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PubMed1990

Analysis of the mechanisms involved in NK resistance induced by a new tumor factor NK-RIF.

The mechanisms involved in susceptibility or resistance of neoplasic cells to lysis by NK cells are not well known. We have recently described a 12-kDa factor (NK-RIF), produced and released by different tumor cell lines, making K562 resistant to NK lysis without affecting the cytotoxic function of NK effector cells. In this paper we further study the mechanism involved in NK resistance of K562 mediated by NK-RIF and its biological implications. The results show that NK-RIF does not affect the binding capacity of target and effector cells nor the levels of HLA class I antigen expression on the target cells, as a proof that resistance to NK-mediated lysis is not always associated with a defect in target effector binding or with an increased MHC class I antigen expression. However NK-RIF-treated K562 loses its capacity to induce NK cell activation and the subsequent capacity to release NKCF and makes K562 resistant to lysis by NKCF. Therefore our results show that induction of resistance to NK cytotoxicity can be the result of the modulation of target structures responsible for inducing effector cell activation without affecting target/effector binding molecules. This indicates that the structures involved in adherence and activation of NK cells have a different nature and that molecules other than HLA participate in NK resistance.

Biological Factors↗

PubMed1992

Superior repositioning of the maxilla combined with mandibular advancement: mandibular RIF improves stability.

Postsurgical changes in 24 patients who had rigid internal fixation (RIF) of the mandible with screws after combined superior repositioning of the maxilla and mandibular advancement were compared with 53 patients who underwent the same surgery but who had intraosseous wire fixation, skeletal suspension wires, and 8 weeks of maxillomandibular fixation (MMF). During the first 8 weeks after surgery, the mean posterior relapse of the mandible was greater in the MMF group than in the RIF group (for example, -1.1 mm versus 0.15 mm at B point), and the percentage of patients with clinically significant vertical and horizontal changes was greater in the MMF group. By 1 year, there had been slight additional mean relapse in the MMF group (-1.5 mm net relapse at B point, with 42% of the patients showing 2 mm or more relapse). In the RIF group, the mandible was more likely to be repositioned forward than posteriorly (net mean change at B point, 0.7 mm forward; 33% had 2 mm or more forward movement). In the RIF group, all but one of the patients (96%) were judged to have an excellent clinical result; in the MMF group, the corresponding figure was 60%.

Adult↗

PubMed1984

Locus unlinked to alpha-fetoprotein under the control of the murine raf and Rif genes.

The levels of alpha-fetoprotein mRNA in mice are determined by at least two trans-acting, unlinked genes, raf and Rif. raf determines the basal levels of alpha-fetoprotein mRNA in adult mice, while Rif determines its degree of inducibility during liver regeneration. To determine whether these regulatory loci affect other structural genes, we screened a murine fetal liver cDNA library for clones containing mRNA sequences that decrease after birth. One such clone, termed pH19, was identified, and its mRNA was shown to be under the control of both raf and Rif. The single-copy gene for H19 mRNA was localized to chromosome 7, and genetic crosses established that it was unlinked to either raf or Rif. It encodes a 2.5-kilobase mRNA that was identified in those tissues that produce alpha-fetoprotein: visceral endoderm, liver, and fetal gut. The repression of H19 mRNA in neonatal liver occurs several days after the decrease in alpha-fetoprotein mRNA, whereas inductions of both mRNAs during the differentiation of F9 teratocarcinoma cells into visceral endoderm were identical. The tissue-specific expression of H19 mRNA is different from that of alpha-fetoprotein in that H19 mRNA was detected also in both cardiac and skeletal muscle where no alpha-fetoprotein mRNA is produced. Despite the fact that the levels of H19 mRNA decline to 1/10th to 1/20th in cardiac muscle after birth, the adult basal levels are not under the influence of raf. This observation argues that the raf gene is a tissue-specific regulator of mRNA levels.

Animals↗

PubMed1995

Inherent cellular differences may explain the dissimilar survival of RIF-1 and KHT tumour cells under aerobic and hypoxic conditions.

