A TSENet Model for Predicting Cellular Network Traffic.

Wireless sensor networks (WSNs) are gaining traction in the realm of network communication, renowned for their adaptability, configuration, and flexibility. The forthcoming network traffic within WSNs can be forecasted through temporal sequence models. In this correspondence, we present a method (TSENet) that can accurately predict the traffic in the cellular network. TSENet is composed of transformers and self-attention network. We have designed a temporal transformer module specifically for extracting temporal features. This module accomplishes this by modeling the traffic flow within each grid of the communication network at both near-term and periodical intervals. Simultaneously, we amalgamate the spatial features of each grid with information from its correlated grids, generating spatial predictions within the spatial transformer. Furthermore, we employ self-attention aggregation to capture dependencies between external factor features and cellular data features. Empirical assessments performed on a genuine cellular traffic dataset offer compelling evidence substantiating the efficacy of TSENet.

High-level production of nervonic acid in the oleaginous yeast Yarrowia lipolytica by systematic metabolic engineering.

Nervonic acid benefits the treatment of neurological diseases and the health of brain. In this study, we employed the oleaginous yeast Yarrowia lipolytica to overproduce nervonic acid oil by systematic metabolic engineering. First, the production of nervonic acid was dramatically improved by iterative expression of the genes ecoding ß-ketoacyl-CoA synthase CgKCS, fatty acid elongase gELOVL6 and desaturase MaOLE2. Second, the biosynthesis of both nervonic acid and lipids were further enhanced by expression of glycerol-3-phosphate acyltransferases and diacylglycerol acyltransferases from Malania oleifera in endoplasmic reticulum (ER). Third, overexpression of a newly identified ER structure regulator gene YlINO2 led to a 39.3% increase in lipid production. Fourth, disruption of the AMP-activated S/T protein kinase gene SNF1 increased the ratio of nervonic acid to lignoceric acid by 61.6%. Next, pilot-scale fermentation using the strain YLNA9 exhibited a lipid titer of 96.7 g/L and a nervonic acid titer of 17.3 g/L (17.9% of total fatty acids), the highest reported titer to date. Finally, a proof-of-concept purification and separation of nervonic acid were performed and the purity of it reached 98.7%. This study suggested that oleaginous yeasts are attractive hosts for the cost-efficient production of nervonic acid and possibly other very long-chain fatty acids (VLCFAs).

A Refractory Case of CDKN2A/B Loss Metastatic Intrahepatic Cholangiocarcinoma Achieving a Partial Response After First-Line Treatment with Palbociclib.

Intrahepatic cholangiocarcinoma (ICC) is a highly aggressive and malignant subtype of biliary duct tumors. The poor prognosis of advanced ICC brings great challenges to clinical treatment, and chemotherapy-based therapy remains the standard first-line regimen. In recent years, the development of clinical research on targeted therapy for biliary duct tumors has brought new strategies for clinical treatment, but the targets are limited. Herein, we reported a 68-year-old patient with metastasis ICC harboring CDKN2A/B loss, who achieved a partial response (PR) after the first-line treatment with a cyclin-dependent kinases 4 and 6 (CDK4/6) inhibitor called palbociclib, and no obvious side effects were observed. As of the latest follow-up time, the progression-free survival (PFS) had lasted for 20 months. This case reveals the molecular characteristic of ICC patients who respond to palbociclib treatment and illustrates the importance of performing a multiple-gene panel test in ICC patients.

Effects of Enhanced Recovery Rehabilitation Surgery Concepts on the Surgical Process, Postoperative Pain, Complications, and Prognosis of Discectomy in Patients with Lumbar Disc Herniation: A Systematic Review and Meta-Analysis.

Objective: The purpose of this study was to investigate the effect of lumbar disc herniation (LDH) disease degree on lumbar discectomy and to explore the relationship between the degree of intervertebral disc disease and postoperative pain score changes. Methods: We conducted a comprehensive search in China National Knowledge Infrastructure (CNKI), Wanfang Data, PubMed, MEDLINE, Embase, Cochrane database, and other databases, obtained all relevant studies as of April 2017, and then followed strict inclusion and exclusion criteria. Standard screening was performed on the retrieved literature. We extract and analyze key data using Review Manager 5.3 software. Pooled effects were calculated by mean difference or odds ratio and 95% confidence interval analysis, depending on data attributes. Results: Various databases were searched for the results of papers from lumbar discectomy since April 2017 to April 2022. Nine papers from 2502 patients were selected. The average overall follow-up was 52 weeks. There were statistically significant reductions in postoperative pain scores and degree of disc disease. There was a significant correlation between the reduction in pain score after discectomy and the degree of disc disease (r = 0.73, 95%CI = 0.01-1.20, p = 0.005). Conclusions: Decreased disc disease grade is one of the reasons for the lower back pain score after discectomy. Furthermore, region-dependent economic factors must be considered before developing a treatment strategy. Larger, well-defined randomized controlled trials are needed to further confirm these results.

