Current scenario and challenges of clinical pharmacists to implement pharmaceutical care in DRG/DIP payment hospitals in China: a qualitative interview study.

Purpose: The Diagnosis-Related Group (DRG) or Diagnosis-Intervention Packet (DIP) payment system, now introduced in China, intends to streamline healthcare billing practices. However, its implications for clinical pharmacists, pivotal stakeholders in the healthcare system, remain inadequately explored. This study sought to assess the perceptions, challenges, and roles of clinical pharmacists in China following the introduction of the DRG or DIP payment system. Methods: Qualitative interviews were conducted among a sample of clinical pharmacists. Ten semi-structured interviews were conducted, either online or face to face. Thematic analysis was employed to identify key insights and concerns related to their professional landscape under the DRG or DIP system. Results: Clinical pharmacists exhibited variable awareness levels about the DRG or DIP system. Their roles have undergone shifts, creating a balance between traditional responsibilities and new obligations dictated by the DRG or DIP system. Professional development, particularly concerning health economics and DRG-based or DIP-based patient care, was highlighted as a key need. There were calls for policy support at both healthcare and national levels and a revised, holistic performance assessment system. The demand for more resources, be it in training platforms or personnel, was a recurrent theme. Conclusion: The DRG or DIP system's introduction in China poses both opportunities and challenges for clinical pharmacists. Addressing awareness gaps, offering robust policy support, ensuring adequate resource allocation, and recognizing the evolving role of pharmacists are crucial for harmoniously integrating the DRG or DIP system into the Chinese healthcare paradigm.

A Self-Sensing and Self-Powered Wearable System Based on Multi-Source Human Motion Energy Harvesting.

Wearable devices play an indispensable role in modern life, and the human body contains multiple wasted energies available for wearable devices. This study proposes a self-sensing and self-powered wearable system (SS-WS) based on scavenging waist motion energy and knee negative energy. The proposed SS-WS consists of a three-degree-of-freedom triboelectric nanogenerator (TDF-TENG) and a negative energy harvester (NEH). The TDF-TENG is driven by waist motion energy and the generated triboelectric signals are processed by deep learning for recognizing the human motion. The triboelectric signals generated by TDF-TENG can accurately recognize the motion state after processing based on Gate Recurrent Unit deep learning model. With double frequency up-conversion, the NEH recovers knee negative energy generation for powering wearable devices. A model wearing the single energy harvester can generate the power of 27.01 mW when the movement speed is 8 km h-1 , and the power density of NEH reaches 0.3 W kg-1 at an external excitation condition of 3 Hz. Experiments and analysis prove that the proposed SS-WS can realize self-sensing and effectively power wearable devices.

An energy harvesting shock absorber for powering on-board electrical equipment in freight trains.

To realize smart detection and safe operation of freight trains, a continuous and stable energy source is required for electrical equipment on the train. It is a feasible scheme to harvest the vibration energy of train suspension to supply power for on-board electrical equipment. This paper presents an energy-harvesting shock absorber (EHSA) based on the slider-crank mechanism and ratchet-pawl mechanism, which provide a vibration reduction effect and renewable electricity. To determine the damping performance and the power generation performance of EHSA, a dynamic model is established based on MATLAB. According to the tests on the mechanical testing and sensing (MTS) bench, the maximum power generation mechanical efficiency of the EHSA is 67.75%, and the maximum output power of the EHSA is 1.65W. In addition, the charging tests on the MTS bench show that the proposed device is applicable to power on-board electrical equipment on freight trains.

MORN4 protects cardiomyocytes against ischemic injury via MFN2-mediated mitochondrial dynamics and mitophagy.

The imbalance of mitochondrial fission and fusion dynamics causes ischemic cardiomyocyte apoptosis and heart injury by affecting mitophagy. Regulation of mitochondrial dynamics is an important therapeutic strategy for ischemic heart diseases. Considering the important roles of MORN motifs in heart diseases and chloroplast fission, we aimed to investigate the possible role of MORN repeat-containing protein 4 (MORN4) in the progression of myocardial infarction (MI), ischemic cardiomyocyte apoptosis, mitochondrial dynamics, and mitophagy. We found that in the MI mouse, MORN4 knockdown remarkably accelerated cardiac injury and fibrosis with deteriorating cardiac dysfunction. Sphingosylphosphorylcholine (SPC) alleviated ischemic cardiomyocyte apoptosis and heart injury through increased level of MORN4, indicating a vital function of MORN4 in heart with SPC used to clarify the molecular mechanisms underlying the functions of MORN4. Mechanistically, we found that MORN4 directly binds to MFN2 and promotes the phosphorylation of MFN2 S442 through Rho-associated protein kinase 2 (ROCK2), which mediates beneficial mitophagy induced by mitochondrial dynamics, while SPC promoted the binding of MORN4 and MFN2 and the process. Taken together, our data reveal a new perspective role of MORN4 in ischemic heart injury, and report that SPC could regulate myocardial mitochondrial homeostasis by activating the MORN4-MFN2 axis during the ischemic situation, this finding provides novel targets for improving myocardial ischemia tolerance and rescue of acute myocardial infarction.

