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1.
Egyptian Journal of Histology [The]. 2014; 37 (3): 526-536
in English | IMEMR | ID: emr-160229

ABSTRACT

Cigarette smoking is one of the major problems affecting the health of humans. Many studies have been conducted on different organs of the body, but only a few have been conducted on the effect of cigarette smoking on bone. Vitamin E is a potent antioxidant supplement that might alleviate these hazardous effects on bone. The aim of our study was to evaluate the effect of nicotine on bone and whether the addition of vitamin E could protect the bone against nicotine-induced effects. Forty-five animals were used and divided into three groups comprising 15 animals each. Group I served as the control group. Animals in group II received nicotine. Animals in group III received nicotine in addition to vitamin E. At the end of the experiment the animals were sacrificed and the femur bone specimens were dissected and processed. The specimens were subjected to histological study: H and E and scanning electron microscopy. Evaluation of bone mineral density using energy dispersive X-ray was also carried out. Statistical analysis was carried out for all data recorded. Animals of group II showed thinning out of compact bone and trabeculae of cancellous bone of the proximal end of the femur. An increase in adipocytes in adjacent bone marrow was also detected. Cracking and microfracture of bone were apparent, as well as irregular endosteal pores. There was decrease in calcium content in the bone. Group III showed improvement in the morphology of bone and mineral content. Statistical analysis confirmed these results. We concluded that nicotine has hazardous effects on bone, and vitamin E has a protective role against nicotine


Subject(s)
Male , Animals, Laboratory , Protective Agents , Vitamin E , Bone and Bones/ultrastructure , Microscopy, Polarization/statistics & numerical data , Microscopy, Electron, Scanning/statistics & numerical data , Spectrometry, X-Ray Emission/statistics & numerical data , Rats
2.
Egyptian Journal of Histology [The]. 2012; 35 (1): 87-94
in English | IMEMR | ID: emr-126546

ABSTRACT

Smoking is associated with many dermatological conditions, including poor wound healing and premature skin aging. Nigella sativa, commonly known as black seed or black cumin, is used in folk herbal medicine all over the world for the treatment and prevention of a number of diseases. the aim of the work is to investigate the effect of smoking on the histological structure of the skin and to evaluate the possible protective role of the nigella sativa oil [NSO]. Twenty adult male albino rats were divided into four equal groups: group I [the control group] was placed 10 min twice daily for 4 weeks in a chamber without cigarette smoke exposure and was given a single dose of saline, 10ml/kg BW [body weight] orally and daily, group II [the NSO group] was given a single dose of NSO, 10ml/kg BW orally and daily, group III [the passive smoking group] was exposed to both side stream and main stream smoke for 10min twice daily for 4 weeks, and group IV [the protected group [was exposed to both side stream and main stream smoke for 10min twice daily for 4 weeks simultaneously with a single dose of NSO, 10ml/kg BW orally and daily. Exposure of male albino rats to cigarette smoke for 4 weeks produced some histological changes in the skin in the form of a significant decrease in the thickness of the epidermis and flattening of the epidermal-dermal junction. There was also a significant decrease in the collagen fibers in the dermis and an apparent decrease in the cytokeratin intermediate filaments in the keratinocytes, whereas the histological structure of the skin in the animals that received black seeds oil concomitant with smoke exposure [group IV] was almost similar to that of the control. It was concluded that exposure to cigarette smoke produced some histological changes in the skin similar to that occurring in old age, and administration of black seed oil could protect against these changes in adult male albino rats


Subject(s)
Male , Animals, Laboratory , Skin/pathology , Histology , Immunohistochemistry , Protective Agents , Nigella sativa , Plant Oils , Treatment Outcome , Rats , Male
3.
Egyptian Journal of Histology [The]. 2011; 34 (3): 538-545
in English | IMEMR | ID: emr-135760

