README.md

---
tags:
- sentence-transformers
- sentence-similarity
- feature-extraction
- generated_from_trainer
- dataset_size:34441
- loss:MultipleNegativesRankingLoss
base_model: ibm-granite/granite-embedding-107m-multilingual
widget:
- source_sentence: inhibitors antiviral, antibacterial is as in with and Tzds. not
    been combination with insulin. sitagliptin resulted an HbA of effects rate of
    (upper tract and urinary (when (when combined with sulfonylurea), hypersensitivity
    facial administered insulin agogue insulin may to be lowered to hypoglycemia.
    is and to properties to sitagliptin tin. is use as with glimepiride, pioglitazone.
    COMBINATION THERAPY—ORAL AGENTS & MEDICATION in Type 2 Mellitus Failure maintain
    good over owing to a decrease beta-cell physical lean or increase ectopic the
    manage- of type diabetes. required to glycemic Unless is a contraindication, be
    initiated with a biguanide. If metformin agent or is added. drug be secret- incretin-based
    therapy, amylin glucosi- given to sulfonylureas or insulin cost, include metformin,
    other oral a noninsulin injectable and intensified insulin
  sentences:
  - inhibitors such as antiviral, antifungal, and certain antibacterial agents. Saxagliptin
    is approved as monotherapy and in combination with biguanides, sulfonylureas,
    and Tzds. It has not been studied in combination with insulin. During clinical
    trials, mono- and combination therapy with sitagliptin resulted in an HbA 1c reduc-
    tion in the range of 0.4–0.9%. Adverse effects include an increased rate of infections
    (upper respiratory tract and urinary tract), headaches, peripheral edema (when
    combined with a Tzd), hypoglycemia (when combined with a sulfonylurea), and hypersensitivity
    reactions (urticaria, facial edema). The dose of a concurrently administered insulin
    secret- agogue or insulin may need to be lowered to prevent hypoglycemia. Linagliptin
    is the most recently introduced drug in this class and appears to have properties
    similar to sitagliptin and saxaglip- tin. It is approved for use as monotherapy
    and in combination with metformin, glimepiride, and pioglitazone. COMBINATION
    THERAPY—ORAL ANTIDIABETIC AGENTS & INJECTABLE MEDICATION Combination Therapy in
    Type 2 Diabetes Mellitus Failure to maintain a good response to therapy over the
    long term owing to a progressive decrease in beta-cell mass, reduction in physical
    activity, decline in lean body mass, or increase in ectopic fat deposition remains
    a disconcerting problem in the manage- ment of type 2 diabetes. Multiple medications
    may be required to achieve glycemic control. Unless there is a contraindication,
    medical therapy should be initiated with a biguanide. If clinical failure occurs
    with metformin monotherapy, a second agent or insulin is added. The second-line
    drug can be an insulin secret- agogue, Tzd, incretin-based therapy, amylin analog,
    or a glucosi- dase inhibitor; preference is given to sulfonylureas or insulin
    because of cost, adverse effects, and safety concerns. Third-line therapy can
    include metformin, multiple other oral medications, or a noninsulin injectable
    and metformin and intensified insulin
  - 'of the integrity of membranes in cells and organelles. A. Nervous System The
    developing central nervous system of the fetus and young child is the most sensitive
    target organ for lead’s toxic effect. Epidemiologic studies suggest that blood
    lead concentrations even less than 5 mcg/dL may result in subclinical deficits
    in neurocog- nitive function in lead-exposed young children, with no demon- strable
    threshold for a “no effect” level. The dose response between TABLE 57–1 Toxicology
    of selected arsenic, lead, and mercury compounds. Form Entering Body Major Route
    of Absorption Distribution Major Clinical Effects Key Aspects of Mechanism Metabolism
    and Elimination Arsenic Inorganic arsenic salts Gastrointestinal, respiratory
    (all mucosal surfaces) Predominantly soft tissues (highest in liver, kidney).
    Avidly bound in skin, hair, nails Cardiovascular: shock, arrhythmias. CNS: encephalopathy,
    peripheral neuropathy. Gastroenteritis; pan- cytopenia; cancer (many sites) Inhibits
    enzymes; interferes with oxidative phosphorylation; alters cell signaling, gene
    expression Methylation. Renal (major); sweat and feces (minor) Lead Inorganic
    lead oxides and salts Gastrointestinal, respiratory Soft tissues; redistributed
    to skeleton (> 90% of adult body burden) CNS deficits; peripheral neuropathy;
    ane- mia; nephropathy; hypertension; reproductive toxicity Inhibits enzymes; interferes
    with essential cations; alters membrane structure Renal (major); feces and breast
    milk (minor) Organic (tetraethyl lead) Skin, gastrointesti- nal, respiratory Soft
    tissues, especially liver, CNS Encephalopathy Hepatic dealkylation (fast) → trialkyme-
    tabolites (slow) → dissociation to lead Urine and feces (major); sweat (minor)
    Mercury Elemental mercury Respiratory tract Soft tissues, especially kidney, CNS
    CNS: tremor, behavioral (erethism); gingivo'
  - '61. Glucocorticoids for gastrointestinal use: See Chapter 62. REFERENCES Alesci
    S et al: Glucocorticoid-induced osteoporosis: From basic mechanisms to clinical
    aspects. Neuroimmunomodulation 2005;12:1. Bamberger CM, Schulte HM, Chrousos GP:
    Molecular determinants of gluco- corticoid receptor function and tissue sensitivity
    to glucocorticoids. Endocr Rev 1996;17:245. Charmandari E, Kino T: Chrousos syndrome:
    A seminal report, a phylogenetic enigma and the clinical implications of glucocorticoid
    signaling changes. Eur J Clin Invest 2010;40:932. Charmandari E, Tsigos C, Chrousos
    GP: Neuroendocrinology of stress. Ann Rev Physiol 2005;67:259. Chrousos GP: Stress
    and disorders of the stress system. Nat Endocrinol Rev 2009;5:374. Chrousos GP,
    Kino T: Glucocorticoid signaling in the cell: Expanding clinical implications
    to complex human behavioral and somatic disorders. In: Glucocorticoids and mood:
    Clinical manifestations, risk factors, and molecular mechanisms. Proc NY Acad
    Sci 2009;1179:153. Elenkov IJ, Chrousos GP: Stress hormones, TH1/TH2 patterns,
    pro/anti-in- flammatory cytokines and susceptibility to disease. Trends Endocrinol
    Metab 1999;10:359. Elenkov IJ et al: Cytokine dysregulation, inflammation, and
    wellbeing. Neuroimmunomodulation 2005;12:255. Franchimont D et al: Glucocorticoids
    and inflammation revisited: The state of the art. Neuroimmunomodulation 2002–03;10:247.
    Graber AL et al: Natural history of pituitary-adrenal recovery following long-term
    suppression with corticosteroids. J Clin Endocrinol Metab 1965;25:11. Hochberg
    Z, Pacak K, Chrousos GP: Endocrine withdrawal syndromes. Endocrine Rev 2003;24:523.
    Kalantaridou S, Chrousos GP: Clinical review 148:'
- source_sentence: Against Gram-Negative Carbapenems Cephalosporins Chloramphenicol
    Daptomycin Tigecycline Oxazolidinones Penicillins Streptogramins Trimethoprim
    TABLE 51–5 agents that dosage or are contraindicated patients hepatic Dosage Adjustment
    in Impairment Renal Impairment Dosage Needed Hepatic Impairment Acyclovir, aztreonam,
    carbapenems, clarithromycin, colistin, cycloserine, daptomycin, didanosine, ethionamide,
    famciclovir, foscarnet, ganciclovir, penicillins,3 stavudine, telithromycin, tenofovir,
    trimethoprim- Cidofovir, tetracyclines2 Amprenavir, atazanavir, erythromycin,
    1Except 2Except doxycycline minocycline. 3Except antistaphylococcal penicillins
    (eg, dicloxacillin). That Alter Antimicrobi
  sentences:
  - the body to colonize various organs in the process called metastasis. Such tumor
    stem cells thus can express clonogenic (colony-forming) capability, and they are
    characterized by chromosome abnormalities reflecting their genetic instability,
    which leads to progressive selection of subclones that can survive more readily
    in the multicellular environment of the host. This genetic instability also allows
