With the development of clinical related disciplines, the update and establishment of relevant standards/guidelines at home and abroad, GBZ 185-2006 Diagnostic Criteria for Occupational Medicamentose-like Dermatitis due to Trichloroethylene (hereinafter referred to as “GBZ 185-2006”) was unable to meet clinical needs. Therefore, the GBZ 185-2006 was revised based on the principles of evidence-based medicine, in accordance with relevant laws/regulations and relevant standards/guidelines in combination with review of research data on occupational medicamentose-like dermatitis due to trichloroethylene (OMDT) home and abroad, and the development of clinical practice and clinical related disciplines. The main modifications include: adding terms and definitions of OMDT, modifying the description of clinical manifestations of the diagnostic principles, adjusting the description of latency, deleting the diagnostic requirement of the incidence probability, adding the specific allergen patch test as the etiological diagnostic index, standardizing the application scope, operating procedure and precautions of the specific allergen patch test. In addition, the relevant content of “Basic Characteristics and Clinical Types of Skin Damage of Medicamentose-like Dermatitis due to Trichloroethylene” in Appendix A is improved, the treatment principles are revised, and the content of new progress in treatment, artificial liver application, are added. The revised GBZ 185-2024 Diagnostic Standard for Occupational Medicamentose-like Dermatitis due to Trichloroethylene is more scientific and practical, and can provide technical basis for the standardized diagnosis and treatment of OMDT in medical and health institutions.

Objective To analyze the clinical manifestations of delayed serological transfusion reactions(DSTR)after platelet transfusion in tumor patients,and to explore the transfusion strategy.Methods Clinical data and laboratory test re-sults of patients with positive antibody screening were analyzed after platelet transfusion in our hospital from January 1,2015 to June 30,2023,and the incidence rate,clinical characteristics and transfusion strategy of patients with DSTR were ana-lyzed.Results A total of 2 553 patients with 6 057 platelet transfusions were reviewed.Eight patients developed DSTR and received a total of 21 therapeutic amounts of platelets,and 5 patients were subsequently transfused with red blood cells.Rh system antibodies were detected in 7 cases(4 anti-E,1 anti-c/E,1 anti-C and 1 anti-c)and Kell system antibodies in 1 case.Conclusion Tumor patients may also develop DSTR after platelet transfusion.It is necessary to pay close attention to the antibody situation and perform matched transfusion when transfusing blood again.

Patients with severe trauma require an extremely timely treatment and transfusion plays an irreplaceable role in the emergency treatment of such patients. An increasing number of evidence-based medicinal evidences and clinical practices suggest that patients with severe traumatic bleeding benefit from early transfusion of low-titer group O whole blood or hemostatic resuscitation with red blood cells, plasma and platelet of a balanced ratio. However, the current domestic mode of blood supply cannot fully meet the requirements of timely and effective blood transfusion for emergency treatment of patients with severe trauma in clinical practice. In order to solve the key problems in blood supply and blood transfusion strategies for emergency treatment of severe trauma, Branch of Clinical Transfusion Medicine of Chinese Medical Association, Group for Trauma Emergency Care and Multiple Injuries of Trauma Branch of Chinese Medical Association, Young Scholar Group of Disaster Medicine Branch of Chinese Medical Association organized domestic experts of blood transfusion medicine and trauma treatment to jointly formulate Chinese expert consensus on blood support mode and blood transfusion strategies for emergency treatment of severe trauma patients ( version 2024). Based on the evidence-based medical evidence and Delphi method of expert consultation and voting, 10 recommendations were put forward from two aspects of blood support mode and transfusion strategies, aiming to provide a reference for transfusion resuscitation in the emergency treatment of severe trauma and further improve the success rate of treatment of patients with severe trauma.

