The role of platelets in central hubs of inflammation: A literature review.

Platelets are increasingly recognized for their multifaceted roles in inflammation beyond their traditional involvement in haemostasis. This review consolidates knowledge on platelets as critical players in inflammatory responses. This study did an extensive search of electronic databases and identified studies on platelets in inflammation, focusing on molecular mechanisms, cell interactions, and clinical implications, emphasizing recent publications. Platelets contribute to inflammation via surface receptors, release of mediators, and participation in neutrophil extracellular trap formation. They are implicated in diseases like atherosclerosis, rheumatoid arthritis, and sepsis, highlighting their interaction with immune cells as pivotal in the onset and resolution of inflammation. Platelets are central to regulating inflammation, offering new therapeutic targets for inflammatory diseases. Future research should explore specific molecular pathways of platelets in inflammation for therapeutic intervention.

Evaluating the impact of school-based influenza vaccination programme on absenteeism and outbreaks at schools in Hong Kong: a retrospective cohort study protocol.

INTRODUCTION: Seasonal influenza causes annual school breaks and student absenteeism in Hong Kong schools and kindergartens. This proposal aims to conduct a retrospective cohort study to evaluate the impact of a school-based influenza vaccination (SIV) programme on absenteeism and outbreaks at schools in Hong Kong. METHODS: The study will compare schools that implemented the SIV programme with schools that did not. The data will be sourced from school records, encompassing absenteeism records, outbreak reports, and vaccination rates. We will recruit 1000 students from 381 schools and kindergartens in 18 districts of Hong Kong starting June 2024. The primary outcome measures will include absenteeism rates due to influenza and school influenza outbreaks. Secondary outcomes will consist of vaccination coverage rates and the impact of the SIV programme on hospitalisations due to influenza-like illness. A t-test will be conducted to compare the outcomes between schools with and without the SIV programme. ETHICS AND DISSEMINATION: The school completed signing the participants' informed consent form before reporting the data to us. Our study has been approved by the Hospital Authority Hong Kong West Cluster IRB Committee (IRB No: UW 17-111) and was a subtopic of the research "The estimated age-group specific influenza vaccine coverage rates in Hong Kong and the impact of the school outreach vaccination program". TRIAL REGISTRATION: This study will be retrospectively registered.

Chrysophanol improves memory impairment and cell injury by reducing the level of ferroptosis in Aß25-35 treated rat and PC12 cells.

Alzheimer's disease (AD) is a common age-related chronic and neurodegenerative disease that has become a global health problem. AD pathogenesis is complex, and the clinical efficacy of commonly used anti-AD drugs is suboptimal. Recent research has revealed a close association between AD-induced damage and the activation of ferroptosis signaling pathways. Chrysophanol (CHR) the principal medicinal component of Rhubarb, has been reported to have anti-AD effects and can reduce ROS levels in AD-damaged models. AD has been linked to the activation of ferroptosis signaling pathways, which has an important feature of higher levels of reactive oxygen species (ROS). Therefore, the present study explored whether CHR had an anti-AD effect by regulating the ferroptosis levels in AD injury models. Morris water maze, novel object recognition test, Y-maze test, Hematoxylin-eosin (H&E) staining, western blotting, ROS measurement, GPx activity measurement, LPO measurement, transmission electron microscopy, live/dead cell staining were used to investigate the changes in spatial memory level and ferroptosis level in AD model, and the intervention effect of CHR. CHR improved the spatial memory level of AD rat models, reduced the level of hippocampal neuron damage, and improved the survival rate of PC12 cells damaged by ß-amyloid (Aß). Meanwhile, CHR increased glutathione peroxidase-4 (GPX4) protein expression, GPx activity, and GSH, decreased ROS and LPO levels in AD rat models and Aß-damaged PC12 cells, and improved mitochondrial pathological damage. Our findings suggest that CHR may play a protective role in AD injury by lowering ferroptosis levels, which may provide a potential pathway for developing drugs for AD. However, the mechanism of CHR's role requires further investigation.

Enhanced biocompatibility of silk sericin/caffeic acid nanoparticles by red blood cell membranes cloaking.

