The factors influencing the occurrence of post-ischemic stroke depression and its relationship with the burden score of cerebral small vessel disease.

OBJECTIVE: This study explored the determinants of post-stroke depression (PSD) in ischemic stroke (AIS) patients and its association with the burden score of cerebral small vessel disease (CSVD). PATIENTS AND METHODS: We analyzed 374 AIS patients treated between January 2020 and January 2022. Patients were categorized into 90 with PSD and 284 without PSD, enabling an investigation into PSD risk factors and the CSVD-PSD relationship. RESULTS: There was no significant difference in health factors between PSD and non-PSD patients (p>0.05). However, significant disparities were noted in age, gender, initial Barthel Index (BI), Mini-Mental State Examination (MMSE) score, plasma fibrinogen, homocysteine, red cell distribution width, National Institutes of Health Stroke Scale (NIHSS) score, and CSVD burden score (p<0.05). Regression analysis indicated that these variables were pivotal PSD predictors (OR>1, p<0.05). Surprisingly, a positive correlation with PSD occurrence was found for age, NIHSS score, plasma fibrinogen, homocysteine levels, red cell distribution width, CSVD burden score (r=0.565, 0.615, 0.482, 0.514, 0.572, 0.608, respectively; p<0.05). Meanwhile, the MMSE score and BI index were inversely related to PSD onset (r=-0.604, -0.590; p<0.05). The ROC curve analysis of the combination model based on MMSE, NIHSS and CSVD score revealed an AUC of 0.926 and Youden's index of 0.744. CONCLUSIONS: Age, MMSE score, BI index, NIHSS score, plasma fibrinogen concentration, homocysteine level, red blood cell distribution width, and CSVD burden score are all major influencing factors in the occurrence of PSD. The combination model based on MMSE, NIHSS, and CSVD scores presented a valuable approach to predicting PSD.

[Early results of left ventricular assist device implantation for the treatment of heart failure].

Twenty-four male patients who underwent left ventricular assist device (LVAD) implantation due to advanced heart failure in Union Hospital, Fujian Medical University from June 2019 to June 2022 were retrospectively included. The age of patients was 32-61 (48.4±8.4) years. Everheat-Ⅰ, HeartCon and Corheart 6 left ventricular assist systems were used in 10, 6 and 8 cases, respectively. All patients were discharged successfully without mechanical failure, thrombosis or secondary thoracotomy for hemostasis. Early postoperative hemodynamics were significantly improved, left ventricular systolic diameter was reduced, left ventricular ejection fraction was gradually improved, and no hemolysis occurred. The patients were followed up for 3 to 39 (17.9±8.6) months, the cardiac function was restored to grade Ⅰ to Ⅱ, and the 6-minute walking test distance increased significantly. Therefore, satisfactory early results can be achieved with left ventricular assist device implantation for the treatment of heart failure.

The new-generation proteasome inhibitor oprozomib increases the sensitivity of cervical cancer cells to cisplatin-induced apoptosis.

This study aimed to evaluate the anti-tumor effect of a new generation of protease inhibitor, oprozomib (OPZ), used alone and in combination with cisplatin, also called CDDP, on cervical cancer. Five different types of cervical cancer cell lines - HeLa, Caski, HeLa-CDDP, C33a, and SiHa - and one nontransformed cervical cell line - HaCaT -were treated with OPZ alone or in combination with cisplatin. The inhibitory effects of OPZ and cisplatin on the proliferation of cervical cancer cells were then analyzed using cytotoxicity tests, flow cytometry, and Western blotting. It was found that OPZ alone or in combination with cisplatin can reduce the proliferation of the five types of cancer cells by enhancing the lysis of caspase-3 and PARP and inducing cancer cell apoptosis. In the combined treatment, OPZ was found to inhibit the degradation of inhibitory factor κB alpha induced by cisplatin, thereby inhibiting the activation of NF-κB, which causes cisplatin resistance, and enhancing the sensitivity of the tumor cells to cisplatin. Moreover, OPZ promoted the phosphorylation of the apoptosis signaling pathway JNK that was activated by cisplatin, thereby inducing tumor cell apoptosis. These findings provide a theoretical basis for the clinical use of OPZ alone and in combination with cisplatin in the treatment of cervical cancer.

The relationship between endoplasmic reticulum stress and liver function, insulin resistance and vascular endothelial function in patients with non-alcoholic fatty liver disease.

