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Biomedical subjects

M A Ayoub

Publications and source records attributed to M A Ayoub.

10 recordsLinked to original sources
PubMed1997

Presence of RNase A causes aberrant DNA band shifts.

RNase A, which is routinely added during DNA purification to reduce contaminating RNA, causes shifting of DNA bands in agarose gels. DNA band sizes on agarose gels increase as much as 10%-20% when RNase A is present. The low concentrations of RNase A typically used to purify DNA cause shifting of select DNA bands, in contrast to higher concentrations of RNase A where all band are shifted and smeared. The binding of RNase A to the DNA is specific and the degree of the shift varies; not all DNA bands are retarded, and the deviation is more pronounced in certain buffers. Other proteins, such as bovine serum albumin or proteinase K, do not induce DNA band shift, suggesting the interaction is specific. The binding of RNase A to DNA is reversible. The formation of RNase:DNA complexes may affect experiments involving DNA:protein interactions such as gel shift, footprinting and filter binding assays. Researchers performing DNA characterization from miniprep protocols should be aware that RNase may cause the apparent sizes of DNA fragments to be altered and obscure the presence of very small cloned fragments.

Buffers↗
PubMed1993

Inhibitory effect of bovine follicular fluid on in vitro maturation of bovine oocytes.

To investigate its inhibitory properties, bovine follicular fluid was collected at different stages of the estrous cycle from small, medium, and large follicles. Follicular fluids were incubated with germinal vesicle stage, bovine oocytes aspirated from small follicles. Nuclear maturation was determined at 24 h. Bovine follicular fluid inhibited the spontaneous maturation of bovine oocytes. The inhibition was reversed when follicular fluid was removed from oocyte cultures by 24 h. Follicular fluid varied in its ability to inhibit germinal vesicle breakdown according to follicle size and estrual stage. Follicular fluid from both small and medium follicles at estrus had the greatest ability to prevent germinal vesicle breakdown but became less potent postestrus. Follicular fluid from large follicles at estrus had less ability to inhibit germinal vesicle breakdown than fluid from small and medium follicles. Strong germinal vesicle breakdown inhibiting activity was present in large, probably atretic follicles at late metestrus, early diestrus, and mid diestrus. However, follicular fluid from large follicles had less germinal vesicle breakdown inhibiting activity at proestrus than follicular fluid from large follicles at late metestrus, early diestrus, and mid diestrus. This proestrual activity was similar to that in Graafian follicles at estrus.

Animals↗
PubMed1993

Parthenogenetic activation of in vitro matured bovine oocytes.

Bovine germinal vesicle oocytes were collected from 2- to 4-mm follicles. Oocytes were matured in medium 199 containing 10% bovine follicular fluid, FSH, and estradiol. Matured oocytes were cocultured for 2 to 24 h with dead bovine sperm in either Tyrode's medium without albumin or with 40% follicular fluid. After removal of sperm, oocytes were cultured an additional 48 to 72 h in synthetic oviduct fluid or medium 199 containing 10% follicular fluid without hormones. Oocyte activation rates (pronucleus to 8 cells), after exposure to dead sperm for 2, 4, 6, 12, or 24 h, in protein-free Tyrode's medium before embryo culture in synthetic oviductal fluid were 11, 17, 41, and 41%. Activation rates were decreased to 3, 9, 8, 27, and 34% for these same times by the addition of estrual follicular fluid to the protein-free Tyrode's medium. Substitution of bovine serum albumin for follicular fluid in the Tyrode's medium resulted in 47% oocyte activation. Activation depended on time and composition of media, occurred with high frequency with matured bovine oocytes under common in vitro culture conditions, and decreased in the presence of bovine follicular fluid. Therefore, because cleavage is not a sufficient measure of embryo quality, parthenogenetic controls must be run.

Animals↗
PubMed1990

Ergonomic deficiencies: I. Pain at work.

This is Part I of a three-part series that examines various aspects of ergonomic deficiencies at work. This paper deals with pain at work and the association between such pain or discomfort and a poorly designed workplace or poorly structured job. Neglect of ergonomic principles brings inefficiency and pain to the workplace. An ergonomically deficient workplace may not cause immediate pain, because the human body has a great capacity for adapting to a poorly designed workplace or structured job. However, in time, the compounding effect of job and/or workplace deficiencies will surpass the body's coping mechanisms, causing the inevitable: physical symptoms, emotional stress, low productivity, and poor quality of work.

Ergonomics↗
PubMed1990

Ergonomic deficiencies: III. Root causes and their correction.

This is Part III of a three-part series that examines various aspects of ergonomic deficiencies at work. Part I examined pain at work and the association between such pain or discomfort and a poorly designed workplace or poorly structured job. Part II considered causes of ergonomic deficiencies and their identification and assessment through the use of checklists. Part III demonstrates that treating the symptoms or apparent proximate causes does not assure correction of the root causes, and suggests strategies for correcting ergonomic deficiencies.

Environment Design↗
PubMed1990

Ergonomic deficiencies: II. Probable causes.

This is Part II of a three-part series that examines various aspects of ergonomic deficiencies at work. Part I examined pain at work and the association between such pain or discomfort and a poorly designed workplace or poorly structured job. Part II considers causes of ergonomic deficiencies and their identification and assessment through the use of checklists. Part III demonstrates that treating the symptoms or apparent proximate causes does not assure correction of the root causes, and suggests strategies for correcting ergonomic deficiencies.

Causality↗
PubMed1982

Control of manual lifting hazards: II. Job redesign.

Job content and workplace components can be altered to assure that lifting stresses remain within the acceptable limits defined for the industrial population-at-large. The plan for redesign advocates (1) maintaining the weight handled within the recommended limits; (2) modifying the workplace to enhance postural stability and to avoid handling weights and excessive physical loading; and (3) increasing available job time by reducing frequency of lifts and/or introducing appropriate rest periods. Limits recommended by the National Institute for Occupational Safety and Health on acceptable loads are reviewed.

Accidents, Occupational↗
PubMed1982

Control of manual lifting hazards: III. Preemployment screening.

In the control of manual lifting hazards an alternative to job redesign is preemployment screening and selection. With a screening procedure, lifting stresses can be controlled by effecting a match between job demands and human work capacity. This is predicated on the principle that jobs cannot be redesigned or changed to lower their demands. Accordingly, the hazard control strategy becomes one of selecting only those individuals with the capacity to perform the given job without excessive risk. An integrative screening program suited for physically demanding jobs is presented. Prerequisites for implementation of the program include (1) step testing at submaximal levels; (2) strength testing using three standard postures (arms, back and legs); and (3) determination of job demands expressed in terms of work output and strength requirements. The criteria for screening are based on the level of utilization of each of the principal determinants of human work capacity (energy expenditure, heart rate, and strength capability).

Biomechanical Phenomena↗