Temporal Trends in Telehealth Availability in Mental Health Treatment Settings: Differences in Growth by State Rurality, 2015-2020.

We sought to investigate temporal trends in telehealth availability among outpatient mental health treatment facilities and differences in the pace of telehealth growth by state urbanicity and rurality. We used the National Mental Health Services Survey (2015-2020) to identify outpatient mental health treatment facilities in the US (N = 28,989 facilities; 2015 n = 5,018; 2020 n = 4,889). We used logistic regression to model telehealth, predicted by time, state rurality (1 to 10% rural, 10 to < 20%, 20 to < 30%, or [Formula: see text] 30%), and their interaction, and adjusted for relevant covariates. We estimated the predicted probability of telehealth based on our model. We estimated effects with and without data from 2020 to assess whether the rapid and widespread adoption of telehealth during the COVID-19 pandemic changed the rural/urban trajectories of telehealth availability. We found that telehealth grew fastest in more urban states (year*rurality interaction p < 0.0001). Between 2015 and 2020, the predicted probability of telehealth in more urban states increased by 51 percentage points (from 9 to 61%), whereas telehealth in more rural states increased by 38 percentage points (from 23 to 61%). Predicted telehealth also varied widely by state, ranging from more than 75% of facilities (RI, OR) to below 20% (VT, KY). Health systems and new technological innovations must consider the unique challenges faced by urban populations and how best practices may be adapted to meet the growing urban demand. We framed our findings around the need for policies that minimize barriers to telehealth.

Comparing blastocyst quality and live birth rates of intravaginal culture using INVOcell™ to traditional in vitro incubation in a randomized open-label prospective controlled trial.

PURPOSE: The purpose of this study is to to compare the efficacy of intravaginal culture (IVC) of embryos in INVOcell™ (INVO Bioscience, MA, USA) to traditional in vitro fertilization (IVF) incubators in a laboratory setting using a mild pre-determined stimulation regimen based solely on anti-mullerian hormone (AMH) and body weight with minimal ultrasound monitoring. The primary endpoint examined was total quality blastocysts expressed as a percentage of total oocytes placed in incubation. Secondary endpoints included percentage of quality blastocysts transferred, pregnancy, and live birth rates. METHODS: In this prospective randomized open-label controlled single-center study, 40 women aged <38 years of age with a body mass index (BMI) of <36 and an AMH of 1-3 ng/mL were randomized prior to trigger to receive either IVC or IVF. Controlled ovarian stimulation was administered with human menopausal gonadotropin (hMG) in a fixed gonadotropin-releasing hormone (GnRH) agonist cycle based solely on AMH and body weight. A single ultrasound-monitoring visit was performed on the 10th day of stimulation. One or two embryos were transferred following 5 days of culture. RESULTS: IVF produced a greater percentage of total quality embryos as compared to IVC (50.6 vs. 30.7 %, p = 0.0007, respectively). There was no significant difference between in IVF and IVC in the percentage of quality blastocysts transferred (97.5 vs. 84.9 %, p = 0.09) or live birth rate (60 % IVF, 55 % IVC). CONCLUSIONS: IVF was shown to be superior to IVC in creating quality blastocysts. However, both IVF and IVC produced identical blastocysts for transfer resulting in similar live birth rates. IVC using INVOcell™ is effective and may broaden access to fertility care in selected patient populations by ameliorating the need for a traditional IVF laboratory setting. Further studies will help elucidate the potential physiological, psychological, geographic, and financial impact of IVC on the delivery of fertility care.

Dose responses for adaption to low doses of (60)Co gamma rays and (3)H beta particles in normal human fibroblasts.