Objective:Hereditary neuropathy with liability to pressure palsy(HNPP)is a rare autosomal dominant peripheral neuropathy,usually caused by heterozygous deletion mutations in the peripheral myelin protein 22(PMP22)gene.This study aims to investigate the clinical and molecular genetic characteristics of HNPP. Methods:HNPP patients in the Department of Neurology at Third Xiangya Hospital of Central South University from 2009 to 2023 were included in this study.The general clinical data,nervous electrophysiological and molecular genetic examination results were collected and analyzed.Molecular genetic examination was to screen for deletion of PMP22 gene using multiplex ligation-dependent probe amplification(MLPA)after extracting genomic DNA from peripheral blood;and if no PMP22 deletion mutation was detected,next-generation sequencing was used to screen for PMP22 point mutations.The related literatures of HNPP were reviewed,and the clinical and molecular genetic characteristics of HNPP patients were analyzed. Results:A total of 34 HNPP patients from 24 unrelated Chinese Han families were included in this study,including 25 males and 9 females.The average age at illness onset was 22.0 years.Sixty-two point five percent of the families had a positive family history.Among them,30 patients had symptoms of peripheral nerve paralysis.Patients often presented with paroxysmal single limb weakness with(or)numbness(25/30),and some patients had paroxysmal unilateral recurrent laryngeal nerve(vagus nerve)paralysis(2/30).Physical examination revealed muscle weakness(23/29),hypoesthesia(9/29),weakened or absent ankle reflexes(20/29),distal limb muscle atrophy(8/29)and high arched feet(5/29).Most patients(26/30)could fully recover to normal after an acute attack.Thirty-one patients in our group underwent nervous electrophysiological examination,and showed multiple demyelinating peripheral neuropathies with both motor and sensory nerves involved.Most patients showed significantly prolonged distal motor latency(DML),mild to moderate nerve conduction velocity slowing,decreased amplitude of compound muscle action potential(CMAP)and sensory nerve action potential(SNAP),and sometimes with conduction block.Nerve motor conduction velocity was(48.5±5.5)m/s,and the CMAP amplitude was(8.4±5.1)mV.Nerve sensory conduction velocity was(37.4±10.5)m/s,and the SNAP amplitude was(14.4±15.2)μV.There were 24 families,23 of whom had the classical PMP22 deletion,the last one had a heterozygous pathogenic variant in the PMP22 gene sequence(c.434delT).By reviewing clinical data and genetic testing results of reported 1 734 HNPP families,we found that heterozygous deletion mutation of PMP22 was the most common pathogenic mutation of HNPP(93.4%).Other patients were caused by PMP22 small mutations(4.0%),PMP22 heterozygous gross deletions(0.6%),and PMP22 complex rearrangements(0.1%).Thirty-eight sorts of HNPP-related PMP22 small mutations was reported,including missense mutations(10/38),nonsense mutations(4/38),base deletion mutations(13/38),base insertion mutations(3/38),and shear site mutations(8/38).HNPP patients most often presented with episodic painless single nerve palsy.Common peroneal nerve,ulnar nerve,and brachial plexus nerve were the most common involved nerves,accounting for about 75%.Only eighteen patients with cranial nerve involved was reported. Conclusion:Heterozygous deletion mutation of PMP22 is the most common pathogenic mutation of HNPP.Patients is characterized by episodic and painless peripheral nerve paralysis,mainly involving common peroneal nerve,ulnar nerve,and other peripheral nerves.Nervous electrophysiological examination has high sensitivity and specificity for the diagnosis of HNPP,which is manifested by extensive demyelinating changes.For patients with suspected HNPP,nervous electrophysiological examination and PMP22-MLPA detection are preferred.Sanger sequencing or next generation sequencing can be considered to detect other mutations of PMP22.

Objective:To investigate the mechanism of human placenta derived mesenchymal stem cells (hPMSCs) in the inhibition of TNF-α secretion in CD4 + IFN-γ + T cells (Th1) through CD73/nuclear factor-erythroid 2-related factor 2(Nrf2) pathway to reduce liver injury in mice with graft versus-host disease (GVHD). Methods:Flow cytometry (FCM) was used to analyze the expression of TNF-α in Th1 cells and the expression of PD-1 on CD4 + IFN-γ + TNF-α + T cells (TNF-α + Th1 cells) isolated from peripheral blood and liver tissues of mice with GVHD. Hematoxylin-hosin (HE) staining, Masson staining and immunofluorescence staining were used to observe the pathological changes in liver tissues of GVHD mice in each group. HE staining was also used to observe the pathological changes in skin and lung tissues of GVHD mice. A nonconditional protocol to induce the differentiation of peripheral blood mononuclear cells (PBMCs) into Th1 cells in vitro was established. The proportion of TNF-α + Th1 cells and the mean fluorescence intensity (MFI) of Nrf2 and phosphorylated nuclear factor-kappa B (p-NF-κB) in this T cell subgroup were detected. Results:Compared with the normal control group, the proportion of TNF-α + Th1 cells and the expression of PD-1 on this T cells in peripheral blood and liver tissues of mice in the GVHD high group increased significantly ( P<0.01). The proportion of TNF-α + Th1 cells in peripheral blood and liver tissues decreased after hPMSCs treatment ( P<0.001), but the expression of PD-1 on this T cell subset was promoted in peripheral blood and liver tissues ( P<0.01, P<0.001). However, the intervention effects of shCD73 on TNF-α + Th1 cells in peripheral blood and liver tissues were significantly weakened ( P<0.05, P<0.01). Liver histopathological analysis showed that the proportion of TNF-α + Th1 cells in liver was positively correlated with Suzuki′s score, collagen area and the MFI of α-SMA ( P<0.001). Similarly, histopathological analysis of skin and lung tissues also showed that the proportion of TNF-α + Th1 cells in peripheral blood was positively correlated with skin Marina score and lung Shukai Qiao score ( P<0.001). In vitro experiment also showed that hPMSCs down-regulated the proportion of TNF-α + Th1 cells ( P<0.01) and up-regulated the expression of PD-1 on them ( P<0.05). Further analysis showed that hPMSCs could enhance the MFI of Nrf2 ( P<0.05) and weaken the MFI of p-NF-κB ( P<0.01) in TNF-α + Th1 cells. Conclusions:hPMSCs could up-regulate the expression of PD-1 through CD73/Nrf2 pathway to inhibit the formation of TNF-α + Th1 cells, thereby alleviating liver injury in GVHD mice.

