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PubMed1984

Colonization of a human intestine by four different genotypes of Lactobacillus acidophilus.

To understand the effect on a human host suffering from intestinal disorders we supplied non fat milk cultures of Lactobacillus acidophilus for 25 days. The picture of the faeces bacterial count was completely different before and after treatment and we noticed increases in lactobacilli, bifidobacteria and coliforms while the clostridia decreased. The lactobacilli treatment solved the diarrohea problem. Of the four genetic lines of L. acidophilus supplied only D179, isolated from calf faeces, and ATCC 4356 of human origin were found able to colonize the intestine of the little girl, while 255S isolated from swine and D328 isolated from calf faeces, did not find favourable growth conditions.

Animals↗
PubMed1998

A model to investigate postoperative ileus with strain gauge transducers in awake rats.

BACKGROUND: Postoperative ileus influences patients well-being, hospital stay, and health cost, and postoperative inhibition of colonic motility is a major contributor to postoperative ileus. Experimental models for investigating postoperative ileus are needed. In particular, recording of postoperative colonic motility in awake rats has not been described yet. MATERIAL AND METHODS: Gastric, small intestinal, and colonic motility were recorded with strain gauge transducers in awake rats, and the effects of anesthesia and abdominal surgery on gastrointestinal motility were investigated. RESULTS: Ether anesthesia increased gastric motility and inhibited small intestinal motility, while enflurane anesthesia had only minor effects on gastrointestinal motility. Abdominal surgery inhibited gastric, small intestinal, and colonic motility, and a detailed analysis of gastrointestinal motility in our postoperative ileus model is given. CONCLUSIONS: We established a model to record gastric, small intestinal, and colonic motility in awake rats postoperatively. We could demonstrate that enflurane anesthesia had little effect on gastrointestinal motility, while laparotomy and short manipulation of the cecum produced a prolonged inhibition of gastrointestinal motility. Our model could be used to investigate postoperative ileus, particularly of the colon, in awake rats.

Abdomen↗
PubMed2000

Assessment of intestinal permeability in rats by permeation of inulin-fluorescein.

The measurement of intestinal permeability is widely used to assess different aspects of mucosal barrier disorders and related disease states, and has been proposed for evaluation of disease activity. To provide a simple method for assessment of intestinal permeability, we examined the permeation of inulin-fluorescein (InFl) in rat models of small intestinal injury and colitis. Small intestinal or colonic inflammation was induced by either i.p. administration of indomethacin or rectal administration of trinitrobenzene sulfonic acid (TNBS), respectively. For monitoring of intestinal permeability, InFl was administered orally or rectally to rats with small intestinal or colonic inflammation, respectively, and its level in blood was determined by the fluorescence intensity in the plasma. In small intestinal injury, InFl reached its peak in plasma 3 h after oral administration, while in colitis the InFl peak was reached 1 h after rectal administration. The highest permeability was observed at 72 h or 12 h after induction of small intestinal or colonic inflammation, respectively. In small intestinal injury the InFl permeation, as measured by its plasma level prior to sacrifice, was in agreement with intestinal damage evaluated after sacrifice. In colitis, the permeability at 12 h after induction of the disease correlated well with mortality. These findings demonstrate that InFl can be used as a novel, safe and easy-to-use probe for the evaluation of gut permeation and follow-up of gastrointestinal injury.

Animals↗
PubMed1992

Second-generation monoclonal antibodies to intestinal MUC2 peptide reactive with colon cancer.