Although previous work has shown striking differences in radiobiological hypoxic fraction between KHT and RIF-1 murine sarcomas, intravascular oxyhaemoglobin (HbO2 saturations have revealed less substantial variations. Using quantitative histological techniques, we have also found minor differences in the distributions of distances between tumour cells and the nearest bloods vessel for KHT versus RIF-1 sarcomas. We report here, the results of an investigation of the inherent ability of these tumour cells to withstand conditions of hypoxia by in vitro culturing under aerobic and anoxic conditions. Tumours were dissociated, seeded into culture dishes, and placed in air-tight aluminium chambers. These chambers were repeatedly evacuated and refilled with a mixture of 95% N2 and 5% CO2 over a 2.5-h period. Following anoxic exposure, cells were removed and replated, and the in vitro plating efficiency (PE) was determined using a colony survival assay. After normalizing to aerobic controls, KHT tumour cells had a significantly lower PE, following a 16-hour exposure to anoxic conditions (0.4), than RIF-1 (0.6). Increasing the hypoxic exposure to 40 h resulted in normalized PEs of 0.07 for KHT versus 0.4 for RIF-1. Although these results support the hypothesis that the two tumour lines have different inherent abilities to withstand hypoxia, they do not explain the failure of direct measures of tumour oxygenation to correlate with the radiobiological hypoxic fraction. Additional factors such as differences in oxygen diffusivity or oxygen consumption rates between tumour lines may also be involved.

Aerobiosis↗

PubMed1994

Mouse alpha-fetoprotein gene 5' regulatory elements are required for postnatal regulation by raf and Rif.

The mouse alpha-fetoprotein (AFP) gene is expressed at high levels in the yolk sac and fetal liver and at low levels in the fetal gut. AFP synthesis decreases dramatically shortly after birth to low levels that are maintained in the adult liver and gut. AFP expression can be reactivated in the adult liver upon renewed cell proliferation such as during liver regeneration or in hepatocellular carcinomas. Previously, two unlinked genetic loci that modulate postnatal AFP levels were identified. The raf locus controls, at least in part, basal steady-state AFP mRNA levels in adult liver. Rif influences the extent of AFP mRNA induction during liver regeneration. Transgenic mice were used to examine the role of 5' AFP regulatory regions in raf- and Rif-mediated control. A fragment of the AFP 5' region containing enhancer element I, the repressor, and the promoter was linked to the mouse class I H-2Dd structural gene. We demonstrate that this hybrid AFP-Dd transgene is expressed in the appropriate tissues. In addition, it is postnatally repressed and reactivated during liver regeneration in parallel with the endogenous AFP gene. Therefore, proper transcriptional control does not require the AFP structural gene. Furthermore, the AFP 5' control region is sufficient to confer raf and Rif responsiveness to the linked H-2Dd structural gene, suggesting that raf and Rif act at the level of transcriptional initiation.

Alleles↗

PubMed2002

Induction of adaptive response by low-dose radiation in RIF cells transfected with Hspb1 (Hsp25) or inducible Hspa (Hsp70).

An adaptive response results in a reduced effect of a high challenging dose of a stressor after a smaller, inducing dose has been applied a few hours earlier. Radiation-induced fibrosarcoma (RIF) cells did not show an adaptive response, i.e. a reduced effect from a high challenging dose (2 Gy) of a radiation after a priming dose (1 cGy) had been applied 4 or 7 h earlier, but cells of a thermoresistant clone (TR) derived from RIF cells did. Since the expression of inducible Hspa (also known as Hsp70) and Hspb1 (also known as Hsp25) was different in these two cell lines, the role of inducible Hspa and Hspb1 in the adaptive response was examined. When RIF cells were transfected with inducible Hspa or Hspb1, both radioresistance measured by clonogenic assays and a reduction of apoptosis were detected. The adaptive response was also acquired by these two cell lines. The inducible Hspa transfectant showed a more pronounced adaptive response than the Hspb1 transfectant. Based on these results, it appears that inducible Hspa and Hspb1 are at least partly responsible for the induction of the adaptive response in these cells. Moreover, when inducible Hspa or Hspb1 was transfected into RIF cells, co-regulation of the two genes was detected. Heat-shock factor (Hsf) was found to be at least partially responsible for the induction of the adaptive response in these cells.

Adaptation, Physiological↗

PubMed1989

31P-nuclear magnetic resonance studies of the effect of recombinant human interleukin 1 alpha on the bioenergetics of RIF-1 tumors.