Genome-wide identification and expression profiling of Wnt gene family in Neocaridina denticulata sinensis.

Wnt proteins are a class of hydrophobic secreted glycoproteins involved in diverse important biological processes, such as tissue formation and regeneration, embryonic development and innate immunity. The Wnt gene family has an early origin and is present in all deuterostomes. In the process of evolution, the phenomenon of gene expansion, contraction and adaptive evolution occurs in the Wnt gene family. In the current study, eleven Wnt genes (NdWnt1-2, NdWnt4-7, NdWnt9-11, NdWnt16, and NdWntA) belonging to different subfamilies were obtained based on the genomic and transcriptomic data of Neocaridina denticulata sinensis. Then the expression patterns of all NdWnts were analyzed in various tissues, at different developmental stages and under different stresses. The expression profiles of NdWnts at different developmental stages showed that most NdWnt genes were initially expressed at gastrula stage, and the expression of NdWnt5 and NdWnt16 throughout all developmental stages. The spatial expression of NdWnt genes presented tissue specificity. They were mainly expressed in four tissues, namely gill, intestines, ovary and eyestalk. After Vibrio parahemolyticus infection and under copper exposure, the expression levels of five NdWnts (NdWnt1, NdWnt5, NdWnt10, NdWnt16 and NdWntA) were variable. Our findings enrich the research on the Wnt gene family of N. denticulata sinensis and provide valuable insights into relationship between structure and function of Wnt genes in crustaceans.

RNA-seq analysis revealing the immune response of Neocaridina denticulata sinensis gill to Vibrio parahaemolyticus infection.

Vibrio parahaemolyticus causes serious economic losses to the shrimp farming industry. There is still a lack of adequate understanding of the changes in the overall response of N. denticulata sinensis caused by V. parahaemolyticus, particularly with respect to gill tissue, which is severely damaged by the pathogen. In this study, a total of 1358 differentially expressed genes were identified between the PBS control and Vibrio stimulation groups using transcriptome sequencing techniques. After further screening and analysis, many immune-related genes were obtained, involving lysosome pathway, metabolic process, chitin-binding protein, and serine protease family members. In addition, we randomly selected six DEGs in the lysosome pathway for qRT-PCR verification, and the results showed that their expression patterns were consistent with the RNA-seq. The results demonstrate the molecular regulation of the gill tissue response to V. parahaemolyticus infection in N. denticulata sinensis, contributing to the understand of the complex and efficient innate immune system and defense mechanisms in crustaceans.

An extracellular Cu/Zn superoxide dismutase from Neocaridina denticulata sinensis: cDNA cloning, mRNA expression and characterizations of recombinant protein.

Neocaridina denticulata sinensis possesses characters of rapid growth, tenacious vitality, short growth cycle, transparent, and easy feeding. Therefore, it is gradually being developed into an animal model for basic research on decapod crustaceans. Herein, a Cu/Zn superoxide dismutase (Cu/Zn-SOD), named as Nd-ecCu/Zn-SOD, was identified and characterized from N. denticulata sinensis. The full-length cDNA sequence of Nd-ecCu/Zn-SOD is 829 bp containing a 684 bp open reading frame, which encodes a protein of 227 amino acid residues with a typical Sod_Cu domain. The quantitative real-time PCR analysis showed that Nd-ecCu/Zn-SOD mRNA was expressed in all the tested tissues. Under challenge with copper, the mRNA expression of Nd-ecCu/Zn-SOD reached the maximum at 6 h, and decreased until 24 h. After 24 h of exposure, its expression was up-regulated significantly at 36 h. After then its expression sharply decreased with a comeback at 48 h. The result indicated that Nd-ecCu/Zn-SOD might play an important role in the stress response of N. denticulata sinensis. The expression of Nd-ecCu/Zn-SOD in gills challenged with Vibrio parahaemolyticus changed in a time-dependent manner. Nd-ecCu/Zn-SOD was lowly expressed in early developmental stages by RNA-Seq technology, yet it showed that a cyclical rise and fall occurred between middle stages and late stages. In addition, Nd-ecCu/Zn-SOD was recombinantly expressed using E. coli and the recombinant protein was purified as a single band on SDS-PAGE. The recombinant Nd-ecCu/Zn-SOD (rNd-ecCu/Zn-SOD) existed enzymatic activity under a wide range of temperature and pH. The exposure of metal ions was found that Zn2+, Mg2+, Ca2+, Ba2+, and Cu2+ could inhibit the enzymatic activity of rNd-ecCu/Zn-SOD, and Mn2+ increased the enzymatic activity of rNd-ecCu/Zn-SOD. These results indicate that Nd-ecCu/Zn-SOD may play a pivotal role in resistant against oxidative damage and act as a biomarker under stressful environment.

