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Biomedical subjects

J M Jacobs

Publications and source records attributed to J M Jacobs.

At least 73 records · Page 4Linked to original sources
PubMed1990

Axonal atrophy in the painful peripheral neuropathy in AIDS.

We compared the sural nerves from patients with AIDS; four with the painful peripheral neuropathy (PPN), three patients with non-painful distal symmetrical peripheral neuropathy (DSPN), one without clinical peripheral nerve involvement and two human immunodeficiency virus negative controls. Fibre diameter distributions showed a slight reduction in larger fibres in all patients with AIDS compared with controls. No significant difference was found in the relative frequency distribution of the lamellae counts between any of the groups. The relative frequency distribution of axonal area of myelinated fibres did not differ between controls, non-painful DSPN or the patient without peripheral nerve involvement; however, all patients with PPN showed marked reduction in the number of axons of myelinated fibres of larger area which was significant when compared to each patient from the other groups (P less than 0.0001). This indicates that the reduction in larger fibres in PPN is mostly due to axonal atrophy rather than selective fibre loss. Axonal atrophy is associated with painful peripheral neuropathy in AIDS but not with those without pain. The possible role of axonal atrophy as a pathological substrate for pain is discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Peripheral neuropathy in Leigh's disease.

Sural nerves were examined in 3 childhood cases of Leigh's disease (from 2 families), each with electrophysiological documentation of peripheral neuropathy. Postmortem confirmation of Leigh's disease was made in 2 cases; the third had characteristic CT scan appearances. Myelinated fibre densities were within normal limits, with no evidence of degeneration or regeneration. The myelin sheaths, however, appeared thin and this was confirmed quantitatively. In teased fibres there was no demyelination in 2 cases but some in 1 case. The findings suggest that there is hypomyelination of peripheral nerves leading eventually to demyelination.

Brain↗
PubMed1990

Spongiform encephalopathy transmitted experimentally from Creutzfeldt-Jakob and familial Gerstmann-Sträussler-Scheinker diseases.

A comparison was made of the effects of experimental intracerebral inoculation into marmosets of brain homogenates from a case of Creutzfeldt-Jakob disease (CJD) and from a member of the Wo. family with cerebral amyloid and spongiform encephalopathy--the Gerstmann-Sträussler-Scheinker (GSS) syndrome. All the inoculated marmosets developed spongiform encephalopathy (SE) after incubation times of 20-23 months in the CJD group and 25-32 months in the GSS group. Subsequent passage from 1 affected animal in each group resulted in SE developing after 17 months incubation. In every animal inoculated with CJD or GSS material and in the 2 passage experiments the most severely affected region of the brain was the thalamus which in all cases was almost totally occupied by vacuoles. Other grey matter masses were less severely and less consistently affected. Vacuolation was observed in the cerebellar granule cell layer as well as in the molecular layer and the brain stem was finely vacuolated in all cases. There were only minor and inconsistent differences between the disease transmitted from CJD compared with GSS and some differences between the original transmissions and the SE caused by passaged inocula. Severe astrocytic gliosis accompanied the spongiform changes but no amyloid was identified in any of the marmosets with experimentally transmitted disease. The pathogenesis of the spongiform change in the thalamus was studied in a series of marmosets by light and electron microscopy 3-22 months after the intracerebral inoculation of CJD or GSS homogenates and was compared with controls. Dilated irregularly-shaped cisternae and the large complex vacuoles typical of SE, present in abundance after 18 and 22 months incubation, were considered most probably to be derived from cisternae of neuronal smooth endoplasmic reticulum.

Animals↗
PubMed1990

Pulsatile tinnitus and the vascular tympanic membrane: CT, MR, and angiographic findings.

The radiologic studies of 107 patients with pulsatile tinnitus or a vascular retrotympanic mass were retrospectively reviewed. Of the 100 patients with pulsatile tinnitus, 25 had objective tinnitus. A vascular tympanic membrane was present in 37 cases (35%). Normal vascular variants were present in 23 patients (21%). Twenty-seven patients (25%) had acquired vascular lesions. Temporal bone tumors were found in 33 patients (31%). No abnormality was identified in 21 cases (20%). To ensure optimal radiologic examination, it is imperative to know the nature of the tinnitus (objective vs subjective) and the appearance of the tympanic membrane. All patients with subjective pulsatile tinnitus or a vascular retrotympanic mass should undergo high-resolution computed tomography of the temporal bone as the initial imaging study. Angiography is recommended for patients with objective tinnitus and a normal tympanic membrane. The role of MR imaging, even with the addition of gradient-echo techniques, remains limited and secondary.

