Automatic identification of individuals using deep learning method on panoramic radiographs.

Abstract Background/purpose: The dentition shows individual characteristics and dental structures are stable with respect to postmortem decomposition, allowing the dentition to be used as an effective tool in forensic dentistry. We developed an automatic identification system using panoramic radiographs (PRs) with a deep learning method. Materials and methods: In total, 4966 PRs from 1663 individuals with various changes in image characteristics due to various dental treatments were collected. In total, 3303 images were included in the data set used for model training. Vgg16, Vgg19, ResNet50, ResNet101, and EfficientNet models were applied for identification. The precision curves were evaluated. Results: The matching precision rates of all models (Vgg16, Vgg19, ResNet50, ResNet101, and EfficientNet) were examined. Vgg16 was the best model, with a precision of around 80-90% on 200 epochs, using the Top-N metrics concept with 5-15 candidate labels. The model can successfully identify the individual even with low quantities of dental features in 5-10 s. Conclusion: This identification system with PRs using a deep learning method appears useful. This identification system could prove useful not only for unidentified bodies, but also for unidentified wandering elderly people. This project will be beneficial for police departments and government offices and support disaster responses.

Molecular mechanism of cerebral edema improvement via IL-1RA released from the stroke-unaffected hindlimb by treadmill exercise after cerebral infarction in rats.

Cerebral edema following cerebral infarction can be severe and directly affect mortality and mobility. Exercise therapy after cerebral infarction is an effective therapeutic approach; however, the molecular mechanism remains unclear. Myokines such as interleukin-1 receptor antagonist (IL-1RA) are released during skeletal muscle contraction with effects on other organs. We hypothesized that myokine release during exercise might improve brain edema and confirmed the hypothesis using transient middle cerebral artery occlusion (tMCAO) model rats. Rats subjected to tMCAO were divided according to the severity of illness and further assigned to exercise and non-exercise groups. Treadmill exercises were performed at a speed of 2-8 m/min for 10 min from 1-6 days post-reperfusion after tMCAO. Exercise significantly reduced edema and neurological deficits in severely ill rats, with a reduction in aquaporin-4 (AQP4) expression in the ischemic core and increased blood IL-1RA release from the stroke-unaffected hindlimb muscle after tMCAO. Administration of IL-1RA into the lateral ventricles significantly reduced edema and AQP4 expression in the ischemic core. In conclusion, treadmill exercise performed in the early phase of stroke onset alleviated the decrease in blood IL-1RA following ischemic stroke. IL-1RA administration decreased astrocytic AQP4 expression in the ischemic core, suppressing brain edema.

Activated microglia-derived macrophage-like cells exacerbate brain edema after ischemic stroke correlate with astrocytic expression of aquaporin-4 and interleukin-1 alpha release.

Brain edema following brain infarction affects mobility and mortality. The mechanisms underlying this process remain to be elucidated. Animal studies have shown that aquaporin-4 (AQP4) expression in astrocytes increases after stroke, and its deletion significantly reduces brain swelling. Recently, two kinds of cells, resident microglia-derived macrophage-like cells (MG-MΦ) and bone marrow-derived macrophages (BM-MΦ), have been reported to accumulate in the ischemic core and stimulate adjacent astrocytes. Therefore, we hypothesized that these cells play crucial roles in the expression of AQP4 and ultimately lead to exacerbated brain edema. To verify this hypothesis, we investigated the role of MG- or BM-MΦ in brain edema using a rat model of transient middle cerebral artery occlusion and rat astrocyte primary cultures. AQP4 expression significantly increased in the peri-infarct tissue at 3-7 days post-reperfusion (dpr) and in the core tissue at 5 and 7 dpr, which synchronized with the expression of Iba1, Il1a, Tnf, and C1qa mRNA. Interleukin (IL)-1α treatment or coculture with MG- and BM-MΦ increased AQP4 expression in astrocytes, while an IL-1 receptor type I antagonist reduced these effects. Furthermore, aggravated animals exhibited high expression of Aqp4 and Il1a mRNA in the ischemic core at 7 dpr, which led to the exacerbation of brain edema. MG-MΦ signature genes were highly expressed in the ischemic core in aggravated rats, while BM-MΦ signature genes were weakly expressed. These findings suggest that IL-1α produced by MG-MΦ induces astrocytic AQP4 expression in the peri-infarct and ischemic core tissues, thereby exacerbating brain edema. Therefore, the regulation of MG-MΦ may prevent the exacerbation of brain edema.

