Similar hospital profits with robotic-assisted paraesophageal hiatal hernia repair, despite higher or supply costs.

INTRODUCTION: Robotic-assisted laparoscopic surgery has emerged as an alternative to traditional laparoscopy and may offer some clinical benefits when performing complex hiatal hernia repairs. Many institutions may choose to not invest in robotic surgery because of perceived higher costs, and when they already have proficient laparoscopic surgeons. We hypothesized that the robotic approach would yield lower profits overall due to higher supply costs, while offering comparable outcomes to the traditional laparoscopic approach. METHODS: Financial and outcomes data from a single quaternary academic center was retrospectively reviewed from a prospectively collected database from July 2020 to May 2021. Laparoscopic hiatal hernia repairs and robotic-assisted repairs were compared for metrics including length of stay, operative time, hospital and supply cost, payments, and profits. Metrics of these two groups were compared using t-test analyses with significance set to p < 0.05. RESULTS: Seventy-three patients were included with 31 in the robotic group (42.5%) and 42 in the laparoscopic group (57.5%). There were no significant differences in length of stay (robotic mean 2.0 days, laparoscopic 2.55 days, p = 0.09) or operative time (257.6 min vs 256.7 min, p = 0.48) between the two approaches. The robotic approach was associated with higher supply costs ($2,655 vs $2,028, p < 0.001) and patient charges ($63,997 vs $56,276, p < 0.05). Despite higher costs associated with robotics, hospital profits were not different between the two groups ($7,462 vs $7,939, p = 0.42). CONCLUSION: Despite higher supply costs and charges for robotic-assisted hiatal hernia repair, hospital profits were similar when comparing robotic and laparoscopic approaches. Short-term clinical outcomes were also similar. Programs should do their own analysis to understand their individual cost issues.

U.S. medical student knowledge and interest in asylum seeker medical care.

CONTEXT: Asylum seekers face significant and unique healthcare challenges, requiring healthcare practitioners, specifically in primary care, to be trained to care for this patient population. However, there is limited understanding of medical students' interest in and future ability to care for the population of asylum seekers in the United States. PROJECT AIMS: We aim to understand U.S. medical students' interest, experience, and knowledge in providing care for asylum seekers to assess the need for change in the ways in which medical schools introduce asylum seeker care to learners. DESCRIPTION: A 23-question survey was administered to U.S. medical students at four institutions with asylum programmes affiliated with Physicians for Human Rights (PHR) from June 2020 to March 2021, querying various aspects of providing care to asylum seekers. OUTCOMES: Of the approximately 2846 students who received the survey, 436 students (15%) completed it in its entirety. Most respondents desired training about caring for asylum seekers (91%). Over half (52%) rated their knowledge of asylum issues overall as 'poor' or 'none', and 73% thought their medical school's curriculum on asylum seeker health needed improvement. CONCLUSIONS: Medical students at schools with affiliated asylum clinics desire to care for asylum seeker patients but feel unprepared to do so, highlighting an unmet need for formal asylum education in U.S. medical schools.

Factors influencing scalp cooling discussions and use at a large academic institution: a single-center retrospective review.

PURPOSE: Chemotherapy-induced alopecia (CIA) is a stigmatizing and psychologically devasting side effect of cancer treatment. Scalp cooling therapy (SCT) is the most effective method to reduce CIA, yet it is underutilized. We investigated factors that may impact scalp cooling discussion and use. METHODS: We performed a retrospective review of cancer patients from 2000 to 2019 who had documentation of SCT discussion in the electronic medical record. The University of Michigan Rogel Cancer Center registry was used to identify the total number of cancer patients eligible for SCT during 2015-2019. Chi-square tests were used for outcome and patient characteristic comparisons (p < 0.05). RESULTS: From 2000 to 2019, 194 patients had documentation of SCT discussion. Of those, 72 (43.6%) used SCT, 93 (47.9%) did not use SCT, and the remaining 29 (17.8%) had unknown SCT use. A total of 5615 cancer patients were eligible for SCT from 2015 to 2019. As compared to those who did not have documented SCT discussions, patients who had documentation of SCT discussions in that period (n = 161, 3.0%) were more likely to be female, have breast cancer, be less than 45 years old, and live in a zip code with average income > US $100,000 (all p < 0.0001). Between 2015 and 2019, 57 patients (1.02%) used SCT. On univariate analysis, patient-initiated conversation about SCT (p = 0.01) and age less than 65 (p = 0.03) were significantly associated with decision to use SCT. CONCLUSION: There were distinctions in the types of patients who have documented discussions about SCT. Improving patient knowledge about the availability of SCT and increasing access to this technology for all eligible cancer patients may enable more patients to achieve improved quality of life by reducing or preventing CIA.

Reuterin in the healthy gut microbiome suppresses colorectal cancer growth through altering redox balance.

