ฝึกพูดภาษาอังกฤษด้วยเทคนิค Shadowing จากวิดีโอ: Antibiotics: Cell Wall Synthesis Inhibitors: Part 1

เลือกโหมดฝึก

แต่ละโหมดจะเปิดห้องฝึกแบบเต็มจอ

320 ประโยค

หากประโยคสั้นหรือยาวเกินไป กดที่ Edit เพื่อปรับแก้

Alright engineers, in this video we're going to talk about antibiotics.

Alright, so the way we're going to do this is we're going to go through multiple different types of antibiotics.

We're not going to cover all of them.

It would just be impossible to cover all of them and all their different effects and mechanisms of action.

We're going to start off by looking at antibiotics that are affecting the cell wall.

So let's go ahead and start there.

So if you look here, now bacteria, if we're talking about gram positive or gram negative bacteria, we'll make a video on this,

but gram negative and gram positive bacteria really just differ and they're overall, like if I were to have, let's say I take for example here,

I take two bacterial cells, just real quickly.

Let's say here's a bacteria and here's a bacteria.

Let's say this is gram negative and let's say that this is gram positive.

The real big difference between gram negative and gram positive is that when you look at gram negative bacteria, they have a very thin peptidoglycan layer.

So their peptidoglycan layer that we're going to talk about that is very thin.

And another thing is that they have a cell membrane, an outer cell membrane surrounding that peptidoglycan layer.

And they have little porins inside of it, right?

So little porins.

A gram positive bacteria is the exact opposite.

It has a very very thick peptidoglycan layer, a very thick peptidoglycan layer.

Okay and that is going to be our gram positive.

So when we're looking at gram positive

and gram negative bacteria

it really is important to kind of have a basic idea of what their overall cell wall looks like

and overall cell structure is consisting of.

Okay so again one more time gram negative has a very thin peptidoglycan layer but has an outer cell membrane.

And it also has what's called lipopolysaccharides with lipid A and lipopolysaccharides and stuff like that that are the toxins.

And then over here, gram -positive bacteria just has a very thick peptidoglycan layer, but no outer cell membrane.

Okay, so now that we know that, let's go ahead and dig into antibiotics.

So the first antibiotics that we're going to talk about here, we're going to talk about the beta -lactams.

Okay, so we're going to focus here on our beta -lactams.

Now what is a beta -lactam?

Now just really really quickly it has a specific structure.

So if you look at a beta -lactam usually you have a five ring structure here

and then you have a little four ring structure right here

and then you have a little carbonyl and then you have this little nitrogen group here.

So it's kind of like a cyclic amide.

This right here is the beta -lactam, this component here, this is the beta -lactam.

So these beta -lactam antibiotics usually have this beta -lactam ring which is incorporated into it.

The beta -lactams we're going to focus on here, we're going to focus specifically on the penicillins.

So we'll talk about penicillin, specifically like penicillin G, and then we're going to talk about amoxicillin,

so amoxicillin, and then we're going to talk about cephalosporins.

And we'll talk about all the generations of cephalosporins okay before I do

that let's take a look at the overall cell wall structure

again just a little bit more in depth zooming in on

that peptidoglycan layer

if we look in the peptidoglycan layer what is a peptidoglycan

you see these blue structures right here those blue structures are specific derivatives of carbohydrates like glucose

so what do I mean they're made up of structures which is called NAM and NAG.

So they're just derivatives of glucose.

NAM, NAM, stands for N -acetylmuramic acid.

NAG stands for N -acetylglucosamine.

All these are, these blue structures here, they're just derivatives of our carbohydrates, like glucose.

Okay?

Now coming up off of these carbohydrate residues you see this like a violet structure coming up out of this

that right there is like peptide bonds actually a pentapeptide

and then across from

that again you're gonna have another what would this be this would be another anacetylmuramic acid

and this could be another anacetylglucosamine

these black proteins are coming downwards from this part too this is another pentapeptide

and if you look there this little orange structure that's the cross link between them that's the peptide bond between them

So this is the basic structure of our peptidoglycine layer in a zoomed look.

You see this little orange guy just kind of sitting down?

That's our penicillin binding protein.

So that little red structure right there, which is actually going to be sitting down there on the cell membrane,

is going to be the penicillin binding protein.

So what is this guy here called?

He's called the penicillin binding protein.

