PubMed Health⌕ Search

Biomedical subjects

H Moe

Publications and source records attributed to H Moe.

At least 19 recordsLinked to original sources
PubMed1993

Prevalence of sexually transmitted diseases among female drug abusers in Malaysia.

The prevalence of sexually transmitted diseases (STD) among female drug abusers was determined by screening 130 new inmates of a rehabilitation centre. The majority of the subjects (77.7%) were self-confessed sex workers. A high prevalence of syphilis (50.8%), hepatitis B (52.2%), moniliasis (23.8%) and trichomoniasis (19.2%) were noted. Gonorrhoea vaginitis was seen in 8.5%, which was low compared to previous studies. Six subjects were seropositive for human immunodeficiency virus (HIV), with 5 of them admitting to needle sharing and working as prostitutes. More than half of them harboured 2 or more STD. A rich reservoir of STD was seen among the drug abusers. With more evidence now available concerning the ease of HIV transmission associated with ulcerative STD, a stage could be set for greater heterosexual HIV transmission. As part of the rehabilitation process, female drug abusers need a thorough screening for STD followed by aggressive treatment regimens.

Adolescent↗
PubMed1991

Fireworks related injuries during Hari Raya festival in Hospital Universiti Sains Malaysia--1986 to 1990.

A total of 38 cases of fireworks related injuries from Hospital USM over a 5-year period from 1986 to 1990 during Hari Raya festival were analysed. The majority (68.5%) of the patients were teenagers, between 10 to 19 years of age. All the cases were Malays and most of the accidents occurred before the Hari Raya Idilfitri festive seasons. Fourteen cases were caused by self-made fireworks and another 16 cases were due to modified fire-works. Twenty-four cases suffered permanent disabilities mostly finger amputations. Such injuries could be prevented by law enforcement coupled with public health education to modify social behaviour especially when the ban against the use of fireworks is lifted on religious grounds.

Accident Prevention↗
PubMed1985

Progressive involution and physiological death of smooth muscle cells of rat incisal arterioles.

The sequential morphology of vascular smooth muscle cell involution and physiological cell death was studied by electron microscopy on rat incisors. Concurrently with changes in the pulp of the continuously growing incisor, its arterioles pass through a cycle of growth, remodeling, regression and decay. During the cycle, smooth muscle cells of the arterioles were observed to involute by segregation of cytoplasmic components, formation of autophagic and digestive vacuoles and shedding of cell fragments. Phagocytic vacuoles were found in neighbouring muscle cells and in adventitious macrophages. Concomitant with the involution in some cells, physiological death was observed among other smooth muscle cells. This appears as an apoptosis with sequential transformations of polyribosomes into monoribosomes, nuclear and cytoplasmic condensation, and finally fragmentation followed by phagocytosis mainly by adventitious macrophages. Knowledge of the features of physiological involution and cell death of the vascular smooth muscle cells may be of importance not only in studies of functional remodeling and adaption, but also in the interpretation of vascular lesions.

Acid Phosphatase↗
PubMed1981

Adaptation of arterioles to moving capillaries.

The capillary network of the enamel organ of the continuously growing mandibular incisor of the rat is supplied by a series of arteries which, after penetrating the bone, are disposed in a row in the periodontium along the tooth and linked together by anastomoses. The branches from these arteries are subjected to adaptive changes consistent with a forward movement of the capillaries in relation to the arteries. The mechanism which renders this movement possible appears to be the following: Each artery in the row supplies a section of the passing plexus by coupling and uncoupling short-lived arterioles, which go through a cycle of proliferation, elongation and degeneration. Proliferation takes place at the posterior end of the section, where new arterioles replace discarded arterioles from the preceding artery. By growing in length, the arterioles keep pace with the migrating capillary network. When the capillaries are within reach of the next artery, the arterioles disconnect. Thereafter they become obliterated and die in the intermediate zone of the periodontium, to which they have been gradually displaced by proliferation of the inner-tooth-related layer of the periodontal connective tissue.

Adaptation, Physiological↗
PubMed1979

Physiological cell death of secretory ameloblasts in the rat incisor.

The migration of the ameloblasts in the continuously erupting incisors of the rat is accompanied by cell loss. Ameloblasts degenerate near the mesial and lateral cemento-enamel junctions in the secretory zone and in the middle two thirds of the region of postsecretory transition, degeneration being most marked where these areas merge. These findings support the hypothesis that the prism decussation in the enamel results from alternating transverse rows of secretory ameloblasts sliding past each other whilst elaborating their rods. The distribution of the degenerating cells suggests, however, that the sliding cell rows are not exactly transverse but arcuate, with the opening facing incisally. The progress of structural alterations of the nuclei in the degenerating ameloblasts appears to follow the pattern earlier described in vinblastine-damaged ameloblasts.

Ameloblasts↗
PubMed1979

Structural alterations in proliferating, remodeling, and regressing tooth pulp arterioles.