Adolescent↗
PubMed1990

Trigeminal neuralgia (tic douloureux): MR imaging assessment.

The magnetic resonance (MR) imaging studies and clinical records of 29 patients with typical or atypical trigeminal neuralgia (TN) were retrospectively reviewed and compared with the MR studies of 30 patients imaged for reasons unrelated to the fifth cranial nerve. The symptomatic patients were in three groups. Group 1 included those without masses or multiple sclerosis (MS) and those who had not undergone microvascular decompression; group 2, those who underwent microvascular decompression; and group 3, those with masses or MS. Twenty-seven percent of the control group and 57% of the symptomatic patients without masses or MS showed vessel contact with the root entry zone of the preganglionic segment of the fifth cranial nerve. Vessel contact in the symptomatic groups was generally indistinguishable from that seen in the normal group. Fifteen percent of the patients had MS or masses. It is concluded that MR imaging is useful in evaluating patients with TN by facilitating identification of MS or masses but is not helpful in selecting patients with vascular contact who might benefit from microvascular decompression.

Humans↗
PubMed1990

Familial multiple symmetric lipomatosis with peripheral neuropathy.

We describe coexisting peripheral neuropathy and multiple symmetric lipomatosis in 4 of 7 siblings. The absence of either condition in 3 other generations of this family suggests autosomal recessive inheritance. None of the affected siblings were alcoholic, a factor some have proposed to explain the frequent occurrence of peripheral neuropathy in sporadic multiple symmetric lipomatosis. Serum lipid studies, including apoprotein A levels, were normal. Sural nerve biopsy from 1 patient showed nerve fiber loss, predominantly affecting large myelinated fibers. The relationship between myelin sheath thickness and axon diameter was normal, arguing that this neuropathy is not due to primary axonal atrophy.

Adult↗
PubMed1989

Association of painful peripheral neuropathy in AIDS with cytomegalovirus infection.

12 AIDS patients with a clinically, electrophysiologically, and pathologically homogeneous painful peripheral neuropathy had a significantly higher rate of any or active clinical cytomegalovirus (CMV) infection than did a group of 30 AIDS controls. In 9 patients this syndrome began in close temporal association with clinical infection with CMV. Painful peripheral neuropathy in AIDS may be caused by a CMV dorsal root ganglionitis.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Effects of iron-EDTA on uroporphyrinogen oxidation by liver microsomes.

Uroporphyrinogen oxidation by hepatic microsomes from chick embryos or mice pretreated with methylcholanthrene was increased by addition of iron-EDTA. This increase was partially prevented by catalase, mannitol, ketoconazole and piperonyl butoxide, whereas only ketoconazole and piperonyl butoxide inhibited the oxidation in the presence and absence of iron-EDTA. These data suggest that the oxidations of uroporphyrinogen in the presence and absence of added iron occur by different mechanisms.

Animals↗
PubMed1989

Characteristics of purified protoporphyrinogen oxidase from barley.

The membrane bound enzyme oxidizing protoporphyrinogen to protoporphyrin, a step in heme and chlorophyll synthesis, was purified to a single prominent polypeptide band on SDS/PAGE from barley mitochondrial fractions. It contained a variety of lipids including 0.66 mg of phosphatidyl ethanolamine and 0.46 mg of free fatty acid per mg of protein. Iron, but no flavins or cytochromes, was detected. In the presence of glutathione, enzymatic oxidation was inhibited by the iron chelator o-phenanthroline but was stimulated by iron EDTA. The purified enzyme was inhibited by reductants such as glutathione, ascorbate, NADH and NADPH. These findings are compatible with some direct or indirect involvement of lipids and iron in this oxidation in plants.

Chelating Agents↗
PubMed1989

Oxidation of uroporphyrinogen by methylcholanthrene-induced cytochrome P-450. Essential role of cytochrome P-450d.