The dose response for adaption to radiation at low doses was compared in normal human fibroblasts (AG1522) exposed to either (60)Co gamma rays or (3)H beta particles. Cells were grown in culture to confluence and exposed at either 37 degrees C or 0 degrees C to (3)H beta-particle or (60)Co gamma-ray adapting doses ranging from 0.1 mGy to 500 mGy. These cells, and unexposed control cells, were allowed to adapt during a fixed 3-h, 37 degrees C incubation prior to a 4-Gy challenge dose of (60)Co gamma rays. Adaption was assessed by measuring micronucleus frequency in cytokinesis-blocked, binucleate cells. No adaption was detected in cells exposed to (60)Co gamma radiation at 37 degrees C after a dose of 0.1 mGy given at a low dose rate or to 500 mGy given at a high dose rate. However, low-dose-rate exposure (1-3 mGy/min) to any dose between 1 and 500 mGy from either radiation, delivered at either temperature, caused cells to adapt and reduced the micronucleus frequency that resulted from the subsequent 4-Gy exposure. Within this dose range, the magnitude of the reduction was the same, regardless of the dose or radiation type. These results demonstrate that doses as low as (on average) about one track per cell (1 mGy) produce the same maximum adaptive response as do doses that deposit many tracks per cell, and that the two radiations were not different in this regard. Exposure at a temperature where metabolic processes, including DNA repair, were inactive (0 degrees C) did not alter the result, indicating that the adaptive response is not sensitive to changes in the accumulation of DNA damage within this range. The results also show that the RBE for low doses of tritium beta-particle radiation is 1, using adaption as the end point.

Multivariate Analysis of Triadic Relationst.

To analyze variance in a triadic variable, Bond, Horn, and Kenny (1997) have proposed a Triadic Relations Model. Here we extend this model to analyze the covariances between triadic variables. A bivariate version of the Triadic Relations Model is specified, and estimation methods are presented. These can be used to decompose the covariance between two triadic variables into thirty-three covariance components. Interpretations and an example of this analysis are offered. Applications of this model and alternative techniques are noted.

Adaptation of human fibroblasts to radiation alters biases in DNA repair at the chromosomal level.

PURPOSE: To determine whether adaptation to ionizing radiation biases repair of radiation-induced chromosomal breaks. MATERIALS AND METHODS: Normal human fibroblasts were radiation-adapted by exposure to 10 cGy of gamma-radiation. FISH probes for chromosomes 2, 4, 7, 18 and 19 were used to determine the chromosomal origin of the DNA in micronuclei resulting from a subsequent 4Gy exposure of these cells, and corresponding non-adapted cells. RESULTS: Compared with 4 Gy exposed but non-adapted cells, the radiation-adapted cells subsequently exposed to 4 Gy showed an overall decrease in the frequency of micronuclei. However, the micronuclei that did form in the adapted cells had a decreased frequency of DNA originating from chromosomes 2 and 18, an increased frequency of DNA from chromosome 19 and no change in frequency of DNA from chromosomes 4 and 7. CONCLUSIONS: Adaptation to radiation increased the overall cellular repair of radiation-induced chromosomal breaks, but also created a repair bias such that some chromosomes were preferentially repaired or discriminated against, while the repair of others was unbiased.

Role of apoptosis and apoptosis-related proteins in the cisplatin-resistant phenotype of human tumor cell lines.

Since apoptosis is the primary mode of cell death induced by cisplatin, the role of apoptosis and apoptosis-related gene products in cisplatin resistance was investigated in four human cisplatin-resistant cell lines of different tumour type. A common feature of the resistant sublines was a reduced susceptibility to drug-induced apoptosis compared to parental sensitive lines. Loss of wild-type p53 function was not a general event associated with the development of drug resistance. An increased bcl-2 expression was found in resistant cells characterized by mutant p53 (A431/Pt and IGROV-1/Pt), whereas in osteosarcoma (U2-OS/Pt) and in ovarian carcinoma (A2780/CP) cells with wild-type p53, bcl-2 levels were markedly reduced. U2-OS/Pt cells had a 16-fold increase in the level of Bcl-xL protein. Stable transfection of U2-OS cells with bcl-xL cDNA conferred a low level of drug resistance to cisplatin, suggesting that overexpression of this gene contributes to the cisplatin-resistant phenotype of this osteosarcoma cell system. In conclusion, these observations suggest a variable contribution of apoptosis-related genes to cisplatin resistance depending on the biological background of the cell system and presumably reflecting different pathways of apoptosis.