Polymyalgic presentation of enterovirus infection: a cause of diagnostic confusion.
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Biomedical subjects
Publications and source records attributed to R J Stevens.
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The effect of thyroid hormone on the expression of mitochondrial proteins was evaluated during development by measuring cytochrome c oxidase (CYTOX) activity and cytochrome c protein and mRNA levels in heart and skeletal muscle of control and hypothyroid rats. Animals were killed at the late fetal, early, and late postnatal stages up to 56 days of age. In heart, CYTOX activity increased 2.3-fold above the fetal level throughout development, most of which occurred prior to 2 days of age. No increase was observed in muscle. CYTOX activity was reduced in hypothyroid animals throughout development in heart compared to controls (by 50% at 56 days), but in muscle no effect of hypothyroidism was observed. In muscle and heart 4- and 1.5-fold increases in cytochrome c above the fetal level were evident by 1 day of age, with further increases to 8.5- and 2.7-fold by 56 days, respectively. The increase in cytochrome c differed from the increase in CYTOX, indicating changes in mitochondrial composition. Hypothyroidism reduced cytochrome c in muscle by 30-35% at 56 days, but had no effect in heart, indicating a muscle type-specific effect of thyroid hormone on cytochrome c protein expression. Cytochrome c mRNA increased rapidly to 4-5 fold above the fetal level in both heart and muscle by 6 h post-partum. Between 7 and 56 days of age, further increases to 6- and 25-fold were observed in muscle and heart, respectively. In muscle, the 6-fold developmental increase in mRNA paralleled that of the protein, suggesting transcriptional regulation.(ABSTRACT TRUNCATED AT 250 WORDS)
In this review, current understanding of the aetiopathogenesis of giant cell arteritis is examined. Possible explanations for the late age of onset and striking responsiveness to steroid therapy.
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OBJECTIVE: To identify if an actual increase in children born with gastroschisis is occurring in Oklahoma. To compare findings with historical and current literature concerning the incidence of this congenital malformation of the abdominal wall. DATA: Derived from Children's Hospital of Oklahoma (CHO) medical records, inventory sheets completed by nurses and resident physicians on admission of gastroschisis infants at CHO, hospital records of Tulsa pediatric surgeons (Subramania Jegathesan, MD, and Richard Ranne, MD), and the state health departments of Oklahoma and Iowa. FINDINGS: 1. Increase in number of gastroschisis children born in Oklahoma. 2. Comparable findings in the state of Iowa. 3. No specific maternal or environmental factor to account for increase. CONCLUSIONS: Children born with gastroschisis in Oklahoma and other areas of the country, as well as internationally, have shown an increase in number over the past two decades. This increase cannot be attributed to any one identifiable factor.
Dog bites, a common cause of traumatic injury, tend to be a greater source of morbidity and mortality in children than in adults. We evaluated 13 children, who, during a 10-year period, required surgical intervention for dog bites. The greatest cause of morbidity in these children was the penetrating component of the dog bite. Most initial evaluations focused on the crushing component of the bite, but in children with serious dog bites, wounds must be evaluated with respect to both the crushing and penetrating injury components.
Two mitochondrial fractions, termed intermyofibrillar (IMF) and subsarcolemmal (SS), were isolated from skeletal muscle, and their biochemical properties were related to differences in respiration and mitochondrial protein synthesis. State III respiration was 2.3- to 2.8-fold greater in IMF than in SS mitochondria. Site 1 inhibition of respiration with rotenone reduced this difference to 1.4-fold. When sites 1 and 2 were inhibited with antimycin, the 1.4-fold differences remained. The activities of cytochrome-c oxidase (CYTOX) and succinate dehydrogenase (SDH) could account for some of these differences, since CYTOX was 20% greater (P < 0.05) in IMF mitochondria, and SDH was 40% greater (P < 0.05) in SS mitochondria. Cytochromes a, b, c, and c1 contents were similar in the two fractions. Cardiolipin (CL) content was higher (P < 0.05) in SS mitochondria, indicating a less dense mitochondrial fraction with respect to CL. In vitro [3H]leucine incorporation was 1.8-fold higher (P < 0.05) in IMF than in SS mitochondria. Thus compositional differences between IMF and SS fractions exist, perhaps representing mitochondria at different stages of biogenesis. The biochemical and functional differences could not solely be due to differences in mitochondrial protein synthesis but could also be due to nuclear-directed protein synthesis specific to each mitochondrial fraction.