【Objective】 To evaluate the detection and distribution characteristics of anti-P1 in tumor patients, so as to aid in blood screening and transfusion safety. 【Methods】 The clinical data of 112 658 tumor patients who underwent blood preparation and transfusion in our hospital from January 2014 to December 2021 were retrospectively analyzed, and column agglutination technique was used to perform transfusion compatibility test. 【Results】 A total of 1 079 (0.96%, 1 079/112 658) cases were detected with unexpected antibodies, of which 71 (6.58%, 71/1 079) were identified as anti-P1. In anti-P1 cases, 59.15% (42/71) were males; 60.56% had no pregnancy history (P<0.01); 29.58% (21/71), 52.11%(37/71), 12.68%(9/71) and 5.63%(4/71) of anti-P1 patients were with type A, B, O and AB, respectively. 57 cases of anti-P1 patients (80.28%) had difficulty in ABO blood group identification. The incidence of interfering in patients with type B was higher than that of other blood types (P<0.05), as the frequency of w+ in reverse blood typing was higher than other reactive patterns (P<0.05). The incidence of gastric tumor and brain space-occupying lesion in patients with anti-P1 was higher than that in patients with other alloantibodies, while the incidence of gynecological tumors was lower (P<0.05). 【Conclusion】 Anti-P1 affects the ABO blood group identification of tumor patients, and most of them had difficulty in ABO blood group identification. Compared with patients with other alloantibodies, patients with anti-P1 are more likely to be male and suffer from gastric and brain tumors, but less likely from gynecological tumors.

Since the global COVID-19 pandemic, SARS-CoV-2 infection, which causes COVID-19, has been associated with a range of diseases whose atypical manifestations have been increasingly reported. The mild encephalitis or encephalopathy associated with reversible corpus callosum lesions or mild encephalitis/encephalopathy with reversible splenial lesion (MERS) is a rare clinical and radiographic syndrome. At present, the pathogenesis of MERS caused by COVID-19 is still unclear, and its pathogenesis may include hypoxic damage, inflammatory response, immune disorders, changes in osmotic pressure, excitatory amino acid toxicity, oxidative stress and functional abnormalities of renin-angiotensin system. This paper reports a case of severe COVID-19 complicated with MERS, and discusses the pathogenesis from a pathophysiological point of view.

