Hyperlactatemia associated with diabetic ketoacidosis in pediatric intensive care unit.

BACKGROUND: Children with diabetic ketoacidosis often have elevated lactate. In this study, we investigated the clinical variables associated with hyperlactatemia in children with diabetic ketoacidosis. METHODS: We designed a single-center retrospective descriptive study of children with diabetic ketoacidosis in a pediatric intensive care unit. RESULTS: Of the 107 patients with diabetic ketoacidosis included in the analysis, 61 developed hyperlactatemia. Multivariate logistic regression analysis showed that heart rate (p = 0.003),diastolic blood pressure (p = 0.001) and stage of severity (p = 0.042) were independently associated with the development of hyperlactatemia in diabetic ketoacidosis. We found that lactate level was not significantly associated with length of hospital stay (p = 0.115) or the length of time to diabetic ketoacidosis resolution (p = 0.143). CONCLUSIONS: Children with diabetic ketoacidosis presenting with severer stage, elevated heart rate and higher diastolic blood pressure may be prone to hyperlactatemia. Hyperlactatemia was not associated with length of time to DKA resolution and length of hospital stay.

Dandy-Walker malformation in methylmalonic acidemia: a rare case report.

BACKGROUND: Methylmalonic acidemia is an organic acid metabolism disorder that usually has nonspecific clinical manifestations. CASE PRESENTATION: A 3-month-old female infant was admitted to the hospital for developmental retardation. Her prenatal and birth history was unremarkable. After admission, she developed dyspnea and severe anemia and was subsequently transferred to the intensive care unit. Magnetic resonance imaging of her brain showed a Dandy-Walker malformation, and metabolic screening indicated methylmalonic acidemia. Thus, she was diagnosed with methylmalonic acidemia and Dandy-Walker malformation. The patient underwent treatment including acidosis correction, blood transfusion, antibiotics, mechanical ventilation and heat preservation. Unfortunately, her condition progressively worsened and she died of metabolic crisis. CONCLUSIONS: Dandy-Walker malformation may be a clinical manifestation of methylmalonic acidemia. Additionally, the co-existence of methylmalonic acidemia and Dandy-Walker malformation may be an uncharacterized syndrome which needs to be studied further.

Hippocalcin-like 1 suppresses hepatocellular carcinoma progression by promoting p21(Waf/Cip1) stabilization by activating the ERK1/2-MAPK pathway.

UNLABELLED: Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death. However, the underlying mechanism during hepatocarcinogenesis remains unclarified. Stable isotope labeling by amino acids in cell culture (SILAC) is a powerful quantitative strategy for proteome-wide discovery of novel biomarkers in cancers. Hippocalcin-like 1 (HPCAL1) is a calcium sensor protein. However, the biological function of HPCAL1 is poorly understood in cancers, including HCC. Herein, HPCAL1 was identified by SILAC as a novel hepatocarcinogenesis suppressor down-regulated in HCC cell lines and tissues. Importantly, lost expression of HPCAL1 was associated with worse prognosis of HCC patients. Interestingly, secreted HPCAL1 protein in the plasma dropped dramatically in HCC patients compared with healthy donors. Receiver operating characteristic curve analysis showed that serum HPCAL1 at a concentration of 8.654 ng/mL could better predict HCC. Furthermore, ectopic expression of HPCAL1 suppresses cell proliferation, while depletion of HPCAL1 led to increased cell growth both in vitro and in vivo. Mechanistically, HPCAL1 directly interacted with p21(Waf/Cip1) in the nucleus, which requires the EF-hand 4 motif of HPCAL1 and the Cy1 domain of p21. This interaction stabilized p21(Waf/Cip1) in an extracellular signal-regulated kinase 1/2-mitogen-activated protein kinase-dependent manner, which subsequently prevented p21(Waf/Cip1) proteasomal degradation by disrupting SCF(Skp2) and CRL4(Cdt2) E3 ligase complexes, resulting in increased protein stability and inhibitory effect of p21(Waf/Cip1). Notably, the tumor suppressive function of HPCAL1 was dependent on p21 in vitro and in vivo. Consistent with this observation, expression of HPCAL1 and p21(Waf/Cip1) was positively correlated in HCC tissues. CONCLUSION: These findings highlight a novel tumor suppressor upstream of p21(Waf/Cip1) in attenuating cell cycle progression and provide a promising diagnostic and prognostic factor, as well as a potential therapeutic target for HCC.