OBJECTIVE: The aim of the study was to investigate the relationship between ER stress and liver function, insulin resistance and vascular endothelial function in patients with non-alcoholic fatty liver disease. PATIENTS AND METHODS: A total of 95 patients with non-alcoholic fatty liver disease were selected. They were admitted to our hospital from November 2016 to January 2019. A total of 90 cases of obese patients without fatty liver were selected as control group during the same period. The levels of ER stress marker protein were compared between the two groups, and the relationship between ER stress and liver function, insulin resistance, and vascular endothelial function was analyzed. RESULTS: The protein level of ER stress markers in the test group was significantly higher than that in the control group (p<0.05). The liver function index and insulin resistance level were significantly higher than those in the control group (p<0.05). The level of vascular endothelial function was significantly lower than that of the control group (p<0.05). Pearson correlation analysis showed that ER stress marker protein was positively correlated with liver function and insulin resistance (p<0.05), while ER marker protein was negatively correlated with vascular endothelial function (p<0.05). CONCLUSIONS: Liver function and insulin resistance are closely related to ER stress in patients with non-alcoholic fatty liver disease. Insulin resistance is one of the factors inducing and aggravating endothelial dysfunction.

[Mechanism of nano-indium-tin oxide inducing pulmonary alveolar proteinosis in Sprague-Dawley rats].

Objective: To investigate the pathogenesis of pulmonary alveolar proteinosis in rats induced by nano-indium-tin oxide exposure, and to provide a basis for further determining the limit of occupational exposure to indium and developing related protection measures. Methods: In August 2018, a total of 40 specific pathogen-free Sprague-Dawley rats, with an age of 6-8 weeks and a body weight of (200±10) g, were randomly divided into control group, low-dose group (1.2 mg/kg) , middle-dose group (3 mg/kg) , and high-dose group (6 mg/kg) , with 10 rats in each group. After 1 week of routine feeding, the rats were given non-exposed intratracheal instillation twice every week, with an interval of 3 days, for 12 consecutive weeks. Body weight was measured every week during exposure to observe the change in body weight; The rats were anesthetized and sacrificed by chloral hydrate after the exposure ended, and lung tissue and serum were collected; Hematoxylin-eosin staining and periodic acid-Schiff (PAS) staining were performed for lung tissue to observe pathological results; Inductively coupled plasma mass spectrometry was used to measure the serum level of indium; ELISA was used to measure the levels of surfactant protein A (SP-A) , surfactant protein D (SP-D) , and the type II alveolar cell surface antigen Krebs von den Lungen-6 (KL-6) in lung tissue and the serum level of granulocyte-macrophage colony-stimulating factor (GM-CSF) . Results: The pathological results showed that the rats in the control group had basically complete alveolar structure, and after intratracheal instillation of nano indium-tin oxide, uniform, eosinophilic, and unstructured granular substances were observed in the alveolar space of the low-, middle-, and high-dose exposure groups, with macrophage proliferation and an increase in macrophages, especially in the high-dose group. Negative PAS staining was observed in the control group, while substances with positive PAS staining were observed in lung tissue in each exposure group. The three exposure groups had a significantly higher serum level of indium than the control group (P<0.05) . Compared with the control group, the three exposure groups had significant increases in SP-A, SP-D, and KL-6 in lung tissue and a significant reduction in GM-CSF in serum (P<0.05) . Conclusion: Pulmonary alveolar proteinosis in rats may be associated with the destruction of alveolar macrophages caused by nano-indium-tin oxide and the aggregation of pulmonary surfactants due to disorders in the metabolism and clearance of pulmonary surfactants by macrophages.

[Gastric adenocarcinoma with enteroblastic differentiation and elevated serum alpha fetoprotein].

