Characterization of blood inflammatory markers in patients with non-small cell lung cancer.

OBJECTIVE: To investigate the differences and correlation between blood inflammatory indexes such as monocytes (MONO), lymphocytes (LYM), haemoglobin (HGB), neutrophils (NEU), platelets (PLT), ultrasensitive C-reactive protein, albumin and platelet/lymphocyte ratio (PLR), NEU/LYM ratio (NLR), MONO/LYM ratio (MLR) and clinicopathologic characteristics of patients with non-small cell lung cancer (NSCLC). METHODS: 187 patients with NSCLC who were first diagnosed in 2017-2023 and 102 with healthy check-ups during the same period (control group) were retrospectively selected as study subjects to compare the differences in inflammatory indexes between the two groups and the levels of inflammatory indexes in NSCLC patients with different clinicopathologic characteristics. RESULTS: Correlation analysis between blood inflammatory indexes and clinicopathologic features in NSCLC group showed that C-reactive protein, CAR, and PLR values were different in different pathologic types (P<0.05). The values of NEU, MONO, C-reactive protein, MLR, NLR, CAR and albumin were different among various degrees of differentiation (P<0.05). There were differences in LYM, albumin, MLR, NLR, CAR, and C-reactive protein among M stage subgroups (P<0.05). Analysis of the efficacy of early diagnosis of non-small cell lung cancer has been shown, the AUC of NLR was 0.796, sensitivity of 0.679, specificity of 0.176, 95% CI=0.743-0.849 (P<0.001). The AUC of albumin was 0.977, the sensitivity was 0.941, the specificity was 0.941, and 95% CI was 0.959-0.994 (P<0.001). CONCLUSION: Blood inflammatory indexes are closely associated with NSCLC and vary according to pathologic features. Blood inflammatory indices can predict tumor pathologic staging and guide treatment for patients with NSCLC.

Effects of Anesthetics on Proliferation and Apoptosis of Drug-Resistant Human Colon Cancer Cells.

In recent years, people's living standards are getting higher and higher, and life pressure is also increasing, and there are also many problems in eating habits. This is also the direct cause of colon cancer. The aim of this paper was to investigate whether anesthetic drugs could positively affect the proliferation and apoptosis of colon cancer cells. In this paper, the significance of anesthetic drugs is proposed, and an artificial neural network algorithm based on artificial intelligence is proposed. It is well known that artificial neural networks play an important role in medicine. The experimental results of this paper show that the incidence of colon cancer in 2020 will be in the range of 5%-35%, and the incidence of colon cancer in 2021 will be in the range of 7%-30%. While colon cancer rates in 2021 do not appear to be as high as colon cancer rates in 2020, they are generally much higher than colon cancer rates in 2020. It can be seen that as the population ages, the number of colon cancer patients is increasing due to the lack of emphasis on health. This also means that the incidence of colon cancer is getting higher and higher, and traditional drug chemotherapy has been unable to play a good role in inhibiting the proliferation of colon cancer cells. Therefore, this paper investigated the effects of anesthetic drugs on the proliferation and apoptosis of human colon cancer cells.

Effects of oral non-protein calorie supplements on nutritional status among maintenance hemodialysis patients with protein-energy wasting: a multi-center randomized controlled trial.

