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Objective To study relationship between gene status [epidermal growth factor receptor（EGFR）, anaplastic lymphoma kinase (ALK) and ROS proto-oncogene 1, receptor tyrosine kinase (ROS1)] in cases with pathological lung adenocarcinoma lesion of maximum diameter ≤1 cm. Methods A total of 1 232 patients with lung adenocarcinoma lesion of maximum diameter ≤1 cm were enrolled in the Pathology department of Huadong Hospital from January 2013 to October 2020. For patients with multiple lesions, only the biggest lesion was selected. The gene status of EGFR, ALK and ROS1 were identified and clinicopathological characteristics were retrospectively analyzed. Results There were 387 males and 845 females，with a mean age of 54 years.There were 182 (14.8%) cases of adenocarcinomas in situ, 778 (63.1%) cases of minimal invasive adenocarcinomas, 249(20.2%) invasive non-mucinous adenocarcinomas, and 23 (1.9%) invasive mucinous adenocarcinomas. It revealed that 43.1% (352/817 cases) had EGFR gene mutations, of which 46.9% (165/352 cases) were 21L858R mutations and 40.6% (143/352 cases) were 19Del mutations, and 0.9% (3/352 cases) were 18G719X/20S768I and 21L858R/20S768I double mutations. The rate of EGFR mutation were 31.0% (40/129), 42.0% (208/495), 58.4% (104/178), and 0 (0/15) for adenocarcinoma in situ, minimal invasive adenocarcinoma, invasive non-mucinous adenocarcinoma, and invasive mucinous adenocarcinoma, respectively.And 23.1% (3/13 cases) had different EGFR mutation detected for different lesions in the same patient (In 13 cases with 2 lesions of lung adenocarcinoma successively, 2 cases were positive for 19Del mutation in the first postoperative lesion and EGFR wild-type in the second lesion: one case was EGFR wild type in the first postoperative lesion and 21L858R mutation in the second lesion). The rate of EGFR mutations was correlated with histological type and age, and not associated with sex or smoking. EGFR mutations was more likely to occur in the age group over 60 years and in invasive non-mucinous adenocarcinomas. It showed that 1.9% (22/1168 cases) were positive for ALK rearrangements, with a positive rate of 5.2% in invasive non-mucinous adenocarcinomas and of 2.6% in patients ≤60 years. The positive rate of ALK rearrangement in adenocarcinomas with solid components (22.2%, 4/18) was significantly higher than that in invasive non-mucinous adenocarcinomas (5.2%, 12/233) and adenocarcinomas without solid components (1.1%, 12/1095). It showed that 0.8% (6/795 cases) were positive for ROS1 rearrangements, independent of sex, age, smoking and histological type. A total of 382 cases were tested for EGFR, ALK and ROS1 simultaneously, of which 40.6% (155/382) of the tumours containing one of these three mutations or rearrangements status, and no co-exist in either or all three. Conclusions In this single-center study, minimal invasive adenocarcinomas accounts for the majority (63.1%) of lung adenocarcinomas with a lesion size ≤1 cm. At least 40% of them have mutations or rearrangements in one of the three genes (EGFR, ALK and ROS1)， and none of which were significantly associated with sex or smoking. The most common EGFR mutations are 21L858R and 19Del, which occur more frequently in invasive non-mucinous adenocarcinomas in the >60 age group, while ALK rearrangements occur more frequently in solid-component adenocarcinomas in the ≤60 age group. The incidence of ROS1 rearrangements is low. The molecular change may be different in the same patien to with multiple adenocarcinomas，molecular testing foci is necessary for each lesion.

In this study, we report a case of hydroa vacciniforme lymphoproliferative disorder (HVLPD). The patient, who was 21 years old at the time of initial consultation，suffering from recurrent papules, vesicular rashes, bleeding and black scabs on the neck, face and trunk. Serum EBV-DNA was significantly increased (2.88×107 copies/mL). The patient underwent skin biopsies twice within 2 years. The pathology of the first skin biopsy showed partial degeneration and loosening of the epidermal stratum spinosum, intraepidermal blister formation, partial epidermal detachment, and multifocal small abscesses seen in the blisters and stratum spinosum. Patchy infiltration of small lymphocytes, plasma cells, histiocytes, and eosinophils in the dermis, with no significant atypia of lymphocytes, EBER in situ hybridization was negative, which made it difficult to make a definitive diagnosis on pathology. The pathology of the second skin biopsy showed blisters visible within the patient's epidermis， and atypical lymphoid cells infiltrate around the hair follicles, sweat glands and blood vessels in the dermis. The immunohistochemical analysis indicated that lymphoid cells were positive for CD3, CD5, CD4, CD8, granzyme B and TIA-1, while CD56 and Perforin were negative, and the proliferation rate of Ki-67 was approximately 10%. EBER was positive by in situ hybridization consistent with clinicopathologic features of HVLPD. More than 1 year after receiving symptomatic treatment, the patient's rash worsened, with sometimes fever and left eyelid edema. The third skin biopsy performed in the other hospital showed that atypical lymphoid cells infiltrated the subcutaneous adipose tissue, and the proliferation rate of Ki-67 was 60%. The disease progressed to EBER-positive T-cell lymphoma. After 2 courses of chemotherapy with gemcitabine, cisplatin, dexamethasone and pegaspargase, the patient's edema subsided and the rash healed. This report demonstrates the clinical and pathologic features of the disease during its evolution and progression, with a view to enriching its diagnostic and therapeutic experience.

