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Biomedical subjects

M H Kaufman

Publications and source records attributed to M H Kaufman.

At least 55 records · Page 3Linked to original sources
PubMed1997

The gunner with the silver mask: observations on the management of severe maxillo-facial lesions over the last 160 years.

We would like to present a case of severe maxillo-facial trauma occurring over 150 years ago. The case involves a French artillery gunner, Monsieur Alphonse Louis, who received shrapnel injuries from an exploding shell at the Siege of Antwerp in 1832. He sustained near fatal injuries. The fact that he survived is probably due to his rapid evacuation from the battle site, as the French did not like to leave their wounded lying in 'no man's land', prompt surgery and subsequent expert medical and nursing care. M. Louis' maxillo-facial injuries included loss of the entire mandible. As a consequence, the patient had a grotesque appearance and was unable to eat or talk properly. At this time the surgeons of the day had no specialist knowledge of how to reconstruct the lower jaw. Where specialist knowledge or facilities were absent, then as now, improvisation was called for. A silversmith was duly approached and asked to construct a mask to act as a replacement for the deficient lower face. We describe here what an excellent cosmetic and functional result the mask gave, and how it led to the patient being successfully rehabilitated. Almost a century later, during the First World War, pioneering work by Major Harold (later Sir Harold) Gillies and his colleagues led to the first attempts at anatomical mandibular reconstruction. His patients, like M. Louis, were soldiers injured in battle. We will describe his techniques and compare them with how this problem is approached in the modern era, although most reconstructive surgery to the maxillo-facial region these days follows the removal of comparably extensive areas of soft tissue and bone as a result of invasive tumour.

Europe↗
PubMed1996

The safety and efficacy of chronically implanted subdural electrodes: a prospective study.

BACKGROUND: The popularity of subdural electrodes for the presurgical evaluation of patients with intractable seizures is increasing. However, few reports have prospectively dealt with their efficacy and safety. METHODS: We conducted a 5-year prospective study of patients evaluated by the California Comprehensive Epilepsy Program, who subsequently underwent subdural electrode implantation at one of two institutions. Efficacy was examined by ultimate outcome with regards to postsurgery resection seizure frequency. Fifty-five patients underwent 58 implant procedures and postresection outcomes were available in 47 patients. Safety was defined by the incidence of expected and unexpected complications, and neuropathologic examination of tissue specimens. RESULTS: The most common expected adverse effects during implant were fever < or = 102 degrees (41%), cerebrospinal fluid leakage (19%), headache (15%), and nausea (4%). There were no infections. Unexpected adverse events included fever > 102 degrees F (5%), migraine (5%), iatrogenic electrode dysfunction (5%), and temporalis muscle fibrosis (5%). The incidence of pathologic findings suggestive of foreign body reaction was 10%. There were no permanent sequelae. Surgical outcomes were excellent in all (> or = 75% seizure reduction) with 50% seizure free regardless of the focus. CONCLUSIONS: Subdural electrodes are a safe, easy, and efficacious tool for evaluating seizure foci prior to resective surgery. They should no longer be considered investigational devices.

Anticonvulsants↗
PubMed1996

The ontogeny of 11 beta-hydroxysteroid dehydrogenase type 2 and mineralocorticoid receptor gene expression reveal intricate control of glucocorticoid action in development.

Glucocorticoids play important roles in development and 'fetal programming'. Fetal exposure to excess glucocorticoids reduces birth weight and causes later hypertension. To investigate these processes further we have determined the detailed category of 11 beta-hydroxysteroid dehydrogenase type2 (11 beta-HSD2, which potently inactivates glucocorticoids) and the mineralocorticoid receptor (MR) by in situ hybridisation from embryonic day 9.5 (E9.5, term = E19) until after birth in the mouse. Widespread abundant 11 beta-HSD2 mRNA expression from E9.5-E12.5 changes dramatically at approximately E13 to a limited tissue-specific pattern (kidney, hindgut, testis/bile ducts, lung and a few brain regions (later seen in cerebellum, thalamus, roof of midbrain, neuroepithelial regions in pons and near the subicular hippocampus)). Placenta (labyrinthine zone) and extra-embryonic membranes express abundant 11 beta-HSD2 mRNA until E15.5 but this ceases = E16.5. It is unclear to what extent rodent term placental 11 beta-HSD activity is due to persisting 11 beta-HSD2 protein. Convincing MR mRNA expression is seen from E13.5 and includes pituitary, heart, muscle and meninges with expression later in gut, kidney, thymus, discrete areas of lung and several brain regions (including hippocampus, rhinencephalon and hypothalamus). 11 beta-HSD2 and MR clearly co-localise = E18.5 in kidney and colon and might do so in discrete areas of lung (E14-15) and neuroepithelia near the subicular hippocampus. Probably elsewhere MR are non-selective and 11 beta-HSD2 is involved in protecting glucocorticoid receptors in fetal fetal tissues. Comparison with previous enzymology studies suggest the changing pattern of 11 beta-HSD2 mRNA is likely to be translated into enzyme activity and have significant parallels in human development.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1996

