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Maternal mortality is defined as the number of deaths related to complications during or after childbirth. Food deserts are defined as regions that have limited access to affordable and healthy food options. This study utilized R to analyze data from the United States Department of Agriculture Economic Research Service’s Food Access Research Atlas and maternal mortality rates from the UCSF paper “Maternal Morbidity and Outcomes Including Mortality, California 2001-2006.” to search for an association between the two variables. The research atlas maps areas in Northern California with low access to grocery stores, as well as provides information on food access throughout the United States using census tracts. The independent variable in this study is food access and the dependent variable is maternal mortality. After analyzing the data collected using R, correlation graphs were created and intercepts and R values were identified. This information was used to further understand the relationship between food access and maternal mortality. For this study, we focused our scope on the Bay Area counties of Alameda, Contra Costa, Marin, San Francisco, Santa Clara, Solano, and Sonoma, which are located in Northern California.

fMRI imaging measures brain activity by detecting changes in the brain that are associated with blood flow and can be used in order to determine the size and location of visual field maps. This study measured BOLD responses in humans to understand spatial summation by showing them spatial contrast pattern images through vertical and horizontal apertures.Nonlinear responses can be computed from the visual field responses, from which the spatial summation ratio is calculated. A ratio of less than one indicates a smaller response to exposure to a full aperture or contrast image than predicted by the linear model. Datasets were analyzed using MATLAB, producing eccentricity maps of the visual cortices from stimuli. BOLD response curves identify the intensity of the maps within a particular voxel. The eccentricity maps can then be overlain on anatomical representations of the brain, characterizing the various visual field cortices. Methods of fMRI data analysis are confirmed with the results of this study.

Earthquakes, one of nature's most spectacular events, can have far-reaching consequences for the population, including fatalities and injuries. Secondary effects, most notably landslides, tsunamis, and considerable ground motion and coseismal occurrences, are blamed for the ensuing calamities. These factors have the potential to exacerbate the already dire situation by creating conditions favourable to the spread of infectious diseases, which could cause even more casualties and delay relief efforts. This review presents a thorough narrative analysis of the literature on infectious diseases triggered by earthquakes in different regions of the world. It includes discussing the symptoms, causative agents, risk factors, and prevention strategies. Infections of the respiratory system, digestive system, and skin, as well as those transmitted by vectors, are the most common types of sickness among persons affected by the earthquake. In addition, methods are proposed for effectively preventing infectious diseases brought on by earthquakes. A robust channel for tracking and monitoring is required to detect infectious diseases in case of disaster before and after their occurrence. This strategy significantly aids in tracking epidemics, checking the accuracy of early warnings, and bolstering relief and restoration efforts. [ABSTRACT FROM AUTHOR]

Ginseng (Panax ginseng Meyer) is a popular traditional herbal medicine used worldwide. Patients often take ginseng preparations with other medicines where the ginseng dose could exceed the recommended dose during long‐term administration. However, ginseng–drug interactions at high doses of ginseng are poorly understood. This study showed the possibility of herb–drug interactions between the Korean red ginseng (KRG) extract and cytochrome P450 (CYP) substrates in higher administration in mice. The CYP activities were determined in vivo after oral administration of KRG extract doses of 0.5, 1.0, and 2.0 g/kg for 2 or 4 weeks by monitoring the concentration of five CYP substrates/metabolites in the blood. The area under the curve for OH‐midazolam/midazolam catalysed by CYP3A was increased significantly by the administration of 2.0 g/kg KRG extract for 2 and 4 weeks. CYP3A‐catalysed midazolam 1ʹ‐hydroxylation also increased significantly in a dose‐ and time‐dependent manner in the S9 fraction of mouse liver which was not related to induction by transcription. Whereas CYP2D‐catalysed dextromethorphan O‐deethylation decreased in a dose‐ and time‐dependent manner in vivo. In conclusion, interactions were observed between KRG extract and CYP2D and CYP3A substrates at subchronic–high doses of KRG administration in mice. [ABSTRACT FROM AUTHOR]

1. Glycyrol is a coumestan derivative that is isolated from roots of Glycyrrhiza uralensis. Glycyrol exhibits several biological effects, including anti-oxidative and anti-inflammatory effects. 2. Herein, we characterized glycyrol metabolism by cytochrome P450 enzymes (CYPs) and UDP-glucuronosyltransferases (UGTs) using human liver microsomes (HLM), human liver cytosol, human intestinal microsomes, or human recombinant cDNA-expressed CYPs and UGTs. The analysis was conducted using high resolution mass spectroscopy (HR-MS) on a Q ExactiveTM HF Hybride Quadrupole-Orbitrap mass spectrometer. 3. NADPH-supplemented HLM generated six glycyrol metabolites (M1–M6) via hydroxylation, oxidation, and hydration; both NADPH- and UDPGA-supplemented liver microsomes generated three glucuronides (M7–M9). Reaction phenotyping revealed that CYP1A2 is the primary enzyme responsible for phase I metabolism, with minor involvement of the CYP3A4/5, CYP2D6, and CYP2E1 enzymes. Glucuronidation of glycyrol was primarily mediated by UGT1A1, UGT1A3, UGT1A9, and UGT2B7. 4. In conclusion, glycyrol undergoes the efficient metabolic hydroxylation and glucuronidation reactions in human liver microsomes, which are predominantly catalyzed by CYP1A2, UGT1A1/3/9, and UGT2B7. [ABSTRACT FROM AUTHOR]