Okay, he's a pretty important structure here because he's really what a lot of these actual beta -lactams are binding onto.

Alright, next thing.

If you look here, these brown scissors, those are little autolytic enzymes.

We're going to talk about them.

And then these little C -like orange enzymes there, they're called beta -lactamases.

Okay, so this little orange structure up here, this orange structure here is called beta -lactamase.

and then these little brown structures there are actually going to be called autolytic enzymes.

Okay now that we've done that let's go over these antibiotics here.

All right penicillin first.

So penicillin it's it is able to treat in general gram -positive and gram -negative bacteria.

However However, over the past years,

certain bacteria have become resistant to penicillin.

Okay?

How have they become resistant to penicillin?

Okay.

This beta -lactamase, there's a specific part of its name, beta -lactamase.

So it's an enzyme, right?

So look what it can actually do.

I'm going to draw that beta -lactam ring over here.

And it's got that double bond right there with the NH and then it's got that little five -membered ring there.

This is our penicillin.

If we give someone penicillin who already has bacteria that are very resistant to the penicillin, what do I mean?

Maybe they have plasmids that allow for them to produce this enzyme called beta -lactamase.

What will the beta -lactamase do?

Boom.

It'll break the beta -lactam ring.

If it cuts the beta -lactam ring, this penicillin is not going to be able to bind to this penicillin binding protein and mediate its effects.

So because of this would be rendered ineffective.

So that is the importance as a certain bacteria become resistant by developing these beta -lactamases.

So really it's more effective now just being able to treat gram -positive bacteria with a little bit of gram -negative coverage.

So what type of bacteria is it able to cover?

It can cover streptococcal, okay that's the main one.

It can cover streptococcal bacteria.

100

So any type of streptococcal bacteria.

101

It was able to develop in the past treat staphylococcal bacteria but again they've developed resistance also.

102

So streptococcal bacteria it's also able to treat syphilis.

103

So just a little bit on the penicillin.

104

So what is penicillin actually do?

105

How does it mediate these effects that it can actually kill these bacteria because it's bactericidal meaning it can kill the bacteria.

106

So let's say here here's the penicillin.

107

What the penicillin does is it comes in and it binds on to this penicillin binding protein.

108

So let's say that we draw that here.

109

Here's the penicillin and he binds on to this penicillin binding protein.

110

When he binds to the penicillin binding protein he stimulates the penicillin binding protein

111

and what this penicillin binding protein does is it takes its hand

112

and it comes up there and it stimulates these brown enzymes.

113

So then what does it do?

114

It comes up here and stimulates these autolytic enzymes.

115

If these autolytic enzymes are activated, what are they gonna do?

116

They're gonna start cutting up these bonds, these peptide bonds, these glycosidic bonds, and it's gonna start altering the overall structure of the cell wall.

117

That's one thing that happens.

118

Second thing that happens, there's a lot of other enzymes here.

119

There is other enzymes that actually link these peptide bonds together between these little pentapeptides, so you're having different types of transpeptidase enzymes,

120

whenever the penicillin binding protein is stimulated, he inhibits the transpeptidases from cross -linking these pentapeptides.

121

And if these are no longer cross -linked, the cell wall starts becoming disrupted.

122

Now, when the cell wall is disrupted, it allows for water to start leaking into the bacterial cells.

123

And when water leaks into the bacteria cell eventually can cause the cell to lice.

124

That is the way penicillin works.

125

So again one more time because all the rest of them are gonna do the same thing.

126

So once we know penicillin we know what these functions are too.

127

So one more time what does penicillin do?

128

Penicillin comes in binds onto the penicillin binding protein, stimulates him.

129

When he becomes stimulated he stimulates these autolytic enzymes who start cleaving and breaking up the cell wall.

130

Then he also inhibits, let's say that I draw this enzyme out here I'm just gonna draw some little dude out here.

131

Here's this little dude and he's got his hand in this bond right there.

132

Okay these are transpeptidase enzymes.

133

What are these transpeptidase enzymes doing?

134

They're helping to link these actual pentapeptides.

135

He will inhibit these transpeptidase enzymes.

136

So now they can no longer cross -link these little peptide chains and because that the cell wall will be disrupted.

137

Once it's disrupted water can leak in.

138

When water leaks in to cell lysis.

139

Okay so we're set there.