Observations on Barclay's elephant.

This account attempts to trace the fate of the skeleton of an elephant that was gifted by George Ballingall to Dr John Barclay, one of the most important teachers of Anatomy in Edinburgh during the early 19th century. In his will, Barclay gifted his human and comparative anatomy collections, including the elephant, to the Royal College of Surgeons of Edinburgh on two conditions, that a hall should be built to house the collection, and that it should be associated with his name in perpetuity. In the 1830s, the comparative collection, but particularly the skeleton of the elephant, was the pride of the College. Unfortunately, interest in the comparative material rapidly diminished, and, due to constraints on space, while the elephant's skull was retained the rest of the skeleton was disposed of. An unpublished poem written at the time of the Burke trial, in 1829, testifies to the fact that Barclay's elephant was closely associated in the minds of the public with the activities of Dr Robert Knox, the then Conservator of the College museum.

Anatomy, Comparative↗
PubMed1996

Limb and other postcranial skeletal defects induced by amniotic sac puncture in the mouse.

A mouse model for studying the teratogenic effects of amniotic sac puncture has recently been established (MacIntyre et al. 1995), and the anomalies encountered included cleft palate, limb and tail abnormalities, and postural deformities. In order to investigate the underlying mechanism(s) involved, mouse embryos subjected to amniotic sac puncture on day 13 of gestation were examined externally on day 19, then 'cleared' and bulk stained with alizarin red S and Alcian blue to reveal, respectively, their bony and cartilaginous elements. This procedure allowed a comparison to be made between the incidence of soft tissue anomalies of the distal parts of the limbs and the appearance of the underlying skeletal elements. Despite a high incidence of soft tissue (principally digital) anomalies, relatively few skeletal anomalies were encountered. Measurements of intact long bones, and regions of ossification, were made in the major long bones of 'nonexperimental' and 'internal' controls and 'experimental' fetuses that displayed external morphological malformations to establish whether the experimental procedure had a greater effect on the proximal or distal components of the limb skeleton. No significant difference was observed when the ratios of proximal: distal length were compared with those obtained from the control series. The degree of severity of 'clubhand' and 'clubfoot' deformity was determined, and a comparison made between the severity observed on the right and left sides. This analysis revealed that for 'clubhand', the left forelimb was more severely affected than the right forelimb. The incidence of 'clubfoot' deformity was similar between the 2 sides. A possible explanation for this asymmetric effect is provided. An unexpected finding was the abnormal pattern of ossification seen in the sternum of two thirds of the 'experimental' fetuses that displayed external morphological malformations. This abnormal pattern was seen in none of the controls nor in fetuses in the 'experimental' series that displayed no external morphological malformations.

Amnion↗
PubMed1996

Postnatal development of the optic nerve in (C57BL x CBA)F1 hybrid mice: general changes in morphometric parameters.

A morphometric analysis of the optic nerve in different age groups of (C57BL x CBA)F1 hybrid mice was carried out. Morphometric parameters examined were mean nerve cross-sectional area (csa), mean myelinated nerve fibre count, mean myelinated nerve fibre density and myelinated nerve fibre size distribution. The findings revealed that the optic nerve continues to develop well into adult life. Growth in calibre was very rapid during the early stage of postnatal life, but progressively slowed with age thereafter. No myelinated nerve fibres were observed before the 5th day of postnatal life. Similarly, once myelination was initiated, it progressed very rapidly during the early stage of postnatal development and, as for the csa, it slowed thereafter. Peak level of myelination within the optic nerve, which corresponded with the age when the maximum number of myelinated nerve fibres, i.e. 94213 +/- 1799 (S.E.M.) was measured, occurred at the 16th week of postnatal life. The earliest myelinated nerve fibres seen were predominantly large in diameter, but with increasing age, fibres of smaller diameter dominated the myelinated nerve fibre spectrum in the nerve. The highest mean myelinated nerve fibre density was observed in mice at the age of peak myelination.