The effect of a single injection of human recombinant interleukin 1 alpha (IL-1 alpha) on s.c. RIF-1 tumors in mice was studied by in vivo 31P nuclear magnetic resonance spectroscopy. Spectra were obtained before and up to 24 h after IL-1 alpha. At 2, 4, 6, and 8 h after IL-1 alpha injection, RIF-1 tumors exhibited a reduction in bioenergetic status compared to untreated controls. The Pi to beta-nucleoside triphosphate and the phosphomonoester to beta-nucleoside triphosphate ratios increased, while the phosphocreatine to Pi and phosphodiester to phosphomonoester ratios decreased. Tumor blood flow, estimated by 86RbCl uptake, decreased within 30 min after IL-1 alpha treatment. Minimum perfusion was detected at 4 h, with recovery between 6 and 12 h after IL-1 alpha treatment. Histological sections of the RIF-1 tumors revealed intravascular congestion by 2 h, extravascular hemorrhage by 4 h, and necrosis by 12 h after treatment with IL-1 alpha. The time course of bioenergetic changes in RIF-1 tumors determined by 31P-NMR spectroscopy was found to parallel the reduction and subsequent recovery of tumor blood flow.

Animals↗

PubMed1992

31P NMR spectroscopic study of the effects of gamma-irradiation on RIF-1 tumor cells perfused in vitro.

In order to examine the mechanisms underlying radiation-induced changes in phosphorus metabolite levels observed in RIF-1 tumors in vivo, RIF-1 cells in culture were perfused for up to 70 h following gamma-irradiation with 0-25 Gy and monitored continuously by 31P NMR spectroscopy at 8.5 T. Cells immobilized in the sample volume by incorporation into calcium alginate beads were bioenergetically stable, but did not replicate at the cell density used. Following an initial increase in PCr and NTP, which occurred in both control and irradiated cells, a dramatic decline in high-energy phosphates was detected beginning 24-30 h after irradiation with 15 or 25 Gy. In contrast, unirradiated cells or cells treated with 10 Gy remained metabolically stable for up to 72 h. The metabolic changes induced by irradiation of the cultured cells, which reflected cell death and lysis, were distinctly different from those observed in RIF-1 tumors in vivo during the same postirradiation time interval--an increase in high-energy relative to low-energy phosphates. This suggests that the spectral changes in vivo do not result from direct modification of cellular energy metabolism by radiation injury.

Animals↗

PubMed1991

Time-dependent effects of anesthetic agents on 31P NMR high-energy phosphates in KHT and RIF-1 fibrosarcomas.

Previous studies have reported significant radiobiological and hemodynamic effects associated with sodium pentobarbital (PB) anesthetization. The present work contrasts the effects of PB with azaperone-ketamine (AZ) in RIF-1 and KHT tumors while animal body core temperature is maintained at 37 degrees C. The primary aims were to evaluate both agents in terms of: (i) duration of anesthetic; (ii) effect on absolute levels of 31P NMR phosphocreatine (PCr) + beta-nucleoside triphosphate (beta-NTP)/inorganic phosphate (Pi) ratios; and (iii) effect on temporal variability of PCr + beta-NTP/Pi ratios. In terms of overall duration, AZ was the clear preference. Although the maintenance of 37 degrees C core temperature significantly reduced overall durations for both anesthetics, AZ animals invariably remained immobile for a minimum of 80 min. For PB, durations were highly unpredictable. With AZ, mean PCr + beta-NTP/Pi ratios were constant over the entire 80 min period for both lines. With PB, PCr + beta-NTP/Pi ratios were lower in relation to AZ for KHT at select timepoints, but highly variable among RIF-1 tumours. Since ratios under PB varied substantially with time for RIF-1 lines, measurements taken with PB are clearly not representative of the control state. Furthermore, in light of the consistent and reproducible results obtained with AZ, this anesthetic is considered a marked improvement over PB for animal studies of this nature.

Anesthetics↗

PubMed2005

Label-free characterization of cell adhesion using reflectometric interference spectroscopy (RIfS).