ABSTRACT

Today, about half of the world's population, even at a very young age, owns microwaveproducing mobile phones. As mobile phones are held in close proximity to the head, the microwaves emitted may exert many effects on the brain. This study aimed to evaluate the effects of long-term exposure to mobile phone emissions on the thalamic neurons and the integrity of its blood barrier. This study also aimed to investigate whether ascorbic acid could ameliorate microwave-induced thalamic changes. Forty adult male albino rats were used; they were divided into four equal groups. Group I served as a control group. In group II, rats were exposed to 0.043-0.135 W/kg for 42 days [4 h/day in the light]. The microwave radiation was produced by a mobile test phone [model NOKIA 3110]. Rats of group III were subjected to mobile waves as in group II and they concomitantly received oral ascorbic acid at a dose of 250 mg/kg/day. Group IV received ascorbic acid only. The thalamic neurons of wave-exposed animals showed significant morphological necrotic changes. Some appeared markedly vacuolated ; others were irregular in shape, with densely stained nuclei. Ultrastructurally, the cytoplasm of some neurons showed prominent cytoplasmic vacuolization. A significant decrease in the mean area percentage of tight junction protein occludin expression in thalamic microvessels was also detected. In contrast, sections obtained from rats of group III showed a significant improvement of the microwave-produced changes but never reverted to the same state as the controls. Chronic microwave exposure could have a marked effect on the thalamic neurons and its blood barrier. Administration of ascorbic acid resulted in a significant improvement, but it was not sufficient to gain a normal histological appearance


Subject(s)
Male , Animals, Laboratory , Thalamus/ultrastructure , Microscopy, Electron , Protective Agents , Ascorbic Acid , Treatment Outcome , Rats , Male
4.
Egyptian Journal of Histology [The]. 2010; 33 (1): 68-80
in English | IMEMR | ID: emr-136376

ABSTRACT

The prevalence of asthma is rising. Consequently, there is an increased need for the development of new agents for its treatment, especially for patients who respond poorly to conventional therapy. The current study aim to establish whether statins could modulate inflammatory responses in a model of allergic asthma in guinea pig or not. Thirty six male guinea pigs were used. The animals were divided into two groups: Control group I and asthmatic group II. In group II, asthma was induced by sensitization and challenging with ovalbumin [OVA]. Group II was further divided into: Subgroup IIa which was just asthmatic subgroup, subgroup lib was given montelukast, subgroup Ic was given simvastatin and subgroup lid was given pravastatin. The duration of experiment was 3 weeks at the end of the experiment bronchoalveolar lavage [BAL] was performed and lung specimens were obtained, processed and subjected to different histological staining techniques. Lungs of asthmatic animals showed thick interalveolar septa due to inflammatory cells migration. Goblet cells were increased in number with more mucous secretion. Narrow airways were apparent due to inflammatory edema, mucous secretion and desquamated cells. There was statistically significant increase in mean thickness of interalveolar septa and mean number of goblet cells. Also there was significant increase in mean number of alveolar macrophages, eosinophils, lymphocytes and neutrophils. In simvastatin subgroup, there was partial improvement while in pravastatin subgroup there was similar picture as that of montelukast subgroup and control group. Statins could be used as anti-inflammatory in treatment of bronchial asthma. Moreover. Pravastatin [hydrophilic lipid lowering agents] could produce more anti-inflammatory effect better than simvastatin [hydrophobic lipid lowering agents]

5.
Egyptian Journal of Histology [The]. 2009; 32 (2): 368-378
in English | IMEMR | ID: emr-136363

ABSTRACT

Dysfunctions of the gastrointestinal system are more common complaints of the elderly. Enteric neurons are known to be vulnerable to age related cell death. So, the aim of this study was to study the effect of diet restriction on the histological changes in the myenteric neurons of jejunum of aged male albino rat. Thirty male albino rats of 6 months were used. Group I was the control group. Subgroup Ia included 5 rats of 6 months and subgroups Ib and Ic included 5 animals each and were continued to live up to the age of 12 and 18 months, respectively. Group II included 10 rats which were early fed the restricted diet [25 gm diet/rat! day] and subdivided into two subgroups five animals each. Subgroup ha were fed the restricted diet starting from 6 to 12 months. Subgroup IIb were fed the restricted diet starting from 6 to 18 months. Group III included 5 rats that were lately fed the restricted diet from 12 to 18 months. At time of sacrifice all the animals were anaesthetized, the jejunum was dissected out and specimens were processed for histological examination. Immunohistochemical expression of the pan-neuronal marker PGP 9.5 and neuronal nitric oxide synthase [nNOS] was investigated. As age advances in subgroup lb and Ic there was increased neuronal loss and obvious gaps in the myenteric ganglia with significant decrease in the number of PGP positive neurons. Animals of subgroup ha and llb showed that most of the myenteric neurons maintained their usual structural arrangement and expression of PGP. In group III rats showed neuronal loss and significant decrease in the PGP positive neurons. There was non significant decrease in the number of nNOS positive neurons in all groups. The results of the current study revealed that age related change involved mainly the cholinergic neurons and starting diet restriction early at 6 months age might slow or delay the age related damage of the rat myenteric neurons

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