140

Amoxicillin, same mechanism of action.

141

Cephalosporin, same mechanism of action.

142

But now, Amoxicillin, he is very, very susceptible to these beta -lactamases.

143

Very, very susceptible.

144

So when you give someone Amoxicillin, you usually want to give it to them with clavulonic acid.

145

Clavulonic acid.

146

Why do you want to give that?

147

Because clavulonic acid is a beta -lactamase inhibitor.

148

So if you give them clavulonic acid, what is it going to do?

149

It's going to inhibit the beta -lactamase enzyme.

150

If the beta -lactamase is inhibited, now this amoxicillin is going to have more available to start exhibiting this effect.

151

Okay, so that's the job of clavulonic acid.

152

What can amoxicillin treat?

153

It can treat a lot of different things.

154

So amoxicillin is good at being able to treat urinary tract infections.

155

He's good at being able to treat respiratory tract infections.

156

He's also good at being able to treat meningitis.

157

and he can also treat infections that are caused by salmonella too.

158

So he can also treat infections caused by salmonella, and he's also really good at being able to treat middle ear infections, otitis media too.

159

So otitis media, middle ear infections, right?

160

Okay, so that is going to be the amoxicillin.

161

So he's good at being able to treat urinary tract infections, respiratory tract infections, meningitis, salmonella, otitis media, okay?

162

Cephalosporins, mechanism of action, same thing, activates the penicillin binding proteins and exerts all those effects.

163

Cephalosporins though are very interesting.

164

Okay, so there's four generations of cephalosporins, right?

165

So let's go ahead and go over those real quickly.

166

So they're first generation, so we could say first generation.

167

So first generation is actually going to be, we could take for example, Cephalexin.

168

So Cephalexin is one example here of a first generation Cephalosporum.

169

Then we could take for example a second generation.

170

Now a second generation would be like Cephiroxine.

171

Okay and then we could take for example a third generation Cephalosporum.

172

So a third generation Cephalosporum could be like ceftriaxone.

173

And then there's even fourth generation.

174

So fourth generation would be like cefepine.

175

So fourth generation would be like cefepine.

176

Now why am I mentioning this?

177

Well the reason why is cephalosporins, the first and second generation,

178

are really only good at being able to treat mainly gram positive bacteria.

179

So these are really only good at being able to treat gram positive bacteria.

180

Okay whereas what's happened over the years is that the ceftriaxone

181

and the sepapine have actually had a little bit more ability to treat more of the gram negative bacteria.

182

Okay so again first generation could be like cefalexan

183

and second generation could be like cefiroxan but But the big takeaway is these aren't really used anymore, but they're good to treat gram -positive.

184

Third generation, fourth generation have a little bit more gram -negative coverage.

185

So like ceftriaxone and cefepine.

186

Okay, so what would be the coverage?

187

So for example, let's say that I used cefalexan and cefiroxine.

188

They really only have gram -positive coverage.

189

So what would I really use these guys for?

190

I would probably use these guys for more of your Staphylococcus aureus and Streptococcus pyogenes.

191

So even Streptococcus pyogenes.

192

Okay?

193

Now if we use Ceftriaxone and Cefepime, they can treat Gram -negative.

194

So what could I use that for?

195

I could use that to treat, they have a lot of things that they could treat.

196

Pseudomonas is a really big one.

197

They can treat Pseudomonas, so like Pseudomonas aeruginosa.

198

They can treat certain types of bacteria that cause meningitis.

199

They're also pretty good at being able to treat infections caused by Klebsiella.

200

So Klebsiella, which is very common bacteria that can cause pneumonia.

201

So pneumonia, this is actually a bacteria that can cause pneumonia.

202

More commonly, it can cause other infections, but more commonly pneumonia.

203

and even other different types of enterobacteria.

204

So even different types of enterobacteria.

205

All right.

206

So that's our cephalosporins.

207

There is other beta -lactams and different types of penicillin derivatives that I could have mentioned, like Piptazo.

208

I could even have mentioned carbopanems.

209

You know, Piptazo can treat pseudomonas.

210

Carbopanems are actually good at being able to treat very, very...

211

problematic abdominal infections so they can treat that too.

212

Alright but that's pretty much going to cover our beta -lactam

213

so quick review and then we're gonna move on to the next ones.

214

Really?

