As a traditional Chinese medicine, wolfberry (Lycium barbarum) has a long cultivation history and a good industrial development foundation. With the development of wolfberry production, the expansion of cultivation area and the increased attention of governments and consumers on food safety, the quality and safety requirement of wolfberry is higher demanded. The quality tracing and traceability system of production entire processes is the important technology tools to protect the wolfberry safety, and to maintain sustained and healthy development of the wolfberry industry. Thus, this article analyzed the wolfberry quality management from the actual situation, the safety hazard sources were discussed according to the HACCP (hazard analysis and critical control point) and GAP (good agricultural practice for Chinese crude drugs), and to provide a reference for the traceability system of wolfberry.
The present study investigated enhancement of apoptosis induction and the mechanisms underlying calcium overload on C6 glioma cells in vitro, stimulated by low-level ultrasound in combination with hematoporphyrin monomethyl ether (HMME). The optimum frequency of ultrasound was determined by 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The apoptotic rate, reactive oxygen species concentration and decreased mitochondrial membrane potential (MMP) were analyzed by flow cytometry. Morphological changes were detected by a transmission electron microscope, and the concentration of intracellular Ca2+, [Ca2+]i, was detected by a confocal laser scanning microscope. In addition, the release of cytochrome c (cyt-c) was measured by western blot analysis. The results revealed that an increased apoptotic effect was induced by sonodynamic therapy (SDT), and this was found to correlate with the overloaded [Ca2+]i, derived from the intra- and extracellular sources in the early apoptotic process. The results also revealed an increased level of ROS production, a decreased MMP and an increased release of cyt-c. The present study indicated that low-level ultrasound in combination with HMME improved the apoptotic effect in C6 glioma cells. The overloaded [Ca2+]i was involved in the mechanism by which apoptosis was stimulated and enhanced by SDT.
Abstract: The calcium‐sensing receptor (CaR) is a G protein‐coupled receptor. The CaR stimulation elicits phospholipase C‐mediated inositol triphosphate formation, leading to an elevation in the level of intracellular calcium released from endoplasmic reticulum (ER). Depletion of ER Ca 2+ leads to ER stress, which is thought to induce apoptosis. Intracellular calcium overload‐induced apoptosis in cardiac myocytes during hypoxia–reoxygenation (H/Re) has been demonstrated. However, the links between CaR, ER stress and apoptosis during H/Re are unclear. This study hypothesized that the CaR could induce apoptosis in neonatal rat cardiomyocytes during H/Re via the ER stress pathway. Neonatal rat cardiomyocytes were subjected to 3 hr of hypoxia, followed by 6 hr of reoxygenation. CaR expression was elevated and the number of apoptotic cells was significantly increased, as shown by transferase‐mediated dUTP nick end‐labelling, with exposure to CaCl 2 , a CaR activator, during H/Re. The intracellular calcium concentration was significantly elevated and the Ca 2+ concentration in the ER was dramatically decreased during H/Re with CaCl 2 ; both intracellular and ER calcium concentrations were detected by laser confocal microscopy. Expression of GRP78 (glucose‐regulated protein 78), the cleavage products of ATF6 (activating transcription factor 6), phospho‐PERK [pancreatic ER kinase (PKR)‐like ER kinase], the activated fragments of caspase‐12, and phospho‐JNK (c‐Jun NH 2 ‐terminal kinase) were increased following exposure to CaCl 2 during H/Re. Our results confirmed that the activated CaR can induce cardiomyocyte apoptosis via ER stress‐associated apoptotic pathways during H/Re.
Cytomegalovirus (CMV) infections in the population are mostly subclinical, inapparent, or latent. However, it is rare in brain tissue. Most reported CMV encephalitis cases were patients with immunodeficiency. The diagnosis and detection rate of CMV encephalitis in patients with normal immune function needs to be further improved.An 86-year-old male was admitted due to a sudden onset of unconsciousness for 3 h. The patient developed status epilepticus and was relieved after antiepileptic treatment. Encephalitis was considered due to the high signals of diffusion-weighted imaging sequences in the right central region by magnetic resonance imaging. Metagenomic next-generation sequencing (mNGS) of blood and cerebrospinal fluid revealed CMV, with unique reads number being 614 and 1, respectively. Simultaneous quantitative PCR results showed CMV positive in blood samples and negative in cerebrospinal fluid samples. The patient was finally diagnosed as CMV encephalitis with status epilepticus. After the antiviral, hormonal, and γ-globulin pulse therapy, the patient's condition improved, and he was finally discharged.mNGS could be a reliable approach for the diagnosis of CMV encephalitis, with high efficiency, sensitivity, and specificity.