Reflectometric interference spectroscopy (RIfS) is a label-free, time-resolved technique for detecting interactions of molecules immobilized on a surface with ligands in solution. Here we show that RIfS also permits the detection of the adhesion of tissue culture cells to a functionalized surface in a flow system. Interactions of T cells with other leukocytes or epithelial cells of blood vessels are crucial steps in the regulating immune response and inflammatory reactions. Jurkat T cell leukemia cells rapidly attached to a transducer functionalized with a monoclonal antibody directed against the T cell receptor (TCR)/CD3 complex, followed by activation-dependent cell spreading. RIfS curves were obtained for the Jurkat derivative JCaM 1.6 (which lacks the key signaling protein Lck), cells preincubated with cytochalasin D (an inhibitor of actin polymerization), and for surfaces functionalized with an antibody directed against the coreceptor CD28. These curves differed with respect to the maximum signal and the initial slope of the increase in optical thickness. The testing of chemical inhibitors, cell surface molecules and gene products relevant to a key event in T cell immunity illustrates the potential of label-free techniques for the analysis of activation-dependent cell-surface contacts.

Antibodies↗

PubMed1984

NMR study of in vivo RIF-1 tumors. Analysis of perchloric acid extracts and identification of 1H, 31P and 13C resonances.

Perchloric acid extracts of radiation-induced fibrosarcoma (RIF-1) tumors grown in mice have been analyzed by multinuclear NMR spectroscopy and by various chromatographic methods. This analysis has permitted the unambiguous assignment of the 31P resonances observed in vivo to specific phosphorus-containing metabolites. The region of the in vivo spectra generally assigned to sugar phosphates has been found in RIF-1 tumors to contain primarily phosphorylethanolamine and phosphorylcholine rather than glycolytic intermediates. Phosphocreatine was observed in extracts of these tumor cells grown in culture as well as in the in vivo spectra, indicating that at least some of the phosphocreatine observed in vivo arises from the tumor itself and not from normal tissues. In the 31P-NMR spectra of the perchloric acid extract, resonances originating from purine and pyrimidine nucleoside di- and triphosphate were resolved. HPLC analyses of the nucleotide pool indicate that adenine derivatives were the most abundant components, but other nucleotides were present in significant amounts. The 1H and 13C resonance assignments of the majority of metabolites present in RIF-1 extracts have also been made. Of particular importance is the ability to observe lactate, the levels of which may provide a noninvasive measure of glycolysis in these cells in both the in vitro states. In addition, the aminosulfonic acid, taurine, was found in high levels in the tumor extracts.

Animals↗

PubMed2005

The Rho family GTPase Rif induces filopodia through mDia2.

Eukaryotic cells produce a variety of specialized actin-rich surface protrusions. These include filopodia-thin, highly dynamic projections that help cells to sense their external environment. Filopodia consist of parallel filaments of actin, bundled by actin crosslinking proteins. The filaments are oriented with their rapidly growing "barbed" ends at the protruding tip and their slowly growing "pointed" ends at the base. Extension occurs by polymerization at the tip and is controlled by regulation of filament capping. The Rho GTPase Cdc42 is a key mediator of filopodia formation, which it regulates through binding CRIB domain-containing effectors. Cdc42 binds and activates the WASP proteins, which in turn activate the actin-nucleating complex Arp2/3. It also binds and activates IRSp53, which recruits the Ena/WASP family protein Mena to the filopodial tip and protects elongating actin filaments from capping. Previously, we identified another Rho family GTPase, Rif, as a potent stimulator of filopodial protrusion through a mechanism that does not require Cdc42. Here we characterize the differences between filopodia induced by these two small GTPases and show that the Rif effector in this pathway is the Diaphanous-related formin mDia2. Thus, Rif and Cdc42 represent two distinct routes to the induction of filopodia-producing structures with both shared and unique properties.

Animals↗

PubMed2004

DNA-modified carbon paste electrode applied to the study of interaction between rifampicin (RIF) and DNA in solution and at the electrode surface.

Rifampicin (RIF) is an antibiotic widely used against tuberculosis and a DNA intercalator. The interaction of RIF with double-stranded (ds) and single-stranded (ss) calf thymus DNA was studied in solution as well as at the electrode surface by means of transfer voltammetry using differential pulse as stripping mode with carbon paste electrode (CPE) at 0.2M acetate buffer at pH 5.0 and at 0.2M phosphate buffer pH 7.4. Differentiations in the above-mentioned interaction at different pH values are presented and compared in order to optimize the detection of Rifampicin (RIF).

Animals↗

PubMed1999

Yeast Ku protein plays a direct role in telomeric silencing and counteracts inhibition by rif proteins.

