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Biomedical subjects

M Richardson

Publications and source records attributed to M Richardson.

At least 217 records · Page 12Linked to original sources
PubMed1993

Virological investigations of specimens from buffaloes affected by buffalopox in Maharashtra State, India between 1985 and 1987.

Isolates of poxviruses were made from thirteen of eighteen specimens of scabs taken from pox lesions on buffaloes in five different districts of Maharashtra State, India, between December, 1985 and February, 1987. The biological characters of twelve of the isolates resembled those of the Hissar strain of buffalopox virus; the thirteenth isolate appeared to be vaccinia. The Hin dIII restriction profiles of DNA from all 13 isolates and from the Hissar strain were typical of those given by vaccinia strains. DNA from all twelve Maharashtra buffalopox (BPV) isolates gave identical profiles with each of three additional endonucleases; these viruses appear to be repeated isolations of a single strain of BPV. The DNA profile of this strain was not the same as that of the Hissar strain of BPV and both could readily be distinguished from each of the three strains of vaccinia virus which had been used in India. The thirteenth Maharashtra isolate was indistinguishable from vaccinia in its biological properties, but the restriction profile of its DNA differed from those of three vaccinia strains and the BPV isolates. These observations, made 6-8 years after cessation of smallpox vaccination indicate that BPV is an emerging enzootic virus and is a subspecies of vaccinia virus.

Animals↗
PubMed1993

Nutrition interventions for intensive therapy in the Diabetes Control and Complications Trial. The DCCT Research Group.

As part of an intensive treatment regimen that had as its goal achieving and maintaining blood glucose levels in the normal range in individuals with insulin-dependent diabetes mellitus, dietitians in the Diabetes Control and Complications Trial implemented varying nutrition intervention strategies to counsel patients to attain normoglycemia. Dietary management encompassed recommendations on altering insulin dosages for varying food intake. Nutrition intervention was tailored to best meet a participant's life-style, motivation, ability to grasp information, diet history, and specific intensive insulin therapy. Dietitians were integral participants in the team management of individuals in the intensive treatment group. Selected nutrition interventions--Healthy Food Choices, exchange systems, carbohydrate counting, and total available glucose--and behavior management approaches were coupled with intensive insulin therapy. Case presentations illustrate each nutrition intervention in the attainment of normoglycemia.

Adult↗
PubMed1993

Purification and amino acid sequences of six Tx3 type neurotoxins from the venom of the Brazilian 'armed' spider Phoneutria nigriventer (Keys).

Six neurotoxic peptides (Tx3-1 to Tx3-6) were purified from the venom of the spider Phoneutria nigriventer by a combination of gel filtration, reverse phase FPLC on PEP-RPC and PRO-RPC columns, reverse phase HPLC on Vydac C18, and ion exchange HPLC on cationic and anionic columns. These toxins caused different neurological symptoms in mice after intracerebroventricular injection. At dose levels of 5 micrograms/mouse, Tx3-3 and Tx3-4 caused rapid general flaccid paralysis followed by death in 10-30 min; Tx3-2 induced immediate clockwise gyration and flaccid paralysis after 6 hr; Tx3-1, Tx3-5 and Tx3-6 produced paralysis only in the posterior limbs and gradual decreases in movement and aggression during 24 hr. The mol. wt of these cystine-rich peptides were found to be in the range of 3500-8500 by mass spectroscopy and SDS-PAGE. The complete amino acid sequences of the neurotoxins Tx3-1 (40 residues), Tx3-2 (34 residues) and Tx3-6 (55 residues), and the N-terminal sequences of Tx3-3 (34 res.), Tx3-4 (40 res.) and Tx3-5 (36 res.) were established by direct automated Edman degradation, and manual DABITC/PITC microsequence analyses of peptides obtained from digests with various proteases. The structures of these Tx3 neurotoxins from Phoneutria nigriventer exhibited sequence similarities to one another and to the neurotoxins from the venoms of the spiders Hololena curta and Agelenopsis aperta, which were most evident in the location of the Cys residues.

Amino Acid Sequence↗
PubMed1993

Congenital cytomegalovirus infection and neonatal auditory screening.

Auditory screening of newborn infants has been recommended on the basis of the presence of risk criteria, including congenital infection. We assessed the ability of risk criteria-based neonatal auditory brain stem response to identify infants with hearing loss resulting from congenital cytomegalovirus (CMV) infection. Data from 6 1/2 years of risk criteria-based neonatal auditory screening were compared with the results of screening of all newborn infants for congenital CMV infection. Infants with congenital CMV infection received follow-up hearing evaluations. Congenital CMV infection was found in 167 (1.3%) of 12,371 infants; 134 had follow-up hearing evaluations, and 14 (10.4%) had confirmed sensorineural hearing loss. The rate of sensorineural hearing loss resulting from congenital CMV infection was 14 per 12,371 infants, of 1.1 per 1000 live births; the rate of bilateral loss > or = 50 dB was 0.6 per 1000. Although 2036 infants received auditory screening because of risk criteria, only 34 (20%) of 167 infants with congenital CMV infection were included. Only 2 (14%) of 14 children with sensorineural hearing loss caused by CMV were identified by risk criteria-based screening. We conclude that congenital CMV infection is an important cause of hearing impairment. Neonatal auditory screening based on the presence of risk criteria will fail to identify the majority of cases of sensorineural hearing loss caused by congenital CMV infection.