Animals↗
PubMed1995

High-frequency developmental abnormalities in p53-deficient mice.

BACKGROUND: Several strains of mice carrying null mutations of the tumour suppressor gene p53 have been developed. It has been reported that homozygous mice from all of these strains develop normally to birth, but then succumb rapidly to neoplasia. RESULTS: Here, we report that a significant proportion of female p53-/- mice die during embryogenesis or in the period between birth and weaning, being subject to a spectrum of abnormalities. In a significant proportion (23%) of p53-/- female embryos, the normal process of neural tube closure failed, leading to exencephaly and subsequent anencephaly. Although this phenomenon was predominantly associated with females, we observed one affected male embryo. In addition to a spectrum of neural tube defects, many of these embryos exhibited a range of craniofacial malformations, including ocular abnormalities and defects in upper incisor tooth formation. We observed a significant reduction in the number of p53-/- female progeny of p53+/- x p53+/- matings, and also in an in utero analysis of the p53+/- female progeny of p53-/- x p53+/+ matings. When male mice were exposed to irradiation prior to mating, a significant increase in the rate of abnormality was seen in the progeny, which was specifically associated with p53 deficiency. CONCLUSIONS: We have identified a high rate of developmental abnormalities associated with p53 deficiency. This manifests itself as a spectrum of lesions, predominantly female-associated defects in neural tube closure. These defects may arise either because p53 plays a physiological role at the time of neural tube closure, or because of an abnormally high frequency of mutation within the haploid gametes of p53-null parents.

Animals↗
PubMed1995

Teratogenic effects of amniotic sac puncture: a mouse model.

The possibility of an association between chorionic villus sampling (cvs) and limb abnormalities has prompted a review of the relevant experimental data. Although a vascular aetiology is favoured by many at present, the possibility exists that a proportion of cases may be caused by oligohydramnios secondary to inadvertent amniotic sac puncture. A mouse model of amniotic puncture syndrome has been developed to study the craniofacial and limb abnormalities produced by this procedure. Pregnant mice were anaesthetised and a laparotomy performed. One uterine horn was exteriorised, and the amniotic sacs punctured through the wall of the uterus with either a 21 gauge or a 25 gauge needle. The conceptuses in the contralateral uterine horn acted as controls. The mice were all killed on d 19 of pregnancy (day of finding a vaginal plug = d 1 of pregnancy) by cervical dislocation, and the morphological features of the embryos examined in detail. In a preliminary study, amniotic sac puncture was carried out on d 12, 13, 14, 15 or 16 of pregnancy, with either a 21 or a 25 gauge needle. Since the highest rates of palatal defects and limb deformities were observed following amniotic sac puncture using a 21 gauge needle, when this procedure was carried out on either d 13 or 14 of pregnancy, the main study was undertaken using a 21 gauge needle on these two days of pregnancy. Of 102 embryos in which amniotic sac puncture was carried out on d 13, 53% survived to d 19. Of the latter, 35% had a cleft palate, 61% had one or more morphologically abnormal limbs, and 43% had an abnormal tail. When amniotic sac puncture was carried out on d 14 of pregnancy, of 83 embryos subjected to this procedure, 81% survived to d 19. Of the latter, 27% had a cleft palate, 39% had one or more morphologically abnormal limbs, and 19% had an abnormal tail. In the controls, of 86 and 61 embryos isolated respectively from the d 13 and 14 mice, the survival rates were 97 and 90%, respectively. Palatal, limb and tail abnormalities were not observed in the control series. Tentative relationships are drawn between cvs and amniocentesis-associated abnormalities, the Robin sequence and their rodent phenocopies.

Amnion↗
PubMed1995

Craniofacial abnormalities in homozygous Small eye (Sey/Sey) embryos and newborn mice.

