In the cerebrospinal fluid and serum the activity was determined of phosphocreatine kinase (CPK), lactic dehydrogenase (LDH), aspartate transaminase (AspAT) and alanine transaminase (AlAT) in 107 cases of multiple sclerosis. The results were compared with those in a control group of neurosis and a highly significant (three times) increase was observed in the activity of CPK and LDH in the cerebrospinal fluid as a result of organic damage to the brain tissue. By chromatographic method direct data were obtained indicating that increased CPK activity in the cerebrospinal fluid was connected with the CK-BB isoenzyme, that is with the cerebral fraction of the enzyme.

Creatine kinase (ATP: creatine N-phosphotransferase, EC 2.7.3.2, CK) BB isoenzyme from stomach tumor tissue was partially purified and its characteristics were compared with those from healthy tissue. Molecular mass of tumor CK-BB was estimated to be 82 000 by polyacrylamide gel electrophoresis. Tumor CK-BB was separated into 2 main subbands around pH 4.5 and 11, minor subbands around pH 5-7.5 by agarose isoelectric focusing. The isoenzyme reacted with anti-human brain CK-BB antibodies and formed a hybrid, CK-MB, with CK-MM prepared from healthy human skeletal muscle. The above physicochemical and immunological characteristics of tumor CK-BB were the same as those of normal CK-BB from normal stomach tissue. Optimum pH of tumor CK-BB was more acidic than that of normal CK-BB. Affinity for creatine phosphate and heat sensitivity of tumor CK-BB were slightly lower than those of normal CK-BB. Tumor CK-BB was more stable after iodoacetamide and urea treatments.

A new commercial enzyme immunoassay kit for quantification of creatine kinase-MB (CK-MB) isoenzyme was compared with its electrophoretic determination with respect to efficacy in diagnosis of acute myocardial infarction. Enzygnost CK-MB (Behring Diagnostics) is a solid-phase "sandwich"-type enzyme immunoassay with antibodies to the B-subunit coated on plastic tubes and peroxidase-conjugated antibodies to the M-subunit added after incubation with sample. This kit is designed to measure only CK-MB and not CK-MM, CK-BB, adenylate kinase, or atypical CK molecules. The linear-regression equation comparing the two methods was: Enzygnost = 0.98 . electrophoresis - 0.72, with a correlation coefficient of r = 0.967 (n = 143). For 51 patients admitted for diagnosis of possible acute myocardial infarction, the Enzygnost kit achieved 100% sensitivity, specificity, and efficiency in predicting the correct diagnosis. Corresponding values for the electrophoretic assay were: 95.5% sensitivity, 93.1% specificity, and 94.1% efficiency. We conclude that this kit method provides an excellent alternative to electrophoresis.

More than 300 laboratories participated in an interlaboratory survey of creatine kinase (CK, EC 2.7.3.2) determinations in which they analyzed seven lyophilized samples for total CK and CK isoenzymes and furnished information about their methodology. The samples were not necessarily intended to mimic typical patients' specimens but rather to determine the analytical ability of the laboratories to distinguish isoenzyme fraction CK-MB from CK-BB and to detect small but abnormal amounts of CK-BB. For total CK measurement, most laboratories used an NADP+ reduction method monitored at 340 nm (89%), and reported results in units per liter (U/L) (99%) at either 30 degrees C (34%) or 37 degrees C (60%). Despite the variety of analytical conditions, most laboratories (89%) correctly reported results within their normal range for all samples. The 287 laboratories that reported isoenzyme distributions in the samples used either cellulose acetate (37%) or agarose (44%) electrophoresis, ion-exchange chromatography (9%), or immunoinhibition (7%). Results from laboratories that used nonspecific CK-MB immunoinhibition techniques were biased when a significant amount of CK-BB isoenzyme was present.

