[Relationship between the neutrophil-to-lymphocyte ratio and estimated glomerular filtration rate in patients with primary aldosteronism: a cross-sectional study].

Objective: To investigate the associations between neutrophil-to-lymphocyte ratio (NLR) and estimated glomerular filtration rate (eGFR) in patients with primary aldosteronism (PA). Methods: This study was a cross-sectional study. Consecutive patients diagnosed with PA and admitted to the Second Affiliated Hospital of Nanchang University from October 2017 to April 2022 were enrolled. General information, blood routine, renal function, and other clinical data of the patients were collected. Based on the median NLR of the enrolled patients, NLR

Screening the Fusarium graminearum inhibitory mutant strain from Bacillus subtilis by atmospheric-pressure plasma jet.

AIMS: The aim of this study was to improve the antagonistic activity of Bacillus subtilis JA towards Fusarium graminearum by screening high-yielding mutant using the atmospheric-pressure plasma jet (APPJ). METHODS AND RESULTS: Atmospheric-pressure plasma jet was applied as mutagenic source for breeding high-yielding mutant strain. Helium was used as APPJ operating gas. The mutation effects of different treatment times of APPJ were studied. The mutant strain designated as B. subtilis B06 was successfully screened out, which showed higher antagonistic activity against F. graminearum in vitro. Its inhibition zone against the indicator fungus increased by 23% compared to the original one. HPLC and ESI (electrospray ionization) mass spectrometry analysis indicated that antifungal compounds produced by the mutant and original strain belonged to the lipopeptide, surfactin and iturin families. The mutant strain showed favourable properties of faster growth in the fermentation process and higher production of antibiotics. The lipopeptide production of the mutant was 2.3-fold as that of the original strain. CONCLUSIONS: A mutant strain with strong antagonistic activity and high yielding of antibiotics was obtained by APPJ in this study. The mutant could be used as a promising biocontrol agent in agriculture. SIGNIFICANCE AND IMPACT OF STUDY: This study provides a novel mutagenic source for breeding high-yielding microbial mutant, which would be very useful in the application of some valuable metabolites from micro-organism.

Propofol improves intestinal ischemia-reperfusion injury in rats through NF-κB pathway.

OBJECTIVE: The aim of this study was to investigate the effects of propofol on intestinal ischemia-reperfusion injury in rats through the nuclear factor-kappa B (NF-κB) pathway. MATERIALS AND METHODS: A total of 24 Sprague-Dawley rats were selected and randomly divided into three groups, including sham operation group, ischemia group and propofol group. Rats in sham operation group were only treated with isolation of superior mesenteric artery, which was clipped for 1 h and reperfused for 2 h in ischemia group. Meanwhile, propofol (60 mg/kg) was injected into the femoral vein 1 h before ischemia in propofol group. TUNEL assay was performed to detect cell apoptosis of intestinal tissues. Real-time quantitative polymerase chain reaction (RT-qPCR) was conducted to measure the expression levels of malondialdehyde (MDA), superoxide dismutase (SOD), myeloperoxidase (MPO), caspase-3 and B-cell lymphoma-2 (Bcl-2) in rats of each group. Western blotting was utilized to detect the protein expression levels of NF-κB pathway related molecules, such as myeloid differential protein-88 (MyD88), v-rel avian reticuloendotheliosis viral oncogene homolog A (RelA) and NF-κB. Furthermore, changes in plasma cytokine levels were determined via enzyme-linked immunosorbent assay (ELISA). RESULTS: The number of apoptotic cells in ischemia group was remarkably higher than that in sham operation group (p<0.05). However, it decreased notably in propofol group compared with ischemia group (p<0.05). In comparison with sham operation group, significantly up-regulated expression of caspase-3 and down-regulated expression of Bcl-2 were observed in the intestinal tissues of rats in ischemia group (p<0.05). Caspase-3 was lowly expressed, while Bcl-2 was highly expressed in the intestinal tissues of rats in propofol group compared with ischemia group (p<0.05). In addition, no statistically significant differences were observed in the expression level of SOD among sham operation group, ischemia group and propofol group (p>0.05). The expression levels of MDA and MPO were overtly higher in the intestinal tissues of rats in ischemia group than those in sham operation group and propofol group (p<0.05). Besides, the protein expression levels of MyD88, RelA and NF-κB in the intestinal tissues of rats in ischemia group were remarkably higher than those in sham operation group and propofol group (p<0.05). The activity of the NF-κB pathway in the intestinal tissues of rats in propofol group significantly declined compared with ischemia group (p<0.05). Moreover, compared with sham operation group, plasma levels of TNF-α, interleukin (IL)-2, IL-6 and IL-4 increased significantly in rats of ischemia group (p<0.05). However, they were markedly lower in propofol group than those in ischemia group (p<0.05). CONCLUSIONS: Propofol protects rats from intestinal ischemia-reperfusion injury through the NF-κB pathway.

Cloning and characterization of G protein-gated inward rectifier K+ channel (GIRK1) isoforms from heart and brain.

A G protein-gated inward rectifier potassium (K+) channel (GIRK1a) has been cloned from different tissues (Kubo et al., 1993b; Dascal et al., 1993). Here we report the cloning of three additional novel isoforms of GIRK1a from rat atria and and one from human brain. These isoform cDNAs code for proteins that have identical N-termini, M1-H5-M2 (predicted transmembrane and pore domains), and post-M2 amino acid regions to GIRK1a (1-501 amino acids), but they have shorter C-termini (GIRK1b (1-309), GIRK1c (1-308), GIRK1d (1-235), and GIRK1e (1-253). These results indicated that isoforms were generated by alternative splicing and partial genomic analysis confirmed the presence of exons and introns in the rat GIRK1 gene. RNase protection analysis and immunoblot analysis indicated that the isoforms were expressed in both rat atria and brain but at lower levels versus GIRK1a. The physiological role that the isoforms may play in atrial and brain physiology remains to be determined.

