scholarly journals Correlation between Azole Susceptibilities, Genotypes, and ERG11 Mutations in Candida albicans Isolates Associated with Vulvovaginal Candidiasis in China

2010 ◽  
Vol 54 (8) ◽  
pp. 3126-3131 ◽  
Author(s):  
Shu-Hua Ge ◽  
Zhe Wan ◽  
Juan Li ◽  
Jianping Xu ◽  
Ruo-Yu Li ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Amino Acid ◽  
Oral Cavity ◽  
Target Gene ◽  
Chinese Women ◽  
Missense Mutations ◽  
Statistical Support ◽  
Strain Sc5314 ◽  
The Relationship ◽  
Susceptibility Patterns

ABSTRACT The relationship between susceptibilities to fluconazole and itraconazole and microsatellite CAI genotypes were examined from a total of 154 Candida albicans isolates (97 isolates causing vulvovaginitis in Chinese women and 6 vaginal isolates and 51 oral cavity isolates from asymptomatic carriers). The two dominant genotypes, CAI 30-45 (45 isolates) and CAI 32-46 (33 isolates), associated with vulvovaginitis showed significantly different azole susceptibility patterns with strong statistical support. CAI 32-46 isolates were usually less susceptible to both fluconazole and itraconazole than CAI 30-45 isolates and than the oral isolates with other diversified CAI genotypes. Remarkably different mutation patterns in the azole target gene ERG11 were correspondingly observed among C. albicans isolates representing different genotypes and sources. Isolates with the same or similar CAI genotypes usually possessed identical or phylogenetically closely related ERG11 sequences. Loss of heterozygosity in ERG11 was observed in all the CAI 32-46 isolates but not in the CAI 30-45 isolates and most of the oral isolates sequenced. Compared with the ERG11 sequence of strain SC5314 (X13296), two homozygous missense mutations (G487T and T916C) leading to two amino acid changes (A114S and Y257H) in Erg11p were found in CAI 32-46 isolates. The correlation between azole susceptibility and C. albicans genotype may be of potential therapeutic significance.

scholarly journals The polymorphism of rs6505162 in the MIR423 coding region and recurrent pregnancy loss

Reproduction ◽  
2015 ◽  
Vol 150 (1) ◽  
pp. 65-76 ◽  
Author(s):  
Xing Su ◽  
Yi Hu ◽  
Ying Li ◽  
Jing-Li Cao ◽  
Xue-Qin Wang ◽  
...  
Keyword(s):  
Pregnancy Loss ◽  
Target Gene ◽  
Recurrent Pregnancy Loss ◽  
Chinese Women ◽  
Luciferase Assay ◽  
Coding Region ◽  
Functional Polymorphisms ◽  
Group 4 ◽  
Migratory Capacity ◽  
The Relationship

Although the relationship between polymorphisms in microRNAs (miRNAs) and recurrent pregnancy loss (RPL) has been studied, there is very little data available in the literature. In the present study, we scanned 55 potentially functional polymorphisms in the miRNA coding region in Chinese women with unexplained RPL (URPL; no. 2011-10). The rs6505162 C>A in theMIR423coding region was found to be significantly associated with the occurrence of human URPL. The rare A allele contributed to an increase in the expression of matureMIR423. C to A substitution in the polymorphism rs6505162 in pre-MIR423repressed cell proliferation and migratory capacity. Further investigations showed thatMIR423could inversely regulate the expression of proliferation-associated 2 group 4 (PA2G4) by binding the 3′-UTR ofPA2G4. Dual-luciferase assay indicated that the A allele in the polymorphism rs6505162 could more effectively suppress the expression ofPA2G4than the C allele could. Collectively, the present data suggest that rs6505162 C>A in pre-MIR423may contribute to the genetic predisposition to RPL by disrupting the production of matureMIR423and its target gene, which consequently interferes withMIR423functioning.

scholarly journals Assessing Resistance to the Echinocandin Antifungal Drug Caspofungin in Candida albicans by Profiling Mutations in FKS1

2006 ◽  
Vol 50 (6) ◽  
pp. 2058-2063 ◽  
Author(s):  
Sergey V. Balashov ◽  
Steven Park ◽  
David S. Perlin
Keyword(s):  
Candida Albicans ◽  
Amino Acid ◽  
Molecular Beacon ◽  
Rapid Identification ◽  
Heterozygous Mutation ◽  
Allele Specific ◽  
Double Amino Acid ◽  
Echinocandin Resistance ◽  
Spontaneous Mutants ◽  
The Relationship