The Small eye (Sey) gene in the mouse is lethal in the homozygous state. It is located on chromosome 2, is a mutation in the Pax-6 gene, and is genetically homologous with the human aniridia 2 (AN2) gene mutation. Numerous studies over the last few years, using genetic and molecular biological approaches, have investigated both the location of the gene as well as its possible mode of action. In the homozygous state, the primary defect appears to be limited to the failure of differentiation of the presumptive lens and nasal placodes. Such mice therefore display a characteristic phenotype; they possess neither eyes nor any nasal derivatives. Their heterozygous (Sey/+) and normal (+/+) littermates may be distinguished before birth only by a detailed examination of their eyes. Few detailed morphological/histological studies have been undertaken to date in the Sey/Sey embryos and newborn, and in the present study we describe a variety of craniofacial abnormalities that have not previously been reported. We observed, with one exception, delayed closure of the palate, and the presence in 80% of mice of an abnormal complement of upper incisor teeth, so that 35% possessed 1 supernumerary tooth while 45% possessed 2 supernumerary teeth. In these mice, a total of either 3 or 4, rather than the normal complement of 2, upper incisor teeth were present. Possibly the most unexpected finding, however, was the presence of a median cartilaginous rod-like structure which protruded between the 2 maxillae to give the Alizarin red S and Alcian blue-stained 'cleared' skulls of the newborn mice a characteristic 'unicorn-like' appearance. While this structure appeared to be a rostral extension of the chondrocranium, its exact derivation is unclear.

Animals↗
PubMed1995

The timing of ossification of the limb bones, and growth rates of various long bones of the fore and hind limbs of the prenatal and early postnatal laboratory mouse.

In order to study the pattern of ossification of the skeletal components of the fore and hind limb of the mouse, intact embryos were isolated between days (d) 15 and 19 of pregnancy (the morning of finding a vaginal plug is termed d 1 of pregnancy), and postnatal animals isolated on d 1 (newborns), 7 and 14 after birth. The total number of fore and hind limbs studied for each day of pregnancy or postnatal day for the bone growth study is given in parentheses: d 15 (2), d 16, 17, 18 and 19 of pregnancy (5 specimens for each of these days), d 1 (newborn), wk 1 and 2, postnatal (4 specimens analysed at each of these times), since only the right limbs were studied. For the study involving the time of first appearance of ossification centres, either the right or the left limb of each of these prenatal and postnatal specimens was analysed. All specimens were fixed in 80% ethanol, bulk-stained using alizarin and Alcian blue, in order to stain ossification centres and cartilage, respectively, and cleared. The limbs were then disarticulated from the axial skeleton at the sternoclavicular and sacroiliac joints to facilitate (1) the determination of the sequential pattern of ossification in the various cartilage primordia analysed, and (2) the analysis of the pattern of growth of the humerus, ulna, femur and tibia. The latter values were plotted graphically, and the individual growth rate of each of the long bones studied was then deduced and also plotted graphically. The findings demonstrated that, with the exception of the femur and ulna, all of the long bones studied had significantly different growth patterns. The time of appearance of the various centres of ossification in the skeletal elements studied proceeded in a similar order to that described by previous authors, though there was some discrepancy in the exact time of first appearance of certain ossification centres. Of particular interest was the somewhat unusual pattern of ossification of the first digits of both the fore and hind limb compared with that of the other digits. The data presented here provide useful baseline information on the normal sequential pattern of ossification in the fore and hind limb, and the characteristic growth pattern of the individual long bones of the limbs in this species.

Animals↗
PubMed1995

Optic nerve hypoplasia in the fetal alcohol syndrome: a mouse model.

Optic nerve hypoplasia is commonly observed in children affected by the fetal alcohol syndrome, and is believed to contribute to their poor visual acuity. We have used a 'binge' model of alcohol abuse in an attempt to recreate this hypoplasia in a mouse model. Pregnant female (C57BL/6 x CBA)F1 mice were injected intraperitoneally with a single dose of a 25% solution of ethanol (v:w), either on d 11 or d 12 of gestation. Optic nerves were prepared for transmission electron microscopy from offspring at 3, 6, 9 and 15 wk of age (n = 64). A systematic random sampling technique was used to analyse both the cross-sectional areas of the optic nerves from semithin sections, and the numbers and cross-sectional areas of myelinated axons from thin sections. We found no significant differences either in the cross-sectional area or in the number of axons in the optic nerves between 3 and 9 wk from control and alcohol-treated groups. From 9 to 15 wk, alcohol-treated groups showed a loss of approximately 25% of myelinated axons (65,931 +/- 2806-49,186 +/- 3194: mean number of axons +/- S.E.M., respectively). Over the same period the number of axons in control groups was relatively stable (62,087 +/- 2043-64,703 +/- 3607). This resulted in an optic nerve with statistically significantly fewer myelinated axons at 15 wk in the alcohol-treated group, and was reflected in a trend towards a smaller cross-sectional area of the optic nerve in alcohol-treated groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