Caffeic acid (CA) is an antioxidant phenolic compound that enriched in coffee beans, however, its administration often restrains by the instability and low solubility. Nanoparticle encapsulation is an effective approach to improve the therapeutic activity of CA. For example, silk sericin (SS), a natural biomaterial finds applications in food, cosmetics and biomedical fields, is proved here to be an appropriate encapsulation agent for CA, and a SS/CA composite nanoparticle has been fabricated. To further improve the biocompatibility of SS/CA, a red blood cell membranes (RM) cloaking strategy is adopted. The as-formed SS/CA/RM preserves the antioxidant activity of CA, and shows satisfactory biocompatibility especially under high concentration. Hope this can provide a potential appropriative strategy to adjust the chemical stability of insoluble drugs and to improve their biocompatibility.

Optimization of empty container allocation for inland freight stations considering stochastic demand.

In the post-COVID-19 epidemic era (PCEE), the supply of empty containers will face stronger uncertainty. Estimating the amount of self-owned and leased empty containers that need to be allocated to each inland freight station in a specific area becomes a critical issue for liner companies in PCEE. However, owing to the high degree of unpredictability of the demand and the limited flexibility of empty container relocation, the abovementioned issue has not been fully addressed. This paper provides a model for empty container allocation without knowing the probability distribution function of empty container demand in advance. The abovementioned model can jointly optimize the quantities of self-owned empty containers and leased containers allocated to each inland freight station. To solve the model, a largest-debt-first policy is adopted to simplify the complicated model, and a differential evolutionary (DE) algorithm is developed to solve the simplified model. Compared with some commonly used algorithms, DE has advantages considering the ability to explore the optimal solution. In addition, the utility of the largest-debt-first policy proposed in this paper is compared with that of the traditional method. Experimental results show that in the case of high demand fluctuations, the proposed policy is better in controlling the operational and management costs. Overall, the theory and method proposed in this paper can effectively help the carrier set a reasonable regional empty container stock level and determine the number of self-owned and leased empty containers.

Coexistence of Pituitary Adenoma and Primary Pituitary Lymphoma: A Case Report and Review of the Literature.

In the pituitary sella, the coexistence of pituitary adenoma and primary pituitary lymphoma is exceedingly rare. Thus far, only six cases have been reported. Here, we present the seventh case of coexisting pituitary adenoma and primary pituitary lymphoma, which was difficult to differentiate from other sellar tumors. To our knowledge, this is the first case of the prolactin subtype of the pituitary adenoma in literature. We have also systematically reviewed the literature and summarized the characteristics of coexisting pituitary adenoma and lymphoma. We believe this report provides a new clinical reference for the diagnosis and treatment of collision tumors of pituitary adenoma and lymphoma.

Rhein incorporated silk fibroin hydrogels with antibacterial and anti-inflammatory efficacy to promote healing of bacteria-infected burn wounds.

Advanced dressings that can simultaneously prevent bacterial colonization/infection and reduce inflammation are highly desired. A simple strategy was developed to incorporate an anti-inflammatory and antibacterial drug rhein into the structure of silk fibroin (SF) matrix to fabricate a hydrogel dressing. The SF/Rhein hydrogels showed fibrous network nanostructure, high water content (~90%), high water adsorption ability (>2 folds of its own weight), acceptable mechanical strength, biocompatibility and antibacterial properties, suitable as dressings for the treatment of bacterial infected wounds. The SF/Rhein hydrogels enhanced the healing rate of burn wounds by reducing inflammation, expediting angiogenesis, and promoting skin appendages formation, being a promising candidate as wound dressings.

The Role of NF-kB in the Downregulation of Organic Cation Transporter 2 Expression and Renal Cation Secretion in Kidney Disease.

Organic cation transporter 2 (OCT2), encoded by the SLC22A2 gene, is the main cation transporter on the basolateral membrane of proximal tubular cells. OCT2 facilitates the entry step of the vectorial transport of most cations from the peritubular space into the urine. OCT2 downregulation in kidney disease models is apparent, yet not clear from a mechanistic vantage point. The aim of this study was to explore the role of inflammation, a common thread in kidney disease, and NF-kB in OCT2 modulation and tubular secretion. Among the OCTs, OCT2 was found consistently downregulated in the kidney of rats with chronic kidney disease (CKD) or acute kidney injury (AKI) and in patients diagnosed with CKD, and it was associated with the upregulation of TNFα renal expression. Exposure to TNFα reduced the expression and function of OCT2 in primary renal proximal tubule epithelial cells (RPTEC). Silencing or pharmacological inhibition of NF-kB rescued the expression of OCT2 in the presence of TNFα, indicating that OCT2 repression was NF-kB-dependent. In silico prediction coupled to gene reporter assay demonstrated the presence of at least one functional NF-kB cis-element upstream the transcription starting site of the SLC22A2 gene. Acute inflammation triggered by lipopolysaccharide injection induced TNFα expression and the downregulation of OCT2 in rat kidney. The inflammation did reduce the active secretion of the cation Rhodamine 123, with no impairment of the glomerular filtration. In conclusion, the NF-kB pathway plays a major role in the transcriptional regulation of OCT2 and, in turn, in the overall renal secretory capacity.

