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Post-COVID-19 conditions (PCC) may include pulmonary sequelae, fatigue and other symptoms, but its mechanisms are not fully elucidated.
This study investigated the correlation between fatigue and the presence of pulmonary abnormalities in PCC patients with respiratory involvement 6–12 months after hospitalisation.
Cross-sectional study.
A tertiary hospital in Brazil.
315 patients, aged ≥18 years, were considered eligible based on SARS-CoV-2 infection confirmed by reverse transcription-PCR.
Pulmonary function tests (PFT), cardiopulmonary exercise tests (CPET), chest CT and hand grip were performed. The following scales were applied: Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-F) scale, Euroqol 5 Dimensions quality of life (EQ-5D) and Hospital Anxiety and Depression Scale (HADS). Participants were divided between the fatigue group (FACIT-F≤30) and the non-fatigue group (FACIT-F>30). For the statistical analysis, the primary outcome was the difference in the diffusing capacity of the lungs for carbon monoxide (DLCO) between groups. Considered secondary outcomes were differences in PFT, CPET, chest CT, hand grip, EQ-5D and HADS.
The fatigue group had 81 patients (25.7%) against 234 (74.3%). PFT and CPET showed no significant difference in DLCO and oxygen consumption peak values between groups. The fatigue group had a lower workload (mean 55.3±21.3 watts vs 66.5±23.2 watts, p=0.003), higher breathing reserve (median 41.9% (33.8–52.5) vs 37.7% (28.9–47.1), p=0.028) and lower prevalence of ground glass opacity (60.8% vs 77.7%, p=0.003) and reticulation (36.7% vs 54.9%, p=0.005) in chest CT. The fatigue group had higher anxiety (57% vs 24%, p
Fatigue in patients with PCC 6–12 months after hospitalisation is relatively common and had weak correlation with pulmonary disorders. Our results suggested fatigue could be strongly related with peripheral disorders such as reduced musculoskeletal strength or psychosocial limitations.
by Diane C. Lim, Cheng-Bang Chen, Ankita Paul, Yujie Wang, Jinyoung Kim, Soonhyun Yook, Emily Y. Kim, Edison Q. Kim, Anup Das, Medhi Wangpaichitr, Virend K. Somers, Chi Hang Lee, Phyllis C. Zee, Toshihiro Imamura, Hosung Kim
ObjectiveTo quantitate hypoxemia severity.
MethodsWe developed the Weighted Hypoxemia Index to be adapted to different clinical settings by applying 5 steps to the oxygen saturation curve: (1) Identify desaturation/resaturation event i by setting the upper threshold; (2) Exclude events as artifact by setting a lower threshold; (3) Calculate weighted area for each i, as (Δi × Φi); (4) Calculate a normalization factor Ω for each subject; (5) Calculate the Weighted Hypoxemia Index as the summation of all weighted areas multiplied by Ω. We assessed the Weighted Hypoxemia Index predictive value for all-cause mortality and cardiovascular mortality using the Sleep Heart Health Study (enrollment 1995–1998, 11.1 years mean follow-up).
ResultsWe set varying upper thresholds at 92%, 90%, 88%, and 86%, a lower threshold of 50%, calculated area under the curve and area above the curve, with and without a linear weighted factor (duration of each event i), and used the same normalization factor of total sleep time Conclusion
The Weighted Hypoxemia Index offers a versatile and clinically relevant method for quantifying hypoxemia severity, with potential applications to evaluate mechanisms and outcomes across various patient populations.
by Masayoshi Terayama, Yu Imamura, Toru Kitazawa, Naoki Miyazaki, Misuzu Ishii, Kumi Takagi, Kengo Kuriyama, Naoki Takahashi, Masahiro Tamura, Akihiko Okamura, Jun Kanamori, Masayuki Watanabe
BackgroundPostoperative hyperglycemia in diabetic patients is a widely known risk factor for postoperative infectious complications (PICs) after esophagectomy; however, the significance of glycemic control in non-diabetic patients is less clear. In diabetic patients, early postoperative management of esophagectomy favors low-carbohydrate enteral nutrition (EN) over standard EN to suppress the risk of glycemic spike. Our single-center, randomized phase II trial seeks to test the hypothesis that low-carbohydrate EN can suppress hyperglycemia in non-diabetic patients who undergo esophagectomy. Herewith we present the study protocol.
MethodsA total of 50 patients will be enrolled and randomly assigned (1:1 ratio) to standard or low-carbohydrate EN. Randomization will be stratified by operation time (≥560 vs. blood glucose level of 180 mg/dL), and is indicative of the frequency and duration of hyperglycemia. AUC, which identifies periods of hyperglycemia and provides a comprehensive picture of glucose variability and control in diabetes management, is defined as the area under the curve over blood glucose level of 180 mg/dL on CGM monitoring.
DiscussionThis study is the first to investigate the impact of a low-carbohydrate EN formula on hyperglycemic control during perioperative nutritional management of esophageal cancer. These results will help to outline whether glycemic control should be also considered for non-diabetic patients during hospital care.
Trial registrationThis trial has been registered in the Japanese Registry of Clinical Trials (jRCTs031240081).
by Hisako Takigawa-Imamura, Katsumi Fumoto, Hiroaki Takesue, Takashi Miura
The lung airways exhibit distinct features with long, wide proximal branches and short, thin distal branches, crucial for optimal respiratory function. In this study, we investigated the mechanism behind this hierarchical structure through experiments and modeling, focusing on the regulation of branch length and width during the pseudoglandular stage. To evaluate the response of mouse lung epithelium to fibroblast growth factor 10 (FGF10), we monitored the activity of extracellular signal-regulated kinase (ERK). ERK activity exhibited an increase dependent on the curvature of the epithelial tissue, which gradually decreased with the progression of development. We then constructed a computational model that incorporates curvature-dependent growth to predict its impact on branch formation. It was demonstrated that branch length is determined by the curvature dependence of growth. Next, in exploring branch width regulation, we considered the effect of apical constriction, a mechanism we had previously proposed to be regulated by Wnt signaling. Analysis of a mathematical model representing apical constriction showed that branch width is determined by cell shape. Finally, we constructed an integrated computational model that includes curvature-dependent growth and cell shape controls, confirming their coordination in regulating branch formation. This study proposed that changes in the autonomous property of the epithelium may be responsible for the progressive branch morphology.
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