Protective effect of propolis on manganese chloride neurotoxicity of olfactory bulb in adult male albino rat.

BACKGROUND: Manganese (Mn) is widely used for industrial purposes and exposure to high levels of Mn may cause an irreversible brain disease. Propolis is a natural plant product; it acts as a powerful reactive oxygen species scavenger and improves the neurodegeneration process. MATERIALS AND METHODS: In this study 40 adult male albino rats were divided randomly into four groups 10 rats each: group I (control group), group II manganese chloride (MnCl2) received 10 mg/kg/day/orally for 4 weeks by intra-gastric tube, group III (propolis group) received 50 mg/kg/day/orally for 4 weeks by intra-gastric tube, and group IV (MnCl2 + propolis group) received the same doses with the same duration and route as in groups II and III. Rats were sacrificed after 24 h of last dose. The olfactory bulbs removed, the right bulb cut to be processed for haematoxylin and eosin, immunohistochemical staining and the left cut for electron microscopic studies. RESULTS: Results revealed that rat olfactory bulb from MnCl2 group showed darkly stained mitral cells with dark pyknotic nuclei, some show pericellular spaces and vacuolation, dark apoptotic cells in granular cells, neuropil vacuolation and pyknotic astrocyte. Electron microscopic examination showed abnormal granular cell with irregular damaged nuclear membrane, rupture of myelin fibre. Mitral nerve cell with destructed nucleus, many cytoplasmic vacuoles, swollen rough endoplasmic reticulum, vacuolated mitochondria and neuropil were observed. Manganese chloride + propolis group showed improvement compared to MnCl2 group. CONCLUSIONS: It was concluded that propolis can ameliorate the toxic changes of manganese chloride on rat olfactory bulb.

Role of Nigella sativa seed oil on corneal injury induced by formaldehyde in adult male albino rats.

Formaldehyde is frequently used in occupational environments, its toxicity concerns to all who work closely with it such as anatomists. Nigella sativa is an amazing herb with a rich historical and religious background; its seeds are the source of its active ingredients. The purpose of the present study was to evaluate the role of Nigella sativa oil on corneal injury induced by formaldehyde in adult male albino rats. Forty adult male albino rats were divided randomly to four groups 10 rats each: I - Control group, II - Formaldehyde exposed group, III - Nigella sativa oil group (40 mg/kg/day) via intragastric tube daily for 2 weeks and IV - Formaldehyde and Nigella sativa group. Rats were sacrificed with ether, the corneas were extracted, one processed for haematoxylin and eosin stain and the other was used for transmission electron microscopic examination. Our results in group II revealed marked disorganisation, erosion, vacuolation and necrosis of epithelial cells with loss of parts of epithelial layer. Large congested invasion of blood vessels with separation and disorganisation of stromal fibrils. The corneas of group IV showed intact layers of epithelial cells with appearance close to control group. Star shaped cells (limbal stem cells) were obviously noticed in basal and intermediate layer with intact Bowman's membrane. Stroma showed regular parallel collagen, limbal stem cells were also noticed in group III. We concluded that Nigella sativa oil can ameliorate the toxic changes of formaldehyde on rat corneas. (.

Risk factors for nutritional rickets among children in Kuwait.

AIM: To assess the risk factors for nutritional rickets among children in Kuwait. METHODS: One hundred and three children with rickets and 102 control children matched for age and socioethnic characteristics were recruited over a 2 year period (January 1995 to January 1997) in Al-Adan Hospital in Kuwait. Diagnosis was made on clinical, radiologic and biochemical parameters. A specially designed questionnaire was administered by one of the investigators to both mothers of patients and mothers of control subjects to assess the role of social, nutritional and other related factors in the pathogenesis of nutritional rickets. Biochemical investigations included estimation of hemoglobin, serum calcium, serum phosphorus, serum alkaline phosphatase and serum 25-hydroxy vitamin D. RESULTS: The mean birthweights of rickets patients and control subjects were 3.20 +/- 0.46 and 3.19 +/- 0.45 kg, respectively. At the time of diagnosis, bodyweights of the patients and controls were 9.36 +/- 1.50 and 10.15 +/- 2.10 kg, respectively. Heights at the time of diagnosis were 73.58 and 77.24 cm for the patients and the controls, respectively. Mean hemoglobin, serum calcium and serum phosphate were significantly lower in the patients compared with the controls. Alkaline phosphatase was higher among the patients (P < 0.0001). The mean serum 25-hydroxy vitamin D level of the patients was 26.5 nmol/L, compared with 83.5 nmol/L in the controls. The mean age of starting semisolid feeds for the patients was 8.12 months, compared with 5.7 months in the controls. The nutritional quality of semisolid feeds was adequate among 71.6% of the controls as opposed to 13.6% of the patients. CONCLUSION: Nutritional rickets is a multifactorial condition. However, several factors seem to make important contributions. Among these, lack of exposure to sunlight, prolonged breast feeding without supplementation and inadequate weaning practices are important. Maternal education is important as it can influence all of the above factors.