BACKGROUND: Antitumor antibodies have traditionally been made to whole tumors or tumor extract. The use of defined synthetic antigens would be desirable for producing monoclonal antibodies. PURPOSE: Our purpose was to determine if antipeptide antibody to MUC2 had antitumor activity and specificity. METHODS: A 29-amino-acid peptide to MUC2 was synthesized and monoclonal antibodies were produced after immunizing BALB/c mice with peptide-keyhole-limpet hemocyanin in complete Freund's adjuvant, and the monoclonal antibodies were tested on peptides and human tissues. RESULTS: CCP31, CCP37, and CCP58 monoclonal antibodies were produced using MUC2 MI-29 (KYPTTTPISTTTMVTPTPTPTGTQTPTTT) containing one repeat unit of 23 amino acids and part of the next repeat of four amino acids. These antibodies reacted with the MUC2-derived peptide but not with MUC1- or MUC3-derived peptides. One of the monoclonal antibodies, CCP58, reacted strongly with human colon cancer and normal intestine in both fresh and formalin-fixed tissues; two other antibodies, CCP37 and CCP31, reacted only with fresh human tissues of normal colon and malignant colon tumors by immunoperoxidase staining. In addition, CCP37 and CCP58 reacted strongly with human gastric cancer; all antibodies reacted weakly with human salivary gland, and none reacted with tissues from normal human lung, kidney, stomach, pancreas, or endometrium. By analysis of mucin molecules by Western blotting, the antigen detected by monoclonal antibodies CCP37 and CCP58 was found to be of a high relative molecular mass (520 kd). CONCLUSIONS: Anti-MUC2 peptide antibodies appear to be relatively tissue specific and represent a new method of producing antitumor antibodies.

Amino Acid Sequence↗
PubMed2000

Chemoprevention of familial adenomatous polyposis development in the APC(min) mouse model by 1,4-phenylene bis(methylene)selenocyanate.

Epidemiological and experimental studies have suggested that dietary supplementation with selenium can inhibit the development of cancers at several organ sites. We have consistently shown that 1, 4-phenylene bis(methylene) selenocyanate (p-XSC) is a highly effective cancer chemopreventive agent against the development of chemically induced cancers in several laboratory animal species. This is the first report describing the preventive effects of p-XSC in an animal model of familial adenomatous polyposis (FAP) containing a germline mutation of the APC gene. Six-week old male (heterozygous) C57BL/6J-APC(min) or wild-type mice were fed high fat diets containing 0, 10 or 20 p.p.m. p-XSC. After 80 days, the mice were killed and their intestines were excised and evaluated for polyps. Multiple samples were also harvested from normal appearing small intestine and colon for molecular analysis. Both the mucosa and polyps from the intestine and colon were assayed for beta-catenin, cyclooxygenase (COX)-2 expression and COX isoform activities. Administration of p-XSC in the diet significantly decreased the rate of formation of small intestinal tumors (P < 0. 0001) and colon tumors (P < 0.002) in APC(min) mice. p-XSC produced a dose-dependent inhibition of tumors in both small intestine (P < 0. 0001) and colon (P < 0.035). Mice fed 20 p.p.m. p-XSC had significantly lower levels of beta-catenin expression and COX-2 activity in polyps. These observations demonstrate for the first time that the synthetic organoselenium compound p-XSC possesses antitumor activity against genetically predisposed neoplastic lesions, such as FAP. While the exact mechanism(s) for this antitumor activity of p-XSC remains to be elucidated, it appears that modulation of beta-catenin expression and COX-2 activity is associated with inhibition of intestinal polyps.

Adenomatous Polyposis Coli↗
PubMed2002

Dietary inulin suppresses azoxymethane-induced aberrant crypt foci and colon tumors at the promotion stage in young Fisher 344 rats.

This study was designed to determine the effect of 10% dietary long-chain inulin on the azoxymethane (AOM)-induced colonic preneoplastic aberrant crypt foci (ACF) and small intestinal and colon tumors at the initiation (I), promotion (P) and I + P stages (20 rats per treatment) in Fisher 344 male weanling rats. After an acclimatization period of 1 wk, groups of Fisher 344 male weanling rats were assigned to consume AIN 93G diet (control) or AIN 93G diet containing 10% inulin. All the rats received 16 mg/kg body AOM dissolved in saline subcutaneously at 7 wk of age followed by a second injection at 8 wk of age. An additional group of five rats received only saline and consumed the control diet. The rats received the assigned diets until asphyxiation by CO(2) at 16 wk of age for the ACF experiment and 45 wk for the end-point tumor experiment. Feed intake, weight gain, diarrheal index, cecal weight, cecal pH, ACF and tumors in the colon were determined. Rats fed inulin had diarrhea after 2 wk of feeding and recovered by approximately 4 wk. Cecal weight was greater in rats fed inulin and cecal pH was lower. The inulin group had more than 66% fewer aberrant crypts and 60% fewer ACF compared with the control group. Tumor incidences in the small intestine and colon of rats in the control, I, P and I + P groups were: 78, 31, 0 and 11% and 90, 73, 69 and 50%, respectively. The corresponding values for the distal portion of the colon were 87, 63, 45 and 33%, respectively. Colon tumors per tumor-bearing rat were 4.2, 3.09, 1.36 and 1.2 for the control, I, P and I + P groups, respectively. All groups differed, P < 0.05. The results of this study indicate that dietary long-chain inulin suppresses AOM-induced ACF formation, an early preneoplastic marker of colon tumorigenesis in rats, and colon tumors, particularly at the promotion stage.

