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Biomedical subjects

D Hogan

Publications and source records attributed to D Hogan.

At least 19 recordsLinked to original sources
PubMed1996

Physical injuries and fatalities resulting from the Oklahoma City bombing.

OBJECTIVE: To provide an epidemiologic description of physical injuries and fatalities resulting from the April 19, 1995, bombing of the Alfred P. Murrah Federal Building in Oklahoma City. DESIGN AND SETTING: Descriptive epidemiologic study of all persons injured by the bombing and of all at-risk occupants of the federal building and 4 adjacent buildings. Data were gathered from hospital emergency and medical records departments, medical examiner records, and surveys of area physicians, building occupants, and survivors. STUDY POPULATION: All persons known to have been exposed to the blast. MAIN OUTCOME MEASURES: Characteristics of fatalities and injuries, injury maps, and injury rates by building location. RESULTS: A total of 759 persons sustained injuries, 167 persons died, 83 survivors were hospitalized, and 509 persons were treated as outpatients. Of the 361 persons who were in the federal building, 319 (88%) were injured, of whom 163 (45%) died, including 19 children. Persons in the collapsed part of the federal building were significantly more likely to die (153/175, 87%) than those in other parts of the building (10/186, 5%) (risk ratio [RR], 16.3; 95% confidence interval [CI], 8.9-29.8). In 4 adjacent buildings, injury rates varied from 38% to 100%; 3 persons in these buildings and 1 person in an outdoor location died. The most frequent cause of death was multiple injuries. Among survivors, soft tissue injuries, fractures, sprains, strains, and head injuries were most common; these injuries were most often caused by flying glass and other debris and collapsed ceilings. CONCLUSIONS: The Oklahoma City bombing resulted in the largest number of fatalities of any terrorist act in the United States, and there were 4 times as many nonfatal injuries as fatalities. Disaster management plans should include the possibility of terrorist bombing, and medical preparedness should anticipate that most injuries will be nonfatal. The role of building collapse in fatal injuries should be considered in the design of buildings at high risk of being bombed so as to reduce injuries.

Cause of Death↗
PubMed1996

Evaluation of a self-medication program.

OBJECTIVE: To determine the effect of an inpatient self-medication program (SMP) on the ability to self-medicate, patient medication knowledge, compliance, and patient morale. DESIGN: Randomized controlled clinical trial. POPULATION: One hundred seven consecutive patients admitted to a geriatric assessment and rehabilitation program were randomized to either participate in the SMP or to receive standard care. INTERVENTION: The SMP was a three-stage program in which patients were given increasing responsibility for the administration of their own medications. MEASUREMENTS: Ability to self-medicate on discharge from hospital; medication compliance at 1 month; patient medication knowledge; Philadelphia Morale Scale. MAIN RESULTS: Participation in the self-medication program did not increase the proportion of patients who were able to self-medicate on discharge from hospital. Compliance was improved by the program. On a proportional basis, the self-medication group made significantly fewer medication errors than the control group at 1-month follow-up (0.045 vs 0.086, P < .001). There were no significant differences in morale or medication knowledge between the SMP and control groups, although both groups made significant gains in knowledge about the names, administration times, and purposes of their medications from admission to follow-up (P < .001). CONCLUSIONS: A SMP can improve compliance in geriatric patients who are discharged to the community. Participation in a SMP does not improve patients' morale nor does it improve their medication knowledge more than pharmacy counselling alone. Participation in a SMP is unlikely to increase the probability that patients will be able to self-medicate on discharge. Cognitive factors limit patients' ability to self-medicate.

Aged↗
PubMed1996

The relationship between capsid protein (VP2) sequence and pathogenicity of Aleutian mink disease parvovirus (ADV): a possible role for raccoons in the transmission of ADV infections.

