Uncommon presentation of gastric mucosa-associated lymphoid tissue lymphoma in a 13-year-old girl: acute vomiting of blood as the initial symptom.

Introduction and importance: Extranodal marginal zone lymphoma (EMZL lymphoma), also known as mucosa-associated lymphoid tissue (MALT) lymphoma, is a rare B-cell lymphoma that rarely affects children. The involvement of infectious agents, especially H. pylori, has been observed in the formation and progression of MALT lymphoma in the stomach. Hematemesis as the primary clinical manifestation is uncommon, highlighting the need for case studies with this presentation. This article uses SCARE2023 criteria as a framework to sort out a case report in order. Case presentation: A 13-year-old female patient was admitted in August 2022 with an episode of hematemesis. She had a prior diagnosis of anaemia and was found positive for H. pylori. Despite treatment, she developed symptoms of chronic non-atrophic gastritis and had recurring episodes of hematemesis. Physical and diagnostic examinations revealed B-cell lymphoma localized in the gastric antrum. The primary diagnosis was extranodal MALT lymphoma with unique plasma cell differentiation. Clinical discussion: The presentation of gastric MALT lymphoma can be variable, with definitive diagnosis often achieved via endoscopic biopsy. H. pylori plays a significant role in the onset and progression of this lymphoma, emphasizing the importance of its eradication for treatment. Effective outcomes can be achieved through anti-H. pylori treatment, although it is essential for clinicians to ensure its complete eradication post-treatment. Conclusion: Paediatric presentation of gastric MALT lymphoma, especially with hematemesis as the primary symptom, is rare and can be easily misdiagnosed. Compared to adults, children generally exhibit a better prognosis with effective H. pylori treatment. It is vital for medical professionals to recognize the differences in presentation between children and adults to ensure accurate diagnosis and treatment.

Efficacy of Faecal Microbiota Transplantation for the Treatment of Autism in Children: Meta-Analysis of Randomised Controlled Trials.

Objective: Evidence-based research methods were applied to assess the efficacy of faecal microbiota transplantation (FMT) for the treatment of autism in children. Methods: We searched the Chinese Biomedical Literature, CNKI, Wanfang, PubMed, Embase, Web of Science, and the Cochrane Library databases to collect randomised controlled trials on faecal microbiota transplantation for the treatment of autism in children. The search included studies published from the creation of the respective database to 5 April 2022. Literature screening, data extraction, and quality evaluation were implemented by three investigators according to the inclusion and exclusion criteria. The meta-analysis was performed using the RevMan 5.1 software. Results: Nine studies with population-based subjects and four studies with animal-based subjects were included. Five papers were screened for the meta-analysis. The results showed that FMT markedly reduced Autism Behaviour Checklist (ABC) scores in children with autism spectrum disorder (weighted mean difference (WMD) = -14.96; 95% confidence intervals (CI), -21.68 to -8.24; P < 0.001; I 2 = 0%). FMT also reduced Childhood Autism Rating Scale (CARS) scores (WMD = -6.95; 95% CI, -8.76 to -5.14; P < 0.001; I 2 = 28.1%). Conclusion: Our results indicate that FMT can benefit children with autism by reducing ABC and CARS scores, but more high-quality studies are needed to verify these results.

Long-chain Non-coding RNA MIR4435-2HG Expression Correlates With Size of Intestinal Polyps in Children and With Metastasis of Colon Cancer.

BACKGROUND/AIM: To determine if long-chain non-coding RNA (lncRNA) MIR4435-2HG (MIR4435) expression is associated with pre-malignant colon polyps and colon cancer. MATERIALS AND METHODS: Children's colonic-polyp specimens were sequenced for MIR4435 expression. LncRNA MIR4435 expression data in colorectal cancer and normal intestinal tissues were retrieved from The Cancer Genome Atlas (TCGA). The proliferation, adhesion, and invasion ability of human colon-cancer cell line HCT116 with or without MIR4435 knockdown was analyzed. The expression of Smad4, desmoplakin, and ß-catenin genes was detected by western blotting in HCT116 cells. RESULTS: MIR4435 expression correlated with the size of intestinal polyps in children. Expression of MIR4435 was up-regulated in colorectal cancer. MIR4435 knockdown in HCT116 cells inhibited their proliferation, adhesion, and invasion ability. Smad4 and desmoplakin were up-regulated and ß-catenin was down-regulated in HCT116 cells by MIR4435 knockdown. CONCLUSION: MIR4435 expression correlated with the size of intestinal polyps in children and with the proliferation, adhesion, and invasion ability of colon-cancer cells and was upregulated in colon cancer.