Yku70p/Yku80p, the yeast Ku protein homologue, is a DNA end-binding heterodimer involved in non-homologous end joining. It also binds to telomeres, where it plays an important role in the maintenance of telomeric DNA structure [1] [2] [3] [4] [5]. Ku protein, together with Rap1p, a telomeric DNA (TG(1-3) repeat)-binding protein, is also required to initiate transcriptional silencing, or telomere-position effect (TPE). Here, we provide evidence for a direct role of Ku in TPE, which is most likely to be in either the recruitment or activation of Sir4 protein at the telomere. Surprisingly, however, the essential role of Ku in TPE is to overcome the inhibitory effect of two Rap1p-interacting proteins, Rif1p and Rif2p, both of which also play an important role in telomere length regulation [6] [7]. Previous studies showed that Rif and Sir proteins compete for binding to the carboxyl terminus of Rap1p [7] [8] [9]. In the absence of this competition, for example, when RIF genes are mutated, Ku is no longer necessary for TPE, whereas the Rap1p carboxyl terminus is still absolutely required. We show that Rif1p is localized to telomeres, indicating that its inhibitory effect on TPE is direct. Our data implicate a role for Ku in the competition between Sir and Rif proteins for access to the telomeric array of Rap1p molecules, which results in a balance between telomeric silencing and telomere length control.

Antigens, Nuclear↗

PubMed1982

Sensitivity of normal mouse marrow and RIF-1 tumour to hyperthermia combined with cyclophosphamide or BCNU: a lack of therapeutic gain.

The effect of simultaneous whole-body heat (45 min 41 degrees C) on cyclophosphamide (CTX) and BCNU toxicity to normal mouse marrow stem cells and to the RIF-1 tumour in C3H/He mice has been studied. Marrow stem-cell survival was assayed by the spleen-colony technique at both 2 and 24 h after treatment, and also by following peripheral WBC count during the weeks after treatment. Heat potentiation of CTX toxicity to marrow stem cells was similar at both times and 24 h after treatment heat was dose-modifying with a DMF of 2.0. The heat potentiation of BCNU toxicity to stem cells was much greater at 24 h than at 2 h, and at 24 h had a DMF of 2.1. Peripheral WBC counts supported the results from 24 h assay for both drugs. RIF-1 tumour response was assayed by clonogenic cell survival measured 24 h after treatment, and by growth delay. For clonogenic tumour-cell survival after CTX, heated and unheated curves were parallel at doses above 75 mg/kg, yielding DMFs varying between 1.9 and 1.4 according to dose. DMFs for BCNU were also dose-dependent, lying between 2.0 and 1.6, the RIF-1 tumour being much less sensitive to BCNU than to CTX. Growth-delay data agreed with clonogenic cell survival. Therapeutic ratios for the combination of heat with CTX or BCNU fell in the range 0.91--0.69, according to dose, i.e. no gain or even therapeutic loss under the conditions of this study.

Bone Marrow↗

PubMed2003

Spatial heterogeneity and temporal kinetics of photosensitizer (AlPcS2) concentration in murine tumors RIF-1 and MTG-B.

In this study we compared the photosensitizer concentration in two experimental murine tumors using an in situ fluorescence detection instrument to examine temporal and spatial variations, after intravenous versus intratumor injection. Also, the variations in the estimate as detected by large area sampling and micro-region sampling are compared, in order to determine what the inter-tissue and inter-animal variations are, and how the method of sampling affects this estimate. The latter study was carried out ex vivo in the same tumors, which had been harvested and frozen after in vivo measurements were made. The photosensitizer, disulphonated aluminum phthalocyanine (AlPcS2) was injected either intravenously (IV) or directly into the tumor (ITu), using two murine models, MTG-B (mammary adenocarcinoma) and RIF-1 (radiation-induced fibrosarcoma) grown subcutaneously on the flank. An in situ microsampling fluorescence probe was used to assess photosensitizer concentration, through real-time measurement of the remitted intensity. The photosensitizer concentration was evaluated at 8 time endpoints between 15 min and 48 h post-injection. Inter-tumor and intra-tumor variations were assessed by repeated samples from the tumor tissues. The average photosensitizer level reaches a peak between 3 to 6 h in both tumor and normal tissues using IV administration, but peaks within 1 h following ITu administration. MTG-B tumors demonstrated a factor of 2 higher uptake than RIF-1 tumors. The pharmacokinetic uptake rates of the RIF-1 tumor were 3 times faster than for MTG-B, while there was no statistical difference in their clearance rates. Preferential uptake of AlPcS2 by both tumors compared to contra-lateral flank subcutaneous normal tissue was documented, with ITu injection exceeding IV injection by a factor of 10 in the tumor to normal tissue ratio. Inter-animal standard deviation in the mean fluorescence was near 76% for both routes of administration, but estimates of the variation within tumor were near 16% standard deviation when a large sampling volume was used. In contrast, microscopic intra-tumor standard deviation in the mean estimate was near 76%, with IV injection, indicating that high heterogeneity exists in the photosensitizer concentration on a smaller distance scale. The inter-tumor variation was reduced by ITu injection, but at the expense of increasing intra-tumor variation.

