Short bowel syndrome (SBS) is a condition that results from a reduction in the length of the intestine or its functional capacity. SBS patients can have significant side effects and complications, the etiology of which remains ill-defined. Thus, facilitating intestinal adaptation in SBS remains a major research focus. Emerging data supports the role of the gut microbiome in modulating disease progression. There has been ongoing debate on defining a “healthy” gut microbiome, which has led to many studies analyzing the bacterial composition and shifts that occur in gastrointestinal disease states such as SBS and the resulting systemic effects. In SBS, it has also been found that microbial shifts are highly variable and dependent on many factors, including the anatomical location of bowel resection, length, and structure of the remnant bowel, as well as associated small intestinal bacterial overgrowth (SIBO). Recent data also notes a bidirectional communication that occurs between enteric and central nervous systems called the gut–brain axis (GBA), which is regulated by the gut microbes. Ultimately, the role of the microbiome in disease states such as SBS have many clinical implications and warrant further investigation. The focus of this review is to characterize the role of the gut microbiota in short bowel syndrome and its impact on the GBA, as well as the therapeutic potential of altering the microbiome.

Bioinformatic methodologies play a crucial role in the assessment of gut microbiota, offering advanced tools for analyzing complex microbial communities. These methodologies involve high-throughput sequencing technologies, such as 16S rRNA gene sequencing and metagenomics, which generate vast amounts of data on microbial diversity and functional potential, as well as whole-genome sequencing, which, while being more costly, has a more expansive potential. Bioinformatics tools and algorithms process these data to identify microbial taxa and quantify and elucidate their roles within the microbiome. Advanced statistical and computational models further enable the identification of microbiota patterns associated with various diseases and health conditions. Overall, bioinformatic approaches are essential for deciphering the complexities of gut microbiota so that, in the future, we may be able to discover treatments and technologies aimed at restoring or optimizing the microbiome. The goal of this review is to describe the differences in methodology and utilization of 16S versus whole-genome sequencing to address the increased understanding of the role that the gut microbiome plays in human physiology and pathology.

Short bowel syndrome (SBS) is a particularly serious condition in which the small intestine does not absorb sufficient nutrients for biological needs, resulting in severe illness and potentially death if not treated. Given the important role of the gut in many signaling cascades throughout the body, SBS results in disruption of many pathways and imbalances in various hormones. Due to the inability to meet sufficient nutritional needs, an intravenous form of nutrition, total parental nutrition (TPN), is administered. However, TPN presents difficulties such as severe liver injury and altered signaling secondary to the continued lack of luminal contents. This manuscript aims to summarize relevant studies into the systemic effects of TPN on systems such as the gut–brain, gut-lung, and gut-liver axis, as well as present novel therapeutics currently under use or investigation as mitigation strategies for TPN induced injury.

Hepatic ischemia–reperfusion injury (IRI) is a major cause of postoperative hepatic dysfunction and liver failure involving cellular damage to previously ischemic tissues to which blood flow is restored. The reestablishment of blood flow is essential for salvaging ischemic tissues. The reperfusion itself, however, can paradoxically lead to further cellular damage, which involves a multi-factorial process resulting in extensive tissue damage, which can threaten the function and viability of the liver and other organ systems. The following review outlines multiple models for in-lab analysis of the various hepatic IRI mechanisms, including murine, porcine, cell lines, and machine perfusion models.

Social Determinants of Health (SDOH) impact nearly half of health outcomes, surpassing the influence of human behavior, clinical care, and the physical environment. SDOH has five domains: Economic Stability, Education Access and Quality, Health Care Access and Quality, Neighborhood and Built Environment, and Social and Community Context. Any adversity arising out of these interlinked domains predominantly affects children due to their greater susceptibility, and the adverse outcomes may span generations. Unfavorable SDOH may cause food insecurity, malnutrition, unbalanced gut microbiome, acute and chronic illnesses, inadequate education, unemployment, and lower life expectancy. Systematic screening by health care workers and physicians utilizing currently available tools and questionnaires can identify children susceptible to adverse childhood experiences, but there is a deficiency with respect to streamlined approach and institutional support. Additionally, current ameliorating supplemental food programs fall short of pediatric nutritional requirements. We propose a nutrition-based Surveillance, Screening, Referral, and Reevaluation (SSRR) plan encompassing a holistic approach to SDOH with a core emphasis on food insecurity, coupled with standardizing outcome-based interventions. We also propose more inclusive use of Food Prescription Programs, tailored to individual children’s needs, with emphasis on education and access to healthy food.

Background: Homozygosity for LIMS1 rs893403-GG genotype is linked to an increased risk of allograft rejection after kidney transplantation. Ischemia-reperfusion of the kidney allograft leads to long term infiltration of activated and effector-memory T lymphocytes and resulting in rejection and long-term fibrosis. However, the genotype, LIMS1 expression under ischemic conditions and the long-term histopathological relationships remain ill-defined. Methods: We examined the impact of the recipient’s LIMS1-rs893403 genotype with transplant kidney histopathology. The association of the LIMS1-rs893403 genotype and LIMS1 and GCC2 mRNA expression in ischemic donor kidneys were also examined. Recipients who underwent transplant kidney biopsy were genotyped for the LIMS1-rs893403 variant and associated deletion. Histopathological findings were compared between recipients with LIMS1 risk and non-risk genotypes. Real-time PCR and immunofluorescence staining for LIMS1 and GCC2 expression were performed in non-utilized donor kidneys. Results: Demographic, clinical, and treatment characteristics and the histopathological diagnosis were similar between recipients with rs893403 GG and AA/AG genotype. The Banff tubulitis score was higher in GG recipients (n = 24) compared to AA/AG (n = 86) recipients (1.42 ± 0.65 vs. 1.12 ± 0.66, p = 0.03). Ischemic kidneys with GG showed higher LIMS1 and GCC2 mRNA expression than kidneys with AG. Kidneys with rs893403-GG had higher tubular LIMS1 and GCC2 immunohistochemical staining compared to kidneys with rs893403-AG. Conclusions: Our data supports the role of the LIMS1 locus in kidney transplant rejection, particularly in lymphocyte infiltration into the internal aspect of the tubular basement membranes. Increased LIMS1 and GCC2 expression in ischemic donor kidneys with the GG genotype require further studies.