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1.
PLoS One ; 19(5): e0302570, 2024.
Article in English | MEDLINE | ID: mdl-38709749

ABSTRACT

University students are at high risk of sexually transmitted infections due to the lack of adequate sexual education, as well as multiple associated factors, which lead to risky sexual practices. It is important to update data about sexual behaviors to identify the main factors associated with sexually risky behaviors. The present study aimed to evaluate the current prevalence of sexually risky practices in medical students. A cross-sectional study was conducted among medical students through an anonymous self-administered online questionnaire including demographic characteristics and sexual behaviors. We used descriptive statistics and multivariable regression to analyze the data collected. A total of 1520 undergraduate medical students aged between 18 and 28 years old were included in the study. Sixty percent of the students were sexually active with a higher proportion in men (70%), likewise, they had an earlier sexual debut (16.5 vs 16.9 years old), and a greater number of lifetime sexual partners than women (3.8 vs 2.2). The main sexual activity in both groups was vaginal sex with high use of condoms (75%), however, most of them (67%) reported having unprotected oral sex. Logistic regression analysis showed that condomless sex was associated with having oral sex, anal sex, and being female. The findings of this study showed that medical university students are involved in risky sexual behaviors, the major risk factor was unprotected oral sex. Based on these results, we recommended designing interventions to improve sexual education and preventive approaches from early stages such as in middle school students to mitigate sexually transmitted infections among medical university students.


Subject(s)
Risk-Taking , Sexual Behavior , Students, Medical , Humans , Male , Female , Students, Medical/statistics & numerical data , Students, Medical/psychology , Mexico/epidemiology , Adolescent , Adult , Young Adult , Sexual Behavior/statistics & numerical data , Prevalence , Cross-Sectional Studies , Surveys and Questionnaires , Sexually Transmitted Diseases/epidemiology , Unsafe Sex/statistics & numerical data
2.
Genes (Basel) ; 14(4)2023 04 09.
Article in English | MEDLINE | ID: mdl-37107645

ABSTRACT

BACKGROUND: Ellis-van Creveld syndrome (EvCS) is an autosomal recessive ciliopathy with a disproportionate short stature, polydactyly, dystrophic nails, oral defects, and cardiac anomalies. It is caused by pathogenic variants in the EVC or EVC2 genes. To obtain further insight into the genetics of EvCS, we identified the genetic defect for the EVC2 gene in two Mexican patients. METHODS: Two Mexican families were enrolled in this study. Exome sequencing was applied in the probands to screen potential genetic variant(s), and then Sanger sequencing was used to identify the variant in the parents. Finally, a prediction of the three-dimensional structure of the mutant proteins was made. RESULTS: One patient has a compound heterozygous EVC2 mutation: a novel heterozygous variant c.519_519 + 1delinsT inherited from her mother, and a heterozygous variant c.2161delC (p.L721fs) inherited from her father. The second patient has a previously reported compound heterozygous EVC2 mutation: nonsense mutation c.645G > A (p.W215*) in exon 5 inherited from her mother, and c.273dup (p.K92fs) in exon 2 inherited from her father. In both cases, the diagnostic was Ellis-van Creveld syndrome. Three-dimensional modeling of the EVC2 protein showed that truncated proteins are produced in both patients due to the generation of premature stop codons. CONCLUSION: The identified novel heterozygous EVC2 variants, c.2161delC and c.519_519 + 1delinsT, were responsible for the Ellis-van Creveld syndrome in one of the Mexican patients. In the second Mexican patient, we identified a compound heterozygous variant, c.645G > A and c.273dup, responsible for EvCS. The findings in this study extend the EVC2 mutation spectrum and may provide new insights into the EVC2 causation and diagnosis with implications for genetic counseling and clinical management.


Subject(s)
Ellis-Van Creveld Syndrome , Membrane Proteins , Humans , Female , Membrane Proteins/genetics , Intercellular Signaling Peptides and Proteins/genetics , Ellis-Van Creveld Syndrome/genetics , Ellis-Van Creveld Syndrome/diagnosis , Pedigree , Mutation , Codon, Nonsense
3.
Int J Mol Sci ; 24(4)2023 Feb 13.
Article in English | MEDLINE | ID: mdl-36835161