    them to become resistant to chemotherapy and radiotherapy. The invasive and metastatic
    processes as well as a series of metabolic abnormalities associated with the cancer
    result in tumor-related symptoms and eventual death of the patient unless the
    neoplasm can be eradicated with treatment. 54 CAUSES OF CANCER The incidence,
    geographic distribution, and behavior of specific types of cancer are related
    to multiple factors, including sex, age, race, genetic predisposition, and exposure
    to environmental car- cinogens. Of these factors, environmental exposure is probably
    most important. Exposure to ionizing radiation has been well documented as a significant
    risk factor for a number of cancers, including acute leukemias, thyroid cancer,
    breast cancer, lung cancer, soft tissue sarcoma, and basal cell and squamous cell
    skin cancers. Chemical carcinogens (particularly those in tobacco smoke) as well
    as azo dyes, aflatoxins, asbestos, benzene, and radon have all been well documented
    as leading to a wide range of human cancers. Several viruses have been implicated
    in the etiology of various human cancers. For example, hepatitis B and hepatitis
    C are asso- ciated with the development of hepatocellular cancer; HIV is associated
    with Hodgkin’s and non-Hodgkin’s lymphomas; human papillomavirus is associated
    with cervical cancer and head and neck cancer; and Ebstein-Barr virus is associated
    with nasopharyn- geal cancer. Expression of virus-induced neoplasia may also depend
    on additional host and environmental factors that modu- late the transformation
    process. Cellular genes are known that are homologous to the transforming genes
    of the retroviruses, a family
  - Against Gram-Positive Cocci Against Gram-Negative Bacilli Aminoglycosides Aminoglycosides
    Carbapenems Carbapenems Cephalosporins Chloramphenicol Chloramphenicol Quinolones
    Clindamycin Rifampin Daptomycin Tetracyclines Glycopeptide antibiotics Tigecycline
    Ketolides Macrolides Oxazolidinones Penicillins Quinolones Rifampin Streptogramins
    Sulfonamides Tetracyclines Tigecycline Trimethoprim TABLE 51–5 Antimicrobial agents
    that require dosage adjustment or are contraindicated in patients with renal or
    hepatic impairment. Dosage Adjustment Needed in Renal Impairment Contraindicated
    in Renal Impairment Dosage Adjustment Needed in Hepatic Impairment Acyclovir,
    amantadine, aminoglycosides, aztreonam, carbapenems, cephalosporins,1 clarithromycin,
    colistin, cycloserine, daptomycin, didanosine, emtricitabine, ethambutol, ethionamide,
    famciclovir, fluconazole, flucytosine, foscarnet, ganciclovir, lamivudine, penicillins,3
    pyrazinamide, quinolones, 4 rimantadine, stavudine, telavancin, telbivudine, telithromycin,
    tenofovir, terbinafine, trimethoprim- sulfamethoxazole, valacyclovir, vancomycin,
    zidovudine Cidofovir, methenamine, nalidixic acid, nitrofurantoin, sulfonamides
    (long-acting), tetracyclines2 Amprenavir, atazanavir, chloram- phenicol, clindamycin,
    erythromycin, fosamprenavir, indinavir, metronida- zole, rimantadine, tigecycline
    1Except ceftriaxone. 2Except doxycycline and possibly minocycline. 3Except antistaphylococcal
    penicillins (eg, nafcillin and dicloxacillin). 4Except moxifloxacin. Conditions
    That Alter Antimicrobi
  - host disease after allogeneic stem cell trans- plantation. Cyclosporine has also
    proved useful in a variety of autoimmune disorders, including uveitis, rheumatoid
    arthritis, psoriasis, and asthma. Its combination with newer agents is show- ing
    considerable efficacy in clinical and experimental settings where effective and
    less toxic immunosuppression is needed. Newer for- mulations of cyclosporine have
    been developed that are improving patient compliance (smaller, better tasting
    pills) and increasing bioavailability. Tacrolimus Tacrolimus (FK 506) is an immunosuppressant
    macrolide antibi- otic produced by Streptomyces tsukubaensis. It is not chemically
    related to cyclosporine, but their mechanisms of action are similar. Both drugs
    bind to cytoplasmic peptidylprolyl isomerases that are abundant in all tissues.
    While cyclosporine binds to cyclophilin, tacrolimus binds to the immunophilin
    FK-binding protein (FKBP). Both complexes inhibit calcineurin, which is necessary
    for the activation of the T-cell-specific transcription factor NF-AT. On a weight
    basis, tacrolimus is 10–100 times more potent than cyclosporine in inhibiting
    immune responses. Tacrolimus is utilized for the same indications as cyclosporine,
    particularly in organ and stem cell transplantation. Multicenter studies in the
    USA and in Europe indicate that both graft and patient survival are similar for
    the two drugs. Tacrolimus has proved to be effective therapy for preventing rejection
    in solid-organ transplant patients even after failure of standard rejection therapy,
    including anti-T- cell antibodies. It is now considered a standard prophylactic
    agent (usually in combination with methotrexate or mycophenolate mofetil) for
    graft-versus-host disease. Tacrolimus can be administered orally or intravenously.
    The half-life of the intravenous form is approximately 9–12 hours. Like cyclosporine,
    tacrolimus is metabolized primarily by P450 enzymes in the liver, and there is
    potential for drug interactions. The dosage is determined by trough blood level
    at
- source_sentence: Antiprotozoal 923 therapy many strains of P and is a of recommended
    chemopro- for in malaria-endemic with chloroquine-resistant is a synthetic 4-quinoline
    is related to quinine. It only be given orally because local with parenteral It
    is absorbed, and peak reached 18 Mefloquine is extensively distrib- uted and eliminated
    treat- ment The terminal elimination about 20 days, weekly dosing ing, steady-state
    levels are over a weeks; this shortened beginning a with consecutive although
    is stan- practice. slowly mainly the The can in the after of & Mefloquine has
    P falciparum vivax, but not against The mechanism of action is to mefloquine from
    areas. appears regions Mefloquine quinine with Clinical Uses A. Chemoprophylaxis
    Mefloquine prophylaxis most
  sentences:
  - CHAPTER 52 Antiprotozoal Drugs 923 MEFLOQUINE Mefloquine is effective therapy
    for many chloroquine-resistant strains of P falciparum and against other species.
    Although toxicity is a concern, mefloquine is one of the recommended chemopro-
    phylactic drugs for use in most malaria-endemic regions with chloroquine-resistant
    strains. Chemistry & Pharmacokinetics Mefloquine hydrochloride is a synthetic
    4-quinoline methanol that is chemically related to quinine. It can only be given
    orally because severe local irritation occurs with parenteral use. It is well
    absorbed, and peak plasma concentrations are reached in about 18 hours. Mefloquine
    is highly protein-bound, extensively distrib- uted in tissues, and eliminated
    slowly, allowing a single-dose treat- ment regimen. The terminal elimination half-life
    is about 20 days, allowing weekly dosing for chemoprophylaxis. With weekly dos-
    ing, steady-state drug levels are reached over a number of weeks; this interval
    can be shortened to 4 days by beginning a course with three consecutive daily
    doses of 250 mg, although this is not stan- dard practice. Mefloquine and acid
    metabolites of the drug are slowly excreted, mainly in the feces. The drug can
    be detected in the blood for months after the completion of therapy. Antimalarial
    Action & Resistance Mefloquine has strong blood schizonticidal activity against
    P falciparum and P vivax, but it is not active against hepatic stages or gametocytes.
    The mechanism of action of mefloquine is unknown. Sporadic resistance to mefloquine
    has been reported from many areas. At present, resistance appears to be uncommon
    except in regions of Southeast Asia with high rates of multidrug resistance (especially
    border areas of Thailand). Mefloquine resis- tance appears to be associated with
