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PubMed2006

Peripheral proteasome and caspase activity in Parkinson disease and Alzheimer disease.

BACKGROUND: Defects of the ubiquitin-proteasome (UP) system, a multicatalytic complex degrading polyubiquitinated proteins, may intervene in the pathogenesis of neurodegenerative disorders characterized by intracellular formation of protein aggregates such as Parkinson disease (PD) and Alzheimer disease (AD) by inducing proapoptotic conditions. METHODS: The authors measured the activity of proteolytic UP core, proteasome 20S, and of proapoptotic caspase-3 and -9 in peripheral blood lymphocytes (PBLs) of PD and AD patients to establish whether changes in these systems are detectable peripherally. RESULTS: Proteasome 20S activity was reduced in PBLs of treated PD patients vs healthy controls (mean +/- SEM: 1.0 +/- 0.1 vs 2.3 +/- 0.2 nmol 7-amino-4-methylcoumarin (AMC)/10(6) cells, p < 0.001), whereas marked increases in caspase-3 activity (1370 +/- 153 vs 586 +/- 104 pmol AMC/10(6) cells, p < 0.001) and caspase-9 activity (873 +/- 86 vs 304 +/- 27 U/10(6) cells, p < 0.001) were found. Increased caspase-9 activity was also detected in PBLs of untreated PD patients (900 +/- 193 U/10(6) cells). PD duration and severity (Unified Parkinson's Disease Rating Scale score) were inversely correlated with proteasome 20S activity and directly correlated with caspase-3 activity. An inverse correlation was also observed in PD patients between caspase-3 activity and proteasome 20S activity. No significant changes in proteasome 20S or caspase activity or correlations between biochemical and clinical variables were found in patients with AD. CONCLUSIONS: A decrease in proteasome activity, possibly related to caspase activation, is detectable in peripheral blood lymphocytes of patients with Parkinson disease but not patients with Alzheimer disease, suggesting that these variables may be considered for the development of peripheral biomarkers of Parkinson disease.

Aged↗
PubMed1998

The U.S. EPA Conference on Preventable Causes of Cancer in Children: a research agenda.

On 15-16 September 1997, the U.S. Environmental Protection Agency sponsored the Conference on Preventable Causes of Cancer in Children. The conference was convened to examine rising trends in reported incidence of childhood cancer and the association of these trends with environmental exposures. This paper summarizes recommendations for future research offered by participants. These recommendations included more collaborative research integrating epidemiology, molecular biology, toxicology, and risk assessment; the development of better protocols for toxicologic testing including carcinogenicity using young animals; and research focused on specific periods of development during which susceptibility to environmental agents may be enhanced. Also recommended was enhanced use and development of molecular biomarkers for identification of susceptible populations, and documentation of exposures and effects in epidemiologic and toxicologic studies. Although toxicologic testing is considered essential to determine the effects of potential carcinogens on biological organisms, participants emphasized the need to link these findings with epidemiologic and exposure assessment research.

Age Factors↗
PubMed2003

Molecular targets as therapeutic strategies in the management of breast cancer.

Although the molecular and genetic determinants of most sporadic breast cancers remain unknown, increasing understanding of molecular and genetic events affecting breast carcinogenesis has provided information about the potential roles of specific biomarkers in tumour development and spread. It is now recognised that mutations of some tumour suppressor genes appear to play important early roles in the formation of some breast cancers. In addition, alterations in proto-oncogenes may contribute to the development of some breast cancers. The study of breast tumour biology at the molecular level has led to the development of targeted drug design, which provides a variety of agents targeted at specific molecules for the prevention, diagnosis and treatment of breast cancer. This review will describe the recognised molecular targets in breast cancer.

Angiogenesis Inhibitors↗
PubMed2004

The efficacy of a brief alcohol intervention combined with %CDT feedback in patients being treated for type 2 diabetes and/or hypertension.

