METHODS: This study evaluated Malaysian Gelam honey as a nutraceutical alternative to estrogen HRT (ERT) in alleviating VVA. A total of 24 female 8-weekold Sprague Dawley rats underwent bilateral oophorectomy. A minimum of 14 days elapsed from the time of surgery and administration of the first dose of Gelam honey to allow the female hormones to subside to a stable baseline and complete recovery from surgery. Vaginal tissues were harvested following a 2-week administration of Gelam honey, the harvested vagina tissue underwent immunohistochemistry (IHC) analysis for protein localization and qPCR for mRNA expression analysis.
RESULTS: Results indicated that Gelam honey administration had increased the localization of Aqp1, Aqp5, CFTR and Muc1 proteins in vaginal tissue compared to the menopause group. The effect of Gelam honey on the protein expressions is summarized as Aqp1>CFTR>Aqp5>Muc1.
DISCUSSION: Gene expression analysis reveals Gelam honey had no effect on Aqp1 and CFTR genes. Gelam honey had up-regulated Aqp5 gene expression. However, its expression was lower than in the ERT+Ovx group. Additionally, Gelam honey up-regulated Muc1 in the vagina, with an expression level higher than those observed either in the ERT+Ovx or SC groups. Gelam honey exhibits a weak estrogenic effect on the genes and proteins responsible for regulating water in the vaginal tissue (Aqp1, Aqp5 and CFTR). In contrast, Gelam honey exhibits a strong estrogenic ability in influencing gene and protein expression for the sialic acid Muc1. Muc1 is associated with mucous production at the vaginal epithelial layer. In conclusion, the protein and gene expression changes in the vagina by Gelam honey had reduced the occurrence of vaginal atrophy in surgically-induced menopause models.
Objectives: Brain volume reduction occurs with age, especially in Parkinson plus syndrome or psychiatric disorders. We searched to define the degree of volume discrepancy in advanced IPD patients and correlate the anatomical volumetric changes to motor symptoms and cognitive function.
Methods: We determined the magnetic resonance imaging (MRI)-based volumetry of deep brain nuclei and brain structures of DBS-IPD group and matched controls.
Results: DBS-IPD group had significant deep nuclei atrophy and volume discrepancy, yet none had cognitive or psychobehavioural disturbances. Globus pallidus volume showed positive correlation to higher mental function.
Conclusion: The morphometric changes and clinical severity discrepancy in IPD may imply a more complex degenerative mechanism involving multiple neural pathways. Such alteration could be early changes before clinical manifestation.
METHODS: 3-T brain MRI and DTI (diffusion tensor imaging) were performed on 26 PD and 13 MSA patients. Regions of interest (ROIs) were the putamen, substantia nigra, pons, middle cerebellar peduncles (MCP) and cerebellum. Linear, volumetry and DTI (fractional anisotropy and mean diffusivity) were measured. A three-node decision tree was formulated, with design goals being 100 % specificity at node 1, 100 % sensitivity at node 2 and highest combined sensitivity and specificity at node 3.
RESULTS: Nine parameters (mean width, fractional anisotropy (FA) and mean diffusivity (MD) of MCP; anteroposterior diameter of pons; cerebellar FA and volume; pons and mean putamen volume; mean FA substantia nigra compacta-rostral) showed statistically significant (P < 0.05) differences between MSA and PD with mean MCP width, anteroposterior diameter of pons and mean FA MCP chosen for the decision tree. Threshold values were 14.6 mm, 21.8 mm and 0.55, respectively. Overall performance of the decision tree was 92 % sensitivity, 96 % specificity, 92 % PPV and 96 % NPV. Twelve out of 13 MSA patients were accurately classified.
CONCLUSION: Formation of the decision tree using these parameters was both descriptive and predictive in differentiating between MSA and PD.
KEY POINTS: • Parkinson's disease and multiple system atrophy can be distinguished on MR imaging. • Combined conventional MRI and diffusion tensor imaging improves the accuracy of diagnosis. • A decision tree is descriptive and predictive in differentiating between clinical entities. • A decision tree can reliably differentiate Parkinson's disease from multiple system atrophy.
MATERIAL AND METHODS: Three databases including MEDLINE, Scopus and the Cochrane Central Register of Controlled Trials were from inception to August 2017.
RESULT: Two systematic reviews and 11 RCTs were included in the overview. According to the findings, isoflavones increased the maturation value and attenuated the vaginal atrophy in the post-menopausal women. Topical isoflavones had beneficial effects on the vaginal atrophy. Similar efficacy was found in Pueraria mirifica and conjugated estrogen cream on dryness ( p = 0.277), soreness ( p = 0.124) and irritation ( p = 0.469), as well as discharge ( p = 0.225) and dyspareunia ( p = 0.089). However, the conjugated estrogen cream was more effective compared to Pueraria mirifica ( p > 0.005) regarding maturation index improvement. Comparison of fennel 5% vaginal cream and placebo gel showed significant difference in superficial cells ( p
METHODS: Blinded assessors coded baseline images for acute ischaemic signs (presence, extent, swelling and attenuation of acute lesions; and hyperattenuated arteries) and pre-existing changes (atrophy, leucoaraiosis and old ischaemic lesions). Logistic regression models assessed associations between imaging features and death at 7 and 90 days; good recovery (modified Rankin Scale scores 0-2 at 90 days) and sICH. Data are reported with adjusted ORs and 95% CIs.