Age Factors↗
PubMed1994

[Volvulus of the transverse colon: a rare cause of intestinal obstruction].

Volvulus of the transverse colon is rare, given its short and fixed mesentery and the normal fixation of the hepatic and splenic flexures of the colon. The case reported herein brings the total of reported cases to 72. Various predisposing factors have been identified, most notably congenital abnormalities, physiologic disturbances and mechanical obstruction; in our case these three factors were present. The possible role of colonoscopy in diagnosis and/or therapy is unclear. In our patient, colonoscopy proved to be of no use for diagnosis or treatment.

Adult↗
PubMed1995

Attenuation of vasoactive intestinal peptide enhancement of colon carcinogenesis by ornithine decarboxylase inhibitor.

The effects of combined administration of vasoactive intestinal peptide (VIP) and the ornithine decarboxylase (ODC) inhibitor, 1,3-diaminopropane (DAP), on development of colon tumors induced by azoxymethane (AOM), on ODC activity of the colon wall, and on the labelling index of colon epithelial cells were investigated in inbred Wistar rats. Rats received weekly subcutaneous injections of AOM for 10 weeks and subcutaneous injections of VIP every other day and drinking water containing DAP (2.5 milligrams) ad libitum until the end of the experiment at week 45. Administration of VIP significantly increased the incidence of colon tumors at week 45. It also resulted in significant increases in colon ODC activity and in the labelling index during administration of AOM, but not after its cessation. Administration of both DAP and VIP significantly reduced the enhanced colon carcinogenesis by VIP. The DAP significantly attenuated the VIP enhancement of colon ODC activity and of the labelling index during AOM administration. These findings indicate that ODC inhibition attenuated enhancement of colon carcinogenesis, and suggest that enhancement of colon carcinogenesis by VIP may be mediated through its polyamine biosynthesis.

Adenocarcinoma↗
PubMed2006

Vibrio cholerae virulence regulator-coordinated evasion of host immunity.

To successfully propagate and cause disease, pathogenic bacteria must modulate their transcriptional activities in response to pressures exerted by the host immune system, including secreted immunoglobulins such as secretory IgA (S-IgA), which can bind and agglutinate bacteria. Here, we present a previously undescribed flow cytometry-based screening method to identify bacterial genes expressed in vitro and repressed during infections of Vibrio cholerae, an aquatic Gram-negative bacterium responsible for the severe diarrheal disease cholera. We identified a type IV mannose-sensitive hemagglutinin (MSHA) pilus that is repressed specifically in vivo. We showed that bacteria that failed to turn off MSHA biosynthesis were unable to colonize the intestines of infant mice in the presence of S-IgA. We also found that V. cholerae bound S-IgA in an MSHA-dependent and mannose-sensitive fashion and that binding of S-IgA prevented bacteria from penetrating mucus barriers and attaching to the surface of epithelial cells. The ability of V. cholerae to evade the non-antigen-specific binding of S-IgA by down-regulating a surface adhesin represents a previously undescribed mechanism of immune evasion in pathogenic bacteria. In addition, we found that repression of MSHA was mediated by the key virulence transcription factor ToxT, indicating that V. cholerae is able to coordinate both virulence gene activation and repression to evade host defenses and successfully colonize intestines.

Animals↗
PubMed1993

The role of cyclosporine on Ia antigen expression on gut epithelium in nude mice.

