Objective To explore the differences in stress distribution and stability of the planta pedis in the patients with unilateral and bilateral plantar fasciitis(PF)through plantar stress and center of pressure(COP)analysis.Methods A total of 100 patients with PF visiting in this hospital were enrolled,among them 50 cases were unilateral heel pain(unilateral heel pain group)and 50 cases were bilateral heel pain(bilateral heel pain).Meanwhile,50 healthy subjects were included(healthy group).In the health group and bilateral heel pain groups,the average stress value of both planta pedis surfaces of each subject was taken and named as the J0 group and H2 group,respectively.In the unilateral heel pain group,the plantar stress in 50 healthy feet and 50 affected feet were named as the J1 group and H1 group,respectively.The plantar pedis was divided into 10 regions for analysis and comparison[the first foot toe(T1),T2-5,the first-fifth metatarsal bones(M1-M5),the mid foot(MF),heel medial side(MH),heel lateral side(LH)].The subjects in 3 groups conducted the static and dynamic tests respectively,and the differences in plantar stress distribution and COP parameters among the J1,H1,H2 and J0 groups were compared respectively.Results In the static tests,the maximum pressure of the LH regions in the group J1 was increased when compared with the group J0,the contact area of LH regions in the group H1 was reduced when compared with the group J0,the maximum pressure of the M2 and M3 regions in the H1 group was increased when compared with the group J0,the contact areas of the MH and LH regions in the H2 group were decreased when compared with the group J0,the maximum pressure of the M1 region was increased when compared with the group J0,and the differences were statistically significant(P<0.05).In the dynamic tests,the maximum pressure of the T2-5 regions in the J1 group was increased when compared with the J0 group,the maximum pressure of the M3 region in the group H1 was increased when compared with the group J0,the maximum pressure of the M3 and M4 region in the group H2 was in-creased when compared with the group J0,and the differences were statistically significant(P<0.05).The COP 95%confidence ellipse area in the health group was the smallest,followed by the bilateral heel pain group,and finally the unilateral heel pain group,and the differences among 3 groups were statistically signifi-cant(P<0.05),there was also statistically significant difference between pairwise comparisons in 3 groups(P<0.05).Conclusion In the static condition,the pressure of the healthy heel and affected forefoot in the patients with PF is increased;while in the dynamic condition,the pressure of the toes of the healthy foot and forefoot of the affected foot in the patients with PF is also increased.The distribution of plantar stress in the patients with PF has larger difference compared with the healthy population,and the stability is poor.Meas-ures can be taken to improve the abnormal force on the foot,reduce pain and reduce the risk of falling.

Objective To investigate the impact of minocycline(MC)on myocardial cell damage in rats with chronic heart failure(CHF)by regulating the hypoxia-inducible factor 1α(HIF-1α)/B-cell lymphoma-2/adenovirus E1B 19-kDa interacting protein(BNIP3).Methods All rats were randomly divided into Sham,CHF,positive drug(LP),low dose MC,high dose MC(HMC),and HMC+HIF-1α activator(DMOG)groups.Cardiac function was detected using echocardiography.HE staining,transmission electron microscopy,and TUNEL assay were used to evaluate myocardial pathology and apoptosis.Enzyme-linked immunosorbent assay was applied to quantify tumor necrosis factor α(TNF-α),interleukin-1β,superoxide dismutase(SOD),and malondialdehyde(MDA).Quantitative real-time PCR was used to detect the mRNA levels of Bcl-2 and Bcl-2-related X protein(Bax),while Western blotting was applied to detect the expres-sion of HIF-1α,BNIP3,Beclin-1,and microtubule-associated protein 1 light chain 3(LC3)proteins.Results Compared to rats in the sham group,rats from the CHF group exhibited increased left ventricular end-diastolic diameter(LVEDD),left ventricular end-systolic diameter(LVESD),cell apoptosis rate,TNF-α,IL-1β,MDA,Bax,HIF-1α,BNIP3,Beclin-1,and LC3Ⅱ/Ⅰwith decreased left ventricular ejection fraction(LVEF),left ventricular shortening fraction(LVFS),SOD,and Bcl-2 levels(P<0.05).Compared with CHF group,rats from LP group,LMC group and HMC group exhibited decreased levels of LVEDD,LVESD,apoptosis rate,TNF-α,IL-1β,MDA,Bax,HIF-1α,BNIP3,Beclin-1,LC3Ⅱ/Ⅰ,and increased levels of LVEF,LVFS,SOD and Bcl-2(P<0.05).DMOG attenuated the protective effect of high-dose MC on myocardial cell damage in rats of the CHF group(P<0.05).Conclusion MC improves myocardial cell damage in rats of CHF group by inhibiting the HIF-1α/BNIP3 signaling pathway.

