Partial Purification of Anti-Tumor and Antioxidant Components from Uvaria Narum (Dunal) Wall Seed

Uvaria is a genus of flowering plants in the soursop family (Padmaja et al.,1993), Annonaceae. The generic name Uvaria is derived from the Latin uva meaning grape, because the edible fruits of some species in this genus resemble grapes. Scandent shrubs, branchlets sparsely hairy. It is a large climbing shrub with woody stems. Uvaria is a large woody stellately pubescent straggling shrub with dark bluish green leaves. Uvaria narum (Tran et al., 2013) is mainly used in eczema, itching, varicose vein, haemorrhoids, jaundice, inflammation and fever. Leaves are recommended in rheumatic swellings, jaundice, biliousness and fevers. Root is used in the treatment of jaundice, fever, biliousness and typhoid. A decoction of the root bark is given to women to control fits at the time of delivery. It is also used in rheumatism, bowel complaints of Children, for eczema and used in skin diseases. Oil Extracted from the root reduces burning sensation of the Liver. The whole root extract of Uvaria narum could be medicinally employed as a possible free radical scavenger. The plant may also be considered against ageing and other disease caused by free radicals. The aerial parts of Uvaria are used in stomach disorder. OBJECTIVES: 1. Preparation of oil extract and its fractions of Uvaria narum seed. 2. Screening of Phytochemical constituents of seed oil extract using standard assays as well as purification by Thin Layer Chromatography. 3. Analysis of antioxidant activity of seed oil extract and its selected fractions using various In vitro assays. 4. Analysis of In vivo antitumor activity of oil extract of seeds of Uvaria narum in mice using DLA induced solid tumor model. CONCLUSION: The seed oil fraction of Uvaria narum possesses significant cytotoxic effect towards malignat cells than normal cells. In the present study two cytotoxic fractions one positive to alkaloid stains and the other positive to anthraquinone in TLC could be purified. Both these fractions exhibited siginificant cytotoxicity towards tumor cells however they are less toxic to normal cells. The alkaloid fraction reduce DLA induced tumor progression in mice but does not show weight loss, decrease in WBC count and haemoglobin level in the tumor bearing animals suggesting a promising antitumor property. The other two fractions, Fraction-III (positive to terpenoids) and Fraction-IV (positive to tannins and phenolics) are also obtained from this seed oil extract of Uvaria narum of which Fraction-IV exhibits significant antioxidant potential. Overall partial purification of promising antitumor alkaloids and antioxidant tannin/phenolic has been achieved from Uvaria narum seeds. It is expected that further level of purification of these fractions may yield pharmacologically important phytochemicals

The clinical utility of echocardiography as a cardiological diagnostic tool in poor resource settings

Background: There has been a decline in the auscultatory and other clinical skills of physicians especially in developed countries. The advent of echocardiography has revolutionized the diagnosis of cardiovascular diseases and made up for the decline in clinical skills.Objective: To assess the sensitivity and specificity of auscultatory and clinical skills in the diagnosis of cardiovascular diseases using echocardiography as the gold standard.Materials and Methods: All the adult echocardiographic studies (321) performed over a 1.year period were collated for analysis. The clinical indications of the studies were compared with the final diagnoses by echocardiography. The sensitivity and specificity of the clinical diagnosis of hypertensive heart disease (HHD), rheumatic heart disease (RHD), and the cardiomyopathies were determined.Results: Of the 244 (76.0%) clinically diagnosed as HHD, 188 (58.6%) were confirmed by echocardiography. For RHD 9 (2.8%) were diagnosed clinically while on echocardiography, 13 (4.1%) were diagnosed. All the 31 (9.7%) cases of dilated cardiomyopathy were confirmed on echocardiography. No case of ischemic heart disease was confirmed.Seventy.one (22.0%) had normal studies. The sensitivity of clinical  diagnosis for RHD was low (41.7%) while for HHD and dilated  cardiomyopathy, sensitivity was high, 95.7% and 75.0%, respectively. Specificity was high for all three cardiovascular diseases analyzed.Conclusion: Auscultatory and clinical skills are still sensitive and specific tools in the diagnosis of cardiovascular diseases in developing countries and should be sustained. However, echocardiography is indispensable in the diagnosis of cases with subtle clinical signs and should be made more available and affordable.Key words: Cardiovascular diseases, clinical diagnosis, echocardiograph

Vitamin D3 Receptor Activation Rescued Corticostriatal Neural Activity and Improved Motor-Cognitive Function in −D2R Parkinsonian Mice Model

