Effects of Hot Water Immersion on Storage Quality of Fresh Broccoli Heads

Freshly harvested broccoli heads were immersed for 0, 1, 4 or 8 min into hot water at 45 °C, and then were hydrocooled rapidly for 10 min at 10 °C. Following these treatments, the broccoli were air-dried for 30 min, then packed in commercial polymeric film bags, and, finally, stored for 16 days at –1, 1, and 12 °C. The samples treated with hot water maintained high contents of chlorophyll concentrations, their yellowing rate was delayed, and fungal infection and chilling or freezing injury were inhibited markedly. Compared to non-heat-treated broccoli, a lower level of peroxidase activity with a relatively higher chlorophyll concentration was observed when broccoli were treated with hot water. Among these heat treatments, immersion in hot water for 4 min at 45 °C was the most effective for maintaining the quality of harvested broccoli heads

A screening analysis of the GJB2 c.176 del 16 mutation responsible for hereditary deafness in a Chinese family

AbstractObjectiveTo determine whether a new-born child from a family carrying a deafness gene needs cochlear implantation to avoid dysphonia by screening and sequencing a deafness-related gene.ResultsBoth screening and sequencing results confirmed that the new born child had a normal GJB2 gene despite the fact that she has a brother suffering from hearing loss triggered by an allelic GJB2 c.176 del 16 mutation. We cloned the GJB2 genes derived from their respective blood genomic DNA into GFP fused plasmids and transfected those plasmids into the 293T cell line to test for gene function. While the mutated GJB2 gene (GJB2 c.176 del 16) of her deaf brother was found to be unable to form the gap junction structure between two adjacent cells, the baby girl's GJB2 gene ran into no such problems.ConclusionThe screening and sequencing as well as the GJB2 gene function tests invariably showed results consistent with the ABR tested hearing phenotype, which means that the child, with a normal wild type GJB2 gene, does not need early intervention to prevent her from developing hearing loss and dysphonia at a later stage in life

HSPA12B Attenuated Acute Myocardial Ischemia/reperfusion Injury via Maintaining Endothelial Integrity in a PI3K/Akt/mTOR-dependent Mechanism

Endothelial damage is a critical mediator of myocardial ischemia/reperfusion (I/R) injury. HSPA12B is an endothelial-cell-specifically expressed heat shock protein. However, the roles of HSPA12B in acute myocardial I/R injury is unknown. Here we reported that myocardial I/R upregulated HSPA12B expression in ventricular tissues, and endothelial overexpression of HSPA12B in transgenic mice (Tg) limited infarct size, attenuated cardiac dysfunction and improved cardiomyocyte survival compared with their wild type littermates. These improvements were accompanied with the diminished myocardial no-reflow phenomenon, decreased microvascular leakage, and better maintained endothelial tight junctions. The I/R-evoked neutrophil infiltration was also suppressed in Tg hearts compared with its wild type (WT) littermates. Moreover, Tg hearts exhibited the enhanced activation of PI3K/Akt//mTOR signaling following I/R challenge. However, pharmacological inhibition of PI3K abolished the HSPA12B-induced cardioprotection against myocardial I/R injury. The data demonstrate for the first time that the endothelial HSPA12B protected hearts against myocardial I/R injury. This cardioprotective action of HSPA12B was mediated, at least in part, by improving endothelial integrity in a PI3K/Akt/mTOR-dependent mechanism. Our study suggests that targeting endothelial HSPA12B could be an alternative approach for the management of patients with myocardial I/R injury

Dual-factor Synergistically Activated ESIPT-based Probe:Differential Fluorescence Signals to Simultaneously Detect α-Naphthyl Acetate and Acid α-Naphthyl Acetate Esterase