To investigate the protective effects of ginkgo diterpene lactone meglumine injection (GDLMI) on cerebral focal ischemia reperfusion injury induced by middle cerebral artery occlusion (MCAO) in rats, and explore its possible mechanism. One hundred and forty male SD rats were randomly divided into sham operation group, model group, ginkgo biloba extract injection (Ginaton, 1.0 mL•kg⁻¹) group, nimodipine (0.4 mg•kg⁻¹) group, and GDLMI (5.2, 2.6, 1.3 mg•kg⁻¹) groups; All of rats received corresponding drugs by tail vein injection 4 days before operation (normal saline in model group and sham operation group). Except the sham operation group, the cerebral ischemic stroke model was established by MCAO method in right brain of the other rats. After 3 h of ischemia, all the animals received intravenous administration again. The neurobehavioral scores of rats after ischemia-reperfusion were evaluated and the infarct rate of brain tissue was observed by TTC staining. The super oxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA) and lactic acid (LA) contents in brain tissue homogenate and the concentration of Ca2+, glutamate (Glu) and aspartate (Asp), creatine phosphate kinase (CK-BB) and lactate dehydrogenase (LDH) content changes in cerebrospinal fluid were measured. As compared with the sham operation group, the cerebral infarction rate was increased significantly in the model group; the content of MDA and LA in the homogenate of brain tissue was increased, and the content of GSH and SOD was decreased; in cerebrospinal fluid, Ca2+ concentration was decreased, and the content of Glu and Asp, CK-BB and LDH increased significantly. As compared with the model group, the high and medium dose GDLMI groups can significantly reduce the cerebral infarction rate and improve the symptoms of neurological impairment; increase SOD and GSH activity, reduce MDA and LA content in serum; increase Ca2+ concentration in cerebrospinal fluid and decrease the content of neurotransmitter Glu and Asp as well as CK-BB and LDH. GDLMI could obviously improve neurologic impairment in model rats, and the mechanism may be related to recovering the blood brain barrier, scavenging free radicals, decreasing free Ca2+ inflow into the cells and the content of excitatory amino acid in cerebrospinal fluid to improve its protective effect on cerebral ischemia.

In recent years the determination of serum enzyme activities has played an increasing role in clinical chemical diagnosis. Because the enzyme composition of single organs is qualitatively and, to a certain extent, quantitatively similar, the diagnostic value of enzyme activity determinations is often diminished. Each serum enzyme can be separated into isoenzymes which stem from different organs and make specific organ diagnoses possible. This separation is possible through chemico-physical and immunological methods. Electrophoretic, chromatographic and immunological methods for the determination of creatine phosphokinase isoenzymes the immunological method is superior to the electrophoretic method in precision and accuracy. Artefacts through storage do not occur in the immunological method. New aspects of the clinical value of the determination of isoenzymes of alkaline phosphatase (AP, E.C. 3.1.3.1), creatine phosphokinase (CK, E.C. 2.7.3.2) and lactate dehydrogenase (LDH, E.C. 1.1.1.27) were studied in the following 8 patient groups: 1. The value of AP isoenzymes for determining liver damage due to chronic alcoholism. 2. The distribution of AP isoenzymes in dialysis patients with special regard to the intestinal isoenzyme. 3. The immunological demonstration of carcino-placental antigen of AP in tumours of the lung. 4. The demonstration of intestinal isoenzymes of AP in chylous effusions. 5. The profile of LDH isoenzymes in pulmonary alveolar proteinosis in serum and in lung lavage-fluid. 6. The usefulness of CK-MB isoenzyme as proff of cardiotoxicity of pharmaceuticals. 7. The profile of CK isoenzymes in central and peripheral nervous system diseases, especially the appearance of CK-BB in serum and the behaviour of CK at the blood spinal fluid barrier. 8. The appearance of unusual isoenzyme patterns in newborn infants and in pregnant women in comparison with normal adults. The determination of isoenzymes is of great clinical importance, even if the total serum activity of the particular enzyme is not elevated.

