Biomedical subjects
J Green
Publications and source records attributed to J Green.
The survival game.
This paper describes a flexible and enjoyable learning game and summarizes our experiences of using it (including the medical students' own evaluation of the game). The description is sufficiently detailed to encourage readers to reproduce and adapt the game to fit their own requirements.
Employees provide free housing.
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Bailey-Boushay House: a home with a heart for people living with AIDS.
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Stimulation of renal prostanoid synthesis by potassium loading in the rat.
In vitro we measured the urinary excretion and synthesis of prostaglandins (PGE2, 6-keto-PGF1 alpha, thromboxane B2 and PGF2 alpha) by isolated glomeruli, cortical homogenates, medulla and papilla in KCl-loaded rats (KCl+, average K intake: 17 mmol/day for 20 days) and in rats loaded with non-Cl K salts (KCl-, average K intake: 21 mmol/day) as compared with control rats. In 2 separate groups of rats (KCl+ and KCl-) the urinary excretion of prostaglandins was measured after variations of K intake from an average of 4 to 20 mmol/day in 5-day periods. Glomerular PGE2 synthesis tended to decrease in KCl+, whereas it increased in KCl- rats. 6-Keto-PGF1 alpha and TXB2 did not vary, and PGF2 alpha decreased in both K-loaded groups. In the cortex, KCl loading decreased PGE2 synthesis. In KCl-, cortical TXB2 decreased. In the medulla, KCl loading increased the synthesis of TXB2 and PGF2 alpha, but not that of PGE2 and 6-keto-PGF1 alpha. In KCl- rats, TXB2 but not PGF2 alpha increased and PGE2 synthesis was also elevated. In the papilla, TXB2 synthesis increased in both KCl+ and KCl- rats. The urinary excretion of 6-keto-PGF1 alpha and TXB2 increased in both KCl+ and KCl- rats, whereas PGF2 alpha increased only in KCl+ rats. The changes of glomerular prostaglandin synthesis during K loading could dilate the glomerular vasculature, in keeping with the known vasoactive effects of the cation.(ABSTRACT TRUNCATED AT 250 WORDS)
An operation for the removal of the eye-ball, together with the entire conjunctival sac and lid margins.
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Evidence of cross-reactivity between olive, ash, privet, and Russian olive tree pollen allergens.
In a clinical investigation, 103 Michigan residents with symptoms suggestive of allergic rhinitis or asthma were skin tested with olive (Olea europaea) pollen extract. Nineteen had positive reactions. Since the olive tree is not native to nor grown in Michigan, this study was undertaken to determine whether the skin test reactivity was the result of cross-reactivity among tree pollen allergens. ELISAs were developed to measure olive, ash (Fraxinus americana), privet (Ligustrum vulgare), and Russian olive (Elaeagnus angustifolia) specific IgE antibodies. Inhibition studies were performed to determine whether pollen extracts from each of these tree species could inhibit IgE antibody binding to olive extracts. Eleven of the 19 skin test-positive patients were olive-ELISA positive, eight either were ELISA-positive to ash, seven to privet and ten to Russian olive. There were significant correlations between the ELISA results to olive and each of the other three pollens. The inhibition studies demonstrated that all three of the tree pollens were capable of inhibiting the binding of IgE to olive extract in a dose-response fashion. IgE-immunoblot studies demonstrated several proteins common to olive, ash, and privet. Twelve of the olive skin test-positive patients were contacted and 75% were exposed to one or more of the studied trees in their yards. Five patients had traveled to areas where olive trees are grown. We conclude that there is a high degree of cross-reactivity among allergens from native Michigan trees and from olive trees. This cross-reactivity is the most likely reason for skin test reactivity to olive pollen extract in Michigan.
Programmed instruction: cancer care. Basic cancer concepts.
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Blunt traumatic iliac vein laceration without pelvic fracture: a rare entity.
Most blunt traumatic pelvic venous injuries are associated with pelvic fractures. We report the case of a 32-year-old man who suffered a common iliac vein laceration, without a pelvic fracture, during a motor vehicle accident. Laparotomy and venous repair were undertaken.