Molecular mechanisms of Wischnewski spot development on gastric mucosa in fatal hypothermia: an experimental study in rats.

Numerous dark-brown-coloured small spots called "Wischnewski spots" are often observed in the gastric mucosa in the patients dying of hypothermia, but the molecular mechanisms through which they develop remain unclear. We hypothesised that hypothermia may activate the secretion of gastric acid and pepsin, leading to the development of the spots. To investigate this, we performed experiments using organotypic rat gastric tissue slices cultured at 37 °C (control) or 32 °C (cold). Cold loading for 6 h lowered the extracellular pH in the culture medium. The mRNA expression of gastrin, which regulates gastric acid secretion, increased after cold loading for 3 h. Cold loading increased the expression of gastric H+,K+-ATPase pump protein in the apical canalicular membrane and resulted in dynamic morphological changes in parietal cells. Cold loading resulted in an increased abundance of pepsin C protein and an elevated mRNA expression of its precursor progastricsin. Collectively, our findings clarified that cold stress induces acidification by activating gastric H+,K+-ATPase pumps and promoting pepsin C release through inducing progastricsin expression on the gastric mucosa, leading to tiny haemorrhages or erosions of the gastric mucosa that manifest as Wischnewski spots in fatal hypothermia.

A case of severe soft tissue infection due to Streptococcus tigurinus diagnosed by necropsy in which genomic analysis was useful for clarifying its pathogenicity.

Post-mortem detection of pathogenetic microorganisms in severe infectious death is significantly important for diagnosing the cause of death as well as for public health. However, it is difficult to recognize whether a microorganism detected from post-mortem materials is truly pathogenic or not. We report a case of severe soft tissue infection due to Streptococcus oralis subsp. tigurinus (S. tigurinus), a recently reported species, in which whole-genome analysis was performed to clarify its pathogenicity. A 46-year-old woman had died with symptoms of a severe infectious disease. A post-mortem examination was performed by a medical examiner. The external findings suggested a soft tissue infection; subsequently, pathological specimens sampled by necropsy revealed findings compatible with necrotizing fasciitis. In the post-mortem bacterial test, S. tigurinus was detected from the localized autopsy sample. Whole-genome sequencing was performed to analyze its pathogenicity and detected a strain of S. tigurinus with genetic determinants that were specific and unique to its highly virulent strains as a result of gene annotation. Utilizing various technologies, such as whole-genome sequencing, may be a powerful tool for diagnosing the cause of infectious death accurately and safely.

Whole-Genome Sequence of Streptococcus tigurinus Strain osk_001, Isolated from Postmortem Material.

Streptococcus tigurinus was recently described as a novel species, and some strains are highly virulent. We detected S. tigurinus in infected tissue sampled by necropsy. In order to characterize and confirm the virulence of this species, whole-genome sequencing of the pure cultured bacterium was performed. We found that the strain has specific and unique genetic elements contained in highly virulent strains of S. tigurinus.

Ethanol increases astrocyte aquaporin-4 expression under hyper-sodium condition.

Ethanol increases brain aquaporin-4 (AQP4) expression after traumatic brain injury (TBI), leading to augment mortality and morbidity after TBI. AQP4 is regulated by sodium ion channels/transporters. Ethanol affects the ion channels/transporters. From these findings, we hypothesized that ethanol may have different effects on AQP4 expression in hypo- or hyper-sodium condition. In this study, rat primary astrocytes were incubated in iso-, hypo- or hyper-sodium MEM medium with 10% calf serum. Ethanol was added to each medium simultaneously. And to check whether hypo/hyper-sodium condition could change AQP4 expression after ethanol exposure or not, astrocytes were incubated in iso-sodium with ethanol, followed by changed to hypo/hyper-sodium with the same concentration of ethanol. Astrocyte AQP4 expression was increased in hypo-sodium exposure. Hypo-sodium with ethanol did not change AQP4 expression significantly, on the other hand, hyper-sodium with ethanol decreased AQP4 expression for short time exposure, and increased it for long time exposure. Hyper-sodium changing increased astrocyte AQP4 expression under EtOH exposure. These findings suggest that AQP4 expression is regulated by sodium ion or ion channels/transporters. And ethanol affects sodium ion channels/transporters, which is involved in AQP4 expression under ethanol.