Increased expression of class II antigens (HLA-DR, human:Ia murine) on epithelial cells (EC) such as keratinocytes and gut EC suggests a role of the epithelium in the inflammatory response. It has been shown that injection of normal mouse serum (NMS) into nude mice caused an induction of Ia antigen by keratinocytes of the nude mice. The aim of the present study was to determine whether such induction could be observed in gut EC and whether it can be inhibited by cyclosporine A (CyA). Forty nude mice were divided into 4 groups of 10 each, designated A-D. Group A was injected with 0.1 ml of NMS; groups B and C were also injected with NMS and treated with oral CyA for 10 days. The dosage in group B was 30 g/ml and in group C 60 g/ml of drinking water. Group D was injected with serum of nude mice and served as a control group. Biopsies of small intestine and colon were obtained from each mouse and analyzed by indirect immunoperoxidase to identify Ia expression. Small intestine and colon EC were induced to express Ia antigen in most of the mice in groups A and B. A striking reduction in Ia expression was noted in group C. The differences between groups A and C concerning Ia expression on small intestine and colon EC were statistically significant. Our results demonstrate that the nude mouse may serve as a model for the study of Ia expression on gut EC, and that CyA can suppress the expression of Ia antigen also in the gut.

Animals↗
PubMed2002

Direct effect of croton oil on intestinal epithelial cells and colonic smooth muscle cells.

AIM: To investigate the direct effect of croton oil (CO) on human intestinal epithelial cell (HIEC) and guinea pig colonic smooth muscle cells in vitro. METHODS: Growth curves of HIEC were drawn by MTT colorimetry. The dynamics of cell proliferation was analyzed with flow cytometry, and morphological changes were observed under light and electron microscopy after long-term (6 weeks) treatment with CO. Expression of cyclooxygenase-2 (COX-2) mRNA was detected by dot blot in HIEC treated with CO. Genes related to CO were screened by DD-PCR, and the direct effect of CO on the contractility of isolated guinea pig colonic smooth muscle cells was observed. RESULTS: High concentration (20-40 mg x L(-1)) CO inhibited cell growth significantly (1, 3, 5, 7d OD sequence: (20 mg x L(-1)) 0.040+/-0.003, 0.081+/-0.012, 0.147+/-0.022,0.024+/-0.016; (40 mg x L(-1)) 0.033+/-0.044, 0.056+/-0.012, 0.104+/-0.010, 0.189+/-0.006; OD control 0.031+/-0.008, 0.096+/-0.012, 0.173+/-0.009, 0.300+/-0.016, P<0.01), which appeared to be related directly to the dosage. Compared with the control, the fraction number of cells in G1 phase decreased from 0.60 to 0.58, while that in S phase increased from 0.30 to 0.34 and DNA index also increased after 6 weeks of treatment with CO (the dosage was increased gradually from 4 to 40 mg x L(-1)). Light microscopic observation revealed that cells had karyomegaly, less plasma and karyoplasm lopsidedness. Electron microscopy also showed an increase in cell proliferation and in the quantity of abnormal nuclei with pathologic mitosis. Expression of COX-2 mRNA decreased significantly in HIEC treated with CO. Thirteen differential cDNA fragments were cloned from HIEC treated with CO, one of which was 100 percent homologous with human mitochondrial cytochrome C oxidase subunit II. The length of isolated guinea pig colonic smooth muscle cells was significantly shortened after treatment with CO (P<0.05). CONCLUSION: At a high CO concentration (>20 mg x L(-1)), cell growth and proliferation are inhibited in a dosage-dependent manner. Increase in cell proliferation and in malignant conversion of the cellular phenotype is observed in cells cultured chronically with CO. COX-2 mRNA expression decreases significantly, while human mitochondrial cytochrome C oxidase subunit IImRNA expression increases significantly in HIEC treated with CO. CO also has a direct effect on the contractility of Guinea pig colonic smooth muscle cells.

Animals↗
PubMed2005

The SrtA Sortase of Streptococcus agalactiae is required for cell wall anchoring of proteins containing the LPXTG motif, for adhesion to epithelial cells, and for colonization of the mouse intestine.

