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Purpose The purpose of this paper is to explore the impact of ambidextrous leadership on employees’ innovative behaviors in public museums based on the ambidexterity theory of leadership for innovation. It also examines the mediating mechanism of organizational climate for innovation in public museums. Design/methodology/approach Multisource survey data were obtained from 30 human resource managers, 74 department managers and 237 employees of Taiwanese public museums. Multilevel path analysis was conducted to test the proposed model. Findings Ambidextrous leadership has the most significant effect on employees’ innovative behaviors. Moreover, organizational climate for innovation has a mediating effect on the relationship between ambidextrous leadership and employees’ innovative behaviors. Practical implications This study provides a new perspective on dynamic and complementary ambidextrous leadership, thereby providing important practical implications for innovation management in public museums. Specifically, leaders should apply ambidextrous leadership behaviors in their daily operations to develop an organizational climate for innovation and facilitate employees’ innovative behaviors. Originality/value This study is the first to explore the influence of ambidextrous leadership in a museum. In addition, it examines the mediating effect of organizational climate for innovation to explain the effect of ambidextrous leadership on employees’ innovative behaviors. The findings provide valuable insights for both researchers and managers of public and private entities.

Background Loss of ovarian function, as in menopause or after ovariectomy (OVX), is closely associated with obesity and white adipose tissue (WAT) inflammation. Estrogen replacement protects against postmenopausal obesity but increases the risks of carcinogenesis. In the present study, we investigated the effects of long-term treatment of raloxifene (RAL), a selective estrogen receptor modulator, on the features of estrogen deficiency-induced obesity and explored the involvement of canonical and non-canonical Wnt regulation in vivo and in vitro. Methods Adult female rats received bilateral OVX and divided into 5 groups: (1) Sham, (2) OVX, (3) OVX + E 2 : OVX rats were administered with E 2 (50 μg/kg, s.c., 3 times/week), (4) OVX + RAL: OVX rats were treated with RAL (gavage, 1 mg/kg/day) suspended in 0.8% carboxymethylcellulose (CMC), (5) OVX + CMC: 0.8% CMC as vehicle control. All treatments were given for 8 weeks beginning at 1 week after OVX. In 3 T3-L1 cells, the effects of RAL on adipogenesis and lipopolysaccharide (LPS)-induced inflammation were evaluated. Results Treatment with RAL significantly decreased body weight, visceral fat pad mass, adipocyte size and plasma levels of glucose but increased plasma adiponectin. RAL reduced the elevation of HIF-1α, VEGF-A and proinflammatory cytokines (MCP-1 and TNF-α) expression by inhibition of NF-κB p65 and JNK cascades in retroperitoneal WAT. This anti-inflammatory capacity of RAL may result from upregulation of secreted frizzle-related protein 5 (SFRP5), an adipokine that repressed Wnt5a signaling. Furthermore, RAL inhibited adipogenic factors such as PPAR-γ, C/EBP-α, and FABP4, and preserved canonical Wnt10b/β-catenin protein expression. In 3 T3-L1 adipocytes, RAL (20 μM) diminished lipid accumulation and inhibited adipogenic factors accompanied with the induction of β-catenin, which were effectively reversed by the β-catenin inhibitor IWR-1-endo. In addition, RAL reduced LPS-induced NF-κB p65 and p-IκB expression as well as TNF-α secretion. Suppression of SFRP5 by small interfering RNA significantly abrogated the anti-inflammatory effects of RAL. Conclusions Distinct activation of canonical β-catenin on inhibition of adipogenesis and non-canonical SFRP5 on suppression of WAT inflammation may contribute to the beneficial effects of RAL. Therefore, this study provides a rationale for the therapeutic potential of RAL for postmenopausal obesity.

Sepsis is defined as a life-threatening organ dysfunction syndrome with high morbidity and mortality caused by bacterial infection. The major characteristics of sepsis are systemic inflammatory responses accompanied with elevated oxidative stress, leading to multiple organ dysfunction syndrome (MODS), and disseminated intravascular coagulation (DIC). As a molecular chaperon to repair unfolded proteins, heat shock protein 70 (HSP70) maintains cellular homeostasis and shows protective effects on inflammatory damage. HSP 90 inhibitors were reported to exert anti-inflammatory effects via activation of the heat shock factor-1 (HSF-1), leading to induction of HSP70. We evaluated the beneficial effect of HSP 90 inhibitor NVP-AUY 922 (NVP) on multiple organ dysfunction syndrome induced by lipopolysaccharide (LPS) and further explored the underlying mechanism. NVP (5 mg/kg, i.p.) was administered 20 h prior to LPS initiation (LPS 30 mg/kg, i.v. infusion for 4 h) in male Wistar rats. Results demonstrated that pretreatment with NVP significantly increased survival rate and prevented hypotension at 6 h after LPS injection. Plasma levels of ALT, CRE and LDH as well as IL-1β and TNF-α were significantly reduced by NVP at 6 h after LPS challenge. The induction of inducible NO synthase in the liver, lung and heart and NF-κB p-p65 and caspase 3 protein expression in the heart were also attenuated by NVP. In addition, NVP markedly induced HSP70 and HO-1 proteins in the liver, lung and heart after LPS injection. These results indicated that NVP possessed the anti-inflammatory and antioxidant effects on LPS-induced acute inflammation, which might be associated with HSP70 and HO-1, leading to prevent MODS in sepsis. NVP might be considered as a novel therapeutic strategy in the prevention of sepsis-induced MODS.