Plume-ridge interaction induced migration of the Hawaiian-Emperor seamounts.

The history of the Hawaiian hotspot is of enduring interest in studies of plate motion and mantle flow, and has been investigated by many researchers using the detailed history of the Hawaiian-Emperor Seamount chain. One of the unexplained aspects of this history is the apparent offset of several Emperor seamounts from the Hawaii plume track. Here we show that the volcanic migration rates of the Emperor seamounts based on existing data are inconsistent with the drifting rate of the Pacific plate, and indicate northward and then southward "absolute movements" of the seamounts. Numerical modeling suggests that attraction and capture of the upper part of the plume by a moving spreading ridge led to variation in the location of the plume's magmatic output at the surface. Flow of the plume material towards the ridge led to apparent southward movement of Meiji. Then, the upper part of the plume was carried northward until 65 Ma ago. After the ridge and the plume became sufficiently separated, magmatic output moved back to be centered over the plume stem. These changes are apparent in variations in the volume of seamounts along the plume track. Chemical and isotopic compositions of basalt from the Emperor Seamount chain changed from depleted (strong mid-ocean ridge affinity) in Meiji and Detroit to enriched (ocean island type), supporting declining influence from the ridge. Although its surface expression was modified by mantle flow and by plume-ridge interactions, the stem of the Hawaiian plume may have been essentially stationary during the Emperor period.

Ibrexafungerp: An orally active ß-1,3-glucan synthesis inhibitor.

We previously reported medicinal chemistry efforts that identified MK-5204, an orally efficacious ß-1,3-glucan synthesis inhibitor derived from the natural product enfumafungin. Further extensive optimization of the C2 triazole substituent identified 4-pyridyl as the preferred replacement for the carboxamide of MK-5204, leading to improvements in antifungal activity in the presence of serum, and increased oral exposure. Reoptimizing the aminoether at C3 in the presence of this newly discovered C2 substituent, confirmed that the (R) t-butyl, methyl aminoether of MK-5204 provided the best balance of these two key parameters, culminating in the discovery of ibrexafungerp, which is currently in phase III clinical trials. Ibrexafungerp displayed significantly improved oral efficacy in murine infection models, making it a superior candidate for clinical development as an oral treatment for Candida and Aspergillus infections.

MK-5204: An orally active ß-1,3-glucan synthesis inhibitor.

Our previously reported efforts to produce an orally active ß-1,3-glucan synthesis inhibitor through the semi-synthetic modification of enfumafungin focused on replacing the C2 acetoxy moiety with an aminotetrazole and the C3 glycoside with a N,N-dimethylaminoether moiety. This work details further optimization of the C2 heterocyclic substituent, which identified 3-carboxamide-1,2,4-triazole as a replacement for the aminotetrazole with comparable antifungal activity. Alkylation of either the carboxamidetriazole at C2 or the aminoether at C3 failed to significantly improve oral efficacy. However, replacement of the isopropyl alpha amino substituent with a t-butyl, improved oral exposure while maintaining antifungal activity. These two structural modifications produced MK-5204, which demonstrated broad spectrum activity against Candida species and robust oral efficacy in a murine model of disseminated Candidiasis without the N-dealkylation liability observed for the previous lead.

Analgesic Mechanism of Sinomenine against Chronic Pain.

Purified from the roots of the plant Sinomenium acutum, sinomenine is traditionally used in China and Japan for treating rheumatism and arthritis. Previously, we have demonstrated that sinomenine possessed a broad analgesic spectrum in various chronic pain animal models and repeated administration of sinomenine did not generate tolerance. In this review article, we discussed sinomenine's analgesic mechanism with focus on its role on immune regulation and neuroimmune interaction. Sinomenine has distinct immunoregulative properties, in which glutamate, adenosine triphosphate, nitric oxide, and proinflammatory cytokines are thought to be involved. Sinomenine may alter the unbalanced neuroimmune interaction and inhibit neuroinflammation, oxidative stress, and central sensitization in chronic pain states. In conclusion, sinomenine has promising potential for chronic pain management in different clinical settings.