    resistance to quinine and halofantrine but not with resistance to chloroquine.
    Clinical Uses A. Chemoprophylaxis Mefloquine is effective in prophylaxis against
    most strain
  - 938 SECTION VIII Chemotherapeutic Drugs Clinical Uses Albendazole is administered
    on an empty stomach when used against intraluminal parasites but with a fatty
    meal when used against tissue parasites. A. Ascariasis, Trichuriasis, and Hookworm
    and Pinworm Infections For adults and children older than 2 years of age with
    ascariasis and hookworm infections, the treatment is a single dose of 400 mg TABLE
    53–1 Drugs for the treatment of helminthic infections. 1 Infecting Organism Drug
    of Choice Alternative Drugs Roundworms (nematodes) Ascaris lumbricoides (roundworm)
    Albendazole or pyrantel pamoate or mebendazole Ivermectin, piperazine Trichuris
    trichiura (whipworm) Mebendazole or albendazole Ivermectin Necator americanus
    (hookworm); Ancylostoma duodenale (hookworm) Albendazole or mebendazole or pyrantel
    pamoate Strongyloides stercoralis (threadworm) Ivermectin Albendazole or thiabendazole
    Enterobius vermicularis (pinworm) Mebendazole or pyrantel pamoate Albendazole
    Trichinella spiralis (trichinosis) Mebendazole or albendazole; add corticosteroids
    for severe infection Trichostrongylus species Pyrantel pamoate or mebendazole
    Albendazole Cutaneous larva migrans (creeping eruption) Albendazole or ivermectin
    Thiabendazole (topical) Visceral larva migrans Albendazole Mebendazole Angiostrongylus
    cantonensis Albendazole or mebendazole Wuchereria bancrofti (filariasis); Brugia
    malayi (filariasis); tropical eosinophilia; Loa loa (loiasis) Diethylcarbamazine
    Ivermectin Onchocerca volvulus (onchocerciasis) Ivermectin Dracunculus medinensis
    (guinea worm) Metronidazole Thiabendazole or mebendazole Capillaria philippinensis
    (intestinal capillariasis) Albendazole Mebendazole Flukes (trematodes) Schistosoma
    haematobium (bilharziasis)
  - safely and effectively combined with 5-FU-, irinotecan-, and oxaliplatin-based
    chemotherapy in the treatment of metastatic colorectal cancer. Bevacizumab is
    FDA approved as a first-line treatment for metastatic colorectal cancer in combination
    with any intravenous fluoropyrimidine-contain- ing regimen and is now also approved
    in combination with che- motherapy for metastatic non-small lung cancer and breast
    cancer. One potential advantage of this antibody is that it does not appear to
    exacerbate the toxicities typically observed with cytotoxic che- motherapy. The
    main safety concerns associated with bevacizumab include hypertension, an increased
    incidence of arterial throm- boembolic events (transient ischemic attack, stroke,
    angina, and myocardial infarction), wound healing complications, gastrointes-
    tinal perforations, and proteinuria. Sorafenib is a small molecule that inhibits
    multiple receptor tyrosine kinases (RTKs), especially VEGF-R2 and VEGF-R3, platelet-derived
    growth factor-β (PDGFR-β), and raf kinase. It was initially approved for advanced
    renal cell cancer and is also approved for advanced hepatocellular cancer. Sunitinib
    is similar to sorafenib in that it inhibits multiple RTKs, although the specific
    types are somewhat different. They include PDGFR-α and PDGFR-β, VEGF-R1, VEGF-R2,
    VEGF-R3, and c-kit. It is approved for the treatment of advanced renal cell cancer
    and for the treatment of gastrointestinal stromal tumors (GIST) after disease
    progression on or with intolerance to imatinib. Pazopanib is a small molecule
    that inhibits multiple RTKs, espe- cially VEGF-R2 and VEGF-R3, PDGFR-β, and raf
    kinase. This oral agent is approved for the treatment of advanced renal cell cancer.
    Sorafenib, sunitinib, and pazopanib are metabolized in the liver by the CYP3A4
    system, and elimination is primarily hepatic with excretion in feces. Each of
    these agents has potential interac-
- source_sentence: Endocrine is gland, increases phate reduce the enhanced feedback
    regulation the effect PTH to calcium and reduce Likewise, and at levels the D
    kidney increase amount produced. High reducing PTH works by FGF23 1,25(OH) 2 raises
    phosphate, whereas 2 D has such is appropriate. 1,25(OH) D of on serum inhibitory
    effect negative feedback patients producing 1,25(OH) loss feedback coupled with
    impaired and intestinal calcium leads to hyperparathyroidism. The of 2 D inhibit
    being exploited with analogs serum calcium their drugs are useful roidism accompanying
    chronic disease in of primary 1,25(OH) also stimulates production completes negative
    feedback loop inhibits 1,25(OH) production while promoting hypophosphatemia, which
    turn production 1,25(OH) D production. SECONDARY HOMEOST
  sentences:
  - 774 SECTION VII Endocrine Drugs that is detected by the parathyroid gland, increases
    in serum phos- phate levels reduce the ionized calcium, leading to enhanced PTH
    secretion. Such feedback regulation is appropriate to the net effect of PTH to
    raise serum calcium and reduce serum phosphate levels. Likewise, both calcium
    and phosphate at high levels reduce the amount of 1,25(OH) 2 D produced by the
    kidney and increase the amount of 24,25(OH) 2 D produced. High serum calcium works
    directly and indirectly by reducing PTH secretion. High serum phosphate works
    directly and indirectly by increasing FGF23 levels. Since 1,25(OH) 2 D raises
    serum calcium and phosphate, whereas 24,25(OH) 2 D has less effect, such feedback
    regulation is again appropriate. 1,25(OH) 2 D directly inhibits PTH secretion
    (independent of its effect on serum calcium) by a direct inhibitory effect on
    PTH gene transcription. This pro- vides yet another negative feedback loop. In
    patients with chronic renal failure who frequently are deficient in producing
    1,25(OH) 2 D, loss of this 1,25(OH) 2 D-mediated feedback loop coupled with impaired
    phosphate excretion and intestinal calcium absorption often leads to secondary
    hyperparathyroidism. The ability of 1,25(OH) 2 D to inhibit PTH secretion directly
    is being exploited with calcitriol analogs that have less effect on serum calcium
    because of their lesser effect on intestinal calcium absorption. Such drugs are
    proving useful in the management of secondary hyperparathy- roidism accompanying
    chronic kidney disease and may be useful in selected cases of primary hyperparathyroidism.
    1,25(OH) 2 D also stimulates the production of FGF23. This completes the negative
    feedback loop in that FGF23 inhibits 1,25(OH) 2 D production while promoting hypophosphatemia,
    which in turn inhibits FGF23 production and stimulates 1,25(OH) 2 D production.
    SECONDARY HORMONAL REGULATORS OF BONE MINERAL HOMEOST
  - ke). Equine and ovine antivenoms are available for rattle- snake envenomations,
    but only equine antivenom is available for coral snake bite. The ovine antivenom
    is a Fab preparation and is less immunogenic than whole equine IgG antivenoms,
    but retains the ability to neutralize the rattlesnake venom. MONOCLONAL ANTIBODIES
    (MABs ) Recent advances in the ability to manipulate the genes of immu- noglobulins
    have resulted in development of a wide array of humanized and chimeric monoclonal
    antibodies directed against therapeutic targets. The only murine elements of humanized
    monoclonal antibodies are the complementarity-determining regions in the variable
    domains of immunoglobulin heavy and light chains. Complementarity-determining
    regions are primarily responsible for the antigen-binding capacity of antibodies.
    Chimeric antibodies typically contain antigen-binding murine variable regions
    and human constant regions. The following are brief descriptions of the engineered
    antibodies that have been approved by the FDA. Antitumor MABs Alemtuzumab is a
    humanized IgG 1 with a kappa chain that binds to CD52 found on normal and malignant
    B and T lymphocytes, NK cells, monocytes, macrophages, and a small population
