Non-rigid point cloud registration for middle ear diagnostics with endoscopic optical coherence tomography.

PURPOSE: Middle ear infection is the most prevalent inflammatory disease, especially among the pediatric population. Current diagnostic methods are subjective and depend on visual cues from an otoscope, which is limited for otologists to identify pathology. To address this shortcoming, endoscopic optical coherence tomography (OCT) provides both morphological and functional in vivo measurements of the middle ear. However, due to the shadow of prior structures, interpretation of OCT images is challenging and time-consuming. To facilitate fast diagnosis and measurement, improvement in the readability of OCT data is achieved by merging morphological knowledge from ex vivo middle ear models with OCT volumetric data, so that OCT applications can be further promoted in daily clinical settings. METHODS: We propose C2P-Net: a two-staged non-rigid registration pipeline for complete to partial point clouds, which are sampled from ex vivo and in vivo OCT models, respectively. To overcome the lack of labeled training data, a fast and effective generation pipeline in Blender3D is designed to simulate middle ear shapes and extract in vivo noisy and partial point clouds. RESULTS: We evaluate the performance of C2P-Net through experiments on both synthetic and real OCT datasets. The results demonstrate that C2P-Net is generalized to unseen middle ear point clouds and capable of handling realistic noise and incompleteness in synthetic and real OCT data. CONCLUSIONS: In this work, we aim to enable diagnosis of middle ear structures with the assistance of OCT images. We propose C2P-Net: a two-staged non-rigid registration pipeline for point clouds to support the interpretation of in vivo noisy and partial OCT images for the first time. Code is available at: https://gitlab.com/nct_tso_public/c2p-net.

Progression from different blood glucose states to cardiovascular diseases: a prospective study based on multi-state model.

AIMS: To quantify the trajectories from normoglycaemia to pre-diabetes, subsequently to type 2 diabetes mellitus (T2DM), cardiovascular diseases (CVD), and cardiovascular death, and the effects of risk factors on the rates of transition. METHODS AND RESULTS: We used data from the Jinchang Cohort of 42 585 adults aged 20-88 free of coronary heart disease (CHD) and stroke at baseline. A multistate model was applied for analysing the progression of CVD and its relation to various risk factors. During a median follow-up of 7 years, 7498 participants developed pre-diabetes, 2307 developed T2DM, 2499 developed CVD, and 324 died from CVD. Among 15 postulated transitions, transition from comorbid CHD and stroke to cardiovascular death had the highest rate (157.21/1000 person-years), followed by transition from stroke alone to cardiovascular death (69.31/1000 person-years) and transition from pre-diabetes to normoglycaemia (46.51/1000 person-years). Pre-diabetes had a sojourn time of 6.77 years, and controlling weight, blood lipids, blood pressure, and uric acid within normal limits may promote reversion to normoglycaemia. Among transitions to CHD alone and stroke alone, transition from T2DM had the highest rate (12.21/1000 and 12.16/1000 person-years), followed by transition from pre-diabetes (6.81/1000 and 4.93/1000 person-years) and normoglycaemia (3.28/1000 and 2.39/1000 person-years). Age and hypertension were associated with an accelerated rate for most transitions. Overweight/obesity, smoking, dyslipidaemia, and hyperuricaemia played crucial but different roles in transitions. CONCLUSION: Pre-diabetes was the optimal intervention stage in the disease trajectory. The derived transition rates, sojourn time, and influence factors could provide scientific support for the primary prevention of both T2DM and CVD.

Former single-outcome studies on the relationship between glycaemia and cardiovascular disease (CVD) may ignore the complexity and multi-transformations across the multiple stages from normoglycaemia to CVD in real-world setting. We aimed to quantify the trajectories from normoglycaemia to pre-diabetes, subsequently to type 2 diabetes, CVD, and cardiovascular death. Pre-diabetes was the optimal intervention stage in the disease trajectory. Transitions from CVD to death had much higher rates than other transitions. Age and hypertension were associated with an accelerated rate for most transitions. Overweight/obesity, smoking, dyslipidaemia, and hyperuricaemia played crucial but different roles in transitions.

Fasting plasma glucose and alanine aminotransferase on the risk of hepatocellular carcinoma: A nested case-control study.