Objective:To investigate the influence of TGF-β1 on the malignant transformation of bystander cells after proton irradiation simulating space radiation, and its underlying mechanism.Methods:Normal human bronchial epithelial cells BEAS-2B were exposed to proton irradiation at 0, 0.2, 0.5, and 1.0 Gy to simulate space radiation. Supernatants from cell culture media were collected as a conditioned medium (CM) for treating bystander BEAS-2B cells. The enzyme-linked immunosorbent assay (ELISA) was employed to detect TGF-β1 levels within the CM. The soft agar colony formation assay was performed to assess the rate of malignant transformation of bystander cells. Immunofluorescence and Western blot techniques were utilized to examine the localization of β-arrestin1 in CM-treated bystander cells, with or without the TGF-β1 receptor inhibitor SB525334. The malignant transformation of bystander cells was assessed via soft agar colony formation assay under CM treatment, combined with either a TGF-β1 receptor inhibitor or β-arrestin1 knockdown. Additionally, mRNA and protein levels of epithelial-mesenchymal transition(EMT)-related genes (e.g., E-cadherin, N-cadherin, Fibronectin1, and Vimentin) were analyzed through qRT-PCR and Western blot, respectively.Results:Contrasting with the 0 Gy group, the proton irradiation groups exhibited a dose-dependent increase in TGF-β1 secretion after 24 h ( t=3.38, 8.32, 10.96, P<0.05), and a corresponding rise in the soft agar colony formation rate of CM-treated bystander cells ( t=5.04, 7.20, 10.78, P<0.05). Immunofluorescence and Western blot results indicated that with escalating doses, CM-treated bystander cells showed increased β-arrestin1 into nuclei ( t=7.57, 7.51, P<0.05), being stimulated by TGF-β1 and inhibited by SB525334. The SB525334 application or β-arrestin1 knockdown significantly inhibited the malignant transformation and EMT induced by proton irradiation in bystander cells. This inhibition further reduced the soft agar colony formation rate ( t=2.84, 3.39, P<0.05), and increased mRNA and protein levels of the E-cadherin gene in CM-treated bystander cells exposed to 1 Gy proton irradiation ( t=7.33, 5.38, P<0.05) while reducing the mRNA and protein levels of N-cadherin, Fibronectin1, and Vimentin genes ( t=4.37, 4.10, 5.29, 10.65, 5.15, 3.11, P<0.05). Conclusions:Proton irradiation simulating space radiation can enhance TGF-β1 secretion from lung epithelial cells, inducing β-arrestin1 into nuclei in bystander cells, thereby spurring the malignant transformation of cells. The TGF-β1/β-arrestin1 pathway plays a crucial role in this process.

Objective:To investigate the differential responses of the endoplasmic reticulum stress-to-apoptosis cascade induced by proton ultra-high dose rate (FLASH) irradiation between lung epithelial and lung cancer cells.Methods:Human lung epithelial cells (KT) and lung adenocarcinoma cells (A549) were irradiated with protons, and divided into Ctrl, CONV and FLASH groups. Survival curves were generated using colony formation assay. Protein and mRNA expressions of the endoplasmic reticulum (ER) stress and apoptosis regulators were assessed via Western blot and RT-qPCR. The concentration of IL-6 secreted into the culture supernatant was determined by enzyme-linked immunosorbent assay(ELISA).Results:In KT cells, compared to the CONV group, FLASH irradiation resulted in a significantly higher survival fraction ( P<0.05), increased GRP78 protein expression ( t= 7.52, P < 0.05) and UPR-related genes PERK, ATF4, and CHOP. In A549, the cell survival rate did not differ significantly between the CONV and FLASH groups ( P > 0.05). UPR pathway was not activated in either group. However, both CONV and FLASH irradiation significantly promoted secretion of IL-6 ( t=4.31, 4.47, P<0.05), while no difference was identified between two groups. In KT, both irradiation promoted secretion of IL-6 ( t=7.43, 3.07, P<0.05) while IL-6 concentration in FLASH group was significantly lower than that in CONV group ( t=7.63, P<0.05). Additionally, a pro-apoptotic propensity in KT cells following FLASH irradiation and in A549 cells following both FLASH and CONV irradiation was identified. Conclusions:In KT cells, FLASH irradiation cleared misfolded proteins through activating UPR pathway, promoted apoptosis of damaged cells, suppressed IL-6 secretion to attenuate inflammatory injury, and ultimately enhanced cell survival. Furthermore, proton FLASH irradiation bypasses ER stress activation in A549 cells, instead directly priming an apoptotic disposition with concomitant IL-6 hypersecretion. This paracrine damage amplification cascade potentiates radiation-induced tumoricidal efficacy through sustained cytotoxic microenvironment remodeling.