Highly Efficient Production of l-Histidine from Glucose by Metabolically Engineered Escherichia coli.

l-Histidine is a functional amino acid with numerous therapeutic and ergogenic properties. It is one of the few amino acids that is not produced on a large scale by microbial fermentation due to the lack of an efficient microbial cell factory. In this study, we demonstrated the engineering of wild-type Escherichia coli to overproduce histidine from glucose. First, removal of transcription attenuation and histidine-mediated feedback inhibition resulted in 0.8 g/L histidine accumulation. Second, chromosome-based optimization of the expression levels of histidine biosynthesis genes led to a 4.75-fold increase in histidine titer. Third, strengthening phosphoribosyl pyrophosphate supply and rerouting the purine nucleotide biosynthetic pathway improved the histidine production to 8.2 g/L. Fourth, introduction of the NADH-dependent glutamate dehydrogenase from Bacillus subtilis and the lysine exporter from Corynebacterium glutamicum enabled the final strain HW6-3 to produce 11.8 g/L histidine. Finally, 66.5 g/L histidine was produced under fed-batch fermentation, with a yield of 0.23 g/g glucose and a productivity of 1.5 g/L/h. This is the highest titer and productivity of histidine ever reported from an engineered strain. Additionally, the metabolic strategies utilized here can be applied to engineering other microorganisms for the industrial production of histidine and related bioproducts.

Antinociceptive Effects of Sinomenine Combined With Ligustrazine or Paracetamol in Animal Models of Incisional and Inflammatory Pain.

The management of postoperative and inflammatory pain has been a pressing challenge in clinical settings. Sinomenine (SN) is a morphinan derived alkaloid with remarkable analgesic properties in various kinds of pain models. The aim of the current study is to investigate if SN can enhance the effect of ligustrazine hydrochloride (LGZ) or paracetamol (PCM) in animal models of postoperative and inflammatory pain. And to determine if the combined therapeutic efficacies can be explained by pharmacokinetics changes. Pharmacological studies were performed using a rat model of incisional pain, and a mouse model of carrageenan induced inflammatory pain. Pharmacokinetic studies were performed using a microdialysis sampling and HPLC-MS/MS assay method to quantify SN, LGZ, and PCM levels in blood and extracellular fluid in brain. We found that SN plus LGZ or SN plus PCM produced marked synergistic analgesic effects. However, such synergy was subjected to pain modalities, and differed among pain models. Pharmacological discoveries could be partially linked to pharmacokinetic alterations in SN combinations. Though further evaluation is needed, our findings advocate the potential benefits of SN plus LGZ for postoperative pain management, and SN plus PCM for controlling inflammatory pain.

Exploratory study data for determining the adverse effects of sinomenine plus gabapentin or ligustrazine hydrochloride and the pharmacokinetic insights of sinomenine in plasma and CNS tissue.

This paper contains data that can be used in interpretation of the pharmacological effects of sinomenine combined with gabapentin or ligustrazine hydrochloride on chronic pain. The data can be divided into two parts. The first part is regarding if there were noticeable side effects accompanying drug applications of sinomenine plus gabapentin or ligustrazine hydrochloride. These side effects include sedation and change of core body temperature as well as tissue edema and sustained itch. The data were acquired from the open field test in mice, and provided insights for the effects of drug combination therapy on locomotive activities, rearing behaviors and body temperature. The second part is regarding whether sinomenine could be accumulated in the central nervous system (CNS) tissue following repeated drug administration. The data were acquired using microdialysis, which illustrated the pharmacokinetic properties of sinomenine, by showing relative concentrations of sinomenine in blood and CNS tissue, following single or repeated drug application. Data presented here is related to and supportive of the research article by Gao et al., "Sinomenine facilitates the efficacy of gabapentin or ligustrazine hydrochloride in animal models of neuropathic pain"[1], where interpretation of the research data presented here is available.

Multi-terrane structure controls the contrasting lithospheric evolution beneath the western and central-eastern Tibetan plateau.

The Tibetan plateau is manifested by contrasting along-strike lithospheric structures, but its formation mechanism and the relationship with the heterogeneous multi-terrane configuration is a challenging problem. Here we conduct systematic numerical modeling to explore the roles of width, density, and rheological properties of the multiple terranes in the lithospheric evolution of the Tibetan plateau, which reveals two distinct collision modes. In Mode-I, the lithospheric mantles of both the strong and weak terranes in the Tibetan plate are completely detached, followed by the underthrusting of Indian lithosphere beneath the whole plateau. Alternatively, Mode-II is characterized by full detachment of the weak terranes, but (partial) residue of the strong terranes during collision. These two contrasting modes, broadly consistent with the lithospheric structures of western and central-eastern Tibetan plateau, respectively, are strongly dependent on the along-strike variation of the width of the strong Lhasa-Qiangtang terranes.