OBJECTIVE: Alcohol biomarkers are being developed to improve a physician's ability to identify and intervene with patients with chronic medical problems adversely affected by heavy alcohol use. This article reports the findings of a brief intervention trial which included feedback to patients of their carbohydrate-deficient transferrin (CDT) test results. METHOD: A pilot study was conducted to test the efficacy of brief clinician advice to reduce alcohol use and improve health status in a sample of 151 patients being treated for Type 2 diabetes and hypertension. The intervention included informing patients of their CDT levels. The patients were randomized to a usual care or brief intervention group. RESULTS: There were no significant differences at baseline between the two groups in alcohol use, CDT levels, addiction rates, age, gender, socioeconomic status or health status measures. Following brief intervention, significant differences were observed in the intervention group in alcohol use and CDT: The proportion of heavy drinkers at the 12-month follow-up compared with baseline decreased from 35.8% to 24.7% in the intervention group, with no change in the control group (p < .044). CDT levels decreased as well from 2.79% to 2.41% (16% change) in the control group and 3.05% to 2.35% (28% change) in the intervention group, with significantly more intervention-group patients reducing their CDT level by at least 25% (p < .006). CONCLUSIONS: The study provides new information suggesting brief intervention, combined with feedback on CDT levels, can reduce alcohol use and %CDT in a sample of primary care patients being treated for Type 2 diabetes and hypertension.

Adult↗
PubMed2005

Stimulus frequency dependence of the central and peripheral somatosensory evoked activity in rats treated with various pesticides.

Rats were treated with a combination of insecticide agents in different timing schemes. In acute administration, 1/5 LD50 of the three insecticides: dimethoate, propoxur and cypermethrin, or their combination, was given once by gavage. In the developmental model, female rats received oral doses of 1/25 LD50 of the above insecticides in combination in three timing schemes including pregnancy and lactation. Responses in the somatosensory cortex and in the tail nerve, evoked by peripheral electric stimulation, were recorded in acute preparation under urethane anesthesia. It was tested whether the parameters of the cortical and peripheral evoked response are dependent on the frequency and whether this dependence is different in control and treated animals. The latency increase of the cortical responses with increasing stimulation frequency was significantly stronger in rats treated acutely with cypermethrin and the combination, and in rats receiving the combination during both intra- and extrauterine development. On the duration, the effects were less clear. Frequency dependent increase of the tail nerve action potential latency was significantly intensified by cypermethrin, and the amplitude decrease, by cypermethrin and dimethoate. Fatigue of this response during a stimulation series was also altered by the insecticides. Frequency dependence and fatigue possibly reflect the actual state of the nervous system and may have the potency to be developed to functional biomarkers.

Action Potentials↗
PubMed2006

Developing a tool for noninvasive monitoring of renal allografts.

Renal transplantation has emerged as the therapy of choice for many patients with end-stage renal disease. One of the major goals is to tailor immunosuppressive therapy to the individual needs of every patient at every time point post transplant, balancing the risk for rejection and over-immunosuppression. Such individualized treatment will require assays that can detect harmful processes in the allograft early and that can be measured repeatedly. In this review, advantages and disadvantages of current assays to monitor renal allografts noninvasively and how proteomic technology might contribute to the development of novel biomarkers to improve patient management will be discussed.

Animals↗
PubMed2003

Noninvasive molecular detection of cancer -- the bench and the bedside.

The more profound understanding of the genetics and molecular pathways driving human tumorigenesis is paralleled by an ongoing interest to translate this knowledge into development of cancer biomarkers, termed molecular tumor markers. The molecular changes observed in tumors frequently constitute early events which are detectable as signatures of malignancy in body fluids and their occurrence may precede clinical cancer diagnosis. Thus, beyond applicability on tissue samples, molecular markers for tumor signatures should allow noninvasive or minimally invasive diagnosis in blood and/or other body fluid samples. However, to qualify as a clinically useful molecular tumor marker for initial diagnosis and detection of recurrent disease, a molecular tumor marker must have better test characteristics (sensitivity, specifity) than currently applied tumor markers. A molecular tumor marker should also be suitable for screening purposes by defining the subset of individuals for which definite cancer diagnosis by more invasive and/or expensive additional investigations is indicated. In addition, there is a demand for molecular tumor markers to be used as reliable surrogate endpoints in cancer prevention trials. Recommendation for the use of individual molecular tumor markers within evidence-based medicine criteria should ideally be derived from their overall efficacy to reduce tumor-specific mortality. This review focuses on DNA based, RNA based and proteomics based molecular methods of noninvasive cancer detection in bodily fluids and assess the value of these methods for the current and future clinical management of cancer patients.