Objective: To study the proportion and clinicopathological characteristics of gastric adenocarcinoma with enteroblastic differentiation (GAED) in gastric cancers showing an elevated serum alpha fetoprotein(AFP). Methods: A total of 724 resected gastric adenocarcinomas were collected from 2008 to 2018 at the 904 Hospital of Joint Service Support Force, and cases with pre-operative serum AFP>10 µg/L were screened. From the cases with elevated serum AFP, GAED cases were further evaluated based on morphology. Then the clincopathological features and immunohistochemical phenotypes of GAED were reviewed. In addition, the amplification of HER2 gene was detected with fluorescence in situ hybridization(FISH). When overall survival (OS) and progression-free survival (PFS) of GAED were analyzed, 289 cases ordinary gastric adenocarcinoma with normal serum AFP were employed as a control. Results: The percentage of GAED was 44% (11/25) in gastric cancers with elevated serum AFP. GAED was histologically tubular or papillary with clear cytoplasm, and some GAED cases showed cystadenoid structure similar to embryo sac (5 cases), homogeneous eosinophilic granules (4 cases) and intragland ulareosinophilic material (6 cases). All 11 GAED cases had lymph node metastasis. Liver metastasis and vascular thrombus were observed in 2 cases and 5 cases respectively. GAED was immunohistochemically positive for CDX2 (11/11), CD10 (8/11) and MUC2(3/11), which were intestinal epithelium differentiation markers. Meanwhile, primitive markers SALL4 (8/11), GPC3 (7/11) and AFP (5/11) were also expressed in GAED, and HER2 gene amplification was found in 3 cases (3/11) of GAED. Lastly, the PFS of GAED were significantly shorter than that of the control group (P=0.02), while OS was not statistically different between these two groups (P=0.99). Conclusions: Patients with GAED usually have a higher rate of elevated serum AFP in gastric adenocarcinoma, and the cancer exhibites features of both intestinal and primitive differentiation. As GAED is highly invasive, the prognosis of GAED may be poor. For GAED, the diagnosis of well-differentiated or moderately-differentiated adenocarcinoma should be avoided, because this diagnosis leads to underestimated malignant potential.

Element Specificity of Transient Extreme Ultraviolet Magnetic Dichroism.

In this work we combine theory and experiment to study transient magnetic circular dichroism (TRMCD) in the extreme ultraviolet spectral range in bulk Co and CoPt. We use the ab initio method of real-time time-dependent density functional theory to simulate the magnetization dynamics in the presence of short laser pulses. From this we demonstrate how TRMCD may be calculated using an approximation to the excited-state linear response. We apply this approximation to Co and CoPt and show computationally that element-specific dynamics of the local spin moments can be extracted from the TRMCD in the extreme ultraviolet energy range, as is commonly assumed. We then compare our theoretical prediction for the TRMCD for CoPt with experimental measurement and find excellent agreement at many different frequencies including the M_{23} edge of Co and N_{67} and O_{23} edges of Pt.

[Contrast-enhanced CT and texture analysis of mass-forming pancreatitis and cancer in the pancreatic head].

Objective: To explore the value of contrast-enhanced CT combined with texture analysis in differentiating pancreatic cancer from mass-forming pancreatitis in pancreatic head. Methods: A retrospective study collected 21 patients with pancreatic head mass-forming pancreatitis confirmed by surgery or biopsy and 47 patients with pancreatic ductal adenocarcinoma confirmed by surgery. The patients visited the Affiliated Hospital of Nanjing University of Chinese Medicine and the First Affiliated Hospital of Wannan Medical College between January 2014 and December 2017. Gender, age and CT findings were collected. The parenchymal phase was selected for texture analysis. The minimum absolute shrinkage and selection operator (LASSO) method was applied for dimensionality reduction.Two independent sample t-tests or Mann-Whitney U test were used for continuous variables based on the Shapiro-Wilks normality test results. Categorical variables were tested by Chi-square or Fisher test. By multivariable regression analysis, CT findings, CT texture analysis, CT findings combined with texture analysis prediction models were established. The receiver operating characteristic (ROC) curve was used to evaluate the diagnostic performance of individual indicators and each prediction model. The Delong test was used to compare the area under the curve (AUC) of each model. Results: The CT findings prediction model consisted of CT value of lesion on pancreatic parenchymal phase and pancreatic duct penetrating sign. The texture analysis prediction model consists of root mean square and low grey level run emphasis_angle135. The AUC of them were not statistically different (Z=0.150,P>0.05). The combined predictive model had the better diagnostic performance (AUC 0.944, sensitivity 83.0%, specificity 95.2%, +LR 17.43, -LR 0.18) than CT sign prediction model (Z=2.008, P<0.05) and texture analysis prediction model(Z=2.236, P<0.05) were significantly different. Conclusions: The CT findings model and the texture analysis model have equivalent diagnostic performance in the differentiation of mass-forming pancreatitis and pancreatic cancer. The enhanced CT combined with texture analysis model has the best diagnostic efficiency and can further improve the diagnostic ability.