Sphingosylphosphorylcholine ameliorates doxorubicin-induced cardiotoxicity in zebrafish and H9c2 cells by reducing excessive mitophagy and mitochondrial dysfunction.

Doxorubicin (DOX, C27H29NO11), is an anthracycline tumor chemotherapy drug, which has significant side effects on many organs including the heart. In recent years, mitochondrial dysfunction caused by DOX was identified as an important reason for cardiotoxic injury. Sphingosylphosphorylcholine (SPC) is essential for mitochondrial homeostasis in our previous report, however, its role in DOX-caused cardiomyopathy has remained elusive. Herein, DOX treated zebrafish embryos (90 µM) and adult fish (2.5 µM/g) were used to simulate DOX-induced cardiotoxic damage. Histopathological and ultrastructural observations showed that SPC (2.5 µM) significantly ameliorated DOX-induced pericardial edema, myocardial vacuolization and apoptosis. Furthermore, SPC (2.5 µM) can significantly inhibit DOX-induced apoptosis and promote cell proliferation in DOX treated H9c2 cells (1 µM), which is dependent on the restoration of mitochondrial homeostasis, including restored mitochondrial membrane potential, mitochondrial superoxide and ATP levels. We finally confirmed that SPC restored mitochondrial homeostasis through ameliorating DOX-induced excessive mitophagy. Mechanistically, SPC reduced calmodulin (CaM) levels and thus inhibiting Parkin activation and Parkin-dependent mitophagy. These results suggest that reducing the cardiotoxicity of chemotherapeutic drugs by targeting SPC may be a new solution to rescue chemotherapy injury.

Pancreaticoduodenectomy Is the Best Surgical Procedure for Zollinger-Ellison Syndrome Associated with Multiple Endocrine Neoplasia Type 1.

AIM: The aim of this research was to evaluate the long-term outcome of pancreaticoduodenectomy (PD) versus other duodenopancreatic resections (non-PD) for the surgical treatment of the Zollinger-Ellison syndrome (ZES) in patients with multiple endocrine neoplasia type 1 (MEN1). METHODS: Prospectively recorded patients with biochemically confirmed MEN1-ZES who underwent duodenopancreatic surgery were retrospectively analyzed in terms of clinical characteristics, complications, cure rate, and long-term morbidity, including quality of life assessment (EORTC QLQ-C30). RESULTS: 35 patients (16 female, 19 male) with MEN1-ZES due to duodenopancreatic gastrinomas with a median age of 42 (range 30-74) years were included. At the time of diagnosis, 28 (80%) gastrinomas were malignant, but distant metastases were only present in one (3%) patient. Eleven patients (31.4%) underwent pancreatoduodenectomy (PD) as the initial procedure, whereas 24 patients underwent non-PD resections involving duodenotomy with gastrinoma excision, enucleation of the pNEN from the head of the pancreas, and peripancreatic lymphadenectomy, either with or without distal pancreatectomy (i.e., either Thompson procedure, n = 12, or DUODX, n = 12). There was no significant difference in perioperative morbidity and mortality between the two groups (p ≥ 0.05). One (9%) patient of the PD group required reoperation for recurrent or metastatic ZES compared to eight (22.8%) patients of the non-PD resection groups. After a median follow-up time of 134 months (range 6-480) nine of 11 (82%) patients in the PD group, two of 12 (16%) patients in the Thompson procedure group, and three of 12 (25%) patients in the DUODX group had normal serum gastrin levels. In addition, the global health QoLScore was better in the PD group (76.9) compared to the Thompson procedure (57.4) and DUODX (59.5) groups. CONCLUSIONS: Initial PD seems to be the superior surgical procedure for MEN1-ZES, resulting in a long-term cure rate of about 80%, fewer duodenopancreatic reoperations, and an acceptable quality of life.