Loxoprofen is a prodrug that exerts strong analgesic and anti‐inflammatory effects through its active trans‐alcohol metabolite, which is produced in the liver by carbonyl reductase. Previous metabolic studies have evaluated loxoprofen, but its sulfate and taurine conjugates have not yet been studied. We characterized the metabolomic profile of loxoprofen in rat plasma, urine, and feces using high‐resolution mass spectrometry. We identified 17 metabolites of loxoprofen in the three different biological matrices, 13 of which were detected in plasma and feces and 16 in urine. Amongst these metabolites, two novel taurine conjugates (M12 and M13) and two novel acyl glucuronides (M14, M15) were identified for the first time in rats. In addition, we detected three novel sulfate conjugates (M9, M10, and M11) of loxoprofen. Further study of these metabolites of loxoprofen is essential in order to assess their potency and toxicity. [ABSTRACT FROM AUTHOR]

1. Leelamine is a diterpene compound found in the bark of pine trees and has garnered considerable interest owing to its potent anticancer properties. The aim of the present study was to investigate the metabolic profile of leelamine in human liver microsomes (HLMs) and mice using liquid chromatography-tandem mass spectrometry (LC-MS/MS). 2. We found that leelamine undergoes only Phase I metabolism, which generates one metabolite that is mono-hydroxylated at the C9 carbon of the octahydrophenanthrene ring (M1) both in vitro and in vivo. The structure and metabolic pathway of M1 were determined from the MSn fragmentation obtained by collision-induced dissociation using LC-MS/MS in HLMs. 3. Cytochrome p450 (CYP) 2D6 was found to be the dominant CYP enzyme involved in the biotransformation of leelamine to its hydroxylated metabolite, whereas CYP2C19, CYP1A1, and CYP3A4 contributed to some extent. 4. Moreover, we identified only one metabolite M1, in the urine, but none in the feces. In conclusion, leelamine was metabolized to a mono-hydroxyl metabolite by CYP2D6 and mainly excreted in the urine. [ABSTRACT FROM AUTHOR]

Loxoprofen (LOX) is a non-selective cyclooxygenase inhibitor that is widely used for the treatment of pain and inflammation caused by chronic and transitory conditions. Its alcoholic metabolites are formed by carbonyl reductase (CR) and they consist of trans-LOX, which is active, and cis-LOX, which is inactive. In addition, LOX can also be converted into an inactive hydroxylated metabolite (OH-LOXs) by cytochrome P450 (CYP). In a previous study, we reported that CYP3A4 is primarily responsible for the formation of OH-LOX in human liver microsomes. Although metabolism by CYP3A4 does not produce active metabolites, it can affect the conversion of LOX into trans-/cis-LOX, since CYP3A4 activity modulates the substrate LOX concentration. Although the pharmacokinetics (PK) and metabolism of LOX have been well defined, its CYP-related interactions have not been fully characterized. Therefore, we investigated the metabolism of LOX after pretreatment with dexamethasone (DEX) and ketoconazole (KTC), which induce and inhibit the activities of CYP3A, respectively. We monitored their effects on the PK parameters of LOX, cis-LOX, and trans-LOX in mice, and demonstrated that their PK parameters significantly changed in the presence of DEX or KTC pretreatment. Specifically, DEX significantly decreased the concentration of the LOX active metabolite formed by CR, which corresponded to an increased concentration of OH-LOX formed by CYP3A4. The opposite result occurred with KTC (a CYP3A inhibitor) pretreatment. Thus, we conclude that concomitant use of LOX with CYP3A modulators may lead to drug–drug interactions and result in minor to severe toxicity even though there is no direct change in the metabolic pathway that forms the LOX active metabolite. [ABSTRACT FROM AUTHOR]