Recent advances in microfluidics-based cell migration research.

Cell migration is crucial for many biological processes, including normal development, immune response, and tissue homeostasis and many pathological processes such as cancer metastasis and wound healing. Microfluidics has revolutionized the research in cell migration since its inception as it reduces the cost of studies and allows precise manipulation of different parameters that affect cell migratory response. Over the past decade, the field has made great strides in many directions, such as techniques for better control of the cellular microenvironment, application-oriented physiological-like models, and machine-assisted cell image analysis methods. Here we review recent developments in the field of microfluidic cell migration through the following aspects: 1) the co-culture models for studying host-pathogen interactions at single-cell resolution; 2) the spatiotemporal manipulation of the chemical gradients guiding cell migration; 3) the organ-on-chip models to study cell transmigration; and 4) the deep learning image processing strategies for cell migration data analysis. We further discuss the challenges, possible improvement and future perspectives of using microfluidic techniques to study cell migration.

Exogenous pancreatic kininogenase protects against tacrolimus-induced renal injury by inhibiting PI3K/AKT signaling: The role of bradykinin receptors.

BACKGROUND: Tissue kallikrein offers a wide spectrum of biological activity in the protection against various types of injury. However, information on its role in tacrolimus (TAC)-induced renal injury is limited. OBJECTIVES: This study aimed to assess the beneficial effects of pancreatic kininogenase (PK) in a rat model of chronic TAC nephrotoxicity and in vitro. METHODS: Sprague Dawley rats were treated daily with either TAC or PK or a combination of the two for four weeks. The influence of PK on renal injury was examined in terms of renal function, histopathology, cytokine expression, oxidative stress, intracellular organelles, programmed cell death, and PI3K/AKT signaling. Human kidney proximal tubular (HK-2) cells and mouse mesangial (SV40 MES13) cells treated with TAC and PK were also studied. RESULTS: PK treatment improved renal function and histopathology. This effect was paralleled by downregulation of proinflammatory and profibrotic cytokine expression. TAC-induced oxidative stress was closely associated with endoplasmic reticulum stress and mitochondrial dysfunction, resulting in excessive programmed cell death (apoptosis and autophagy) that was significantly abrogated by concurrent PK interference with PI3K/AKT signaling. PK also stimulated bradykinin receptor 1 (B1R) and B2R mRNA synthesis and increased bioactive nitric oxide (NO) and cAMP concentrations in TAC-treated kidneys. Blockade of either B1R or B2R eliminated the renoprotective effects of PK. In HK-2 and SV40 MES13 cells, PK decreased TAC-induced overproduction of intracellular reactive oxygen species and inhibited apoptotic cells, whereas cell viability was improved. Moreover, activated PI3K/AKT signaling in HK-2 cells was inhibited by PK and the PI3K inhibitor, LY294002. CONCLUSIONS: These findings indicate that PK treatment protects against chronic TAC nephrotoxicity via inhibition of PI3K/AKT signaling.

Nicotine exacerbates tacrolimus-induced renal injury by programmed cell death

Background/Aims@#Cigarette smoking is an important modifiable risk factor in kidney disease progression. However, the underlying mechanisms for this are lacking. This study aimed to assess whether nicotine (NIC), a major toxic component of cigarette smoking, would exacerbates tacrolimus (TAC)-induced renal injury. @*Methods@#Sprague-Dawley rats were treated daily with NIC, TAC, or both drugs for 4 weeks. The influence of NIC on TAC-caused renal injury was examined via renal function, histopathology, oxidative stress, mitochondria, endoplasmic reticulum (ER) stress, and programmed cell death (apoptosis and autophagy). @*Results@#Both NIC and TAC significantly impaired renal function and histopathology, while combined NIC and TAC treatment aggravated these parameters beyond the effects of either alone. Increased oxidative stress, ER stress, mitochondrial dysfunction, proinf lammatory and profibrotic cytokine expressions, and programmed cell death from either NIC or TAC were also aggravated by the two combined. @*Conclusions@#Our observations suggest that NIC exacerbates chronic TAC nephrotoxicity, implying that smoking cessation may be beneficial for transplant smokers taking TAC.

