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  - sentence-transformers
  - sentence-similarity
  - feature-extraction
  - generated_from_trainer
  - dataset_size:34441
  - loss:MultipleNegativesRankingLoss
base_model: ibm-granite/granite-embedding-107m-multilingual
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      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:
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        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
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        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
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        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:
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      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
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        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
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        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
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        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
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      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
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        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
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        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)
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        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-
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      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
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        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
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        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
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        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
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      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
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        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
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        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 model finetuned from 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
Maximum Sequence Length: 512 tokens
Output Dimensionality: 384 dimensions
Similarity Function: Cosine Similarity

Model Sources

Documentation: Sentence Transformers Documentation
Repository: Sentence Transformers on GitHub
Hugging Face: Sentence Transformers on Hugging Face

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:

pip install -U sentence-transformers

Then you can load this model and run inference.

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]

Training Details

Training Dataset

Unnamed Dataset

Size: 34,441 training samples
Columns: anchor and positive
Approximate statistics based on the first 1000 samples:
anchor positive
type string string
details
min: 4 tokens
mean: 99.53 tokens
max: 279 tokens

min: 14 tokens
mean: 245.16 tokens
max: 512 tokens

	anchor	positive
type	string	string
details	min: 4 tokens mean: 99.53 tokens max: 279 tokens	min: 14 tokens mean: 245.16 tokens max: 512 tokens

Samples:

anchor	positive
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 #	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...
`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.`	`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`
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, ,	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...

Loss: MultipleNegativesRankingLoss with these parameters:

{
    "scale": 20.0,
    "similarity_fct": "cos_sim"
}

Evaluation Dataset

Unnamed Dataset

Size: 3,827 evaluation samples
Columns: anchor and positive
Approximate statistics based on the first 1000 samples:
anchor positive
type string string
details
min: 15 tokens
mean: 175.44 tokens
max: 258 tokens

min: 55 tokens
mean: 432.79 tokens
max: 512 tokens

	anchor	positive
type	string	string
details	min: 15 tokens mean: 175.44 tokens max: 258 tokens	min: 55 tokens mean: 432.79 tokens max: 512 tokens

Samples:

anchor	positive
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	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, ...
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	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...
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	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...

Loss: MultipleNegativesRankingLoss with these parameters:

{
    "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

Click to expand

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

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

@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

@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}
}