Streptococcus agalactiae (group B streptococcus [GBS]) is the leading cause of neonatal pneumonia, sepsis, and meningitis. An in silico genome analysis indicated that GBS strain NEM316 encodes 35 proteins containing an LPXTG motif which are thought to be covalently linked to the peptidoglycan by an enzyme called sortase. The role of these cell wall-anchored proteins in GBS pathogenesis was evaluated on a global level by inactivating the srtA gene. This gene encodes the major sortase SrtA that anchors most of the LPXTG-containing proteins. We chose the C5a peptidase (ScpB) and Alp2, an abundant immunogenic protein, as prototypical LPXTG-containing proteins. As expected, the SrtA knockout mutant was unable to anchor the C5a peptidase (ScpB) and Alp2 to the cell wall. Complementation with plasmid-borne srtA inserted into the chromosome restored the correct surface localization of both ScpB and Alp2. Interestingly, the SrtA mutant was impaired for binding to the major extracellular matrix components fibronectin and fibrinogen and displayed a significant reduction in adherence to human (A549, HeLa, and Caco-2) and murine (L2) epithelial cells compared to the parental wild-type strain. Surprisingly, the inactivation of srtA had no effect on the virulence of the type III strain of GBS in a neonatal rat model (measured by the 50% lethal dose and lung colonization) but strongly impaired the capacity of the strain to colonize the intestines of gnotobiotic mice in a competition assay. These results demonstrate that LPXTG-containing proteins are involved in cell adhesion and GBS persistence in vivo.

Amino Acid Motifs↗
PubMed1993

Localization of Vibrio cholerae O1 in the intestinal tissue.

Colonization of V. cholerae O1 in vivo is known to be a non-invasive type which the vibrios are confined only to the intestinal tissues. The pathway by which the vibrio antigens reach the lymphoid cells and subsequently give rise to the immune responses is not entirely clear. Thus, experiments were performed in experimental rats by inoculating live V. cholerae O1 into the ligated ileal loops. The fate of the vibrios in the intestinal tissues was then studied by transmission electron microscopy at different times after the inoculation. It was concluded that live V. cholerae O1 were initially taken up by the M cells which overlay Peyer's patches and which subsequently delivered the intact vibrios to phagocytic cells in the Peyer's patches. These phagocytic cells processed (digested) the vibrios while the lymphocytes and plasma cells infiltrated around them. During the late period of infection (12-15 hours after inoculation of the vibrios), vibrios were also found passing through the loose intercellular spaces between the absorptive epithelial cells into the underlying intestinal tissues.

Animals↗
PubMed2003

Requirement of the Yersinia pseudotuberculosis effectors YopH and YopE in colonization and persistence in intestinal and lymph tissues.

The gram-negative enteric pathogen Yersinia pseudotuberculosis employs a type III secretion system and effector Yop proteins that are required for virulence. Mutations in the type III secretion-translocation apparatus have been shown to cause defects in colonization of the murine cecum, suggesting roles for one or more effector Yops in the intestinal tract. To investigate this possibility, isogenic yop mutant strains were tested for their ability to colonize and persist in intestinal and associated lymph tissues of the mouse following orogastric inoculation. In single-strain infections, a yopHEMOJ mutant strain was unable to colonize, replicate, or persist in intestinal and lymph tissues. A yopH mutant strain specifically fails to colonize the mesenteric lymph nodes, but yopE and yopO mutant strains showed only minor defects in persistence in intestinal and lymph tissues. While no single Yop was found to be essential for colonization or persistence in intestinal tissues in single-strain infections, the absence of both YopH and YopE together almost eliminated colonization of all tissues, indicating either that these two Yops have some redundant functions or that Y. pseudotuberculosis employs multiple strategies for colonization. In competition infections with wild-type Y. pseudotuberculosis, the presence of wild-type bacteria severely hindered the ability of the yopH, yopE, and yopO mutants to persist in many tissues, suggesting that the wild-type bacteria either fills colonization niches or elicits host responses that the yop mutants are unable to withstand.

Animals↗
PubMed1990

Central nervous system action of peptides to influence gastrointestinal motor function.

