performed either in m. tibialis anterior or m. vastus lateralis. Electromyographic recordings (macro EMG) were made from the m. tibialis anterior motor units. Psychiatric ratings included the PANSS and extrapyramidal side effects. RESULTS: Seven of the muscle biopsy specimens from the patients and one from the control subjects were classified as abnormal (p =.049). The most frequent abnormality was atrophic muscle fibers. Eight patients and no control subjects exhibited pathological macro EMG (p =.032). The findings were present in chronic as well as in first-episode patients with schizophrenia. CONCLUSIONS: In approximately 50% of the patients, neuromuscular abnormalities were found either in the muscle biopsy or the macro EMG investigations. The results indicate that either a common pathologic process or different pathological processes are at hand in the neuromuscular system in patients with schizophrenia. The findings are compatible with a disturbed cell membrane function.

Acute Disease↗
PubMed2000

Early and selective loss of neuromuscular synapse subtypes with low sprouting competence in motoneuron diseases.

The addition or loss of synapses in response to changes in activity, disease, or aging is a major aspect of nervous system plasticity in the adult. The mechanisms that affect the turnover and maintenance of synapses in the adult are poorly understood and are difficult to investigate in the brain. Here, we exploited a unique anatomical arrangement in the neuromuscular system to determine whether subtypes of synapses can differ in anatomical plasticity and vulnerability. In three genetic mouse models of motoneuron disease of diverse origin and severity, we observed a gradual and selective loss of synaptic connections that begun long before the onset of clinical deficits and correlated with the timing of disease progression. A subgroup of fast-type (fast-fatiguable) neuromuscular synapses was highly vulnerable and was lost very early on. In contrast, slow-type synapses resisted up to the terminal phase of the disease. Muscle-specific differences were also evident. Similar selective losses were detected in aged mice. These selective vulnerability properties of synapses coincided with hitherto unrecognized major differences in stimulus-induced anatomical plasticity that could also be revealed in healthy mice. Using paralysis and/or growth-associated protein 43 overexpression to induce synaptic sprouting, we found that slow-type, disease-resistant synapses were particularly plastic. In contrast, fast-type synapses with the highest vulnerability failed to exhibit any stimulus-induced change. The results reveal pronounced subtype specificity in the anatomical plasticity and susceptibility to loss of neuromuscular synapses and suggest that degenerative motoneuron diseases involve a common early pathway of selective and progressive synaptic weakening also associated with aging.

Aging↗
PubMed2000

Macro-EMG and muscle biopsy of paretic foot dorsiflexors in Charcot-Marie-Tooth disease.

Twelve patients with Charcot-Marie-Tooth disease type 1 (CMT1) and 11 with type 2 (CMT2), with a clinically similar range of muscle weakness of foot dorsiflexion, were subjected to macroelectromyographic (macro-EMG) examination and muscle biopsy of the tibialis anterior (TA) muscle in order to elucidate the denervation-reinnervation process in the two CMT forms. The macro-EMG examination showed higher median amplitude values and median area values for the CMT1 patients, with a mean value of 1,515 +/- 1,222 microV and 3,953 +/- 2,613 microV. ms, respectively, than for the CMT2 patients, with a mean value of 865 +/- 971 microV and 2,525 +/- 2,575 microV. ms, respectively. When corrected for muscle fiber area, the difference was statistically significant for amplitude (P < 0.01) and area (P < 0.05). For CMT1 patients, the increase of macro-EMG potentials varied from 2 to 14 times and for CMT2 patients from less than 1 to 8 times larger than corresponding age-matched values. Muscle biopsies of TA showed that the type I fiber percentage was significantly higher (P < 0.05) in the CMT1 patients (99 +/- 2.2%) than in the CMT2 patients (86 +/- 12.3%). Morphometric data showed a significantly higher (P < 0.05) mean type I fiber area in the CMT2 patients (8,130 +/- 4,721 microm(2)) when compared with the CMT1 patients (5,066 +/- 3,431 microm(2)). The present data indicate that denervation in CMT1 is associated with prominent collateral reinnervation but only minor muscle fiber changes, whereas in CMT2 there is only minor collateral reinnervation but prominent muscle fiber changes including significant muscle fiber hypertrophy.