The activity of creatine kinase isoenzyme BB (CK-BB) was determined in serum of healthy adults and in patients undergoing maintenance hemodialysis and with kidney transplant. In the healthy adults examined, an activity of 0.56 +/- 0.16 U/l (mean +/- SD) was found. The arithmetic mean of CK-BB activity in patients with renal insufficiency under hemodialysis was 1.42 +/- 0.87 U/l and differed from that of the healthy group. The CK-BB activity in patients with kidney transplant was not different from that of the control group. The occurrence of CK-BB in serum is discussed from diagnostic and methodological point of view.

Biochars are widely used to improve soil macropore structures. However, the size-dependent effects of biochars in affecting macropore structure still remain unclear. In this study, the modification of soil macropore structure following biochar addition was investigated by high-resolution X-ray tomography (CT) and advanced data analytical methods. Quantification of soil macropore structure (>52 μm) was based on the intact soil cores (5 cm in diameter and 7 cm in height) collected from biochar-amended paddy soil. The treatments were: (a) control (CK), (b) rice straw biochar (RSB), (c) corn straw biochar (CSB), and (d) bamboo biochar (BB). The application rate of biochar was 25 Mg ha^-1 (w/w). Results revealed that the biochars affected the soil macropores through both "occupying effect" and "expansion effect". The "occupying effect" means that the biochar particles occupy the original pore space of the soil and reduce the soil porosity, while the "expansion effect" means that the biochar particles produce additional pore space in the soil matrix and increase the soil porosity. For all the biochar treatments in our study, the "occupying effect" was dominated. Therefore, the connected- and isolated porosity of biochar-treated soils were significantly lower than those of CK. The size-dependent effects of biochar in modifying soil macropores were observed. For RSB treatment, the "expansion effect" predominated at the size of <1200 μm and >1800 μm, while both the "occupying effect" and "expansion effect" were observed at the size of 1200-1800 μm. For CSB and BB treatments, the "expansion effect" predominate only at the size of 600-1200 μm; whereas both the "occupying effect" and "expansion effect" were observed at the size of <600 μm and >1800 μm. Our results indicated that the effects of biochar on soil macroporosity were dependent on the combined effects the "occupying effect" and "expansion effect". In conclusion, all the biochar types in this study have adverse effects in increasing the soil macroporosity.

Platelet-derived endothelial cell growth factor (PD-ECGF) is linked to angiogenesis in human cancer. Direct studies have demonstrated that PD-ECGF is a potent mitogen for endothelial cells in vivo. Because endothelial repair and smooth muscle cell proliferation are two processes that affect arterial wall structure and tone, we analyzed the effects of PD-ECGF on DNA synthesis and creatine kinase BB-specific activity (CK) in human umbilical artery smooth muscle cells (SMC) and in a human umbilical endothelial cell line (E304). In SMC, PD-ECGF (0.001 to 10 U/mL) inhibited DNA synthesis dose dependently (-24% + 6% to -63% + 15%) assessed by 3[H]thymidine incorporation into DNA, whereas in E304 it stimulated DNA synthesis dose dependently (30% + 4% to 100% + 4%). In both SMC and E304, however, PD-ECGF elicited an increase in CK-specific activity by 54% to 130% and 79% to 163%, respectively. These effects were reversed by a specific anti-PD-ECGF antibody. In E304 cells PD-ECGF enhanced 17beta-estradiol (E2) or dihydrotestosterone (DHT)-induced DNA synthesis from 56% to 122% and from 127% to 359%, and CK activity from 70% to 180% and from 90% to 190%, respectively. In SMC PD-ECGF, an inhibitor of 3[H]thymidine incorporation by itself, markedly enhanced the stimulatory effect of low concentrations of E2 and DHT on 3[H]thymidine incorporation. It also increased E2 and DHT CK induction from 40% to 140% and from 52% to 120%, respectively. In both E304 and SMC, PD-ECGF inhibited the proliferative and the CK-inducing effects of platelet-derived growth factor (PDGF) and immunoglobulin F1 (IGF1). Thus, PD-ECGF, an established growth promoter for endothelial cells, is a potent inhibitor of DNA synthesis in human arterial SMC. However, in both E304 endothelial cells and SMC, PD-ECGF enhances the stimulatory effect of low concentrations of gonadal steroids on 3[H]thymidine incorporation. PD-ECGF antagonizes PDGF- and IGF1-induced DNA synthesis in both E304 and SMC cells. By inhibiting arterial SMC proliferation and accelerating endothelial cell replication, PD-ECGF may buffer the effect of PDGF and favorably modulate arterial wall response to injury.