Downregulated Trophinin-Associated Protein Plays a Critical Role in Human Hepatocellular Carcinoma Through Upregulation of Tumor Cell Growth and Migration.

Trophinin-associated protein (TROAP) was a protein first identified to mediate the process of embryo transplantation and later found to be involved in microtubule regulation. However, little is known about the role of TROAP in hepatocellular carcinoma (HCC). In the present study, we reported that both TROAP mRNA and protein expressions were downregulated in human HCC samples as well as cell lines. A high level of TROAP was associated with small tumor size (p < 0.05), minor tumor nodules (p < 0.01), and mild vein invasion (p < 0.05). We further constructed in vitro TROAP depletion and overexpression HCC cell models. TROAP depletion significantly enhanced the proliferation and colony formation abilities, whereas TROAP overexpression had an inhibitory effect on the growth of HCC cells. The G1/S phase arrest by TROAP overexpression correlated with increased cell cycle inhibitors p21 and p27, and declined cell cycle promoting kinase complex CDK6/cyclin D1. Depressed TROAP expression enhanced the migration ability, while the opposite influence was observed in TROAP-overexpressed HCC cells. Taken together, these results indicate that TROAP suppresses cellular growth and migration in HCC. This discovery will further our understanding of the pathogenic mechanisms of human HCC.

Efficacy and Safety of Zhuanggu Joint Capsules in Combination with Celecoxib in Knee Osteoarthritis: A Multi-center, Randomized, Double-blind, Double-dummy, and Parallel Controlled Trial.

BACKGROUND: Knee osteoarthritis (KOA) is a chronic joint disease that manifests as knee pain as well as different degrees of lower limb swelling, stiffness, and movement disorders. The therapeutic goal is to alleviate or eliminate pain, correct deformities, improve or restore joint functions, and improve the quality of life. This study aimed to evaluate the efficacy and safety of Zhuanggu joint capsules combined with celecoxib and the benefit of treatment with Zhuanggu alone for KOA. METHODS: This multi-center, randomized, double-blind, double-dummy, parallel controlled trial, started from December 2011 to May 2014, was carried out in 6 cities, including Beijing, Shanghai, Chongqing, Changchun, Chengdu, and Nanjing. A total of 432 patients with KOA were divided into three groups (144 cases in each group). The groups were treated, respectively, with Zhuanggu joint capsules combined with celecoxib capsule simulants, Zhuanggu joint capsules combined with celecoxib capsules, and celecoxib capsules combined with Zhuanggu joint capsule simulants for 4 weeks consecutively. The improvement of Western Ontario and McMaster Universities Osteoarthritis (WOMAC) index and the decreased rates in each dimension of WOMAC were evaluated before and after the treatment. Intergroup and intragroup comparisons of quantitative indices were performed. Statistically significant differences were evaluated with pairwise comparisons using Chi-square test (or Fisher's exact test) and an inspection level of α = 0.0167. RESULTS: Four weeks after treatment, the total efficacies of Zhuanggu group, combination group, and celecoxib group were 65%, 80%, and 64%, respectively, with statistically significant differences among the three groups (P = 0.005). Intergroup pairwise comparisons showed that the total efficacy of the combination group was significantly higher than that of the Zhuanggu (P = 0.005) and celecoxib (P = 0.003) groups. The difference between the latter two groups was not statistically significant (P > 0.0167). Four weeks after discontinuation, the efficacies of the three groups were 78%, 95%, and 65%, respectively, with statistically significant differences (P < 0.0001). Intergroup pairwise comparisons revealed that the efficacy of the combination group was significantly better than that of the Zhuanggu and the celecoxib groups (P < 0.0001). The difference between the latter two groups was not statistically significant (P > 0.0167). The incidences of adverse events in Zhuanggu group, combination group, and celecoxib group were 8.5%, 8.5%, and 11.1%, respectively, with insignificant differences (P > 0.05). CONCLUSIONS: Zhuanggu joint capsules alone or combined with celecoxib showed clinical efficacy in the treatment of KOA. The safety of Zhuanggu joint capsules alone or combined with celecoxib was acceptable. TRIAL REGISTRATION: Chinese Clinical Trial Registry, ChiCTR-IPR-15007267; http://www.medresman.org/uc/project/projectedit.aspx?proj=1364.