Gliomas, with their infiltrative growth and malignant potential, present considerable therapeutic challenges. Maximal safe resection is essential for optimizing patient survival and quality of life. Despite this, existing intraoperative visualization techniques suffer from limited sensitivity and accuracy. Label-free Raman spectroscopy has emerged as a non-invasive, rapidly diagnostic, and highly accurate technique. It accurately diagnoses tumors, identifies infiltration margins, and classifies molecular subtypes, enhancing the precision of glioma surgery. This review summarizes the latest advances and applications of label-free Raman spectroscopy in glioma surgery.

Gliomas, with their infiltrative growth and malignant potential, present considerable therapeutic challenges. Maximal safe resection is essential for optimizing patient survival and quality of life. Despite this, existing intraoperative visualization techniques suffer from limited sensitivity and accuracy. Label-free Raman spectroscopy has emerged as a non-invasive, rapidly diagnostic, and highly accurate technique. It accurately diagnoses tumors, identifies infiltration margins, and classifies molecular subtypes, enhancing the precision of glioma surgery. This review summarizes the latest advances and applications of label-free Raman spectroscopy in glioma surgery.

Objective To investigate the impact of minocycline(MC)on myocardial cell damage in rats with chronic heart failure(CHF)by regulating the hypoxia-inducible factor 1α(HIF-1α)/B-cell lymphoma-2/adenovirus E1B 19-kDa interacting protein(BNIP3).Methods All rats were randomly divided into Sham,CHF,positive drug(LP),low dose MC,high dose MC(HMC),and HMC+HIF-1α activator(DMOG)groups.Cardiac function was detected using echocardiography.HE staining,transmission electron microscopy,and TUNEL assay were used to evaluate myocardial pathology and apoptosis.Enzyme-linked immunosorbent assay was applied to quantify tumor necrosis factor α(TNF-α),interleukin-1β,superoxide dismutase(SOD),and malondialdehyde(MDA).Quantitative real-time PCR was used to detect the mRNA levels of Bcl-2 and Bcl-2-related X protein(Bax),while Western blotting was applied to detect the expres-sion of HIF-1α,BNIP3,Beclin-1,and microtubule-associated protein 1 light chain 3(LC3)proteins.Results Compared to rats in the sham group,rats from the CHF group exhibited increased left ventricular end-diastolic diameter(LVEDD),left ventricular end-systolic diameter(LVESD),cell apoptosis rate,TNF-α,IL-1β,MDA,Bax,HIF-1α,BNIP3,Beclin-1,and LC3Ⅱ/Ⅰwith decreased left ventricular ejection fraction(LVEF),left ventricular shortening fraction(LVFS),SOD,and Bcl-2 levels(P<0.05).Compared with CHF group,rats from LP group,LMC group and HMC group exhibited decreased levels of LVEDD,LVESD,apoptosis rate,TNF-α,IL-1β,MDA,Bax,HIF-1α,BNIP3,Beclin-1,LC3Ⅱ/Ⅰ,and increased levels of LVEF,LVFS,SOD and Bcl-2(P<0.05).DMOG attenuated the protective effect of high-dose MC on myocardial cell damage in rats of the CHF group(P<0.05).Conclusion MC improves myocardial cell damage in rats of CHF group by inhibiting the HIF-1α/BNIP3 signaling pathway.