Greatly improved survival and neuroprotection in aquaporin-4-knockout mice following global cerebral ischemia.

Aquaporin-4 (AQP4), the principal water channel in astrocytes, is involved in brain water movement, inflammation, and neuroexcitation. In this study, there was strong neuroprotection in mice lacking AQP4 in a model of global cerebral ischemia produced by transient, bilateral carotid artery occlusion (BCAO). Survival and neurological outcome were greatly improved in the AQP4(-/-) vs. AQP4(+/+) mice after occlusion, with large and robust differences in both outbred (CD1) and inbred (C57bl/6) mouse strains without or with mechanical ventilation. Improved survival was also seen in mice lacking the scaffold protein α-syntrophin, which manifest reduced astrocyte water permeability secondary to defective AQP4 plasma membrane targeting. Intracranial pressure elevation and brain water accumulation were much reduced in the AQP4(-/-) vs. AQP4(+/+) mice after carotid artery occlusion, as were blood-brain barrier (BBB) disruption and neuronal loss. Brain slices from AQP4(-/-) mice showed significantly reduced cell swelling and cytotoxicity in response to oxygen-glucose deprivation, compared with slices from AQP4(+/+) mice. Our findings suggest that the neuroprotective effect of AQP4 deletion in global cerebral ischemia involves reduced astrocyte swelling and brain water accumulation, resulting in reduced BBB disruption, inflammation, and neuron death. AQP4 water transport inhibition may improve survival and neurological outcome after cardiac arrest and in other conditions associated with global cerebral ischemia.

Experimental rat model for alcohol-induced osteonecrosis of the femoral head.

Alcohol-induced osteonecrosis of the femoral head (ONFH) is observed in alcohol abusers and patients with alcoholic fatty liver disease. It has been reported that Toll-like receptor 4 (TLR4) signalling plays a crucial role in the pathogenesis of alcoholic fatty liver disease. We previously reported a corticosteroid-induced ONFH rat model, and suggested that TLR4 signalling contributes to the pathogenesis of ONFH. Thus, it is thought that the pathogenesis of alcohol-induced ONFH is probably similar to that of corticosteroid-induced ONFH. The aim of this study was to develop a new animal model for alcohol-induced ONFH and to evaluate the relationship between the pro-inflammatory response via TLRs and the development of ONFH in rats. Male Wistar rats were fed a Lieber-DeCarli liquid diet containing 5% ethanol (experimental group) or dextran (control group) for 1-24 weeks. Histopathological and biochemical analyses were performed. Feeding the ethanol-containing liquid diet resulted in the development of ONFH with hepatic steatosis, hepatic dysfunction and hyperlipidaemia, whereas feeding the dextran-containing diet did not cause ONFH. However, we could not recognize any relationship between the pro-inflammatory response via TLR4 and the development of alcohol-induced ONFH. Thus in this study we have developed a new rat model for alcohol-induced ONFH based on the feeding of an ethanol liquid diet. ONFH was observed within seven days from the start of feeding with 5% ethanol-containing liquid diet. Although this was linked to hepatic steatosis, a TLR4 association was not a feature of this model.

Postmortem computed tomography lung findings in fatal of hypothermia.

To identify lung findings specific to fatal hypothermia on postmortem computed tomography (CT) imaging. Whole body CT scans were performed followed by full autopsy to investigate causes of death. There were 13 fatal hypothermia cases (group A) and 118 with other causes of death (group B). The chest cavity (CC), dead space including fluid/pneumothorax (DS), aerated lung volume (ALV), percentage aerated lung (%ALV), and tracheal aerated volume (ATV) were measured. Autopsy findings of groups A and B were compared. Receiver operating characteristics (ROC) curves were used to identify factors specific to fatal hypothermia. There were no differences in age, sex, number with emphysema, or time from death to CT examination between the 2 groups. CC, DS, ALV, %ALV, and ATV were 2601.0±247.4 (mL), 281.1±136.5 (mL), 1564.5±281.1 (mL), 62.1±6.2(%), and 21.8±2.7 (mL) in group A and 2339.2±67.7 (mL), 241.1±38.0 (mL), 739.9±67.0 (mL), 31.4±2.3(%), and 15.9±0.8 (mL) in group B, respectively. There were statistically significant differences between groups A and B in ALV, %ALV and ATV. The multiple comparison procedure revealed that ALV and %ALV differed significantly between fatal hypothermia and other causes of death (p<0.05). Using ROC evaluation, %ALV had the largest area under the curve (0.819). This study demonstrates that the %ALV is greater in fatal hypothermia cases than in those with other causes of death on postmortem CT chest imaging. Based on CT, hypothermia is very likely to be the cause of death if the %ALV is >70%.