Aleutian mink disease parvovirus (ADV) DNA was identified by PCR in samples from mink and raccoons on commercial ranches during an outbreak of Aleutian disease (AD). Comparison of DNA sequences of the hypervariable portion of VP2, the major capsid protein of ADV, indicated that both mink and raccoons were infected by a new isolate of ADV, designated ADV-TR. Because the capsid proteins of other parvoviruses play a prominent role in the determination of viral pathogenicity and host range, we decided to examine the relationship between the capsid protein sequences and pathogenicity of ADV. Comparison of the ADV-TR hypervariable region sequence with sequences of other isolates of ADV revealed that ADV-TR was 94 to 100% related to the nonpathogenic type 1 ADV-G at both the DNA and amino acid levels but less than 90% related to other pathogenic ADVs like the type 2 ADV-Utah, the type 3 ADV-ZK8, or ADV-Pullman. This finding indicated that a virus with a type 1 hypervariable region could be pathogenic. To perform a more comprehensive analysis, the complete VP2 sequence of ADV-TR was obtained and compared with that of the 647-amino-acid VP2 of ADV-G and the corresponding VP2 sequences of the pathogenic ADV-Utah, ADV-Pullman, and ADV-ZK8. Although the hypervariable region amino acid sequence of ADV-TR was identical to that of ADV-G, there were 12 amino acid differences between ADV-G and ADV-TR. Each of these differences was at a position where other pathogenic isolates also differed from ADV-G. Thus, although ADV-TR had the hypervariable sequence of the nonpathogenic type 1 ADV-G, the remainder of the VP2 sequence resembled sequences of other pathogenic ADVs. Under experimental conditions, ADV-TR and ADV-Utah were highly pathogenic and induced typical AD in trios of both Aleutian and non-Aleutian mink, whereas ADV-Pullman was pathogenic only for Aleutian mink and ADV-G was noninfectious. Trios of raccoons experimentally inoculated with ADV-TR and ADV-Utah all became infected with ADV, but only a single ADV-Pullman-inoculated raccoon showed evidence of infection. Furthermore, none of the ADV isolates induced pathological findings of AD in raccoons. Finally, when a preparation of ADV-TR prepared from infected raccoon lymph nodes was inoculated into mink and raccoons, typical AD was induced in Aleutian and non-Aleutian mink, but raccoons failed to show serological or pathological evidence of infection. These results indicated that raccoons can become infected with ADV and may have a role in the transmission of virus to mink but that raccoon-to-raccoon transmission of ADV is unlikely.

Aleutian Mink Disease↗
PubMed1995

Analysis of the retinas and optic nerves of achiasmatic Belgian sheepdogs.

An autosomal recessive mutation carried in a family of black Belgian sheepdogs eliminates the optic chiasm--all retinal ganglion cell axons extend directly into the ipsilateral optic tract. One key issue we are trying to resolve is whether the retina or the chiasm is the principal site of mutant gene action. In this study, we have examined retinas of mutants to discover any associated changes in retinal structure. Retinas of mutant animals are relatively normal. Inner and outer nuclear layers are qualitatively indistinguishable from those of normal dogs. The principal difference is that the area centralis of mutants is smaller and had a lower peak ganglion cell density than that of normal dogs (8,100 vs 10,500/mm2, P < 0.05). This mutant phenotype is similar to that seen in retinas of Siamese cats and albino ferrets. Beyond area centralis, the central-to-peripheral gradient in ganglion cell density is normal in mutants. The size of the optic nerves, density of axons, and total number of axons do not differ between mutant and normal dogs. One of three mutant dogs had a small abnormal optic chiasm. Retrograde labeling of ganglion cells demonstrated that the residual crossed projection originated from cells in a widespread region in nasal retina and not solely from the peripheral nasal region, as might be expected of an anti-albino. Although our analysis does not rule out the retina as a site of mutant gene action, the modest differences between mutant and normal retinas suggest that the mutation either acts outside the retina or exerts a highly specific effect on ganglion cell trajectories alone.

Animals↗
PubMed1995

A comparison of diagnosis, evaluation, and treatment of patients with dermatologic disorders.

BACKGROUND: Managed care in the American health care system may limit access to health care specialists. OBJECTIVE: We assessed primary care providers' abilities at diagnosing and treating patients with a previously undiagnosed skin disorder. METHODS: Patients with previously undiagnosed skin disorders were seen and examined sequentially by three groups of physicians: (1) internal medicine residents, (2) board-certified internal medicine attending physicians and (3) dermatology faculty. The internal medicine residents and attending physicians' diagnoses were compared with the dermatologists'. Appropriateness of therapy ordered by the internal medicine residents and attending physicians was assessed. RESULTS: Medical residents' diagnoses were correct in 43% of the patients whereas the attending physicians diagnosed 52% of cases correctly. Attending physicians and residents frequently ordered therapy inappropriate for the patient's diagnosis. Internal medicine residents and attending physicians were more likely to order skin biopsies than dermatologists. CONCLUSIONS: Our results confirm earlier studies that nondermatologists perform poorly in the diagnosis and treatment of skin disease. Primary care providers should receive more training in dermatology, or dermatologists should be permitted to act as primary caregivers to patients with skin disease.

