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Biomedical subjects

J B Myers

Publications and source records attributed to J B Myers.

At least 19 recordsLinked to original sources
PubMed1997

The laboratory diagnosis of cytomegalovirus infections.

Rapid and accurate diagnosis of cytomegalovirus (CMV) infection is imperative with the advent of effective antiviral therapy (gangiclovir, foscarnet, CMV hyperimmune globin). Applications of conventional cell culture (CC), shell vial assay (SV), serological testing, antigenemia assay (AG) as well as molecular methods [polymerase chain reaction (PCR), branch DNA (b-DNA) and hybrid capture (HC)] to various patient populations and specimen types are discussed. A three year study of 670 specimens [354 urines, 205 peripheral blood leukocytes (PBLs), 56 upper respiratory and 55 tissues] compared CMV CC and SV isolation rates. Of the total, 124 (18.5%) were positive by either or both techniques. For each specimen type the number of positives detected by SV was greater than CC (urine 28 vs 15, PBLs, 12 vs 2). However, of 124 positives, 21 were solely CC positive. A comparison of SV to AG in 230 PBLs yielded a sensitivity of 100% and specificity of 68.3%. The low specificity when compared to SV may be due to the increased sensitivity of AG. Fifty-nine PBLs were examined for differing immunostaining techniques [immunoperoxidase (IP) vs Immunofluorescence (IF)]. IF stained PBLs showed an increased number of positive cells per preparation and greater stain intensity for ease of interpretation.

Cytomegalovirus↗
PubMed1995

Pyoderma gangrenosum and cranial osteolysis: case report and review of the paediatric literature.

Pyoderma gangrenosum is a poorly understood, ulcerating cutaneous disorder which is rarely seen in the paediatric age-group. We report a 3-year-old boy who developed an ulcer over the left frontoparietal scalp at the age of 1 year. A 9-cm area of underlying cranial bone was destroyed. The appearance on radiographs and CT scan was suggestive of eosinophilic granuloma, osteomyelitis, or other destructive processes. Biopsies of the scalp lesion and calvaria showed granulation tissue and degenerating bone. After the biopsies the scalp lesion increased in size, and wound dehiscence occurred. Ulceration developed at the site of a PPD skin test, which on biopsy was consistent with the diagnosis of pyoderma gangrenosum. Pyoderma gangrenosum should be added to the differential diagnosis of cutaneous disorders which can result in osteolytic/osteonecrotic defects.

Humans↗
PubMed1994

Biopty gun testis needle biopsy: a preliminary clinical experience.

OBJECTIVE: To assess the reliability, safety and patient satisfaction of transcutaneous Biopty (Bard Urological, Covington, GA, USA) gun testis biopsies. PATIENTS AND METHODS: Nineteen young men who were referred for evaluation of azoospermia were included in the study. The procedure was performed in an outpatient setting, under local anaesthesia and without sedation. Two passes of the Biopty gun spring-loaded needle were performed unilaterally in each patient. RESULTS: An average of 38.9 seminiferous tubules were evaluable per patient. The procedure was extremely well-tolerated by all patients and most felt that the procedure was no more distressing than simple phlebotomy. CONCLUSION: Transcutaneous testis needle biopsy performed with the Biopty gun is safe, rapid and cost-effective. This technique may represent a viable alternative to the open method of testis biopsy.

Adult↗
PubMed1990

Phorbol ester-stimulated human neutrophil membrane depolarization is dependent on Ca2(+)-regulated Cl- efflux.

The ionic basis of phorbol 12-myristate 13-acetate (PMA)-stimulated membrane depolarization in the human neutrophil has not previously been established. Alterations in cation permeability are probably not directly responsible for the depolarization response, since the rate or Rb+ influx or efflux is unchanged upon PMA stimulation, and although Na+ fluxes are increased, depolarization is not changed by either the addition of ouabain or reduction of extracellular Na+ from 140 to 0 meq. Furthermore, the enhanced Na+ influx in stimulated cells is blocked by amiloride at 10(-3) M, but not by 10(-5) M, suggesting Na+ influx proceeds through the electroneutral Na(+)-H+ antiporter and is therefore not responsible for depolarization. Upon stimulation, Cl- content of PMA-stimulated neutrophils decreases without change in Na+ or K+ content, as determined by electron probe analysis. In addition, acute reduction in extracellular Cl- enhances the rate and extent of depolarization induced by PMA. This change in intracellular Cl- and effect of reduction in extracellular Cl- concentration on depolarization can best be accounted for by an enhanced efflux via an electrogenic mechanism. Thus enhanced conductive Cl- efflux can account for the observed depolarization. That Ca2+ regulates depolarization is evidenced by the dependence of depolarization on external Ca2+ (Cao2+). Depolarization is absent in Ca2(+)-depleted cells [internal Ca2+ (Cai2+) less than 15 nM] and is restored with titration of extracellular Ca2+, exhibiting a 50% effective dose (ED50) of 100 mM. Thus PMA-initiated depolarization is regulated by Ca2+, either from intra- or extracellular sources, but the Ca2(+)-dependent activity responsible for control of Cl- efflux is as yet uncharacterized.