215

Here we go.

216

Penicillins.

217

What do they actually do?

218

They're gonna come down here, bind onto the penicillin binding proteins, then what?

219

Activate the autolytic enzymes which are gonna cut up some of the cell wall structures, disrupting the cell wall.

220

Also penicillin binding proteins are going to inhibit these enzymes which are called transpeptidases.

221

So if you inhibit them they can't cross -link these actual peptide chains.

222

Cell walls disrupted.

223

What happens as a result?

224

Water leaks in and then eventually causes the cell to lice and kills the cell.

225

So these are bactericidal, meaning they kill the bacteria.

226

What could be certain types of beta -lactams?

227

Penicillin, amoxicillin, cephalosporins, right?

228

And I could even include carbapandums or pipericillin with tazobactam like piptazo.

229

But again, what is penicillin treating?

230

Gram positive and gram negative, mainly streptococcal because there's staphylococcal bacteria become resistant.

231

He can also treat syphilis.

232

What about amoxicillin?

233

He's very very sensitive to the beta -lactamases who cleave the beta -lactam rings.

234

So in order to make them effective, what do you give them with?

235

Calavulonic acid.

236

What can they treat?

237

UTIs, respiratory tract infections, bacteria that cause meningitis, salmonella, otitis media.

238

Okay, and then cephalosporins we said there are four main generations.

239

There is five.

240

Fifth I said can treat MRSA.

241

First generation and second generation are mainly for gram -positive.

242

First generation could be like cephalexin, second generation could be like cefiroxime, so they can treat staphylococcus aureus and streptococcus pyogenes.

243

Okay, and then third and fourth generation are more for the gram -negative coverage, and so those third generations would be like ceftriaxone

244

and cefepime, right? what can they treat like Pseudomonas aeruginosa meningitis Klebsiella

245

which can cause pneumonia as well as enterobacteria okay what other kind of drugs affect the cell wall

246

because there is other drugs besides these ones very very powerful one

247

we have to mention this one this very very powerful one is actually called it's a glycopeptide

248

so let's actually put that down

249

so let's actually this is actually a group under the glycopeptides so what glycopeptides Glycopeptide is this.

250

This glycopeptide is very very strong.

251

This is called vancomycin.

252

And vancomycin is actually really good at being able to treat MRSA.

253

What is MRSA?

254

MRSA stands for Methicillin Resistant Staphylococcus Aureus.

255

Now Methicillin is an antibiotic but they don't really use that anymore.

256

okay but certain bacteria have become resistant right to penicillins

257

or methicillin so you have to get vanco because

258

that can kill the MRSA okay

259

now vanco is actually really good mainly at being able to treat gram -positive bacteria okay

260

so like MRSA and C diff so Clostridium difficile colitis

261

so it's good at being able to treat C diff

262

so C diff is the one that makes you pee out your butthole all right

263

so it's really nasty one really really infectious diarrhea

264

and it also can treat certain types of bacteria

265

which are like resistant resistant coagulase

266

so coagulase negative now remember I'm saying negative resistant coagulase negative bacteria okay

267

and this is vanco

268

so vanco is a pretty powerful antibiotic

269

now what is vancomycin do he does something different he has the overall same effect as these beta -lactams

270

but different mechanism of action what exactly is he doing?

271

Vanko is very very interesting so you know

272

that every protein usually has what's called a carboxy terminus

273

and then it has an amino terminus right and then really

274

if I were to show this peptide bond correctly

275

it's really what's linking this part together right here's what's interesting let's say I take Vanko if I give someone vanco,

276

look what it's doing.

277

It's binding onto this carboxyl end.

278

When it binds onto the carboxyl end, this can't form a peptide bond.

279

So now what happens is vancomycin binds onto the carboxyl end of these actual peptide chains.

280

And if it blocks onto it, it hysterically hinders that peptide bond formation.

281

So now if you can't form a peptide bond, this cell wall is disrupted.

282

If the cell wall is disrupted what happens?

283

Water flows in.

284

As water flows in what happens?

285

The cell lysis.

286

So this is a bacteriocidal antibiotic.

287

Okay so one more time.

288

What is vanco doing?

289

It's binding onto the carboxyl end of these peptide chains.

290

As it binds onto the carboxyl end it sterically hinders this amine group from being able to form a peptide bond.