Adenocarcinoma↗

PubMed1992

In vitro and in vivo studies using BW12C: toxicity, haemoglobin modification and effects on the radiosensitivity of normal marrow and RIF-1 tumours in mice.

BW12C binds to haemoglobin, shifting the oxygen saturation curve to the left, and is under investigation as an inducer of tumour hypoxia. The intrinsic cellular toxicity of the drug to RIF-1 and EMT6 cells in monolayer culture was studied, and IC50 values of 100 micrograms ml-1 for 24 h exposure and 10 micrograms ml-1 for 4-day exposure were measured. The LD50 (95% CL) in C3H mice was shown to be 124 (118-130) mg kg-1 for normal, rapid i.v. injection of the drug, and 173 (164-181) mg kg-1 for slow injection. The well-tolerated dose of 70 mg kg-1, used for all subsequent studies, was shown to produce a maximum haemoglobin modification of 70% 5 min after i.v. administration. This effect decayed with a half-life (+/- 2 se) of 76 +/- 8 min, giving 50% modification at 30 min and 22-25% modification at 2 h after administration. A dose of 70 mg kg-1 BW12C administered 30 min before irradiation protected animals against lethality, and increased the radiation LD50 (95% CL) from 7.16 (7.05-7.27) to 7.86 (7.70-8.02) Gy, representing a DMF of 1.1. In contrast the same drug dose and schedule did not alter normal marrow CFUs radiosensitivity at doses up to 6 Gy. The dose of 70 mg kg-1 did, however, cause marked radioprotection in RIF-1 intramuscular leg tumours. Four- to seven-fold increases in survival were measured by clonogenic cell survival immediately or 24 h after treatment. Protection was maximal 15 to 30 min after administration, and absent by 2 h. The drug did not protect RIF-1 cells in culture against radiation damage, indicating that the in vivo effect is indirect. BW12C is therefore an effective tumour radioprotector in this tumour model, in a manner consistent with an increase in tumour hypoxic fraction, although factors other than changes in blood chemistry may also be involved.

Animals↗

PubMed1997

Evaluation of the INNO-LiPA Rif. TB assay, a reverse hybridization assay for the simultaneous detection of Mycobacterium tuberculosis complex and its resistance to rifampin.

Mycobacterium tuberculosis resistance to rifampin results from nucleotide changes in the gene encoding the beta-subunit of the RNA polymerase (rpoB). We developed a reverse hybridization-based line probe assay (LiPA; the INNO-LiPA Rif. TB) carrying one oligonucleotide probe for the detection of M. tuberculosis complex strains and nine probes designed to detect nucleotide changes in the relevant part of rpoB. This assay was evaluated with 107 M. tuberculosis isolates with known rpoB sequences, 52 non-M. tuberculosis complex strains, and 61 and 203 clinical isolates found to be sensitive and resistant, respectively, by in vitro testing. The results indicated that (i) the M. tuberculosis complex probe was 100% specific, (ii) when compared to the results of nucleotide sequencing, no discrepancies with the results of INNO-LiPA Rif. TB were observed, (iii) all strains sensitive by in vitro susceptibility testing were correctly identified, and (iv) among the strains resistant by in vitro susceptibility testing, only 4 (2%) yielded conflicting results. The INNO-LiPA Rif. TB is therefore a reliable and widely applicable assay and a valuable tool for routine diagnostic use, given its simplicity and rapid performance.

Antibiotics, Antitubercular↗