JNK-dependent phosphorylation and nuclear translocation of EGR-1 promotes cardiomyocyte apoptosis.

Myocardial apoptosis induced by myocardial ischemia and hyperlipemia are the main causes of high mortality of cardiovascular diseases. It is not clear whether there is a common mechanism responsible for these two kinds of cardiomyocyte apoptosis. Previous studies demonstrated that early growth response protein 1 (EGR-1) has a pro-apoptotic effect on cardiomyocytes under various stress conditions. Here, we found that EGR-1 is also involved in cardiomyocyte apoptosis induced by both ischemia and high-fat, but how EGR-1 enters the nucleus and whether nuclear EGR-1 (nEGR-1) has a universal effect on cardiomyocyte apoptosis are still unknown. By analyzing the phosphorylation sites and nucleation information of EGR-1, we constructed different mutant plasmids to confirm that the nucleus location of EGR-1 requires Ser501 phosphorylation and regulated by JNK. Furthermore, the pro-apoptotic effect of nEGR-1 was further explored through genetic methods. The results showed that EGR-1 positively regulates the mRNA levels of apoptosis-related proteins (ATF2, CTCF, HAND2, ELK1), which may be the downstream targets of EGR-1 to promote the cardiomyocyte apoptosis. Our research announced the universal pro-apoptotic function of nEGR-1 and explored the mechanism of its nucleus location in cardiomyocytes, providing a new target for the "homotherapy for heteropathy" to cardiovascular diseases.

MicroRNA-155-5p/EPAS1/interleukin 6 pathway participated in the protection function of sphingosylphosphorylcholine to ischemic cardiomyocytes.

AIM: Previous research in our laboratory found that a biologically active sphingomyelin metabolite, sphingosylphosphorylcholine (SPC), can inhibit myocardial cell apoptosis caused by ischemia with an unknown mechanism. Here, we aimed to study the possible participation of EPAS1 in the protection process of SPC. METHODS: The rat cardiomyocytes deprived of serum were used to mimic ischemic-caused apoptosis, then treated with or without SPC. The expression and nuclear shift of EPAS1 were detected by western blot and immunofluorescence, and its function was studied using its siRNA. KEY FINDING: Our research shows that SPC inhibited serum starvation caused cardiomyocyte apoptosis, accompanied by the up-regulation and nucleus translocation of EPAS1. EPAS1 levels did not change when its transcript was blocked by Actinomycin D, which prompted us to search for a post-transcription mechanism for its increased expression, and finally found that miR-155-5p, regulated by STAT3, was a new post-transcription regulator to EPAS1. Further investigation found that EPAS1 participated in the protective effect of SPC is mainly achieved by activating the downstream target gene, interleukin-6 (IL-6). SIGNIFICANCE: Our results expand our understanding of the biological functions of SPC, and bring a new pathway as a potential therapeutic target to the treatment of cardiovascular diseases caused by myocardial apoptosis.

Sphingosylphosphorylcholine alleviates hypoxia-caused apoptosis in cardiac myofibroblasts via CaM/p38/STAT3 pathway.

Blockade of hypoxia-caused nonmyocytes apoptosis helps improve survival and mitigate ventricular remodeling and dysfunction during the chronic stage of myocardial infarction. But tools affecting nonmyocyte apoptosis are very rare. Sphingosylphosphorylcholine (SPC), a naturally occurring bioactive sphingolipid in plasma, was proved to protect cardiomyocyte against apoptosis in an ischemic model in our previous study. Here, we showed that SPC also inhibited hypoxia-induced apoptosis in myofibroblasts, an important type of nonmyocytes in the heart. Calmodulin (CaM) is an identified receptor of SPC. We clarified that SPC inhibited myofibroblast apoptosis through CaM as evidenced by decreased cleaved caspase 3, PARP1 and condensed nucleus. Furthermore, the employment of inhibitor and agonist of p38 and STAT3 suggests that SPC inhibits myofibroblast apoptosis by regulating the phosphorylation of p38 and STAT3, and they act as downstream of CaM. The present work may provide new evidence on the regulation of myofibroblasts apoptosis by SPC and a novel target for heart remodeling after hypoxia.