Improving power conversion efficiency in luminescent solar concentrators using nanoparticle fluorescence and scattering.

Large-size luminescent solar concentrators (LSCs), which act as a complement to silicon-based photovoltaic (Si-PV) systems, still suffer from low power conversion efficiency (PCE). How to improve the performance of LSCs, especially large ones, is currently a hot research topic. Traditional LSCs have only a single transmission mode of fluorescence from the luminescent materials to the Si-PV, but here we introduce a new idea to improve the absorption of Si-PV by employing dual transmission modes of both fluorescence and scattering light. To prepare LSCs with dual mode transmission, Si-PV systems are coupled around the edges of a light-harvesting slice, which is prepared by ultraviolet light-induced polymerization of methyl methacrylate (MMA) solution containing both luminescent CsPbBr3 and TiO2 nanocrystals (NCs). When the sun light or incident light is coupled into the light-harvesting slice, CsPbBr3 NCs can convert the incident light into fluorescence, and then partly transmit to Si-PV at the edges, where the light is finally converted into electrical energy. Besides the traditional fluorescence transmission mode, the addition of TiO2 brings another transmission mode, namely the scattering of incident light to Si-PV, leading to an increase in PCE. In comparison to that of pure CsPbBr3-based LSCs without the addition of TiO2 (0.97%), the PCE of TiO2-doped LSCs with a large size of 20 cm × 20 cm is improved to 1.82%. The maximal PCE appears for LSCs with a size of 5 cm × 5 cm, reaching 2.62%. The reported method of dual transmission modes is a new alternative way to improve the performance of LSC devices, which does not need to change the optical properties of luminescent materials. Moreover, the production process is simple, low-cost and suitable for preparing large area LSCs, further promoting the application of LSCs.

Clinicopathologic significance of CXCR4 expressions in patients with esophageal squamous cell carcinoma.

AIMS: This study was designed to investigate the biological function of CXCR4 in esophageal squamous cell carcinoma and to explore the underlying mechanism to provide potential targets for esophageal squamous cell carcinoma. METHODS: A total of 101 patients with esophageal squamous cell carcinoma were included, and the relationship between CXCR4 and clinicopathological factors was analyzed. Laser scanning confocal microscopy was used to observe numbers of autophagosomes in TE-1 cell line and the ability of proliferation and invasion were evaluated meanwhile. RESULTS: CXCR4 is overexpressed in ESCC specimens and is associated with poor differentiation and lymphocyte metastasis. In the survival analysis, CXCR4 predicted a poor overall survival prognosis. The number of autophagosomes in the siR-CXCR4 group was decreased compared with negative group (P < 0.05), while was increased in the pcDNA3.1-CXCR4 group (P < 0.05).Western blot result show upregulation of LC3II, the ratio of LC3II/LC3I and Beclin1 in pcDNA3.1-CXCR4 group and decreased expression of LC3II, the ratio of LC3II/LC3I and Beclin1 in siR-CXCR4 group. Transwell assay show CXCR4 overexpression promote the invasion of TE-1 cells and was attenuated by autophagy inhibitor 3-Methyladenine.On the contrary, invasion cell numbers decreased in siR-CXCR4 group and was rescued by autophagy inducer Rapamycin. CONCLUSION: CXCR4 is an indicator of poor prognosis for ESCC. CXCR4 promote autophagy and regulate cell invasion through autophagy in ESCC. Our study provides new insights for the treatment of esophageal squamous cell carcinoma and CXCR4 may serve as a therapeutic target for ESCC.

The blockage of Notch signalling promoted the generation of polymorphonuclear myeloid-derived suppressor cells with lower immunosuppression.