旨在为脂肪酸高产菌株的筛选和构建奠定理论基础，研究谷氨酸棒杆菌脂肪酸合成酶A（FasA）对大肠杆菌脂肪酸合成的影响，利用生物信息学软件预测分析了FasA的性质并构建过表达载体pXMJ19-fasA，转化至大肠杆菌进行表达,对表达诱导剂异丙基-β-D-硫代吡喃半乳糖苷（IPTG）浓度进行考察，并测定了异源表达后的脂肪酸组成。结果表明，重组菌株在IPTG浓度为1 mmol/L下诱导20 h，棕榈油酸和油酸产量分别达到1.735、2.325 mg/g，与对照菌株相比分别提高了53.95%和59.68%。研究结果说明FasA对大肠杆菌合成棕榈油酸和油酸有促进作用。 In order to lay a theoretical foundation for screening and constructing fatty acid high-yielding strains, the effects of Corynebacterium glutamicum fatty acid synthase A (FasA) on the synthesis of fatty acids in E. coli were studied, the properties of FasA were predicted and analyzed using bioinformatics software, moreover the overexpression vector pXMJ19-fasA was constructed and transformed into E. coli for expression, the concentration of expression inducer isopropyl-β-D-thiogalactoside (IPTG) was investigated and the fatty acid composition after heterologous expression was determined.The results showed that when the recombinant strain was induced under the IPTG concentration of 1 mmol/L for 20 h，the yield of palmitoleic acid and oleic acid reached 1.735，2.325 mg/g ，which increased by 53.95% and 59.68% respectively compared with the control strain. These results indicate that FasA can promote the synthesis of palmitoleic acid and oleic acid by E. coli.

Background The prevalence of anticancer drug-induced kidney injury is increasing, but related renal pathology studies are still rare. Objective To analyze the clinicopathological characteristics of patients with anticancer drug-related kidney injury. Methods We selected 112 cancer inpatients aged 18 years or older with kidney injury (kidney injury occurred after cancer or nearly at the same time as cancer, and may be directly or indirectly associated with anticancer treatment) detected by kidney biopsy from Department of Nephrology, the Fourth Hospital of Hebei Medical University from October 2013 to August 2021. We assigned those (n=65) who were previously treated with chemotherapy, molecularly targeted drugs or immune checkpoint inhibitors and other systemic treatments to an anticancer drug group, and other cases (n=47) to a non-use anticancer drug group. We collected their demographics, laboratory examination and pathological data, and analyzed the clinical features and pathological characteristics of kidney of those with anticancer drug-related kidney injury. Results In the anticancer drug group, acute kidney injury (AKI) occurred in 30 (50.8%) out of 59 cases of solid cancer, and in 4 out of 6 cases of hematological cancer. In non-use anticancer drug group, AKI occurred in 11 (31.4%) out of 35 cases of solid cancer, and in 6 (50.0%) out of 12 cases of hematological cancer. The serum creatinine level increased after treatment in the anticancer drug group (P0.05) . Solid cancer patients with anticancer drug treatment had higher prevalence of tubulointerstitial injury (P=0.023) and lower prevalence ofmembranous nephrosis (P=0.004) compared with those without anticancer drug treatment. Renal tubulointerstitial injury was the main pathological manifestations in the anticancer drug group〔34 cases (52.3%) 〕. Membranous nephropathy〔18 cases (38.3%) 〕and tubulointerstitial injury〔18 cases (38.3%) 〕were main pathological manifestations in the non-use anticancer drug group. Conclusion There are various clinical and pathological types of anticancer drug-induced kidney injury. The application of anticancer drug may cause damage to renal function, so priority should be given to the prevention of renal tubulointerstitial injury during the treatment.