Calcium↗
PubMed1989

Priming of human neutrophils with N-formyl-methionyl-leucyl-phenylalanine by a calcium-independent, pertussis toxin-insensitive pathway.

Resting neutrophils may be "primed" to augmented effector function, eg, superoxide (O2-) production in the respiratory burst, upon a second stimulation with a variety of soluble agonists including formylated methionyl-leucyl-phenylalanine (FMLP) and phorbol myristate acetate (PMA). At priming concentrations of FMLP (5 x 10(-9) mol/L) that did not initiate O2- generation, two metabolic activities were noted: (1) approximately a threefold increase in the baseline intracellular calcium (Ca++i) level, that was not dependent on extracellular Ca++, and (2) a rapid rise in intracellular pH that was blocked by 5-(N,N-dimethyl) amiloride (DA), that had no effect on the Ca++i response to priming. Furthermore, there were no significant increases in inositol metabolites in cells primed and stimulated with FMLP compared with cells receiving the stimulating dose of FMLP alone and pretreatment with pertussis toxin (PT) (before the addition of the priming -5 x 10(-9) mol/L dose of FMLP), whereas abolishing the response to FMLP during the second stage of stimulation, had (1) no effect on FMLP-primed cells subsequently stimulated with PMA, and (2) only partially ablated the rise in Ca++i initiated with FMLP. That FMLP priming involved distinctive processes to those of the well characterized FMLP-coupled Ca++-dependent activation cascade was shown by the full priming effect attained in a Ca++-free buffer, which did not sustain an O2- response to a second-stage FMLP stimulation, but sustained a primed response to PMA. These data demonstrate that FMLP primes human neutrophils by a Ca++-independent and PT-insensitive pathway, offering a functional model for studying heterogeneous FMLP receptor-coupled reactions.

Calcium↗
PubMed1989

Reduced sodium chloride intake normalises blood pressure distribution.

The blood pressure distribution of 172 healthy normotensive subjects aged 3-77 years receiving diets containing different amounts of sodium are presented. On their usual intake of sodium (154 +/- 63 mmol Na+/day) and after two weeks on a high sodium intake (201 +/- 92 mmol Na+/day) supine systolic and supine diastolic blood pressure distribution were positively skewed to the right. After two weeks on a reduced sodium diet (77 +/- 37 mmol Na+/day) the blood pressure distribution was normal. An incremental effect of sodium on diastolic blood pressure occurred in 22% of the subjects. The fall in blood pressure on the reduced sodium diet in these 'sodium sensitive' subjects reduced the mean blood pressure level, which was associated with 'normalisation' of the blood pressure distribution.

Adolescent↗
PubMed1988

Effects of influenza A virus on human neutrophil calcium metabolism.

Bacterial superinfection in influenza A virus-related illness may in part be explained by virus-induced neutrophil dysfunction. We here provide evidence that this effect is related to abnormal calcium metabolism of virus-infected cells. Neutrophils exposed to influenza virus for 0.5 h at 37 degrees C showed depressed O2- generation and release of radiolabeled arachidonic acid upon stimulation with FMLP. The peak cytosolic Ca2+ level achieved by virus-infected neutrophils after FMLP stimulation was significantly depressed as is efflux of 45Ca2+. This deficient Ca2+ mobilization could not be attributed to alterations of inositol phosphate production or Ca2+ influx in response to FMLP, both of which were unaffected by prior virus infection. Given these findings, the immediate effects of influenza virus on neutrophil Ca2+ metabolism were examined. The virus itself caused a rise in cytosolic Ca2+ and an efflux of 45Ca2+ without any corresponding 45Ca2+ influx. Total cell Ca2+ however was not depleted as measured by atomic absorption. Influenza virus, therefore, causes neutrophil activation leading to significant perturbations in Ca2+ metabolism and later to impaired mobilization of Ca2+ stores. This system offers a model for phagocyte deactivation and an opportunity to define control mechanisms of signal transduction.

Arachidonic Acid↗
PubMed1987

'Sodium sensitivity' in man.

Increased cell membrane permeability to sodium is proposed as the initial event leading to high blood pressure in susceptible subjects when sodium intake is increased. All cells, including circulating cells, would be affected, but a key role for endothelial cells in the pathophysiology of the diastolic blood pressure elevation is proposed. Involvement of capillary endothelium could increase capillary permeability to proteins, and thereby would contribute to the altered fluid distribution on the high sodium diet which has been observed. If movement of fluid into the interstitium raised interstitial fluid pressure, venous capacitance would fall and right atrial pressure would rise. Several mechanisms would cause vascular smooth muscle tone to increase. Altered fluid distribution correlates with the rise in diastolic blood pressure from reduced sodium to high sodium diet, but arteriolar constriction would reduce capillary flow so altered fluid distribution occurs first. Arteriolar constriction could serve as a negative feedback to the raised atrial filling pressure by reducing raised capillary flow, which would decrease both altered fluid distribution and interstitial fluid pressure rise. Consequently, diastolic blood pressure would be chronically raised in 'sodium sensitive' subjects taking increased amounts of sodium in the diet. The relationship of the findings to "essential" hypertension and to premorbid cardiovascular sequelae, and the key role of capillary endothelium in the development of "essential" hypertension is discussed.

