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1.
Medicine (Baltimore) ; 103(27): e38630, 2024 Jul 05.
Artigo em Inglês | MEDLINE | ID: mdl-38968489

RESUMO

Dental infections, which include anything from severe periodontal illnesses and abscess forms to routine tooth caries, are a major public health risk. This review article focuses on the pathophysiology and treatment of dental infections. A narrative review was conducted based on several published articles, relevant journals, and books in Google Scholar PubMed using the keywords dental caries, periodontal disease, gingivitis, and related diseases; we excluded duplicated information. Our review illustrated the types of dental infections and the proper antimicrobial drug that is suitable for this disease. Drawing from recent research findings and clinical evidence, we explore the spectrum of bacteria commonly associated with dental infections and their susceptibility profiles to various antibiotics. Emphasis is placed on understanding the mechanisms of antibiotic action and resistance in the context of dental pathogens, shedding light on optimal treatment regimens and potential challenges in clinical management. Additionally, we go over the clinical consequences of antibiotic therapy in dentistry, taking into account factors like patient selection, dose guidelines, and side effects. The management of dental infections through antimicrobial strategies has undergone significant advancements, as evidenced by this updated review. Besides the normal methods, emerging technologies such as 3D printing for drug delivery of antibiotics and disinfectants hold promise in enhancing treatment efficacy and patient outcomes. By leveraging the precision and customization afforded by 3D printing, dentistry can tailor antimicrobial interventions to individual patient needs, optimizing therapeutic outcomes while minimizing adverse effects.


Assuntos
Antibacterianos , Humanos , Antibacterianos/uso terapêutico , Doenças Periodontais/tratamento farmacológico , Doenças Periodontais/microbiologia , Anti-Infecciosos/uso terapêutico
2.
Medicine (Baltimore) ; 103(8): e37297, 2024 Feb 23.
Artigo em Inglês | MEDLINE | ID: mdl-38394496

RESUMO

Multiple sclerosis (MS) is a chronic autoimmune disease with demyelination, inflammation, neuronal loss, and gliosis (scarring). Our object to review MS pathophysiology causes and treatment. A Narrative Review article was conducted by searching on Google scholar, PubMed, Research Gate about relevant keywords we exclude any unique cases and case reports. The destruction of myelinated axons in the central nervous system reserves this brunt. This destruction is generated by immunogenic T cells that produce cytokines, copying a proinflammatory T helper cells1-mediated response. Autoreactive cluster of differentiation 4 + cells, particularly the T helper cells1 subtype, are activated outside the system after viral infections. T-helper cells (cluster of differentiation 4+) are the leading initiators of MS myelin destruction. The treatment plan for individuals with MS includes managing acute episodes, using disease-modifying agents to decrease MS biological function of MS, and providing symptom relief. Management of spasticity requires physiotherapy, prescription of initial drugs such as baclofen or gabapentin, secondary drug options such as tizanidine or dantrolene, and third-line treatment such as benzodiazepines. To treat urinary incontinence some options include anticholinergic medications such as oxybutynin hydrochloride, tricyclic antidepressants (such as amitriptyline), and intermittent self-catheterization. When it comes to bowel problems, one can try to implement stool softeners and consume a high roughage diet. The review takes about MS causes Pathophysiology and examines current treatment strategies, emphasizing the advancements in disease-modifying therapies and symptomatic treatments. This comprehensive analysis enhances the understanding of MS and underscores the ongoing need for research to develop more effective treatments.


Assuntos
Esclerose Múltipla , Humanos , Esclerose Múltipla/epidemiologia , Esclerose Múltipla/etiologia , Esclerose Múltipla/terapia , Resultado do Tratamento , Doença Crônica , Espasticidade Muscular/etiologia
3.
J Pharm Bioallied Sci ; 15(3): 101-106, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-37705854

RESUMO

Background: Clinical pharmacogenetics is a rapidly growing field that focuses on the study of genetic variations and their impact on drug metabolism, efficacy, and safety. Angiotensin II receptor blockers (ARBs) are commonly used to treat hypertension in Iraq but not all patients respond equally to these drugs. Aim: This article aims to review the current evidence on the clinical pharmacogenetics of ARBs in Iraq and its implications for personalized medicine. Materials and Methods: We conducted a literature review of studies on the genetic variations that affect the response to ARBs in Iraq. We also reviewed the prevalence of these genetic variants in the Iraqi population and discussed the potential clinical implications for personalized medicine. Results: The most studied genetic variations associated with ARB response in Iraq are the angiotensin-converting enzyme gene insertion/deletion polymorphism and the angiotensin II type 1 receptor gene A1166C polymorphism. The angiotensin-converting enzyme gene insertion/deletion polymorphism is associated with variability in response to ARBs, while the angiotensin II type 1 receptor A1166C polymorphism is associated with an increased risk of cardiovascular events in patients treated with ARBs. The prevalence of these genetic variants in the Iraqi population varies widely depending on the region and ethnic group. Conclusion: The clinical pharmacogenetics of ARBs in Iraq suggests that pharmacogenetic testing could improve the selection and dosing of ARBs in Iraqi patients, leading to better patient outcomes and cost-effective healthcare.