[Altered serum cytokine expression profile in systemic sclerosis and its regulatory mechanisms].

OBJECTIVE: To analyze the expression profile of serum cytokines in patients with systemic sclerosis (SSc) and explore its possible regulatory mechanisms. METHODS: Serum and DNA of peripheral blood mononuclear cells were collected from 30 SSc patients and 80 normal controls (NCs). According to the presence or absence of interstitial lung disease (ILD) in SSc, the patients were divided into SSc with ILD group and SSc without ILD group. According to the degree of skin involvement, the patients were divided into diffuse systemic scleroderma (dcSSc) group and limited systemic scleroderma (lcSSc) group. According to the presence of anti-topoisomerase-1 antibody (anti-Scl-70 antibody) in the serum of patients with SSc, they were divided into SSc Scl-70 (+) group and SSc Scl-70 (-) group. 27 cytokines in serum were detected by Luminex MAGPIX detection system and Bio-Plex Pro Human Cytokine 27-plex Assay kit: interleukin-1ß (IL-1ß), interleukin-1 receptor antagonist (IL-1ra), IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-9, IL-10, IL-12P70, IL-13, IL-15, IL-17, basic fiber growth factor (BASIC FGF), eotaxin, granulocyte colony stimulating factor (G-CSF), granulocyte-macrophage colony stimulating factor (GM-CSF), interferon-γ (IFN-γ), interferon-gamma induced protein 10(IP-10), monocyte chemotactic protein 1(MCP-1), macrophage inflammatory protein-1α (MIP-1α), macrophage inflammatory protein 1ß(MIP-1ß), platelet-derived growth factor BB (PDGF-BB), regulated on activation in normal T-cell expressed and secreted (RANTES), tumor necrosis factor-α (TNF-α), and vascular endothelial growth factor(VEGF). Methylation sites were detected by Illumina 450K methylation chip. RESULTS: Compared with NCs group, the expression of 12 cytokines (BASIC FGF, eotaxin, G-CSF, GM-CSF, IFN-γ, IL-1ß, IL-1ra, IL-6, IP-10, MCP-1, TNF-α and RANTES) in the SSc group significantly increased (P<0.05), IL-5 was decreased expression in the SSc group (P<0.05), there was no significant difference in the expressions of the other 14 cytokines. Compared with lcSSc group, 9 cytokines (eotaxin, IL-5, MCP-1, IL-2, RANTES, IL17A, IL-8, MIP-1ß and PDGF-BB) increased in dcSSc group, but there was no significant difference. Compared with SSc without ILD group, IL-15 increased in SSC with ILD group [18.2 (172.97) ng/L vs. 2.03(0.05) ng/L, P<0.05]. Compared with SSc Scl-70 (-) group, the expression of IP-10 decreased in SSc Scl-70 (+) group [1 030 (2 196.6) ng/L vs. 1 878 (2 964) ng/L, P<0.05]. The correlation analysis of serum cytokines with erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) showed that IL-6 was positively correlated with ESR (r =0.04, P= 0.017), MCP-1 (r=0.49, P=0.043) and MIP-1ß (r=0.41, P=0.007) positively correlated with CRP. By analyzing the changes of methylation sites of cytokines, it was found that cg17744604 in IL-10 TSS1500 region, cg06111286 in IL-12P70 TSS200 region, cg07935264 in IL-1ß TSS200 region, cg01467417 in IL-1ra TSS1500 region, cg03989987 in IL-1ra 5'UTR region and cg21099624 in VEGF TSS200 region were all hypomethylated. CONCLUSION: There were different cytokines expression profiles in the serum of SSc patients, and the altered cytokines were correlected with the degree of skin damage and pulmonary fibrosis. Many cytokines were regulated by methylation.

FAL1 regulates endothelial cell proliferation in diabetic arteriosclerosis through PTEN/AKT pathway.