Biomarkers, Tumor↗
PubMed2006

Proteomic strategies for individualizing therapy of acute myeloid leukemia (AML).

Acute myeloid leukemia (AML) is an aggressive hematological malignancy characterized by accumulating myeloid precursor cells in the bone marrow, with approximately 2-3 months 50% survival if left untreated. With current treatment modalities the five years overall survival hardly exceeds 50%. Cytogenetics and molecular diagnostics guide the clinician to select individualized therapy in certain subsets of AML, achieving long-term survival above 70% of these cases. However, approximately half of the AML patients have no risk stratifying features, and early reports indicate that proteomic approaches may be utilized for disease classification as well as development of novel biomarkers related to prognosis, diagnosis, and choice of therapeutic regimen. Proteomics, here defined as the analysis of all proteins in a cell, in a cell compartment or in a signaling pathway, has probably its greatest potential in investigating pathways that are easily targeted by small molecules or therapeutic antibodies. The major methodological challenges include detection sensitivity in a limited clinical material, a problem that in some cases can be solved through designated multiplexed protein assays based on single cells or cell extracts. In this review we will discuss pharmacoproteomic studies of drugs regulating leukemia specific targets like all-trans retinoic acid, histone deacetylase inhibitors, proteasome inhibitors and tyrosine kinase inhibitors, as well as studies on drug resistance and graft-versus-host studies during stem cell transplantations. These studies indicate new avenues in AML diagnostics, individualized therapy design and therapy response surveillance for the clinician.

Acute Disease↗
PubMed1998

Voltage dependent calcium channels in mammalian spermatozoa.

Calcium influx is an absolute requirement for the physiological acrosome reaction in sperm from all sources examined, both invertebrate and mammalian. Pharmacological studies suggest that the major channel in the sperm head plasma membrane responsible for modulating calcium entry and intracellular ionized calcium levels could be either an L-type (a class of high voltage-activated) or a T-type (low voltage-activated) voltage-dependent calcium channel. Patch clamp analysis of calcium currents in immature spermatogenic cells demonstrates the presence of T-type currents. Therefore, an argument has been put forth that the acrosome reaction of ejaculated sperm is regulated by a T-type calcium channel. However, indirect analysis of calcium currents in mature sperm after transfer of ion channels to planar lipid bilayers detects three current types, including that similar, but not identical, to an L-type channel, but no T-type currents. Molecular cloning of the alpha-1 pore forming subunit of calcium channels expressed in the male reproductive tract and in ejaculated sperm has resolved this controversy, demonstrating the existence of only high voltage-activated channels. Further analysis of the alpha-1 subunit isoform from rat and human testis and sperm suggests that, as a result of alternate splicing, this L-type alpha-1 subunit could produce calcium currents that were T-like, e.g., transient, rapidly inactivating with slow deactivation. Multiple splice variants of this isoform were detected in human testis, suggesting a correlation with intra-individual variation in the ability of sperm to undergo an induced acrosome reaction and with male infertility. These variants could be developed as useful biomarkers for susceptibility to environmental and occupational toxicants. Knowledge of calcium channels structure will also contribute to design of new male contraceptives based on existing calcium channel antagonists.

Acrosome Reaction↗
PubMed2026

Identification of Critical Genes for Recurrent Aphthous Ulcer by Transcriptome Data Analysis and Mendelian Randomization.

PURPOSE: Recurrent aphthous ulcer (RAU) is a common oral mucosal disorder with a poorly understood etiology, significantly affecting patients' quality of life. This study aims to investigate critical genes linked to RAU and explore their biological mechanisms using transcriptomic data and Mendelian randomization (MR) analysis. MATERIALS AND METHODS: RAU-related gene expression data from the GEO database (GSE37265) were analyzed to identify differentially expressed genes (DEGs). A two-sample MR approach was used to assess the causal impact of expression quantitative trait loci (eQTL) on RAU. Critical genes were identified by intersecting DEGs with significant MR findings. GO and KEGG pathway enrichment analyses were performed, along with GSEA and immune cell infiltration analysis, to investigate the functions and mechanisms of these genes in RAU. RESULTS: A total of 184 differentially expressed genes (DEGs) were identified, while 339 RAU-associated genes were screened through MR analysis. Cross-validation further identified 7 critical genes. Among these, CCR1, ERP27, HCK, MICB, and SLC2A3 showed protective associations with RAU risk, whereas CD177 and IFITM1 were positively associated with increased risk. Enrichment analysis revealed that these genes are involved in specific biological processes, including cell migration, immune response, and metabolic regulation, which are closely linked to RAU pathogenesis. CONCLUSION: This systematic study comprehensively investigates the critical causative genes underlying RAU, emphasizing the intricate relationships between immune regulation and metabolic disturbances in its pathology. These findings lay a solid foundation for the development of novel biomarkers and may inform future research on targeted therapeutic strategies for RAU.