ABSTRACT

Alzheimer's disease (AD) is the most common neurodegenerative disease in the world. It is classified as familial and sporadic. The dominant familial or autosomal presentation represents 1-5% of the total number of cases. It is categorized as early onset (EOAD; <65 years of age) and presents genetic mutations in presenilin 1 (PSEN1), presenilin 2 (PSEN2), or the Amyloid precursor protein (APP). Sporadic AD represents 95% of the cases and is categorized as late-onset (LOAD), occurring in patients older than 65 years of age. Several risk factors have been identified in sporadic AD; aging is the main one. Nonetheless, multiple genes have been associated with the different neuropathological events involved in LOAD, such as the pathological processing of Amyloid beta (Aß) peptide and Tau protein, as well as synaptic and mitochondrial dysfunctions, neurovascular alterations, oxidative stress, and neuroinflammation, among others. Interestingly, using genome-wide association study (GWAS) technology, many polymorphisms associated with LOAD have been identified. This review aims to analyze the new genetic findings that are closely related to the pathophysiology of AD. Likewise, it analyzes the multiple mutations identified to date through GWAS that are associated with a high or low risk of developing this neurodegeneration. Understanding genetic variability will allow for the identification of early biomarkers and opportune therapeutic targets for AD.


Subject(s)
Alzheimer Disease , Neurodegenerative Diseases , Humans , Alzheimer Disease/genetics , Amyloid beta-Peptides/genetics , Amyloid beta-Protein Precursor/metabolism , Genome-Wide Association Study , Mutation , Neurodegenerative Diseases/genetics , Presenilin-1/genetics , Presenilin-2/genetics
4.
Molecules ; 27(17)2022 Sep 01.
Article in English | MEDLINE | ID: mdl-36080417

ABSTRACT

Infections caused by micro-organisms of the genus Candida are becoming a growing health problem worldwide. These fungi are opportunistic commensals that can produce infections-clinically known as candidiasis-in immunocompromised individuals. The indiscriminate use of different anti-fungal treatments has triggered the resistance of Candida species to currently used therapies. In this sense, propolis has been shown to have potent antimicrobial properties and thus can be used as an approach for the inhibition of Candida species. Therefore, this work aims to evaluate the anti-Candida effects of a propolis extract obtained from the north of Mexico on clinical isolates of Candida species. Candida species were specifically identified from oral lesions, and both the qualitative and quantitative anti-Candida effects of the Mexican propolis were evaluated, as well as its inhibitory effect on C. albicans isolate's germ tube growth and chemical composition. Three Candida species were identified, and our results indicated that the inhibition halos of the propolis ranged from 7.6 to 21.43 mm, while that of the MFC and FC50 ranged from 0.312 to 1.25 and 0.014 to 0.244 mg/mL, respectively. Moreover, the propolis was found to inhibit germ tube formation (IC50 ranging from 0.030 to 1.291 mg/mL). Chemical composition analysis indicated the presence of flavonoids, including pinocembrin, baicalein, pinobanksin chalcone, rhamnetin, and biochanin A, in the Mexican propolis extract. In summary, our work shows that Mexican propolis presents significant anti-Candida effects related to its chemical composition, and also inhibits germ tube growth. Other Candida species virulence factors should be investigated in future research in order to determine the mechanisms associated with antifungal effects against them.


Subject(s)
Candida , Propolis , Antifungal Agents/pharmacology , Candida albicans , Humans , Mexico , Microbial Sensitivity Tests , Plant Extracts/chemistry , Propolis/chemistry , Propolis/pharmacology
5.
Hum Vaccin Immunother ; 18(1): 2028514, 2022 12 31.
Article in English | MEDLINE | ID: mdl-35103580

ABSTRACT

Human papillomavirus (HPV) is one of the most common causes of sexually transmitted diseases, and the main etiology of cervical cancer. This study was aimed to assess type-specific cervical HPV prevalence and their association with HPV-specific antibodies in a cohort of female university students. HPV genotyping was performed by amplifying and sequencing a fragment of the L1 protein. A BLAST search was performed to identify HPV types. HPV-specific IgG antibodies were measured by ELISA in serum samples. A total of 129 women participated, with an average age of 21.75 years. The prevalence of vaginal HPV infection was 74.42%. The most predominant high-risk HPV types were 18 (13.95%), 31 (10.85%), and 16 (9.3%). We found that early age at coitarche and a higher number of sexual partners were significantly associated with a high prevalence of HPV infection. In addition to sexual behavior, we observed that the presence of serum-specific IgG antibodies against HPV can impact the prevalence of the virus. Seropositivity to HPV-16 and HPV-18 was associated with a lower prevalence of HPV-16, but not for other HPV types. Of note, there was a lower proportion of HPV-specific seropositivity in women who had the presence of the same HPV type in a cervical specimen, suggesting an immunoregulatory mechanism associated with the viral infection. In conclusion, the prevalence of HPV in university women was higher than expected and it was associated with early age of sexual debut, an increasing number of sexual partners, and a low proportion of HPV seropositivity.