OBJECTIVE: This study aims to investigate the role of FAL1 in the occurrence and progression of diabetic arteriosclerosis and its underlying mechanism. PATIENTS AND METHODS: FAL1 expression in coronary artery disease (CAD) tissues, normal artery tissues, and tumor necrosis factor-α (TNF-α)-induced endothelial cells was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The regulatory effects of FAL1 on cell proliferation, migration, and cell cycle were examined by cell counting kit-8 (CCK-8) assay, transwell assay, and flow cytometry, respectively. Western blot was used to detect protein expressions of proliferation-related gene PCNA (proliferating cell nuclear antigen), cell cycle-related genes cyclin D1, PTEN (phosphatase and tensin homolog deleted on chromosome ten) and AKT (protein kinase B) in HUVECs. Subsequently, rescue experiments were performed to assess whether PTEN/AKT signaling pathway is activated during the process of FAL1-regulated proliferation and migration of HUVECs. RESULTS: FAL1 was highly expressed in CAD tissues and TNF-α-induced endothelial cells compared with that of controls. Overexpression of FAL1 in HUVECs promoted cell cycle, proliferation, and migration. FAL1 activated PTEN/AKT pathway in HUVECs, which was partially reversed by PTEN overexpression. CONCLUSIONS: Highly expressed FAL1 can promote proliferation and migration of endothelial cells through activating PTEN/AKT signaling pathway.

CdS nanoparticles of different lengths induce differential responses in some of the liver functions of mice.

Cadmium sulfide nanoparticles (CdS NPs) are one of important nanoparticle materials which are widely used in photoelectric production, but their potential health hazard to the liver is not clear. This study is aimed at exploring the possible mechanisms of liver injury induced by CdS NPs. Male mice were treated with nanoparticles of 110-130 nm and 80-100 nm cadmium sulfide. The main methods were based on detecting the vigor of superoxide dismutase (SOD) and glutathione (GSH), and content of malondialdehyde (MDA) in both blood and liver tissues as well as on observing the pathological changes in liver tissue. CdS NPs suppressed the activity of SOD and GSH, and increased the serum MDA content (p < 0.05); both effects were observed together in liver tissues of 80-100 nm group (p < 0.05) and were accompanied by an obviously inflammatory response. CdS NPs induced oxidative damage and inflammatory response in liver tissue, which may be an underlying mechanism for its pulmonary toxicity. Additionally, the toxicity of CdS NPs was closely related to the size of nanoparticles. Pathological results showed that the hepatotoxicity of shorter CdS NPs is greater than that of longer CdS NPs (Tab. 6, Fig. 3, Ref. 20).

[Analysis and treatment of postoperative blockage of tympanic ventilation tubes].

Objective:To explore the occurrence and treatment of complications of postoperative blockage of tympanic ventilation tubes.Method:Two hundred and four patients(278 ears)with otitis media with effusion(OME) who received tympanostomy tube insertion from February 2010 to February 2016 were retrospectively analyzed．Ofloxacin ear drops was introduced into 80 ears in 59 patients undergoing myringotomy and ventilation tube insertion. In a follow-up period of 1,3,6,12 months,if the blockage is caused by viscid secretion,blood clot or cerumen,4% of sodium bicarbonate ear drops were used to treat patients. 3% aquae hydrogenii dioxidi and Ofloxacin ear drops were used on the patients with purulent otorrhea.Result:In the 198 ears without Ofloxacin ear drops treatment,postoperative tube obstruction occurred in 16 ears(8 of viscid secretion,3 of blood clot,3 of cerumen and 2 of purulent otorrhea). Of the 59 patients who received Ofloxacin ear drops treatment,seven ears experienced blocked tubes(1 of viscid secretion,1 of blood clot,4 of cerumen and 1 of purulent otorrhea).Conclusion:The complication of postoperative blockage of tympanic ventilation tubes is common. Relative prevention and therapy should be performed during intraoperative and postoperative procedures. Short term treatment of Ofloxacin ear drops can prevent postoperative blockage of tympanic ventilation tubes and infection.

Association between transcription factor 7-like 2 genetic polymorphisms and development of type 2 diabetes in a Chinese population.