Recent reports have suggested that serum creatine kinase isoenzyme BB (CK-BB) may be used as a tumor marker for a variety of malignancies, particularly prostatic carcinoma. Two cases of small cell anaplastic carcinoma of the lung (SCAC) had markedly contrasting levels of CK-BB by serum electrophoresis. Retrospective analysis of the index cases, and four additional autopsy cases of SCAC, included: 1) quantitation of CK-B in postmortem tumor and adjacent non-tumor lung tissue; 2) enzymatic and radioimmunoassay serum levels of CK-B; and 3) CK-B immunoperoxidase staining of tumor and non-tumor tissues for CK-B. Serum CK-BB is a non-specific tumor marker, but its presence, in whatever amount, should alert the clinician to the possibility of an associated malignancy, particularly SCAC or metastatic carcinoma.

The CK-BB isoenzyme is ubiquitous in neoplastic tissue, but with low activity. Accordingly, it might be a nonspecific and insensitive tumor marker. Evaluation of BB isoenzyme in serum might indicate the extent of diseases or the response to therapy. The presence of CK-MB in patients with cancers may cause confusion with AMI. Serial determinations of both CK and lactate dehydrogenase isoenzymes are of great help in differential diagnosis. The presence of mit-CK is a poor prognostic sign in patients with malignancy. The greatest clinical significance of CK-BB and macro-CK isoenzyme lies in their effect on various assays for CK-MB. Macro-CK types 1 and 2 are much more heat stable than are CK-MB and CK-BB, and so by heating samples for 20 min at 45 degrees C the presence of thermostable macro types can be demonstrated. Macro-CK type 2 has a much higher activation energy than macro-CK type 1. If macro-CK is present, determination of the activation energy easily differentiates between types 1 and 2. CK-Bi seems to be glycosylated protein, and it is thought that glycosylation may be a general way of enzyme inactivation. If inactivation inside the cell is postulated, it has to be shown that enzymes indeed pass into the cell compartments where glycosylating enzymes are located. Another possible mechanism is within the circulation. Whether malignant cells themselves produce Ck-Bi or if inactivation occurs in the blood is still unknown. In this connection, one finding is that in plasma of cancer patients, CK-Bi can be reactivated to CK-BB by mercaptoethanol to 95%, whereas in plasma of normal persons there is no reactivation of the much lower CK-Bi concentrations.

CK-MB activity, which is measured by the immunoinhibition method, is an important marker for use in the diagnosis of acute coronary syndromes. In the present study, we evaluated the basal performance of a recently improved CK-MB activity kit, "L-system CK-MB," in which the activity of mitochondrial CK subunits is inhibited. Within-run and between-day precision were in the range of 1.9-2.3% and 3.2-6.0%, respectively. Diluted linearity and limit of detection were determined to be 600 U/L and 0.8 U/L, respectively. The use of L-system CK-MB allowed the inhibition of the activity of 98.1% of sarcomeric mitochondrial CK, 97.7% of ubiquitous mitochondrial CK, and 99.9% of CK-MM. The correlation coefficient (r) between CK-MB activity and CK-MB protein was 0.968. However, we found 4 cases showing CK-MB activity significantly higher than the protein concentration. Increased CK-BB activity was detected by electrophoresis in these cases. In some patients with malignant tumors, the presence of CK-immunoglobulin complex also lead to elevated CK-MB concentrations. Thus, the discrepancy in the CK-MB activity and the protein concentration may be caused by the presence of CK-BB and/or CK-immunoglobulin complex. More attention needs to be focused on samples with high CK-MB protein concentrations, especially when the CK-MB/CK ratio is high.