Previous studies have shown that the apoptosis of vascular smooth muscle cells (VSMCs) underlies the mechanism of pathological calcification in patients with chronic kidney disease (CKD). SET domain-containing protein 8 (SET8) is an efficient protein that modulates apoptosis in hepatocellular carcinoma cells, esophageal squamous cells, and neuronal cells by regulating pathological processes, such as cell cycle progression and transcription regulation. However, whether SET8 is involved in high phosphorus-induced vascular calcification by mediating apoptosis remains unclear. Here, we report that SET8 is located both in the nucleus and cytoplasm and is significantly downregulated in calcification models. SET8 deficiency promoted apoptosis of VSMCs, as indicated by the increased Bax/Bcl-2 and cleaved caspase-3/total caspase-3 ratios. Mechanistically, the PI3K/Akt pathway was mediated by SET8, and inhibition of the PI3K/Akt signaling pathway by administering LY294002 or transfecting the Akt phosphorylation-inactivated mutation plasmid increased apoptosis and calcification. Akt phosphorylation constitutively activated mutations can reduce the apoptosis and calcification of VSMCs. Furthermore, exogenous overexpression of SET8 reversed the effect of PI3K/Akt inhibition on VSMC apoptosis and calcification. In summary, our research suggests that SET8 overexpression ameliorates high phosphorus-induced calcification of VSMCs by activating PI3K/Akt mediated anti-apoptotic effects. Key words: vascular calcification, SET8, PI3K/Akt Pathway, apoptosis. Des etudes anterieures ont montre que l'apoptose des cellules musculaires lisses vasculaires (CMLV) est a la base du mecanisme de calcification pathologique chez les patients atteints de maladie renale chronique (MRC). La proteine SET8 (SET domain-containing protein 8) a ete signalee a titre de proteine efficace pour moduler l'apoptose dans les cellules de carcinome hepatocellulaire, les cellules squameuses de l'oesophage et les cellules neuronales, en regulant des processus pathologiques tels que la progression du cycle cellulaire et la regulation de la transcription. Toutefois, l'implication de SET8 dans la calcification vasculaire induite par une teneur elevee en phosphore, par la mediation de l'apoptose, reste a determiner. Les auteurs ont rapporte ici que SET8 etait localisee a la fois dans le noyau et le cytoplasme, et qu'elle etait significativement regulee a la baisse dans les modeles de calcification. La deficience en SET8 favorisait l'apoptose des CMLV, comme l'indiquait l'augmentation des ratios Bax/Bcl-2 et caspase-3 clivee/caspase-3 totale. Du point de vue du mecanisme, la voie PI3K/Akt etait mediee par SET8 et l'inhibition de la voie de signalisation PI3K/Akt par l'administration de LY294002 ou la transfection d'un plasmide mute ou la phosphorylation d'Akt etait inactivee accroissait l'apoptose et la calcification. Un mutant d'Akt dont la phosphorylation etait activee de facon constitutive pouvait reduire l'apoptose et la calcification des CMLV. De plus, la surexpression exogene de SET8 pouvait renverser l'effet de l'inhibition de PI3K/Akt sur l'apoptose et la calcification des CMLV. En resume, ces recherches suggerent que la surexpression de SET8 favorise la calcification des cellules musculaires lisses vasculaires induite par une haute teneur en phosphore par l'activation des effets anti-apoptotiques medies par PI3K/Akt. [Traduit par la Redaction] Mots-cles : calcification vasculaire, SET8, voie PI3K/Akt, apoptose., Introduction Vascular calcification (VC) is the pathological deposition of calcium and phosphate in the blood vessels, which contributes to increased morbidity and mortality in patients with coronary artery disease (CAD), [...]

Objective. To explore the effect of electric function training instrument for arteriovenous fistula on vascular index of fistula and puncture success rate in patients with autogenous arteriovenous fistulization (AVF). Methods. 60 patients received AVF in the Fourth Hospital of Hebei Medical University from June 2020 to June 2021 were selected as the study subjects, and they were divided into the treatment group (TG, n = 30) and the reference group (RG, n = 30) according to the random number table method. The patients in the RG received routine pressure training by clench fist and tourniquet after surgery, and the TG used electric function training instrument for arteriovenous fistula on the basis of routine clench fist, then comprehensively evaluating the clinical application value of this study protocol by comparing the vascular index of fistula and puncture success rate of the two groups. Results. The depth of cephalic vein to skin at T2 and T3 in the TG was notably lower than the RG (P < 0.05), and the vessel diameter of cephalic vein at T3 in the TG was visibly higher than the RG (P < 0.05), with no overt difference in the rate of fistula complication, one-time puncture success rate and the incidence of puncture injury in both groups (P > 0.05). The score of functional exercise compliance of fistula in the TG was clearly higher than the RG (P < 0.001). Conclusion. The study results suggest that the use of electric function training instrument for arteriovenous fistula after AVF is more effective, so it has certain clinical application value. [ABSTRACT FROM AUTHOR]