Abstract:
The intervertebral disc is avascular. Nutrients and waste are diffused through adjacent vertebral bodies into the disc. As we age, calcified layers form between the disc and vertebral bodies, blocking diffusion of nutrients, oxygen and pH buffer in blood. Under anaerobic conditions, lactic acid is produced, irritating nerve endings and causing nonspecific pain. In addition, the disc begins to starve and flatten. The weight shifts abnormally from disc to the facet joints causing strain and back pain. 
     Lactic acid inhibitor inhibits production of lactic acid from pyruvate within the disc to reduce or alleviate back pain.

Description:
CROSS-REFERENCE 
     This application claims priority of U.S. Provisional Application 61/400,223, entitled Alleviate Back Pain with Lactic Acid Inhibitor, filed on Jul. 23, 2010 by Jeffrey E. Yeung and Teresa T. Yeung. 
    
    
     FIELD OF INVENTION 
     Diffusion of nutrients, oxygen and pH buffer into avascular intervertebral discs is limited to the depths of diffusion zones near superior and inferior endplates. Lactic acid produced anaerobically in the mid layers of the nucleus leaks from the disc to cause acid burn and persistent back pain. This invention relates to chemicals, device and method for inhibiting production of lactic acid within the avascular disc. As a result, back pain from lactic acid burn is reduced or alleviated. 
     BACKGROUND 
     Chronic back pain is an epidemic. Nerve impingement is not seen by CT or MRI in about 85% of back pain patients [Deyo R A, Weinstein J N: Low back pain, N Eng J Med, 344(5) February, 363-370, 2001. Boswell M V, et. al.: Interventional Techniques: Evidence-based practice guidelines in the management of chronic spinal pain, Pain Physician, 10:7-111, ISSN 1533-3159, 2007]. In fact, lumbar disc prolapse, protrusion, or extrusion account for less than 5% of all low back problems, but are the most common causes of nerve root pain and surgical interventions (Manchikanti L, Derby R, Benyamin R M, Helm S, Hirsch J A: A systematic review of mechanical lumbar disc decompression with nucleoplasty, Pain Physician; 12:561-572 ISSN 1533-3159, 2009). The cause of chronic back pain in most patients has been puzzling to both physicians and patients. 
     Studies indicate back pain is correlated with high lactic acid in the disc. Leakage of the acid causes acid burn and persistent back pain. In addition, as the disc degenerates and flattens, the compressive load is shifted from the flattened disc to facet joints, causing pain. Both lactic acid burn and strain of the facet joints are not visible under CT or MRI. 
     SUMMARY OF INVENTION 
     Lactic acid is anaerobically produced within avascular intervertebral discs. Acid hydrolysis of disc matrix creates fissures at the annulus. Lactic acid leaks from the nucleus through fissures to burn surrounding nerves and cause persistent back pain. 
     Lactic acid inhibitor inhibits production of lactic acid from pyruvate within discs to reduce or alleviate back pain. 
     
       
         
               
             
               
               
               
             
           
               
                   
               
               
                 REFERENCE NUMBERS 
               
               
                   
               
             
             
               
                   
               
             
          
           
               
                   
                 100 
                 Intervertebral disc 
               
               
                   
                 105  
                 Endplate 
               
               
                   
                 106A 
                 Superior diffusion zone 
               
               
                   
                 106B 
                 Inferior diffusion zone 
               
               
                   
                 107  
                 Capillaries (blood vessels) 
               
               
                   
                 108  
                 Calcified layers 
               
               
                   
                 114  
                 Annular delamination 
               
               
                   
                 115  
                 Epiphysis 
               
               
                   
                 118  
                 Nerve 
               
               
                   
                 119  
                 Vascular buds at the endplate 
               
               
                   
                 121  
                 Fissure 
               
               
                   
                 122  
                 Buffer or alkaline chemical 
               
               
                   
                 123  
                 Spinal cord 
               
               
                   
                 126  
                 Disc shunt 
               
               
                   
                 128  
                 Nucleus pulposus 
               
               
                   
                 129  
                 Facet joint 
               
               
                   
                 131  
                 Nutrients, oxygen and pH  
               
               
                   
                   
                 buffering solute 
               
               
                   
                 133  
                 Transverse process 
               
               
                   
                 142  
                 Superior articular process 
               
               
                   
                 143  
                 Inferior articular process 
               
               
                   
                 159  
                 Vertebral body 
               
               
                   
                 162  
                 Lactic acid 
               
               
                   
                 163  
                 Lactic acid inhibitor 
               
               
                   
                 193  
                 Muscle 
               
               
                   
                 194  
                 Spinal nerve root 
               
               
                   
                 195  
                 Posterior longitudinal ligament 
               
               
                   
                 276A 
                 Syringe 
               
               
                   
                 276B 
                 Disc injecting needle 
               
               
                   
                 278  
                 Pedicle 
               
               
                   
                 378  
                 Annulus or annular layer 
               
               
                   
                 505  
                 Skin 
               
               
                   
                   
               
             
          
         
       
     
    
    
     