Weight bearing does not contribute to the development of osteonecrosis of the femoral head.

The hip joint is one of the major structures in the human body and the resultant force acting through the hip joint is 300% of body weight. Therefore, weight bearing, as a cause of ischaemia, may contribute to the development of non-traumatic osteonecrosis of the femoral head (ONFH). However, it remains unclear whether weight bearing is related to the development of non-traumatic ONFH. Therefore the aim of this study was to clarify the role of weight bearing in the development of non-traumatic ONFH. Non-weight-bearing (NWB) rats were tail suspended to prevent any weight coming to bear on the hindlimbs from day 1 to the time of sacrifice. The weight-bearing (WB) group rats were also housed individually, although without tail suspension. All rats were injected with lipopolysaccharide and methylprednisolone to promote the development of non-traumatic ONFH. All animals were sacrificed three weeks after the final methylprednisolone injection. Histopathological analysis was performed. Osteonecrosis of the femoral head was observed not only in the NWB but also in the WB rats; however, no osteonecrosis of the humeral head was observed in either group. We confirmed that non-traumatic ONFH developed in NWB rats, suggesting that weight bearing does not contribute to the development of non-traumatic ONFH in rats.

Epigenetic regulation of MIR-124 under ethanol dependence and withdrawal.

Withdrawal from chronic alcohol cause the persistent molecular alteration, such as changes in the release of neurotransmitter and gene expression. The alterations are thought to increase in the risk of relapse. Recent studies suggest that the gene expression regulated by histone acetylation may play an important role in the dependence of abused drugs, including of ethanol. Furthermore, miRNA, another regulator of gene expression, are also important molecules for the dependence. However, changes in the molecules under ethanol withdrawal and its relationship are poorly understood. In the present study, we investigated the expression of acetylated histone H3 and miR-124 in mouse brain at 3 days after ethanol withdrawal. 6-Week ages of C57BL/6J mice were treated with liquid diet containing ethanol for 10 days. Using the escalating ethanol dosage schedule, the mice were fed the ethanol diet as follows: 1st day: 1 w/v%: 2nd and 3rd day: 3 w/v%; 4th and 5th day: 4 w/v% and from the 6th to 10th day: 5 w/v% ethanol diet, respectively. The pair-fed control mice were given the same volume of ethanol-free liquid diet with glucose substituted in isocaloric quantities for ethanol. After feeding alcohol liquid diet, the mice showed severe withdrawal signs. The expression of acetylated histone H3 was significantly decreased in limbic forebrain at 3 days after withdrawal. We found that miR-124 also decreased in the limbic forebrain. It has been reported that Cdc42 regulates neuronal development as a target of miR-124. We found that Cdc42 protein markedly increased in both brain regions at 3 days after withdrawal. Our findings suggest that changes in the expression of miR-124 via histone acetylation leads to change the Cdc42 expression under ethanol withdrawal.

Ethanol-induced hyponatremia augments brain edema after traumatic brain injury.

Alcohol consumption augments brain edema by expression of brain aquaporin-4 after traumatic brain injury. However, how ethanol induces brain aquaporin-4 expression remains unclear. Aquaporin-4 can operate with some of ion channels and transporters. Therefore, we hypothesized that ethanol may affect electrolytes through regulating ion channels, leading to express aquaporin-4. To clarify the hypothesis, we examined role of AQP4 expression in ethanol-induced brain edema and changes of electrolyte levels after traumatic brain injury in the rat. In the rat traumatic brain injury model, ethanol administration reduced sodium ion concentration in blood significantly 24 hr after injury. An aquaporin-4 inhibitor recovered sodium ion concentration in blood to normal. We observed low sodium ion concentration in blood and the increase of brain aquaporin-4 in cadaver with traumatic brain injury. Therefore, ethanol increases brain edema by the increase of aquaporin-4 expression with hyponatremia after traumatic brain injury.

The suppression of TRIM21 and the accumulation of IFN-α play crucial roles in the pathogenesis of osteonecrosis of the femoral head.