RESULTS: 2916 patients (67±13 years, National Institutes of Health Stroke Scale 8 (5-14)) were included. Visible ischaemic lesions, severe hypoattenuation, large ischaemic lesion, swelling and hyperattenuated arteries were associated with 7-day death (OR (95% CI): 1.52 (1.06 to 2.18); 1.51 (1.01 to 2.18); 2.67 (1.52 to 4.71); 1.49 (1.03 to 2.14) and 2.17 (1.48 to 3.18)) and inversely with good outcome. Severe atrophy was inversely associated with 7-day death (0.52 (0.29 to 0.96)). Atrophy (1.52 (1.08 to 2.15)) and severe leucoaraiosis (1.74 (1.20 to 2.54)) were associated with 90-day death. Hyperattenuated arteries were associated with sICH (1.71 (1.01 to 2.89)). No imaging features modified the effect of alteplase dose.
CONCLUSIONS: Non-expert-defined brain imaging signs of brain frailty and acute ischaemia contribute to the prognosis of thrombolysis-treated AIS patients for sICH and mortality. However, these imaging features showed no interaction with alteplase dose.
AIMS: To investigate the ability of intravaginal MP gel treatment to ameliorate VA in sex-steroid deficient condition, mimicking post-menopause.
METHODS: Ovariectomized female Sprague-Dawley rats received MP (100 μg/ml, 250 μg/ml and 500 μg/ml) and estriol (E) gels intravaginally for seven consecutive days. Rats were then euthanized and vagina was harvested and subjected for histological and protein expression and distribution analyses. Vaginal ultrastructure was observed by transmission electron microscopy (TEM).
RESULTS: Thickness of vaginal epithelium increased with increasing intravaginal MP doses. Additionally, increased in expression and distribution of proliferative protein i.e. PCNA, tight junction protein i.e. occludin, water channel proteins i.e. AQP-1 and AQP-2 and proton extruder protein i.e. V-ATPase A1 were observed in the vagina following intravaginal MP and E gels treatment. Intravaginal MP and E gels also induced desmosome formation and approximation of the intercellular spaces between the vaginal epithelium.
CONCLUSIONS: Intravaginal MP was able to ameliorate features associated with VA; thus, it has potential to be used as an agent to treat this condition.
METHODS: Mice were dosed intraperitoneally with mefenamic acid either as a single dose (100 or 200 mg/kg in 10% Dimethyl sulfoxide/Palm oil) or as single daily doses for 14 days (50 or 100 mg/kg in 10% Dimethyl sulfoxide/Palm oil per day). Venous blood samples from mice during the dosing period were taken prior to and 14 days post-dosing from cardiac puncture into heparinized vials. Plasma blood urea nitrogen (BUN) and creatinine activities were measured.
RESULTS: Single dose of mefenamic acid induced mild alteration of kidney histology mainly mild glomerular necrosis and tubular atrophy. Interestingly, chronic doses induced a dose dependent glomerular necrosis, massive degeneration, inflammation and tubular atrophy. Plasma blood urea nitrogen was statistically elevated in mice treated with mefenamic acid for 14 days similar to plasma creatinine.
CONCLUSION: RESULTS from this study suggest that mefenamic acid as with other NSAIDs capable of producing nephrotoxicity. Therefore, the study of the exact mechanism of mefenamic acid induced severe nephrotoxicity can be done in this animal model.
Material and Methods: Patients with ACL re-injury to either knee after successful primary ACLR were included in Group I and those with no further re-injury were included in Group II. Variables including age, gender, side, body mass index (BMI), thigh atrophy, anterior knee laxity difference between both knees measured by KT-1000 arthrometer, mean time of return to sports (RTS), graft type, type of game, mode of injury, Tegner Activity Score, hormone levels, femoral tunnel length (FTL), posterior tibial slope (PTS) and notch width index (NWI) were studied. Binary logistic regression was used to measure the relative association.
Results: A total of 128 athletes were included with 64 in each group. Mean age in Group I and II were 24.90 and 26.47 years respectively. Mean follow-up of Group I and Group II were 24.5 and 20.11 months respectively. Significant correlation was present between ACL re-injury and following risk factors; PTS of >10º, KT difference of >3.0mm, thigh atrophy of >2.50cm and time to RTS <9.50 months P value <0.05). No correlation was found with age, sex, BMI, type of game, Tegner Activity Score, mode of injury, NWI, size of graft, FTL and hormone levels.
Conclusion: Possible risk factors include PTS of ≥ 10º, KT difference of ≥ 3.0mm at 1 year follow-up, thigh atrophy of ≥ 2.50cm at 1 year follow-up and RTS <9.5 months after primary ACLR.