Effects of acetylcholine (ACh) and substance P on the electrical and mechanical activities of the circular muscle layer of the canine proximal colon were studied. Because this muscle layer is bordered by two different pacemaker regions, responses from segments containing either a single pacemaker region or no pacemaker region were compared with responses of the complete muscle layer. Concentration-response relationships for ACh and substance P were similar between the various segments, suggesting that receptors for these agonists are expressed throughout the layer. The dominant contractile pattern induced by ACh and substance P in each segment was a 1- to 3-cycle/min rhythm. In a like manner, these agonists also elicited an electrical pattern in which a long-duration slow wave occurred one to three times per minute between short-duration slow waves. Low concentrations of nifedipine (0.01 microM) selectively antagonized the 1- to 3-cycle/min rhythm. In circular muscles with no pacemaker region, ACh (1 microM) caused depolarization, induced oscillations in membrane potential averaging 24 +/- 5 mV in amplitude and 2.9 +/- 0.9 cycles/min in frequency, and generated rhythmic contractions at the same frequency. This "interior" circular muscle was functionally innervated by cholinergic excitatory nerves. Exposure to ACh (1 microM) did not alter the conduction of slow waves through the thickness of the circular layer. In summary, the excitatory neurotransmitters, ACh and substance P, induce a dominant electrical and contractile rhythm throughout the circular muscle layer that is different from the spontaneous rhythms produced at either the myenteric or submucosal border.
The effects of cromakalim (BRL 34915) and its optical isomer lemakalim (BRL 38227) were investigated in intact tissue and freshly dispersed circular muscle cells from canine proximal colon. Cromakalim and lemakalim hyperpolarized resting membrane potential, shortened the duration of slow waves by abolishing the plateau phase, and decreased the frequency of slow waves. Glyburide, a K channel blocker, prevented the effect of cromakalim on slow-wave activity. The mechanisms of these alterations in slow-wave activity were studied in isolated myocytes under voltage-clamp conditions. Cromakalim and lemakalim increased the magnitude of a time-independent outward K current, but cromakalim also reduced the peak outward K current. Glyburide inhibited lemakalim stimulation of the time-independent background current. Nisoldipine also reduced the peak outward current, and in the presence of nisoldipine, cromakalim did not affect the peak outward component of current. This suggested that cromakalim may block a Ca-dependent component of the outward current. Lemakalim did not affect the peak outward current. We tested whether the effects of cromakalim on outward current might be indirect due to an effect on inward Ca current. Cromakalim, but not lemakalim, was found to inhibit L-type Ca channels; however, glyburide did not alter cromakalim inhibition of inward Ca current. We conclude that the effects of cromakalim and lemakalim on membrane potential and slow waves in colonic smooth muscle appear to result primarily from stimulation of a time-independent background K conductance. The effects of these compounds on channel activity may explain the inhibitory effect of these compounds on contractile activity.
Microelectrode techniques and the fluorescent Ca2+ indicator indo-1 were used to measure membrane potential, cytosolic Ca2+ ([Ca2+]cyt), and muscle tension simultaneously in canine antral smooth muscles. Responses of muscles from the myenteric and submucosal regions were compared, since electrical activity and excitation-contraction coupling in these regions differ. The upstroke phase of electrical slow waves in both regions induced an increase in [Ca2+]cyt. In myenteric muscles the plateau phase of slow waves often caused either a further rise in [Ca2+]cyt or maintenance of the level reached during the upstroke event. In submucosal muscles, the plateau phase was significantly smaller and did not induce a second phase in the Ca2+ transient. Contractions were related to the amplitudes of Ca2+ transients. Acetylcholine (ACh; 3 x 10(-8)-10(-6) M) increased the amplitude and duration of the plateau phase of slow waves in a concentration-dependent manner. ACh also increased the second phase of Ca2+ transients and contractile responses associated with the plateau potential. In submucosal muscles ACh induced a significant increase in the plateau phase of the slow wave and increased the corresponding phase of Ca2+ transient. Nicardipine (10(-6) M) inhibited plateau phase of slow waves and the associated increases in [Ca2+]cyt and muscle tension. BAY K 8644 (10(-7) M) augmented the plateau potential and increased [Ca2+]cyt and muscle tension. These results suggest that dihydropyridine-sensitive Ca2+ currents participate in the plateau potential. Cholinergic stimulation modulates [Ca2+]cyt and therefore force by regulating the amount of Ca2+ entering cells through these channels.