Reduced expression of the chromatin remodeling gene ARID1A enhances gastric cancer cell migration and invasion via downregulation of E-cadherin transcription.

The chromatin remodeling gene AT-rich interactive domain-containing protein 1A (ARID1A) encodes the protein BAF250a, a subunit of human SWI/SNF-related complexes. Recent studies have identified ARID1A as a tumor suppressor. Here, we show that ARID1A expression is reduced in gastric cancer (GC) tissues, which are significantly associated with local lymph node metastasis, tumor infiltration and poor patient prognosis. ARID1A silencing enforces the migration and invasion of GC cells, whereas ectopic expression of ARID1A inhibits migration. The adhesive protein E-cadherin is remarkably downregulated in response to ARID1A silencing, but it is upregulated by ARID1A overexpression. E-cadherin overexpression significantly inhibits GC cell migration and invasion, whereas CDH1 (coded E-cadherin) silencing promotes migration. Restored expression of CDH1 in ARID1A-silenced cell lines restores the inhibition of cell migration. Luciferase reporter assays and chromatin immunoprecipitation indicate that the ARID1A-associated SWI/SNF complex binds to the CDH1 promoter and modulates CDH1 transcription. ARID1A knockdown induces evident morphological changes of GC cells with increased expression of mesenchymal markers, indicating an epithelial-mesenchymal transition. ARID1A silencing does not alter the level of ß-catenin but induces a subcellular redistribution of ß-catenin from the plasma membrane to the cytoplasm and nucleus. Immunohistochemical studies demonstrate that reduced expression of E-cadherin is associated with local lymph node metastasis, tumor infiltration and poor clinical prognosis. ARID1A and E-cadherin expression show a strong correlation in 75.4% of the analyzed GC tissues. They are synergistically downregulated in 23.5% of analyzed GC tissues. In conclusion, ARID1A targets E-cadherin during the modulation of GC cell migration and invasion.

Analysis of the therapeutic effect of synchronous integrated intensity modulated radiotherapy combined with chemotherapy in stage IIIc of cervical cancer.

Objective: To explore the Therapeutic effect of synchronous Integrated intensity modulated radiotherapy combined with chemotherapy in stage IIIc of Cervical Cancer. Methods: A total of 58 patients with stage IIIC cervical cancer (KPS ≥ 80) were analyzed in this study. They were admitted to our hospital between August 2017 and August 2022. Synchronous integrated boost intensity-modulated radiotherapy (SIB-IMRT) and sequential boost intensity-modulated radiotherapy (LCB-IMRT) were used to treat pelvic and/or para-aortic metastatic lymph nodes, with 30 cases in the SIB group and 28 cases in the LCB group. Comparison of short-term and long-term efficacy. Comparison of recurrence and metastasis rates, radiation dose to organs at risk and incidence of adverse drug reactions. Result: 30 patients were treated with simultaneous integrated boost intensity-modulated radiotherapy (SIB-IMRT), and 28 patients were treated with sequential boost intensity-modulated radiotherapy (LCB-IMRT). At the completion of radiotherapy and 3 months after radiotherapy, there was no significant difference in clinical efficacy observed between the two treatment groups. The median overall survival (OS), progression-free survival (PFS), and disease-free survival (DMR) in the SIB-IMRT group were significantly higher compared to the LCB-IMRT group. The SIB-IMRT group demonstrated significantly lower rates compared to the LCB-IMRT group. Furthermore, within 3 years and 5 years, the rates of lymph node recurrence, cervical and vaginal local recurrence, and distant metastasis within the radiotherapy field were significantly lower in the SIB-IMRT group compared to the LCB-IMRT group. There were no significant differences observed between the two groups in terms of the maximum dose to the small intestine (Dmax), dose received by 2cc of the small intestine (D2cc), maximum dose to the rectum (Dmax), and dose received by 1cc of the bladder (D1cc). The incidence of bone marrow toxicity in the SIB-IMRT group was significantly lower compared to the LCB-IMRT group. Moreover, the occurrence of grade III and IV bone marrow toxicity was also significantly lower in the SIB-IMRT group compared to the LCB-IMRT group. Conclusion: The study has concluded that there is no significant differences in in terms of bladder associated adverse events and gastrointestinal toxicity in both Simultaneous Integrated Boost Intensity-Modulated Radiotherapy and Layered Conical Beam Intensity-Modulated Radiation Therapy.

