Delivery of ASCs in poloxamer addresses multiple facets of the complexity of nerve/muscle unit regeneration, representing a promising avenue for further study. Muscle Nerve 58: 251-260, 2018.

Diabetes is a systemic disease in which the body cannot regulate the amount of sugar, namely glucose, in the blood. High glucose toxicity has been implicated in the dysfunction of diabetic wound healing, following insufficient production (Type 1) or inadequate usage (Type 2) of insulin. Chronic non-healing diabetic wounds are one of the major complications of both types of diabetes, which are serious concerns for public health and can impact the life quality of patients significantly. In general, diabetic wounds are characterized by deficient chemokine production, an unusual inflammatory response, lack of angiogenesis and epithelialization, and dysfunction of fibroblasts. Increasing scientific evidence from available experimental studies on animal and cell models strongly associates impaired wound healing in diabetes with dysregulated fibroblast differentiation to myofibroblasts, interrupted myofibroblast activity, and inadequate extracellular matrix production. Myofibroblasts play an important role in tissue repair by producing and organizing extracellular matrix and subsequently promoting wound contraction. Based on these studies, hyperglycaemic conditions can interfere with cytokine signalling pathways (such as growth factor-β pathway) affecting fibroblast differentiation, alter fibroblast apoptosis, dysregulate dermal lipolysis, and enhance hypoxia damage, thus leading to damaged microenvironment for myofibroblast formation, inappropriate extracellular matrix modulation, and weakened wound contraction. In this review, we will focus on the current available studies on the impact of diabetes on fibroblast differentiation and myofibroblast function, as well as potential treatments related to the affected pathways.

This study aimed to evaluate whether the BETA‐2 score is a reliable early predictor of graft decline and loss of insulin independence after islet allotransplantation. Islet transplant procedures were stratified into 3 groups according to clinical outcome: long‐term insulin independence without islet graft decline (group 1, N = 9), initial insulin independence with subsequent islet graft decline and loss of insulin independence (group 2, N = 13), and no insulin independence (group 3, N = 13). BETA‐2 was calculated on day 75 and multiple times afterwards for up to 145 months posttransplantation. A BETA‐2 score cut‐off of 17.4 on day 75 posttransplantation was discerned between group 1 and groups 2 and 3 (area under the receiver operating characteristic 0.769, P = .005) with a sensitivity and negative predictive value of 100%. Additionally, BETA‐2 ≥ 17.4 at any timepoint during follow‐up reflected islet function required for long‐term insulin independence. While BETA‐2 did not decline below 17.4 for each of the 9 cases from group 1, the score decreased below 17.4 for all transplants from group 2 with subsequent loss of insulin independence. The reduction of BETA‐2 below 17.4 predicted 9 (1.5‐21) months in advance subsequent islet graft decline and loss of insulin independence (P = .03). This finding has important implications for posttransplant monitoring and patient care.

Background: This study investigates the psychometric properties of patient-reported outcome instruments for assessing outcomes in postsurgical traumatic digit amputation patients. The authors hypothesize that the Michigan Hand Outcomes Questionnaire (MHQ) and Disabilities of the Arm, Shoulder and Hand (DASH) questionnaire are the most valid and reliable instruments. Methods: The authors studied traumatic digit amputation patients as part of the Finger Replantation and Amputation Challenges in Assessing Impairment, Satisfaction, and Effectiveness (FRANCHISE) study initiated by The Plastic Surgery Foundation. The MHQ, DASH questionnaire, Patient-Reported Outcomes Measurement Information System (PROMIS), and 36-Item Short-Form Health Survey were used to assess patients at least 1 year postoperatively. Internal consistency was measured by Cronbach’s alpha and criterion validity with Pearson correlation coefficient (r). Construct validity was tested with four predefined hypotheses. Discriminant validity was analyzed by receiver operating characteristic curves. Results: One hundred sixty-eight replantation and 74 revision amputation patients met the inclusion criteria. All instruments demonstrated fair to good internal consistency in both cohorts (0.7 < α < 0.9). The MHQ and DASH questionnaire scores correlated strongly (r > 0.60) in both cohorts. The 36-Item Short-Form Health Survey had moderate to weak correlation with the remaining instruments, and its mental component had poor discriminant validity (area under the curve, 0.64 to 0.67). The MHQ, DASH questionnaire, and PROMIS demonstrated good construct validity confirming 75 to 100 percent of predefined hypotheses, whereas the 36-Item Short-Form Health Survey confirmed only 25 percent. Conclusions: The authors recommend using the Michigan Hand Outcomes Questionnaire or the Disabilities of the Arm, Shoulder and Hand questionnaire when assessing patient-reported outcomes in digit amputation patients based on good internal consistency and validity. The Patient-Reported Outcomes Measurement Information System has fair validity and reliability but should be an adjunct instrument. The 36-Item Short-Form Health Survey should not be used as a primary assessment tool, but as an adjunct to assess overall quality of life.

Background Tumor initiation and subsequent progression are usually long-term processes, spread over time and conditioned by diverse aspects. Many cancers develop on the basis of chronic inflammation; however, despite dozens of years of research, little is known about the factors triggering neoplastic transformation under these conditions. Molecular characterization of both pathogenetic states, i.e., similarities and differences between chronic inflammation and cancer, is also poorly defined. The secretory activity of tumor cells may change the immunophenotype of immune cells and modify the extracellular microenvironment, which allows the bypass of host defense mechanisms and seems to have diagnostic and prognostic value. The phenomenon of immunosuppression is also present during chronic inflammation, and the development of cancer, due to its duration, predisposes patients to the promotion of chronic inflammation. The aim of our work was to discuss the above issues based on the latest scientific insights. A theoretical mechanism of cancer immunosuppression is also proposed. Conclusions Development of solid tumors may occur both during acute and chronic phases of inflammation. Differences in the regulation of immune responses between precancerous states and the cancers resulting from them emphasize the importance of immunosuppressive factors in oncogenesis. Cancer cells may, through their secretory activity and extracellular transport mechanisms, enhance deterioration of the immune system which, in turn, may have prognostic implications.