Persistent hyperinsulinaemic hypoglycaemia of infancy (nesidioblastosis): a report from Kuwait.

We report nine Bedouin children from Kuwait with persistent hyperinsulinaemic hypoglycaemia (PHHI) seen over a 13-year period in two regional hospitals. The incidence of PHHI in this inbred community is high (1:20,000); five of them came from two families. All the children presented with seizures associated with severe and recurrent hypoglycaemia, eight presenting in the neonatal period and one at the age of 2 months. One child died soon after birth. All the others received diazoxide initially, which achieved remission in one while two siblings remain dependent on the drug. Long-acting somatostatin analogue (octreotide) was successfully used in one child. Four children underwent pancreatectomy, two showed diffuse and two had localized nesidioblastosis. Two children achieved normal neurodevelopmental milestones, four suffered mental retardation of varying degrees and three died. Early diagnosis and prompt treatment are essential to avoid the neurological damage associated with hypoglycaemia. In some cases, this condition is due to an autosomal recessive pattern of inheritance and it is therefore important to offer genetic counselling to families with one or more affected siblings.

Bartter's syndrome in Arabic children: review of 13 cases.

BACKGROUND: Bartter's syndrome (BS) is an inherited disease of renal potassium wasting characterized by hypokalemic alkalosis, normal blood pressure, vascular insensitivity to pressor agents and elevated plasma concentrations of renin and aldosterone. It is caused by generalized hyperplasia of the juxtaglomerular apparatus at the site of renin production caused by mutations in the Na-K-2Cl cotransporter gene, NKCC2. The objective of our study is to establish the prevalence and incidence of BS in Kuwait and to assess treatment modalities for it. METHODS AND RESULTS: Bartter's syndrome was diagnosed in 13 Kuwaiti children over a 14 year period (1981-1995) with the estimated incidence of 1.7/100,000 live births. The mean age at diagnosis was 9.3 months (range 2-32 months). There were five males and eight females (ratio 1:1.6). The mean duration of follow up was 5.6 years (1-14 years). Both consanguinity and familial history among our patients were high (69 and 54%, respectively). All patients had hypokalemia, hypochloremia with metabolic alkalosis, hyperreninemia and were normotensive. Clinical presentation was essentially similar to that in other series. Eleven patients (85%) had growth failure, two had nephrocalcinosis (15%) and one had renal failure. All patients were treated with supplemental potassium, an aldosterone antagonist (spironolactone) and a prostaglandin synthetase inhibitor (indomethacin or aspirin) sequentially. Significant catch-up of growth (four patients) and increases in serum potassium (eight patients) were recorded after administration of indomethacin therapy. One patient died of severe pneumonia with respiratory failure from hypokalemic myopathy. Clinical presentation, inheritance, complications and therapy of BS are briefly discussed. CONCLUSION: Bartter's syndrome is a rare disease, but should be considered in the differential diagnosis of other disorders with growth failure and/or hypokalemia. Early diagnosis, close follow up and compliance with treatment may lead to appropriate growth and development.

Congenital chloride diarrhoea in Kuwait: a clinical reappraisal.

Congenital chloride diarrhoea (CCD) is a recessively inherited disorder of chloride transport in the distal ileum and colon. Congenital chloride diarrhoea is a common metabolic disorder in Kuwait with an incidence of 1/3200. Clinical findings in 14 children with CCD are reported over a period of 4 years. Maternal polyhydramnios, abdominal distension, watery diarrhoea, and a high faecal chloride level > 90 mmol/l were the cardinal features in the neonatal period. In spite of the classical features of this disease 75 per cent of our cases were diagnosed beyond the neonatal period and all demonstrated chronic diarrhoea and failure to thrive, with hypochloraemia, hypokalaemia, and metabolic alkalosis. The practice of ultrasonic examination for pregnant women with polyhydramnios and, particularly, for those with previously affected siblings led to early identification of new cases among our population recently. The antenatal ultrasonic examination showed dilated intestinal loops which suggest CCD. The diagnosis was confirmed by a high faecal chloride level.