Access to general obstetrics and gynecology care among Medicaid beneficiaries and the privately insured: a nationwide mystery caller study in the USA.

BACKGROUND: The mean wait time for new patient appointments has been growing across specialties, including obstetrics and gynecology, in recent years. This study aimed to assess the impact of insurance type (Medicaid versus commercial insurance) on new patient appointment wait times in general obstetrics and gynecology practices. METHODS: A cross-sectional study used covert mystery calls to general obstetrician gynecologists. Physicians were selected from the American College of Obstetricians and Gynecologists directory and stratified by districts to ensure nationwide representation. Wait times for new patient appointments were collected and analyzed. RESULTS: Regardless of insurance type, the mean wait time for all obstetrician gynecologists was 29.9 business days. Medicaid patients experienced a marginally longer wait time of 4.8% (Ratio: 1.048). While no statistically significant difference in wait times based on insurance type was observed (P=0.39), the data revealed other impactful factors. Younger physicians and those in university-based practices had longer wait times. The gender of the physician also influenced wait times, with female physicians having a mean wait time of 34.7 days compared to 22.7 days for male physicians (P=0.03). Additionally, geographical variations were noted, with physicians in American College of Obstetricians and Gynecologists District I (Atlantic Provinces, CT, ME, MA, NH, RI, VT) having the longest mean wait times and those in District III (DE, NJ, PA) the shortest. CONCLUSIONS: While the type of insurance did not significantly influence the wait times for general obstetrics and gynecology appointments, physician demographic and geographic factors did.

Adaptive responses in uteroplacental metabolism and fetoplacental nutrient shuttling and sensing during placental insufficiency.

Glucose, lactate, and amino acids are major fetal nutrients. During placental insufficiency-induced intrauterine growth restriction (PI-IUGR), uteroplacental weight-specific oxygen consumption rates are maintained, yet fetal glucose and amino acid supply is decreased and fetal lactate concentrations are increased. We hypothesized that uteroplacental metabolism adapts to PI-IUGR by altering nutrient allocation to maintain oxidative metabolism. Here, we measured nutrient flux rates, with a focus on nutrients shuttled between the placenta and fetus (lactate-pyruvate, glutamine-glutamate, and glycine-serine) in a sheep model of PI-IUGR. PI-IUGR fetuses weighed 40% less and had decreased oxygen, glucose, and amino acid concentrations and increased lactate and pyruvate versus control (CON) fetuses. Uteroplacental weight-specific rates of oxygen, glucose, lactate, and pyruvate uptake were similar. In PI-IUGR, fetal glucose uptake was decreased and pyruvate output was increased. In PI-IUGR placental tissue, pyruvate dehydrogenase (PDH) phosphorylation was decreased and PDH activity was increased. Uteroplacental glutamine output to the fetus and expression of genes regulating glutamine-glutamate metabolism were lower in PI-IUGR. Fetal glycine uptake was lower in PI-IUGR, with no differences in uteroplacental glycine or serine flux. These results suggest increased placental utilization of pyruvate from the fetus, without higher maternal glucose utilization, and lower fetoplacental amino acid shuttling during PI-IUGR. Mechanistically, AMP-activated protein kinase (AMPK) activation was higher and associated with thiobarbituric acid-reactive substances (TBARS) content, a marker of oxidative stress, and PDH activity in the PI-IUGR placenta, supporting a potential link between oxidative stress, AMPK, and pyruvate utilization. These differences in fetoplacental nutrient sensing and shuttling may represent adaptive strategies enabling the placenta to maintain oxidative metabolism.NEW & NOTEWORTHY These results suggest increased placental utilization of pyruvate from the fetus, without higher maternal glucose uptake, and lower amino acid shuttling in the placental insufficiency-induced intrauterine growth restriction (PI-IUGR) placenta. AMPK activation was associated with oxidative stress and PDH activity, supporting a putative link between oxidative stress, AMPK, and pyruvate utilization. These differences in fetoplacental nutrient sensing and shuttling may represent adaptive strategies enabling the placenta to maintain oxidative metabolism at the expense of fetal growth.

Clinical spectrum of Cutibacterium acnes infections: The SAPHO syndrome.

Cutibacterium acnes, previously known as Proprionobacterium, is a commensal Grampositive bacterium of the skin commonly implicated in prosthetic joint infections. However, it has been documented to play a role in other conditions, including SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, osteitis), a rare autoinflammatory disorder. Diagnosing SAPHO syndrome is cumbersome, as the clinical manifestations are variable and overlap with many inflammatory joint disorders. Herein, we describe a 56-year-old female patient with a presumed diagnosis of longstanding seronegative rheumatoid arthritis and history of C. acnes prosthetic joint infection following revision arthroplasty of the right shoulder. She presented to our clinic with a rash over the upper extremities and trunk and joint symptoms involving the right shoulder. Treatment was initiated with ceftriaxone followed by doxycycline suppressive therapy, with clinical improvement of joint and skin involvement. Symptoms recurred upon brief cessation of antibiotic therapy due to adverse gastrointestinal effects; however, symptoms abated once again upon re-initiation of treatment. Given the patient's cutaneous lesions and longstanding history of arthritis that improved with antimicrobial therapy against C. acnes, the diagnosis of SAPHO syndrome was entertained. The present case demonstrates the clinical challenges of diagnosing SAPHO syndrome and the importance of its consideration on the differential for a patient with osteoarticular and cutaneous features. Additional literature is needed to improve diagnostic criteria and treatment guidelines.