Evaluation of facial soft tissue thickness in asymmetric mandibular deformities after orthognathic surgery / 대한악안면성형재건외과학회지

Objectives@#The purpose of this study was to compare differences in facial soft tissue thickness in three-dimensional (3D) images before and after orthognathic surgery in patients with skeletal Class III malocclusion and to obtain a better understanding of the relationship between hard and soft tissue changes after surgery.Materials and method: The present retrospective study included 31 patients with skeletal Class III malocclusion with mandibular chin deviation greater than 4 mm who had undergone cone-beam computed tomography before and 6 months after surgery. Seven bilateral points were established. Measurements were taken from software-generated multiplanar reconstructions. The predictor variables were timing (pre- and postoperatively) and side (deviated vs.nondedicated). A regression model and correlation analysis were conducted for statistical analysis. @*Results@#The difference of bilateral facial soft tissue thickness was statistically significantly different between deviated and nondeviated sides (P < 0.05), with lower values observed on the deviated side. The soft tissue thickness has become nearly symmetric at local regions of the lower thirds of the face after orthognathic surgery. However, most measurements showed a negative correlation between changes in soft tissue thickness and changes in bone tissues. @*Conclusions@#Skeletal Class III malocclusion with facial asymmetry is accompanied by differences in soft tissue thickness when comparing Dev and N-Dev sides of the posterior region of the mandible, where soft tissues are thinner on the Dev side. Soft tissue thickness can compensate for or camouflage the underlying asymmetric mandible. In addition, the asymmetric soft tissue thickness on the lower third of the face can be partially improved by orthognathic surgery, but the amount of soft tissue thickness change is not consistent with that of hard tissue positional change.

L-carnitine treatment attenuates renal tubulointerstitial fibrosis induced by unilateral ureteral obstruction

Background/Aims@#Accumulating evidence indicates that L-carnitine (LC) protects against multiorgan damage through its antioxidant properties and preservation of the mitochondria. Little information is available about the effects of LC on renal fibrosis. This study examined whether LC treatment would provide renoprotection in a rat model of unilateral ureteral obstruction (UUO) and in vitro. @*Methods@#Sprague-Dawley rats that underwent UUO were treated daily with LC for 7 or 14 days. The influence of LC on renal injury caused by UUO was evaluated by histopathology, and analysis of gene expression, oxidative stress, mitochondrial function, programmed cell death, and phosphatidylinositol 3-kinase (PI3K)/ AKT/forkhead box protein O 1a (FoxO1a) signaling. In addition, H2O2-exposed human kidney cells (HK-2) were treated with LC. @*Results@#LC treatment inhibited expression of proinflammatory and profibrotic cytokines, and was followed by a significant attenuation of tubulointerstitial inflammation and fibrosis. The increased oxidative stress caused by UUO was associated with mitochondrial dysfunction and excessive apoptosis and autophagy via PI3K/AKT/FoxO1a-dependent signaling, and this was abrogated by administration of LC. In H2O2-exposed HK-2 cells, LC decreased intracellular production of reactive oxygen species, and suppressed expression of profibrotic cytokines and reduced the number of apoptotic cells. @*Conclusions@#LC protects against the progression of tubulointerstitial fibrosis in an obstructed kidney.

The role of bone marrow-derived cells in the origin of liver cancer revealed by single-cell sequencing.