    of granulocytes. Currently, alemtuzumab is approved for the treatment of B-cell
    chronic lymphocytic leukemia in patients who have been treated with alkylating
    agents and have failed fludarabine therapy. Alemtuzumab appears to deplete leukemic
    and normal cells by direct antibody-dependent lysis. Patients receiving this antibody
    become lymphopenic and may also become neutro- penic, anemic, and thrombocytopenic.
    As a result patients should be closely monitored for opportunistic infections
    and hemato- logic toxicity. Bevacizumab is a humanized IgG 1 monoclonal antibody
    that binds to vascular endothelial growth factor (VEGF) and inhibits VEGF from
    binding to its receptor, especially on endothelial cells. It is an antiangiogenic
    drug that
  - rier only when the meninges are inflamed. Concentrations in cerebrospinal fluid
    are highly variable, ranging from 4% to 64% of serum levels in the setting of
    meningeal inflammation. As with all antituberculous drugs, resistance to ethambutol
    emerges rapidly when the drug is used alone. Therefore, ethambutol is always given
    in combination with other antituberculous drugs. Ethambutol hydrochloride, 15–25
    mg/kg, is usually given as a single daily dose in combination with isoniazid or
    rifampin. The higher dose is recommended for treatment of tuberculous menin- gitis.
    The dose of ethambutol is 50 mg/kg when a twice-weekly dosing schedule is used.
    Adverse Reactions Hypersensitivity to ethambutol is rare. The most common serious
    adverse event is retrobulbar neuritis, resulting in loss of visual acuity and
    red-green color blindness. This dose-related adverse effect is more likely to
    occur at dosages of 25 mg/kg/d continued for several months. At 15 mg/kg/d or
    less, visual disturbances are very rare. Periodic visual acuity testing is desirable
    if the 25 mg/kg/d dosage is used. Ethambutol is relatively contraindicated in
    chil- dren too young to permit assessment of visual acuity and red- green color
    discrimination. PYRAZINAMIDE Pyrazinamide (PZA) is a relative of nicotinamide.
    It is stable and slightly soluble in water. It is inactive at neutral pH, but
    at pH 5.5 it inhibits tubercle bacilli at concentrations of approximately 20 mcg/mL.
    The drug is taken up by macrophages and exerts its activity against mycobacteria
    residing within the acidic environ- ment of lysosomes. Pyrazinamide (PZA) N C
    O NH2 N Mechanism of Action & Clinical Uses Pyrazinamide is converted to pyrazinoic
    acid—the active form of the drug—by mycobacterial pyrazinamidase, which is encoded
    by
- source_sentence: Agents 49–1 Agents to or prevent herpes simplex virus and varicella-zoster
    virus (VZV) Route Administration Use Recommended Dosage and Regimen Acyclovir1
    First herpes 400 tid 5 times daily 7–10 days Recurrent genital herpes treatment
    or 200 daily or 800 bid or 800 mg tid × days in the HIV-infected mg 3–5 daily
    days in the HIV-infected mg times Orolabial herpes 400 mg 5 × 5 treatment 800
    qid treatment mg 5 days Intravenous mg/kg Mucocutaneous herpes the host treatment
    q8h × mg/kg × days HSV 10–20 Varicella or zoster in the immunosuppressed host
    × Topical (5% cream) Herpes labialis covering times × 4 days First genital herpes
    500 × Recurrent treatment × 1 Genital in bid Genital herpes herpes suppression
    the mg bid 1500 mg Orolabial suppression 250-500 mg mg tid × 7 treatment 10 days
    Recurrent treatment 500 days Genital in HIV-infected treatment 5–10 herpes herpes
    suppression HIV
  sentences:
  - Primaquine is the drug of choice for the eradication of dormant liver forms of
    P vivax and P ovale and can also be used for chemo- prophylaxis against all malarial
    species. Chemistry & Pharmacokinetics Primaquine phosphate is a synthetic 8-aminoquinoline
    ( Figure 52–2 ). The drug is well absorbed orally, reaching peak plasma levels
    in
  - CHAPTER 49 Antiviral Agents 865 TABLE 49–1 Agents to treat or prevent herpes simplex
    virus (HSV) and varicella-zoster virus (VZV) infections. Route of Administration
    Use Recommended Adult Dosage and Regimen Acyclovir1 Oral First episode genital
    herpes treatment 400 mg tid or 200 mg 5 times daily × 7–10 days Recurrent genital
    herpes treatment 400 mg tid or 200 mg 5 times daily or 800 mg bid × 3–5 days or
    800 mg tid × 2 days Genital herpes in the HIV-infected host treatment 400 mg 3–5
    times daily × 5–10 days Genital herpes suppression in the HIV-infected host 400–800
    mg bid–tid Herpes proctitis treatment 400 mg 5 times daily until healed Orolabial
    herpes treatment 400 mg 5 times daily × 5 days Varicella treatment (age ≥ 2 years)
    800 mg qid × 5 days Zoster treatment 800 mg 5 times daily × 7–10 days Intravenous
    Severe HSV treatment 5 mg/kg q8h × 7–10 days Mucocutaneous herpes in the immunocompromised
    host treatment 10 mg/kg q8h × 7–14 days Herpes encephalitis treatment 10–15 mg/kg
    q8h × 14–21 days Neonatal HSV infection treatment 10–20 mg/kg q8h × 14–21 days
    Varicella or zoster in the immunosuppressed host treatment 10 mg/kg q8h × 7 days
    Topical (5% cream) Herpes labialis treatment Thin film covering lesion 5 times
    daily × 4 days Famciclovir1 Oral First episode genital herpes treatment 500 mg
    tid × 5–10 days Recurrent genital herpes treatment 1000 mg bid × 1 day Genital
    herpes in the HIV-infected host treatment 500 mg bid × 5–10 days Genital herpes
    suppression 250 mg bid Genital herpes suppression in the HIV-infected host 500
    mg bid Orolabial herpes treatment 1500 mg once Orolabial or genital herpes suppression
    250-500 mg bid Zoster 500 mg tid × 7 days Valacyclovir1 Oral First episode genital
    herpes treatment 1000 mg bid × 10 days Recurrent genital herpes treatment 500
    mg bid × 3 days Genital herpes in the HIV-infected host treatment 500–1000 mg
    bid × 5–10 days Genital herpes suppression 500–1000 mg once daily Genital herpes
    suppression in the HIV
  - 708 SECTION VII Endocrine Drugs marked adverse effects because there is a recovery
    period between each dose. The transition to an alternate-day schedule can be made
    after the disease process is under control. It should be done gradu- ally and
    with additional supportive measures between doses. When selecting a drug for use
    in large doses, a medium- or intermediate-acting synthetic steroid with little
    mineralocorticoid effect is advisable. If possible, it should be given as a single
    morning dose. C. Special Dosage Forms Local therapy, such as topical preparations
    for skin disease, oph- thalmic forms for eye disease, intra-articular injections
    for joint disease, inhaled steroids for asthma, and hydrocortisone enemas for
    ulcerative colitis, provides a means of delivering large amounts of steroid to
    the diseased tissue with reduced systemic effects. Beclomethasone dipropionate,
    and several other glucocorti- coids—primarily budesonide, flunisolide, and mometasone
    furoate, administered as aerosols—have been found to be extremely useful in the
    treatment of asthma (see Chapter 20 ). Beclomethasone dipropionate, triamcinolone
    acetonide, budes- onide, flunisolide, and mometasone furoate are available as
    nasal sprays for the topical treatment of allergic rhinitis. They are effec- tive
    at doses (one or two sprays one, two, or three times daily) that in most patients
    result in plasma levels that are too low to influ- ence adrenal function or have
    any other systemic effects. Corticosteroids incorporated in ointments, creams,
    lotions, and sprays are used extensively in dermatology. These preparations are
    discussed in more detail in Chapter 61 . MINERALOCORTICOIDS (ALDOSTERONE, DEOXYCORTICOSTERONE,
    FLUDROCORTISONE) The most important mineralocorticoid in humans is aldosterone.
    However, small amounts of deoxycorticosterone (DOC) are also formed and released.
    Although the amount is normally insignifi- cant, DOC was of some importance therapeut
pipeline_tag: sentence-similarity
library_name: sentence-transformers
---