Hydroxysafflor Yellow A Protects Neurons From Excitotoxic Death through Inhibition of NMDARs.

Excessive glutamate release causes overactivation of N-methyld-aspartate receptors (NMDARs), leading to excitatory neuronal damage in cerebral ischemia. Hydroxysafflor yellow A (HSYA), a compound extracted from Carthamus tinctorius L., has been reported to exert a neuroprotective effect in many pathological conditions, including brain ischemia. However, the underlying mechanism of HSYA's effect on neurons remains elusive. In the present study, we conducted experiments using patch-clamp recording of mouse hippocampal slices. In addition, we performed Ca(2+) imaging, Western blots, as well as mitochondrial-targeted circularly permuted yellow fluorescent protein transfection into cultured hippocampal neurons in order to decipher the physiological mechanism underlying HSYA's neuroprotective effect.Through the electrophysiology experiments, we found that HSYA inhibited NMDAR-mediated excitatory postsynaptic currents without affecting α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor and γ-aminobutyric acid A-type receptor-mediated currents. This inhibitory effect of HSYA on NMDARs was concentration dependent. HSYA did not show any preferential inhibition of either N-methyld-aspartate receptor subtype 2A- or N-methyld-aspartate receptor subtype 2B- subunit-containing NMDARs. Additionally, HSYA exhibits a facilitatory effect on paired NMDAR-mediated excitatory postsynaptic currents. Furthermore, HSYA reduced the magnitude of NMDAR-mediated membrane depolarization currents evoked by oxygen-glucose deprivation, and suppressed oxygen-glucose deprivation-induced and NMDAR-dependent ischemic long-term potentiation, which is believed to cause severe reperfusion damage after ischemia. Through the molecular biology experiments, we found that HSYA inhibited the NMDA-induced and NMDAR-mediated intracellular Ca(2+)concentration increase in hippocampal cultures, reduced apoptotic and necrotic cell deaths, and prevented mitochondrial damage. Together, our data demonstrate for the first time that HSYA protects hippocampal neurons from excitotoxic damage through the inhibition of NMDARs. This novel finding indicates that HSYA may be a promising pharmacological candidate for the treatment of brain ischemia.

Novel orally active inhibitors of ß-1,3-glucan synthesis derived from enfumafungin.

The clinical success of the echinocandins, which can only be administered parentally, has validated ß-1,3-glucan synthase (GS) as an antifungal target. Semi-synthetic modification of enfumafungin, a triterpene glycoside natural product, was performed with the aim of producing a new class of orally active GS inhibitors. Replacement of the C2 acetoxy moiety with various heterocycles did not improve GS or antifungal potency. However, replacement of the C3 glycoside with an aminoether moiety dramatically improved oral pharmacokinetic (PK) properties while maintaining GS and antifungal potency. Installing an aminotetrazole at C2 in conjunction with an N-alkylated aminoether at C3 produced derivatives with significantly improved GS and antifungal potency that exhibited robust oral efficacy in a murine model of disseminated candidiasis.

NMDAR-Mediated Hippocampal Neuronal Death is Exacerbated by Activities of ASIC1a.

NMDARs and ASIC1a both exist in central synapses and mediate important physiological and pathological conditions, but the functional relationship between them is unclear. Here we report several novel findings that may shed light on the functional relationship between these two ion channels in the excitatory postsynaptic membrane of mouse hippocampus. Firstly, NMDAR activation induced by either NMDA or OGD led to increased [Ca(2+)](i)and greater apoptotic and necrotic cell deaths in cultured hippocampal neurons; these cell deaths were prevented by application of NMDAR antagonists. Secondly, ASIC1a activation induced by pH 6.0 extracellular solution (ECS) showed similar increases in apoptotic and necrotic cell deaths; these cell deaths were prevented by ASIC1a antagonists, and also by NMDAR antagonists. Since increased [Ca(2+)](i)leads to increased cell deaths and since NMDAR exhibits much greater calcium permeability than ASIC1a, these data suggest that ASIC1a-induced neuronal death is mediated through activation of NMDARs. Thirdly, treatment of hippocampal cultures with both NMDA and acidic ECS induced greater degrees of cell deaths than either NMDA or acidic ECS treatment alone. These results suggest that ASIC1a activation up-regulates NMDAR function. Additional data supporting the functional relationship between ASIC1a and NMDAR are found in our electrophysiology experiments in hippocampal slices, where stimulation of ASIC1a induced a marked increase in NMDAR EPSC amplitude, and inhibition of ASIC1a resulted in a decrease in NMDAR EPSC amplitude. In summary, we present evidence that ASIC1a activity facilitates NMDAR function and exacerbates NMDAR-mediated neuronal death in pathological conditions. These findings are invaluable to the search for novel therapeutic targets in the treatment of brain ischemia.