Cytomegalovirus Infections↗
PubMed1993

Variation in plasma platelet-activating factor degradation and serum lipids after acute myocardial infarction.

BACKGROUND: Platelet-activating factor is a biologically potent phospholipid that may mediate cell damage in patients with myocardial ischemia. In plasma, its inactivation to lyso-platelet-activating factor is catalyzed by a specific, lipoprotein-associated acetylhydrolase. Because lipoprotein levels decrease after myocardial infarction, a possible reduction was suspected to occur in plasma degradation of platelet-activating factor. METHODS: Degradation of platelet-activating factor was examined in an optimized assay of acetylhydrolase activity and in relation to the in vitro plasma half-life of platelet-activating factor. These, plasma lyso-platelet-activating factor and serum lipids, were measured in 12 men with acute myocardial infarction at presentation and at 2 and 7 days later. RESULTS: Acetylhydrolase activity was depressed at day 2 and at day 7. The corresponding increase in plasma half-life of platelet-activating factor was minimal and insignificant. A significant linear relation existed between the half-life of platelet-activating factor and the reciprocal of acetylhydrolase activity at each time of study, indicating a hyperbolic relation between the two. By day 2, total and low-density lipoprotein cholesterol had decreased but showed no further change by day 7; high-density lipoprotein cholesterol had not decreased at day 2 but was depressed by day 7. Plasma lyso-platelet-activating factor had decreased by day 2 and had returned to its initial level by day 7. CONCLUSIONS: Acute myocardial infarction is associated with depression of plasma acetylhydrolase activity, and because of the hyperbolic relation between the plasma enzyme activity and the half-life of platelet-activating factor, the latter shows negligible change. Hence, the mechanism for the inactivation of any platelet-activating factor that might be released as a consequence of tissue damage is preserved.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1993

Utilization of the mouse large intestine to select an Escherichia coli F-18 DNA sequence that enhances colonizing ability and stimulates synthesis of type 1 fimbriae.

Escherichia coli F-18, a normal human fecal isolate, is an excellent colonizer of the streptomycin-treated mouse large intestine. E. coli F-18 Col-, a derivative of E. coli F-18 which no longer makes the E. coli F-18 colicin, colonizes the large intestine as well as E. coli F-18 when fed to mice alone but is eliminated when fed together with E. coli F-18. Random sequences of E. coli F-18 DNA were cloned into pRLB2, a par-B-stabilized derivative of pHC79. The entire gene library was transformed into E. coli F-18 Col- and fed to streptomycin-treated mice. The mouse large intestine selected a predominant clone which contained a recombinant plasmid (pRLB7) that enhanced E. coli F-18 Col- colonizing ability 100-fold but did not stimulate colicin synthesis. Moreover, pRLB7 simultaneously improved the survival of E. coli F-18 Col- in stationary phase in vitro, utilizing nutrients derived from mouse cecal mucus, and stimulated synthesis of both type 1 fimbriae and three E. coli F-18 Col- outer membrane proteins (74, 71, and 69 kDa). The 6.5-kb E. coli F-18 DNA sequence in pRLB7 does not contain either the fim operon or pilG (hns), both known to be involved in type 1 fimbrial synthesis. The sequence encodes six proteins, all smaller than the three E. coli F-18 Col- outer membrane proteins whose synthesis it stimulates. Collectively, the results suggest that the cloned E. coli F-18 DNA sequence contains one or more regulators of E. coli F-18 Col- operons expressed in the mouse large intestine in vivo and in isolated mouse cecal mucus in vitro.

Animals↗
PubMed1993

Continued platelet interaction with de-endothelialized aortae associated with slower re-endothelialization and more extensive intimal hyperplasia in spontaneously diabetic BB Wistar rats.

Diabetic patients are at increased risk for atherosclerosis and its complications. Platelets contribute to atherosclerosis through effects of factors released from platelets which interact with injured vessels. Diabetic platelets are hypersensitive to agonists in vitro. If diabetic platelets interact more extensively with injured vessels, they could contribute to increased vascular disease in diabetic patients. We examined the effect of spontaneous diabetes in BB Wistar rats on platelet accumulation and turnover, endothelial regeneration and intimal thickening in rat aortae de-endothelialized with a balloon catheter. 51Cr-labelled platelets were injected before or at different times after injury, and platelet accumulation on the aortae was determined at various times after the injection. Platelets rapidly accumulate on the aortae 30 min after injury and the net accumulation is similar in control and diabetic rats. Platelets continue to interact to a similar extent with the aortae of control and diabetic rats up to 4 days after injury, but the extent of interaction is less than that observed initially after injury. After 4 days, aortae of control rats gradually lose their ability to attract new platelets; this phase is delayed in diabetic rats. When 51Cr-platelets are injected 6 days after injury more radioactivity accumulates in a 24-h period on aortae of diabetic (22,050 +/- 6290 plts/mm2) than of control rats (8030 +/- 670 plts/mm2, P < 0.05). Seven days after injury, the percentage of aortic re-endothelialization is less in diabetic (58.2 +/- 7.2) than in control rats (86.8 +/- 6.9, P < 0.01). By 28 days, re-endothelialization is complete in control and diabetic rats. The smooth-muscle-cell-rich neointima is thicker and more extensive in diabetic than in control rats 15 or 28 days after aortic injury. Diabetes in rats is associated with continued platelet interaction with de-endothelialized aortae, slower re-endothelialization, and the formation of a thicker and more extensive smooth-muscle-cell-rich neointima.

Animals↗