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Background Our previous work suggested biological potential alterations in chondrogenic progenitor cells (CPCs) during knee osteoarthritic progression. The Wnt pathway plays a pivotal role in osteoarthritis progression, and Dickkopf-3 (DKK3) is a noncanonical Wnt antagonist. However, it remains unclear whether the DKK3 expression level is involved in the changes of the biological characteristics of CPCs during OA progression. This study aimed to explore the difference of DKK3 expression in osteochondral specimens and corresponding CPCs during osteoarthritis progression. Furthermore, the influence of DKK3 on the in vitro characteristics and in vivo therapeutic efficacy of CPCs was investigated. Methods The expression levels of DKK3 in human paired grade 1–2 and grade 3–4 osteoarthritic cartilage and corresponding CPCs were determined via immunohistochemical staining and western blotting, respectively. CPCs were isolated, cultured and characterized for their self-renewal and multidifferentiation abilities. Then, the CPCs were transfected with Lentiviral-DKK3 or siRNA to overexpress or knock down DKK3, respectively. The chondrogenic potential of the CPCs was examined via pellet staining and gene detection. The expression levels of inflammatory factors in different groups of CPCs were examined via qRT‒PCR and ELISA. The activation status of β-catenin in Wnt signalling was investigated via confocal microscopy. The in vivo chondroprotective effects of LV-DKK3 and Si-DKK3–transgenic CPCs were examined in a rat model of posttraumatic osteoarthritis. Results The DKK3 expression level was significantly increased in Grade 3–4 cartilage compared with Grade 1–2 cartilage. However, the DKK3 expression level was significantly lower in Grade 3–4 CPCs than in Grade 1–2 CPCs. The overexpression of DKK3 significantly increased CPC chondrogenic potential and inhibited the expression of catabolic factors, whereas the knockdown of DKK3 had the opposite effects, decreasing CPC chondrogenic potential and increasing the expression of catabolic factors. Wnt signalling was significantly inhibited by DKK3. The in vivo results suggested that lentivirus-induced LV-dkk3 significantly delayed the progression of experimental OA, whereas lentivirus-mediated Si-DKK3, which aimed to silence endogenous DKK3, accelerated the progression of experimental OA. Conclusion Our results suggest that DKK3 has a chondroprotective effect during osteoarthritis progression and that CPCs may be functional targets. The underlying mechanisms of DKK3 may include enhancing CPC chondrogenic capacity and inhibiting Wnt-mediated expression of catabolic factors and matrix remodelling activities. These findings indicate that DKK3 is a potential therapeutic target for CPC-mediated OA treatment.

Sebaceous carcinoma (SC) of the submandibular gland is extremely rare. Owing to the low morbidity and nonspecific clinical manifestations, diagnosis is commonly delayed, which increases metastasis and mortality. To date, there have been five reported cases of SC of the submandibular gland. Here, we present a new case and review the relevant literature. A 36-year-old woman presented with an enlarged left submandibular gland. Clinical features included a non-tender solitary nodular mass with normal overlying skin. There were no special findings on computed tomography or ultrasound examination except for a swollen mass in the left submandibular gland. The patient underwent surgical resection. Pathological examination confirmed the diagnosis of SC with nerve infiltration. Immunohistochemical examination of this case showed positive staining for P63, P40, CK7, CK8/18, MLH1, MSH2, MSH6, and PMS2. The specimen was negative for androgen receptor, CEA, S-100, CK5/6, SOX-10, SOX-11, SMA, and GCDFP-15. The KI-67 labeling index was determined to be 15%. PAS and anti-epithelial membrane antigen were positive in partial area. The patient is still undergoing follow-up, and no metastasis or recurrence has been observed for 2 months. This case highlighted the fact that despite its rarity, SC should be considered as a differential diagnosis for masses located in the head and face. Early and accurate diagnosis, followed by wide surgical excision, has a favorable prognosis. Therefore, clinicians should be familiar with the clinical and pathological features of this disease.

The existence of H2S has limited the biogas energy promotion. The traditional photodegradation of H2S is usually conducted in the presence of O2, yet this is unsuitable for biogas desulfurization which should be avoided. Therefore, the ultraviolet degradation of H2S in the absence of O2 was investigated for the first time in the present study from a mathematical point of view. Light wavelength and intensity applied were 185 nm and 2.16 × 10−12 Einstein/cm2·s, respectively. Firstly, the mathematical model of H2S photodegradation was established with MATLAB software, including the gas flow distribution model and radiation model of photoreactor, kinetics model, mass balance model, and calculation model of the degradation rate. Then, the influence of the initial H2S concentration and gas retention time on the photodegradation rate were studied, for verification of the mathematical model. Results indicated that the photodegradation rate decreased with the increase in initial H2S concentration, and the maximum photodegradation rate reached 62.8% under initial concentration of 3 mg/m3. In addition, the photodegradation rate of H2S increased with the increase in retention time. The experimental results were in good accordance with the modeling results, indicating the feasibility of the mathematical model to simulate the photodegradation of H2S. Finally, the intermediate products were simulated and results showed that the main photodegradation products were found to be H2 and elemental S, and concentrations of the two main products were close and agreed well with the reaction stoichiometric coefficients. Moreover, the concentration of free radicals of H• and SH• was rather low.

