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Bacterial vaginosis in pregnancy: Evidence-based approaches
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
James A. McGregor, Michael W. McCullough
Intravaginal treatments for bacterial vaginosis are similarly effective at eradication of bacterial vaginosis but have not been shown to improve pregnancy outcomes (38,80,82,84). Metronidazole gel 0.75% one 5-g applicator intravaginally once a day for 5 days or clindamycin 2% one 5-g applicator for 7 days is recommended. Other treatments for bacterial vaginosis have been evaluated: ampicillin, augmentin, ofloxacin, erythromycin, triple sulfa cream, and vaginal acidification (60,84). These treatments are less effective than both oral and vaginal preparations of metronidazole or clindamycin and are not recommended. Similarly, probiotic therapy with microbial products, such as lactobacillus powders and capsules, should be avoided; many of the nondairy products are contaminated with potentially harmful bacteria such as Clostridium sporogenes and Enterococcus species (85). Therapy with yogurt or acidophilus milk is also likely to be of little benefit, since the L. acidophilus strains are not easily established in the vagina (86).
Bacteria and Bioactive Peptides
Published in Prakash Srinivasan Timiri Shanmugam, Understanding Cancer Therapies, 2018
Ameer Khusro, Chirom Aarti, Paul Agastian
This therapy uses anaerobic bacteria that have been transformed with a specific enzyme that converts a nontoxic prodrug into a toxic drug. The enzyme is expressed solely due to the proliferation of the bacteria in the necrotic and hypoxic regions of the tumor and thus, the prodrug is metabolized to the toxic drug only in the tumor. Cytosine deaminase (CD) converts 5-fluorocytosine (5FC) to 5-fluorouracil (5FU), and nitroreductase (NR) converts the prodrug CB1954 to a DNA cross-linking agent. These enzymes have been tested with Clostridium sporogenes, showing satisfactory in vitro results, but in vivo results are disappointing. Recently it was illustrated that CD can be successfully cloned and expressed in the same strain of Clostridium. CD expression was enhanced significantly by combretastatin A-4 phosphate that might be due to the enlargement of the necrotic area in tumors (Theys et al. 2001). Other in vivo studies include the incorporation of NR and CD with Salmonella vector, which is undergoing phase I clinical trials in cancer patients. TAPET (Tumour Amplified Protein Expression Therapy) uses an attenuated strain of S. typhimurium (VNP20009) as a bacterial vector and expresses an E. coli CD in order to deliver anticancer drugs to solid tumors (Luo et al. 2001). The expression of the prodrug-converting enzyme HSV-thymidine kinase (TK) in a purine auxotroph showed enhanced anticancer activity upon the addition of the corresponding prodrug (Pawelek et al. 1997). Transfected B. longum by pBLES100-S-eCD produces cytosine deaminase in the hypoxic tumor, suggesting an effective prodrug-enzyme therapy (Fujimori et al. 2003).
Platelets get gutted by PAG
Published in Platelets, 2020
Iván Parra-Izquierdo, Ryan Bradley, Joseph E. Aslan
Classical and more recent microbiology studies have determined a role for the Clostridium sporogenes gene porA in host metabolism of Phe to PAG. Remarkably, the Hazen lab and colleagues find that transplantation of C. sporogenes mutants engineered to block PAG production lowered thrombosis potential in mice, providing compelling evidence that microbiota-derived PAG fuels platelet hyperactivity in vivo. Finally, through a combination of loss-of-function, gain-of-function and pharmacological experiments, the authors determine that PAG can signal through platelet G protein coupled receptor (GPCR) pathways, and that PAG specifically binds to adrenergic receptors (ADRs). These GPCRs include α2A, α2B and β2 receptors, which are expressed by platelets and known to regulate platelet activation in other contexts. Using a set of specific ADR-blocking agents, the authors further demonstrate that PAG potentiates platelet activation and thrombosis via ADRs in a manner that may explain some of the clinically relevant benefits of ADR inhibitor cardioprotective drugs [6].
Effect of gamma sterilization on the properties of microneedle array transdermal patch system
Published in Drug Development and Industrial Pharmacy, 2020
Honnavar Parthasarathy Swathi, Vishwanath Anusha Matadh, Jhimli Paul Guin, Sathyanarayana Narasimha Murthy, Paranjothy Kanni, Lalit Varshney, Sarasija Suresh, Hagalavadi Nanjappa Shivakumar
Sterility testing of the gamma sterilized MNs was performed on two sterile media namely Fluid Thioglycollate Medium (FTM) and Soyabean Casein Digest Medium (SCDM) by direct inoculation method as per the Indian Pharmacopeia [17] procedure (IP 2007)17. FTM is primarily intended for culture of anaerobic bacteria, whereas SCDM is well suited for the growth of fungi and aerobic bacteria. The sterility test involved two test samples composed of irradiated MNs of PVPK90 and HU. In addition, the test employed six positive controls (three for anaerobic and three for aerobic media) and two negative controls (one each for anaerobic and aerobic media). Three different anaerobic positive controls were used during the test by directly inoculating Staphylococcus aureus, Pseudomonas aeruginosa and Clostridium sporogenes to FTM. Likewise, three different aerobic positive controls were maintained by directly inoculating SCDM with Bacillus subtilis, Aspergillus niger and Candida albicans. The uninoculated FTM and SCDM served as negative controls in the test. After inoculation, FTM was incubated at 30° to 35 °C, while SCDM was incubated at 20 °C to 25 °C under aseptic conditions. The media were observed every week for 14 days for possible turbidity if any that might indicate microbial growth of less than 1 colony-forming unit (CFU).
The gut microbiota – a modulator of endothelial cell function and a contributing environmental factor to arterial thrombosis
Published in Expert Review of Hematology, 2019
Henning Formes, Christoph Reinhardt
The impact that the gut microbiota exerts on carotid artery thrombosis was also confirmed in the ferric chloride injury mouse model [42]. In this study, the microbiota-derived choline metabolite TMAO, the product of the conversion of trimethylamine (TMA) by hepatic flavin monooxygenases (FMOs), was demonstrated to promote platelet hyperreactivity [42]. The enhanced platelet aggregation response in the presence of TMAO was independent of the agonist used, but strictly dependent on choline-enriched diet. Furthermore, the same group recently demonstrated that the TMA-generating gut bacterial CutC and CutD enzymes can be targeted by selective inhibitors to reduce arterial thrombosis resulting from choline-enriched diet, setting the stage for the gut microbiome as a potential drug target in cardiometabolic disease [123]. Furthermore, Hazen and coworkers demonstrated by interspecies fecal microbiota transplantation form humans into germ-free mice and by monoassociation experiments with the TMA generating bacterium Clostridium sporogenes that TMAO-dependent thrombosis potential is a transferrable trait [43,124]. In conclusion, the conversion of microbiota-derived TMA to TMAO by hepatic FMO3 [125] may represent an additional metabolic route that, amongst other effects on cardiovascular physiology [17,126], was suggested to stimulate prothrombotic platelet function and arterial thrombosis (Figure 1).