Adult↗
PubMed1984

Effect of alteration in sodium chloride intake on blood pressure of normotensive subjects.

Sodium intake was altered for 2-week periods in 201 volunteers with no history of hypertension. Systolic and diastolic blood pressure was higher with a high sodium intake (200 mmol) compared with the values for a reduced intake (70 mmol). The rise in supine systolic and diastolic blood pressure in subjects over 50 years was 15/8 mm Hg, which was larger than the increase of 2.5/2.3 mm Hg measured in younger people. In the younger age group blood pressure changed with diet in approximately 15%. Individuals with a family history of hypertension were more likely to have a rise in blood pressure when sodium intake was increased. Patients were subdivided into responders and nonresponders according to the change in blood pressure with a different sodium intake. Creatinine clearance with a reduced sodium intake was lower in the responders compared with the values for the nonresponders. In the responders creatinine clearance increased as sodium intake increased and with the high sodium intake was not different in the two groups. In subjects who had a rise in blood pressure with increasing sodium load, plasma volume fell, while it rose in the nonresponders. These studies demonstrate that increased sodium intake causes blood pressure to rise in normotensive individuals. Renal function is less in those who have a rise in blood pressure when extra sodium is consumed. Changes in plasma volume indicate that the link between sodium intake and hypertension does not involve plasma volume.

Adult↗
PubMed1984

Effect of changes in sodium intake on cell transport parameters.

Changing sodium intake from 70-200 mmol/day elevates blood pressure in normotensive volunteers by 6/4 mmHg. Older people, people with reduced renal function on a low sodium diet and people with a family history of hypertension are more likely to show this effect. The rise in blood pressure was associated with a fall in plasma volume suggesting that plasma volume changes do not initiate hypertension. In normotensive individuals the most common abnormality in membrane sodium transport induced by an extra sodium load was an increased permeability of the red cell to sodium. Some normotensive individuals also had an increase in the level of a plasma inhibitor that inhibited Na-K ATPase. These individuals also appeared to have a rise in blood pressure. Sodium intake and blood pressure are related. The relationship differs in different people and is probably controlled by the genetically inherited capacity of systems involved in membrane sodium transport.

Biological Transport↗
PubMed1982

Biochemical response to change in the environment and the nature of "essential" hypertension.

The abnormality of Na+, K+-cotransport detected in erythrocytes of patients with "essential" hypertension, appears to be an inherited biochemical disorder characteristic of the disease. This explains several features of "essential" hypertension. However, characteristics of the kinetics of this Na+ transport system are similar to characteristics of enzymes in halophilic organisms, which live in a high saline environment. Cell Na+ is increased in patients with "essential" hypertension and in halophilic organisms. This suggests that the enzyme characteristics are response mechanisms to maintain extracellular Na+ concentration within an optimal range. Based on this view two assumptions of biochemical response have been put forward which form the biochemical basis of a general biological theory. The implications of this for understanding the nature of "essential" hypertension are discussed. To explain the nature of the inheritance of the Na+, K+-cotransport defect in erythrocytes of patients with "essential" hypertension, a theory of acquired genetic transmission called "improvisation" theory is proposed. Improvisation may be the mechanism whereby new gene formation occurs, and be the mechanism for evolution of species if successful reproduction of offspring is allowed to continue.

Adaptation, Physiological↗
PubMed1981

Hypertension treated by sodium restriction.

Forty-eight people with hypertension entered a controlled study to observe the effect of sodium (NaCl) restriction on blood pressure. In people with mild hypertension (diastolic blood pressure 90-105 mmHg), sodium restriction reduced blood pressure compared with a control group and 75% obtained a diastolic blood pressure of less than 90 mmHg. In people with more severe hypertension (diastolic blood pressure 4105 mmHg), sodium restriction achieved the same level of control as chlorothiazide (500 mg a day). Restriction of sodium intake is an effective method of reducing blood pressure and should be the first form of therapy in people with mild hypertension.

Adult↗
PubMed1981

Self-poisoning with drugs: a 3 1/2-year study in Newcastle, NSW.

This is a review of 963 cases of self-poisoning with drugs (8.5% of all medical emergencies) treated in the three major Newcastle hospitals over a 3 1/2-year period. The number of patients admitted rose from 243 (July 1976 to June 1977) to 326 (January to December, 1979)-an overall increase of 34%. The most common drugs used were benzodiazepines (34.9% of cases); barbiturates (11.2%); tricyclic depressants (9.2%); paracetamol (8.1%) and phenothiazines (6.2%). In four of 134 cases involving barbiturates, phenobarbitone had been used as part of an anticonvulsant regimen. Six patients died in hospital and 31 who committed suicide with drugs were not admitted to the hospital, but were investigated by the Regional Forensic Pathologist.

Acetaminophen↗