Adult↗
PubMed2000

Prevention of mutant SOD1 motoneuron degeneration by copper chelators in vitro.

An animal model of familial amyotrophic lateral sclerosis (FALS) has been generated by overexpression of human CuZn superoxide dismutase (SOD1) containing a substitution of glycine to alanine at position 93 in transgenic G93A mice. The loss of motoneurons shown in this model has been attributed to a dominant gain of function of this mutated enzyme, which might be due to copper toxicity. This hypothesis was tested in purified spinal motoneurons cultures originating from G93A transgenic embryos. Spinal motoneurons were isolated from E13 embryos by several steps including density gradient centrifugation. The effect of copper chelators on survival and neurite growth of motoneurons was investigated. Survival of G93A motoneurons was decreased by 46% as compared to wild-type motoneurons. Moreover, G93A motoneurons showed reduced neurite outgrowth. Copper chelators strikingly increased viability of G93A motoneurons (by over 200%) but had no effect on wild-type cells. Presence of DDC in the medium increases the length of neurites from G93A motoneurons. The present results suggest the capacity of copper chelators to reduce the effect of reverse function of mutated SOD1 on motoneurons.

Amyotrophic Lateral Sclerosis↗
PubMed2000

Inter-rater reliability of the 1992 international standards for neurological and functional classification of incomplete spinal cord injury.

AIMS: To determine the inter-rater reliability in scoring sensory and motor function and in defining sensory and motor levels in incomplete spinal cord injury, using the revised 1992 International Standards for Neurological and Functional Classification of Spinal Cord Injury (ISCSCI-92) and to determine the effect on raters agreement of one standardising assessment. METHODS: Two physicians and two physiotherapists at the Spinal Cord Injury Unit, Karolinska Hospital, classified 23 patients according to the ISCSCI-92. Kappa values were calculated. RESULTS: Kappa values varied from 0 to 0.83 (poor to very good) for the pin-prick scores, from 0 to 1 for the light touch scores and from 0 to 0.89 for motor function after the standardising assessment. Kappa values for sensory and motor levels were fair to poor after the standardising assessment. The results showed improvement in degree of agreement in 35/46 dermatomes for scoring pin-prick, in 15/42 for light touch, in 14/19 segments for motor function and for three out of four sensory and motor levels. CONCLUSION: This study indicates a weak inter-rater reliability for scoring incomplete SCI lesions using the ISCSCI-92.

Female↗
PubMed2000

Tissue mitochondrial DNA changes. A stochastic system.

Several lines of evidence support the view that the bioenergetic function of the mitochondria in postmitotic tissue deteriorates during normal aging. Skeletal muscle is one such tissue that undergoes age-related fiber loss and atrophy and an age-associated rise in the number of cytochrome c oxidase (COX) deficient fibers. With such metabolic pressure placed on skeletal muscle it would be an obvious advantage to supplement the cellular requirement for energy by up-regulating glycolysis, and alternative pathway for energy synthesis. Analysis of rat skeletal muscle utilizing antibodies directed against key enzymes involved in glycolysis has provided evidence of an age-associated increase in the enzymes involved in glycolysis. Fructose-6-phosphate kinase, aldolase, glyceraldehyde-3-phosphate dehydrogenase, and pyruvate kinase protein levels appeared to increase in the soleus, gracilis, and quadriceps muscle from aged rats. The increase in the level of these proteins appeared to correlate to a corresponding decrease in the amount of cytochrome c oxidase protein measured in the same tissue. Together these results are interpreted to represent a general upregulation of glycolysis that occurs in response to the age-associated decrease in mitochondrial energy capacity. Mitochondrial DNA (mtDNA) damage and mutations may accumulate with advancing age until they reach a threshold level were they impinge on the bioenergy capacity of the cell or tissue. Evidence indicates that mtDNA from the skeletal muscle of both aged rats and humans not only undergoes changes at the nucleotide sequence level (mutations and DNA damage), but also undergoes modifications at the tertiary level to generate unique age-related conformational mtDNA species. One particular age-related conformational form was only detected in aged rat tissues with high demands on respiration, specifically in heart, kidney, soleus muscle, and, to a lesser extent, the quadriceps muscle. The age-related form was not detected in gracilis muscle which is predominantly dependent upon glycolysis with regard to its energy requirements. Finally, a comprehensive hypothesis is presented that features the stochastic nature of the mitochondrial system. The basis of the hypothesis is that a dynamic relationship exists between endogenous mutagen production, DNA repair, mtDNA turnover, and nuclear control of mtDNA copy number and that age-associated changes in the dynamics of this relationship lead to a loss of functional full-length mtDNA that eventually leads to bioenergy decline.