Stomatitis, Aphthous↗
PubMed2026

The role of Epstein-Barr virus in NK/T cell lymphoproliferative disorders: molecular mechanisms and potential therapeutic strategies.

Epstein-Barr virus (EBV) is a widely prevalent lymphotropic &#x3b3;-herpesvirus, with approximately 95% of the population showing evidence of infection at some point during their lifetime. While most infections are asymptomatic or follow a self-limiting clinical course, in certain populations, EBV can lead to a range of lymphoproliferative disorders (LPDs), particularly subtypes originating from T cells and natural killer (NK) cells, which are often characterized by highly aggressive disease progression. This review aims to systematically discuss the molecular basis of EBV infection, covering its viral biological properties, regulation of the latent and lytic cycles, key viral protein functions (e.g., LMP1, LMP2A, EBNA1), miRNA regulatory mechanisms, and the activation of various host signaling pathways (such as NF-&#x3ba;B, PI3K-AKT, JAK-STAT) that contribute to the maintenance of latent infection, cell transformation, and immune evasion. Additionally, the review focuses on the pathogenic contributions of these mechanisms in EBV-related T/NK cell lymphoproliferative diseases. Research highlights include the in-depth analysis of virus-host genome interaction mechanisms, the identification of novel molecular biomarkers, and the development of targeted therapeutic strategies (e.g., PD-1/PD-L1 immune checkpoint inhibitors, EBV-specific T cell therapy). Through this comprehensive review, it is hoped that personalized medicine and artificial intelligence-assisted multimodal decision-making will be applied to the precise prevention and treatment of EBV-related diseases.

Humans↗
PubMed2004

Primer on medical genomics. Part XIV: Introduction to systems biology--a new approach to understanding disease and treatment.

The advent of the "-omics revolution" has forced us to reevaluate our ability to acquire, measure, and handle large data sets. Omic platforms such as expression arrays and mass spectrometry, with their exquisite selectivity, sensitivity, and specificity, are unrivaled technologies for detection, quantitation, and identification of DNA, messenger RNA, proteins, and metabolites derived from complex body tissue and fluids. More recently, attempts have been made to capture the utility of these platform technologies and combine them under the umbrella of systems biology, also referred to as pathway, network, or integrative biology. Applied systems biology is the integrated analysis of genetic, genomic, protein, metabolite, cellular, and pathway events that are in flux and interdependent. It necessitates the use of a variety of analytic platforms as well as biostatistics, bioinformatics, data integration, computational biology, modeling, and knowledge assembly protocols. Such sophisticated analyses may provide new insight into the understanding of disease processes and mechanisms of action of pharmaceutical agents. Ultimately, this requires a perspective on how complex systems behave and are modulated. In this regard, systems biology, more appropriately considered as a process containing a series of modules, aims to provide tools and capabilities to carry out such tasks. We describe the essentials required to carry out systems biology experiments, the method in which integrated data in the form of a systems biology correlation network affords new insight into understanding disease, and the vista of developing more efficient biomarkers and therapeutic agents.

Animals↗
PubMed2000

Morphodensitometric analysis of protein kinase C beta(II) expression in rat colon: modulation by diet and relation to in situ cell proliferation and apoptosis.