ABSTRACT Resistance of clinical isolates of Candida albicans to the echinocandin drug caspofungin is slowly emerging and is linked to mutations in short conserved regions in the FKS1 gene. The most prominent changes occurred at the serine 645 position in Fks1p with substitutions of proline, tyrosine, and phenylalanine. An allele-specific real-time PCR molecular-beacon assay was developed for rapid identification of drug resistance by targeting FKS1 mutations. Mutations altering serine 645 were reliably identified in both heterozygous and homozygous states. The molecular-beacon assay was used to evaluate two large collections of spontaneous mutants from separate strains of C. albicans with resistance (MICs, >16 μg/ml) to caspofungin with the goal of understanding the relationship between FKS1 mutations and echinocandin resistance. Of 85 resistant isolates recovered, all were identified with mutations in FKS1; 93% showed changes at Ser645, with 62% displaying a characteristic S645P substitution expressed as either a homozygous or a heterozygous mutation in FKS1. Two other prominent amino acid substitutions, S645Y and S645F, were found at frequencies of 22% and 8%, respectively. Three new mutations were also identified: T1922C, G1932T, and C1934G, encoding F641S, L644F, and S645C substitutions, respectively. One strain had the double amino acid substitution L644F and S645C. Allele-specific probes were combined in a multiplex assay for reliable screening of known FKS1 mutations. These data support the importance of FKS1p substitutions in echinocandin resistance and demonstrate the feasibility of applying molecular screening for routine resistance assessment.

Surface microhardness of different restorative materials exposed to candida albicans biofilm isolated from the oral cavity of hiv-infected children

2019 ◽  
Vol 4 (1) ◽  
pp. 87-91
Author(s):  
Leandro COSTA ◽  
Larissa SOARES-SILVA ◽  
Paulini Malfei De C. COSTA ◽  
Adrielle MANGABEIRA ◽  
Maristela PORTELA ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Oral Cavity ◽  
Surface Microhardness ◽  
Restorative Materials

MiR-125a-5p Alleviates Dysfunction and Inflammation of Pentylenetetrazol- induced Epilepsy Through Targeting Calmodulin-dependent Protein Kinase IV (CAMK4)

2019 ◽  
Vol 16 (4) ◽  
pp. 365-372 ◽  
Author(s):  
Qishuai Liu ◽  
Li Wang ◽  
Guizhen Yan ◽  
Weifa Zhang ◽  
Zhigang Huan ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Target Gene ◽  
Luciferase Assay ◽  
Enzyme Linked Immunosorbent Assay ◽  
Inflammatory Factor ◽  
Dependent Protein Kinase ◽  
Expression Levels ◽  
Dependent Protein ◽  
Polymerase Chain ◽  
The Relationship

Background: MicroRNAs (miRNA) are known to play a key role in the etiology and treatment of epilepsy through controlling the expression of gene. However, miR-125a-5p in the epilepsy is little known. Epilepsy in rat models was induced by Pentylenetetrazol (PTZ) and miR- 125a-5p profiles in the hippocampus were investigated in our experiment. Also, the relationship between miR-125a-5p and calmodulin-dependent protein kinase IV (CAMK4) was identified and the related mechanism was also illustrated. Methods: The miR-125a-5p mRNA expression levels were evaluated by quantitative real time polymerase chain reaction (qRT-PCR). Western Blot (WB) was used to analyze the CAMK4 protein expression levels. Seizure score, latency and duration were determined based on a Racine scale. The enzyme-linked immunosorbent assay (ELISA) was used to analyze the inflammatory factor expression. The relationship between miR-125a-5p and CAMK4 was detected through dual luciferase assay. Results: Downregulation of miR-125a-5p was observed in the hippocampus of PTZ-induced epilepsy rats. The overexpression of miR-125a-5p attenuated seizure and decreased inflammatory factor level in the hippocampus of PTZ-induced rats. The miR-125a-5p alleviated epileptic seizure and inflammation in PTZ-induced rats by suppressing its target gene, CAMK4. Conclusion: miR-125a-5p may represent a novel therapeutic treatment for PTZ-induced epilepsy by preventing the activation of CAMK4.

scholarly journals Overdiagnosis and overtreatment of nipple and breast candidiasis: A review of the relationship between diagnoses of mammary candidiasis and Candida albicans in breastfeeding women

2021 ◽  
Vol 17 ◽  
pp. 174550652110314
Author(s):  
Pamela Douglas
Keyword(s):  
Candida Albicans ◽  
Human Milk ◽  
Signs And Symptoms ◽  
Breast Pain ◽  
Breastfeeding Support ◽  
Candida Spp ◽  
Healthy Human ◽  
Nipple Areolar Complex ◽  
Areolar Complex ◽  
The Relationship

