Objective: To explore the laboratory testing methods and clinical management strategies for immune hemolytic anemia induced by Ceftizoxime sodium drug-dependent antibodies. Methods: Patient blood samples were subjected to blood typing, direct antiglobulin test, and unexpected antibody identification. Ceftizoxime sodium drug-dependent antibodies were detected using the immune complex method and drug-sensitized red cell method. The properties and titers of the drug antibodies were further assessed. Flow cytometry was used to assess the complement activation capacity of the drug antibodies in vitro. Results: Direct antiglobulin tests (IgG and C3d) were positive. Ceftizoxime sodium drug-dependent antibodies were identified using both the immune complex method and the sensitized red cell method, their titers significantly increased following the addition of the drug. Flow cytometry confirmed the complement activation capability of these antibodies and identified 30 minutes as the optimal time for activation in vitro. The patient's condition improved rapidly after drug withdrawal and supportive transfusion, resulting in a favorable outcome. Conclusion: Ceftizoxime sodium can cause drug-induced immune hemolytic anemia via complement activation mediated by drug-dependent antibodies. Serological testing is essential for diagnosing drug-induced hemolytic anemia. Clinicians should be vigilant for this adverse reaction. The offending drug must be promptly discontinued, and supportive care should be initiated upon the onset of symptoms.

Inflammatory breast cancer(IBC)is a rare but highly aggressive subtype of breast cancer characterized by rapid clinical progression and poor prognosis.Although it accounts for only 2%-4%of all breast cancer cases,it is responsible for 8%-10%of breast cancer-related mortality.The etiology of IBC is multifactorial,involving genetic,hormonal,environmental,and socioeconomic factors.Pathologically,IBC is marked by the presence of dermal lymphatic tumor emboli,and molecular subtypes are predominantly HER2-positive and triple-negative,indicating high tumor invasiveness.Diagnosis relies on characteristic clinical manifestations and histopathological confirmation,while imaging techniques such as MRI and PET/CT play important roles in evaluating disease extent and metastasis.Given that IBC is often diagnosed at a locally advanced or metastatic stage,there is currently no specific treatment protocol.Instead,management generally follows the treatment paradigm of non-IBC,emphasizing systemic therapy within a multidisciplinary framework.HER2-positive IBC benefits from chemotherapy combined with dual-targeted anti-HER2 therapy;triple-negative IBC may respond to immune checkpoint inhibitors;and CDK4/6 inhibitors show potential efficacy in hormone receptor-positive subtypes.Despite advancements,the prognosis remains poor,with a high risk of early recurrence and distant metastasis.Prognostic factors include lymph node involvement,molecular subtype,and response to neoadjuvant therapy.As research into the tumor microenvironment and molecular mechanisms deepens,targeted and individualized therapies hold promise for improving outcomes.This review summarizes the epidemiology,pathology,diagnostic criteria,treatment strategies,and prognostic factors of IBC,aiming to inform clinical practice and future research.

Inflammatory breast cancer(IBC)is a rare but highly aggressive subtype of breast cancer characterized by rapid clinical progression and poor prognosis.Although it accounts for only 2%-4%of all breast cancer cases,it is responsible for 8%-10%of breast cancer-related mortality.The etiology of IBC is multifactorial,involving genetic,hormonal,environmental,and socioeconomic factors.Pathologically,IBC is marked by the presence of dermal lymphatic tumor emboli,and molecular subtypes are predominantly HER2-positive and triple-negative,indicating high tumor invasiveness.Diagnosis relies on characteristic clinical manifestations and histopathological confirmation,while imaging techniques such as MRI and PET/CT play important roles in evaluating disease extent and metastasis.Given that IBC is often diagnosed at a locally advanced or metastatic stage,there is currently no specific treatment protocol.Instead,management generally follows the treatment paradigm of non-IBC,emphasizing systemic therapy within a multidisciplinary framework.HER2-positive IBC benefits from chemotherapy combined with dual-targeted anti-HER2 therapy;triple-negative IBC may respond to immune checkpoint inhibitors;and CDK4/6 inhibitors show potential efficacy in hormone receptor-positive subtypes.Despite advancements,the prognosis remains poor,with a high risk of early recurrence and distant metastasis.Prognostic factors include lymph node involvement,molecular subtype,and response to neoadjuvant therapy.As research into the tumor microenvironment and molecular mechanisms deepens,targeted and individualized therapies hold promise for improving outcomes.This review summarizes the epidemiology,pathology,diagnostic criteria,treatment strategies,and prognostic factors of IBC,aiming to inform clinical practice and future research.