Controlled growth and ion intercalation mechanism of monocrystalline niobium pentoxide nanotubes for advanced rechargeable aluminum-ion batteries.

Rechargeable aluminum-ion batteries (RAIBs) have attracted increasing attention owing to their high theoretical volumetric capacity, high resource abundance, and good safety performance. However, the existing RAIB systems usually exhibit relatively low specific capacities limited by the cathode materials. In this study, we developed a one-step chemical vapor deposition method to prepare single-crystal orthogonal Nb2O5 nanotubes for serving as high-performance electrode materials for RAIBs, showing a high reversible capability of 556 mA h g-1 at 25 mA g-1 and good thermal endurability at elevated temperatures (50 °C). A combination of a series of detailed ex situ structural characterization studies verified the reversible intercalation/deintercalation of chloroaluminate anions (AlCl4-) into/from the (001) planes of monocrystalline Nb2O5 nanotubes. It also revealed that the nanoarchitecture of Nb2O5 nanotubes with thin tube walls, hollow inner space and a short ion transport distance is conducive to the rapid kinetics of the insertion/extraction process. This work provides a promising route to design high-performance electrode materials based on transition metal compounds for RAIBs via the rational modulation of their structure and morphology.

Intermetallic SnSb nanodots embedded in carbon nanotubes reinforced nanofabric electrodes with high reversibility and rate capability for flexible Li-ion batteries.

Tin (Sn) based anode materials have been regarded as promising alternatives for graphite in lithium ion batteries (LIBs) due to their high theoretical specific capacity and conductivity. However, their practical application is severely restrained by the drastic volume variation during cycling processes. Here we report the preparation of intermetallic SnSb nanodots embedded in carbon nanotube reinforced N-doped carbon nanofibers (SnSb-CNTs@NCNFs) as a free-standing and flexible anode for LIBs. In this unique structure, the SnSb nanodots are well protected by the NCNFs and exhibit greatly reduced volume change. The mechanical strength and conductivity of the nanofabric electrode are further improved by the embedded CNTs. Benefiting from these advantages, the SnSb-CNTs@NCNFs anode delivers a high reversible capacity of 815 mA h g-1 at 100 mA g-1, a high rate capability (370 mA h g-1 at 5000 mA g-1) and a long cycle life (451 mA h g-1 after 1000 cycles at 2000 mA g-1). When assembled into flexible pouch cells, the full cells based on SnSb-CNTs@NCNFs anodes also exhibit high flexibility and good lithium storage performances.

Synthesis and Fluorescence Properties of Eu(3+), Tb(3+) Complexes with Schiff Base Derivatives.

Novel Schiff base ligands derived from N'-benzylidene-benzohydrazide (substituted by -H, -CH3, -OCH3, -Cl) and 2-chloro-N-phenylacetamide were synthesized. The solid complexes of rare earth (Eu, Tb) nitrate with these Schiff base ligands were synthesized and characterized by elemental analysis, EDTA titrimetric analysis, thermal analysis, infrared spectra and UV-Vis spectra analysis. The fluorescence properties of rare earth (Eu, Tb) complexes in solid were studied. Under the excitation of ultraviolet light, these complexes exhibited characteristic emission of europium and terbium ions. The results showed that the ligand favored energy transfer to the emitting energy of Eu and Tb ions. Effects of different ligands on the fluorescence intensity of rare earth (Eu, Tb) complexes had been discussed. The electrochemical properties of rare earth (Eu, Tb) complexes were also investigated.

The complete mitochondrial genome sequence of a rat 9L glial neoplasms CNS-1 cell line.

We sequenced a complete mitochondrial genome sequence of a rat 9L glial neoplasms disease CNS-1 cell line for the first time (Accession No. KM657952). The total length of the mitogenome was 16,306 bp and coding 13 protein-coding genes, 2 ribosomal RNA genes, 22 transfer RNA genes. This mitochondrial genome sequence will provide new genetic resource into glial neoplasms disease.

Characterization of sFRP2-like in amphioxus: insights into the evolutionary conservation of Wnt antagonizing function.