Bronchiolitis obliterans associated with toxic epidermal necrolysis induced by infection: A case report and literature review.

Background: Stevens-Johnson syndrome/toxic epidermal necrolysis has a severe impact on patients' eyes, genital mucosa, and many other organs. Bronchiolitis obliterans is a rare complication of Stevens-Johnson syndrome/toxic epidermal necrolysis. Data sources: We report a case of bronchiolitis obliterans associated with toxic epidermal necrolysis in our department. Furthermore, we examined the patients with bronchiolitis obliterans induced by Stevens-Johnson syndrome/toxic epidermal necrolysis and summarized the clinical characteristics, treatment, and prognosis. Databases available online in English including PubMed, Medline, and Web of Science were consulted. Results: We report one case and review 23 published case reports. Of the 24 patients, 13 were female, the oldest patient was 59 years old and the youngest was 5 years old. The time of bronchiolitis obliterans onset after Stevens-Johnson syndrome/toxic epidermal necrolysis varied from 5 days to 5 months. Bronchoscopy examination showed ulceration, exudative lesions, occlusion, and inflammation. The CT of lung manifestation included mosaic perfusion, bronchiectasis, consolidation, air trapping, pneumatocele, pleural thickening, lung collapse, larger central airway dilatation, lung overinflation, oligemia, and pneumomediastinum. Most cases indicated pulmonary function tests with obstructive ventilation dysfunction. The prognosis was poor; six of the patients died. Conclusions: Patients with Stevens-Johnson syndrome/toxic epidermal necrolysis may develop bronchitis obliterans at different stages, so all patients with Stevens-Johnson syndrome/toxic epidermal necrolysis should be followed up for possible respiratory complications.

[Expression of heat shock protein 70 in lung and plasma of rats with pulmonary fibrosis induced by SiO2].

OBJECTIVE: To investigate the dynamic expression of Heat shock protein 70 (Hsp70) in the lungs and plasma of rats with pulmonary fibrosis induced by silicon dioxide (SiO2). METHODS: Forty-eight Wistar rats were randomly divided into the control group exposed to normal solution and group exposed to SiO2 (50 mg/ml) with intratracheal injection. Each group was divided into four subgroups. The animals of SiO2 group and control group were sacrificed and lungs were collected on the 7th, 14th and 28th days after exposure, respectively. The left lung tissues were examined with the histopathologic HE staining. The expression and localization of Hsp70 protein in the lung tissues were examined with western blot assay and immunohistochemistry, respectively. The expression levels of Hsp70 protein in the plasma were measured by ELISA. RESULTS: The expression of Hsp70 in lung tissues of SiO2 group increased on the 7th day and reached the peak value on the 14th day then decreased, but still was significantly higher than that of the control group, the expression of Hsp70 in plasma of SiO2 group still was significantly higher than that of the control group (P < 0.05). The maximum expression level of Hsp70 in plasma of SiO2 group on the 21st day after exposure was 0.216 ± 0.027 µg/ml. CONCLUSION: The expression levels of Hsp70 protein in the lung tissues and plasma of the group exposed to SiO2 significantly increased, which were associated with the process of pulmonary fibrosis. It was suggested that Hsp70 protein may play an important biological role in the pulmonary fibrosis induced by SiO2.

Vehicle Safety-Assisted Driving Technology Based on Computer Artificial Intelligence Environment.

In this paper, we propose an assisted driving system implemented with a Jetson nano-high-performance embedded platform by using machine vision and deep learning technologies. The vehicle dynamics model is established under multiconditional assumptions, the path planner and path tracking controller are designed based on the model predictive control algorithm, and the local desired path is reasonably planned in combination with the behavioral decision system. The behavioral decision algorithm based on finite state machine reasonably transforms the driving state according to the environmental changes, realizes the following of the target vehicle speed, and can take effective emergency braking in time when there is a collision danger. The system can complete the motion planning by the model predictive control algorithm and control the autonomous vehicle to smoothly track the replanned local desired path to complete the lane change overtaking action, which can meet the demand of ADAS. The path planner is designed based on the MPC algorithm, solving the objective function with obstacle avoidance function, planning the optimal path that can avoid a collision, and using 5th order polynomial to fit the output local desired path points. In 5∼8 s time, the target vehicle decelerates to 48 km/h; the autonomous vehicle immediately makes a deceleration action and gradually reduces the speed difference between the two vehicles until it reaches the target speed, at which time the distance between the two vehicles is close to the safe distance, obtained by the simulation test results. The system can still accurately track the target when the vehicle is driving on a curve and timely control the desired speed change of the vehicle, and the target vehicle always maintains a safe distance. The system can be used within 50 meters.