Subject(s)
Papillomavirus Infections , Adult , Antibodies, Viral , DNA, Viral/analysis , Female , Humans , Immunoglobulin G , Mexico/epidemiology , Papillomaviridae , Prevalence , Risk Factors , Seroepidemiologic Studies , Students , Universities , Young Adult
6.
Article in English | MEDLINE | ID: mdl-33563162

ABSTRACT

Knowledge of epidemiology, genetic etiopathogenesis, diagnostic criteria, and management of familial hypercholesterolemia have increased in the last two decades. Several population studies have shown that familial hypercholesterolemia is more frequent than previously thought, making this entity the most common metabolic disease with monogenic inheritance in the world. Identification of causal heterozygous pathogenic variants in LDLR, APOB, and PCSK9 genes has increased diagnostic accuracy of classical criteria (extreme hypercholesterolemia, personal / family history of premature coronary artery disease or other cardiovascular diseases). Genetic screening has been recently introduced in many European countries to detect patients with familial hypercholesterolemia, mainly affected pediatric subjects, asymptomatic or those at the beggining of their disease, to increase surveillance and avoid complications such as cardiovascular diseases. Cholesterol- lowering drugs should be started as soon as the diagnosis is made. Various combinations between drugs can be used when the goal is not achieved. New therapies, including small interference ribonucleic acids (siRNA) are being tested in different clinical trials.


Subject(s)
Anticholesteremic Agents , Cardiovascular Diseases , Hyperlipoproteinemia Type II , Anticholesteremic Agents/therapeutic use , Cardiovascular Diseases/epidemiology , Child , Humans , Hyperlipoproteinemia Type II/diagnosis , Hyperlipoproteinemia Type II/epidemiology , Hyperlipoproteinemia Type II/genetics , Mutation , Phenotype , Proprotein Convertase 9/genetics , Receptors, LDL/genetics
7.
Antioxidants (Basel) ; 10(12)2021 Dec 19.
Article in English | MEDLINE | ID: mdl-34943117

ABSTRACT

The skin is the main external organ. It protects against different types of potentially harmful agents, such as pathogens, or physical factors, such as radiation. Skin disorders are very diverse, and some of them lack adequate and accessible treatment. The photoaging of the skin is a problem of great relevance since it is related to the development of cancer, while psoriasis is a chronic inflammatory disease that causes scaly skin lesions and deterioration of the lifestyle of people affected. These diseases affect the patient's health and quality of life, so alternatives have been sought that improve the treatment for these diseases. This review focuses on describing the properties and benefits of flavonoids from propolis against these diseases. The information collected shows that the antioxidant and anti-inflammatory properties of flavonoids play a crucial role in the control and regulation of the cellular and biochemical alterations caused by these diseases; moreover, flavones, flavonols, flavanones, flavan-3-ols, and isoflavones contained in different worldwide propolis samples are the types of flavonoids usually evaluated in both diseases. Therefore, the research carried out in the area of dermatology with bioactive compounds of different origins is of great relevance to developing preventive and therapeutic approaches.

8.
Biology (Basel) ; 10(5)2021 May 12.
Article in English | MEDLINE | ID: mdl-34065939

ABSTRACT

Infectious diseases are a significant problem affecting the public health and economic stability of societies all over the world. Treatment is available for most of these diseases; however, many pathogens have developed resistance to drugs, necessitating the development of new therapies with chemical agents, which can have serious side effects and high toxicity. In addition, the severity and aggressiveness of emerging and re-emerging diseases, such as pandemics caused by viral agents, have led to the priority of investigating new therapies to complement the treatment of different infectious diseases. Alternative and complementary medicine is widely used throughout the world due to its low cost and easy access and has been shown to provide a wide repertoire of options for the treatment of various conditions. In this work, we address the relevance of the effects of propolis on the causal pathogens of the main infectious diseases with medical relevance; the existing compiled information shows that propolis has effects on Gram-positive and Gram-negative bacteria, fungi, protozoan parasites and helminths, and viruses; however, challenges remain, such as the assessment of their effects in clinical studies for adequate and safe use.