Improvement of natamycin production by engineering of phosphopantetheinyl transferases in Streptomyces chattanoogensis L10.

Phosphopantetheinyl transferases (PPTases) are essential to the activities of type I/II polyketide synthases (PKSs) and nonribosomal peptide synthetases (NRPSs) through converting acyl carrier proteins (ACPs) in PKSs and peptidyl carrier proteins (PCPs) in NRPSs from inactive apo-forms into active holo-forms, leading to biosynthesis of polyketides and nonribosomal peptides. The industrial natamycin (NTM) producer, Streptomyces chattanoogensis L10, contains two PPTases (SchPPT and SchACPS) and five PKSs. Biochemical characterization of these two PPTases shows that SchPPT catalyzes the phosphopantetheinylation of ACPs in both type I PKSs and type II PKSs, SchACPS catalyzes the phosphopantetheinylation of ACPs in type II PKSs and fatty acid synthases (FASs), and the specificity of SchPPT is possibly controlled by its C terminus. Inactivation of SchPPT in S. chattanoogensis L10 abolished production of NTM but not the spore pigment, while overexpression of the SchPPT gene not only increased NTM production by about 40% but also accelerated productions of both NTM and the spore pigment. Thus, we elucidated a comprehensive phosphopantetheinylation network of PKSs and improved polyketide production by engineering the cognate PPTase in bacteria.

Characterization of two polymorphs of lornoxicam.

OBJECTIVES: The aim of the study was to prepare and to characterize two polymorphs of lornoxicam, a water-insoluble non-steroidal anti-inflammatory drug, which has thus far received no exploration of its polymorphs. METHODS: Form I and form II of lornoxicam were prepared by recrystallization and characterized by X-ray powder diffractometry (XRPD), thermal analysis, Fourier transform infrared spectroscopy and scanning electron microscopy. The solubility and dissolution of both polymorphs were also determined and compared to provide the basis for polymorph selection in formulation. KEY FINDINGS: The crystal structures of the two polymorphs were established by the experimental XRPD patterns. Form I was demonstrated to be triclinic with two kinds of intermolecular hydrogen bonds, while form II was orthorhombic with two kinds of intramolecular hydrogen bonds. The morphologies of form I and form II were observed to be rectangle and approximately oval, respectively. CONCLUSIONS: Form II had the significantly higher solubility and dissolution and would be the suitable polymorph for the preparation of oral and injectable dosage forms of lornoxicam.

Development and validation of a stability indicating HPLC method for the analysis of lornoxicam in powder for injection.

A rapid, isocratic stability indicating high performance liquid chromatographic method was developed and validated for the estimation of lornoxicam in its powder for injection. The analysis was performed on a Shimadzu VP-ODS (4. 6 mm x 15 cm, 5 µm) column. The mobile phase consisted of sodium acetate (pH 5.8; 0.05 M) and methanol (45:55) flowed at 1.0 ml/min. Detection was carried out at 290 nm. The developed method had the good ability to separate lornoxicam well from the degradation products. The regression data showed good linear relationship at the concentration range of 4.04-20.20 µ/mL with r(2)=0.9999. Specificity, linearity, accuracy, precision and robustness of the method were evaluated to validate the proposed method. Stressed degradation studies were conducted to provide an indication of its stability indicating property. The limits of detection and quantitation were 9.70 and 33.94 ng /ml, respectively. Lornoxicam was found to be stable in the mobile phase in 24 h. The co-existed excipients had no interference with the analytical procedure. Additional peaks appeared in the chromatograms of five kinds of forced degraded samples (light, heat, acid, base and oxidation degradation). Mean recovery assessed at three levels was from 99. 7 to 100.3%, indicating the good accuracy of the method. Repeatability and inter-day RSD of the method was determined to be 0.38% and 0.81%, respectively. The HPLC method was demonstrated to be robust for intentional minor changes of ratio, pH change, salt concentration and column temperature. The method should be utilized as the routine analysis and quality control of lornoxicam in injectable formulation.