291

And as a result the cell wall is disrupted, water enters in and the cell lysis.

292

So it's a bacteriocidal antibiotic.

293

Okay, so we've covered our glycopeptides.

294

Now let's go over here

295

and let's cover a very weird type of bacteria that's not for gram positive or gram negative bacteria.

296

Okay, so this one that I'm going to talk about is mainly important for being able to treat tuberculosis.

297

Okay, so it's mainly used to treat tuberculosis.

298

So caused by the mycobacterium.

299

Now mycobacterium don't have a cell wall that's made up of peptidoglycans.

300

They are made up of these little orange structures.

301

You know what these orange structures are called?

302

They're called mycolic acid.

303

So, and you see this enzyme right here, this blue enzyme?

304

This blue enzyme is called a mycolic acid synthetase or synthase.

305

It's called isoniazid.

306

and again what is this antibiotic do this antibiotic is mainly treating tuberculosis caused by the mycobacterium

307

so what it does is it has a specific point where it actually here let's say here's the isoniazid

308

it's actually going to come in and inhibit this mycolic acid synthase

309

or synthetase enzyme

310

if this enzyme is inhibited can it synthesize the mycolic acids to make up the cell wall no

311

and if it can't synthesize this mycolic acid the cell wall integrity is altered.

312

If the cell wall's integrity is altered, can that cell survive?

313

No. Water might flush into it and cause the bacteria to die.

314

So again, isoniazid is used to treat tuberculosis caused by the mycobacterium.

315

Its cell walls consisting of these mycolic acid residues.

316

What happens is if you give isoniazid, it inhibits the mycolic acid synthetase or synthase enzyme, which then can no longer synthesize mycolic acid.

317

If it can't synthesize mycolic acid, the cell walls integrity is altered and then what happens the bacterial cell dies.

318

Okay all right guys so that pretty much covers on this part the antibiotics

319

that are treating for specifically the cell wall synthesis and structure.

320

In the next video we're going to talk about the antibiotics that are mainly used to target the folic acid pathway.

ดาวน์โหลดแอป

ทุกอย่างที่ต้องใช้เพื่อพูดได้คล่อง

AI ให้คะแนนการออกเสียงให้คะแนนทุกประโยค

ฝึก IPAเชี่ยวชาญทุกเสียง

คำศัพท์สร้างคลังคำของคุณ

เกมคำศัพท์เล่นไปเรียนไป

สแกน QR

Download on theApp Store Get it onGoogle Play

ช่องเดียวกัน

FOR YOU

วิดีโอแนะนำ

32 ประโยค

Structure and Function of a Prokaryotic Cell (Bacteria)

Daily ConversationUniversity Students

51 ประโยค

Understanding Cervical Ectropion / Cervical Erosion

Daily ConversationUniversity Students

41 ประโยค

Nutrition And Why It Matters

Daily ConversationUniversity Students

158 ประโยค

OWASP Top 10 Explained

Daily ConversationUniversity StudentsWorking Adults

67 ประโยค

Viruses: Components & Shapes - Microbiology Acellular Pre-Nursing, Pre-Med | @LevelUpRN

Daily ConversationUniversity Students

128 ประโยค

Bioprocessing Part 1: Fermentation

Daily ConversationUniversity Students

48 ประโยค

Pharmaceutical Industry Overview | Pharma and Biotech: Distinctions | Understanding Pharmaceuticals

Daily ConversationUniversity StudentsWorking Adults

165 ประโยค

How Gross Was the Past, Really?

Daily ConversationUniversity StudentsWorking Adults

57 ประโยค

Cambridge 10 Test 4 Section 4 Listening

Daily ConversationUniversity Students

28 ประโยค

Explanation of Vaccine Adjuvants

Daily ConversationUniversity Students

คำศัพท์และข้อสังเกตด้านการพูดสำหรับบทเรียนนี้

บทเรียนฝึกพูดนี้ใช้วิดีโอ “Antibiotics: Cell Wall Synthesis Inhibitors: Part 1” เป็นสื่อ คำที่ถูกพูดซ้ำบ่อยที่สุด: penicillin, cell, bacteria, treat, gram วิดีโอนี้มี 320 ประโยค และ 3467 คำ สำหรับฝึกพูดตาม ช่วงที่มีเสียงพูดยาว 22:08 ผู้พูดพูดด้วยความเร็วเป็นธรรมชาติ ประมาณ 157 คำต่อนาที ใกล้เคียงกับบทสนทนาในชีวิตประจำวัน มีเพียง 76% ของคำที่อยู่ใน 3,000 คำที่ใช้บ่อยที่สุดในภาษาอังกฤษ คำศัพท์จึงค่อนข้างยาก

