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如果有人能帮忙。我一直在用 html 和 css 开发我的页面。现在我的这个页面变得冗长乏味,无法滚动并获得您想要的内容。我在 css 上使用 :target
标签将页面分成几个部分,但它在某些浏览器上不起作用。我一直在玩 javascript 但没有成功。任何人都可以帮助我处理我应该在页面中使用的 js 脚本,这样当有人加载页面时,它只显示将用作目录的内部链接,当用户单击内部链接时,仅显示该部分与 div 链接显示或弹出?
或者我可以使用 PHP 吗?
<div>
<ul>
<li><a href="#introduction">Introduction to
antimicrobials</a></li>
<li><a href="#antifungals">Antifungal Drugs</a></li>
<li><a href="#antiprotozoals">Antiprotozoal Drugs</a></li>
<li><a href="#antihelminthics">Antihelminthic Drugs</a></li>
<li><a href="#antibacterials">Antibacterials</a></li>
<li><a href="#aminoglycosides">Aminoglycosides</a></li>
<li><a href="#antifolates">Antifolate Drugs</a></li>
<li><a href="#fluoroquinolones">Fluoroquinolones</a></li>
<li><a href="#antimycobacterials">Antimycobacterial
Drugs</a></li>
</ul>
<div id="introduction">
Viruses: Smallest pathogens, programmed to infect only certain
body cells. Virus uses a body cells to reproduce itself it cannot be
treated with medication.
Bacteria: single celled microorganism, 1000 different bacteria, but 100
cause disease.
- Bacteria can be treated with antibiotics.
- Some bacteria are becoming immune to certain antibiotics.
- Bacterial Diseases: Strep throat, Tuberculosis Gonorrhea, Syphilis
Fungi: single celled or multicellular plantlike organism
- Fungi can cause diseases of the skin, mucous membrane, and lungs.
- Fungi Diseases: Athlete’s foot, Ringworm, Jock itch, Nail infections,
Candidiasis</div>
<div id="antifungals">
Amphotericin B continues to be an important drug for the treatment of
systemic fungal infections. However, several azoles and echinocandins are
proving to be just as effective in some systemic mycoses with less risk of
toxic effects.
</div>
<div id="antiprotozoals">
Drugs for Malaria:
Malaria is one of the most common diseases worldwide and a leading cause of
death. Plasmodium species that infect humans (P falciparum, P malariae, P
ovale, P vivax) undergo a primary developmental stage in the liver and then
parasitize erythrocytes. P falciparum and P malariae have only 1 cycle of
liver cell invasion. The other species have a dormant hepatic stage
responsible for recurrent infections and relapses. Primary tissue
schizonticides (eg, primaquine) kill schizonts in the liver, whereas blood
schizonticides (eg, chloroquine, quinine) kill these parasitic forms only
in the erythrocyte. Sporonticides (proguanil, pyrimethamine) prevent
sporogony and multiplication in the mosquito.
Drugs: Chloroquine, Quinine, Mefloquine, Primaquine, pyrimethamine,
proguanil, Sulfadoxine, Dapsone, Doxycycline, Amodiaquine, Atovaquone,
Halofantrine, Artesunate, Artemether, Dihydroartemisinin
</div>
<div id="antihelminthics">
Antihelminthic drugs have diverse chemical structures, mechanisms of
action, and properties. Most were discovered by empiric screening methods;
many act against specific parasites, and few are devoid of significant
toxicity to host cells. In addition to the direct toxicity of the drugs,
reactions to dead and dying parasites may cause serious toxicity in
patients.
</div>
<div id="antibacterials">
Beta-Lactam Antibiotics & Other Cell Wall Synthesis Inhibitors
Penicillins and cephalosporins are the major antibiotics that inhibit
bacterial cell wall synthesis. They are called beta-lactams because of the
unusual 4-member ring that is common to all their members. The beta-lactams
include some of the most effective, widely used, and well-tolerated agents
available for the treatment of microbial infections. Vancomycin,
fosfomycin, and bacitracin also inhibit cell wall synthesis but are not
nearly as important as the beta-lactam drugs. More than 50 antibiotics that
act as cell wall synthesis inhibitors are currently available, with
individual spectra of activity that afford a wide range of clinical
applications.
</div>
<div id="aminoglycosides">
Aminoglycosides are structurally related amino sugars attached by
glycosidic linkages. They are polar compounds, not absorbed after oral
administration and must be given intramuscularly, or intravenously for
systemic effect. They have limited tissue penetration and do not readily
cross the blood-brain barrier. Glomerular filtration is the major mode of
excretion, and plasma levels of these drugs are greatly affected by changes
in renal function. Excretion of aminoglycosides is directly proportional to
creatinine clearance. With normal renal function, the elimination half-life
of aminoglycosides is 2–3 h. Dosage adjustments must be made in renal
insufficiency to prevent toxic accumulation. Monitoring of plasma levels of
aminoglycosides is important for safe and effective dosage selection and
adjustment. For traditional dosing regimens (2 or 3 times daily), peak
serum levels are measured 30–60 min after administration and trough levels
just before the next dose. With once-daily dosing, peak levels are less
important since they will naturally be high.
</div>
<div id="fluoroquinolones">
The fluoroquinolones interfere with bacterial DNA synthesis by inhibiting
topoisomerase II (DNA gyrase), especially in gram-negative organisms and
topoisomerase IV, especially in gram-positive organisms. They block the
relaxation of supercoiled DNA that is catalyzed by DNA gyrase, a step
required for normal transcription and duplication. Inhibition of
topoisomerase IV by fluoroquinolones interferes with the separation of
replicated chromosomal DNA during cell division. Fluoroquinolones are
usually bactericidal against susceptible organisms. Like aminoglycosides,
the fluoroquinolones exhibit postantibiotic effects, whereby bacterial
growth continues to be inhibited even after the plasma concentration of the
drug has fallen below the minimum inhibitory concentration of the bacterium
</div>
<div id="antimycobacterials">
Drugs for Tuberculosis
The major drugs used in tuberculosis are isoniazid (INH), rifampin,
ethambutol, pyrazinamide, and streptomycin. Actions of these agents on M
tuberculosis are bactericidal or bacteriostatic depending on drug
concentration and strain susceptibility. Appropriate drug treatment
involves antibiotic susceptibility testing of mycobacterial isolates.
Initiation of treatment of pulmonary tuberculosis usually involves a 3- or
4-drug combination regimen depending on the known or anticipated rate of
resistance to isoniazid (INH). Directly observed therapy (DOT) regimens are
recommended in noncompliant patients and in drug-resistant tuberculosis.
</div>
</div>
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