A hospital's emergency physician billing procedures and fee schedules may not have kept pace with changes in the make-up of emergency room personnel. Revisions require thorough analysis of coding procedures, payer and patient data, Medicare rates, and breakdowns of collections. A successful analysis may yield improved collections, increased physician compensation, and separate billing by emergency physicians.
Various empirical indices such as the pulsatility index (PI) are widely used for quantitative analysis of Doppler ultrasound velocity waveforms. The physical interpretation of these indices was studied using a mathematical model. Although the method has more general applicability, this particular study was concerned with the umbilical-placental circulation. A lumped element electrical circuit equivalent was used, with each arterial branch represented by a resistor and a capacitor. The placental villous bed was modelled by a two-step parallel branching structure. Placental vascular disease was modelled either as obliteration of a fraction of the terminal branches, or as a fractional decrease in the radius of the vessels. The main features of both normal and abnormal umbilical artery waveforms can be reproduced by this simple model. Theoretical relationships between the velocity waveform indices and the lumped resistances and capacitance of the system were obtained for different input pressure functions. Over a wide range of physically reasonable conditions, the umbilical artery PI is approximately proportional to the ratio of the placental resistance to the umbilical artery resistance. The PI also depends on the pulsatility of the input pressure waveform. The Fourier pulsatility index was evaluated for an arbitrary pressure function, and shown to behave like (PI)2 for the umbilical artery waveform.
The hypothesis that methylene blue has a direct effect on colonic muscle cells was tested. Intracellular recordings were made from cross-sectional preparations of canine proximal colon. Cells through the circular layer were impaled and membrane potentials ranging from -81 mV at the submucosal surface to -46 mV at the myenteric border were recorded. Methylene blue (10(-5) M) depolarized cells near the submucosal border by an average of 43 mV and slow-wave activity ceased. The loss of slow-wave activity could be explained by the depolarizing effects of methylene blue rather than a specific effect of methylene blue on the pacemaker mechanism. Other experiments suggested that the depolarizing effects of methylene blue were not confined to muscle cells within the submucosal pacemaker region. Depolarization of cells was noted throughout the circular layer, but the magnitude of the depolarization decreased with distance from the submucosal border. After methylene blue, the gradient in resting potential across the circular layer was greatly reduced or abolished. The data suggest that methylene blue is not necessarily a specific probe for interstitial cells and has direct effects on smooth muscle cells in the canine proximal colon. This effect is similar to treatments that are known to block the electrogenic sodium pump.
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Arildone (WIN 38020), a broad spectrum antiviral, aryl-beta-diketone (4-[6-(2-chloro-4-methoxy)phenoxyl]hexyl-3,5-heptanedione), blocks the replication of human cytomegalovirus at a stage prior to the synthesis of virus-specific DNA. Inhibitory action was demonstrated against a number of virus isolates from neonates and immune-compromised patients. Intranuclear sites of virus replication, highlighted by DNA-staining methods or immunofluorescence, were absent after Arildone treatment and corresponded with the lack of ultrastructural changes associated with productive infection. The abundance of early antigens in cells treated with Arildone was evidence for expression of the viral genome and this was confirmed by detection of immediate-early viral proteins in the presence of the drug. The results suggest that Arildone prevents the replication of human cytomegalovirus at a stage after virion uncoating but prior to viral DNA synthesis.
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By testing adjacent sites on the hypothenar eminence of the palm, enriched with bacteria by massaging the forehead, we found that the numbers of bacteria recovered from the skin surface by a wet cotton swab in 30 s were not significantly different from the numbers obtained by a brisk scrubbing with a blunted Teflon policeman for 120 s. This was true of aerobes (gram-positive cocci) and anaerobes (propionibacteria). If the same site on the palm was swabbed two times for 15 s each time, 67 to 94% of the total recovered bacteria were obtained on the first swab. Differential localization of bacteria into surface and subsurface populations was accomplished by first swabbing a test skin site to assay the surface flora and then scrubbing the same site to test for subsurface organisms. On the palm the swab yielded more aerobes and anaerobes than did the subsequent scrub. On the forehead the scrub yielded three to eight times as many anaerobes as the preceding swab. In some tests gram-positive cocci were distributed on the forehead like propionibacteria (large excess in scrub specimen); in other tests their numbers were similar in the swab and scrub specimens or there was a large excess in the swab specimen. These results indicate that there was no substantial subsurface flora on the palm. On the forehead propionibacteria were predominantly in deeper locations in all tests; gram-positive cocci were variable: in some test sites they were largely at the surface, whereas at other sites a predominance of cocci was in subsurface locations.