Osteonecrosis of the femoral head (ONFH), the pathogenesis of which remains unclear, has been observed in autoimmune disease patients treated with corticosteroids. Recently, it has been shown that anti-tripartite motif-containing 21 (TRIM21) autoantibodies, which are often present in patients with systemic lupus erythematosis and Sjögren's syndrome, inhibit the E3 ligase activity of TRIM21. TRIM21 negatively regulates nuclear factor-κB (NF-κB) and interferon regulatory factors (IRFs) 3 and 7, three downstream transcription factors, via toll-like receptor 4 signaling. The aim of this study was to clarify the role of TRIM21 in the pathogenesis of ONFH using an animal model. Male Wistar rats were injected with lipopolysaccharide (LPS) twice and with methylprednisolone (MPSL) or saline three times. N-acetyl cysteine (NAC) was administered either concurrently with MPSL or once daily for the 3 days following the last MPSL injection. The incidence of ONFH in the MPSL group was 23.5%. Co-treatment of NAC and MPSL increased the incidence of ONFH to 55.6%. MPSL treatment decreased the activity of NF-κB in the liver and significantly increased the activity of both IRF3 and IRF7. No significant differences were observed in the activity of any of these three transcription factors between the MPSL and the co-treatment groups. In the femoral head, co-treatment with NAC and MPSL significantly decreased the expression of TRIM21 at 3 h and significantly increased the expression of interferon (IFN)-α at 24 h when compared with the MPSL group. IFN-α is known to induce cell death. These findings suggest that the suppression of TRIM21 in the femoral head causes an accumulation of IFN-α, which in turn leads to the development of ONFH. In conclusion, the suppression of TRIM21 resulting from altered NF-κB and IRF homeostasis accelerates the ONFH in rats treated with corticosteroids following LPS administration.

Expression of aquaporin-4 augments cytotoxic brain edema after traumatic brain injury during acute ethanol exposure.

We previously reported that ethanol consumption affects morbidity and mortality after traumatic brain injury (TBI) by accelerating brain edema via oxidative stress after TBI. Aquaporin-4 (AQP4), a water channel, is involved in brain edema formation. In this study, we found that acute ethanol administration increased AQP4 expression after TBI, leading to severe brain edema in rats. Rats were pretreated with ethanol (3 g/kg) or dl-buthionine-(S,R)-sulfoximine (BSO; 100 mg/kg), an oxidative stressor, before TBI. Acetazolamide, an AQP4 inhibitor, was administered to ethanol-pretreated rats 3 or 12 hours after TBI. Brain edema was increased 24 hours after TBI in both the ethanol- and BSO-pretreated groups. Ethanol pretreatment induced lipid peroxidation 24 hours after TBI. Transcription factors, NF-κB and hypoxia-inducible factor-1α, were activated 3 and 24 hours after TBI in the BSO- and ethanol-pretreated groups, respectively. In the ethanol-pretreated group, AQP4 was accumulated, particularly in astrocyte end feet, 24 hours after TBI. Acetazolamide treatment improved the survival rate to 100% and decreased brain edema and AQP4 in ethanol-pretreated rats. These findings suggest that ethanol induces up-regulation of AQP4, leading to brain edema. The accumulation of AQP4 may play an important role in the augmentation of brain edema after TBI under ethanol consumption.

[Effects of alcohol consumption on traumatic brain injury].

It has been well known that alcohol consumption affects traumatic brain injury. The mechanism of detrimental effect of ethanol on traumatic brain injury has not been clarified. This review focused on the relationship among traumatic brain injury, ethanol and aquaporin-4. We have reported that ethanol increased brain edema after brain contusion and decreased survival rates in rats. It was suggested that increasing brain edema by ethanol after brain contusion may be caused by oxidative stress. Brain edema consists of cytotoxic brain edema, vasogenic brain edema, interstitial brain edema and osmotic edema. Ethanol mainly increases cytotoxic brain edema. Both alcohol consumption and brain contusion cause oxidative stress. Antioxidant treatment decreases cytotoxic brain edema. Aquaporin-4, an water channel, was increased by ethanol 24 hr after traumatic brain injury in rat. The aquaporin-4 inhibitor decreased brain edema after brain contusion and increased survival rates under ethanol consumption. Aquaporin-4 may have strict relation between ethanol and brain edema increasing after brain contusion.