# SentenceTransformer based on ibm-granite/granite-embedding-107m-multilingual

This is a [sentence-transformers](https://www.SBERT.net) model finetuned from [ibm-granite/granite-embedding-107m-multilingual](https://huggingface.co/ibm-granite/granite-embedding-107m-multilingual). It maps sentences & paragraphs to a 384-dimensional dense vector space and can be used for semantic textual similarity, semantic search, paraphrase mining, text classification, clustering, and more.

## Model Details

### Model Description
- **Model Type:** Sentence Transformer
- **Base model:** [ibm-granite/granite-embedding-107m-multilingual](https://huggingface.co/ibm-granite/granite-embedding-107m-multilingual) <!-- at revision 5c793ec061753b0d0816865e1af7db3f675d65af -->
- **Maximum Sequence Length:** 512 tokens
- **Output Dimensionality:** 384 dimensions
- **Similarity Function:** Cosine Similarity
<!-- - **Training Dataset:** Unknown -->
<!-- - **Language:** Unknown -->
<!-- - **License:** Unknown -->

### Model Sources

- **Documentation:** [Sentence Transformers Documentation](https://sbert.net)
- **Repository:** [Sentence Transformers on GitHub](https://github.com/UKPLab/sentence-transformers)
- **Hugging Face:** [Sentence Transformers on Hugging Face](https://huggingface.co/models?library=sentence-transformers)

### Full Model Architecture

```
SentenceTransformer(
  (0): Transformer({'max_seq_length': 512, 'do_lower_case': False}) with Transformer model: XLMRobertaModel 
  (1): Pooling({'word_embedding_dimension': 384, 'pooling_mode_cls_token': True, 'pooling_mode_mean_tokens': False, 'pooling_mode_max_tokens': False, 'pooling_mode_mean_sqrt_len_tokens': False, 'pooling_mode_weightedmean_tokens': False, 'pooling_mode_lasttoken': False, 'include_prompt': True})
  (2): Normalize()
)
```

## Usage

### Direct Usage (Sentence Transformers)

First install the Sentence Transformers library:

```bash
pip install -U sentence-transformers
```

Then you can load this model and run inference.
```python
from sentence_transformers import SentenceTransformer

# Download from the 🤗 Hub
model = SentenceTransformer("RikoteMaster/embedder-granite")
# Run inference
sentences = [
    'Agents 49–1 Agents to or prevent herpes simplex virus and varicella-zoster virus (VZV) Route Administration Use Recommended Dosage and Regimen Acyclovir1 First herpes 400 tid 5 times daily 7–10 days Recurrent genital herpes treatment or 200 daily or 800 bid or 800 mg tid × days in the HIV-infected mg 3–5 daily days in the HIV-infected mg times Orolabial herpes 400 mg 5 × 5 treatment 800 qid treatment mg 5 days Intravenous mg/kg Mucocutaneous herpes the host treatment q8h × mg/kg × days HSV 10–20 Varicella or zoster in the immunosuppressed host × Topical (5% cream) Herpes labialis covering times × 4 days First genital herpes 500 × Recurrent treatment × 1 Genital in bid Genital herpes herpes suppression the mg bid 1500 mg Orolabial suppression 250-500 mg mg tid × 7 treatment 10 days Recurrent treatment 500 days Genital in HIV-infected treatment 5–10 herpes herpes suppression HIV',
    'CHAPTER 49 Antiviral Agents 865 TABLE 49–1 Agents to treat or prevent herpes simplex virus (HSV) and varicella-zoster virus (VZV) infections. Route of Administration Use Recommended Adult Dosage and Regimen Acyclovir1 Oral First episode genital herpes treatment 400 mg tid or 200 mg 5 times daily × 7–10 days Recurrent genital herpes treatment 400 mg tid or 200 mg 5 times daily or 800 mg bid × 3–5 days or 800 mg tid × 2 days Genital herpes in the HIV-infected host treatment 400 mg 3–5 times daily × 5–10 days Genital herpes suppression in the HIV-infected host 400–800 mg bid–tid Herpes proctitis treatment 400 mg 5 times daily until healed Orolabial herpes treatment 400 mg 5 times daily × 5 days Varicella treatment (age ≥ 2 years) 800 mg qid × 5 days Zoster treatment 800 mg 5 times daily × 7–10 days Intravenous Severe HSV treatment 5 mg/kg q8h × 7–10 days Mucocutaneous herpes in the immunocompromised host treatment 10 mg/kg q8h × 7–14 days Herpes encephalitis treatment 10–15 mg/kg q8h × 14–21 days Neonatal HSV infection treatment 10–20 mg/kg q8h × 14–21 days Varicella or zoster in the immunosuppressed host treatment 10 mg/kg q8h × 7 days Topical (5% cream) Herpes labialis treatment Thin film covering lesion 5 times daily × 4 days Famciclovir1 Oral First episode genital herpes treatment 500 mg tid × 5–10 days Recurrent genital herpes treatment 1000 mg bid × 1 day Genital herpes in the HIV-infected host treatment 500 mg bid × 5–10 days Genital herpes suppression 250 mg bid Genital herpes suppression in the HIV-infected host 500 mg bid Orolabial herpes treatment 1500 mg once Orolabial or genital herpes suppression 250-500 mg bid Zoster 500 mg tid × 7 days Valacyclovir1 Oral First episode genital herpes treatment 1000 mg bid × 10 days Recurrent genital herpes treatment 500 mg bid × 3 days Genital herpes in the HIV-infected host treatment 500–1000 mg bid × 5–10 days Genital herpes suppression 500–1000 mg once daily Genital herpes suppression in the HIV',
    '708 SECTION VII Endocrine Drugs marked adverse effects because there is a recovery period between each dose. The transition to an alternate-day schedule can be made after the disease process is under control. It should be done gradu- ally and with additional supportive measures between doses. When selecting a drug for use in large doses, a medium- or intermediate-acting synthetic steroid with little mineralocorticoid effect is advisable. If possible, it should be given as a single morning dose. C. Special Dosage Forms Local therapy, such as topical preparations for skin disease, oph- thalmic forms for eye disease, intra-articular injections for joint disease, inhaled steroids for asthma, and hydrocortisone enemas for ulcerative colitis, provides a means of delivering large amounts of steroid to the diseased tissue with reduced systemic effects. Beclomethasone dipropionate, and several other glucocorti- coids—primarily budesonide, flunisolide, and mometasone furoate, administered as aerosols—have been found to be extremely useful in the treatment of asthma (see Chapter 20 ). Beclomethasone dipropionate, triamcinolone acetonide, budes- onide, flunisolide, and mometasone furoate are available as nasal sprays for the topical treatment of allergic rhinitis. They are effec- tive at doses (one or two sprays one, two, or three times daily) that in most patients result in plasma levels that are too low to influ- ence adrenal function or have any other systemic effects. Corticosteroids incorporated in ointments, creams, lotions, and sprays are used extensively in dermatology. These preparations are discussed in more detail in Chapter 61 . MINERALOCORTICOIDS (ALDOSTERONE, DEOXYCORTICOSTERONE, FLUDROCORTISONE) The most important mineralocorticoid in humans is aldosterone. However, small amounts of deoxycorticosterone (DOC) are also formed and released. Although the amount is normally insignifi- cant, DOC was of some importance therapeut',
]
embeddings = model.encode(sentences)
print(embeddings.shape)
# [3, 384]

# Get the similarity scores for the embeddings
similarities = model.similarity(embeddings, embeddings)
print(similarities.shape)
# [3, 3]
```