Protein-energy wasting (PEW) is prevalent in maintenance hemodialysis (MHD) patients, and is one of the major risk factors for poor outcomes and death. This study aimed to investigate the effects of non-protein calorie supplements on the nutritional status of MHD patients with PEW. MHD patients with PEW were enrolled in this multi-center, open-label, randomized controlled trial. Then, they were randomly assigned to the intervention group to receive the non-protein calorie supplements containing 280 kcal of energy every day for 6 months or the control group to complete all aspects of the study without receiving supplements. Patients in both groups received dietary counselling from dietitians. Data on nutritional assessments, anthropometric measurements, blood analysis and dietary recall were collected at the baseline and at six months from both groups. Statistical analyses were performed using analysis of covariance (ANCOVA) adjusted for sex and baseline values. Ninety-two MHD patients completed the study. A significant increase in the subjective global assessment (SGA) score was found in the intervention group compared with the control group (4.88 ± 1.41 vs. 4.40 ± 1.16, p = 0.044). The ratio of PEW patients (diagnosed with SGA ≤5) in the intervention group (61.2%) was also significantly lower than that in the control group (83.7%) (p < 0.001). Moreover, significant improvements in body mass index (20.81 ± 2.46 kg m-2vs. 19.51 ± 2.60 kg m-2, p < 0.001), nutrition risk screening 2002 (2.45 ± 1.40 vs. 3.12 ± 1.37, p = 0.038), mid-upper arm circumference (23.30 ± 2.78 cm vs. 21.75 ± 2.87 cm, p = 0.001), and mid-arm muscle circumference (20.51 ± 2.32 cm vs. 19.06 ± 2.92 cm, p = 0.005) were observed in the intervention group compared with the control group. Patients in the intervention group took in more dietary energy than the control group (26.96 ± 4.75 kcal per kg body weight per day vs. 24.33 ± 2.68 kcal per kg body weight per day, p < 0.001). In conclusion, non-protein calorie supplements may improve the nutritional status of MHD patients with PEW.

Administration of rTMS Alleviates Stroke-Induced Cognitive Deficits by Modulating miR-409-3p/CTRP3/AMPK/Sirt1 Axis.

Cognitive deficit is a typical complication induced by stroke injuries. Repetitive transcranial magnetic stimulation (rTMS) is a technique that can both attenuate neuropsychiatric disorders and influence miR levels. We attempted to assess effects of rTMS on post-stroke cognitive deficit (PSCD) by focusing on the activity of miR-409-3p/CTRP3/AMPK/Sirt1 axis. PSCD was induced in rats using middle cerebral artery occlusion (MCAO) method and handled with rTMS. MiRs responding to rTMS administration were determined using microarray method. Changes in cognitive function, brain histological feature, neuron apoptosis, and activity of miR-409-3p/CTR3/AMPK/Sirt1 axis were detected. The interaction between of miR-409-3p and rTMS was verified by inducing its level in MCAO rats. rTMS influenced levels of miRs in MCAO rats, with 104 miRs being upregulated and 249 s miR being downregulated, contributing to the function changes in multiple biological processes. Moreover, the technique improved brain function and structure in model rats. At the molecular level, rTMS inhibited miR-409-3p and activated CTRP3/AMPK/Sirt1 pathway. After the induction of miR-409-3p, effects of rTMS were counteracted, which were represented by the impaired cognitive function and neuron viability in model rats. Collectively, rTMS could protect against stroke-induced cognitive deficits, which depended on the inhibition of miR-409-3p level.

Auxiliary genetic analysis in a Chinese adolescent NPH family by single nucleotide polymorphism screening.

Hereditary nephropathy is a progressive fatal renal disease caused by genetic changes. In this study, genetic screening was used to reveal mutations in a family in Southern China, in which there are two patients with confirmed hereditary nephropathy, who are alive at the time of publication. Imaging tests, including color Doppler ultrasonography and magnetic resonance imaging (MRI), as well as pathological examinations, including hematoxylin­eosin staining, electron microscopy and immunohistochemistry were performed. Target sequencing of nephrosis 2 (NPHS2), wilms tumor 1 (WT1), phospholipase C ε 1 (PLCE1), actinin α 4 (ACTN4), angiotensin I converting enzyme (ACE), uromodulin (UMOD) and nephrocystin 1 (NPHP1) was also carried out. This study indicated that heterozygous genetic variants of NPHS2, WT1, ACTN4, PLCE1 and UMOD found in the patients were gene polymorphisms. A renal biopsy showed sclerosing glomerulonephritis, dilated tubules and lymphocyte/monocyte infiltration in the interstitium of the index patients. Genetic analysis showed vertical transmission of the disease­causing mutations, including a homozygous deletion in NPHP1 and a nonsense mutation in ACE found via PCR­based single nucleotide polymorphism screening. Further network analysis identified direct and indirect co­location genes between NPHP1 and ACE. To conclude, familial adolescent nephronophthisis was diagnosed in two index patients in this study. It is recommended that comprehensive gene mutation screening is used in the diagnosis of complex hereditary diseases.