Myeloid-derived suppressor cells (MDSCs) mostly consisting of polymorphonuclear (PMN)-MDSCs and mononuclear MDSCs have been considered to play critical roles in immunosuppression, angiogenesis, invasion and metastases of various tumours. However, it is still unclear the regulated mechanisms underlying the generation and immunosuppression of two major MDSC subsets. Here, we report Notch signalling was inhibited significantly in tumour-bearing mouse MDSCs, in which PMN-MDSCs were the major population. MDSCs without recombination signal binding protein-Jк (RBP-J), the critical transcription factor mediating signalling from all four mammalian Notch receptors, reduced their ability of inhibiting the proliferation and activation of allogenic T cells. RBP-J-deficient MDSCs could not down-regulate the expression of co-stimulation molecules on dendritic cells (DCs). The antigen presentation capacity of DCs co-cultured with RBP-J-deficient MDSCs was not impaired in contrast to controls. Moreover, we show the blockage of Notch signalling could improve the generation of PMN-MDSCs but inhibit the production of mononuclear MDSCs both in vitro and in vivo. Stat3 pathway was suppressed in MDSCs blocked Notch signalling and Stat3 activation by IL-6 could reverse the phenotype and immunosuppression of Notch signalling-deficient MDSCs. Therefore, targeting Notch signalling may be an effective therapeutic strategy in tumour therapy.

Golgi Phosphoprotein 3 Inhibits the Apoptosis of Human Glioma Cells in Part by Downregulating N-myc Downstream Regulated Gene 1.

BACKGROUND Golgi phosphoprotein 3 (GOLPH3) has been reported to be involved in the development of several human cancers. Our previous study showed that GOLPH3 expression in glioma tissues was related to the severity of the malignancy of the cancer. However, the mechanism by which GOLPH3 affects cell apoptosis is largely unknown. The present study was designed to explore the possible mechanism of GOLPH3 in cell apoptosis. MATERIAL AND METHODS To analyze the biological role of GOLPH3 in glioma cells, we used GOLPH3 small interference RNA in apoptosis of glioma cells. The apoptosis of glioma cells was detected by flow cytometry. The expression level of GOLPH3 and NDRG1 protein was determined by Western blot analyses and immunohistochemical staining, respectively, to evaluate their association with glioma. Tumor tissues were collected from patients with glioma. Normal cerebral tissues were acquired from cerebral trauma patients undergoing internal decompression surgery. RESULTS We confirm that the decrease of GOLPH3 that promotes the apoptosis of glioma cells may be regulated by the activation of NDRG1 and cleaved capcase 3. There was a inverse association between GOLPH3 and NDRG1 in glioma samples. CONCLUSIONS Our findings indicate that GOLPH3 and NDRG1 both play an important role in glioma etiology. Either GOLPH3 or NDRG1 might be a potential candidate for malignant glioma therapy.

Protein phosphatase 4 catalytic subunit is overexpressed in glioma and promotes glioma cell proliferation and invasion.

Protein phosphatase 4 catalytic subunit (PP4C) has been identified to be overexpressed in various solid cancers. However, to date, the role of PP4C in glioma remains elusive. In the present study, we aimed to detect PP4C expression in glioma patients and explore its function in glioma and prognostic significance in patients with glioma. The expression levels of PP4C mRNA and protein in 30 glioma tissue specimens and 10 non-cancerous brain tissue specimens were detected by qRT-PCR and Western blot analysis. Moreover, immunohistochemistry was performed to assess PP4C expression in 120 glioma patients. The effects of siRNA-mediated PP4C silencing on the proliferation, migration, and invasion of U251 and U87 glioma cells were assessed. We found that PP4C was upregulated in glioma tissue at both mRNA and protein levels compared with non-cancerous brain tissue. Univariate and multivariate analyses indicated that high PP4C expression was an independent prognostic factor for poor survival of glioma patients. Knockdown of PP4C reduced the proliferation, migration, and invasion of U251 and U87 cells. In conclusion, our findings suggest that PP4C plays an oncogenic role in glioma development and progression and might serve as a prognostic biomarker as well as a potential therapeutic target for glioma.

Protective effects of butyrate on intestinal ischemia-reperfusion injury in rats.