Background: Breastfeeding mothers commonly experience nipple pain accompanied by radiating, stabbing or constant breast pain between feeds, sometimes associated with pink shiny nipple epithelium and white flakes of skin. Current guidelines diagnose these signs and symptoms as mammary candidiasis and stipulate antifungal medications. Aim: This study reviews existing research into the relationship between Candida albicans and nipple and breast pain in breastfeeding women who have been diagnosed with mammary candidiasis; whether fluconazole is an effective treatment; and the presence of C. albicans in the human milk microbiome. Method: The author conducted three searches to investigate (a) breastfeeding-related pain and C. albicans; (b) the efficacy of fluconazole in breastfeeding-related pain; and (c) composition of the human milk mycobiome. These findings are critiqued and integrated in a narrative review. Results: There is little evidence to support the hypothesis that Candida spp, including C. albicans, in maternal milk or on the nipple-areolar complex causes the signs and symptoms popularly diagnosed as mammary candidiasis. There is no evidence that antifungal treatments are any more effective than the passage of time in women with these symptoms. Candida spp including C. albicans are commonly identified in healthy human milk and nipple-areolar complex mycobiomes. Discussion: Clinical breastfeeding support remains a research frontier. The human milk microbiome, which includes a mycobiome, interacts with the microbiomes of the infant mouth and nipple-areolar complex, including their mycobiomes, to form protective ecosystems. Topical or oral antifungals may disrupt immunoprotective microbial homeostasis. Unnecessary use contributes to the serious global problem of antifungal resistance. Conclusion: Antifungal treatment is rarely indicated and prolonged courses cannot be justified in breastfeeding women experiencing breast and nipple pain. Multiple strategies for stabilizing microbiome feedback loops when nipple and breast pain emerge are required, in order to avoid overtreatment of breastfeeding mothers and their infants with antifungal medications.

scholarly journals Hsa-miR-494-3p attenuates gene HtrA3 transcription to increase inflammatory response in hypoxia/reoxygenation HK2 Cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Qian Gong ◽  
Zhi-ming Shen ◽  
Zhe Sheng ◽  
Shi Jiang ◽  
Sheng-lin Ge
Keyword(s):  
Cardiac Surgery ◽  
Inflammatory Response ◽  
Target Gene ◽  
Kidney Injury ◽  
Human Kidney ◽  
Luciferase Reporter ◽  
The Relationship ◽  
Hk2 Cells ◽  
Dual Luciferase Reporter Assay ◽  
Hypoxia Reoxygenation

AbstractThe occurrence of cardiac surgery-associated acute kidney injury (CSA-AKI) increases hospital stay and mortality. MicroRNAs has a crucial role in AKI. This objective of the current study is to explore the function of hsa-miR-494-3p in inflammatory response in human kidney tubular epithelial (HK2) cells with hypoxia/reoxygenation. According to KDIGO standard, patients after cardiac surgery with cardiopulmonary bypass were divided into two groups: AKI (n = 10) and non-AKI patients (n = 8). HK2 were raised in the normal and hypoxia/reoxygenation circumstances and mainly treated by overexpression ofmiR-494-3p and HtrA3. The relationship between miR-494-3p and HtrA3 was determined by dual-luciferase reporter assay. Our result showed that Hsa-miR-494-3p was elevated in the serum of patients with CSA-AKI, and also induced in hypoxic reoxygenated HK2 cells. Hsa-miR-494-3p also increased a hypoxia-reoxygenation induced inflammatory response in HK2 cells. Moreover, as a target gene of miR-494-3p, overexpression of HtrA3 downregulated the hypoxia-reoxygenation induced inflammatory response in HK2 cells. Overexpression of hsa-miR-494-3p-induced inflammatory response was inhibited by overexpression of HtrA3. Collectively, we identified that hsa-miR-494-3p, a miRNA induced in both circulation of AKI patients and hypoxia-reoxygenation-treated HK2 cells, enhanced renal inflammation by targeting HtrA3, which may suggest a possible role as a new therapeutic target for CSA-AKI.

scholarly journals Recent Advances in Biomarkers and Regenerative Medicine for Diabetic Neuropathy

2021 ◽  
Vol 22 (5) ◽  
pp. 2301
Author(s):  
Yoshikai Fujita ◽  
Tatsufumi Murakami ◽  
Akihiro Nakamura
Keyword(s):  
Diabetic Neuropathy ◽  
Target Gene ◽  
Pathological Condition ◽  
Nerve Fibers ◽  
Nerve Degeneration ◽  
Limb Amputation ◽  
Sensory Impairment ◽  
Mechanical Stimuli ◽  
Pathological Conditions ◽  
The Relationship

Diabetic neuropathy is one of the most common complications of diabetes. This complication is peripheral neuropathy with predominant sensory impairment, and its symptoms begin with hyperesthesia and pain and gradually become hypoesthesia with the loss of nerve fibers. In some cases, lower limb amputation occurs when hypoalgesia makes it impossible to be aware of trauma or mechanical stimuli. On the other hand, up to 50% of these complications are asymptomatic and tend to delay early detection. Therefore, sensitive and reliable biomarkers for diabetic neuropathy are needed for an early diagnosis of this condition. This review focuses on systemic biomarkers that may be useful at this time. It also describes research on the relationship between target gene polymorphisms and pathological conditions. Finally, we also introduce current information on regenerative therapy, which is expected to be a therapeutic approach when the pathological condition has progressed and nerve degeneration has been completed.

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