The central action of peptides to influence GI motility in experimental animals is summarized in Table 1. TRH stimulates gastric, intestinal, and colonic contractility in rats and in several experimental species. A number of peptides including calcitonin, CGRP, neurotensin, NPY, and mu opioid peptides act centrally to induce a fasted MMC pattern of intestinal motility in fed animals while GRF and substance P shorten its duration. The dorsal vagal complex is site of action for TRH-, bombesin-, and somatostatin-induced stimulation of gastric contractility, and for CCK-, oxytocin- and substance P-induced decrease in gastric contractions or intraluminal pressure. The mechanisms through which TRH, bombesin, calcitonin, neurotensin, CCK, and oxytocin alter GI motility are vagally mediated. An involvement of central peptidergic neurons in the regulation of gut motility has recently been demonstrated in Aplysia, indicating that such regulatory mechanisms are important in the phylogenesis. Alterations of the pattern of GI motor activity are associated with functional changes in transit. TRH is so far the only centrally acting peptide stimulating simultaneously gastric, intestinal, and colonic transit in various animals species. Opioid peptides acting on mu receptor subtypes in the brain exert the opposite effect and inhibit concomitantly gastric, intestinal, and colonic transit. Bombesin and CRF were found to act centrally to inhibit gastric and intestinal transit and to stimulate colonic transit in the rat. The antitransit effect of calcitonin and CGRP is limited to the stomach and small intestine. The delay in GI transit is associated with reduced GI contractility for most of the peptides except central bombesin that increases GI motility. Nothing is known about brain sites through which these peptides act to alter gastric emptying and colonic transit. Regarding brain sites influencing intestinal transit, TRH-induced stimulation of intestinal transit in the rat is localized in the lateral and medial hypothalamus and medial septum. The periaqueductal gray matter is a responsive site for mu receptor agonist- and neurotensin-induced inhibition of intestinal transit. The neural pathways from the brain to the gut whereby these peptides express their stimulatory or inhibitory effects on GI transit is vagal dependent with the exception of calcitonin. It is not known whether the vagally mediated inhibition of GI transit by these peptides results from a decrease activity of vagal preganglionic fibers synapsing with excitatory myenteric neurons or an activation of vagal preganglionic neurons synapsing with inhibitory myenteric neurons. The lack of specific antagonists for these peptides has hampered the assessment of their physiological role.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1999

Turcot syndrome with colonic obstruction and small intestinal invagination: report of a case.

We report herein the case of a 16-year-old boy diagnosed as having Turcot syndrome, otherwise known as glioma-polyposis syndrome. The patient was transferred from the Department of Neurosurgery where he was undergoing investigation of a brain tumor, to the Department of Medicine for investigation of gastrointestinal symptoms. The patient was diagnosed as having Turcot syndrome, and was then transferred to the Department of Surgery for treatment of an obstruction in the sigmoid colon and small intestinal invagination. A subtotal colectomy with side-to-end ileoproctostomy and release of the invaginations was carried out. Multiple polyps were found in the colon, two of which, including a large polyp that obstructed the colonic lumen, were confirmed histologically to be adenocarcinoma. The remaining polyps were adenomas. A biopsy of the brain tumor confirmed a diagnosis of astrocytoma (WHO grade II). This case report describes the characteristic features of Turcot syndrome presented by this patient.

Adenocarcinoma↗
PubMed2005

Expression pattern of Wnt signaling components in the adult intestine.

BACKGROUND & AIMS: In the intestine, the canonical Wnt signaling cascade plays a crucial role in driving the proliferation of epithelial cells. Furthermore, aberrant activation of Wnt signaling is strongly associated with the development of colorectal cancer. Despite this evidence, little is known about the precise identity and localization of Wnts and their downstream effectors in the adult intestine. To address this issue, we examined the expression pattern of all Wnts, Frizzleds (Fzs), low-density lipoprotein receptor-related proteins, Wnt antagonists, and T-cell factors in the murine small intestine and colon and adenomas. METHODS: Embryonic, postnatal, and adult intestinal samples were subjected to in situ hybridization by using specific RNA probes for the various genes tested. RESULTS: Our analysis showed high expression of several signaling components (including Wnt-3, Wnt-6, Wnt-9b, Frizzled 4, Frizzled 6, Frizzled 7, low-density lipoprotein receptor-related protein 5, and secreted Frizzled-related protein 5) in crypt epithelial cells. We also detected Wnt-2b, Wnt-4, Wnt-5a, Wnt-5b, Frizzled 4, and Frizzled 6 in differentiated epithelial and mesenchymal cells of the small intestine and colon. Finally, several factors (Frizzled 4, T-cell factor 1, lymphoid enhancer factor, Dickkopf 2, Dickkopf 3, and Wnt-interacting factor) displayed differential expression in normal vs neoplastic tissue. CONCLUSIONS: Our study predicts a much broader role for Wnt signaling in gut development and homeostasis than was previously anticipated from available genetic studies and identifies novel factors likely involved in promoting canonical and noncanonical Wnt signals in the intestine.

Adult↗