<!--
### Direct Usage (Transformers)

<details><summary>Click to see the direct usage in Transformers</summary>

</details>
-->

<!--
### Downstream Usage (Sentence Transformers)

You can finetune this model on your own dataset.

<details><summary>Click to expand</summary>

</details>
-->

<!--
### Out-of-Scope Use

*List how the model may foreseeably be misused and address what users ought not to do with the model.*
-->

<!--
## Bias, Risks and Limitations

*What are the known or foreseeable issues stemming from this model? You could also flag here known failure cases or weaknesses of the model.*
-->

<!--
### Recommendations

*What are recommendations with respect to the foreseeable issues? For example, filtering explicit content.*
-->

## Training Details

### Training Dataset

#### Unnamed Dataset

* Size: 34,441 training samples
* Columns: <code>anchor</code> and <code>positive</code>
* Approximate statistics based on the first 1000 samples:
  |         | anchor                                                                             | positive                                                                             |
  |:--------|:-----------------------------------------------------------------------------------|:-------------------------------------------------------------------------------------|
  | type    | string                                                                             | string                                                                               |
  | details | <ul><li>min: 4 tokens</li><li>mean: 99.53 tokens</li><li>max: 279 tokens</li></ul> | <ul><li>min: 14 tokens</li><li>mean: 245.16 tokens</li><li>max: 512 tokens</li></ul> |
* Samples:
  | anchor                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           | positive                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 |
  |:-----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------|:---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------|
  | <code>Advanced March 2022 Solving Notes by In this do the following: We Weight Update then use method to This is very fast solving these based on an 11 of in TCS, 2015” written Eggerling on notes Kaul that we last lecture. last lecture In lecture, we to the order to fairly smartly advice of the game-setting with days and N follows: . expert gives some advice: UP predicts, based on of the expert, or DOWN. with knowledge and aggregator’s the UP/DOWN outcome. observes the outcome suffers his was incorrect. by ε (the i w(1) i to 1. (All experts are equally the ning.) At t: based a weighted majority vote , . w(t) N ). • observing the cost vector, set w(t) i i (Discount Last lecture analyzed the case when ε 1/2. same proof Theorem sequence outcomes, duration and expert i #</code> | <code>Advanced Algorithms March 22, 2022 Lecture 9: Solving LPs using Multiplicative Weights Notes by Ola Svensson1 In this lecture we do the following: • We describe the Multiplicative Weight Update (actually Hedge) method. • We then use this method to solve covering LPs. • This is a very fast and simple (i.e., very attractive) method for solving these LPs approximately. These lecture notes are partly based on an updated version of “Lecture 11 of Topics in TCS, 2015” that were written by Vincent Eggerling and Simon Rodriguez and on the lecture notes by Shiva Kaul that we used in the last lecture. 1 Recall last lecture In the previous lecture, we saw how to use the weighted majority method in order to fairly smartly follow the advice of experts. Recall that the general game-setting with T days and N experts was as follows: For t = 1, . . . , T: 1. Each expert i ∈[N] gives some advice: UP or DOWN 2. Aggregator (you) predicts, based on the advice of the expert, UP or DOWN. 3. Adversary, with k...</code> |
  | <code>analyzed the case when = same the following For any outcomes, T, and of of + O(log(N)/ε) These notes for the have not peer-reviewed and may contain inconsistent omit works.</code>                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        | <code>Last lecture we analyzed the case when ε = 1/2. The same proof gives the following Theorem 1 For any sequence of outcomes, duration T, and expert i ∈[N], # of WM mistakes ≤2(1 + ε) · (# of i’s mistakes) + O(log(N)/ε) . 1Disclaimer: These notes were written as notes for the lecturer. They have not been peer-reviewed and may contain inconsistent notation, typos, and omit citations of relevant works. 1</code>                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          |
  | <code>proof by defining function: each t . Φ(t) = i∈[N] i . We lower the Φ(T +1) using of of then bound terms bound: of goes a mistake initial weight is 1, Φ(T +1) = w(T +1) j ≥w(T +1) = (1 −ε)# of i’s mistakes bound: Every errs, at least half the experts (since weighted weights are (1 follows that down factor (1 WM ≤Φ(1) · WM = (1 WM for the equality that N initialized a weight of 1. The above give us (1 i’s mistakes ≤Φ(T WM . logs on then statement. 2 the game: for randomized strategies In you proved that instances for which weighted twice as as expert! is will to of making prediction (that the adversary then create side note this often is to following days and experts: 1, ,</code>                                                                                             | <code>Proof [Sketch] The proof was done by defining a potential function: for each t = 1, . . . , T + 1, let Φ(t) = X i∈[N] w(t) i . We now lower bound the “final” potential Φ(T +1) using the number of mistakes of i. We then upper bound it in terms of our number of mistakes. Lower bound: The weight of expert i goes down by a factor (1 −ε) for each mistake i does. As the initial weight of i is 1, Φ(T +1) = X j∈[N] w(T +1) j ≥w(T +1) i = (1 −ε)# of i’s mistakes . Upper bound: Every time WM errs, at least half the weight of the experts was wrong (since weighted majority was wrong). These weights are then decreased by (1 −ε). It follows that the potential goes down by at least a factor (1 −ε/2) every time WM errs. And so Φ(T +1) ≤Φ(1) · (1 −ε/2)# of WM mistakes = N · (1 −ε/2)# of WM mistakes , where for the equality we used that Φ(1) = N since each expert was initialized with a weight of 1. The above bounds give us (1 −ε)# of i’s mistakes ≤Φ(T +1) ≤N · (1 −ε/2)# of WM mistakes . Taking logs on b...</code> |
* Loss: [<code>MultipleNegativesRankingLoss</code>](https://sbert.net/docs/package_reference/sentence_transformer/losses.html#multiplenegativesrankingloss) with these parameters:
  ```json
  {
      "scale": 20.0,
      "similarity_fct": "cos_sim"
  }
  ```