Evidence for two protein-lipoylation activities in Escherichia coli.
The lipoate acyltransferase subunits of the 2-oxo acid dehydrogenase complexes are post-translationally modified with one or more covalently-bound lipoyl cofactors. Two distinct lipoate-protein ligase activities, LPL-A and LPL-B, have been detected in E. coli by their ability to modify purified lipoyl apo-domains of the bacterial pyruvate dehydrogenase complex. Both enzymes require ATP and Mg2+, use L-lipoate, 8-methyllipoate, lipoyl adenylate and octanoyl adenylate as substrates, and both activate lipoyl-deficient pyruvate dehydrogenase complexes. In contrast, only LPL-B uses D-lipoate and octanoate and there are differences in the metal-ion and phosphate requirements. It is suggested that LPL-B may be responsible for the octanoylation of lipoyl domains observed previously under lipoate-deficient conditions.
Half the aggro.
A project at a London hospital is helping to iron out friction between the A&E department and local GPs, write Judith Green and colleagues.
FNR activates and represses transcription in vitro.
FNR is an iron-binding transcriptional regulator for anaerobic gene expression in Escherichia coli. Footprinting studies with the purified protein have confirmed that it is a site-specific DNA-binding protein. Transcription tests with the positively-regulated FFmelR promoter and the negatively-regulated ndh promoter likewise demonstrated that FNR can activate or repress transcription in vitro. Reducing conditions were not required but activity was abolished by substituting an essential cysteine residue with alanine (C122A) and the affinity for DNA was reduced by iron-depletion. The start point(s) for transcription of the FNR-repressed NADH dehydrogenase II gene (ndh) were identified by transcript mapping and the corresponding promoter (-35 and -10 sequences) was located immediately downstream of the FNR-binding site.
New survey shows 6.7% pay hikes in hospitals.
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Characterization of the FNR protein of Escherichia coli, an iron-binding transcriptional regulator.
FNR is a transcriptional regulator mediating the activation or repression of a variety of Escherichia coli genes in response to anoxia. The FNR protein resembles CRP (the cyclic-AMP receptor protein) except for the presence of a cysteine-rich N-terminal segment which may form part of an iron-binding redoxsensing domain. The FNR protein was purified by a new procedure. It was monomeric (Mr = 30,000) and contained as much as 1.1 mol of iron per monomer when purified in the presence of added iron. This iron was associated with cysteine residues, because there was an inverse relation between iron content and titratable sulphydryl groups. Other physical and chemical properties are reported including evidence for a potential disulphide group or analogous modification. The interaction between FNR protein and target DNA appeared weak and non-specific in gel-retardation assays, but specific binding to the proposed DNA-binding site was shown for the first time in footprinting studies. A role for iron in FNR-mediated gene expression was confirmed by using cultures in which FNR was inactivated by growth in the presence of the specific chelator, ferrozine, but protected by ferrous iron.
Analyzing hospital mortality. The consequences of diversity in patient mix.
Consumers and payers increasingly demand data with which to evaluate health care providers. While publication of risk-adjusted hospital-specific death rates is one response, debate continues over whether higher than predicted mortality is a warning about quality of care or rather a reflection of a hospital's atypical patient population. To help inform this debate, we compared the characteristics of Medicare patients discharged from 187 hospitals that the Health Care Financing Administration (HCFA) had labeled "high-mortality outliers" with those of Medicare patients from 5373 hospitals not so designated. Hospitals were most likely to be flagged as high-mortality outliers by HCFA when they had large shares of very elderly patients (age greater than or equal to 85 years), patients with high-risk diagnoses, or patients requiring nursing home care. After adjustments were made to compensate for these biases, nearly half the hospitals flagged as outliers by HCFA were no longer so designated. Statistics purporting to measure effectiveness of care from hospital death rates should be modified to account for diversity in patient mix.
Voltage-dependent phosphate transport in osteoblast-like cells.