In the continuously growing upper incisor of 100 g rats about 25 arterioles arise from an artery outside the tooth and pass through the apical foramen to run parallel to one another in the central part of the pulp, each supplying a well-defined sector of the migrating odontoblast layer. The arterioles pass through a cycle of proliferation, growth, remodeling, regression and decay, phase displaced in relation to each other. Proliferative and degenerative processes occur in the arteriole wall throughout the cycle, but vary considerably in intensity at different phases. Proliferation takes place by mitosis in the endothelium and the innermost smooth muscle cells. The degenerative process consists of reduction in size of smooth muscle cells by partial autodigestion and by cell death. When the odontoblasts reach the incisal extremity of the tooth, they die, and the associated regressed arteriole disappears. The system of pulpal arterioles has remarkable spatio-temporal features and each of its vessels appears to be in a state of sensitive structural equilibrium.

Animals↗
PubMed1979

Sequential ultrastructural changes in vinblastine-induced cell death of secretory ameloblasts of rat incisors in vivo.

Secretory ameloblasts in the continuously growing incisors of the rat were used to study the sequential changes in a mature cell type degenerating after administration of vinblastine at a dosage of 2 mg per kg body weight. In less than half an hour nearly all microtubules vanished. This was succeeded by progressive displacement of the nuclei and disorganization of the cytoplasmic structure. After 1 to 3 hours attached and free polyribosomes were converted into monoribosomes. All these cytoplasmic changes were seen in viable as well as in necrotic cell. Between 5 and 61/2 hours after application of the drug degeneration of nuclei began; these changes from the outset indicated that a particular ameloblast had been drawn into a sequence of events which would ultimately lead to its death. The progressive alterations of the nucleus and cytoplasm of the degenerating cells and the concurrent fragmentation and elimination of the fragments are described.

Ameloblasts↗
PubMed1977

On the effect of vinblastine on ameloblasts of rat incisors in vivo. 2. Protracted effect on secretory ameloblasts. A light microscopical study.

The effects of vinblastine sulphate at a dosage of 0.2 mg per 100 g body weight on the secretory ameloblasts of rat incisors were studied 3, 6 and 24 hours and 3 and 7 days after administration of the drug. The vinblastine affected the secretion profoundly, caused a reduction in size of the cells and death of many ameloblasts. Most of the surviving ameloblasts restored initially-induced loss of polarity. Many also resumed secretion and deposition of enamel matrix. The Tomes' processess were extremely sensitive to vinblastine and all matrix deposited after administration of the drug appeared abnormal in structure. Ameloblasts not resuming secretory activity were less than half the size (height) of normal cells. In some areas all the ameloblasts were destroyed with the exception of a varying number of surviving ameloblasts parts consisting only of a nucleus and a small amount of cytoplasm. The ameloblasts which had re-established secretory activity, and most of the ameloblasts which had not, retained their ability to transform into transporting ameloblasts. Large amounts of ameloblast debris present 3 and 6 hours after administration of the vinblastine were effectively engulfed and digested by the cells of the striatum intermedium within 24 hours.

Ameloblasts↗
PubMed1977

Light microscopical and ultrastructural observations on the effect of vinblastine on ameloblasts of rat incisors in vivo. I. Short-term effect on secretory ameloblasts.

The highly polarized secretory ameloblasts in the incisors of rats fixed by perfusion with glutaraldehyde two or three hours after intravenous administration of vinblastine sulfate at a dosage of 5 mg per 100 g body weight were studied in the light microscope and the electron microscope. The following effects were observed: 1. All cytoplasmic microtubules in the ameloblasts had vanished. This was not accompanied by the appearance of paracrystals of microtubular protein or macrotubules. 2. The ameloblasts preserved their external features of polarized cells but lost their ability to maintain normal orderly segregation of the cell constituents; i.e. their normal internal compartmentalization and polarity had vanished. 3. The ameloblasts lost their capability of directional translocation of the secretory granules towards the cell apex. 4. Secretory granules already translocated to the cell apex regurgitated in the cell and a probably delayed discharge of secretory material had started in abnormal site at the surface. 5. The normal arrangement of ribosomes into polyribosomes on the membranes of the rough endoplasmic reticulum was no longer present; the ribosomes were apparently distributed at random. 6. New secretion was inhibited or brought to a standstill but secretory material already present in the Golgi complex appeared to be transported normally. 7. The centriole had started to develop into a cilium in many of the cells. 8. The number of autophagic vacuoles had increased.

Ameloblasts↗
PubMed1977

On the effect of vinblastine on ameloblasts of rat incisors in vivo. 3. Acute and protracted effect on differentiating ameloblasts. A light microscopical study.

The acute effect of vinblastine sulphate at a dosage of 0.2 mg per 100 g body weight on ameloblasts in the progress of differentiation in rat incisors, and the ability of these cells to develop into secretory ameloblasts after exposure to the drug, were studied under the light microscope. In the early stages of differentiation (exclusively dividing cells) no changes were seen. In more advanced stages of differentiation the cell apices were altered and the nuclei normally placed near the cell base were located at all levels in the ameloblast layer. These changes were reversible and the cells developed into secretory ameloblasts of normal appearance and function. Ameloblasts in the most advanced stage of differentiation in which secretion had begun were severely damaged, and the mature secretory ameloblast population derived from these cells was decimated and produced enamel matrix with abnormal structure. It is concluded that differentiating ameloblasts are relatively invulnerable to vinblastine, whereas in secretory ameloblasts the organelles directly engaged in the secretory processes are particularly exposed to damage from the drug.

Ameloblasts↗