Attenuation of antigen-induced airway hyperresponsiveness and inflammation in CXCR3 knockout mice.

BACKGROUND: CD8+ T cells participate in airway hyperresponsiveness (AHR) and allergic pulmonary inflammation that are characteristics of asthma. CXCL10 by binding to CXCR3 expressed preferentially on activated CD8+ T cells, attracts T cells homing to the lung. We studied the contribution and limitation of CXCR3 to AHR and airway inflammation induced by ovalbumin (OVA) using CXCR3 knockout (KO) mice. METHODS: Mice were sensitized and challenged with OVA. Lung histopathological changes, AHR, cellular composition and levels of inflammatory mediators in bronchoalveolar lavage (BAL) fluid, and lungs at mRNA and protein levels, were compared between CXCR3 KO mice and wild type (WT) mice. RESULTS: Compared with the WT controls, CXCR3 KO mice showed less OVA-induced infiltration of inflammatory cells around airways and vessels, and less mucus production. CXCR3 KO mice failed to develop significant AHR. They also demonstrated significantly fewer CD8+ T and CD4+ T cells in BAL fluid, lower levels of TNFα and IL-4 in lung tissue measured by real-time RT-PCR and in BAL fluid by ELISA, with significant elevation of IFNγ mRNA and protein expression levels. CONCLUSIONS: We conclude that CXCR3 is crucial for AHR and airway inflammation by promoting recruitment of more CD8+ T cells, as well as CD4+ T cells, and initiating release of proinflammatory mediators following OVA sensitization and challenge. CXCR3 may represent a novel therapeutic target for asthma.

Translation and Validation: Chinese Version of the HIV-Related Social Support Scale.

PURPOSE: Social support is increasingly recognized to be important in care of people living with HIV/AIDS (PLWH), we firstly translate and validate the disease-targeted social support instrument in Chinese and to explore the correlation with WHOQOL-HIV. PATIENTS AND METHODS: We established content validity for HIV-related social support scale (HSSS) and administered the resultant questionnaire to 310 PLWH. Descriptive statistics were generated for each of the variables of general characteristics; student t-test was used to compare the different groups. RESULTS: The HSSS demonstrated a high level of internal consistency, both within each subscale and with the total score; all Cronbach's α values exceeded a priori threshold of ≥0.70. The HSSS cores were positively correlated with WHOQOL-HIV total scores (Pearson correlation: 0.39, P < 0.001). We also found that higher educational level, personal income, CD4 cell count, and shorter duration of antiretroviral therapy are significantly associated with a higher level of social support (P < 0.05). CONCLUSION: Social support may improve quality of life for PLWH, Chinese version of HIV-related social support scale can be used in future clinical practice.

Synthesis and Characterization of Anatase TiO2 Microspheres Self-Assembled by Ultrathin Nanosheets.

In this paper, we report a novel anCd simple method for synthesizing the microspheres self-assembled from ultrathin anatase TiO2 nanosheets with a high percentage of (001) facets via the hydrolysis process of the single-reagent (potassium fluorotitanate). We then used optical microscopy, scanning electron microscopy, and high-resolution confocal laser Raman spectroscopy to characterize the microspheres generated under different conditions. The study found that the size of the anatase TiO2 microspheres synthesized was 0.5-3 µm. As the synthesis time increased, the corroded surface of the microspheres gradually increased, resulting in the gradual disappearance of the edges and corners of the anatase nanosheets. The exposure percentage of the (001) facets of ultrathin anatase nanosheets synthesized for 2 h at 180-200 °C are close to 100%. The microsphere whose surface is completely covered by these anatase nanosheets also has nearly 100% exposed (001) facets. This new anatase nanosheet-based self-assembled microsphere will have great application potential in pollution prevention, environmental protection, and energy fields.

Enhancement of E-cadherin expression and processing and driving of cancer cell metastasis by ARID1A deficiency.