4.
Pharmaceuticals (Basel) ; 15(12)2022 Nov 26.
Artigo em Inglês | MEDLINE | ID: mdl-36558919

RESUMO

NeuroAid II, a folk Chinese Medicine, is currently used in Asia for the treatment of stroke. An experimental study demonstrated that NeuroAid enables neuronal cells to be more resistant to glutamate toxicity. This research was constructed to evaluate the efficacy of NeuroAid in the prevention of epilepsy (EP). Forty healthy adult male mice were used and divided into four groups (10 mice/group): normal control group; positive control group; NeuroAid-treated group (10 mg/kg); topiramate-treated group (10 mg/kg). The treatment continued for 7 days, and on the last day, EP was induced using strychnine at a dose of 2 mg/kg via intraperitoneal (ip) administration. Seizure severity, latency to the seizure onset, the number of seizures, and the duration of each seizure episode were observed for one hour. The death and protection rates over the next twenty-four hours were recorded. Brain specimens from surviving animals were extracted and examined pathologically for quantification of glutamate receptor (GluR) gene expression in the isolated hippocampus employing real-time PCR analysis. Treatment with NeuroAid resulted in a significant reduction in seizure severity, prolonged the onset of seizures, decreased the number and duration of episodes, reduced brain insult, and decreased mortality rate. Reductions in the gene expression of GluRs in the hippocampus with minor histopathological changes were observed in the NeruoAid- and topiramate-treated groups. It is concluded that NeuroAid has a potential antiepileptic effect (EP) with the ability to prevent convulsion through its effect on the glutamate receptor.

5.
Asian Pac J Cancer Prev ; 23(9): 3151-3156, 2022 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-36172678

RESUMO

OBJECTIVE: Monitoring the result of miR 409 3p and its response to tumor proliferation and its mechanism of action on some types of lung cancer in vitro (A549 cell line). METHODS: Two A549 cell line group negative control group with oligonucleotide cultured under conventional conditions and transfected with positive control nucleotides. Experiments Based on the control group, chemically synthesized miR 409 3p mimics were used in the positive group with liposome transfection to construct A549 cells with high miR-409-3p expression. RESULT: miR4093p expression was estimated using the qPCR method in the two groups after 48 h. Later, the miR-409-3p expression in A549 cells obviously increased significantly with a positive attitude in the positive control group that was transfected by miR-409-3p (mimics) (P<0.20). As a result of this investigation, a significant increase in the percentage of total cell apoptosis was significantly increased in the positive group compared to the control group (22.68% ± 4.62%), (7.79%±1.94%) respectively, (P<0.05). However, in terms of the G1 phase, the rate is obviously low compared to the control group (40.22%±5.36%); (56.08%±5.21%) (P<0.05). endogenous ELF2 was considerably reduced after overexpression of the miR-409-3p mimic (P<0.05). CONCLUSION: miR-409-3p may prevent non-small cell lung cancer (NSCLC) by affecting ELF2 transcription and other cellular regulators to regulate A549 cell division and induce apoptosis.


Assuntos
Carcinoma Pulmonar de Células não Pequenas , Neoplasias Pulmonares , MicroRNAs , Apoptose/genética , Carcinoma Pulmonar de Células não Pequenas/patologia , Linhagem Celular , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células/genética , Regulação Neoplásica da Expressão Gênica , Humanos , Lipossomos , Neoplasias Pulmonares/patologia , MicroRNAs/genética , MicroRNAs/metabolismo , Nucleotídeos , Oligonucleotídeos
6.
Front Pharmacol ; 13: 905828, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35814241

RESUMO

Doxorubicin (DOX) is an anticancer agent for treating solid and soft tissue malignancies. However, the clinical use of DOX is restricted by cumulative, dose-dependent cardiotoxicity. Therefore, the present study aimed to assess the cardioprotective effects of P. ginseng C. A. Mey, febuxostat, and their combination against DOX-induced cardiotoxicity. Thirty-five Sprague Dawley male rats were used in this study. The animals were randomly divided into five groups, with seven rats per group. The control group received normal saline, the induced group received DOX only, and the treated group received P. ginseng, febuxostat, and their combination before DOX treatment. Biomarkers of acute cardiac toxicity were assessed in each group. Results showed that treatment with the combination of febuxostat and P. ginseng before DOX led to a significant improvement in the biomarkers of acute DOX-induced cardiotoxicity. In conclusion, the combination of P. ginseng and febuxostat produced more significant cardioprotective effects against DOX-induced cardiotoxicity when compared to either P. ginseng or febuxostat when used alone. The potential mechanism of this combination was mainly mediated by the anti-inflammatory and antioxidant effects of P. ginseng and febuxostat.

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