BACKGROUND: Butyrate is normally fermented from undigested fiber by intestinal microflora. The goal of the present study was to determine the effects of butyrate and its underlying mechanisms on intestinal injury in a rat model of ischemia and reperfusion (I/R). METHODS: Male Sprague-Dawley rats were subjected to warm ischemia for 45 min by clamping the superior mesenteric artery after treatment with butyrate, followed by 6 and 72 h of reperfusion. Pathologic histology analysis, enzyme-linked immunosorbent assay, immunofluorescence, and Western blot were performed. RESULTS: Butyrate preconditioning markedly improved intestinal injury. The inflammatory factor levels and leukocyte infiltration were attenuated by butyrate. Butyrate also maintained the intestinal barrier structures, increased the expression of tight junction proteins, and decreased endotoxin translocation. CONCLUSIONS: We conclude that butyrate administration attenuates intestinal I/R injury, which is associated with preservation of intestinal tight junction barrier function and suppression of inflammatory cell infiltration in the intestinal mucosa. This suggests butyrate as a potential strategy to prevent intestinal I/R injury.

Genetic variants in microRNA target sites of 37 selected cancer-related genes and the risk of cervical cancer.

OBJECTIVES: Single nucleotide polymorphisms (SNPs) in putative microRNA binding sites (miRSNPs) modulate cancer susceptibility via affecting miRNA binding. Here, we sought to investigate the association between miRSNPs and cervical cancer risk. METHODS: We first genotyped 41 miRSNPs of 37 cancer-related genes in 338 patients and 334 controls (Study 1), and replicated the significant associations in 502 patients and 600 controls (Study 2). We tested the effects of miRSNPs on microRNA-mRNA interaction by luciferase reporter assay. RESULTS: Five SNPs displayed notable association with cervical cancer risk in Study 1. Only IL-16 rs1131445 maintained a significant association with cervical cancer (CT/CC vs. TT, adjusted OR = 1.51, P = 0.001) in Study 2. This association was more evident in the combined data of two studies (adjusted OR = 1.49, P = 0.00007). We also found that miR-135b mimics interacted with IL-16 3'-UTR to reduce gene expression and that the rs1131445 T to C substitution within the putative binding site impaired the interaction of miR-135b with IL-16 3'-UTR. An ELISA indicated that the serum IL-16 of patients with cervical cancer was elevated (vs. controls, P = 0.001) and correlated with the rs1131445 genotype. Patients who carried the rs1131445 C allele had higher serum IL-16 than non-carriers (P<0.001). CONCLUSIONS: These results support our hypothesis that miRSNPs constitute a susceptibility factor for cervical cancers. rs1131445 affects IL-16 expression by interfering with the suppressive function of miR135b and this variant is significantly associated with cervical cancer risk.

miR-196a targets netrin 4 and regulates cell proliferation and migration of cervical cancer cells.

Recent research has uncovered tumor-suppressive and oncogenic potential of miR-196a in various tumors. However, the expression and mechanism of its function in cervical cancer remains unclear. In this study, we assess relative expression of miR-196a in cervical premalignant lesions, cervical cancer tissues, and four cancer cell lines using quantitative real-time PCR. CaSki and HeLa cells were treated with miR-196a inhibitors, mimics, or pCDNA/miR-196a to investigate the role of miR-196a in cancer cell proliferation and migration. We demonstrated that miR-196a was overexpressed in cervical intraepithelial neoplasia 2-3 and cervical cancer tissue. Moreover, its expression contributes to the proliferation and migration of cervical cancer cells, whereas inhibiting its expression led to a reduction in proliferation and migration. Five candidate targets of miR-196a chosen by computational prediction and Cervical Cancer Gene Database search were measured for their mRNA in both miR-196a-overexpressing and -depleted cancer cells. Only netrin 4 (NTN4) expression displayed an inverse association with miR-196a. Fluorescent reporter assays revealed that miR-196a inhibited NTN4 expression by targeting one binding site in the 3'-untranslated region (3'-UTR) of NTN4 mRNA. Furthermore, qPCR and Western blot assays verified NTN4 expression was downregulated in cervical cancer tissues compared to normal controls, and in vivo mRNA level of NTN4 inversely correlated with miR-196a expression. In summary, our findings provide new insights about the functional role of miR-196a in cervical carcinogenesis and suggested a potential use of miR-196a for clinical diagnosis and as a therapeutic target.

[Estimation of postmortem interval using FTIR spectroscopy in rats' cardiac muscle].