[Image: see text] α-Naphthyl acetate esterase (α-NAE) and acid α-naphthyl acetate esterase (ANAE), a class of special esterases, are important for lymphocyte typing and immunocompetence-monitoring. As such, the simultaneous detection of α-NAE and ANAE has become a target to effectively improve the accuracy in lymphocyte typing. Therefore, we developed a dual-factor synergistically activated ESIPT-based probe (HBT-NA) to detect α-NAE and ANAE sensitively, rapidly, and simultaneously in a differential manner. HBT-NA exhibits differential fluorescence signal outputs toward small changes of α-NAE and ANAE activities. HBT-NA displays a weak fluorescence signal at 392 nm over a pH range from 6.0 to 7.4. However, when it interacts with α-NAE (0–25 U) at pH = 7.4, the fluorescence intensity at 392 nm enhanced linearly within 60 s (F(392 nm)/F0(392 nm) = 0.042 C(α-NAE) + 1.1, R(2) = 0.99). Furthermore, HBT-NA emits ratiometric fluorescence signals (F(505 nm)/F(392 nm)) for ANAE (0–25 U) at pH = 6.0 within 2.0 min, exhibiting a good linear relationship (F(505 nm)/F(392 nm) = 0.83C(ANAE) – 1.75, R(2) = 0.99). The differential fluorescence signals can be used to simultaneously detect the activities of α-NAE and ANAE in solutions and complex living organisms. More importantly, based on the differential fluorescence signals toward α-NAE and ANAE, T lymphocytes and B lymphocytes could be successfully typed and differentiated among nontyped lymphocytes, facilitating the real-time evaluation of their immune functions using flow cytometry. Hence, HBT-NA could be used for the ultrasensitive detection of the enzyme activities of α-NAE and ANAE, the real-time precise typing of lymphocytes, and the monitoring of immunocompetence

HSPA12A Attenuates Lipopolysaccharide-Induced Liver Injury Through Inhibiting Caspase-11-Mediated Hepatocyte Pyroptosis via PGC-1α-Dependent Acyloxyacyl Hydrolase Expression

Liver dysfunction is strongly associated with poor survival of sepsis patients. Cytosolic lipopolysaccharide (LPS) sensing by Caspase-4/5/11 for pyroptosis activation is a major driver of the development of sepsis. Studies in macrophages and endothelial cells have demonstrated that LPS is inactivated by acyloxyacyl hydrolase (AOAH) and leading to desensitizing Caspase-4/5/11 to LPS. However, little is known about the cytosolic LPS-induced pyroptosis in hepatocytes during sepsis. Heat shock protein 12A (HSPA12A) is a novel member of the HSP70 family. Here, we report that LPS increased HSPA12A nuclear translocation in hepatocytes, while knockout of HSPA12A (Hspa12a−/−) in mice promoted LPS-induced acute liver injury. We also noticed that the LPS-induced Caspase-11 activation and its cleavage of gasdermin D (GSDMD) to produce the membrane pore-forming GSDMDNterm (markers of pyroptosis) were greater in livers of Hspa12a−/− mice compared with its wild type controls. Loss- and gain-of-function studies showed that HSPA12A deficiency promoted, whereas HSPA12A overexpression inhibited, cytosolic LPS accumulation, Caspase-11 activation and GSDMDNterm generation in primary hepatocytes following LPS incubation. Notably, LPS-induced AOAH expression was suppressed by HSPA12A deficiency, whereas AOAH overexpression reversed the HSPA12A deficiency-induced promotion of LPS-evoked and Caspase-11-mediated pyroptosis of hepatocytes. In-depth molecular analysis showed that HSPA12A interacted directly with peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) and increased its nuclear translocation, thereby inducing AOAH expression for cytosolic LPS inactivation, which ultimately leading to inhibition of the Caspase-11 mediated pyroptosis of hepatocytes. Taken together, these findings revealed HSPA12A as a novel player against LPS-induced liver injury by inhibiting cytosolic LPS-induced hepatocyte pyroptosis via PGC-1α-mediated AOAH expression. Therefore, targeting hepatocyte HSPA12A represents a viable strategy for the management of liver injury in sepsis patients

UniBrain: Universal Brain MRI Diagnosis with Hierarchical Knowledge-enhanced Pre-training

Magnetic resonance imaging~(MRI) have played a crucial role in brain disease diagnosis, with which a range of computer-aided artificial intelligence methods have been proposed. However, the early explorations usually focus on the limited types of brain diseases in one study and train the model on the data in a small scale, yielding the bottleneck of generalization. Towards a more effective and scalable paradigm, we propose a hierarchical knowledge-enhanced pre-training framework for the universal brain MRI diagnosis, termed as UniBrain. Specifically, UniBrain leverages a large-scale dataset of 24,770 imaging-report pairs from routine diagnostics. Different from previous pre-training techniques for the unitary vision or textual feature, or with the brute-force alignment between vision and language information, we leverage the unique characteristic of report information in different granularity to build a hierarchical alignment mechanism, which strengthens the efficiency in feature learning. Our UniBrain is validated on three real world datasets with severe class imbalance and the public BraTS2019 dataset. It not only consistently outperforms all state-of-the-art diagnostic methods by a large margin and provides a superior grounding performance but also shows comparable performance compared to expert radiologists on certain disease types