Aging↗
PubMed2000

Monte Carlo study of correction factors for Spencer-Attix cavity theory at photon energies at or above 100 keV.

To develop a primary standard for 192Ir sources, the basic science on which this standard is based, i.e., Spencer-Attix cavity theory, must be established. In the present study Monte Carlo techniques are used to investigate the accuracy of this cavity theory for photons in the energy range from 20 to 1300 keV, since it is usually not applied at energies below that of 137Cs. Ma and Nahum [Phys. Med. Biol. 36, 413-428 (1991)] found that in low-energy photon beams the contribution from electrons caused by photons interacting in the cavity is substantial. For the average energy of the 192Ir spectrum they found a departure from Bragg-Gray conditions of up to 3% caused by photon interactions in the cavity. When Monte Carlo is used to calculate the response of a graphite ion chamber to an encapsulated 192Ir source it is found that it differs by less than 0.3% from the value predicted by Spencer-Attix cavity theory. Based on these Monte Carlo calculations, for cavities in graphite it is concluded that the Spencer-Attix cavity theory with delta = 10 keV is applicable within 0.5% for photon energies at 300 keV or above despite the breakdown of the assumption that there is no interaction of photons within the cavity. This means that it is possible to use a graphite ion chamber and Spencer-Attix cavity theory to calibrate an 192Ir source. It is also found that the use of delta related to the mean chord length instead of delta = 10 keV improves the agreement with Spencer-Attix cavity theory at 60Co from 0.2% to within 0.1% of unity. This is at the level of accuracy of which the Monte Carlo code EGSnrc calculates ion chamber responses. In addition, it is shown that the effects of other materials, e.g., insulators and holders, have a substantial effect on the ion chamber response and should be included in the correction factors for a primary standard of air kerma.

Air↗
PubMed1999

Compensatory mechanism of motor defect in SOD1 transgenic mice by overactivation of striatal cholinergic neurons.

Expression of a mutant superoxide dismutase 1 (SOD1) gene in transgenic mice induces a gradual degeneration of cholinergic motor neurons in the spinal cord, causing progressive muscle weakness and hindlimb paralysis. Transgenic mice over-expressing the human SOD1 gene containing a Gly-->Ala substitution at position 93 (G93A) were employed to explore the effects of the SOD1 mutation on choline acetyltransferase (ChAT) expression in the striatum, and in the lumbar and cervical spinal cord. These mice showed a progressive loss of their spinal cord motor neurons, and at 130 days of age showed an up-regulation of ChAT mRNA expression in the striatum. On the other hand, ChAT mRNA decreased in cervical and lumbar motor neurons. These findings suggest that cholinergic interneurons in striatum in SOD1 transgenic mice are over-activated in an attempt to compensate for the death of spinal motor neurons.

Adaptation, Physiological↗
PubMed1999

Respiratory response to exercise in postpolio patients with severe inspiratory muscle dysfunction.