OBJECTIVE: FTIR (Fourier transform infrared) spectroscopy was applied to observe the process of postmortem degradation in rats' cardiac muscle and provided a new method for the estimation of post-mortem interval (PMI). METHODS: The rats were sacrificed by cervical dislocation and the bodies were kept in a controlled environmental chamber set at (20 +/- 2) degrees C. The FTIR spectra was applied to measure the changes of different chemical group from rats' left ventricle muscle at the different time point postmortem. RESULTS: There were not obvious changes for the main FTIR absorbance peaks. But the different FTIR absorbance at the wave-number (cm(-1)) indicated the three types: increase, decrease, stable. The various absorbance ratios also demonstrated the similar changes. CONCLUSION: FTIR spectroscopy may be potentially used as an effective method for estimating PMI in forensic practice using cardiac muscle tissue.

[The changes of Fourier transform infrared spectroscopy in rat's brain].

OBJECTIVE: To apply Fourier transform infrared (FTIR) spectroscopy to study the process of postmortem degradation of the rat brain and to provide a new way for the estimation of postmortem interval (PMI). METHODS: The rats were sacrificed by cervical dislocation and the bodies were kept in a controlled environmental chamber set at (30 +/- 2) degrees C. To measure the content of the chemical groups in postmortem rat brains at the different time points from 0 to 36 h using the FTIR spectrograph. RESULTS: With prolongation of PMI, the peak position of main absorbance bands in the FTIR spectra showed no significant changes, while the peak levels showed dramatic changes: (1) The relative peak intensity of 1080 cm(-1), 1238 cm(-1) (I1080/I1398, I1238/I1398) associated with nucleic acid decreased obviously; (2) The peak intensity ratio at Amide I, II (I1647/I1541) decreased; (3) The peak intensities at 1456 cm(-1) and 1398 cm(-1) showed a decreased and an increased trend, respectively; (4) Compared to the peak intensity of 1647 cm(-1), the peak intensities at 2852 cm(-1), 2871 cm(-1), 2923 cm(-1), and 2958 cm(-1) tended to increase, with only a slightly increased tendency in peak intensity of 2871 cm(-1). CONCLUSION: FTIR spectroscopy may be potentially used as an effective method for estimating the PMI in medicolegal practice using brain tissue sample.

[The correlation between postmortem interval and Fourier transform infrared spectra in rat's brain].

In the present study, FTIR spectroscopy was applied to observe the process of postmortem degradation in rat's brain and a lot of useful data for the estimation of postmortem interval (PMI) were provided. Sprague-Dawley male rats (weight 240 +/- 10 g) were chosen and sacrificed by cervical dislocation. The bodies were kept in a controlled environmental chamber set at (20 +/- 2) degrees C, and their brain cortex as the measuring sample which was extracted at 0, 12, 24, 48, 72, 96, 120, 144 and 168 h from the 8 rats. The tissues were freeze dried in a vacuum at -50 degrees C overnight in order to dehydrate them. About 2 mg freeze dried tissues were mixed with 200 mg KBr and then ground in an agate mortar for 5 min. The mixture then was pressed into a pellet with a thickness of 0. 4 mm and a diameter of 12 mm. The FTIR spectra were quantitatively recorded at room temperature in the range 4 000-400 cm(-1) on a Shimadzu 8400S spectrometer (Shimadzu, Japan). IR solution 1.10 software (Shimadzu, Japan) was used for the analysis of the FTIR spectra and for recording the data from the spectra. With the PMI increasing, the peak position of main absorbance bands in the FTIR spectra showed no significant difference, but there was a dramatic variance in the intensity: (1) The relative intensity at 1 080 and 1 238 cm(-1) (I1 080/I1 398 and I1 238/I 398) related with nucleic acid tended to decrease obviously. (2) The intensity ratio at amide II and I (I1 541/I1 647) increased with the PMI increasing. The intensity at 1 338 and 1 313 cm(-1) varied slightly, but their intensity ratio to 1 398 cm(-1) decreased. (3) The intensity at 1 456 and 1 398 cm(-1) showed a trend of decreasing and increasing respectively. (4) Compared with the intensity at 2 871 cm(-1), the intensity at 2 852, 2 871, 2 923 and 2 958 cm(-1) tended to increase, but the increasing tendency at 2 871 cm(-1) was slight. It is concluded that FTIR spectroscopy is going to be an effective method for estimating the PMI in medicolegal practice and the brain tissue may be a suitable marker as a potential sample.