We have previously shown that uroporphyrinogen is oxidized to uroporphyrin by microsomes (microsomal fractions) from 3-methylcholanthrene-pretreated chick embryo liver [Sinclair, Lambrecht & Sinclair (1987) Biochem. Biophys. Res. Commun. 146, 1324-1329]. We report here that a specific antibody to chick liver methylcholanthrene-induced cytochrome P-450 (P-450) inhibited both uroporphyrinogen oxidation and ethoxyresorufin O-de-ethylation in chick-embryo liver microsomes. 3-Methylcholanthrene-pretreatment of rats and mice markedly increased uroporphyrinogen oxidation in hepatic microsomes as well as P-450-mediated ethoxyresorufin de-ethylation. In rodent microsomes, uroporphyrinogen oxidation required the addition of NADPH, whereas chick liver microsomes required both NADPH and 3,3',4,4'-tetrachlorobiphenyl. Treatment of rats with methylcholanthrene, hexachlorobenzene and o-aminoazotoluene increased uroporphyrinogen oxidation and P-450d, whereas phenobarbital did not increase either. The contribution of hepatic P-450c and P-450d to uroporphyrinogen oxidation and ethoxyresorufin O-de-ethylation in methylcholanthrene-induced microsomes was assessed by using specific antibodies to P-450c and P-450d. Uroporphyrinogen oxidation by methylcholanthrene-induced rat liver microsomes was inhibited up to 75% by specific antibodies to P-450d, but not by specific antibodies to P-450c. In contrast, ethoxyresorufin de-ethylation was inhibited only 20% by anti-P450d but 70% by anti-P450c. Methylcholanthrene-induced kidney microsomes which contain P-450c but non P-450d did not oxidize uroporphyrinogen. These data indicate that hepatic P-450d catalyses uroporphyrinogen oxidation. We suggest that the P-450d-catalysed oxidation of uroporphyrinogen has a role in the uroporphyria caused by hexachlorobenzene and other compounds.

Animals↗
PubMed1989

Reduced numbers of calcitonin gene-related peptide-(CGRP-) and tachykinin-immunoreactive sensory neurones associated with greater enkephalin immunoreactivity in the dorsal horn of a mutant rat with hereditary sensory neuropathy.

The mutilated foot rat is a mutant with autosomal recessive sensory neuropathy and frequent mutilation of the hindlimbs. Decreased numbers of dorsal root ganglion cells and diminished sensitivity to painful stimuli are characteristics of these animals. By use of immunocytochemistry, changes in the distributions of peptides involved in sensory and/or autonomic regulation, i.e., calcitonin gene-related peptide (CGRP), tachykinins, enkephalin and neuropeptide Y in spinal cord, dorsal root ganglia and skin of these animals, were studied. In comparison with normal litter-mate controls, the dorsal horn of mutilated foot rats contained substantially fewer CGRP- and tachykinin-immunoreactive fibres but more fibres immunoreactive for enkephalin. Many enkephalin-immunoreactive cell bodies were also found in the dorsal horn of the mutants, by contrast none were visible in control animals. Neuropeptide Y immunoreactivity was, however, unchanged in the spinal cord of the mutants. In the dorsal root ganglia of the mutants, the number of CGRP- or tachykinin-immunoreactive cells and their proportion to total neuronal numbers were significantly less in comparison with normal controls. The diameter range of CGRP- and tachykinin-immunoreactive cells shifted from small (15-25 microns) to medium size (25-45 microns) as revealed by frequency distribution histograms. The skin from the affected fore- and hindlimbs of the mutant rats, in keeping with fewer CGRP- and tachykinin-immunoreactive cells in the dorsal root ganglia, contained substantially less fibres immunoreactive for CGRP and tachykinins; a difference that was not seen in skin of unaffected areas (whiskers and snout). By contrast, neuropeptide Y-immunoreactive fibres showed a normal distribution around blood vessels and sweat glands of mutilated foot rats. The data suggest that diminished pain perception in the mutilated foot rat is related to loss of peptide-containing sensory neurones. Furthermore, the intraspinal increase of enkephalinergic neurons in the dorsal horn, concomitant with the decreased number of primary sensory neurones, may also play a contributory rôle in reducing pain thresholds.