Objective:To investigate the influence of TGF-β1 on the malignant transformation of bystander cells after proton irradiation simulating space radiation, and its underlying mechanism.Methods:Normal human bronchial epithelial cells BEAS-2B were exposed to proton irradiation at 0, 0.2, 0.5, and 1.0 Gy to simulate space radiation. Supernatants from cell culture media were collected as a conditioned medium (CM) for treating bystander BEAS-2B cells. The enzyme-linked immunosorbent assay (ELISA) was employed to detect TGF-β1 levels within the CM. The soft agar colony formation assay was performed to assess the rate of malignant transformation of bystander cells. Immunofluorescence and Western blot techniques were utilized to examine the localization of β-arrestin1 in CM-treated bystander cells, with or without the TGF-β1 receptor inhibitor SB525334. The malignant transformation of bystander cells was assessed via soft agar colony formation assay under CM treatment, combined with either a TGF-β1 receptor inhibitor or β-arrestin1 knockdown. Additionally, mRNA and protein levels of epithelial-mesenchymal transition(EMT)-related genes (e.g., E-cadherin, N-cadherin, Fibronectin1, and Vimentin) were analyzed through qRT-PCR and Western blot, respectively.Results:Contrasting with the 0 Gy group, the proton irradiation groups exhibited a dose-dependent increase in TGF-β1 secretion after 24 h ( t=3.38, 8.32, 10.96, P<0.05), and a corresponding rise in the soft agar colony formation rate of CM-treated bystander cells ( t=5.04, 7.20, 10.78, P<0.05). Immunofluorescence and Western blot results indicated that with escalating doses, CM-treated bystander cells showed increased β-arrestin1 into nuclei ( t=7.57, 7.51, P<0.05), being stimulated by TGF-β1 and inhibited by SB525334. The SB525334 application or β-arrestin1 knockdown significantly inhibited the malignant transformation and EMT induced by proton irradiation in bystander cells. This inhibition further reduced the soft agar colony formation rate ( t=2.84, 3.39, P<0.05), and increased mRNA and protein levels of the E-cadherin gene in CM-treated bystander cells exposed to 1 Gy proton irradiation ( t=7.33, 5.38, P<0.05) while reducing the mRNA and protein levels of N-cadherin, Fibronectin1, and Vimentin genes ( t=4.37, 4.10, 5.29, 10.65, 5.15, 3.11, P<0.05). Conclusions:Proton irradiation simulating space radiation can enhance TGF-β1 secretion from lung epithelial cells, inducing β-arrestin1 into nuclei in bystander cells, thereby spurring the malignant transformation of cells. The TGF-β1/β-arrestin1 pathway plays a crucial role in this process.

Objective:To investigate the differential responses of the endoplasmic reticulum stress-to-apoptosis cascade induced by proton ultra-high dose rate (FLASH) irradiation between lung epithelial and lung cancer cells.Methods:Human lung epithelial cells (KT) and lung adenocarcinoma cells (A549) were irradiated with protons, and divided into Ctrl, CONV and FLASH groups. Survival curves were generated using colony formation assay. Protein and mRNA expressions of the endoplasmic reticulum (ER) stress and apoptosis regulators were assessed via Western blot and RT-qPCR. The concentration of IL-6 secreted into the culture supernatant was determined by enzyme-linked immunosorbent assay(ELISA).Results:In KT cells, compared to the CONV group, FLASH irradiation resulted in a significantly higher survival fraction ( P<0.05), increased GRP78 protein expression ( t= 7.52, P < 0.05) and UPR-related genes PERK, ATF4, and CHOP. In A549, the cell survival rate did not differ significantly between the CONV and FLASH groups ( P > 0.05). UPR pathway was not activated in either group. However, both CONV and FLASH irradiation significantly promoted secretion of IL-6 ( t=4.31, 4.47, P<0.05), while no difference was identified between two groups. In KT, both irradiation promoted secretion of IL-6 ( t=7.43, 3.07, P<0.05) while IL-6 concentration in FLASH group was significantly lower than that in CONV group ( t=7.63, P<0.05). Additionally, a pro-apoptotic propensity in KT cells following FLASH irradiation and in A549 cells following both FLASH and CONV irradiation was identified. Conclusions:In KT cells, FLASH irradiation cleared misfolded proteins through activating UPR pathway, promoted apoptosis of damaged cells, suppressed IL-6 secretion to attenuate inflammatory injury, and ultimately enhanced cell survival. Furthermore, proton FLASH irradiation bypasses ER stress activation in A549 cells, instead directly priming an apoptotic disposition with concomitant IL-6 hypersecretion. This paracrine damage amplification cascade potentiates radiation-induced tumoricidal efficacy through sustained cytotoxic microenvironment remodeling.