We conducted a hospital-based case-control study to evaluate the relationship between the transcription factor 7-like 2 (TCF7L2) rs7903146 polymorphism and type 2 diabetes mellitus risk in a Chinese population. Genotyping of TCF7L2 rs7903146 was carried out using the polymerase chain reaction-restriction fragment length polymorphism method. A chi-square test revealed a statistically significant difference between the distributions of rs7903146 genotypes in type 2 diabetes mellitus patient and control groups (chi-square = 10.49, P = 0.005). Using unconditional logistic regression analysis, we observed that the TT genotype of this polymorphism was significantly correlated with increased risk of developing type 2 diabetes mellitus compared to the CC genotype [odds ratio (OR) = 2.31, 95% confidence interval (CI) = 1.33-4.04]. Furthermore, we found that the rs7903146 sequence variation was also significantly associated with susceptibility to this disease under dominant (OR = 1.58, 95%CI = 1.09-2.28) and recessive models  (OR = 2.11, 95%CI = 1.25-3.62). We conclude that the TCF7L2 rs7903146 genetic polymorphism is independently associated with the risk of developing type 2 diabetes mellitus under co-dominant, dominant, and recessive models.

Arraying Autoantibodies in SLE - Lessons Learned.

Systemic lupus erythematosus (SLE) is a chronic autoimmune connective tissue disease characterized by the production of a large number of autoantibodies, but the etiology is complex and poorly understood. A range of different platforms have served as screening methods for the determination of autoantibody specificities over the past few decades. Proteomic microarray is a relatively new high-throughput technology which is playing an increasingly important role in autoantibody diagnostics. In this article, we review different platforms for assaying autoantibodies in SLE, and highlight the use of autoantigen arrays as powerful tools for autoantibody exploration in SLE.

Correlation analysis of the PNPLA7 gene polymorphism and susceptibility to menstrual disorder.

We examined the correlation between PNPLA7 gene polymorphisms at the rs61754920 and rs11137410 loci and menstrual disorder in women of reproductive age in the Central Plain. Genomic DNA was extracted from peripheral blood; polymerase chain reaction-ligase detection reaction and SNaPshot genotyping were used to detect polymorphisms in the rs61754920 and rs11137410 gene loci, respectively. The results for the 2 loci in individuals of different blood types were statistically analyzed. The proportion of the AA homozygote at the rs61754920 locus in the PNPLA7 gene was the lowest, while the proportion of the CC homozygote at the rs11137410 locus in the PNPLA7 gene was the highest. There were no statistical differences in the frequency distribution of genotypes and alleles at the 2 loci between control and test groups. The frequency of the TT genotype at the rs11137410 locus in women with type O blood was significantly lower in the test group than in the control group. Frequencies of the C and T alleles were significantly different between the 2 groups. There may be an association between the PNPLA7 gene and type O blood or a combined effect of the 2 genes.

Resistin as a potential marker of renal disease in lupus nephritis.

Systemic lupus erythematosus (SLE) and lupus nephritis (LN) have strong concomitance with cardiovascular disease that cannot be explained fully by typical risk factors. We examined the possibility that serum or urine expression of adipokines may act as biomarkers for LN, as these proteins have been associated previously with cardiovascular disease as well as SLE. Antibody arrays were performed on serum and urine from lupus patients and matched controls using a cross-sectional study design. From the initial array-based screening data of 15 adipokines, adiponectin, leptin and resistin were selected for validation by enzyme-linked immunosorbent assay (ELISA). Correlations were determined between adipokine expression levels and measures of disease activity or lupus nephritis. The expression of adiponectin and resistin was increased in both sera and urine from LN patients, while leptin was increased in LN patient sera, compared to matched controls. Serum resistin, but not urine resistin, was correlated with measures of renal dysfunction in LN. Serum resistin expression may be useful as a marker of renal dysfunction in patients with LN, although longitudinal studies are warranted. Further studies are necessary to determine if resistin has functional consequences in LN.

Microstructural fingerprints of phase transitions in shock-loaded iron.

The complex structural transformation in crystals under static pressure or shock loading has been a subject of long-standing interest to materials scientists and physicists. The polymorphic transformation is of particular importance for iron (Fe), due to its technological and sociological significance in the development of human civilization, as well as its prominent presence in the earth's core. The martensitic transformation α→ε (bcc→hcp) in iron under shock-loading, due to its reversible and transient nature, requires non-trivial detective work to uncover its occurrence. Here we reveal refined microstructural fingerprints, needle-like colonies and three sets of {112}<111> twins with a threefold symmetry, with tell-tale features that are indicative of two sequential martensitic transformations in the reversible α→ε phase transition, even though no ε is retained in the post-shock samples. The signature orientation relationships are consistent with previously-proposed transformation mechanisms, and the unique microstructural fingerprints enable a quantitative assessment of the volume fraction transformed.