We have recently demonstrated that overexpression of PKC beta(II) renders transgenic mice more susceptible to carcinogen-induced colonic hyperproliferation and aberrant crypt foci formation. In order to further investigate the ability of PKC beta(II) to modulate colonocyte cytokinetics, we determined the localization of PKC beta(II) with respect to cell proliferation and apoptosis along the entire colonic crypt axis following carcinogen and diet manipulation. Rats were provided diets containing either corn oil [containing n-6 polyunsaturated fatty acids (PUFA)] or fish oil (containing n-3 PUFA), cellulose (non-fermentable fiber) or pectin (fermentable fiber) and injected with azoxymethane (AOM) or saline. After 16 weeks, an intermediate time point when no macroscopic tumors are detected, colonic sections were utilized for immunohistochemical image analysis and immunoblotting. Cell proliferation was measured by incorporation of bromodeoxyuridine into DNA and apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling. In the distal colon, PKC beta(II) staining was localized to the upper portion of the crypt. In comparison, proximal crypts had more (P < 0.05) staining in the lower tertile. AOM enhanced (P < 0.05) PKC beta(II) expression in all regions of the distal colonic crypt (upper, middle and lower tertiles). There was also an interaction (P < 0.05) between dietary fat and fiber on PKC beta(II) expression (corn/pectin > fish/cellulose, fish/pectin > corn/cellulose) in all regions of the distal colonic crypt. With respect to colonic cell kinetics, proliferation paralleled the increase in PKC beta(II) expression in carcinogen-treated animals. In contrast, apoptosis at the lumenal surface was inversely proportional to PKC beta(II) expression in the upper tertile. These results suggest that an elevation in PKC beta(II) expression along the crypt axis in the distal colon is linked to enhancement of cell proliferation and suppression of apoptosis, predictive intermediate biomarkers of tumor development. Therefore, select dietary factors may confer protection against colon carcinogenesis in part by blocking carcinogen-induced PKC beta(II) expression.

Animals↗
PubMed2001

Diminished expression of S100A2, a putative tumor suppressor, at early stage of human lung carcinogenesis.

To identify and understand early events in lung carcinogenesis, we used a cDNA array to screen for genes that are expressed differentially in normal human bronchial epithelial (NHBE) cells and a tumorigenic cell line (1170-I) derived from immortalized HBE cells after exposure to cigarette smoke condensate in vivo. Among these genes, we have identified the S100A2 gene, which encodes a nuclear calcium-binding protein, as being down-regulated in the 1170-I cells. Because this gene has been implicated as a tumor suppressor in breast cancer, we examined its potential role as a tumor suppressor in lung carcinogenesis. Levels of S100A2 transcript and protein, which were high in NHBE cells, decreased by up to 50% in immortalized HBE cells (BEAS-2B and 1799) and to low to nearly undetectable levels in transformed (1198) and tumorigenic (1170-I) HBE cells. Furthermore, S100A2 mRNA and protein were undetectable in 8 and expressed at a reduced level in 3 of 11 non-small cell lung cancer (NSCLC) cell lines. Positive immunohistochemical staining of S100A2 was detected in the majority (75-83%) of normal and hyperplastic lung tissues, whereas it was detected in <10% of metaplastic lung tissues, squamous cell carcinoma, and adenocarcinoma. Treatment of 1170-I HBE and NSCLC cells with 5-aza-2'-deoxycytidine resulted in partial restoration of S100A2 expression in seven of eight cell lines. Indeed, CpG methylation was detected in the promoter region of the S100A2 gene. Our results suggest that S100A2 expression is suppressed early during lung carcinogenesis, possibly by hypermethylation of its promoter, and that its loss may be a contributing factor in lung cancer development or a biomarker of early changes in this process.

Animals↗
PubMed2000

[Applications of aryl hydrocarbon hydroxylase in diagnosis of lung cancer].

OBJECTIVE: To develop a new biomarker and improve early diagnosis of lung cancer in clinic. METHODS: Aryl hydrocarbon hydroxylase (AHH) activity in peripheral lymphocytes was detected using spectrofluorometer in 51 healthy subjects, 30 patients with benign lung diseases, 93 patients with lung cancer (including 30 patients with lung adenocarcinoma, 30 with lung squamous carcinoma, 33 with small cell lung cancer, 28 of them were at I, II stage, 35 at III stage, 30 at IV stage), and the results were compared with carcinoembryonic antigen(CEA). RESULTS: AHH activity in peripheral lymphocytes was (4.9 +/- 2.1) pmol.min-1 x 10(-6) cells in patients with lung cancer, (7.3 +/- 1.9) pmol.min-1 x 10(-6) cells in patients with lung squamous carcinoma, (1.1 +/- 0.7) and (1.2 +/- 0.6) pmol.min-1 x 10(-6) cells in healthy subjects and patients with benign lung diseases respectively. It is indicated that AHH activity in peripheral lymphocytes was significantly increased in patients with lung cancer, especially with lung squamous cancer. Of patients with lung cancer, AHH activity was (3.7 +/- 1.4) pmol.min-1 x 10(-6) cells in patient at stage I, II, (5.1 +/- 2.1), (7.1 +/- 1.8) pmol.min-1 x 10(-6) cells at stage III and stage IV, and AHH activity increased when patients deteriorated, vice versa. Diagnosis evaluation test indicated that AHH was over 80% in both sensitivity and specificity. AHH relative risk to lung cancer was 2.83. CONCLUSIONS: AHH is a promising marker of lung cancer which is special for lung squamous carcinoma, it can be used in clinical diagnosis, mornitoring and prognosis estimating in patients with lung cancer.

