RESUMO
Background: Tuberculosis (TB), caused by Mycobacterium tuberculosis (MTB), is one of the top infectious killer diseases in the world. The emergence of drug-resistant MTB strains has thrown challenges in controlling TB worldwide. This study investigated the prevalence of drug-resistant tuberculosis in the states of Nigeria and the risk factors that can increase the incidence of tuberculosis. Methods: The study is a cross-sectional epidemiological research carried out in the six senatorial districts of Ekiti and Ondo states, Nigeria, between February 2019 and January 2020. A structured questionnaire was administered to 1203 respondents for socio-demographic information, and sputum samples were collected from them for TB investigation. GeneXpert technique was used to diagnose TB from the sputum samples, followed by bacterial isolation using Löweinstein-Jensen medium and antibiotic susceptibility testing. Results: Prevalence of TB in the two states combined was 15 â%; with 13.8 â% for Ekiti state and 16.1 â% for Ondo State. The distribution of TB in the senatorial districts was such that: Ondo South â> âEkiti Central â> âEkiti South â> âOndo North â> âEkiti North â> âOndo Central. The risk factors identified for TB prevalence in two states were gender, male â> âfemale (OR â= â0.548, p â= â0.004); overcrowding (OR â= â0.733, p â= â0.026); room size (OR â= â0.580, p â= â0.002); smoking (OR â= â0.682, p â= â0.019) and dry and dusty season (OR â= â0.468, p â= â0.005). The prevalence of MDR-TB in Ekiti and Ondo States were 1.2 â% and 1.3 â% respectively. The identified risk factors for MDR were education (OR â= â0.739, p â= â0.017), age (OR â= â0.846, p â= â0.048), religion (OR â= â1.95, p â= â0.0003), family income (OR â= â1.76, p â= â0.008), previous TB treatment (OR â= â3.64, p â= â0.004), smoking (OR â= â1.33, p â= â0.035) and HIV status (OR â= â1.85, p â= â0.006). Rifampicin monoresistant was reported in 6.7 â% of the rifampicin-resistant strains, while 93.3 â% were rifampicin polyresistant strains. Two (13.3 â%) of the MDR-TB strains were resistant to all the 3 first-line antimycobacterial agents. All the Rifampicin-resistant TB strains were susceptible to the aminoglycosides (Amikacin, Capreomycin and Kanamycin), also with high susceptibility to the fluoroquinilones: Moxifloxacin (100 â%) and Levofloxacin (86.7 â%). Sixteen (94.1 â%) of the 17 Rifampicin-susceptible strains were susceptible to all the eight antibiotics tested, while one (5.9 â%) was susceptible to Rifampicin and Isoniazid but resistant to the rest antibiotics. Conclusion: The study showed that there is high prevalence of TB and MDR-TB in Ekiti and Ondo States Nigeria, hence, to meet the SDG Target 3.3 of ending TB epidemic by 2030, culturing and antibiotic susceptibility testing should be carried out on every TB-positive sputum and the patients treated accordingly.
RESUMO
Obesity (OBS) has been established as a link to male hypogonadism with consequent infertility. Previous studies have shown that melatonin (MEL) modulates hypothalamic-pituitary-gonadal function. The present study therefore investigated the hypothesis that MEL supplementation would attenuate spermatogenic and steroidogenic dysfunctions associated with obesity induced by high-fat diet (HFD). Twenty-four adult male Wistar rats (n = 6/group) were used: control group received vehicle (normal saline), obese group received 40% high-fat diet and distilled water, MEL-treated group received MEL (4 mg/kg), and OBS + MEL group received MEL and 40% HFD and the treatment lasted for 12 weeks. HFD caused increased body weight, glucose intolerance, plasma triglyceride and low-density lipoprotein cholesterol/ very low-density lipoprotein cholesterol and malondialdehyde, as well as decreased antioxidant capacity, high-density lipoprotein cholesterol, gonadotrophin-releasing hormone, follicle-stimulating hormone and testosterone and altered sperm parameters. However, all these alterations were attenuated when supplemented with MEL. Taken together, these results indicate that HFD exposure causes endocrine dysfunction and disrupted sperm parameters in obese animals, which are accompanied by lipid peroxidation/defective antioxidant capacity. In addition, the present results suggest that melatonin supplementation restores endocrine function and sperm integrity in obese rat model by suppression of oxidative stress-dependent mechanism.
Assuntos
Dieta Hiperlipídica , Melatonina , Animais , Dieta Hiperlipídica/efeitos adversos , Masculino , Melatonina/farmacologia , Melatonina/uso terapêutico , Obesidade/tratamento farmacológico , Obesidade/etiologia , Estresse Oxidativo , Ratos , Ratos Wistar , EspermatozoidesRESUMO
We investigated the hypothesis that acetate ameliorates brain-adipose metabolic dysfunction (BAMED) in high fat diet (HFD)-induced obesity, possibly by modulation of peroxisome proliferator-activated receptor-γ (PPAR-γ). Ten-week-old male Wistar rats were randomly assigned into four groups (n = 6/group): Control, acetate and obese with or without acetate groups received vehicle (distilled water; po), acetate (200 mg/kg, po) and 40% HFD with or without acetate respectively. The treatments lasted for 12 weeks. Obese animals showed increase in body weight, visceral fat mass, insulin and triglyceride-glucose index and a reduction in insulin sensitivity. In addition, obese animals also showed increase in plasma/hypothalamic and adipose pyruvate dehydrogenase kinase-4, lactate-pyruvate ratio, malondialdehyde, γ-glutamyl transferase, and a decrease in glucose-6-phosphate dehydrogenase, glutathione, nitric oxide and PPAR-γ. HFD also elevated plasma/hypothalamic lipid and decreased adipose lipid profile, increased hypothalamic and adipose tumor necrosis factor-α, interleukin-6 and histone deacetylase (HDAC), and elevated plasma/adipose leptin. These alterations were reversed by concomitant administration of acetate. The present results demonstrate that obesity is characterized by BAMED, which is accompanied by altered HDAC/PPAR-γ. The results in addition suggest that acetate, an HDAC inhibitor rescues BAMED with consequent normalization of body weight and visceral fat mass by modulation of PPAR-γ and suppression of oxidative stress.