It has been shown that prostaglandin (PG) E 2 synthesized in the lateral parabrachial nucleus (LPBN) is involved in lipopolysaccharide-induced fever. But the neural mechanisms of how intra-LPBN PGE 2 induces fever remain unclear. In this study, we investigated whether the LPBN-preoptic area (POA) pathway, the thermoafferent pathway for feed-forward thermoregulatory responses, mediates fever induced by intra-LPBN PGE 2 in male rats. The core temperature (T core ) was monitored using a temperature radiotelemetry transponder implanted in rat abdomen. We showed that microinjection of PGE 2 (0.28 nmol) into the LPBN significantly enhanced the density of c-Fos-positive neurons in the median preoptic area (MnPO). The chemical lesioning of MnPO with ibotenate or selective genetic lesioning or inhibition of the LPBN-MnPO pathway significantly attenuated fever induced by intra-LPBN injection of PGE 2 . We demonstrated that EP3 receptor was a pivotal receptor for PGE 2 -induced fever, since microinjection of EP3 receptor agonist sulprostone (0.2 nmol) or EP3 receptor antagonist L-798106 (2 nmol) into the LPBN mimicked or weakened the pyrogenic action of LPBN PGE 2 , respectively, but this was not the case for EP4 and EP1 receptors. Whole-cell recording from acute LPBN slices revealed that the majority of MnPO-projecting neurons originating from the external lateral (el) and dorsal (d) LPBN were excited and inhibited, respectively, by PGE 2 perfusion, initiating heat-gain and heat-loss mechanisms. The amplitude but not the frequency of spontaneous and miniature glutamatergic excitatory postsynaptic currents (sEPSCs and mEPSCs) in MnPO-projecting LPBel neurons increased after perfusion with PGE 2 ; whereas the frequency and amplitude of spontaneous inhibitory postsynaptic currents (sIPSCs) and the A-type potassium ( I A ) current density did not change. In MnPO-projecting LPBd neurons, neither sEPSCs nor sIPSCs responded to PGE 2 ; however, the I A current density was significantly increased by PGE 2 perfusion. These electrophysiological responses and the thermoeffector reactions to intra-LPBN PGE 2 injection, including increased brown adipose tissue thermogenesis, shivering, and decreased heat dissipation, were all abolished by L-798106, and mimicked by sulprostone. These results suggest that the pyrogenic effects of intra-LPBN PGE 2 are mediated by both the inhibition of the LPBd-POA pathway through the EP3 receptor-mediated activation of I A currents and the activation of the LPBel-POA pathway through the selective enhancement of glutamatergic synaptic transmission via EP3 receptors.

The effect of steel strip-feeding ratio and superheat degree of molten steel on density and segregation of casting ingot is investigated by an original position analysis. It indicates that under the same degree of superheat condition, with the increase of feeding ratio, the average density of the casting ingot increases and the central segregation of the ingot decreases. Under the same feeding ratio conditions, the density and the central segregation increase with the increase of the degree of superheat.

To determine the dopamine (DA) content in the striatum and the expression changes of the apoptosis-associated proteins Bad and Bcl-2 in the substantia nigra compacta (SNc) in elderly rats with abnormal behavior. Fifty three Sprague–Dawley rats were divided into three groups: adult, age-motorplus (normal behavior) and aged-motorminus (abnormal behavior) using the hanger test. The DA content in the striatum and the expression of tyrosine hydroxylase (TH), Bad and Bcl-2 in the SNc were measured by HPLC/MS (high performance liquid chromatogram–mass spectra) and Western Blot. (1) The results from the hanger test demonstrated that the scores and latency of aged-motorminus group were lower than the age-motorplus group. (2) Results from HPLC-MS showed that, compared with the age-motorplus and adult group, the content of DA in elderly rat striata decreased significantly, with a statistically significant difference. (3) The Western Blot demonstrated that, compared with the adults, the expression of TH in elderly rats significantly decreased, but the difference was not significant between the aged-motorminus group and the age-motorplus group. Compared with the age-motorplus and the adult group, the expression of Bad increased but Bcl-2 decreased in the aged-motorminus group. The decrease in TH content in the SNc correlated with the aging of rats. The decrease in DA content in the striatum may correlate with the abnormal behavior in elderly rats, which could be ascribed to the variations in Bad and Bcl-2.