Objective: Epithelial cancers often originate from progenitor cells, while the origin of hepatocellular carcinoma (HCC) is still controversial. HCC, one of the deadliest cancers, is closely linked with liver injuries and chronic inflammation, which trigger massive infiltration of bone marrow-derived cells (BMDCs) during liver repair. Methods: To address the possible roles of BMDCs in HCC origination, we established a diethylnitrosamine (DEN)-induced HCC model in bone marrow transplanted mice. Immunohistochemistry and frozen tissue immunofluorescence were used to verify DEN-induced HCC in the pathology of the disease. The cellular origin of DEN-induced HCC was further studied by single cell sequencing, single-cell nested PCR, and immunofluorescence-fluorescence in situ hybridization. Results: Studies by using single cell sequencing and biochemical analysis revealed that HCC cells in these mice were coming from donor mice BMDCs, and not from recipient mice. Furthermore, the copy numbers of mouse orthologs of several HCC-related genes previously reported in human HCC were also altered in our mouse model. DEN-induced HCCs exhibited a similar histological phenotype and genomic profile as human HCCs. Conclusions: These results suggested that BMDCs are an important origin of HCC, which provide important clues to HCC prevention, detection, and treatments.

cPLA2α reversibly regulates different subsets of cancer stem cells transformation in cervical cancer.

Cervical cancer stem cells (CCSCs) are considered major causes of chemoresistance/radioresistance and metastasis. Although several cell surface antigens have been identified in CCSCs, these markers vary among tumors because of CSC heterogeneity. However, whether these markers specifically distinguish CCSCs with different functions is unclear. Here, we demonstrated that CCSCs exist in two biologically distinct phenotypes characterized by different levels of cytosolic phospholipase A2α (cPLA2α) expression. Overexpression of cPLA2α results in a CD44+ CD24- phenotype associated with mesenchymal traits, including increased invasive and migration abilities, whereas CCSCs with cPLA2α downregulation express CD133 and show quiescent epithelial characteristics. In addition, cPLA2α regulates the reversible transition between mesenchymal and epithelial CCSC states through PKCζ, an atypical protein kinase C, which governs cancer cell state changes and the maintenance of various embryonic stem cell characteristics, further inhibiting ß-catenin-E-cadherin interaction in membrane and promoting ß-catenin translocation into the nucleus to affect the transcriptional regulation of stemness signals. We propose that reversible transitions between mesenchymal and epithelial CCSC states regulated by cPLA2α are necessary for cervical cancer metastasis and recurrence. Thus, cPLA2α might be an attractive therapeutic target for eradicating different states of CCSCs to eliminate tumors more effectively.

Cytosolic phospholipase A2α modulates cell-matrix adhesion via the FAK/paxillin pathway in hepatocellular carcinoma.

OBJECTIVE: To explore the effect of cytosolic phospholipase A2α (cPLA2α) on hepatocellular carcinoma (HCC) cell adhesion and the underlying mechanisms. METHODS: Cell adhesion, detachment, and hanging-drop assays were utilized to examine the effect of cPLA2α on the cell-matrix and cell-cell adhesion. Downstream substrates and effectors of cPLA2α were screened via a phospho-antibody microarray. Associated signaling pathways were identified by the functional annotation tool DAVID. Candidate proteins were verified using Western blot and colocalization was investigated via immunofluorescence. Western blot and immunohistochemistry were used to detect protein expression in HCC tissues. Prognosis evaluation was conducted using Kaplan-Meier and Cox-proportional hazards regression analyses. RESULTS: Our findings showed that cPLA2α knockdown decreases cell-matrix adhesion but increases cell-cell adhesion in HepG2 cells. Microarray analysis revealed that phosphorylation of multiple proteins at specific sites were regulated by cPLA2α. These phosphorylated proteins were involved in various biological processes. In addition, our results indicated that the focal adhesion pathway was highly enriched in the cPLA2α-relevant signaling pathway. Furthermore, cPLA2α was found to elevate phosphorylation levels of FAK and paxillin, two crucial components of focal adhesion. Moreover, localization of p-FAK to focal adhesions in the plasma membrane was significantly reduced with the downregulation of cPLA2α. Clinically, cPLA2α expression was positively correlated with p-FAK levels. Additionally, high expression of both cPLA2α and p-FAK predicted the worst prognoses for HCC patients. CONCLUSIONS: Our study indicated that cPLA2α may promote cell-matrix adhesion via the FAK/paxillin pathway, which partly explains the malignant cPLA2α phenotype seen in HCC.

Periostin mediates epithelial-mesenchymal transition through the MAPK/ERK pathway in hepatoblastoma.