In this work we have considered CK isoenzymes (CKBB-CKMT) as tumoral markers. The statistical comparison of the results (x2) executed on thirty neoplastic patients selected at random, has proved that CKBB and/or CKMT frequency is the same as the CEA one (CEA vs BB = N.S.; CEA VS MT = N.S.; CEA VS BB + MT = N.S.) and higher than AFP one (AFP VS BB = P less than 0.001; AFP VS MT = P less than 0.01). The isoenzymes' determination was executed by electrophoretic method (Helena) which is sensitive, specific and swift.

Around the world, species from the genus Tilia are commonly used because of their peripheral and central medicinal effects; they are prepared as teas and used as tranquilizing, anticonvulsant, and analgesic agents. In this study, we provide evidence of the protective effects of organic and aqueous extracts (100 mg/kg, i.p.) obtained from the leaves of Tilia americana var. mexicana on CCl4-induced liver and brain damage in the rat. Protection was observed in the liver and brain (cerebellum, cortex and cerebral hemispheres) by measuring the activity of antioxidant enzymes and levels of malondialdehyde (MDA) using spectrophotometric methods. Biochemical parameters were also assessed in serum samples from the CCl4-treated rats. The T. americana var. mexicana leaf extracts provided significant protection against CCl4-induced peripheral and central damage by increasing the activity of antioxidant enzymes, diminishing lipid peroxidation, and preventing alterations in biochemical serum parameters, such as the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), γ-globulin (γ-GLOB), serum albumin (ALB), total bilirubin (BB), creatinine (CREA) and creatine kinase (CK), relative to the control group. Additionally, we correlated gene expression with antioxidant activity in the experimental groups treated with the organic and aqueous Tilia extracts and observed a non-statistically significant positive correlation. Our results provide evidence of the underlying biomedical properties of T. americana var. mexicana that confer its neuro- and hepatoprotective effects.

Creatine kinase isoenzyme I(BB) is generally not detectable in normal serum, and its occurrence in serum has been documented in only a few disease states. In particular, increased activity of this isoenzyme has been reported in association with chronic renal failure, hemodialysis, and renal transplantation. The present study demonstrates that the apparent creatine kinase observed in the serum of such renal patients is an artifact, observed as a result of measuring creatine kinase isoenzymes by fluorescence. Our observations resemble those of McKenzie et al. [Clin. Chim. Acta 70, 333(1976)] concerning an artifact in the fluorometric determination of lactate dehydrogenase isoenzymes in the sera of patients with end-stage renal failure. The artifact binds to albumin, is not a protein, and occurs in some normal sera at very low concentrations. This artifact can be mistakenly identified as isoenzyme I in renal-disease patients if CK isoenzymes are determined fluorometrically.

Objective: To investigate the diagnostic value of plasma miRNA-497, cardiac troponin I (cTnI), fatty acid binding protein 3 (FABP3), glycogen phosphorylase isoenzyme BB (GPBB) in pediatric sepsis complicated with myocardial injury.

Methods: From August 2018 to February 2020, 82 children with sepsis admitted to our hospital and 50 health children who came for physical examination (defined as control group) were enrolled in this study. Children with sepsis and myocardial injury were enrolled in the combined group (n=35), and those without myocardial injury were enrolled in the sepsis group (n=47). General data of three groups were collected, and the levels of miRNA-497, FABP3, GPBB, creatine kinase isoenzyme MB (CK-MB), procalcitonin (PCT), C-reactive protein (CRP), cTnI and N-terminal pro-B-type natriuretic peptide (NT-proBNP) were detected and the cardiac function was measured. The diagnostic value of plasma miRNA-497, cTnI, FABP3 and GPBB in pediatric sepsis complicated with myocardial injury was analyzed.

