75 research outputs found

    Anti-inflammatory and antioxidant effects of Tualang honey in alkali injury on the eyes of rabbits: Experimental animal study

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    <p>Abstract</p> <p>Background</p> <p>Alkali injury is one of the most devastating injuries to the eye. It results in permanent unilateral or bilateral visual impairment. Chemical eye injury is accompanied by an increase in the oxidative stress. Anti-inflammatory and antioxidant agents play a major role in the treatment of chemical eye injuries. The purpose of this study is to evaluate the anti-inflammatory (clinical and histopathological) and antioxidant effects of Tualang honey versus conventional treatment in alkali injury on the eyes of rabbits.</p> <p>Methods</p> <p>A preliminary study was carried out prior to the actual study to establish the alkali chemical injury on rabbit's cornea and we found that alkali chemical injury with 2 N NaOH showed severe clinical inflammatory features. In actual study, alkali injury with 2 N NaOH was induced in the right eye of 10 New Zealand White rabbits' cornea. The rabbits were divided into two groups, Group A was given conventional treatment and Group B was treated with both topical and oral Tualang honey. Clinical inflammatory features of the right eye were recorded at 12 hours, 24 hours, 72 hours, 5<sup>th </sup>day and 7<sup>th </sup>day post induction of alkali burn on the cornea. The histopathological inflammatory features of the right corneas of all rabbits were also evaluated on day-7. The level of total antioxidant status and lipid peroxidation products in the aqueous humour, vitreous humour and serum at day-7 were estimated biochemically. Fisher's Exact, Chi-Square and Mann-Whitney test were used to analyse the data.</p> <p>Results</p> <p>There was no statistically significant difference in clinical inflammatory features (p > 0.05) between honey treated and the conventional treated group at different times of examination. Histopathological examination of the cornea showed the number of polymorphonuclear leucocytes was below 50 for both groups (mild grade). There was also no significant difference in the level of total antioxidant status as well as lipid peroxidation products in aqueous humour (p = 0.117, p = 0.382 respectively), vitreous humour (p = 0.917, p = 0.248 respectively) and serum (p = 0.917, p = 0.332 respectively) between honey treated and the conventional treated group.</p> <p>Conclusion</p> <p>Tualang honey has almost the equal effects when compared with the conventional treatment in treating alkali injury on rabbit's eye. Future research with more number of rabbits and control group is warranted to explore the anti-inflammatory and antioxidant effects of Tualang honey.</p

    Analysis of the genome and transcriptome of Cryptococcus neoformans var. grubii reveals complex RNA expression and microevolution leading to virulence attenuation.

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    Cryptococcus neoformans is a pathogenic basidiomycetous yeast responsible for more than 600,000 deaths each year. It occurs as two serotypes (A and D) representing two varieties (i.e. grubii and neoformans, respectively). Here, we sequenced the genome and performed an RNA-Seq-based analysis of the C. neoformans var. grubii transcriptome structure. We determined the chromosomal locations, analyzed the sequence/structural features of the centromeres, and identified origins of replication. The genome was annotated based on automated and manual curation. More than 40,000 introns populating more than 99% of the expressed genes were identified. Although most of these introns are located in the coding DNA sequences (CDS), over 2,000 introns in the untranslated regions (UTRs) were also identified. Poly(A)-containing reads were employed to locate the polyadenylation sites of more than 80% of the genes. Examination of the sequences around these sites revealed a new poly(A)-site-associated motif (AUGHAH). In addition, 1,197 miscRNAs were identified. These miscRNAs can be spliced and/or polyadenylated, but do not appear to have obvious coding capacities. Finally, this genome sequence enabled a comparative analysis of strain H99 variants obtained after laboratory passage. The spectrum of mutations identified provides insights into the genetics underlying the micro-evolution of a laboratory strain, and identifies mutations involved in stress responses, mating efficiency, and virulence

    Differential diagnosis of suspected multiple sclerosis: a consensus approach

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    BACKGROUND AND OBJECTIVES: Diagnosis of multiple sclerosis (MS) requires exclusion of diseases that could better explain the clinical and paraclinical findings. A systematic process for exclusion of alternative diagnoses has not been defined. An International Panel of MS experts developed consensus perspectives on MS differential diagnosis. METHODS: Using available literature and consensus, we developed guidelines for MS differential diagnosis, focusing on exclusion of potential MS mimics, diagnosis of common initial isolated clinical syndromes, and differentiating between MS and non-MS idiopathic inflammatory demyelinating diseases. RESULTS: We present recommendations for 1) clinical and paraclinical red flags suggesting alternative diagnoses to MS; 2) more precise definition of "clinically isolated syndromes" (CIS), often the first presentations of MS or its alternatives; 3) algorithms for diagnosis of three common CISs related to MS in the optic nerves, brainstem, and spinal cord; and 4) a classification scheme and diagnosis criteria for idiopathic inflammatory demyelinating disorders of the central nervous system. CONCLUSIONS: Differential diagnosis leading to MS or alternatives is complex and a strong evidence base is lacking. Consensus-determined guidelines provide a practical path for diagnosis and will be useful for the non-MS specialist neurologist. Recommendations are made for future research to validate and support these guidelines. Guidance on the differential diagnosis process when MS is under consideration will enhance diagnostic accuracy and precision

    The red eye

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    Snake venom ophthalmia and blindness caused by the spitting cobra (Naja nigricollis) in Nigeria.

