Social needs screening during the COVID-19 pandemic.

BACKGROUND: Millions of Americans lost their jobs as a result of the COVID-19 pandemic, placing immeasurable stress on families and making it difficult for parents to support their children's basic needs. Research shows that screening for social determinants of health is an important part of a child's well visit, noting that awareness of these factors leads to more holistic and improved quality of care. Due to increased precautions during the COVID-19 pandemic and a significant decrease in well-child visits and in-person appointments, there was a marked decrease in the number of face-to-face opportunities for these screenings. In a time of increased need, methods such as telephone screenings represent an opportunity to assess needs and connect patients and families with helpful resources. METHODS: This study occurred in Baltimore, Maryland at the University of Maryland Pediatrics at Midtown outpatient practice (PAM). Five paediatric resident physicians and 17 medical students developed a telephone welfare screening tool and called families receiving primary care at the clinic over a 9-week period. The team documented identified needs and used a community resources database to provide resources to families over the phone. Data regarding the identified needs was collected and analysed throughout the screening process. RESULTS: Volunteers contacted 671 families using our finalized screening tool. Of those, 349 answered the telephone call (52%), and 328 (49%) agreed to participate in the screening. Results showed that families commonly identified food insecurity (20%) and symptoms of depression (18%). This was consistent across families' home locations as analysed by postal ZIP code. CONCLUSIONS: This study suggests that telephone screening is a feasible and informative method for identifying and addressing the social needs of paediatric primary care patients and their families. Furthermore, our study supports the notion that there are significant and widespread social needs resulting from the COVID-19 pandemic.

Hypogammaglobulinemia in a pediatric tertiary care setting.

Hypogammaglobulinemia has been described as a secondary consequence of many disorders. It is also the seminal finding in many primary immune deficiencies. There are few studies examining the global etiologies of hypogammaglobulinemia. This study undertook a database discovery of all cases of laboratory-defined hypogammaglobulinemia identified in a large tertiary care pediatric hospital setting between August of 1990 until June of 2006. Eight thousand three hundred and four IgG levels were sent during that time frame. One thousand two hundred and ninety-five specimens from 680 individual patients exhibited hypogammaglobulinemia and these patients represent the study population. The majority of cases in whom an identifiable cause was found had pre-existing conditions and the IgG level was sent as part of a monitoring process. Of the 366 patients who had an IgG level obtained for diagnostic purposes, nearly half were found to have an immune deficiency. One hundred and seventy-two patients with an immune deficiency were identified. Seven percent of these had severe combined immune deficiency. Seventy-four percent of the immune deficient patients identified required active intervention with IVIG, bone marrow transplantation or other management (not including prophylactic antibiotics). Evaluating all patients with IgG levels less than half of the lower limit for age revealed 122 patients of whom 33% had a primary immune deficiency. This study provides a framework for considering causes of hypogammaglobulinemia. At the study institution, hypogammaglobulinemia was found most often as a secondary immune deficiency due to chemotherapy or from complex cardiac anomalies. The magnitude of the secondary hypogammaglobulinemia in a tertiary care setting requires public health consideration as these patients have an unknown risk of infection and an unknown risk of prolonged viral shedding; issues which could be important in epidemic settings.

Sensitivity of yeast strains with long G-tails to levels of telomere-bound telomerase.

The Saccharomyces cerevisiae Pif1p helicase is a negative regulator of telomere length that acts by removing telomerase from chromosome ends. The catalytic subunit of yeast telomerase, Est2p, is telomere associated throughout most of the cell cycle, with peaks of association in both G1 phase (when telomerase is not active) and late S/G2 phase (when telomerase is active). The G1 association of Est2p requires a specific interaction between Ku and telomerase RNA. In mutants lacking this interaction, telomeres were longer in the absence of Pif1p than in the presence of wild-type PIF1, indicating that endogenous Pif1p inhibits the active S/G2 form of telomerase. Pif1p abundance was cell cycle regulated, low in G1 and early S phase and peaking late in the cell cycle. Low Pif1p abundance in G1 phase was anaphase-promoting complex dependent. Thus, endogenous Pif1p is unlikely to act on G1 bound Est2p. Overexpression of Pif1p from a non-cell cycle-regulated promoter dramatically reduced viability in five strains with impaired end protection (cdc13-1, yku80Delta, yku70Delta, yku80-1, and yku80-4), all of which have longer single-strand G-tails than wild-type cells. This reduced viability was suppressed by deleting the EXO1 gene, which encodes a nuclease that acts at compromised telomeres, suggesting that the removal of telomerase by Pif1p exposed telomeres to further C-strand degradation. Consistent with this interpretation, depletion of Pif1p, which increases the amount of telomere-bound telomerase, suppressed the temperature sensitivity of yku70Delta and cdc13-1 cells. Furthermore, eliminating the pathway that recruits Est2p to telomeres in G1 phase in a cdc13-1 strain also reduced viability. These data suggest that wild-type levels of telomere-bound telomerase are critical for the viability of strains whose telomeres are already susceptible to degradation.