Results: The infection site of the combined group was not significantly different from that of the sepsis group. The levels of miRNA-497, FABP3, GPBB, CK-MB, PCT, CRP, cTnI, NT-proBNP in the combined group were all higher than those in the sepsis group and the control group (P<0.05), and the left ventricular ejection fraction (LVEF) in the combined group was significantly lower than that in the other two group (P<0.05). The area under the curve (AUC) of the combination of miRNA-497, FABP3, GPBB, and cTnI in the diagnosis of sepsis complicated with myocardial injury was significantly higher than that of CK-MB, PCT, CRP, NT-proBNP alone (P<0.05), but there was no significant difference when compared with miRNA-497, FABP3, GPBB and cTnI alone (P>0.05). When the optimal thresholds of miRNA-497, FABP3, GPBB, and cTnI were set to 2.03, 6.23ng/mL, 4.01ng/mL, 1.23ng/mL, respectively, the sensitivity was 95.65%, 88.89%, 82.61%, 87.50%, respectively; the specificity was 83.33%, 94.12%, 83.33%, 90.91%, respectively; and the accuracy was 91.43%, 91.43%, 82.86%, 88.57%, respectively. Pearson correlation analysis indicating that miRNA-497 was positively correlated with the levels of FABP3, GPBB, and cTnI in the combined group (r=0.821, 0.621, 0.782, P<0.05).

Conclusion: Plasma miRNA-497, cTnI, FABP3, and GPBB levels were increased in pediatric sepsis complicated with myocardial injury, and their combination had high diagnostic value, which was of great clinical significance for early diagnosis and early treatment of pediatric sepsis complicated with myocardial injury.

Keywords: FABP3; GPBB; cTnI; diagnosis; miRNA-497; myocardial injury; pediatric sepsis.

Myocardial infarction (MI) is the most common heart disease, and also, it is one of the leading causes of death from cardiovascular disease. It is well known that MI causes additional injury during blood flow restoration in ischaemic myocardium. Boeravinone B (BB) is a well-known antioxidant and anti-inflammatory drug. We investigated the cardioprotective effect of BB drug against isoproterenol (ISO)-induced MI in rats in this experimental study, along with we analysed its underlying mechanism. Adult Sprague Dawley (SD) rats were treated subcutaneously with ISO (45 mg/kg), then divided into groups and then given BB drug was administered orally. The cardioprotective effect of BB on ISO-induced MI rats was analysed by estimating the heart injury markers, antioxidant pro-inflammatory cytokines and inflammatory parameters. We also detected quantified expression of inflammation and apoptosis-related marker protein family. We estimated the effect of BB drug on GUT microbiota in ISO-induced MI rats and scrutinized the histopathological variations in heart tissues. BB treatment significantly (P < .001) diminished the level of heart markers such as lactate dehydrogenase (LDH), troponin (TnT), creatine kinase (CK) and creatine kinase isoenzymes MB (CK-MB). BB treatment also altered the antioxidant parameters and reduced the pro-inflammatory cytokines in the serum and tissues. Additionally, the histopathological aspects demonstrated that the pathological changes observed in the heart tissue of the ISO group rats were suppressed by the BB treatment to varying degrees. Furthermore, the expressions of caspase-3, p53, caspase-9, Bax, interleukin-6 (IL-6), cytochrome C, neutrophil gelatinase-associated lipocalin (NGAL), tumour necrosis factor-α (TNF-α), nuclear factor kappa B (NF-κB) and interleukin-1β (IL-1β) in the heart tissue were down-regulated whereas the Bcl-2 expression seemed to be enhanced. BB treatment not only alleviated ISO-induced gut dysbiosis by its enhanced specified Firmicutesto-Bacteroidetes (F/B) ratio but also maintained the relative abundance of major bacteria such as Clostridium IV, Butyricicoccus, Clostridium XIVs, Akkermansia and Roseburia. Collectively, our findings showed that the BB drug acted against myocardial infraction and prevented the damage by reducing the oxidative stress and controlling the inflammatory pathways, and gut microbiota.