The ARID1A gene, which encodes a subunit of the SWI/SNF chromatin remodeling complex, has been found to be frequently mutated in many human cancer types. However, the function and mechanism of ARID1A in cancer metastasis are still unclear. Here, we show that knockdown of ARID1A increases the ability of breast cancer cells to proliferate, migrate, invade, and metastasize in vivo. The ARID1A-related SWI/SNF complex binds to the second exon of CDH1 and negatively modulates the expression of E-cadherin/CDH1 by recruiting the transcriptional repressor ZEB2 to the CDH1 promoter and excluding the presence of RNA polymerase II. The silencing of CDH1 attenuated the migration, invasion, and metastasis of breast cancer cells in which ARID1A was silenced. ARID1A depletion increased the intracellular enzymatic processing of E-cadherin and the production of C-terminal fragment 2 (CTF2) of E-cadherin, which stabilized ß-catenin by competing for binding to the phosphorylation and degradation complex of ß-catenin. The matrix metalloproteinase inhibitor GM6001 inhibited the production of CTF2. In zebrafish and nude mice, ARID1A silencing or CTF2 overexpression activated ß-catenin signaling and promoted migration/invasion and metastasis of cancer cells in vivo. The inhibitors GM6001, BB94, and ICG-001 suppressed the migration and invasion of cancer cells with ARID1A-deficiency. Our findings provide novel insights into the mechanism of ARID1A metastasis and offer a scientific basis for targeted therapy of ARID1A-deficient cancer cells.

Atrial thrombus as a complication of SLE and APS in an 8-year-old child.

BACKGROUND: Systemic lupus erythematosus (SLE) is an autoimmune disease involving multiple systems with various clinical manifestations. Renal involvement is common, but intracardiac thrombus is rarely reported as a complication of antiphospholipid syndrome (APS, also known as anticardiolipin syndrome). Anticoagulant therapy is the first-line treatment, and surgery is performed in severe cases. We report a case to improve clinicians' understanding of disease diagnosis. CASE PRESENTATION: An 8-year-old girl was admitted to our hospital because of left costal pain, hematuria and fever. She had obvious edema occult blood 3+, urinary protein 3.2 g/24 h, albumin 17.6 g/L, and total cholesterol 7.21 mmol/L, consistent with a diagnosis of nephrotic syndrome. We continued to track the etiology of nephrotic syndrome and performed a renal biopsy, showing dsDNA 1:10 positivity, low C3, low platelets and hemoglobin, anticardiolipin IgM 12 U/ml, anti-ß2-glycoprotein I (ß2GPI) 223 U/ml; renal pathology suggested lupus nephritis (LN), and the patient was ultimately diagnosed with SLE, secondary APS and LN. The patient was treated with hormones and immunosuppressants. Sixteen weeks later, her urinary protein was 1+, and the quantity of urine protein was less than 0.5 g/d. Echocardiography showed that the mass in the right atrium was thrombotic. Heparin anticoagulant therapy was effective. CONCLUSION: SLE can involve multiple systems and various complications. Thrombus in the right atrium is a rare complication of APS. Early diagnosis and treatment are key to improving the prognosis of children.

Resveratrol Protects Osteoblasts Against Dexamethasone-Induced Cytotoxicity Through Activation of AMP-Activated Protein Kinase.

PURPOSE: Glucocorticoids are used for the treatment of inflammatory diseases, but glucocorticoid treatment is associated with bone damage. Resveratrol is a phytoalexin found in many plants, and we investigated its protective role on dexamethasone-induced dysfunction in MC3T3-E1 cells and primary osteoblasts. MATERIALS AND METHODS: MC3T3-E1 cells and primary osteoblasts were treated with dexamethasone in the presence/absence of different doses of resveratrol for 24 or 48 h. Then, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyltetrazolium (MTT) and lactate dehydrogenase (LDH) assays were used to evaluate cell viability. Apoptosis was analyzed by a flow cytometry. An alkaline phosphatase (ALP) activity assay and Alizarin Red S staining were used to study osteoblast differentiation. Expression of osteoblast-related genes was measured by real-time reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The AMP-activated protein kinase (AMPK) signaling pathway and mitochondrial expression of superoxide dismutase were evaluated by Western blotting. Intracellular reactive oxygen species (ROS), adenosine triphosphate (ATP) content, mitochondrial-complex activity, and mitochondrial DNA content were measured to evaluate mitochondrial function. RESULTS: Resveratrol induced the proliferation and inhibited apoptosis of osteoblasts in the presence of dexamethasone. Resveratrol increased the ALP activity and mineralization of osteoblasts. Resveratrol also attenuated dexamethasone-induced inhibition of mRNA expression of osteogenesis maker genes, including bone morphogenetic protein-2, osteoprotegerin, runt-related transcription factor-2, and bone Gla protein. Resveratrol alleviated dexamethasone-induced mitochondrial dysfunction. Resveratrol strongly stimulated expression of peroxisome proliferator-activated receptor-γ coactivator 1α and sirtuin-3 genes, as well as their downstream target gene superoxide dismutase-2. Resveratrol induced phosphorylation of AMPK and acetyl-CoA carboxylase (ACC). Blockade of AMPK signaling using compound C reversed the protective effects of resveratrol against dexamethasone. CONCLUSION: Resveratrol showed protective effects against dexamethasone-induced dysfunction of osteoblasts by activating AMPK signaling.