Loxoprofen, a propionic acid derivative, non-steroidal anti-inflammatory drug (NSAID) is a prodrug that is reduced to its active metabolite, trans-alcohol form (Trans-OH) by carbonyl reductase enzyme in the liver. Previous studies demonstrated the hydroxylation and glucuronidation of loxoprofen. However, the specific enzymes catalyzing its metabolism have yet to be identified. In the present study, we investigated metabolic enzymes, such as cytochrome P450 (CYP) and UDP-glucuronosyltransferase (UGT), which are involved in the metabolism of loxoprofen. Eight microsomal metabolites of loxoprofen were identified, including two alcohol metabolites (M1 and M2), two mono-hydroxylated metabolites (M3 and M4), and four glucuronide conjugates (M5, M6, M7, and M8). Based on the results for the formation of metabolites when incubated in dexamethasone-induced microsomes, incubation with ketoconazole, and human recombinant cDNA-expressed cytochrome P450s, we identified CYP3A4 and CYP3A5 as the major CYP isoforms involved in the hydroxylation of loxoprofen (M3 and M4). Moreover, we identified that UGT2B7 is the major UGT isoform catalyzing the glucuronidation of loxoprofen and its alcoholic metabolites. Further experimental studies should be carried out to determine the potency and toxicity of these identified metabolites of loxoprofen, in order to fully understand of mechanism of loxoprofen toxicity. [ABSTRACT FROM AUTHOR]

Mitochondrial uncouplers are small molecule protonophores that act to dissipate the proton motive force independent of adenosine triphosphate (ATP) synthase. Mitochondrial uncouplers such as BAM15 increase respiration and energy expenditure and have potential in treating a variety of metabolic diseases. In this study, we disclose the structure-activity relationship profile of 6-substituted [1,2,5]oxadiazolo[3,4- b ]pyridin-7-ol derivatives of BAM15. Utilizing an oxygen consumption rate assay as a measure of increased cellular respiration, SHO1122147 ( 7m ) displayed an EC 50 of 3.6 μM in L6 myoblasts. Pharmacokinetic studies indicated a half-life of 2 h, C max of 35 μM, and no observed adverse effects at 1,000 mg kg -1 dose in mice. In a Gubra-Amylin (GAN) mouse model of MASH, SHO1122147 was efficacious in decreasing body weight and liver triglyceride levels at 200 mg kg -1 day -1 without changes in body temperature. These findings indicate the potential of utilizing novel [1,2,5]oxadiazolo[3,4- b ]pyridin-7-ol mitochondrial uncouplers for treatment of fatty liver disease and obesity.

Autoimmune hepatitis (AIH) is a chronic liver disease characterized by immune-mediated destruction of hepatocytes, leading to inflammation and fibrosis. In recent years, significant advances have been made in understanding the pathogenesis, epidemiology, diagnosis, and treatment of AIH. This comprehensive narrative review aims to provide an up-to-date overview of these advances. The review begins by outlining the historical background of AIH, dating back to its initial recognition in the 1940s, and highlights the evolution of diagnostic criteria and classification based on autoantibody profiles. The epidemiology of AIH is explored, discussing its varying prevalence across different regions and the role of genetic predisposition, viral infections, and drug exposure as risk factors. Furthermore, the review delves into the pathogenesis of AIH, focusing on the dysregulated immune response, involvement of T cells, and potential contribution of the gut microbiome. Clinical presentation, diagnostic criteria, and liver biopsy as crucial tools for diagnosis are also discussed. Regarding management, the review provides an in-depth analysis of the standard first-line treatments involving glucocorticoids and azathioprine, as well as alternative therapies for non-responsive cases. Additionally, emerging second and third-line treatment options are examined. In conclusion, this narrative review highlights the complexity of AIH and underscores the importance of early diagnosis and individualized treatment approaches to improve patient outcomes. Further research and clinical trials are needed to optimize AIH management and ensure a better long-term prognosis for affected individuals., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2023, Yadav et al.)

Introduction and Importance: Bud-Chiari syndrome is an uncommon disease due to obstruction of hepatic venous outflow. Clinical manifestations range from asymptomatic cases to those requiring liver transplants. The study highlights the importance of diagnosing a case of Budd-Chiari syndrome which has been suspected with abdominal tuberculosis where anti-tubercular drugs may themselves damage the liver., Case Presentation: Herein we report a case of 18 years old female presenting with upper abdominal pain along with recurrent abdominal distention, jaundice, and deranged liver function. Also, adenosine deaminase level was raised in both pleural and peritoneal fluids, hence, anti-tubercular treatment was started but could not be continued as she developed adverse reactions to these drugs. CT scan later revealed features suggestive of Budd-Chiari syndrome. Initially, she was managed with balloon angioplasty, but her condition worsened ultimately requiring a liver transplant., Clinical Discussion: Budd Chiari syndrome can present with subtle presentation and since abdominal tuberculosis is very non-specific, the two conditions can be very confusing, particularly in the tubercular endemic region. Detailed clinical assessment along with proper investigations and imaging should be performed for early recognition as both conditions are associated with high morbidity and mortality if not treated timely., Conclusion: The necessity of careful investigation and consideration of Budd-Chiari syndrome as an important cause of ascites with jaundice and deranged liver function in TB endemic regions along with early anticipation of liver transplant is necessary, as in this case., Competing Interests: None., (© 2022 The Author(s).)