Microbial dysbiosis is a colorectal cancer (CRC) hallmark and contributes to inflammation, tumor growth, and therapy response. Gut microbes signal via metabolites, but how the metabolites impact CRC is largely unknown. We interrogated fecal metabolites associated with mouse models of colon tumorigenesis with varying mutational load. We find that microbial metabolites from healthy mice or humans are growth-repressive, and this response is attenuated in mice and patients with CRC. Microbial profiling reveals that Lactobacillus reuteri and its metabolite, reuterin, are downregulated in mouse and human CRC. Reuterin alters redox balance, and reduces proliferation and survival in colon cancer cells. Reuterin induces selective protein oxidation and inhibits ribosomal biogenesis and protein translation. Exogenous Lactobacillus reuteri restricts colon tumor growth, increases tumor reactive oxygen species, and decreases protein translation in vivo. Our findings indicate that a healthy microbiome and specifically, Lactobacillus reuteri, is protective against CRC through microbial metabolite exchange.

Hepcidin sequesters iron to sustain nucleotide metabolism and mitochondrial function in colorectal cancer epithelial cells.

Colorectal cancer (CRC) requires massive iron stores, but the complete mechanisms by which CRC modulates local iron handling are poorly understood. Here, we demonstrate that hepcidin is activated ectopically in CRC. Mice deficient in hepcidin specifically in the colon tumour epithelium, compared with wild-type littermates, exhibit significantly diminished tumour number, burden and size in a sporadic model of CRC, whereas accumulation of intracellular iron by deletion of the iron exporter ferroportin exacerbates these tumour parameters. Metabolomic analysis of three-dimensional patient-derived CRC tumour enteroids indicates a prioritization of iron in CRC for the production of nucleotides, which is recapitulated in our hepcidin/ferroportin mouse CRC models. Mechanistically, our data suggest that iron chelation decreases mitochondrial function, thereby altering nucleotide synthesis, whereas exogenous supplementation of nucleosides or aspartate partially rescues tumour growth in patient-derived enteroids and CRC cell lines in the presence of an iron chelator. Collectively, these data suggest that ectopic hepcidin in the tumour epithelium establishes an axis to sequester iron in order to maintain the nucleotide pool and sustain proliferation in colorectal tumours.

Colorectal cancer cells utilize autophagy to maintain mitochondrial metabolism for cell proliferation under nutrient stress.

Cancer cells reprogram cellular metabolism to maintain adequate nutrient pools to sustain proliferation. Moreover, autophagy is a regulated mechanism to break down dysfunctional cellular components and recycle cellular nutrients. However, the requirement for autophagy and the integration in cancer cell metabolism is not clear in colon cancer. Here, we show a cell-autonomous dependency of autophagy for cell growth in colorectal cancer. Loss of epithelial autophagy inhibits tumor growth in both sporadic and colitis-associated cancer models. Genetic and pharmacological inhibition of autophagy inhibits cell growth in colon cancer-derived cell lines and patient-derived enteroid models. Importantly, normal colon epithelium and patient-derived normal enteroid growth were not decreased following autophagy inhibition. To couple the role of autophagy to cellular metabolism, a cell culture screen in conjunction with metabolomic analysis was performed. We identified a critical role of autophagy to maintain mitochondrial metabolites for growth. Loss of mitochondrial recycling through inhibition of mitophagy hinders colon cancer cell growth. These findings have revealed a cell-autonomous role of autophagy that plays a critical role in regulating nutrient pools in vivo and in cell models, and it provides therapeutic targets for colon cancer.

Interleukin-33-induced expression of PIBF1 by decidual B cells protects against preterm labor.

Preterm birth (PTB) is a leading cause of neonatal death worldwide. Intrauterine and systemic infection and inflammation cause 30-40% of spontaneous preterm labor (PTL), which precedes PTB. Although antibody production is a major immune defense mechanism against infection, and B cell dysfunction has been implicated in pregnancy complications associated with PTL, the functions of B cells in pregnancy are not well known. We found that choriodecidua of women undergoing spontaneous PTL harbored functionally altered B cell populations. B cell-deficient mice were markedly more susceptible than wild-type (WT) mice to PTL after inflammation, but B cells conferred interleukin (IL)-10-independent protection against PTL. B cell deficiency in mice resulted in a lower uterine level of active progesterone-induced blocking factor 1 (PIBF1), and therapeutic administration of PIBF1 mitigated PTL and uterine inflammation in B cell-deficient mice. B cells are a significant producer of PIBF1 in human choriodecidua and mouse uterus in late gestation. PIBF1 expression by B cells is induced by the mucosal alarmin IL-33 (ref. 9). Human PTL was associated with diminished expression of the α-chain of IL-33 receptor on choriodecidual B cells and a lower level of active PIBF1 in late gestation choriodecidua. These results define a vital regulatory cascade involving IL-33, decidual B cells and PIBF1 in safeguarding term pregnancy and suggest new therapeutic approaches based on IL-33 and PIBF1 to prevent human PTL.