### Evaluation Dataset

#### Unnamed Dataset

* Size: 3,827 evaluation samples
* Columns: <code>anchor</code> and <code>positive</code>
* Approximate statistics based on the first 1000 samples:
  |         | anchor                                                                               | positive                                                                             |
  |:--------|:-------------------------------------------------------------------------------------|:-------------------------------------------------------------------------------------|
  | type    | string                                                                               | string                                                                               |
  | details | <ul><li>min: 15 tokens</li><li>mean: 175.44 tokens</li><li>max: 258 tokens</li></ul> | <ul><li>min: 55 tokens</li><li>mean: 432.79 tokens</li><li>max: 512 tokens</li></ul> |
* Samples:
  | anchor                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  | positive                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 |
  |:----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------|:---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------|
  | <code>Adrenocorticosteroids & Adrenocortical Antagonists 707 hypertension occurs. or of hydrocortisone growth occurs in and have than steroid at equivalent in larger amounts, such and effects to glucocorticoid effects, sodium and loss potassium. and function, this leads to a hypochloremic alkalosis and eventually to pressure. In patients hypoproteinemia, renal or also In with even degrees to effects be minimized steroids, of potassium supplements. Adrenal administered more may treatment to appropriate at of stress for 24–48 severe to ten-fold dosage increases 48–72 trauma or major corti- costeroid dosage is to it should be slowly. be quite levels. may take 2–12 months hypothalamic-pituitary-adrenal function acceptably, cortisol levels to another months. The suppression is pituitary and treatment ACTH reduce time required the return function. If the in gluco- for certain disorder, the</code> | <code>CHAPTER 39 Adrenocorticosteroids & Adrenocortical Antagonists 707 hypertension also occurs. In dosages of 45 mg/m 2 /d or more of hydrocortisone or its equivalent, growth retardation occurs in children. Medium-, intermediate-, and long-acting glucocorticoids have greater growth-suppressing potency than the natural steroid at equivalent doses. When given in larger than physiologic amounts, steroids such as cortisone and hydrocortisone, which have mineralocorticoid effects in addition to glucocorticoid effects, cause some sodium and fluid retention and loss of potassium. In patients with normal cardiovas- cular and renal function, this leads to a hypokalemic, hypochloremic alkalosis and eventually to a rise in blood pressure. In patients with hypoproteinemia, renal disease, or liver disease, edema may also occur. In patients with heart disease, even small degrees of sodium retention may lead to heart failure. These effects can be minimized by using synthetic non-salt-retaining steroids, ...</code> |
  | <code>is and treatment ACTH not the for of function. If too in corticoids a of the or in intensity. patients an patients Cushing’s also with These symptoms or ing, weight lethargy, joint or pain, postural many of symptoms reflect true deficiency, may occur presence normal even elevated cortisol gesting glucocorticoid Contraindications A. Special glucocorticoids carefully for development of retention peptic osteopo- rosis, should as as and administration alternate-day) should when therapeutic obtained schedule. on relatively low doses of such are intercurrent or acci- dents B. must with great patients with peptic heart heart cer- osteoporosis, or Selection of Dosage Schedule anti- mineralocorticoid duration action, cost, and dosage forms ( these should selecting the drug used. ACTH Adrenocortical Steroids In patients with used</code>                                                            | <code>is not a pituitary problem, and treatment with ACTH does not reduce the time required for the return of normal function. If the dosage is reduced too rapidly in patients receiving gluco- corticoids for a certain disorder, the symptoms of the disorder may reappear or increase in intensity. However, patients without an underlying disorder (eg, patients cured surgically of Cushing’s disease) also develop symptoms with rapid reductions in cortico- steroid levels. These symptoms include anorexia, nausea or vomit- ing, weight loss, lethargy, headache, fever, joint or muscle pain, and postural hypotension. Although many of these symptoms may reflect true glucocorticoid deficiency, they may also occur in the presence of normal or even elevated plasma cortisol levels, sug- gesting glucocorticoid dependence. Contraindications & Cautions A. Special Precautions Patients receiving glucocorticoids must be monitored carefully for the development of hyperglycemia, glycosuria, sodium retention with ede...</code> |
  | <code>39–1 these factors be taken into drug be ACTH versus In with normal was used in production of similar effects. However, an the use a has in which was be were probably due amounts of corticosteroids the dosage B. Dosage the to be used, the physician the the of be required desired and of In some required for maintenance of the desired less the initial and the lowest dosage should gradually lowering the a small in is noted. When it is continuously elevated corticosteroid to suppress oral doses required. exists respect use of in inflammatory allergic same in a be effective than given in smaller doses in a Severe autoimmune vital organs must aggressively, and undertreatment is as To deposition immune and leukocytes 1 mg/kg/d predni- required initially. This dosage is main- tained the gradually are required alternate-day the may control in</code>                                              | <code>available ( Table 39–1 ), and these factors should be taken into account in selecting the drug to be used. A. ACTH versus Adrenocortical Steroids In patients with normal adrenals, ACTH was used in the past to induce the endogenous production of cortisol to obtain similar effects. However, except when an increase in androgens is desir- able, the use of ACTH as a therapeutic agent has been abandoned. Instances in which ACTH was claimed to be more effective than glucocorticoids were probably due to the administration of smaller amounts of corticosteroids than were produced by the dosage of ACTH. B. Dosage In determining the dosage regimen to be used, the physician must consider the seriousness of the disease, the amount of drug likely to be required to obtain the desired effect, and the duration of therapy. In some diseases, the amount required for maintenance of the desired therapeutic effect is less than the dose needed to obtain the initial effect, and the lowest possible dosage for th...</code> |
* Loss: [<code>MultipleNegativesRankingLoss</code>](https://sbert.net/docs/package_reference/sentence_transformer/losses.html#multiplenegativesrankingloss) with these parameters:
  ```json
  {
      "scale": 20.0,
      "similarity_fct": "cos_sim"
  }
  ```

### Training Hyperparameters
#### Non-Default Hyperparameters

- `eval_strategy`: steps
- `per_device_train_batch_size`: 128
- `per_device_eval_batch_size`: 128
- `learning_rate`: 2e-05
- `num_train_epochs`: 5
- `warmup_ratio`: 0.1
- `fp16`: True
- `dataloader_drop_last`: True
- `dataloader_num_workers`: 2
- `load_best_model_at_end`: True
- `push_to_hub`: True
- `hub_model_id`: RikoteMaster/embedder-granite
- `hub_strategy`: end
- `hub_private_repo`: True