Background: fourth generation antipsychotics have been implicated in the blockade of calcium signalling through inhibition of dopamine receptive sites on dopaminergic D2 Receptor (D2R). As a result of the abnormal calcium signalling associated with D2R inhibition, changes occur in the motor and memory neural axis leading to the observed behavioural deficits after prolonged haloperidol. Thus, Vitamin D3 receptor (VD3R), a calcium controlling receptor in the striatum can be targeted to relief the neurological symptoms associated with haloperidol (−D2R) induced PD. Aim: This study sets to investigate the role of VD3R activation in vitro and in vivo after haloperidolinduced Dopaminergic (D2R) blockade. In addition, we examined the associated neural activity and behavioural changes in parkinsonian and VDRA intervention mice. Methods: Dopaminergic D2R inhibition was investigated in vitro using Melanocytes isolated from the scale of a Tilapia. In four separate set ups, the cells were cultured in calcium free Ringer’s solution as follows; 300 μM haloperidol, 100 μM VD3, 100 mM calcium chloride and a combination of 300 μM haloperidol and 100 μM VD3. Subsequently, dopaminergic vesicle accumulation and calcium signalling were observed in bright field microscopy using blue and green fluorescence probes. In the second phase, PD was induced in adult BALB/c mice (−D2; n = 8) after 14 days of intraperitoneal haloperidol treatment (10 mg/Kg). A set of n = 4 mice were untreated (−D2) while the other group (n = 4) received 100 mg/Kg of VD3 for 7 days (−D2/+VDR). The control groups (n = 4 each) were treated with normal saline (NS) and VD3 (+VDR) for 14 days. At the end of the treatment phase, the animals were assessed in Rotarod, parallel bar-, cylinder-, Y-Maze-, one trial place recognition- and novel object recognition-(NOR) tests. Neural activity was measured using chronic electrode implants placed in the M1 (motor cortex), CPu (striatum), CA1 (hippocampus) and PFC (prefrontal cortex). Neural activity was compared with the outcomes of behavioural tests for memory and motor functions and data was expressed as mean ± SEM (analysed using ANOVA with Tukey post-hoc test, significant level was set at 0.05). Results/Discussion: in vitro outcomes show that VDR increase calcium signalling and reverses the effect of haloperidol; specifically by reducing dopaminergic vesicle accumulation in the cell body. Similarly, in vivo neural recordings suggest an increase in calcium hyperpolarization currents in the CPu and PFC of intervention mice (−D2/+VDR) when compared with the parkinsonian mice (−D2). These animals (−D2/+VDR) also recorded an improvement in spatial working memory and motor function versus the Parkinsonian mice (−D2). These outcomes suggest the role of CPu-PFC corticostriatal outputs in the motor-cognitive decline seen in parkinsonian mice. Similarly, VDRA reduced the neural deficits through restoration of calcium currents (burst activities) in the intervention mice (−D2/+VDR). Conclusion: VDRA treatment reduced the motor-cognitive defects observed in haloperidol induced PD. Our findings suggest the role of VDRA in restoration of calcium currents associated with PFC and CPu corticostriatal outputs seen as burst frequencies in in vivo neural recording

Vitamin D 3 Receptor Activation Rescued Corticostriatal Neural Activity and Improved Motor Function in –D 2 R Tardive Dyskinesia Mice Model

Haloperidol-induced dyskinesia has been linked to a reduction in dopamine activity characterized by the inhibition of dopamine receptive sites on D2-receptor (D2R). As a result of D2R inhibition, calcium-linked neural activity is affected and seen as a decline in motor-cognitive function after prolonged haloperidol use in the treatment of psychotic disorders. In this study, we have elucidated the relationship between haloperidol-induced tardive dyskinesia and the neural activity in motor cortex (M1), basal nucleus (CPu), prefrontal cortex (PFC) and hippocampus (CA1). Also, we explored the role of Vitamin D3 receptor (VD3R) activation as a therapeutic target in improving motor-cognitive functions in dyskinetic mice. Dyskinesia was induced in adult BALB/c mice after 28 days of haloperidol treatment (10 mg/Kg; intraperitoneal). We established the presence of abnormal involuntary movements (AIMs) in the haloperidol treated mice (−D2) through assessment of the threshold and amplitude of abnormal involuntary movements (AIMs) for the Limbs (Li) and Orolingual (Ol) area (Li and Ol AIMs). As a confirmatory test, the dyskinetic mice (−D2) showed high global AIMs score when compared with the VD3RA intervention group (−D2/+VDR) for Li and Ol AIMs. Furthermore, in the behavioral tests, the dyskinetic mice exhibited a decrease in latency of fall (LOF; Rotarod-P < 0.05), climbing attempts (Cylinder test; P < 0.05) and latency of Turning (Parallel bar test; LOT-P < 0.05) when compared with the control. The reduced motor function in dyskinetic mice was associated with a decline in CPu-CA1 burst frequencies and an increase in M1-PFC cortical activity. However, after VD3RA intervention (−D2/+VDR), 100 mg/Kg for 7 days, CPu-CA1 burst activity was restored leading to a decrease in abnormal movement, and an increase in motor function. Ultimately, we deduced that VD3RA activation reduced the threshold of abnormal movement in haloperidol induced dyskinesia