OBJECTIVES: To evaluate the limiting factors of exercise performance and to analyze the respiratory strategies adopted during exercise in postpolio patients with severe inspiratory muscle dysfunction. PATIENTS: Five patients with prior poliomyelitis associated with scoliosis and with respiratory muscle dysfunction (mean vital capacity, 1.74L [range, 1.1 to 2.4]) were studied at rest and during leg or arm cycle exercise. METHODS: Gas exchange was examined by arterial blood gases and mass spectrometry of expired air. Ventilatory mechanics were studied by measurement of esophageal and gastric pressures. RESULTS: Blood gases at rest were normal, except for subnormal PO2 levels in three patients. In all but one patient, ventilatory insufficiency was the limiting factor for exercise. A compensatory breathing pattern with abdominal muscle recruitment during expiration was present already at rest in three of the patients. The pressures generated by the diaphragm were below fatiguing margins, ie, levels that in healthy subjects can be sustained for at least 45 minutes. CONCLUSIONS: The extent of ventilatory dysfunction was not evident in blood gas values at rest; however, it was revealed by blood gas values during the exercise test. Diaphragm fatigue seems to be avoided at the cost of impaired blood gases.

Adult↗
PubMed1999

Spectra and air-kerma strength for encapsulated 192Ir sources.

The photon spectra in vacuum around four types of 192Ir HDR brachytherapy sources are calculated using the Monte Carlo code EGS4 and the most recent spectral information on 192Ir decay. The air-kerma strengths per unit activity are calculated based on the photon fluence around a bare 192Ir source and around each of four types of encapsulated sources using recent mass energy-absorption coefficients. For the full spectrum the bare vs encapsulated difference is up to 23% due to the large air-kerma contribution from the unfiltered low-energy photons. For the penetrating part of the photon spectrum (> 11.3 keV), the air-kerma strength per unit source activity on the transverse axis for a bare source is 2-15% higher than for the encapsulated sources due to the attenuation and absorption in the core and the encapsulating material. The contribution to the air-kerma strength from photons scattered in the capsule and from bremsstrahlung are calculated to increase the air-kerma strength by 2-4% and 0.2-0.3%, respectively. Air-kerma strengths for a variety of sources agree well with previously reported results for sources from Nucletron International, Best Industries, Inc., and Alpha-Omega Services, Inc. In addition we present air-kerma strengths for the present model of the HDR source from Nucletron International and the source from Varian Associates, Inc.

Brachytherapy↗
PubMed1999

Motor neuropathy in porphobilinogen deaminase-deficient mice imitates the peripheral neuropathy of human acute porphyria.

Acute porphyrias are inherited disorders caused by partial deficiency of specific heme biosynthesis enzymes. Clinically, porphyrias are manifested by a neuropsychiatric syndrome that includes peripheral neuropathy. Although much is known about the porphyrias' enzyme defects and their biochemical consequences, the cause of the neurological manifestations remains unresolved. We have studied porphyric neuropathy in mice with a partial deficiency of porphobilinogen deaminase (PBGD). PBGD-deficient mice (PBGD-/-) imitate acute porphyria through massive induction of hepatic delta-aminolevulinic acid synthase by drugs such as phenobarbital. Here we show that PBGD-/- mice develop impairment of motor coordination and muscle weakness. Histologically femoral nerves of PBGD-/- mice exhibit a marked decrease in large-caliber (>8 microm) axons and ultrastructural changes consistent with primary motor axon degeneration, secondary Schwann cell reactions, and axonal regeneration. These findings resemble those found in studies of affected nerves of patients with acute porphyria and thus provide strong evidence that PBGD deficiency causes degeneration of motor axons without signs of primary demyelination, thereby resolving a long-standing controversy. Interestingly, the neuropathy in PBGD-/- mice developed chronically and progressively and in the presence of normal or only slightly (twofold) increased plasma and urinary levels of the putative neurotoxic heme precursor delta-aminolevulinic acid. These data suggest that heme deficiency and consequent dysfunction of hemeproteins can cause porphyric neuropathy.

Acute Disease↗