Adult↗
PubMed1994

Homology between Borrelia burgdorferi OspC and members of the family of Borrelia hermsii variable major proteins.

Synthesis of the Borrelia burgdorferi outer surface protein C (OspC) is quite variable. We have cloned and sequenced the ospC gene from B. burgdorferi isolate CA-11.2A, a clone in which ospC expression varies. The 5' flanking region of the gene contains at least two consensus promoter regions, as well as two large overlapping inverted repeats. Sequence comparison to other OspC proteins indicated that the CA-11.2A OspC is as closely related to OspC from two different genospecies of Lyme disease spirochetes as it is to OspC from the prototype B. burgdorferi strain, B31. Comparisons of the OspC amino acid (aa) sequence with those in aa sequence databases revealed partial identity with the variable major proteins Vmp3 and Vmp24 of B. hermsii, a causative agent of tick-borne relapsing fever. An ospC probe hybridized to B. hermsii restriction fragments and linear plasmids that also were recognized by the vmp3 and vmp24 probes. OspC and these Vmp appear to be related, but their synthesis is regulated differently in the two species of spirochetes. This represents a fascinating example of the evolution of the number, position, regulation and perhaps function of homologous genes in two related pathogens. These parameters may relate to characteristic properties of the pathogens and their separate tick vectors.

Amino Acid Sequence↗
PubMed1994

Target recognition and visual maps in the thalamus of achiasmatic dogs.

Vision is dependent on ordered neuronal representations or maps of visual space. These maps depend on precise connections between retinal axons and their targets cells. In mammals, nerve fibres from right and left eyes produce congruent maps of contralateral visual space in adjacent layers of the lateral geniculate nucleus (LGN). We have identified an autosomal recessive mutation in Belgian sheepdogs that eliminates the optic chiasm. In these mutants, all retinal axons project into the ipsilateral optic tract, including those originating in the nasal hemiretina that normally cross midline. These animals exhibit a pronounced horizontal nystagmus. The abnormal ipsilaterally directed nasal fibres innervate the LGN as if they had successfully crossed the midline, terminating in the appropriate layer of the nucleus. As a consequence, the LGN contains non-congruent, mirror-image maps of visual space in adjacent layers. These results show that there is a robust affinity between nasal and temporal retinal axons and specific LGN layers even when all retinal axons originate from a single eye.

Animals↗
PubMed1994

The development of parvalbumin and calbindin-D28k immunoreactive interneurons in kitten visual cortical areas.

Calbindin-D and parvalbumin are calcium binding proteins which are found in non-overlapping subpopulations of GABA-ergic interneurons in mammalian neocortex. We studied the development of these calcium-binding proteins in interneurons of cat striate and extrastriate cortical areas which have differing patterns of connectivity and follow different developmental timetables. We examined primary visual areas 17 and 18, secondary visual area 19, medial lateral suprasylvian and lateral suprasylvian areas (MLS and LLS) and association areas 7 and the splenial visual area from the day of birth (P0) through P101. Parvalbumin-immunoreactive (ir) interneurons followed the inside-out pattern of maturation of cortical laminae. They were located only in infragranular layers at the earliest ages and were not observed in the overlying cortical plate. At 3 weeks of age, when cortical lamination is mature, parvalbumin stained cells were found in all cortical layers except layer I. The number of stained secondary and tertiary dendrites in the parvalbumin-ir interneuronal population decreased with age. This change was associated with a shift in the molecular weight of parvalbumin detected on Western blots. During the first postnatal week, the area 17/18 border contained more parvalbumin-ir neurons than other visual areas. The developmental pattern of calbindin staining differed considerably from the parvalbumin staining pattern. Very few calbindin-ir interneurons were seen in area 17 during the first 2 weeks of life. In lateral cortical areas, calbindin-ir neurons were located in cortical plate, infragranular layers of cortex and white matter/subplate. Calbindin-ir neurons increased in supragranular layers of secondary cortical areas by P7 and in area 17 by P20. In the mature cortex, the calbindin staining pattern was bilaminar, with a dense band of calbindin-ir cells in layer II and a second band in layers V-VI. There was no difference in the distribution of calbindin-ir neurons among visual areas at maturity.