[Surgical treatment of carcinoma of esophagus and cardia in patients from different nationalities in Xingjiang--a report of 650 cases].

A total of 650 patients including 452 with esophageal and 198 with cardiac cancers from different nationalities in Xingjiang were treated by surgery in this department from 1978 to January 1990. The total resectability was 85.4% (555/650), with a higher in the esophagus group (83.5%) and a lower in the cardia group (78.3%). Postoperative complications happened in 63 (10.5%) cases, including anastomotic leakage in 29 (5.2%) cases and intrathoracic leakage in 19 (3.4%) cases. Operative mortality was 3.4% (22 cases). Finally the incidence rate of the disease among different nationalities, the criteria of selection of patients for operation and the technique of operation were discussed.

[Studies on simultaneous production of chitosanase and chitosan degradation in situ with Trichoderma reesei in convoluted fibrous bed bioreactor].

The cells of Trichoderma reesei were immobilized on a roll of porous polyurethane foam sheet and packed in a bubble column bioreactor for simultaneous production of chitosanase and degradation of chitosan in situ. The average degree of polymerization could be regulated by reaction time. Under the repeated-batch process with 2% soluble chitosan at pH4.8, 28 degrees C, the activity of chitosanase for each batch was above 0.15 IU/mL, the average yield of reducing sugar as D-glucosamine reached 73%. The novel immobilized bioreactor system run stably and effectively in the successive 10 batches lasting 30 days without notable change in the activity and productivity.

Molecular cloning and expression of a Kv1.1-like potassium channel from the electric organ of Electrophorus electricus.

Electrocytes from the electric organ of Electrophorus electricus exhibited sodium action potentials that have been proposed to be repolarized by leak currents and not by outward voltage-gated potassium currents. However, patch-clamp recordings have suggested that electrocytes may contain a very low density of voltage-gated K(+) channels. We report here the cloning of a K(+) channel from an eel electric organ cDNA library, which, when expressed in mammalian tissue culture cells, displayed delayed-rectifier K(+) channel characteristics. The amino-acid sequence of the eel K(+) channel had the highest identity to Kv1.1 potassium channels. However, different important functional regions of eel Kv1.1 had higher amino-acid identity to other Kv1 members, for example, the eel Kv1.1 S4-S5 region was identical to Kv1.5 and Kv1.6. Northern blot analysis indicated that eel Kv1.1 mRNA was expressed at appreciable levels in the electric organ but it was not detected in eel brain, muscle, or cardiac tissue. Because electrocytes do not express robust outward voltage-gated potassium currents we speculate that eel Kv1.1 channels are chronically inhibited in the electric organ and may be functionally recruited by an unknown mechanism.

Expression of Kv1.1 delayed rectifier potassium channels in Lec mutant Chinese hamster ovary cell lines reveals a role for sialidation in channel function.

Kv1.1 potassium (K+) channels contain significant amounts of negatively charged sialic acids. To examine the role of sialidation in K+ channel function, Chinese hamster ovary cell lines deficient in glycosylation (Lec mutants) were transfected with rat brain Kv1.1 cDNA. The K+ channel was functionally expressed in all cell lines, but the voltage dependence of activation (V1/2) was shifted to more positive voltages and the activation kinetics were slower in the mutant cell lines compared with control. A similar positive shift in V1/2 was recorded in control cells expressing Kv1.1 following treatment with sialidase or by raising extracellular Ca2+. In contrast, these treatments had little or no effect on the Lec mutants, which indicates that channel sialic acids appear to be the negative surface charges sensitive to Ca2+. The data suggest that sialic acid addition modifies Kv1.1 channel function, possibly by influencing the local electric field detected by its voltage sensor, but that these carbohydrates are not required for cell surface expression.

G-protein-gated inward rectifier K+ channel proteins (GIRK1) are present in the soma and dendrites as well as in nerve terminals of specific neurons in the brain.

G-protein-gated inward rectifier potassium (GIRK) channels are coupled to numerous neurotransmitter receptors in the brain and can play important roles in modulating neuronal function, depending on their localization in a given neuron. Site-directed antibodies to the extreme C terminus of GIRK1 (or KGA1), a recently cloned component of GIRK channels, have been used to determine the relative expression levels and distribution of the protein in different regions of the rat brain by immunoblot and immunohistochemical techniques. We report that the GIRK1 protein is expressed prominently in the olfactory bulb, hippocampus, dentate gyrus, neocortex, thalamus, cerebellar cortex, and several brain stem nuclei. In addition to the expected localization in somas and dendrites, where GIRK channels may mediate postsynaptic inhibition, GIRK1 proteins were also found in axons and their terminal fields, suggesting that GIRK channels can also modulate presynaptic events. Furthermore, the distribution of the protein to either somatodendritic or axonal-terminal regions of neurons varied in different brain regions, which would imply distinct functions of these channels in different neuronal populations. Particularly prominent staining of the cortical barrels of layer IV of the neocortex, and the absence of this staining with unilateral kainate lesions of the thalamus, suggest that the GIRK1 protein is expressed in thalamocortical nerve terminals in which GIRK channels may mediate the actions of mu opiate receptors.