#### All Hyperparameters
<details><summary>Click to expand</summary>

- `overwrite_output_dir`: False
- `do_predict`: False
- `eval_strategy`: steps
- `prediction_loss_only`: True
- `per_device_train_batch_size`: 128
- `per_device_eval_batch_size`: 128
- `per_gpu_train_batch_size`: None
- `per_gpu_eval_batch_size`: None
- `gradient_accumulation_steps`: 1
- `eval_accumulation_steps`: None
- `torch_empty_cache_steps`: None
- `learning_rate`: 2e-05
- `weight_decay`: 0.0
- `adam_beta1`: 0.9
- `adam_beta2`: 0.999
- `adam_epsilon`: 1e-08
- `max_grad_norm`: 1.0
- `num_train_epochs`: 5
- `max_steps`: -1
- `lr_scheduler_type`: linear
- `lr_scheduler_kwargs`: {}
- `warmup_ratio`: 0.1
- `warmup_steps`: 0
- `log_level`: passive
- `log_level_replica`: warning
- `log_on_each_node`: True
- `logging_nan_inf_filter`: True
- `save_safetensors`: True
- `save_on_each_node`: False
- `save_only_model`: False
- `restore_callback_states_from_checkpoint`: False
- `no_cuda`: False
- `use_cpu`: False
- `use_mps_device`: False
- `seed`: 42
- `data_seed`: None
- `jit_mode_eval`: False
- `use_ipex`: False
- `bf16`: False
- `fp16`: True
- `fp16_opt_level`: O1
- `half_precision_backend`: auto
- `bf16_full_eval`: False
- `fp16_full_eval`: False
- `tf32`: None
- `local_rank`: 0
- `ddp_backend`: None
- `tpu_num_cores`: None
- `tpu_metrics_debug`: False
- `debug`: []
- `dataloader_drop_last`: True
- `dataloader_num_workers`: 2
- `dataloader_prefetch_factor`: None
- `past_index`: -1
- `disable_tqdm`: False
- `remove_unused_columns`: True
- `label_names`: None
- `load_best_model_at_end`: True
- `ignore_data_skip`: False
- `fsdp`: []
- `fsdp_min_num_params`: 0
- `fsdp_config`: {'min_num_params': 0, 'xla': False, 'xla_fsdp_v2': False, 'xla_fsdp_grad_ckpt': False}
- `fsdp_transformer_layer_cls_to_wrap`: None
- `accelerator_config`: {'split_batches': False, 'dispatch_batches': None, 'even_batches': True, 'use_seedable_sampler': True, 'non_blocking': False, 'gradient_accumulation_kwargs': None}
- `deepspeed`: None
- `label_smoothing_factor`: 0.0
- `optim`: adamw_torch
- `optim_args`: None
- `adafactor`: False
- `group_by_length`: False
- `length_column_name`: length
- `ddp_find_unused_parameters`: None
- `ddp_bucket_cap_mb`: None
- `ddp_broadcast_buffers`: False
- `dataloader_pin_memory`: True
- `dataloader_persistent_workers`: False
- `skip_memory_metrics`: True
- `use_legacy_prediction_loop`: False
- `push_to_hub`: True
- `resume_from_checkpoint`: None
- `hub_model_id`: RikoteMaster/embedder-granite
- `hub_strategy`: end
- `hub_private_repo`: True
- `hub_always_push`: False
- `gradient_checkpointing`: False
- `gradient_checkpointing_kwargs`: None
- `include_inputs_for_metrics`: False
- `include_for_metrics`: []
- `eval_do_concat_batches`: True
- `fp16_backend`: auto
- `push_to_hub_model_id`: None
- `push_to_hub_organization`: None
- `mp_parameters`: 
- `auto_find_batch_size`: False
- `full_determinism`: False
- `torchdynamo`: None
- `ray_scope`: last
- `ddp_timeout`: 1800
- `torch_compile`: False
- `torch_compile_backend`: None
- `torch_compile_mode`: None
- `include_tokens_per_second`: False
- `include_num_input_tokens_seen`: False
- `neftune_noise_alpha`: None
- `optim_target_modules`: None
- `batch_eval_metrics`: False
- `eval_on_start`: False
- `use_liger_kernel`: False
- `eval_use_gather_object`: False
- `average_tokens_across_devices`: False
- `prompts`: None
- `batch_sampler`: batch_sampler
- `multi_dataset_batch_sampler`: proportional

</details>

### Training Logs
| Epoch     | Step     | Training Loss | Validation Loss |
|:---------:|:--------:|:-------------:|:---------------:|
| 0.1859    | 50       | 0.3888        | -               |
| 0.3717    | 100      | 0.1835        | -               |
| 0.5576    | 150      | 0.0817        | -               |
| 0.7435    | 200      | 0.0401        | 0.0351          |
| 0.9294    | 250      | 0.0376        | -               |
| 1.1152    | 300      | 0.0332        | -               |
| 1.3011    | 350      | 0.028         | -               |
| 1.4870    | 400      | 0.0285        | 0.0162          |
| 1.6729    | 450      | 0.0246        | -               |
| 1.8587    | 500      | 0.0239        | -               |
| 2.0446    | 550      | 0.0241        | -               |
| 2.2305    | 600      | 0.0237        | 0.0130          |
| 2.4164    | 650      | 0.0222        | -               |
| 2.6022    | 700      | 0.019         | -               |
| 2.7881    | 750      | 0.0235        | -               |
| 2.9740    | 800      | 0.0266        | 0.0120          |
| 3.1599    | 850      | 0.0214        | -               |
| 3.3457    | 900      | 0.024         | -               |
| 3.5316    | 950      | 0.0249        | -               |
| 3.7175    | 1000     | 0.0213        | 0.0113          |
| 3.9033    | 1050     | 0.0233        | -               |
| 4.0892    | 1100     | 0.0213        | -               |
| 4.2751    | 1150     | 0.0202        | -               |
| **4.461** | **1200** | **0.0227**    | **0.0109**      |
| 4.6468    | 1250     | 0.0229        | -               |
| 4.8327    | 1300     | 0.0196        | -               |

* The bold row denotes the saved checkpoint.

### Framework Versions
- Python: 3.10.17
- Sentence Transformers: 4.1.0
- Transformers: 4.52.3
- PyTorch: 2.7.0+cu126
- Accelerate: 1.7.0
- Datasets: 3.6.0
- Tokenizers: 0.21.1

## Citation

### BibTeX

#### Sentence Transformers
```bibtex
@inproceedings{reimers-2019-sentence-bert,
    title = "Sentence-BERT: Sentence Embeddings using Siamese BERT-Networks",
    author = "Reimers, Nils and Gurevych, Iryna",
    booktitle = "Proceedings of the 2019 Conference on Empirical Methods in Natural Language Processing",
    month = "11",
    year = "2019",
    publisher = "Association for Computational Linguistics",
    url = "https://arxiv.org/abs/1908.10084",
}
```

#### MultipleNegativesRankingLoss
```bibtex
@misc{henderson2017efficient,
    title={Efficient Natural Language Response Suggestion for Smart Reply},
    author={Matthew Henderson and Rami Al-Rfou and Brian Strope and Yun-hsuan Sung and Laszlo Lukacs and Ruiqi Guo and Sanjiv Kumar and Balint Miklos and Ray Kurzweil},
    year={2017},
    eprint={1705.00652},
    archivePrefix={arXiv},
    primaryClass={cs.CL}
}
```

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