BACKGROUND: The risk of hepatocellular carcinoma (HCC) is associated with a variety of factors. However, the possible association between the abnormal metabolism of fasting plasma glucose (FPG) and alanine aminotransferase (ALT) and the risk of HCC has not been widely studied. We examined this relationship based on a prospective cohort study. METHODS: 162 first-attack HCC cases during three follow-up periods (2014-2020) were selected as the case group. A control group of 648 participants was obtained by 1:4 matching of age (± 2 years) and sex with noncancer participants in the same period. Conditional logistic regression models, restricted cubic spline models, additive interaction models, and generalized additive models were used to explore the effects of FPG and ALT on the risk of HCC. RESULTS: After correction for confounding factors, we found that abnormal FPG and elevated ALT increased the risk of HCC, respectively. Compared with the normal FPG group, the risk of HCC was significantly increased in the impaired fasting glucose (IFG) (OR = 1.91, 95 %CI: 1.04, 3.50) and diabetes groups (OR = 2.12, 95 %CI: 1.24, 3.63). Compared with the lowest quartile of ALT, subjects in the fourth quartile had an 84 % increased risk of HCC (OR = 1.84, 95 %CI: 1.05-3.21). Moreover, there was an interaction between FPG and ALT on the risk of HCC, and 74 % of the HCC risk could be attributed to their synergistic effect (AP = 0.74, 95 %CI: 0.56-0.92). CONCLUSION: Abnormal FPG and elevated ALT are independent risk factors for HCC, and they have a synergistic effect on the risk of HCC. Therefore, serum FPG and ALT levels should be monitored to prevent the development of HCC.

Liposome-embedded SOD attenuated DSS-induced ulcerative colitis in mice by ameliorating oxidative stress and intestinal barrier dysfunction.

Oxidative stress is generally considered inseparable from the development and exacerbation of ulcerative colitis (UC). Therefore, reducing oxidative stress has become a possible way to alleviate UC. In this study, the therapeutic effects of different doses of liposome-embedded superoxide dismutase (L-SOD) on mice with DSS-induced UC were systematically investigated. The results showed that L-SOD significantly attenuated the signs of colitis in mice, including colonic shortening, diarrhoea, bloody stools, and histopathological changes. L-SOD ameliorated DSS-induced oxidative damage, increased SOD, catalase (CAT), and glutathione (GSH) activities, and decreased malondialdehyde (MDA) levels. In addition, L-SOD ameliorated the inflammatory response by inhibiting the expression of myeloperoxidase (MPO) and pro-inflammatory cytokines and protected barrier function by promoting the expression of the tight junction proteins occludin and ZO-1 in the colon. Importantly, the results demonstrated a bell-shaped distribution of therapeutic effects relative to the administered dose, with an optimal dose of 150 000 U kg-1. These results indicate that L-SOD has great potential as an ingredient in functional foods for the prevention and mitigation of UC.

Association between metabolic syndrome and the risk of colorectal cancer: a prospective study in China.

OBJECTIVE: To evaluate the correlation between metabolic syndrome (MetS) and its components on the incidence of colorectal cancer (CRC) based on data from Jinchang Cohort. METHODS: This is a large prospective cohort study. Between 2011 and 2020, a total of 43 516 individuals from Jinchang Cohort were included for this study. Hazard ratios (HRs) with 95% confidence intervals (CIs) for CRC according to MetS were calculated with the Cox proportional hazard models. The restricted cubic spine models with four knots were conducted to fit the dose-response relationships. RESULTS: MetS was associated with increased risk of CRC (n = 141; HR: 1.64, 95% CI: 1.15-2.33) after adjusting for confounding factors (age, sex, education level, family history of CRC, smoking index and alcohol index). Participants with hyperglycemia had a significantly higher risk of developing incident CRC (HR: 1.70; 95% CI: 1.19-2.43). The positive association between MetS and CRC was observed in males (HR: 1.76; 95% CI: 1.17-2.63), but not in females (HR: 1.24; 95% CI: 0.59-2.64). Furthermore, linear dose-response relationship was found between fasting plasma glucose (FPG) and CRC risk in males (Poverall < 0.05, Pnon-linear = 0.35). When stratified by smoke and drink, MetS was found to increase the incidence of CRC only in the smoke (HR: 2.07, 95% CI: 1.35-3.18) and drink (HR: 2.93, 95% CI: 1.51-5.69) groups. CONCLUSION: MetS was associated with a higher risk of CRC incidence. Hyperglycemia lended strong support to the role of MetS in new-onset CRC, especially in males. Other components of MetS were not found to be associated with increased risk of CRC.