Keywords: Boeravinone B; apoptosis; gut microbiota; isoproterenol; myocardial infarction.

Objectives: Sleep loss may contribute to neuroinflammation, which might increase neuroinflammatory markers such as neuron-specific enolase (NSE), creatine kinase-brain fraction (CK-BB), lactate dehydrogenase brain fraction (LDH-BB) in blood. Hence, we evaluated the effect of REM sleep deprivation and recovery on these markers.

Material and methods: Twenty-four adult male Sprague Dawley rats were grouped as control, environmental control, REM sleep deprivation, and 24 hour sleep recovery. The rats were sleep deprived for 72 hours and recovered for 24 hours. NSE, CK-BB, and LDH-BB levels in serum were measured using ELISA.

Results: The serum NSE, CK-BB, and LDH-BB were significantly higher in 72 hour sleep deprived group compared to control (p<0.01). After 24 hours of sleep recovery, the levels of NSE, CK-BB, and LDH-BB were comparable to control (p>0.05).

Discussion: REM sleep deprivation increased serum NSE, CK-BB, and LDH-BB, which might be due to neural damage. However, 24 hours of sleep recovery restored these markers.

Keywords: Creatine Kinase-Brain Fraction; Inflammation; Lactate Dehydrogenase Brain Fraction; Neuron-Specific Enolase; REM Sleep Deprivation; Sleep Recovery.

The present work studied the influence of bacterial agents (B1, B2) and bamboo biochar (BB) on greenhouse gas emissions and bacterial community during the sewage sludge composting. Results showed that compared with CK, the total methane emissions ofC, B1, B1C, B2, and B2C treatments declined by 16.4%, 25.2%, 45.4%, 7.8%, and 44.4%, respectively. The total N₂O emissions ofC and B1C treatments declined by 5.1% and 3.7% while B1, B2, and B2C treatments increased the total N₂O emissions by 6.7%, 21.6%, and 10.4%, respectively. These results illustrated that the addition of BB is conducive for reducing greenhouse gas emissions while different bacterial agents have various effects. According to pearson correlation analysis, N₂O emissions and Acidimicrobiia, Alphaproteobacteria, Gammaproteobacteria, and Tepidiformia have strong negative correlation while positive correlation with Bacilli and Clostridia. Methane emissions have a strong negative correlation with Actinobacteria. CO₂ emissions have a strong positive correlation with Bacilli.

Keywords: Bacterial agents; Composting; Greenhouse gases; Sewage sludge.

A single, specific, sensitive biochemical biomarker that can reliably diagnose a traumatic brain injury (TBI) has not yet been found, but combining different biomarkers would be the most promising approach in clinical and postmortem settings. In addition, identifying new biomarkers and developing laboratory tests can be time-consuming and economically challenging. As such, it would be efficient to use established clinical diagnostic assays for postmortem biochemistry. In this study, postmortem cerebrospinal fluid samples from 45 lethal TBI cases and 47 controls were analyzed using commercially available blood-validated assays for creatine kinase (CK) activity and its heart-type isoenzyme (CK-MB). TBI cases with a survival time of up to two hours showed an increase in both CK and CK-MB with moderate (CK-MB: AUC = 0.788, p < 0.001) to high (CK: AUC = 0.811, p < 0.001) diagnostic accuracy. This reflected the excessive increase of the brain-type CK isoenzyme (CK-BB) following a TBI. The results provide evidence that CK immunoassays can be used as an adjunct quantitative test aid in diagnosing acute TBI-related fatalities.

Keywords: cerebrospinal fluid; creatine kinase; fatal traumatic brain injury; postmortem biochemistry.