9.
Nutrients ; 13(1)2020 Dec 29.
Article in English | MEDLINE | ID: mdl-33383693

ABSTRACT

The use of alternative medicine products has increased tremendously in recent decades and it is estimated that approximately 80% of patients globally depend on them for some part of their primary health care. Propolis is a beekeeping product widely used in alternative medicine. It is a natural resinous product that bees collect from various plants and mix with beeswax and salivary enzymes and comprises a complex mixture of compounds. Various biomedical properties of propolis have been studied and reported in infectious and non-infectious diseases. However, the pharmacological activity and chemical composition of propolis is highly variable depending on its geographical origin, so it is important to describe and study the biomedical properties of propolis from different geographic regions. A number of chronic diseases, such as diabetes, obesity, and cancer, are the leading causes of global mortality, generating significant economic losses in many countries. In this review, we focus on compiling relevant information about propolis research related to diabetes, obesity, and cancer. The study of propolis could generate both new and accessible alternatives for the treatment of various diseases and will help to effectively evaluate the safety of its use.


Subject(s)
Chronic Disease/drug therapy , Propolis/pharmacology , Animals , Antineoplastic Agents/pharmacology , Bees , Biological Products , Geography , Humans , Noncommunicable Diseases , Obesity , Phytochemicals , Waxes/pharmacology
10.
Int J Dermatol ; 57(8): 965-972, 2018 Aug.
Article in English | MEDLINE | ID: mdl-29855039

ABSTRACT

Hypohidrotic Ectodermal Dysplasia (HED) is a genetic human disorder which affects structures of ectodermal origin. Although there are autosomal recessive and dominant forms, X-linked (XL) is the most frequent form of the disease. This XL-HED phenotype is associated with mutations in the gene encoding the transmembrane protein ectodysplasin-1 (EDA1), a member of the TNFα-related signaling pathway. The proteins from this pathway are involved in signal transduction from ectoderm to mesenchyme leading to the development of ectoderm-derived structures in the fetus such as hair, teeth, skin, nails, and eccrine sweat glands. The aim of this review was to update the main clinical characteristics of HED regarding to recent molecular advances in the comprehension of all the possible genes involved in this group of disorders since it is known that Eda-A1-Edar signaling has multiple roles in ectodermal organ development, regulating their initiation, morphogenesis, and differentiation steps. The knowledge of the biological mechanisms that generate HED is needed for both a better detection of possible cases and for the design of efficient prevention and treatment approaches.


Subject(s)
Ectodermal Dysplasia 1, Anhidrotic/genetics , Ectodysplasins/genetics , Edar Receptor/genetics , Edar-Associated Death Domain Protein/genetics , I-kappa B Kinase/genetics , Anodontia/etiology , Ectodermal Dysplasia 1, Anhidrotic/complications , Ectodermal Dysplasia 1, Anhidrotic/diagnosis , Ectodermal Dysplasia 1, Anhidrotic/pathology , Humans , Hypohidrosis/etiology , Hypotrichosis/etiology , Mutation , Signal Transduction
11.
Acta Reumatol Port ; 42(2): 155-161, 2017.
Article in English | MEDLINE | ID: mdl-28379210

ABSTRACT

AIM: The study has two aims: 1) to evaluate the association of IL-17 polymorphism rs2275913 with RA severity and 2) to evaluate if this particular SNP is associated with susceptibility for RA in Mexican patients. METHODS: Seventy-six RA patients and ninety-four healthy controls were included in the study. RA patients were evaluated according to DAS 28. Treatment with DMARD'S was prescribed and radiological damage was evaluated according to the Larsen method. A case-control study was used. Oral epithelial cells were obtained as source for genetic material. DNA was amplified using PCR. Subsequently, a RFLP was carried out. Finally, in order to confirm the IL-17 SNP rs2275913 presence, direct sequencing of the DNA was performed. RESULTS: A significant difference was observed between the RA patients and controls when the prevalence of IL-17 SNP rs2275913 was compared. There was a statistically significant disparity among the two groups with an OR of 5.6 (95%CI 1.5 - 20.9, P=<0.01). In this study was observed that the RA patients who were positive for the IL-17 polymorphism rs2275913 required 3 DMARDs to control the disease compared to 32% of the patients who were negative for the IL-17 polymorphism rs2275913, OR 6.6 (95%CI 1.6 - 27.0, P<0.01). CONCLUSION: This study draws two main conclusions: 1) The presence of IL-17 polymorphism rs2275913 is closely related to a more severe form of the disease and as a result, a higher number of DMARDs required to control it, 2) The presence of IL-17 polymorphism rs2275913 may confer a risk of developing RA in Mexican carriers.