Changes in lipid profiles of epileptic mouse model.

INTRODUCTION: Approximately 1% of the world's population is impacted by epilepsy, a chronic neurological disorder characterized by seizures. One-third of epileptic patients are resistant to AEDs, or have medically refractory epilepsy (MRE). One non-invasive treatment that exists for MRE includes the ketogenic diet, a high-fat, low-carbohydrate diet. Despite the KD's success in seizure attenuation, it has a few risks and its mechanisms remain poorly understood. The KD has been shown to improve metabolism and mitochondrial function in epileptic phenotypes. Potassium channels have implications in epileptic conditions as they have dual roles as metabolic sensors and control neuronal excitation. OBJECTIVES: The goal of this study was to explore changes in the lipidome in hippocampal and cortical tissue from Kv1.1-KO model of epilepsy. METHODS: FT-ICR/MS analysis was utilized to examine nonpolar metabolome of cortical and hippocampal tissue isolated from a Kv1.1 channel knockout mouse model of epilepsy (n = 5) and wild-type mice (n = 5). RESULTS: Distinct metabolic profiles were observed, significant (p < 0.05) features in hippocampus often being upregulated (FC ≥ 2) and the cortex being downregulated (FC ≤ 0.5). Pathway enrichment analysis shows lipid biosynthesis was affected. Partition ratio analysis revealed that the ratio of most metabolites tended to be increased in Kv1.1-/-. Metabolites in hippocampal tissue were commonly upregulated, suggesting seizure initiation in the hippocampus. Aberrant mitochondrial function is implicated by the upregulation of cardiolipin, a common component in the mitochondrial membrane. CONCLUSION: Generally, our study finds that the lipidome is changed in the hippocampus and cortex in response to Kv1.1-KO indicating changes in membrane structural integrity and synaptic transmission.

Aberrant energy metabolism and redox balance in seizure onset zones of epileptic patients.

Epilepsy is a disorder that affects around 1% of the population. Approximately one third of patients do not respond to anti-convulsant drugs treatment. To understand the underlying biological processes involved in drug resistant epilepsy (DRE), a combination of proteomics strategies was used to compare molecular differences and enzymatic activities in tissue implicated in seizure onset to tissue with no abnormal activity within patients. Label free quantitation identified 17 proteins with altered abundance in the seizure onset zone as compared to tissue with normal activity. Assessment of oxidative protein damage by protein carbonylation identified additional 11 proteins with potentially altered function in the seizure onset zone. Pathway analysis revealed that most of the affected proteins are involved in energy metabolism and redox balance. Further, enzymatic assays showed significantly decreased activity of transketolase indicating a disruption of the Pentose Phosphate Pathway and diversion of intermediates into purine metabolic pathway, resulting in the generation of the potentially pro-convulsant metabolites. Altogether, these findings suggest that imbalance in energy metabolism and redox balance, pathways critical to proper neuronal function, play important roles in neuronal network hyperexcitability and can be used as a primary target for potential therapeutic strategies to combat DRE. SIGNIFICANCE: Epileptic seizures are some of the most difficult to treat neurological disorders. Up to 40% of patients with epilepsy are resistant to first- and second-line anticonvulsant therapy, a condition that has been classified as refractory epilepsy. One potential therapy for this patient population is the ketogenic diet (KD), which has been proven effective against multiple refractory seizure types However, compliance with the KD is extremely difficult, and carries severe risks, including ketoacidosis, renal failure, and dangerous electrolyte imbalances. Therefore, identification of pathways disruptions or shortages can potentially uncover cellular targets for anticonvulsants, leading to a personalized treatment approach depending on a patient's individual metabolic signature.

Temporal discounting correlates with directed exploration but not with random exploration.

The explore-exploit dilemma describes the trade off that occurs any time we must choose between exploring unknown options and exploiting options we know well. Implicit in this trade off is how we value future rewards - exploiting is usually better in the short term, but in the longer term the benefits of exploration can be huge. Thus, in theory there should be a tight connection between how much people value future rewards, i.e. how much they discount future rewards relative to immediate rewards, and how likely they are to explore, with less 'temporal discounting' associated with more exploration. By measuring individual differences in temporal discounting and correlating them with explore-exploit behavior, we tested whether this theoretical prediction holds in practice. We used the 27-item Delay-Discounting Questionnaire to estimate temporal discounting and the Horizon Task to quantify two strategies of explore-exploit behavior: directed exploration, where information drives exploration by choice, and random exploration, where behavioral variability drives exploration by chance. We find a clear correlation between temporal discounting and directed exploration, with more temporal discounting leading to less directed exploration. Conversely, we find no relationship between temporal discounting and random exploration. Unexpectedly, we find that the relationship with directed exploration appears to be driven by a correlation between temporal discounting and uncertainty seeking at short time horizons, rather than information seeking at long horizons. Taken together our results suggest a nuanced relationship between temporal discounting and explore-exploit behavior that may be mediated by multiple factors.