3,3'-Bis(4-nitro-phen-yl)-1,1'-(p-phenyl-ene)dithio-urea dimethyl sulfoxide disolvate.

The asymmetric unit of the title compound, C(22)H(16)N(6)O(6)S(2)·2C(2)H(6)OS, consists of one half-mol-ecule of the centrosymmetric thiourea derivative and one molecule of dimethyl sulfoxide (DMSO). The carbonyl group forms an intra-molecular hydrogen bond with the NH group, creating a six-membered (C-N-C-N-H⋯O) ring. Two other N-H⋯O hydro-gen bonds link one mol-ecule of the thio-urea to two mol-ecules of DMSO.

N-(2-Chloro-benzo-yl)-N'-(3-pyrid-yl)thio-urea.

In the mol-ecule of the title compound, C(13)H(10)ClN(3)OS, the dihedral angles between the plane through the thio-urea group and the pyridine and benzene rings are 53.08 (3) and 87.12 (3)°, respectively. The mol-ecules are linked by inter-molecular N-H⋯N hydrogen-bonding inter-actions to form a supra-molecular chain structure along the a axis. An intra-mol-ecular N-H⋯O hydrogen bond is also present.

2,2'-Dichloro-1,1'-[(propane-1,3-diyldi-oxy)bis-(nitrilo-methyl-idyne)]dibenzene.

The title compound, C(17)H(16)Cl(2)N(2)O(2), assumes a V-shape configuration with a dihedral angle between the two halves of the mol-ecule of 79.60 (4)°. The asymmetric unit comprises one half-mol-ecule with a crystallographic twofold rotation axis passing through the central C atom. There are weak inter-molecular π-π stacking inter-actions between neighbouring benzene rings with inter-molecular plane-to-plane distances of 3.277 (6) and 3.465 (5) Šalong the a and c axes, respectively. In the crystal structure, weak inter-molecular C-H⋯O bonds link each mol-ecule to four others to form an infinite three-dimensional network.

3,3'-Dibromo-1,1'-[ethyl-enedioxy-bis(nitrilo-methyl-idyne)]dibenzene.

In the centrosymmetric title compound, C(16)H(14)Br(2)N(2)O(2), the intra-molecular interplanar distance between the parallel benzene rings is 1.305 (3) Å, while the inter-molecular interplanar distance (between neighbouring mol-ecules) is 3.463 (3) Å, exhibiting obvious strong inter-molecular π-π stacking inter-actions.

Proteome responses of Gracilaria lemaneiformis exposed to lead stress.

Proteome response of plants is an important process that enables them to cope with environmental stress including metal stress. In this study, the proteome of Gracilaria lemaneiformis exposed to lead was investigated. Two-dimensional gel electrophoresis analysis revealed 123 protein spots, among which 14 proteins were significantly differentially expressed and identified using MALDI-TOF MS. Two of the up-regulated proteins were identified and predicted to be involved in photosynthesis and signal transduction, while eleven down-regulated proteins were functionally grouped into five classes including photosynthesis, energy metabolism, protein metabolism, carbohydrate transport and metabolism, and antioxidation proteins. There was also an up-regulation in superoxide dismutase, peroxidase, glutathione s-transferase, and heat-shock protein 70 upon Pb exposure. Proteomic studies provide a better picture of protein networks and metabolic pathways primarily involved in intracellular detoxification and defense mechanisms.