OBJECTIVE: The aim of the present study was to analyze the prognostic factors in patients with hepatoblastoma (HB) in our single center and to evaluate periostin (POSTN) expression in HB and its association with clinicopathological variables. In addition, the underlying mechanism of how POSTN promotes HB progression was discussed. METHODS: POSTN expression was investigated in HB tumors by immunohistochemistry (IHC), immunofluorescence (IF) and Western blot (WB). The association among POSTN expression, clinicopathological features and overall survival (OS) was also evaluated. The migration and adhesion ability of HB cells were measured using chemotaxis and cell-matrix adhesion assays, respectively. Epithelial-mesenchymal transition (EMT)-associated markers and activation of the ERK pathway were detected by WB. RESULTS: HB patients had poor prognosis which displayed lymph node metastasis, vascular invasion, POSTN and vimentin expression. POSTN expression was also associated with lymph node metastasis. Furthermore, overexpressed POSTN promoted migration and the adhesive ability of HB cells in vitro. In addition, we demonstrated that POSTN activated the MAPK/ERK pathway, upregulated the expression of Snail and decreased the expression of OVOL2. Finally, POSTN promoted the expression of EMT-associated markers. CONCLUSIONS: POSTN might modulate EMT via the ERK signaling pathway, thereby promoting cellular migration and invasion. Our study also suggests that POSTN may serve as a therapeutic biomarker in HB patients.

Shen-Kang protects against tacrolimus-induced renal injury

BACKGROUND/AIMS@#Evidence suggests that Shen-Kang (SK), a traditional Chinese herbal medicine, protects against various types of renal injury. In this study, we evaluated whether SK treatment confers renoprotection in a rat model of chronic tacrolimus (TAC) nephropathy.@*METHODS@#Rats were treated daily with TAC (1.5mg/kg, subcutaneously) and SK (450 mg/kg, intravenously) for 4 weeks. The effects of SK on TAC-induced renal injury were assessed by measuring renal function, urine albumin excretion, histopathology, inflammatory cell infiltration, expression of profibrotic (transforming growth factor β1 [TGF-β1] and TGF-β inducible gene-h3 [βig-h3]) and proinflammatory cytokines, oxidative stress, and apoptotic cell death.@*RESULTS@#Administration of SK preserved glomerular integrity (fractional mesangial area and Wilms tumor 1-positive glomeruli), attenuated tubulointerstitial fibrosis, and reduced the number of ectodermal dysplasia 1-positive cells, and this was paralleled by improved urine albumin excretion and renal dysfunction. At the molecular level, SK treatment suppressed expression of TGF-β1/Smad2/3, βig-h3, and proinflammatory cytokines. Oxidative stress and apoptotic cell death were significantly decreased with SK treatment, and apoptosis-related genes were regulated toward cell survival (active caspase-3 and the B-cell lymphoma-2/Bcl2-associated X [Bcl-2/Bax] ratio).@*CONCLUSIONS@#SK protects against TAC-induced renal injury.

HCC-derived exosomes elicit HCC progression and recurrence by epithelial-mesenchymal transition through MAPK/ERK signalling pathway.

Liver cancer is the second most common cause of cancer-related death worldwide. Approximately 70-90% of primary liver cancers are hepatocellular carcinoma (HCC). Currently, HCC patient prognosis is unsatisfactory due to high metastasis and/or post-surgical recurrence rates. Therefore, new therapeutic methods for inhibiting metastasis and recurrence are urgently needed. Exosomes are small lipid-bilayer vesicles that are implicated in tumour development and metastasis. Rab27a, a small GTPase, regulates exosome secretion by mediating multivesicular endosome docking at the plasma membrane. However, whether Rab27a participates in HCC cell-derived exosome exocytosis is unclear. Epithelial-mesenchymal transition (EMT) frequently initiates metastasis. The role of HCC cell-derived exosomes in EMT remains unknown. We found that exosomes from highly metastatic MHCC97H cells could communicate with low metastatic HCC cells, increasing their migration, chemotaxis and invasion. Rab27a knockdown inhibited MHCC97H-derived exosome secretion, which consequently promoted migration, chemotaxis and invasion in parental MHCC97H cells. Mechanistic studies showed that the biological alterations in HCC cells treated with MHCC97H-derived exosomes or MHCC97H cells with reduced self-derived exosome secretion were caused by inducing EMT via MAPK/ERK signalling. Animal experiments indicated that exosome secretion blockade was associated with enhanced lung and intrahepatic metastasis of parental MHCC97H cells, while ectopic overexpression of Rab27a in MHCC97H cells could rescue this enhancement of metastasis in vivo. Injection of MHCC97H cell-derived exosomes through the tail vein promoted intrahepatic recurrence of HLE tumours in vivo. Clinically, Rab27a was positively associated with serum alpha-fetoprotein (AFP) level, vascular invasion and liver cirrhosis. Our study elucidated the role of exosomes in HCC metastasis and recurrence, suggesting that they are promising therapeutic and prognostic targets for HCC patients.