Vitamin D 3 Receptor Activation Rescued Corticostriatal Neural Activity and Improved Motor - Cognitive Function in − D 2 R Parkinsonian Mice Model

fourth generation antipsychotics have been implicated in the blockade of calcium signalling through inhibition of dopamine receptive sites on dopaminergic D 2 Receptor (D 2 R). As a result of the abnormal calcium signalling associated with D 2 R inhibition, changes occur in the m o- tor and memory neural axis leading to the observed behavioural deficits after prolonged halope r- idol. Thus, Vitamin D 3 receptor (VD 3 R), a calcium controlling receptor in the striatum can be ta r- geted to relief the neurological symptoms associated with haloperidol ( − D 2 R) induced PD. Aim: This study sets to investigate the role of VD3R activation in vitro and in vivo after haloperidol - induced Dopaminergic (D 2 R) blockade. In addi tion, we examined the associated neural activity and behavioural changes in parkinsonian and VDRA intervention mice. Methods: Dopaminergic D 2 R inhibition was investigated in vitro using Melanocytes isolated from the scale of a Tilapia. In four separate set ups, the cells were cultured in calcium free Ringer’s solution as follows; 300 μM haloperidol, 100 μM VD 3 , 100 mM calcium chloride and a combination of 300 μM haloperidol and 100 μM VD 3 . Subsequently, dopaminergic vesicle accumulation and calcium signalling were observed in bright field microscopy using blue and green fluorescence probes. In the second phase, PD was induced in adult BALB/c mice ( − D 2 ; n = 8) after 14 days of intraperitoneal haloperidol treatment (10 mg/Kg). A set of n = 4 mice were untreated ( − D 2 ) while the other group (n = 4) r e- ceived 100 mg/Kg of VD 3 for 7 days ( − D 2 /+VDR). The control groups (n = 4 each) were treated with normal saline (NS) and VD 3 (+VDR) fo r 14 days. At the end of the treatment phase, the animals were assessed in Rotarod, parallel bar - , cylinder - , Y - Maze - , one trial place recognition - and novel object recognition - (NOR) tests. Neural activity was measured using chronic electrode implants plac ed in the M1 (motor cortex), CPu (striatum), CA1 (hippocampus) and PFC (prefrontal cortex). Neural activity was compared with the outcomes of behavioural tests for memory and motor fun c- tions and data was expressed as mean ± SEM (analysed using ANOVA with T ukey post - hoc test, significant level was set at 0.05). Results/Discussion: in vitro outcomes show that VDR increase calcium signalling and reverses the effect of haloperidol; specifically by reducing dopaminergic vesicle accumulation in the cell body. Sim ilarly, in vivo neural recordings suggest an increase in calcium hyperpolarization currents in the CPu and PFC of intervention mice ( − D 2 /+VDR) when compared with the parkinsonian mice ( − D 2 ). These animals ( − D 2 /+VDR) also recorded an i m- provement in spatial working memory and motor function versus the Parkinsonian mice ( − D 2 ). These outcomes suggest the role of CPu - PFC corticostriatal outputs in the motor - cognitive decline seen in parkinsonian mice. Similarly, VDRA reduced the neural deficits through restorati on of ca l- cium currents (burst activities) in the intervention mice ( − D 2 /+VDR). Conclusion: VDRA treatment reduced the motor - cognitive defects observed in haloperidol induced PD. Our findings suggest the role of VDRA in restoration of calcium currents assoc iated with PFC and CPu corticostriatal ou t- puts seen as burst frequencies in in vivo neural recording

ICAR: endoscopic skull‐base surgery

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DEVELOPING CAUSAL MODEL OF SOME PSYCHO-ACADEMIC AND SCHOOL VARIABLES FOR MATHEMATICS ACHIEVEMENT IN JUNIOR SECONDARY SCHOOLS IN AKWA IBOM STATE, NIGERIA

ABSTRAC

Predictors of in-hospital mortality among stroke patients in Uyo, Nigeria

Background: Stroke is the third leading cause of death in most industrialized countries. Several reports indicate that it is also becoming a major cause of morbidity and mortality in Nigeria and other developing countries.Aim: To identify risk factors and predictors of in-hospital mortality among patients admitted for stroke in a tertiary health institution in Nigeria.Methods: Case records of all patients admitted for stroke in the University of Uyo Teaching Hospital from January 2004 to December 2008 were retrieved and relevant data extracted and analysed.&nbsp; The diagnosis of stroke was made on clinical grounds only.Results: Three hundred and seven patients with stroke were admitted during the study period. The mean ages were 58.3&plusmn; 10 years and 58.4&plusmn; 11.4 years for males and females respectively (p&gt;0.05) indicating that stroke occurred in the sixth decade in both sexes. Systemic hypertension was the commonest risk factor .The overall in- hospital mortality was 24(7.8%) with majority of the mortality [22(7.2%)] occurring within the first seven days of admission. The duration of hospital stay did not influence mortality (p &gt;0.05).Only the female gender and increasing pulse rate were identified as predictors of in hospital mortality (p &lt;0.05).Conclusion: Most deaths from stroke occur in the first seven days of admission when proper intensive care is critical. The predictors of in-hospital mortality identified in this study add to the previously identified ones and should all be kept in view when managing these patients. The need for the establishment of stroke units especially in our tertiary health institutions is advocated. Keywords:&nbsp; Stroke, Predictors, In-hospital mortality, Nigeri

Concentrations of total protein, albumin and immunoglobulins in undiluted uterine fluid of gynecologically healthy mares

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