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    Venom entered the eyes of 9 patients spat at by the spitting cobra, Naja nigricollis. In 5 the only effect was a simple conjunctivitis but 4 had corneal ulceration, 1 developed anterior uveitis indicating absorption of venom in the anterior chamber, and 2 were permanently blinded. Treatment of this rare emergency is discussed: immediate irrigation of the eye with water, careful examination for corneal abrasion, and prevention of secondary infection are recommended. The value of local specific antivenom is unproven

    Bites by the night adder (Causus maculatus) and burrowing vipers (genus Atractaspis) in Nigeria.

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    Nineteen patients proven to have been bitten by the small African adders Causus maculatus, Atractapis dahomeyensis and A. microlepidota were studied in the Nigerian savanna region. One of the patients bitten by C. maculatus was drowsy, hypotensive and flaccid on admission but recovered without treatment. Mild or moderate local swelling, local lymphadenitis and mild fever were the only other features in this group. None of the patients bitten by Atractaspis had signs of systemic envenoming apart from moderate fever. Local blistering appeared in two cases but did not progress to necrosis. No patient showed any disturbance of blood coagulation, or evidence of spontaneous hemorrhage or of cranial nerve lesions. The small literature on the effects of Causus and Atractaspis venoms in man and in laboratory animals is reviewed. It appears that bites by these species are very unlikely to cause serious ill effects. A few deaths from Atractaspis bites have been reported, but the danger from these species has been exaggerated

    Necrosis, haemorrhage and complement depletion following bites by the spitting cobra (Naja nigricollis).

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    The Spitting Cobra, Naja nigricollis, is widely and densely distributed in Africa. Fourteen patients with proven N. nigricollis bites, who were seen in the savanna region of Nigeria, did not exhibit the neurological signs, such as cranial nerve lesions and respiratory paralysis, expected following Elapid poisoning. All had local swelling, in eight cases involving the entire limb, and ten developed local tissue necrosis. Spontaneous haemorrhage was detected in three cases and was the probable cause of death in one of them; the other death in this series was unexplained. Haematological abnormalities included prolonged clot lysis anf failure of clot retraction due to a platelet defect. There was no specific deficit in clotting factors and a delayed rise in fibrin degradation products was attributed to extensive tissue damage at the site of the bit. Most patients showed depletion of complement component C3 and glycine-rich beta-glycoprotein (GBG), suggesting activation of the alternative pathway of complement fixation. There was evidence of hepatocellular damage in two out of six patients investigated. There was no evidence that specific polyvalent antivenoms, used in doses of up to 80 ml, prevented any of the effects of N. nigricollis venom. Clinical laboratory diagnosis is discussed. In the past many bites were wrongly classified as viper bites on the basis of clinical findings. Immunodiagnosis is a promising method for assessing the true importance of N. nigricollis bite in West Africa

    Poisoning by bites of the saw-scaled or carpet viper (Echis carinatus) in Nigeria.

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    The Saw-scaled or Carpet Viper (Echis carinatus) whose range extends from Senegal to Bengal probably bites and kills more people than any other species of snake. One hundred and fifteen patients with poisoning caused by its bite were studied in the savanna region of Nigeria, where victims of this snake may occupy 10 per cent of hospital beds. Patients showing no signs of envenoming were excluded. All patients had local swelling at the site of the bite. Other features included local blistering (13 per cent), local necrosis (11 per cent), incoagulable blood (93 per cent), and spontaneous systemic bleeding (57 per cent). There was evidence of disseminated intravascular coagulation in all cases; fibrinogen was severely depleted, fibrin degradation products were increased (mean 1711 +/- 904 micron per ml), but significant thrombocytopenia (less than 103 000 per mm3) was seen in only ten severe cases. Clotting factors V, VIII, II and XIII were depleted, while X and VII were usually normal. Fibrinolytic activity was rarely increased, so it seems likely that a procoagulant action (direct activation of prothrombin) is principal effect of E. carinatus venom on blood coagulation in man. Development of the haemostatic defect was observed as early as 75 minutes and as late as 27 hours after the bite. Spontaneous haemorrhage is clinically the most important effect of E. carinatus venom, causing the five deaths in this series. The relative importance of procoagulant and haemorrhagic components of the venom in causing haemorrhage is discussed. Complement activation via the classical and alternative pathways may have contributed to vascular damage. Mortality was reduced from the untreated level of between 10 and 20 per cent to 2.8 per cent in a group of 107 patients treated with 10 to 110 ml of specific antivenom. The dose was controlled using a simple clotting test. Blood coagulability was restored in two to 39 (mean 12) hours after the first dose of antivenom. Immediate-type serum reactions were observed in 21 per cent of cases. Additional treatment included blood transfusion for patients in haemorrhagic shock and ealry surgical débridement of necrotic tissue at the site of the bite
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