Heat stroke (HS) is a life-threatening illness and defined as when body temperature elevates above 40°C accompanied by the systemic inflammatory response syndrome that results in multiple organ dysfunctions. α-Lipoic acid (ALA) acts as a cofactor of mitochondrial enzymes and exerts anti-inflammatory and antioxidant properties in a variety of diseases. This study investigates the beneficial effects of ALA on myocardial injury and organ damage caused by experimental HS and further explores its underlying mechanism. Male Wistar rats were exposed to 42°C until their rectal core temperature reached 42.9°C and ALA was pretreared 40 or 80 mg/kg (i.v.) 1.5 h prior to heat exposure. Results showed that HS-induced lethality and hypothermia were significantly alleviated by ALA treatment that also improved plasma levels of CRE, LDH, and CPK and myocardial injury biomarkers myoglobin and troponin. In addition, ALA reduced cardiac superoxide anion formation and protein expression of cleaved caspase 3 caused by HS. Proinflammatory cytokine TNF-α and NF-κB pathways were significantly reduced by ALA treatment which may be associated with the upregulation of Hsp70. ALA significantly increased the Atg5-12 complex and LC3B II/LC3B I ratio, whereas the p62 and p-mTOR expression was attenuated in HS rats, indicating the activation of autophagy by ALA. In conclusion, ALA ameliorated the deleterious effects of HS by exerting antioxidative and anti-inflammatory capacities. Induction of Hsp70 and activation of autophagy contribute to the protective effects of ALA in HS-induced myocardial injury.

Peritoneal dialysis (PD)-associated peritonitis is a major cause of peritoneal dysfunction and failure. The main issue regarding the treatment is whether to remove the catheter surgically or to treat with antibiotics alone. Notably, PD-associated peritonitis is commonly caused by gram-positive cocci, but rarely by Listeria monocytogenes and Burkholderia cepacia . Here, we report a patient diagnosed with PD-associated peritonitis caused by L. monocytogenes and B. cepacia who presented with a fever, abdominal pain, and turbid dialysate and had been receiving PD for over 20 years. After 2 weeks of antibiotic treatment, the catheter in the patient was surgically removed. Culture and pathology results revealed pathogen growth, foreign body granuloma with chronic inflammation, and inflammatory cells with fibroblast infiltration. The patient was switched to hemodialysis. She eventually recovered and was discharged. The patient presented fair health at the 3-month follow-up. In conclusion, sequential dialysate white blood cell count may help clinicians decide the course of treatment and guide the timing of surgical intervention.

Background Phyllodes tumors (PTs) are well known for local recurrence and progression. Less than 10% of these tumors grow larger than 10 cm. Distant metastases have been reported in up to 22% of malignant PTs, with most metastases being discovered in the lungs. PTs of the breast rarely metastasize to the gastrointestinal tract, and reported cases are scarce. To date, a review of the English literature revealed only 3 cases, including our case, of PTs metastasis to stomach. Case presentation An 82-year-old female patient had 10-year-duration of palpable huge tumor on left breast which was in rapid growth in recent months. Total mastectomy of left breast was performed thereafter, and pathology diagnosis was malignant phyllodes tumor. Adjuvant radiotherapy was suggested while she declined out of personal reasons initially. For PTs recurred locally on left chest wall 2 months later, and excision of the recurrent PTs was performed. She, at length, completed adjuvant radiation therapy since then. Six months later, she was diagnosed of metastasis to stomach due to severe anemia with symptom of melena. Gastrostomy with tumor excision was performed for uncontrollable tumor bleeding. Conclusion For PTs presenting as anemia without known etiologies, further studies are suggested to rule out possible gastrointestinal tract metastasis though such cases are extremely rare. Management of metastatic gastric tumor from PTs should be done on a case-to-case basis, surgical intervention may be needed if there is persistent active bleeding despite medical treatment. Adjuvant radiotherapy is recommended in borderline and malignant PTs with tumor-free margin < 1 cm and high-risk malignant tumors. Adjuvant chemotherapy or target therapy may be helpful for metastatic PTs. Molecular and genomic techniques may predict clinical outcomes of benign and borderline PTs more precisely.