Animals↗
PubMed1994

Oral premedication for local anesthesia in plastic surgery: prospective, randomized, blind comparison of lorazepam and temazepam.

Patients undergoing plastic surgical procedures under local anesthesia as inpatients were entered into a phase III randomized, blind trial designed to compare two commonly used oral premedications, lorazepam and temazepam. The effects of the drugs on each patient's memory, pain, sedation, and anxiety were assessed by questions asked of the patient, the nurse, and the surgeon. Analysis was based on 100 randomized patients. Lorazepam had a significantly greater amnesic effect (p < 0.0001), resulted in less pain with the local anesthetic injection (p = 0.006), and had a greater sedative effect than temazepam (p < 0.0001, patient's assessment; p = 0.005, observers' assessments). There was no significant difference in anxiolysis between the two premedications (p = 0.20). If premedication is indicated, we advocate the use of lorazepam rather than temazepam as premedication for plastic surgical procedures to be performed under local anesthesia, provided there is adequate postoperative supervision.

Administration, Oral↗
PubMed1994

Plasmid location of Borrelia purine biosynthesis gene homologs.

The Lyme disease spirochete Borrelia burgdorferi must survive in both its tick vector and its mammalian host to be maintained in nature. We have identified the B. burgdorferi guaA gene encoding GMP synthetase, an enzyme involved in de novo purine biosynthesis that is important for the survival of bacteria in mammalian blood. This gene encodes a functional product that will complement an Escherichia coli GMP synthetase mutant. The gene is located on a 26-kb circular plasmid, adjacent to and divergent from the gene encoding the outer surface protein C (OspC). The guaB gene homolog encoding IMP dehydrogenase, another enzyme in the purine biosynthetic pathway, is adjacent to guaA. In Borrelia hermsii, a tick-borne relapsing fever spirochete, the guaA and guaB genes are located on a linear plasmid. These are the first genes encoding proteins of known function to be mapped to a borrelial plasmid and the only example of genes encoding enzymes involved in the de novo purine biosynthesis pathway to be mapped to a plasmid in any organism. The unique plasmid location of these and perhaps other housekeeping genes may be a consequence of the segmented genomes in borreliae and reflect the need to adapt to both the arthropod and mammalian environments.

Amino Acid Sequence↗
PubMed1994

2-Chlorodeoxyadenosine is an active salvage therapy in advanced indolent non-Hodgkin's lymphoma.

PURPOSE: To determine the response rate to 2-chlorodeoxyadenosine (2-CdA; cladribine) in patients with advanced indolent non-Hodgkin's lymphoma (NHL) who fail to respond to or progress after a response to standard chemotherapy drugs. PATIENTS AND METHODS: Twenty-one patients were treated with at least one cycle of 2-CdA 0.1 mg/kg/d by continuous infusion for 5 or 7 days. RESULTS: The overall response rate (complete response [CR] and partial response [PR]) was nine of 21 patients (43%; 95% confidence interval, 22% to 64%). Unmaintained durable responses (longest follow-up, 29+ months) have been observed. The treatment was well tolerated by all patients. The major toxicity was related to myelosuppression (predominantly neutropenia) and immunosuppression with infection. CONCLUSION: The purine analog 2-CdA is an active salvage therapy in pretreated patients with indolent NHL, and deserves further assessment in untreated patients and in combination with other chemotherapy agents.

Adolescent↗
PubMed1993

Postpolio syndrome in New Zealand: a survey of 700 polio survivors.

AIMS: To examine the experience of postpolio syndrome amongst a group of survivors of polio currently resident in New Zealand. METHODS: A sample of 700 responded to a request for volunteers to take part in a postal survey concerning their experience of polio and postpolio symptoms. RESULTS: The mean age of respondents was 59 years. Two-thirds of them were women. The year of polio infection was between 1915 and 1962 with the majority (54%) being in the 1945-56 period. Most were under 16 years of age (73%) at the time. Paralysis and weakness in limbs and back were the most common symptoms in the acute phase of the infection. Symptoms of the postpolio syndrome were reported by significant numbers. Increasing weakness in muscle functioning in one or more area was evident amongst 38% of the sample. Generalised muscle weakness was reported by 47%, increasing muscle wastage by 17%, difficulty swallowing by 16% and shortness of breath on waking by 10%. Pain in joints was reported by 60% and excessive tiredness by 48%. After controlling for age there was little evidence that the symptoms increased with years since the acute polio infection. CONCLUSIONS: The experience of postpolio symptoms was common amongst this group of polio survivors. It is estimated that there are between 3,000 and 5,000 polio survivors in New Zealand who may be suffering postpolio symptoms. The implications of this for primary and secondary health care provision are discussed.