A growing amount of evidence has suggested that hydrogen sulfide (H 2 S), as a gasotransmitter, is involved in intensive physiological and pathological processes. More and more research groups have found that H 2 S mediates diverse cellular biological functions related to regulating intracellular calcium concentration. These groups have demonstrated the reciprocal interaction between H 2 S and calcium ion channels and transporters, such as L-type calcium channels (LTCC), T-type calcium channels (TTCC), sodium/calcium exchangers (NCX), transient receptor potential (TRP) channels, β -adrenergic receptors, and N-methyl-D-aspartate receptors (NMDAR) in different cells. However, the understanding of the molecular targets and mechanisms is incomplete. Recently, some research groups demonstrated that H 2 S modulates the activity of calcium ion channels through protein S-sulfhydration and polysulfide reactions. In this review, we elucidate that H 2 S controls intracellular calcium homeostasis and the underlying mechanisms.
As an important cytokine that modulate the cell cycle, the involvement of transforming growth factor beta-1 (TGF-beta1) in carcinogenesis has been extensively studied for many years. Literatures have demonstrated that TGF-beta1 gene polymorphisms may alter the risk of various cancers, such as lung, prostate and breast. To investigate whether polymorphisms of the TGF-beta1 gene can modify the risk of gastric cancer, we conduct this hospital-based, case-control study.One hundred and sixty-seven cases and 193 gender, age-matched healthy controls were enrolled in this case-control study. TGF-beta1 polymorphisms C-509T and T + 869C were identified by PCR-RFLP and ARMS-PCR protocols, respectively.Significantly different distributions of both genes were demonstrated between the case and control. Variant genotypes -509CT, -509TT, +869TC and +869CC were associated with increased risk of gastric cancer (P = 0.001, OR = 2.54; P = 0.016, OR = 2.09; P < 0.001, OR = 3.46; P < 0.001, OR = 4.04, respectively). With haplotype analysis, wild type CT (-509C and +869T) led to a lower frequency in case than that in control (P < 0.001), while haplotype TC was more frequent in case than in control (P < 0.001). Multiple logistic regression analysis revealed that individuals with haplotype TC had an increased likelihood of developing gastric cancer (OR = 3.19, 95%CI = 1.72-5.90).Our findings imply that -509C > T and +869T > C gene polymorphisms in TGF-beta1 may be a critical risk factor of genetic susceptibility to gastric cancer in the Chinese population.
Activation of a calcium‐sensing receptor (Ca‐SR) leads to increased intracellular calcium concentration and altered cellular activities. The expression of Ca‐SR has been identified in both nonexcitable and excitable cells, including neurons and smooth muscle cells. Whether Ca‐SR was expressed and functioning in cardiac myocytes remained unclear. In the present study, the transcripts of Ca‐SR were identified in rat heart tissues using RT‐PCR that was further confirmed by sequence analysis. Ca‐SR proteins were detected in rat ventricular and atrial tissues as well as in isolated cardiac myocytes. Anti‐(Ca‐SR) Ig did not detect any specific bands after preadsorption with standard Ca‐SR antigens. An immunohistochemistry study revealed the presence of Ca‐SR in rat cardiac as well as other tissues. An increase in extracellular calcium or gadolinium induced a concentration‐dependent sustained increase in [Ca 2+ ] i in isolated ventricular myocytes from adult rats. Spermine (1–10 m m ) also increased [Ca 2+ ] i . Pre‐treatment of cardiac myocytes with thapsigargin or U73122 abolished the extracellular calcium, gadolinium or spermine‐induced increase in [Ca 2+ ] i . The blockade of Na + /Ca 2+ exchanger or voltage‐dependent calcium channels did not alter the extracellular calcium‐induced increase in [Ca 2+ ] i . Finally, extracellular calcium, gadolinium and spermine all increased intracellular inositol 1,4,5‐triphosphate (IP 3 ) levels. Our results demonstrated that Ca‐SR was expressed in cardiac tissue and cardiomyocytes and its function was regulated by extracellular calcium and spermine.
Reactive oxygen species (ROS) generation has been suggested to play a vital role in the initiation and progression of diabetic cardiomyopathy, a major complication of diabetes mellitus. Recent studies reveal that spermine possesses proliferative, antiaging and antioxidative properties. Thus, we hypothesized that spermine could decrease apoptosis via suppressing ROS accumulation induced by high glucose (HG) in cardiomyocytes. Cultured neonatal rat ventricle cardiomyocytes were treated with normal glucose (NG) (5 mM) or HG (25 mM) in the presence or absence of spermine for 48 h. The cell activity, apoptosis, ROS production, T-SOD and GSH activities, MDA content and GSSG level were assessed. The results showed that HG induced lipid peroxidation and the increase of intracellular ROS formation and apoptosis in primary cardiomyocytes. Spermine could obviously improve the above-mentioned changes. Western blot analysis revealed that spermine markedly inhibited HG-induced the phosphorylation of p38/JNK MAPKs and JAK2. Moreover, spermine had better antioxidative and anti-apoptotic effects than N-acetyl-L-cysteine (NAC). Taken together, the present data suggested that spermine could suppress ROS accumulation to decrease cardiomyocytes apoptosis in HG condition, which may be attributed to the inhibition of p38/JNK and JAK2 activation and its natural antioxidative property. Our findings may highlight a new therapeutic intervention for the prevention of diabetic cardiomyopathy.
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