Wnt signaling plays a key role in embryonic patterning and morphogenetic movements. The secreted Frizzled-related proteins (sFRPs) antagonize Wnt signaling, but their roles in development are poorly understood. To determine whether function of sFRPs is conserved between amphioxus and vertebrates, we characterized sFRP2-like function in the amphioxus, Branchiostoma belcheri tsingtauense (B. belcheri). As in other species of Branchiostome, in B. belcheri, expression of sFRP2-like is restricted to the mesendoderm during gastrulation and to the anterior mesoderm and endoderm during neurulation. Functional analyses in frog (Xenopus laevis) indicate that amphioxus sFRP2-like potently inhibits both canonical and non-canonical Wnts. Thus, sFRP-2 probably functions in amphioxus embryos to inhibit Wnt signaling anteriorly. Moreover, dorsal overexpression of amphioxus sFRP2-like in Xenopus embryos, like inhibition of Wnt11, blocks gastrulation movements. This implies that sFRP2-like may also modulate Wnt signaling during gastrulation movements in amphioxus.

Prostaglandin E synthase is regulated in postnatal mouse testis.

Prostaglandins have important roles in the male reproductive system. In this study, we report on the distribution and regulation of cPGES during postnatal development of mouse testis. The expression of cPGES was weak in testis 5 days after birth and increased through the 10th and 15th day. From the 20th day onward, the cPGES expression in testis reached the level of adult mice. cPGES was expressed at a constantly low level in Sertoli cells in the testis from infant to adult stages. With the occurrence of meiosis during puberty, a high level of cPGES was detected in the spermatocytes and round spermatids, which was then maintained throughout the adulthood. In addition, cPGES was found highly expressed in the epididymis, seminal vesicles and vas deferens This suggests that cPGES in Sertoli cells in infant to juvenile mouse testis contributes to a basic PGE2 synthesis in seminiferous tubules. However, the high level of cPGES in spermatocytes and spermatids may maintain a high amount of PGE2 in seminiferous tubules, which may be tightly coupled with the spermatogenic cycle.

Distinct gene structure and expression pattern of Smad nuclear interacting protein 1 in amphioxus and zebrafish.

A Smad nuclear interacting protein 1 (SNIP1) homologous gene was identified in amphioxus. Phylogenic analysis showed that SNIP1 proteins from different species share a highly conserved FHA domain at the C-terminus, but their N-terminus varies remarkably. The genomic structure of SNIP1 varies in different species, especially at the 5' end. Through in situ hybridization, we studied SNIP1 expression patterns in amphioxus and zebrafish embryos. Amphioxus SNIP1 transcripts were specifically located in the notochord in larval and adult stages. In zebrafish, however, snip1 transcripts were specifically located not only in the notochord, but also in the rhombencephalic ventricle, otic vesicles and pectoral fin buds. This is the first report of SNIP1 expression pattern in early development, which clearly shows different expression patterns between invertebrates and vertebrates. Previous studies reported that it is the N-terminal domain of human and mouse SNIP1 that functions to inhibit both TGF-ß and the NF-κB pathways. Therefore, it is most likely that the modification of SNIP1 expression pattern is related to the remarkable evolution in the N-terminal sequence. In addition, the difference in SNIP1 expression pattern between amphioxus and zebrafish implies the role of SNIP1 in the vertebrate body structural innovation of brain, otic vesicles and pectoral fins.

Heat stress induces Cdc2 protein decrease prior to mouse spermatogenic cell apoptosis.

Both mitosis and meiosis are driven by M-phase promoting factor (MPF), a complex with Cdc2 and Cyclin B. The concentration of Cdc2 remains relatively constant during the cell cycle, while the concentration of Cyclin B fluctuates periodically. Many studies have demonstrated high expression levels of Cdc2 and Cyclin B in the testis. In some gene knock-out mice insufficient amounts of MPF blocked the spermatocytes at the G2/M transition and this was followed by spermatocyte apoptosis. In this study, we examined the expression and the alteration of Cdc2 in testis during the spermatocyte apoptosis process induced by transient heat stress. The results showed that the spermatogenic cell apoptosis was detectable by the TUNEL assay at 4h post-treatment. At 10h, almost all spermatocytes began apoptosis. In situ hybridization and immunohistochemistry indicated that cdc2 was primarily expressed in spermatocytes. Neither the distribution nor the amount of cdc2 mRNA was significantly influenced by the heat stress. In contrast, the amount of Cdc2 protein decreased significantly at 3h post-treatment, which was detectable before apoptosis. This indicated that Cdc2 was susceptible to heat stress in the testis. Cdc2 levels remained low until 8h post-treatment. It was possible that the swift decline in Cdc2 and the resulting lack of MPF blocked the spermatocytes at G2/M transition. Meiosis in the spermatocytes was disrupted leading to the initiation of apoptosis. The results provide evidence that the lack of Cdc2 might induce spermatocyte apoptosis after transient heat stress.