คำศัพท์สำคัญในวิดีโอนี้

คำที่ควรเรียนรู้ 15 คำจากวิดีโอ พร้อมคำอ่านและความหมาย:

คำศัพท์	คำอ่าน	ความหมาย
gram คำนาม	/ˈɡɹæm/	กรัม
beta คำนาม	/ˈbeɪtə/	บีตา
enzyme คำนาม	/ˈɛn.zaɪm/	เอนไซม์
acid คำนาม	/ˈæsɪd/	กรด
antibiotic คำนาม	/ˌæn.taɪ.baɪˈɑ.tɪk/	ยาปฏิชีวนะ, ปฏิชีวนะ
infection คำนาม	/ɪnˈfɛkʃən/	การติดเชื้อ
layer คำนาม	/ˈleɪ̯ɚ/	ชั้น
mechanism คำนาม	/ˈmɛk.ə.nɪ.zəm/	กลไก, เครื่อง
membrane คำนาม	/ˈmɛm.bɹeɪn/	เยื่อ, เนื้อเยื่อ
pneumonia คำนาม	/njuˈməʊniə/	ปอดบวม
tuberculosis คำนาม	/tʃuːˌbɜː(ɹ)kjʊˈləʊsɪs/	วัณโรค
thin คำคุณศัพท์	/ˈθɪn/	บาง
thick คำคุณศัพท์	/θɪk/	หนา
glucose คำนาม	/ˈɡluː.kəʊz/	กลูโคส
violet คำนาม	/ˈvaɪ.ə.lət/	สีม่วง, ไวโอเล็ต

กริยาวลีที่คุณจะได้ยิน

คำศัพท์	ความหมาย
sit down คำกริยา	นั่ง

ประโยคที่ควรฝึกพูดซ้ำ

ประโยคสั้น ๆ ที่สมบูรณ์จากวิดีโอ ซึ่งนำไปใช้ในบทสนทนาประจำวันได้:

We're not going to cover all of them.
Let's say here's a bacteria and here's a bacteria.
You see this little orange guy just kind of sitting down?
Why do you want to give that?
You know what these orange structures are called?

ไวยากรณ์ในวิดีโอนี้

โครงสร้างที่ผู้พูดใช้บ่อยที่สุด พร้อมคำพูดจริงจากวิดีโอ:

โครงสร้าง	ในวิดีโอ
Passive voice be + กริยาช่อง 3 — เน้นสิ่งที่เกิดขึ้น ไม่ใช่ผู้กระทำ	is incorporated · is called · be called
Present perfect have/has + กริยาช่อง 3 — เหตุการณ์ในอดีตที่ยังเกี่ยวข้องกับปัจจุบัน	we've done · have become · have they become
Relative clauses who / which + อนุประโยค — ข้อมูลเพิ่มเติมเกี่ยวกับคนหรือสิ่งของ	ring which is · structures which is · there, which is

การออกเสียงที่ควรระวัง

ผู้พูดใช้รูปย่อและรูปลดเสียง 61 ครั้ง เช่น we're, they're, gonna ให้พูดแบบสั้นตามที่ได้ยิน

เสียง “th”: thin /ˈθɪn/, thick /θɪk/, synthesis /ˈsɪnθəsɪs/, pathway /ˈpæθˌweɪ/, synthesize /ˈsɪnθəsaɪz/
เสียง “sh” และ “zh”: infection /ɪnˈfɛkʃən/, infectious /ɪnˈfɛk.ʃəs/, flush /ˈflʌʃ/
คำยาว — ลงเสียงหนักให้ถูกพยางค์: antibiotic /ˌæn.taɪ.baɪˈɑ.tɪk/, mechanism /ˈmɛk.ə.nɪ.zəm/, derivative /dɪˈɹɪvətɪv/, tuberculosis /tʃuːˌbɜː(ɹ)kjʊˈləʊsɪs/, integrity /ɪnˈtɛɡɹəti/