Ursolic acid inhibits proliferation and reverses drug resistance of ovarian cancer stem cells by downregulating ABCG2 through suppressing the expression of hypoxia-inducible factor-1α in vitro.

Hypoxia in tumors is closely related to drug resistance. It has not been verified whether hypoxia-inducible factor-1α (HIF-1α) or ABCG2 is related to hypoxia-induced resistance. Ursolic acid (UA), when used in combination with cisplatin can significantly increase the sensitivity of ovarian cancer stem cells (CSCs) to cisplatin, but the exact mechanism is unknown. The cell growth inhibitory rate of cisplatin under different conditions was evaluated using Cell Counting Kit-8 (CCK-8) in adherence and sphere cells (SKOV3, A2780, and HEY). The expression of HIF-1α and ABCG2 was tested using quantitative PCR, western blotting, and immuno-fluorescence under different culture conditions and treated with UA. Knockdown of HIF-1α by shRNA and LY294002 was used to inhibit the activity of PI3K/Akt pathway. Ovarian CSCs express stemness-related genes and drug resistance significantly higher than normal adherent cells. Under hypoxic conditions, the ovarian CSCs grew faster and were more drug resistant than under normoxia. UA could inhibit proliferation and reverse the drug resistance of ovarian CSC by suppressing ABCG2 and HIF-1α under different culture conditions. HIF-1α inhibitor YC-1 combined with UA suppressed the stemness genes and ABCG2 under hypoxic condition. The PI3K/Akt signaling pathway activation plays an important functional role in UA-induced downregulation of HIF-1α and reduction of ABCG2. UA inhibits the proliferation and reversal of drug resistance in ovarian CSCs by suppressing the expression of downregulation of HIF-1α and ABCG2.

Comparison of Early and Late Conversion of Sirolimus in Experimental Model of Chronic Cyclosporine Nephropathy

Sirolimus (SRL) is a promising drug for replacing calcineurin inhibitors. We performed this study to determine the optimal time of conversion from cyclosporine (CsA) to SRL in an experimental model of chronic CsA nephropathy. Three separate studies were performed. In the first study, SRL was given to rats with or without CsA for 4 weeks. In the second study, rats were treated initially with CsA for 1 week, and then switched to SRL (early conversion). In the third study, CsA was given for 4 weeks and then replaced by SRL for 4 weeks treatment of CsA (late conversion). The influence of SRL on CsA-induced renal injury was evaluated by assessing renal function, histopathology (interstitial inflammation and fibrosis), and apoptotic cell death. Combined CsA and SRL treatment significantly impaired renal function, increased apoptosis, and interstitial fibrosis and inflammation compared with CsA or SRL treatment alone. Early conversion to SRL did not change renal function, histopathology, or apoptosis compared with early CsA withdrawal. By contrast, late conversion to SRL significantly aggravated these parameters compared with late CsA withdrawal. In conclusion, early conversion from CsA to SRL is effective in preventing CsA-induced renal injury in a setting of CsA-induced renal injury.