Establishing proteomic biomarkers is critical for characterizing disease pathophysiology, identifying genetic risk factors, and predicting clinical outcomes. However, diseases like cervical spondylomyelopathy have not been actively characterized for molecular significance, leading to questions regarding the pathology's molecular mechanisms. Namely, spondylomyelopathy is a degenerative spinal disease that leads to compression and neurologic deficits in the spinal cord. Analyzing a patient's cerebrospinal fluid (CSF) has been well-known for revealing biomarkers that are associated with diseases of the central nervous system. Therefore, in this review, we will formulate a proteomic profile of spondylomyelopathy through a molecular analysis of the CSF. The proteins found to be upregulated in the CSF include vitamin D-binding protein (VDBP), gelsolin, creatine kinase B-type (CK-BB), and angiotensinogen. Meanwhile, the proteins that were downregulated include pigment epithelium-derived factor (PEDF), prostaglandin-H2 D-isomerase (PGH2), apolipoprotein E (APOE), and clusterin. The cellular functions of these proteins are discussed, along with their relevance in manifesting spondylomyelopathy. However, further studies are warranted, as a lack of human studies is a major limiting factor. Nevertheless, based on the continued progression of the proteomic profile of spondylomyelopathy, new targets can be assessed as candidates for future therapeutic intervention.

Keywords: angiotensinogen; apolipoprotein e; clusterin; creatine kinase b-type; gelsolin; pigment epithelium-derived factor; prostaglandin-h2 d-isomerase; proteomics; spondylomyelopathy; vitamin d-binding protein.

Objective: To explore the inhibitory effects of ginsenoside compound K (CK) on pulmonary arterial smooth muscle cells (PASMCs) proliferation and phenotypic conversion in vitro and investigate its related mechanisms.

Methods: PASMCs cultured in vitro were examined in the study. They were induced with platelet-derived growth factor-BB (PDGF-BB) and then treated with CK. The cells were randomly assigned to the control group (receiving no treatment), the model group (PDGF-BB, 20 ng/mL), and the intervention group (20 ng/mL PDGF-BB+5 μmol/L CK). The cell proliferation was measured by CCK-8 assay (on the basis of the above group assignment, concentrations of CK was set at 1, 3, and 5 μmol/L in the intervention group, and the drug group was added, receiving 1, 3, and 5 μmol/L CK, respectively). Cell cycle and apoptosis were examined by flow cytometry. The levels of mRNA and proteins of α-smooth muscle actin ( α-SMA) and smooth muscle 22α ( SMα), markers of phenotypic conversion, were detected by quantitative real-time PCR and Western blot. The levels of protein expression related to Wnt/β-catenin signaling pathway were examined by Western blot.

Results: Compared with the model group, CK significantly inhibited PDGF-BB-induced proliferation of PASMCs in a dose-dependent way. The results of 5 μmol/L CK intervention were not significantly different from that of the control group ( P>0.05). Hence, 5 μmol/L CK was chosen for subsequent experiments. Separate treatment of PASMCs with CK at doses of 1, 3, and 5 μmol/L did not reveal any cytotoxicity to PASMCs ( P>0.05). CK also arrested the cell cycle of PASMCs at the G ₀/G ₁ phase, promoted the apoptosis of PASMCs, and reversed the mRNA and protein expression of α-SMA and SMα ( P<0.01). In addition, CK down-regulated the expressions of cyclin D1 and β-catenin, while it up-regulated the protein expressions of phosphorylated glycogen synthase kinase-3β (pGSK-3β)/glycogen synthase kinase-3β (GSK-3β) ( P<0.01).

Conclusion: CK was capable of inhibiting the abnormal proliferation of PASMCs and reversing the phenotypic conversion, and its acting mechanism may be related to the Wnt/β-catenin signaling pathway, suggesting the therapeutic potential of CK in controlling pulmonary arterial hypertension.

Keywords: Ginsenoside compound K; Phenotypic conversion; Proliferation; Pulmonary arterial smooth muscle cell; Wnt/β-catenin signaling pathway.