Adrenal myelolipoma is an uncommon, benign, and hormonally non-functioning tumor that is composed of mature adipose tissue and normal hematopoietic tissue. Most cases to date are asymptomatic or have epigastric pain. Acute hemorrhage is the most dramatic manifestation of adrenal myelolipoma; though, it is a rare entity. Hemorrhagic shock due to adrenal myelolipoma, to our knowledge, was much less mentioned so far. Persistent bleeding and uncontrollable hypotension are considered to be absolute indications for immediate surgical operation. Herein we presented a 32-year-old male patient with initial symptoms of nausea, vomiting, and epigastric pain progressing to altered consciousness and hypotension during ER course. Hemorrhagic shock due to a giant adrenal myelolipoma, R’t was diagnosed. Emergent exploratory laparotomy was executed, and en bloc excision of tumor was done. Adrenal myelolipoma might be diagnosed as a adjunction to other main causes of illness; furthermore, adrenal myelolipoma could be asymptomatic in lifetime. In our case, however, manifesting as hemorrhage shock was challenging to diagnose step by step; instead, maintaining vital organs perfusion and identifying bleeding sources were to be done. Management of myelolipoma should be done on a case-to-case basis.

Sepsis can cause myocardial dysfunction, which contributes to the high mortality of sepsis. Hypertonic saline (HS) has been reported to increase myocardial contractility in sepsis. In the present study, mechanisms of action of HS resuscitation (4 mL of 7.5% NaCl per kilogram) on cardiac function have been evaluated in septic rats. HS was administered 1 h after LPS (10 mg/kg, i.v.) challenge. The mean arterial blood pressure significantly decreased 4 h after LPS challenge, and septic shock was observed at the end of experiment (6 h). Posttreatment with HS prevented hypotension caused by LPS and significantly improved cardiac function, evidenced by increases in left ventricular developed pressure, mean +dP/dt and -dP/dt. The amplitude of electrical-stimulated intracellular Ca2+ transient in isolated single cardiomyocytes was significantly reduced after 6 h LPS insult, which was recovered by HS. In addition, LPS resulted in significant increases in neutrophil myeloperoxidase activity, macrophage migration inhibitory factor (MIF), and NF-κB phospho-p65 protein levels in myocardium at 6 h, which were significantly attenuated by HS. In conclusion, HS improved myocardial contractility and prevented circulatory failure induced by endotoxemia, which may attribute to improvement of intracellular calcium handling process and inhibitory effects on neutrophil infiltration and MIF production in hearts.

Pyruvate kinase M2 (PKM2) is a key enzyme involved in glycolysis, yet its role in cancer extends far beyond metabolic flux. Unlike its isoform PKM1, PKM2 exhibits unique regulatory properties due to alternative splicing and dynamic structural plasticity, enabling it to translocate into the nucleus. Once nuclear, PKM2 functions as a signal receiver, gene programmer, and metabolic modulator by acting as a co-transcriptional activator and protein kinase. In this capacity, nPKM2 (nuclear PKM2) orchestrates the transcription of genes involved in glycolysis, lipogenesis, redox homeostasis, and cell cycle progression, thereby reinforcing the Warburg effect and promoting tumor growth, metastasis, and resistance to stress. In this regard, nPKM2 can be considered as the oncogenic component of PKM2. This review consolidates current knowledge on the structural basis of PKM2 assembly and the post-translational modifications that govern its oligomeric state and nuclear import. We also explore emerging therapeutic strategies aimed at targeting nPKM2, including small-molecule modulators that stabilize its cytosolic tetrameric form or disrupt its nuclear functions. Ultimately, the multifaceted roles of nuclear PKM2 underscore its significance as a critical oncoprotein and a promising target for precision cancer therapy.

Most cancer cells reprogram their glucose metabolic pathway from oxidative phosphorylation to aerobic glycolysis for energy production. By reducing enzyme activity of pyruvate kinase M2 (PKM2), cancer cells attain a greater fraction of glycolytic metabolites for macromolecule synthesis needed for rapid proliferation. Here we demonstrate that hydrogen sulfide (H 2 S) destabilizes the PKM2 tetramer into monomer/dimer through sulfhydration at cysteines, notably at C326, leading to reduced PKM2 enzyme activity and increased PKM2-mediated transcriptional activation. Blocking PKM2 sulfhydration at C326 through amino acid mutation stabilizes the PKM2 tetramer and crystal structure further revealing the tetramer organization of PKM2-C326S. The PKM2-C326S mutant in cancer cells rewires glucose metabolism to mitochondrial respiration, significantly inhibiting tumor growth. In this work, we demonstrate that PKM2 sulfhydration by H 2 S inactivates PKM2 activity to promote tumorigenesis and inhibiting this process could be a potential therapeutic approach for targeting cancer metabolism. Low level of pyruvate kinase M2 (PKM2) activity in cancer cells is essential for the dependence on aerobic glycolysis. Here the authors show that PKM2 sulfhydration by hydrogen sulfide destabilizes the PKM2 tetramer, leading to reduced PKM2 enzyme activity and enhanced proliferation of breast cancer cells.