Prior ethanol injection promotes brain edema after traumatic brain injury.

Alcohol consumption prior to traumatic brain injury (TBI) promotes morbidity and mortality although the mechanisms involved remain unclear. The morbidity and mortality caused by TBI, especially brain contusion, are known to be closely associated with brain edema. Here we examined the effects of ethanol pretreatment on brain edema, inflammatory responses, and oxidative stress after brain contusion. Male Wistar rats were given 3 g/kg ethanol intraperitoneally and 1 h later were subjected to brain contusion. The ethanol-pretreated group had a significantly decreased survival rate. Magnetic resonance imaging showed ethanol pretreatment significantly augmented the volume of cytotoxic brain edema after contusion. In the ethanol-pretreated rat, the activities of NF-kappaB and AP-1 were reduced 6 h after contusion and COX-2 mRNA expression was increased 24 h after contusion. These findings suggest that ethanol augmented cerebral edema and mortality in rats with brain contusion, possibly through actions on cell survival pathways or COX-2 expression. In addition, antioxidant treatment at 3 h post-injury significantly attenuated some markers of oxidative stress, mortality, and volume of edema at 24 h after ethanol treatment and contusion.

The discrepant severity of external and internal injuries in a traffic accident: The cushioning effect via a human body against direct impact: Autopsy cases.

Traffic accidents cause unexpectedly severe injuries of internal organs despite tiny injuries observed on the external body. A 51-year-old woman (subject 1) and a 54-year-old man (subject 2) were found dead on a road. Subject 1 had subcutaneous and intramuscular bleeding with décollement on the posterior aspect of her body, including upper cervical spine dislocation. Subject 2 did not exhibit any apparent findings on autopsy that were indicative of a direct injury by a motor vehicle, but had severe internal organ injuries, including the transection at the pontomedullary junction. We surmise that subjects 1 and 2 were walking in line with the vehicle which collided with them from behind, and then the body of subject 1 cushioned the direct impact of the vehicle against subject 2. This report illustrates the need of forensic autopsy for victims with no severe external injuries.

Ethanol-induced JNK activation suppressed via active Akt in hepatocytes.

Ethanol induces c-Jun N-terminal kinase (JNK) activation leading to cell death in hepatocytes. However, acute alcohol exposure does not induce remarked cell death in hepatocytes. We hypothesized that active Akt may suppress JNK activation. To clarify this point, we evaluated the role of active Akt in JNK activation under treatment with hepatocyte growth factor (HGF) and compared it with ethanol treatment. Primary rat hepatocytes were treated with 10 ng/ml HGF. 10 min after that, 5 microM insulin, an activator of the Akt pathway, and/or 5 microM LY294002, an inhibitor of the pathway, were added. Hepatocytes were treated with 100 mM ethanol and LY294002. HGF treatment increased JNK activities in hepatocytes. This JNK activation was accumulated by addition of LY294002. These finding suggest that active Akt suppresses JNK activation induced by HGF. On the other hand, addition of insulin did not decrease the JNK activity, showing that insulin-induced Akt activation may rather increase JNK activity. Ethanol also induced JNK activation and this JNK activation was enhanced by LY294002 similar to HGF treatment. We found that active Akt suppressed JNK activation induced by ethanol as well as HGF in hepatocytes. JNK activation may be suppressed by prolonged active Akt or basal active Akt, rather than peaked activation of Akt induced by insulin stimulation. Our results suggest that the suppression of JNK by active Akt may prevent cell death in acute alcohol intoxication.

Saturated and monounsaturated fatty acids increase interleukin-10 production in rat hepatocytes.

Interleukin-10 (IL-10) is a potent anti-inflammatory cytokine, but it still remains unknown whether saturated or unsaturated fatty acid affects IL-10 production in hepatocytes that contribute to lipid metabolism. Primary rat hepatocyte cultures were treated with different fatty acids (18:0 stearic acid, 18:1 oleic acid; 18:2 linoleic acid, 18:3 linolenic acid) at 300 microM for 24 hours. The concentrations of IL-2, IL-10, GM-CSF and IFN-gamma in the medium were detected by multiplex cytokine array. IL-10 was significantly increased with treatment of stearic acid and oleic acid. Production of IL-10 by saturated and monounsaturated fatty acids in hepatocytes may be one of the reasons why the lard oil had less inflammation in the hepatic steatosis animal models.