Inhibition of TRPC6 Signal Pathway Alleviates Podocyte Injury Induced by TGF-ß1.

BACKGROUND/AIMS: Transforming growth factor beta 1 (TGF-ß1) plays a critical role in the pathogenesis of glomerulosclerosis. The purpose of this study was to examine the effects of inhibition of transient receptor potential cation channel C6 (TRPC6) on podocyte injury induced by TGF-ß1 via nephrin and desmin mechanisms. METHODS: A rat model of nephropathy was first induced by intravenous injections of adriamycin to determine TRPC6 signal pathway engaged in glomerulosclerosis in vivo. Conditionally immortalized podocytes were cultured in vitro and they were divided into four groups: control; TGF-ß1 treatment; TGF-ß1 with TRPC6 knockdown and TGF-ß1 without TRPC6 knockdown. Real time RT-PCR and Western blot analysis were employed to determine the mRNA and protein of expression of nephrin, desmin and caspase-9, respectively. Flow cytometry was used to examine the apoptotic rate of podocytes and DAPI fluorescent staining was used to determine apoptotic morphology. RESULTS: In vivo experiment, adriamycin significantly upregulated the protein expression of TGF-ß1, TRPC6, desmin and caspase-9, and decreased nephrin. Consistent with the latter results, in vitro experiment mRNA and protein expression of desmin and caspase-9 was increased in cultured TGF-ß1-treated podocytes, whereas nephrin was declined as compared with the control group. Importantly, TRPC6 knockdown significantly attenuated the upregulated desmin and caspase-9, and alleviated impairment of nephrin induced by TGF-ß1. Moreover, typical morphologic features were presented in apoptotic podocytes. The number of apoptotic podocytes was increased after exposure to TGF-ß1 and this was alleviated after TRPC6 knockdown. TRPC6 knockdown also decreased an apoptosis rate of TGF-ß1-treated podocytes. Note that negative TRPC6 transfection control failed to alter an increase of the apoptosis rate in TGF-ß1-treated podocytes. CONCLUSIONS: TGF-ß1 induced by glomerulosclerosis impairs the protein expression of nephrin and amplifies the protein expression of desmin and caspase -9 via TRPC6 signal pathway. Inhibition of TRPC6 alleviates these changes in podocytes-treated with TGF-ß1 and attenuated apoptosis of podocytes. Our data suggest that TRPC6 signal plays an important role in mediating TGF-ß1-induced podocyte injury via nephrin, desmin and caspase-9. Results of the current study also indicate that blocking TRPC6 signal pathway has a protective effect on podocyte injury. Targeting one or more of these signaling molecules may present new opportunities for treatment and management of podocyte injury observed in glomerulosclerosis.

Activation of TLR5 induces podocyte apoptosis.

The apoptosis plays a critical role in a number of inflammatory disorders. Bacterial infection is one of the causes inducing apoptosis. This study aims to investigate the mechanism by which activation of TLR5 induces podocyte apoptosis. In this study, a podocyte cell line was cultured in RPMI1640 medium. The expression of TLR5 was assessed by real-time PCR and Western blotting. The Fas ligand gene transcription was assessed by immunoprecipitation and chromatin immunoprecipitation assay. The results showed that the expression of TLR5 was observed in the podocytes at both mRNA and protein levels. Exposure to TLR5 ligand, flagellin, induced Fas ligand expression and podocyte apoptosis. p300, one of the histone acetyltransferases, mediated the Fas ligand gene transcription in podocytes. In conclusion, TLR5 activation plays an important role in the induction of podocyte apoptosis.