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Kohlschmidt, J.

Publications and source records attributed to Kohlschmidt, J..

2 recordsLinked to original sources

Gender imbalances in citation rates are mediated by field specific author gender distributions

Gender biases are well documented in science and typically favor male scientists. In this context, a particularly pervasive gender bias is undercitation of publications authored by women, resulting in profound negative effects on academic visibility and career advancement. This bias has been well documented in fields where author gender distributions are strongly skewed towards men (e.g., astronomy, physics, neuroscience). By investigating citation practices in a field that has traditionally been more accessible to female scientists (Speech and Language Pathology, SLP), we demonstrate that gendered citation practices are mediated by author gender distribution, rather than being a universal pattern. Specifically, our results revealed a citation pattern in SLP that (a) overall tends to favor female authors, (b) persists after controlling for potential confounding factors and, (c) is particularly strong when female authors are citing publications involving female first and senior author teams. This research also implies that the implementation of effective measures to increase the number and influence of underrepresented individuals in specific fields of science may be suitable to mitigate downstream disadvantages for career advancement of either sex.

scientific communication and education↗

Immunosuppression and Outcomes in Acute Myeloid Leukemia

Acute myeloid leukemia (AML) patients rarely have long first remissions (> 5 years) after standard-of-care chemotherapy, unless classified as favorable risk at presentation. Identification of the mechanisms responsible for long vs. more typical, short remissions may help to define prognostic determinants for chemotherapy responses. Using exome sequencing, RNA-sequencing and functional immunologic studies, we characterized 28 Normal Karyotype (NK)-AML patients with >5 year first remissions after chemotherapy (Long First Remissions, LFR) and compared them to a well-matched group of 31 NK-AML patients who relapsed within 2 years (Standard First Remissions, SFR). Our combined analyses indicated that genetic risk profiling at presentation (as defined by ELN 2017 Criteria) was not sufficient to explain the outcomes of many SFR cases. Single cell RNA-sequencing studies of 15 AML samples showed that SFR AML cells differentially expressed many genes associated with immune suppression. The bone marrow of SFR cases had significantly fewer CD4+ Th1 cells; these T-cells expressed an exhaustion signature and were resistant to activation by T-cell receptor stimulation in the presence of autologous AML cells. T-cell activation could be restored by removing the AML cells, or blocking the inhibitory MHC Class II receptor, LAG3. Most LFR cases did not display these features, suggesting that their AML cells were not as immunosuppressive. These findings were confirmed and extended in an independent set of 50 AML cases representing all ELN 2017 risk groups. AML cell-mediated suppression of CD4+ T-cell activation at presentation is strongly associated with unfavorable outcomes in AML patients treated with standard chemotherapy.

cancer biology↗