เสียงที่คนไทยมักออกเสียงยาก:

เสียงท้ายคำ — ออกเสียงให้ครบ ไม่เปลี่ยนเป็นตัวสะกดแบบไทย: derivative /dɪˈɹɪvətɪv/, tuberculosis /tʃuːˌbɜː(ɹ)kjʊˈləʊsɪs/, glucose /ˈɡluː.kəʊz/, bacterial [bækˈtɪəɹiəɫ], sensitive /ˈsɛn.sɪt.ɪv/
/v/ — ไม่ใช่ /w/ ให้ฟันบนแตะริมฝีปากล่าง: derivative /dɪˈɹɪvətɪv/, activate /ˈæktɪˌveɪt/, sensitive /ˈsɛn.sɪt.ɪv/, violet /ˈvaɪ.ə.lət/, ineffective /ˌɪn.ɪˈfɛk.tɪv/
/z/ — เสียงก้อง ไม่ใช่ /s/: enzyme /ˈɛn.zaɪm/, resistant /ɹəˈzɪstənt/, mechanism /ˈmɛk.ə.nɪ.zəm/, glucose /ˈɡluː.kəʊz/, zoom /zuːm/

วิธีฝึกกับวิดีโอนี้

ฟังวิดีโอให้จบหนึ่งรอบโดยยังไม่ต้องพูด แล้วจดคำที่ยังไม่รู้จัก
เริ่มที่ความเร็ว 0.75× พูดตามทีละประโยค แล้วกลับไปใช้ความเร็วปกติเมื่อเริ่มคล่อง
อัดเสียงตัวเองแล้วเทียบกับต้นฉบับ โดยสังเกตคำอย่าง gram, beta, enzyme เป็นพิเศษ

เทคนิค Shadowing คืออะไร?

Shadowing เป็นเทคนิคการเรียนรู้ภาษาที่ได้รับการรับรองทางวิทยาศาสตร์ พัฒนาขึ้นสำหรับการฝึกนักแปลมืออาชีพ วิธีการนี้เรียบง่ายแต่ทรงพลัง: คุณฟังเสียงภาษาอังกฤษจากเจ้าของภาษาและพูดตามทันที — เหมือนเงาที่ตามผู้พูดด้วยช่วงเวลาห่าง 1-2 วินาที การวิจัยแสดงว่าเทคนิคนี้ปรับปรุงความแม่นยำในการออกเสียง ทำนองเสียง จังหวะ การเชื่อมเสียง การฟังเข้าใจ และความคล่องแคล่วในการพูดได้อย่างมีนัยสำคัญ

เทคนิค shadowing: อ่านคู่มือฉบับเต็มทีละขั้นตอน →

ฝึกพูดภาษาอังกฤษด้วยเทคนิค Shadowing จากวิดีโอ: Antibiotics: Cell Wall Synthesis Inhibitors: Part 1

เลือกโหมดฝึก

ดาวน์โหลดแอป

Cell Biology | Cell Structure & Function

Metabolism | Electron Transport Chain: DETAILED | Part 1

Antimycobacterials | Anti-TB Drugs

Homeostasis

Neurology | Facial Nerve: Cranial Nerve VII

Anatomy of the Heart and Coronary Circulation

Pharmacokinetics | Drug Absorption

Structure and Function of a Prokaryotic Cell (Bacteria)

Understanding Cervical Ectropion / Cervical Erosion

Nutrition And Why It Matters

OWASP Top 10 Explained

Viruses: Components & Shapes - Microbiology Acellular Pre-Nursing, Pre-Med | @LevelUpRN

Bioprocessing Part 1: Fermentation

Pharmaceutical Industry Overview | Pharma and Biotech: Distinctions | Understanding Pharmaceuticals

How Gross Was the Past, Really?

Cambridge 10 Test 4 Section 4 Listening

Explanation of Vaccine Adjuvants

คำศัพท์และข้อสังเกตด้านการพูดสำหรับบทเรียนนี้

คำศัพท์สำคัญในวิดีโอนี้

กริยาวลีที่คุณจะได้ยิน

ประโยคที่ควรฝึกพูดซ้ำ

ไวยากรณ์ในวิดีโอนี้

การออกเสียงที่ควรระวัง

วิธีฝึกกับวิดีโอนี้

เทคนิค Shadowing คืออะไร?