With the extensive application of highly sensitive genetic techniques in the field of prenatal diagnosis, prenatal chromosomal mosaicisms including true fetal mosaicisms and confined placental mosaicisms are frequently identified in clinical settings, and the diagnostic criteria and principle of genetic counseling and clinical management for such cases may vary significantly among healthcare centers across the country. This not only has brought challenges to laboratory technician, genetic counselor and fetal medicine doctor, but can also cause confusion and anxiety of the pregnant woman and their family members. In this regard, we have formulated a consensus over the prenatal diagnosis and genetic counseling for chromosomal mosaicisms with the aim to promote more accurate and rational evaluation for fetal chromosomal mosaicisms in prenatal clinics.
Consensus ; Female ; Genetic Counseling ; Humans ; Mosaicism ; Placenta ; Pregnancy ; Prenatal Diagnosis/methods*

Genomic disorders caused by pathogenic copy number variation (pCNV) have proven to underlie a significant proportion of birth defects. With technological advance, improvement of bioinformatics analysis procedure, and accumulation of clinical data, non-invasive prenatal screening of pCNV (NIPS-pCNV) by high-throughput sequencing of maternal plasma cell-free DNA has been put to use in clinical settings. Specialized standards for clinical application of NIPS-pCNV are required. Based on the discussion, 10 pCNV-associated diseases with well-defined conditions and 5 common chromosomal aneuploidy syndromes are recommended as the target of screening in this consensus. Meanwhile, a standardized procedure for NIPS-pCNV is also provided, which may facilitate propagation of this technique in clinical settings.
Aneuploidy ; Cell-Free Nucleic Acids/genetics* ; Consensus ; DNA Copy Number Variations ; Female ; High-Throughput Nucleotide Sequencing ; Humans ; Pregnancy ; Prenatal Diagnosis

Objective To study the glycosylated hemoglobin in the level difference between different age,sex and provide a reference for the prevention,early diagnosis and treatment of diabetes.Methods 9 094 cases in clinic of population data were included in this study,according to the different age groups were divided into 30 years old or less group (464 cases),30 ～40 years old group (715 cases),41～50 years old group (1 939 cases),51～60 years old group (1 754 cases),61～ 70 (2 290 cases),71～80 years old group (1 497 cases) and ＞80 years old group (435 cases),7 groups of extraction of venous blood tested glycated hemoglobin and compared,analysis of glycosylated hemoglobin levels between different age groups and different gender differences.Results All subjects crowd glycosylated hemoglobin levels were ≤30 years old group (5.42± 0.841) ％,31 ～40 years old group (5.61 ± + 1.088) ％,41 ～ 50 years old group (5.93 ± 1.264) ％,51 ～ 60 years old group (6.18±1.298) ％,61～ 70 years old group (6.21 ± 1.232) ％,71 ～ 80 years old group (6.29 ± 1.270) ％,＞ 80 years old group (6.35 ± 1.314)％ all were a trend of increase with the increase of age,the difference was statistically significant(F=63.81,P＜0.001).The level of glycosylated hemoglobin was significantly higher in male than in female within 70 years of age,and there was significant difference in HbA1c level between 18～50 years old (P＜0.05).Conclusion There was a correlation between the level of glycosylated hemoglobin with different age,sex and increasing with age.It is suitable for physical examination and screening,and in particular,monitoring of glycosylated hemoglobin levels in middle aged and old age.

Background and objective Tumor necrosis factor-related apoptosis-inducting ligand (TRAIL) can in-duce apoptosis of tumor cells, however, various of tumor cells may survive because of resistance to TRAIL-mediated apoptosis. This study is to observe the proliferation inhibition effect of TRAIL sensitized by thioridazine on PC9 cells through endoplas-mic reticulum (ER) stress mediated up-regulation of death receptor 5 (DR5) and investigate its mechanism.Methods PC9 cells were treated with different concentrations of thioridazine and TRAIL alone or in combination. Cell proliferation was mea-sured by MTT assay, and cell apoptosis and cell-surface DR5 were detected by flow cytometry. Western blotting was utilized to measure the expressions of ER stress-related proteins glucose regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), p-PKR-like ER kinase (PERK), p-eukaryotic initiation factor-2α (eIF2α), activating transcription factor 4 (ATF4) and apoptosis-related proteins caspase-3, caspase-9, caspase-8, PARP, DR5.Results Thioridazine inhibited the proliferation of PC9 cells in a dose-dependent manner (P<0.05). Thioridazine increased the inhibition and apoptosis of PC9 cells and up-regulated the expression of cell-surface DR5 induced by TRAIL. Flow cytometry showed that compared with TRAIL group,combination group of TRAIL and thioridazine increased cell apoptotic rates significantly (P<0.05). Western blotting indicated that compared with TRAIL group, expressions of Cleaved-caspase-8, Cleaved-PARP and DR5 increased significantly in combi-nation group of TRAIL and thioridazine. The induction of DR5 and pro-apoptotic effect were mediated through activation of ER stress accompanying by increased synthesis of GRP78 and CHOP, which can be blocked by adding of ER stress inhibitor 4-PBA.Conclusion Thioridazine enhanced proliferation inhibition effect of TRAIL in PC9 cells may be facilitated through ER stress mediated upregulation of DR5.