Systemic inflammation, which can be induced by metabolic endotoxemia, and corresponding high-fat diet-mediated metabolic disorders are associated with gut microbiota. In the present study reverse transcription-polymerase chain reaction, immunofluorescence, pyrosequencing, ELISA and Oil Red O staining were performed to assess whether berberine can protect against diet-induced obesity, through modulating the gut microbiota and consequently improving metabolic endotoxemia and gastrointestinal hormone levels. Alterations in the gut microbiota induced by berberine resulted in a significant reduction in bacterial lipopolysaccharide levels in portal plasma. Levels of inflammatory and oxidative stress markers, as well as the mRNA expression levels of macrophage infiltration markers in visceral adipose tissue, were also reduced by berberine. Inhibition of the inflammatory response was associated with a reduction in intestinal permeability and an increase in the expression of tight junction proteins. In addition, berberine was reported to restore aberrant levels of gut hormones in the portal plasma, such as glucagon-like peptide-1 and −2, peptide YY, glucose-dependent insulinotropic polypeptide and pancreatic polypeptide. The present findings indicated that berberine, through modulating gut microbiota, restored the gut barrier, reduced metabolic endotoxemia and systemic inflammation, and improved gut peptide levels in high-fat diet-fed rats. The present study suggests that berberine may be an effective therapeutic strategy for the treatment of obesity and insulin resistance.

Cr-coated diamond/Cu composites were prepared by spark plasma sintering. The effects of sintering pressure, sintering temperature, sintering duration, and Cu powder particle size on the relative density and thermal conductivity of the composites were investigated in this paper. The influence of these parameters on the properties and microstructures of the composites was also discussed. The results show that the relative density of Cr-coated diamond/Cu reaches ~100% when the composite is gradually compressed to 30 MPa during the heating process. The densification temperature increases from 880 to 915℃ when the diamond content is increased from 45vol% to 60vol%. The densification temperature does not increase further when the content reaches 65vol%. Cu powder particles in larger size are beneficial for increasing the relative density of the composite.

It has been shown that prostaglandin (PG) E synthesized in the lateral parabrachial nucleus (LPBN) is involved in lipopolysaccharide-induced fever. But the neural mechanisms of how intra-LPBN PGE induces fever remain unclear. In this study, we investigated whether the LPBN-preoptic area (POA) pathway, the thermoafferent pathway for feed-forward thermoregulatory responses, mediates fever induced by intra-LPBN PGE in male rats. The core temperature (T ) was monitored using a temperature radiotelemetry transponder implanted in rat abdomen. We showed that microinjection of PGE (0.28 nmol) into the LPBN significantly enhanced the density of c-Fos-positive neurons in the median preoptic area (MnPO). The chemical lesioning of MnPO with ibotenate or selective genetic lesioning or inhibition of the LPBN-MnPO pathway significantly attenuated fever induced by intra-LPBN injection of PGE . We demonstrated that EP3 receptor was a pivotal receptor for PGE -induced fever, since microinjection of EP3 receptor agonist sulprostone (0.2 nmol) or EP3 receptor antagonist L-798106 (2 nmol) into the LPBN mimicked or weakened the pyrogenic action of LPBN PGE , respectively, but this was not the case for EP4 and EP1 receptors. Whole-cell recording from acute LPBN slices revealed that the majority of MnPO-projecting neurons originating from the external lateral (el) and dorsal (d) LPBN were excited and inhibited, respectively, by PGE perfusion, initiating heat-gain and heat-loss mechanisms. The amplitude but not the frequency of spontaneous and miniature glutamatergic excitatory postsynaptic currents (sEPSCs and mEPSCs) in MnPO-projecting LPBel neurons increased after perfusion with PGE ; whereas the frequency and amplitude of spontaneous inhibitory postsynaptic currents (sIPSCs) and the A-type potassium (I ) current density did not change. In MnPO-projecting LPBd neurons, neither sEPSCs nor sIPSCs responded to PGE ; however, the I current density was significantly increased by PGE perfusion. These electrophysiological responses and the thermoeffector reactions to intra-LPBN PGE injection, including increased brown adipose tissue thermogenesis, shivering, and decreased heat dissipation, were all abolished by L-798106, and mimicked by sulprostone. These results suggest that the pyrogenic effects of intra-LPBN PGE are mediated by both the inhibition of the LPBd-POA pathway through the EP3 receptor-mediated activation of I currents and the activation of the LPBel-POA pathway through the selective enhancement of glutamatergic synaptic transmission via EP3 receptors.

（38vo1% SiCp ＋ 2vo1% A1203f）/2024 A1 composites were fabricated by pressure infiltration. Graphite powder was introduced as a forming filler in preform preparation, and the effects of the powder size on the microstructures and mechanical properties of the final com- posites were investigated. The results showed that the composite with 15 μm graphite powder as a forming filler had the maximum tensile strength of 506 MPa, maximum yield strength of 489 MPa, and maximum elongation of 1.2%, which decreased to 490 MPa, 430 MPa, and 0.4%, respectively, on increasing the graphite powder size from 15 to 60 μm. The composite with 60 μm graphite powder showed the highest elastic modulus, and the value decreased from 129 to 113 GPa on decreasing the graphite powder size from 60 to 15 μm. The differences between these properties are related to the different microstructures of the corresponding composites, which determine their failure modes.