Subject(s)
Antirheumatic Agents/administration & dosage , Arthritis, Rheumatoid/drug therapy , Arthritis, Rheumatoid/genetics , Interleukin-17/genetics , Polymorphism, Single Nucleotide , Arthritis, Rheumatoid/epidemiology , Case-Control Studies , Female , Humans , Male , Mexico , Middle Aged , Prospective Studies
12.
Chem Biol Interact ; 238: 170-9, 2015 Aug 05.
Article in English | MEDLINE | ID: mdl-26148435

ABSTRACT

Cellular response to arsenic is strongly dependent on p53 functional status. Primarily arresting the cell cycle in G1 or G2/M phases, arsenic treatment also induces an increase in the S-phase time in wild-type p53 cells. In contrast, cells with a non-functional p53 display only a subtle increase in the S phase, indicating arsenic differentially affects the cell cycle depending on p53 status. Importantly, it has been reported that arsenic induces reactive oxygen species (ROS), a process counteracted by p53. To evaluate the participation of p53 in the lengthening of the S phase and the connection between the transient cell cycle arrest and oxidative stress, we evaluated the cell response to arsenic in MCF-7 and H1299 cells, and analyzed p53's role as a transcription factor in regulating genes involved in ROS reduction and S phase transition. Herein, we discovered that arsenic induced an increase in the population of S phase cells that was dependent on the presence and transcriptional activity of p53. Furthermore, for the first time, we demonstrate that arsenic activates p53-dependent transcription of ROS detoxification genes, such as SESN1, and by an indirect mechanism involving ATF3, genes that could be responsible for the S phase cell cycle arrest, such as CDC25A.


Subject(s)
Arsenites/toxicity , Reactive Oxygen Species/metabolism , S Phase Cell Cycle Checkpoints/drug effects , Signal Transduction/drug effects , Sodium Compounds/toxicity , Tumor Suppressor Protein p53/metabolism , cdc25 Phosphatases/genetics , cdc25 Phosphatases/metabolism , Activating Transcription Factor 3/genetics , Activating Transcription Factor 3/metabolism , Cell Line, Tumor , Down-Regulation/drug effects , Heat-Shock Proteins/genetics , Heat-Shock Proteins/metabolism , Humans , MCF-7 Cells , Promoter Regions, Genetic , Protein Binding , RNA, Messenger/metabolism , Transcription, Genetic/drug effects , Tumor Suppressor Protein p53/genetics
13.
Int J Dermatol ; 54(7): 790-4, 2015 Jul.
Article in English | MEDLINE | ID: mdl-25626993

ABSTRACT

BACKGROUND: Hypohidrotic ectodermal dysplasia (HED) is a human genetic disorder that affects structures of ectodermal origin such as hair, teeth, and sweat glands. Although there are autosomal recessive and dominant forms, X-linked (XL) is the most frequent form of the disease. This XL-HED phenotype is associated with mutations in the gene encoding the transmembrane protein ectodysplasin-1 (EDA1). We report the clinical and molecular analysis of a novel mutation in exon 1 affecting the transmembrane domain of the protein. METHODS: We have screened 20 members of a family from Yucatán, México, nine men and 11 women, searching clinical and histopathological signs of HED. We searched mutations in EDA1 gene from patients with XL-HED, carriers, and controls. RESULTS: We identified seven men with clinical characteristics of HED showing short toes and plantar hyperkeratosis not reported previously in patients with HED. A mutational study of the EDA1 gene showed that all seven patients with HED carry a novel missense mutation of the nucleotide 409 (c.409T>C) in exon 1, which changes p.Leu56-Pro in the protein amino acid sequence; five women are heterozygous compatible with carrier status. CONCLUSIONS: We found a novel missense mutation in exon 1 of the EDA1 gene in a putative Mayan family from México with XL-HED. We identified in this population some novel clinical signs of HED.


Subject(s)
Ectodermal Dysplasia 1, Anhidrotic/genetics , Ectodysplasins/genetics , Mutation, Missense , Exons , Female , Heterozygote , Humans , Keratoderma, Palmoplantar/genetics , Male , Pedigree , Toes/abnormalities
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