Adult↗
PubMed1993

Transient expression of calbindin-D28k immunoreactivity in layer V pyramidal neurons during postnatal development of kitten cortical areas.

Calbindin-D28k is a 28 kDa calcium binding protein that has been shown to colocalize with a specific subpopulation of gamma-aminobutyric acid inhibitory interneurons in mammalian neocortex. We have examined the ontogeny of calbindin in neonatal kitten cortex in areas 17,18,19,7, medial and lateral suprasylvian visual areas, splenial visual area and cingulate cortex from the day of birth (P0) through maturation of the brain (P101). Transient staining of immature layer V pyramidal cells was seen in kittens six weeks old and younger. This transient staining of pyramidal cells was most intense and the stained neurons were most numerous in cingulate cortex. Apical dendrites of pyramidal cells in cingulate cortex were prominently stained and could be followed to layer I, where they were seen to branch extensively. There were very few calbindin immunoreactive pyramidal cells in primary cortical areas postnatally. Transient staining in extrastriate visual cortical areas disappeared first from the lateral suprasylvian areas, and persisted longest in area 7. Pyramidal neurons in the cingulate gyrus expressed calbindin longest, but calbindin expression by pyramidal neurons ceased by the sixth postnatal week in all areas of the brain.

Aging↗
PubMed1993

The development of somatostatin immunoreactive neurons in cat visual cortical areas.

The development of somatostatin immunoreactive (SOM-ir) neurons in cat striate and extrastriate cortex was studied to determine whether temporal changes in the morphology, distribution and density of SOM-ir neurons during development would provide clues to the emergence of specific cortical areas. The visual cortical areas examined included areas 17-19 and 7, posteromedial lateral suprasylvian, posterolateral lateral suprasylvian cortex and splenial visual area. We observed that the pattern of SOM-ir neurons in the cortical plate reflects the maturation of the cortical plate. At 1 week of age, SOM-ir neurons were only found in layers V and VI of the developing cortex; by 2 weeks of age, SOM-ir neurons were found in layer IV; and by 3 weeks of age, SOM-ir neurons were located in all layers of the cortex except layer I. SOM-ir neurons in the subplate were much more numerous under lateral cortical areas than under medial areas. This difference decreased over the first 2 postnatal weeks and by the 14th day after birth (P14), the distribution and numbers of SOM-ir neurons in the subplate/white matter had reached the adult pattern. The timing of exuberant SOM expression in the subplate suggests a function in the formation of visual corticocortical connections which begin to develop during the first postnatal week in the kitten.

Animals↗
PubMed1992

The development of neuropeptide Y immunoreactive neurons in cat visual cortical areas.

The development of NPY-ir neurons and fibers in cat striate and extrastriate cortex was studied to determine whether temporal changes in the morphology, distribution and density of NPY-ir neurons during development would provide clues to the emergence of specific cortical areas. No differences in the number or distribution of NPY-ir neurons were observed at any age among the five visual cortical areas examined, area 17, 18, 19, posteromedial lateral suprasylvian and posterolateral lateral suprasylvian cortex. The number of NPY-ir neurons in cat visual cortical areas was higher in adult animals than in kittens. The proportion of NPY-ir neurons found in layer VIb was constant throughout life, suggesting that NPY immunoreactivity is not a marker for the transient neurons of the subplate. NPY-ir neuronal morphology was seen to 'flatten' in older animals with the development of sulci and increasing density of the brain. In contrast to the pattern observed with NPY-ir neurons, NPY-ir processes exhibited area-dependent differences during development. NPY-ir fibers grew into area 17 earlier and with a radial orientation which was not consistently observed laterally. This radial orientation was still apparent in adult brains in layer IV of area 17, though there was no orientation of fibers in the other laminae or other visual areas of the adult.

Aging↗