Adult↗
PubMedDate not supplied

Biological effects of EMF exposure on Ets genes.

Ets genes are transcription factors expressed in different tissues. Biochemical pathways interfering with the intracellular calcium ion concentration are known to influence members of this gene family. Considering experimental observations and previous reports, we proposed a hypothetical model of interaction between EMF and Ets, based on possible interference in pathways involving calcium as a second messenger. This approach comprehend different hypothesis and may contribute to clarify EMF biological effects, providing an experimental model and a procedure based on gene expression analysis. Additional knowledge on biological mechanisms is required to support these promising results. Further experiments are in progress to assess the role of EMF in modulating gene expression and its biological meaning. Identification of early endpoints is needed for mechanism understanding and development of sensitive biomarkers for molecular epidemiology studies.

Animals↗
PubMed2004

Gene expression and prognostic significance in ovarian cancer.

Epithelial ovarian cancer (EOC) is the leading cause of death from gynecological malignancies in the United States. Most patients with EOC will respond to surgical debulking followed by platinum and paclitaxel based chemotherapy. Unfortunately, the relapse rate within 2 years is more than 70%. The molecular events leading to the development of EOC and the molecular factors that may predict response to treatment are not well established. Such knowledge would not only improve the understanding of the biology of EOC, but may help in the identification of new tumor markers and the design of molecular therapies for EOC. A literature review was conducted using MEDLINE to delineate studies that investigated gene expression in ovarian cancer correlated with outcome. A review is presented of the expression and role of the BRCA1 and 2 genes, p53, amplification of Her2/neu, PIK3CA, AKT2, K-ras, c-myc, BRCA1, p53, p16, and p27 in ovarian cancer. Additionally, a review of the use of microarray technology is presented and its use in determining expression patterns in ovarian cancer. The accumulation of data derived from new technologies, as well as that obtained from well-established methods, has provided new insights into gene expression profiles in EOC. The utilization of novel technologies that allow high throughput analysis of thousands of genes may lead to the development of new biomarkers or novel therapies that are urgently needed in this deadly disease.

Female↗
PubMed2005

Soil health -- a new challenge for microbiologists and chemists.

Soil health refers to the biological, chemical, and physical features of soil that are essential to long-term, sustainable agricultural productivity with minimal environmental impact. Thus, soil health provides an overall picture of soil functionality. Although it cannot be measured directly, soil health can be inferred by measuring specific soil properties (e.g. organic matter content) and by observing soil status (e.g. fertility). There is also increased interest in studying soil microorganisms in their particular environments, as microbial diversity is intimately related to soil structure and function. One of the key objectives in determining soil health is to acquire indicators that can be used to evaluate the soil's current status and hence to develop sustainable agricultural systems. In this regard, significant progress has been made over the last few years in the development of specific biomarkers and macromolecular probes, enabling rapid and reliable measurements of soil microbial communities. In addition, modern molecular biological techniques, such as fluorescence in situ hybridization (FISH), reverse transcriptase polymerase chain reaction (RT-PCR), denaturing gradient gel electrophoresis (DGGE), and terminal restriction fragment length polymorphism (T-RFLP), have facilitated the analysis of microbial biodiversity and activity, whereas the application of modern analytical techniques, such as nuclear magnetic resonance (NMR) and pyrolysis-gas chromatography-mass spectrometry (Py-GC-MS), have provided data on soil chemistry. The combination of these two approaches offers promise in determining soil health status.

Bacteria↗