Animals↗
PubMed1989

Cytomembranous inclusions in the peripheral nerves in AIDS.

We report finding tubuloreticular inclusions (TRI) in the endothelial cells of endo- and epineurial vessels in the sural nerve of 11 patients with AIDS. Six patients had a painful peripheral neuropathy, one a non-painful sensory neuropathy, one an acute inflammatory demyelinating polyradiculoneuropathy and one a thalidomide-related neuropathy. Two patients had no clinical evidence of neuropathy. The TRI are not specific to one neuropathy and are unlikely to contribute to the pathogenesis of peripheral nerve syndromes in AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1989

The radiologic evaluation of pulsatile tinnitus and the vascular tympanic membrane.

PT may be the only symptom signalling a need for imaging the temporal bone region. Since a wide variety of processes may be responsible for this symptom, the goal of the radiologist should be to ensure a complete, cost-effective work-up. This evaluation is best directed by the type of tinnitus, objective v subjective, and the presence or absence of a vascular retrotympanic mass. HRCT is the initial examination of choice in the majority of instances. Normal vascular variants can be confidently differentiated from paragangliomas with this study. While angiography continues to play an important role in the initial evaluation of a select group of these patients, the role of MR should be adjunctive.

Carotid Arteries↗
PubMed1988

Changes in denervated skeletal muscle of amiodarone-fed mice.

Prolonged dosing of mice with amiodarone produced a myopathy characterized by autophagic vacuolation and phospholipid inclusions. A previous morphological study had shown that amiodarone did not affect the rate of nerve regeneration after sciatic nerve crush. In the present study, reinnervation was assessed by the reappearance of miniature endplate potentials that confirmed that axonal regeneration and motor reinnervation was not affected by amiodarone. However, there was a marked delay in the recovery of motor function in the amiodarone-treated mice. Denervation was found to induce an extensive necrosis of muscle fibers in the deeper parts of fast-twitch muscles. Histochemical studies showed that type 1 fibers were spared, necrosis affecting mainly type 2 fibers with relatively high oxidative enzyme activity (fast-twitch oxidative fibers). Biochemical studies showed a significant increase in the amount of amiodarone and its metabolite in denervated muscle of amiodarone-treated mice when compared with contralateral, normally innervated muscles.

Amiodarone↗
PubMed1988

The pathology of early leprous neuropathy.

A qualitative and quantitative study was made of early changes in nerves from 10 patients with tuberculoid or lepromatous type of leprosy. Five nerve biopsies, taken from sites remote from skin lesions, were considered to be unaffected when examined by paraffin histology but showed abnormalities in semi-thin resin sections and by electron microscopy; 5 showed mild to moderate involvement by paraffin histology. Changes in 'unaffected' nerves in both types of leprosy included the presence of subperineurial oedema; occasional evidence of fibre regeneration, sometimes with atypical features; increased numbers of small myelinated fibres, possibly a consequence of axonal atrophy; a few thinly remyelinated fibres, probably due to secondary demyelination, and some loss of unmyelinated axons. In more affected nerves there was variable loss of axons, both myelinated and unmyelinated. Demyelination was not a conspicuous feature; there was evidence of axonal atrophy in some fibres. Similarities in some of the changes observed in tuberculoid and lepromatous types of leprosy suggest a common mechanism of nerve damage, at least in the early stages. The presence of abnormalities in nerves at a distance from skin lesions implies a more diffuse nerve involvement than might have been expected in both types of leprosy.

Adolescent↗
PubMed1988

Benign lymphoepithelial parotid cysts and hyperplastic cervical adenopathy in AIDS-risk patients: a new CT appearance.

The contrast material-enhanced computed tomographic (CT) scans of 18 patients at risk for acquired immunodeficiency syndrome (AIDS) who had painless facial swelling were reviewed. All scans demonstrated parotid cysts and diffuse homogeneous cervical adenopathy. The cysts were bilateral in all but three cases. Eleven of 13 patients tested had antibodies to the human immunodeficiency virus (HIV), and two of the five untested patients later developed AIDS. The authors believe that the CT findings of multiple parotid cysts and cervical adenopathy suggest that the patient may be infected with the HIV virus, and the radiologist should alert the referring physician so that appropriate precautions and treatment may be initiated.

AIDS-Related Complex↗