Phosphate ion (Pi) in sufficient concentrations is crucial for bone mineralization. The osteoblast (OB) may be responsible for the transport of Pi into the bone interstitium, where mineralization occurs. We previously characterized a Na(+)-dependent Pi transporter (NaPi) in the osteoblastic UMR-106-01 cell line. In the present study, the alteration of Na(+)-dependent Pi transport by changes in membrane potential was investigated. Depolarizing the cells with increasing concentrations of ambient K+ and valinomycin resulted in a progressive decline in Na(+)-dependent Pi uptake to a maximum of 28% at a membrane potential of -18 mV compared to control Na(+)-dependent Pi uptake at a membrane potential of approximately -60 mV. Hyperpolarizing the cells with SCN- increased Na(+)-dependent Pi uptake over control by 50% at an SCN- concentration of 70 mM. Determination of membrane potential by using the fluorescent probe, DiSC3(5), showed that the addition of Pi to cells in Na(+)-containing medium resulted in a small depolarization. These data show that NaPi activity can be altered by membrane potential changes and that the initiation of Na(+)-dependent Pi uptake is associated with depolarization of the plasma membrane of UMR-106-01 cells. Taken together, the cotransport of Na+ and Pi results in the movement of a net positive charge into the cell.
Prevalence of HPV cervical infection in a family planning clinic determined by polymerase chain reaction and dot blot hybridisation.
The overall prevalence of human papillomavirus (HPV) cervical infection in 131 women attending a family planning clinic was 7% (HPV 6/11, 16, 18, 31) by dot blot hybridisation, 53% (HPV 11, 16, 31) by polymerase chain reaction (PCR), and 56% by the two methods combined. HPV 16 and 18 were the commonest types (4% each) by dot blot, HPV 16 (39%) by PCR. Fifteen percent of subjects had mildly abnormal cervical cytology (grades 1A, 2A, or 3). There was no significant correlation between cytological abnormality and HPV positivity, or between cytological or HPV status and other postulated risk factors for cervical neoplasia. It is concluded that PCR is considerably more sensitive than dot blot DNA hybridisation in detecting HPV cervical infection in such a "low risk" setting, where HPV copy number may be low. Firm conclusions cannot be drawn from our results regarding a causal role for HPV or other factors in the development of cervical neoplasia.
Prostaglandins enhance parathyroid hormone-evoked increase in free cytosolic calcium concentration in osteoblast-like cells.
Prostaglandins (PGs) are autocrine or paracrine hormones that may interact with circulating hormones such as parathyroid hormone (PTH) in bone. We examined the interaction of the PGs, PGF2 alpha, PGE2, and 6-keto-PGF1 alpha with PTH to enhance the rapid, initial transient rise in free cytosolic calcium ([Ca2+]i) and cAMP levels stimulated by PTH. Pretreatment of UMR-106, MC3T3-E1, and neonatal rat calvarial osteoblast-like cells by PGs resulted in an enhancement of the early transient rise in [Ca2+]i stimulated by PTH. PGF2 alpha was approximately 100 times more potent than PGE2. PGE2 itself was more potent than 6-keto-PGF1 alpha in enhancing PTH-stimulated rise in [Ca2+]i. Near-maximal augmentation was achieved at PGF2 alpha doses of 10 nM and PGE2 of 1 microM. The degree of augmentation in [Ca2+]i by PGF2 alpha was independent of preincubation time. PGF2 alpha pretreatment did not alter the EC50 for the PTH-induced [Ca2+]i increase but only the extent of rise in [Ca2+]i at each dose of PTH. The augmented increase in [Ca2+]i was mostly due to enhanced PTH-mediated release of Ca2+ from intracellular stores. PGF2 alpha did not stimulate an increase in PTH receptor number as assessed by [125I]-PTH-related peptide binding. PG pretreatment partially reversed PTH inhibition of cell proliferation, suggesting that an increase in [Ca2+]i may play a role in tempering the anti-proliferative effect of PTH mediated by cAMP. These studies suggest a new mode by which PGs can affect cellular activity.