Objective:To investigate the mechanism of IL-6 affecting the expression of CD73 on human placenta-derived mesenchymal stem cells (hPMSCs) and regulating their migration, adhesion and proliferation.Methods:Flow cytometry (FCM) and Western blot were used to analyze the effects of exogenous IL-6 or IL-6 secreted by hPMSCs on the expression of CD73 on hPMSCs. The influence of IL-6 on the phosphorylation of signal transducer and activator of transcription 3 (p-STAT3) in hPMSCs was detected by monoclonal antibody blocking test and Western blot. Real-time cellular analysis (RTCA) was used to analyze the changes in the migration, adhesion and proliferation of hPMSCs after knockdown of CD73 expression or APCP pretreatment.Results:FCM and Western blot showed that both exogenous and autocrine IL-6 from hPMSCs promoted the expression of CD73 on hPMSCs ( P<0.001, P<0.01). Moreover, CD73 expression decreased significantly with the presence of IL-6R inhibitor ( P<0.01). IL-6 could up-regulate the levels of both p-STAT3 and CD73 in hPMSCs ( P<0.05, P<0.01), while CD73 expression decreased after adding STAT3 inhibitor ( P<0.01). RTCA showed that knockdown of CD73 expression on hPMSCs significantly inhibited the adhesion and proliferation ability of hPMSCs( P<0.01, P<0.05), but promoted the migration ability of hPMSCs ( P<0.05). Similarly, inhibiting the hydrolase activity of CD73 on hPMSCs by APCP also resulted in a significant decrease in the adhesion and proliferation capacities of hPMSCs, and an increase in the migration capacity of hPMSCs ( P<0.05). Conclusions:IL-6 enhanced the expression of CD73 on hPMSCs via the JAK/STAT3 pathway, thus affecting the migration, adhesion and proliferation of hPMSCs.

【Objective】 To analyze ABO subtype samples from tumor patients using both blood group serology and molecular biology technology. 【Methods】 32 samples of ABO subtype, identified by routine blood group serology in the Department of Transfusion, of solid tumor patients treated in Cancer Hospital of Chinese Academy of Medical Sciences from July 2014 to December 2019 were analyzed by sequence specific primer polymerase chain reaction (PCR-SSP) and gene sequencing (PCR-SBT). 5 samples were detected by PCR-SSP, 28 PCR-SBT, 1 both PCR-SSP and PCR-SBT. The serological and genotyping results were comparatively analyzed. 【Results】 66% (21/32) of the samples in this study were confirmed as ABO subtypes or harbored mutations by genotyping assays, including 7 cases of B(A).04, 2 of B(A).02, 1 of cis AB.01, 3 of BW.12, 4 of BEL.03, 1 of AEL.02, 1 of B 974G>C, 1 of A 797insT, and 1 of A 617C>G. Among the 21 subtype samples or harbored mutations, 15 had the same blood group serology and genotyping results, and 6 had no A or B antigen detected in the serological adsorption-elution test. An additional 34% (11/32) of the samples had no variants in the gene responsible for ABO subtype detected by molecular analysis. 【Conclusion】 Molecular biology techniques can assist in the identification of difficult ABO blood types caused by weakened antigens or antibodies, and subtypes in solid tumor patients, which is an important auxiliary method for accurate identification of difficult ABO blood group.

Objective:To investigate the role of IL-1β in regulating human placenta-derived mesenchymal stem cells (hPMSCs) to induce the differentiation of activated peripheral blood mononuclear cells (PBMCs) into CD8 + IL-10 + T cell subset in patients with rheumatoid arthritis (RA). Methods:Serum IL-1β levels in RA patients were detected by CBA kit. hPMSCs were isolated from healthy subjects by enzyme digestion. PBMCs that were isolated from RA patients and healthy subjects by Ficoll density gradient centrifugation were activated with PHA and CD3/CD28 monoclonal antibody (McAb) and then co-cultured with hPMSCs. Flow cytometry (FCM) was used to analyze the ability of hPMSCs to induce the differentiation of activated PBMCs into CD8 + IL-10 + T cell subset with the presence of programmed death ligand 1 (PD-L1) and/or PD-L2 McAb and IL-1β. Expression of PD-L1 and PD-L2 on hPMSCs under IL-1β stimulation was analyzed by RT-PCR and FCM. Results:Serum IL-1β levels were significantly higher in RA patients than in healthy subjects. After the activation by PHA and CD3/CD28 McAb, the proportion of CD8 + IL-10 + T cells in PBMCs of RA patients was significantly lower than that of healthy subjects. Moreover, the proportion of CD8 + IL-10 + T cells significantly increased after co-cultured with hPMSCs. The ability of IL-1β-treated hPMSCs to induce activated PBMCs to differentiate into CD8 + IL-10 + T cells was significantly enhanced compared to untreated hPMSCs. IL-1β could up-regulate the expression of PD-L1 and PD-L2 on hPMSCs. Blocking the expression of PD-L1 and/or PD-L2 on hPMSCs significantly reduced the ability of hPMSCs to induce activated PBMCs to differentiate into CD8 + IL-10 + T cells. Conclusions:IL-1β enhanced the capacity of hPMSCs to induce activated PBMCs to differentiate into CD8 + IL-10 + T cells in RA patients by up-regulating the expression of PD-L1 and PD-L2.