Preventive measures significantly reduced the risk of nosocomial infection in elderly inpatients during the COVID-19 pandemic.

In December 2019, there was an outbreak of pneumonia of unknown causes in Wuhan, China. The etiological pathogen was identified to be a novel coronavirus, named severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19). The number of infected patients has markedly increased since the 2019 outbreak and COVID-19 has also proven to be highly contagious. In particular, the elderly are among the group of patients who are the most susceptible to succumbing to COVID-19 within the general population. Cross-infection in the hospital is one important route of SARS-CoV-2 transmission, where elderly patients are more susceptible to nosocomial infections due to reduced immunity. Therefore, the present study was conducted to search for ways to improve the medical management workflow in geriatric departments to ultimately reduce the risk of nosocomial infection in elderly inpatients. The present observational retrospective cohort study analysed elderly patients who were hospitalised in the Geriatric Department of the First Affiliated Hospital with Nanjing Medical University (Nanjing, China). A total of 4,066 elderly patients, who were admitted between January and March in 2019 and 2020 and then hospitalised for >48 h were selected. Among them, 3,073 (75.58%) patients hospitalised from January 2019 to March 2019 were allocated into the non-intervention group, whereas the remaining 933 (24.42%) patients hospitalised from January 2020 to March 2020 after the COVID-19 outbreak were allocated into the intervention group. Following multivariate logistic regression analysis, the risk of nosocomial infections was found to be lower in the intervention group compared with that in the non-intervention group. After age stratification and adjustment for sex, chronic disease, presence of malignant tumour and trauma, both inverse probability treatment weighting and standardised mortality ratio revealed a lower risk of nosocomial infections in the intervention group compared with that in the non-intervention group. To rule out interference caused by changes in the community floating population and social environment during this 1-year study, 93 long-stay patients in stable condition were selected as a subgroup based on 4,066 patients. The so-called floating population refers to patients who have been in hospital for <2 years. Patients aged ≥65 years were included in the geriatrics program. The incidence of nosocomial infections during the epidemic prevention and control period (24 January 2020 to 24 March 2020) and the previous period of hospitalisation (24 January 2019 to 24 March 2019) was also analysed. In the subgroup analysis, a multivariate analysis was also performed on 93 elderly patients who experienced long-term hospitalisation. The risk of nosocomial and pulmonary infections was found to be lower in the intervention group compared with that in the non-intervention group. During the pandemic, the geriatric department took active preventative measures. However, whether these measures can be normalised to reduce the risk of nosocomial infections among elderly inpatients remain unclear. In addition, the present study found that the use of an indwelling gastric tube is an independent risk factor of nosocomial pulmonary infection in elderly inpatients. However, nutritional interventions are indispensable for the long-term wellbeing of patients, especially for those with dysphagia in whom an indwelling gastric tube is the most viable method of providing enteral nutrition. To conclude, the present retrospective analysis of the selected cases showed that enacting preventative and control measures resulted in the effective control of the incidence of nosocomial infections.

Snail modulates JNK-mediated cell death in Drosophila.

Cell death plays a pivotal role in animal development and tissue homeostasis. Dysregulation of this process is associated with a wide variety of human diseases, including developmental and immunological disorders, neurodegenerative diseases and tumors. While the fundamental role of JNK pathway in cell death has been extensively studied, its down-stream regulators and the underlying mechanisms remain largely elusive. From a Drosophila genetic screen, we identified Snail (Sna), a Zinc-finger transcription factor, as a novel modulator of ectopic Egr-induced JNK-mediated cell death. In addition, sna is essential for the physiological function of JNK signaling in development. Our genetic epistasis data suggest that Sna acts downstream of JNK to promote cell death. Mechanistically, JNK signaling triggers dFoxO-dependent transcriptional activation of sna. Thus, our findings not only reveal a novel function and the underlying mechanism of Sna in modulating JNK-mediated cell death, but also provide a potential drug target and therapeutic strategies for JNK signaling-related diseases.