DNA-Based Identification of Necrophagous Fly Species Using Abdominal-B (Abd-B) Homeobox Sequence / 대한법의학회지

In medicolegal investigations, correct identification of the necrophagous fly species collected around and on the corpse is an essential step for estimating the postmortem interval (PMI). Therefore, forensic pathologists and entomologists investigating deaths due to violent crimes need a rapid, easy-to-use protocol to identify fly species found on corpses. A rapid and robust DNA-based tool that can distinguish between various immature and mature species from the Calliphoridae, Muscidae, and Sarcophagidae families would be ideal for such investigations. To date, the DNA barcode initiative is the best approach for identifying species-specific nucleotide sequences. We have developed 3 sequence-characterized amplified region (SCAR)-based identification systems derived from the Abdominal-B homeobox sequences of 17 fly species belonging to the Muscidae and Sarcophagidae. The flies used in this study were collected in Korea. These assay systems can classify 17 forensically important fly species into the dipteran family group and reliably distinguish them from inter- and intraspecific fly species through a 2-step multiplex PCR. This novel approach may also be used as an alternative to conventional DNA-based identification methods.

Higher infiltration by Th17 cells compared with regulatory T cells is associated with severe acute T-cell-mediated graft rejection

The aim of this study was to evaluate whether the Th17 and Treg cell infiltration into allograft tissue is associated with the severity of allograft dysfunction and tissue injury in acute T cell-mediated rejection (ATCMR). Seventy-one allograft tissues with biopsy-proven ATCMR were included. The biopsy specimens were immunostained for FOXP3 and IL-17. The allograft function was assessed at biopsy by measuring serum creatinine (Scr) concentration, and by applying the modified diet in renal disease (MDRD) formula, which provides the estimated glomerular filtration rate (eGFR). The severity of allograft tissue injury was assessed by calculating tissue injury scores using the Banff classification. The average numbers of infiltrating Treg and Th17 cells were 11.6 +/- 12.2 cells/mm2 and 5.6 +/- 8.0 cells/mm2, respectively. The average Treg/Th17 ratio was 5.6 +/- 8.2. The Treg/Th17 ratio was significantly associated with allograft function (Scr and MDRD eGFR) and with the severity of interstitial injury and tubular injury (P < 0.05, all parameters). In separate analyses of the number of infiltrating Treg and Th17 cells, Th17 cell infiltration was significantly associated with allograft function and the severity of tissue injury. By contrast, Treg cell infiltration was not significantly associated with allograft dysfunction or the severity of tissue injury. The results of this study show that higher infiltration of Th17 cell compared with Treg cell is significantly associated with the severity of allograft dysfunction and tissue injury.

Homicidal Fall from Height with 'Tram-line' Bruise at Buttocks / 대한법의학회지

A teenaged female was found dead in front of a three story building. Blunt force injuries were found mainly in the right upper-posterior part of the body. Autopsy findings revealed basal skull fracture, multiple rib fractures of the right thoracic cage, both scapular fractures and right iliac bone fracture. Additionally, typical so-called 'tramline'bruises were bilaterally noted at buttocks. The hymen was intact, but showed mucosal hemorrhage. After the personal identity was revealed, the police could find a witness who heard the detailed description of the criminal acts from one of the suspects. According to the witness, the deceased was pushed by two other teenaged girls from the concrete fence of the roof floor after the suspects molested the genitalia of the deceased and beat on the buttocks with a wooden stick. Mathematical estimation of the height of fall based on the severity of injuries correlates with that of the three story building. Authors suggest that a careful examination of injury patterns is required to differentiate homicidal falls from suicidal or accidental ones. Furthermore, application of mathematical model might be helpful to estimate the height of falls or correlate the assumed height of fall with severity of injuries.

Study of three-dimensional model on biomechanical characteristics of mandibular fractures in different site / 华西口腔医学杂志

<p><b>OBJECTIVE</b>To determine the biomechanical characteristics of mandibular fractures in different site.</p><p><b>METHODS</b>Nine adult mandibular specimens were measured precisely. The data was used to establish a three-dimensional model. When mandibular was under functional loading, the bending and torsion moment as well as shear force of angle, body and symphyseal fracture was calculated. The data were analyzed by Origin 6.0 software.</p><p><b>RESULTS</b>Angle fracture had relatively high positive bending moment and high shear force. Body fracture had positive as well as negative bending moment and the highest torsion moments. Symphyseal fracture had only negative bending moment and relatively low shear force.</p><p><b>CONCLUSION</b>Angle, body and symphyseal fractures each have a biomechanics characteristic. These biomechanics characteristic should have an important meaning in the treatment of mandibular fractures and instructing patient how to bite correctly.</p>