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Biomedical subjects

M K Hassan

Publications and source records attributed to M K Hassan.

8 recordsLinked to original sources
PubMed2001

Transition from random to ordered fractals in fragmentation of particles in an open system.

We consider the fragmentation process with mass loss and discuss self-similar properties of the arising structure both in time and space, focusing on dimensional analysis. This exhibits a spectrum of mass exponents theta, whose exact numerical values are given for which x(-theta) or t(theta z) has the dimension of particle size distribution function psi(x,t), where z is the kinetic exponent. We obtained conditions for which the scaling and fragmentation process altogether breaks down, and we give an explicit scaling solution for a special case. Finally, we identify a new class of fractals ranging from random to nonrandom and show that the fractal dimension increases with increasing order and a transition to a strictly self-similar pattern occurs when randomness completely ceases.

Journal Article↗
PubMed2001

Risk factors for severe pneumonia in children in Basrah.

A case-control study was undertaken in Basrah Maternity and Children Hospital, Iraq. We studied 148 children who were admitted to hospital with severe pneumonia according to the World Health Organization (WHO) criteria and the controls were 250 children attending the out-patient department for non-severe respiratory infections. Significant risk factors were younger age (2-6 months), low parental education, smoking at home, prematurity, weaning from breast milk at < 6 months, a negative history of diphtheria, pertussis and tetanus vaccination, anaemia and malnutrition.

Case-Control Studies↗
PubMed1995

The development of an eluted stain bioassay (ESTA) for human growth hormone.

The basic characteristics of MTT-formazan production by both quiescent Nb2 cells and those activated by fetal calf serum or human growth hormone (hGH) are described. These characteristics are exploited for the development of an MTT-ESTA bioassay for purified preparations of lactogens such as growth hormone. The resulting in vitro bioassay is sensitive and precise, with a detection limit of about 0.05 mU hGH/l (19 ng/l) and a within-assay imprecision of 2.5% in the presence of 0.3 mU hGH/l (114 ng/l). When utilizing quiescent Nb2 cells for bioassays, large magnitudes of response are observed. The major component of the response is clearly derived from metabolic activation of the cells, rather than increased cell proliferation. The response was abolished by anti-human growth hormone. Delayed addition of the latter demonstrated that the presence of the hormone is required for the entire 96 h of the recommended bioassay incubation period to obtain the maximum response. At high doses, the dose-response relationship reaches a prolonged plateau which covers 4 orders of magnitude of incremental hormone concentrations. A decline in response is observed at the highest dose tested, 10(6) mU hGH/l (385 mg/l). This auto-inhibition is consistent with recent reports of a reduction in response due to stoichiometric blockade of sequential receptor dimerisation which is crucial for activation of both somatogenic and lactogenic receptors by hGH.

Animals↗
PubMedDate not supplied

Influence of the host system on the pathogenicity, immunogenicity, and antigenicity of infectious bursal disease virus.

The effect of the host system on the pathogenicity, immunogenicity, and antigenicity of infectious bursal disease virus (IBDV) was investigated. One classic (SAL) and one variant strain (IN) of IBDV were passaged separately six times in three host systems, namely BGM-70 continuous cell line, primary chicken embryo fibroblast (CEF) cells, or embryonating chicken eggs (embryos) or one time in the bursa of Fabricius (BF) of specific-pathogen-free (SPF) chickens. Passage in BGM-70 cells or CEF cells resulted in loss of pathogenicity, but viruses passaged in embryos or BF maintained their pathogenicity. For the immunogenicity study, the viruses described above were used to prepare live and inactivated vaccines, containing 10(3) mean embryo infectious doses (EID50s) and 10(5) EID50s respectively. These vaccines induced different levels of protection. It was concluded that the antigen titration methodology employing embryonating chicken eggs was not suitable for titration of viruses propagated in other host systems because of varying degrees of adaptation and/or pathogenicity of the viruses resulting in variability in antigen mass of the tested vaccines. To test this assumption, an antigen-capture enzyme-linked immunosorbent assay was used as a titration system to compare the antigenicity of viruses propagated in BGM-70 cells or BF. Preparations containing similar antigen masses were inactivated then inoculated into two age groups of SPF chickens and antibody titers were monitored. During the experimental period, the geometric mean virus-neutralizing (VN) antibody titers of the vaccinated groups did not differ significantly (P > 0.05).

Animals↗
PubMedDate not supplied

Comparison between antigen-capture ELISA and conventional methods used for titration of infectious bursal disease virus.

Two antigen-capture enzyme-linked immunosorbent assays (polyclonal and monoclonal AC-ELISAs) were developed and evaluated for titration of infectious bursal disease viruses (IBDVs) propagated in different host systems, namely BGM-70 continuous cell line, primary chicken embryo fibroblast cells, and chicken bursa of Fabricius. The polyclonal system was more sensitive (P < 0.05) than the monoclonal system but both were specific as indicated by the negative results obtained with three non-IBDVs. The results revealed that the conventional systems used for titration of IBDVs (cell cultures and embryonating chicken eggs) were more sensitive than the polyclonal AC-ELISA.

Animals↗
PubMedDate not supplied

Pathogenicity, attenuation, and immunogenicity of infectious bursal disease virus.

An investigation was conducted in specific-pathogen-free chickens on the pathogenicity of bursa-derived and tissue culture-attenuated classic (STC) and variant (IN) serotype 1 strains of infectious bursal disease virus. The IN bursa-derived virus caused bursal inflammation, necrosis, and atrophy earlier than the bursa-derived STC virus. Both viruses lost their pathogenicity after four passages in BGM-70 cells. A statistically significant level (P < 0.05) of protection was observed in SPF chickens vaccinated with the attenuated IN virus used as a live or inactivated vaccine followed by homologous (IN) and heterologous (STC) challenge with bursa-derived viruses.

Animals↗
PubMedDate not supplied

Antigenicity, pathogenicity, and immunogenicity of small and large plaque infectious bursal disease virus clones.

A serotype 1 variant strain of infectious bursal disease virus designated IN was passaged 40 times in BGM-70 cell line. A small plaque (SP) clone and a large plaque (LP) clone were then isolated and plaque purified four times. The SP and LP viruses formed circular plaques about 0.5 mm and 6.0 mm in diameter, respectively. Both clones lost their pathogenicity for specific-pathogen-free (SPF) chickens and did not elicit significant levels of virus-neutralizing antibody titers. However, the SP and LP clones maintained their immunogenicity when used as inactivated vaccines in SPF chickens. The restriction enzyme profiles of both clones were similar. Back passage of the SP and LP clones in SPF chickens resulted in loss of their phenotypic characteristics.

Animals↗