Clinical data of 23 locally recurrent rectal cancer patients underwent radical anterior resection and 69 controls matched by age and gender was retrospectively analyzed to find out the risk factors related to local recur-rence after radical anterior resection of rectal carcinoma. Univariate analysis showed that tumor size, number of positive lymph nodes, distance between tumor and the anal verge and T stage were risk factors for locally recurrent rectal cancer after radical anterior resection. The results of logistic regression analysis showed that T stage ( T4 stage) was an independent risk factor correlated with the tumor recurrence after radical anterior resection and loca-tion of tumor( distance of tumor from the anal verge being less than 5 cm) seemed to be an independent risk factor correlated with the tumor recurrence.

Background and objectiveRecent research shows thioridazine which is a kind of phenothiazine anti-psychotic drugs can inhibit the proliferation of various tumor cellsin vitro, but the role of thioridazine on lung cancer has not been reported. So we choose PC9 cell lines as the research object, the aim is to oberve the killing effect of thioridazine on PC9 cells and investigate its possible mechanism.MethodsAtfer being treated with different concentrations of thioridazine, the proliferation of PC9 cells was determined by methyl thiazolyltetrazolium (MTT) assay. Flow cytometry was used to measure the cell cycle distribution and apoptosis. The expressions of cell cycle-associated protein CyclinD1 and apoptosis-related proteins Caspase-3, Caspase-8, Caspase-9, Bcl-2, Bax and Bcl-xl were detected by Western blot.Results hTe proliferation of PC9 cells was signiifcantly inhibited by thioridazine in a dose- and time-dependent manner. Flow cytometry showed that cell cycle was arrested in G0/G1 phase and the apoptotic rates were signiifcantly increased with the increasing concentration of thioridazine. Compared with the control group, the differences were statistically signiifcant (P<0.05). Western blot analysis showed that, compared with the control group, thioridazine reduced the expressions of CyclinD1, Bcl-2 and Bcl-xl (P<0.01) and increased the expression of Bax (P<0.01). In the mean time, thioridazine promoted the activities of Caspase-3, Caspase-8 and Caspase-9 (P<0.01).ConclusionhTe mechanism of thioridazine inhibiting the proliferation of PC9 cells may be related to stimulation of Caspase apoptotic pathway, down-regulation of CyclinD1, Bcl-2, Bcl-xl and up-regulation of Bax.

Objective To investigate the prevalence and risk factor of Ofloxacin resistance among the tuberculosis patients in Shanghai.Methods Totally 447 isolates resistant to anyone of first-line drug (Isoniazid,Rifampicin,Streptomycin and Ethambutol) and 151 randomly selected isolates susceptible to all above drugs were collected from district tuberculosis(TB) hospitals in Shanghai during 2009 to 2010.All 598 isolates were subject to Ofloxacin sensitive test.Logistic regression analysis was conducted to determine risk factors of Ofloxacin resistance.DNA sequencing was applied to study the mutation characteristics in gyrA and gyrB among Ofloxacin resistant isolates.Results Seventy-two(16.1%) of the 447 drug-resistant isolates were found resistant to Ofloxacin,and the Ofloxacin resistant rate among multiple drug-resistant (MDR) isolates was 39.6%(44/111).Ofloxacin resistance was also found in 4(2.6%) of the 151 drug sensitive isolates.Logistic regression analysis showed that first-line drug-resistance MDR(resistant to at least rifampin and isoniazid) and poly-drug resistance(resistance to two or more first-line drugs but not MDR) had significant effect on Ofloxacin resistance(OR = 19.5、5.6,95% CI:6.4 - 59.4、1.7 - 18.1,all P＜ 0.05);re-treatment(OR = 2.3,95 % CI:1.2 -4.0,P＜ 0.05),and a higher age(OR = 1.03,95 % CI:1.0 1 - 1.05,P＜ 0.05)were also significantly associated with Ofloxacin resistance.Resistance mutations in the gyrA and gyrB genes were detected in 62 of 76(81.6%) isolates with phenotypic Ofloxacin-resistance. Conclusions The Ofloxacin resistance rate in Shanghai MDR-TB patients is significantly higher than the pan-susceptible TB patients.Risk factors of ofloxacin resistance are MDR,poly-resistant,retreated patients,age.Among them,MDR has the highest strength of association.