       DESCRIPTION OF THE DRAWINGS 
         FIG. 1  shows a cut-away spinal segment, showing vascular buds  119  of capillaries  107  embedded in endplates  105  to nourish cells in the avascular disc  100 . 
         FIG. 2  shows a longitudinal view of a healthy spinal segment with nutrients  131  supplied through vascular buds of capillaries  107  at the endplates  105  to feed the cells within the disc  100 . 
         FIG. 3  shows a graph of distance from endplate versus oxygen concentration. 
         FIG. 4  shows calcified layers  108  accumulated at the endplates  105 , partially blocking diffusion of nutrient/oxygen  131  from capillaries  107 , leading to anaerobic production of lactic acid  162  to irritate nerves  118 . 
         FIG. 5  shows leakage of lactic acid  162  through a fissure  121  burning or irritating the spinal nerve  194 . 
         FIG. 6  shows anaerobic metabolism of pyruvate to lactate by oxidizing nicotinamide adenine dinucleotide (NADH), catalyzed by lactate dehydrogenase (enzyme) in the avascular disc. 
         FIG. 7  showing the oxidized nicotinamide adenine dinucleotide NAD+ is reduced by 2 electrons and two protons to NADH, capable of metabolizing pyruvate to lactate. 
         FIG. 8  shows a lactic inhibitor inhibiting the conversion of pyruvate to lactate. The inhibitor can be irreversible, reversible, competitive, non-competitive, un-competitive or mixed inhibitor. 
         FIG. 9  shows intra-discal injection of lactic acid inhibitor  163  into the painful and degenerated disc  100 . 
         FIG. 10  shows a longitudinal view of intra-discal injection of lactic acid inhibitor  163  to inhibit production of lactic acid, especially within the mid-layer of the avascular disc  100 . 
         FIG. 11  shows combination intra-discal injection of alkaline/buffer chemical  122  and lactic acid inhibitor  163  to neutralize and inhibit production of the lactic acid within the avascular disc  100 . 
         FIG. 12  shows intra-discal injection of lactic acid inhibitor  163  into a disc-shunted disc  100  to preserve pyruvate for aerobic metabolism into carbon dioxide and adenosine triphosphate (ATP). 
         FIG. 13  shows the lactic acid inhibitor  163  can be delivered through intra-vertebral body injection to alleviate back pain. 
     
    
    
     DETAILED DESCRIPTION OF THE EMBODIMENTS 
     Intervertebral discs are avascular (no blood vessels). Nutrients, oxygen and pH buffer  131  essential for disc cells are supplied by the capillaries  107  in the vertebral bodies  159  and diffused from both superior and inferior endplates  105  into the disc  100 , as shown in  FIGS. 1 and 2 . Normal blood pH is tightly regulated between 7.35 and 7.45, mainly by the pH buffering bicarbonate dissolved in blood plasma diffused through capillaries  107  and vascular buds  119  into the disc  100 . 
     However, depth of diffusion is shallow into thick human discs  100 . The calculated depth of oxygen diffusion from the endplates  105  is summarized in  FIG. 3  (Stairmand J W, Holm S, Urban J P G: Factor influencing oxygen concentration gradients in disc, Spine, Vol. 16, 4, 444-449, 1991). 
     Similarly, calculated depths of glucose diffusion are less than 3 mm from superior and inferior endplates (Maroudas A, Stockwell R A, Nachemson A, Urban J: Factors involved in the nutrition of the human lumbar intervertebral disc: Cellularity and diffusion of glucose in vitro, J. Anat., 120, 113-130, 1975). Nearly all animals have thin discs; depths of diffusion of nutrients and oxygen seem to be sufficient. Lumbar discs of a large sheep weighing 91 kg (200 pounds) are less than 4 mm thick. However, human lumbar discs are about 7-12 mm thick. Mid layers of our thick discs  100  are highly vulnerable to severe nutritional and oxygen deficiency. 
     As we age, calcified layers  108  form and accumulate at the endplates  105 , blocking capillaries  107  and further limiting the depth of diffusion of nutrients/oxygen/pH buffer  131  into the disc  100 , as shown in  FIG. 4 . The depth of diffusion of nutrients/oxygen/pH buffer  131  is mainly limited to superior diffusion zone  106 A, about zero to 2 mm from the superior endplate  105 , and inferior diffusion zone  106 B, about zero to 2 mm from the inferior endplate  105 . Cell death, matrix degradation and lactic acid  162  accumulation due to starvation and anaerobic conditions are common in the mid layers of the avascular discs  100 . Degradation of glycosaminoglycans may provide sugars to fuel the production of lactic acid  162 . [Urban J P, Smith S, Fairbank J C T: Nutrition of the Intervertebral Disc, Spine, 29 (23), 2700-2709, 2004. Benneker L M, Heini P F, Alini M, Anderson S E, Ito K: Vertebral endplate marrow contact channel occlusions &amp; intervertebral disc degeneration, Spine V30, 167-173, 2005. Holm S, Maroudas A, Urban J P, Selstam G, Nachemson A: Nutrition of the intervertebral disc: solute transport and metabolism, Connect Tissue Res., 8(2): 101-119, 1981]. 
     When glycosaminoglycans diminish, water content and swelling pressure of the nucleus pulposus  128  decrease. The nucleus  128  with reduced swelling pressure can no longer distribute forces evenly against the circumference of the inner annulus  378  to keep the annulus bulging outward. As a result, the inner annulus  378  sags inward while the outer annulus  378  bulges outward, creating annular delamination  114  and weakened annular layers  378 , possibly initiating fissure  121  formation depicted in  FIGS. 4 and 5 . 
     High lactic acid content in discs  100  correlates with back pain. In fact, dense fibrous scars and adhesions, presumably from lactic acid  162  burn, can be found around nerve roots  194  during spinal surgery [Diamant B, Karlsson J, Nachemson A: Correlation between lactate levels and pH of patients with lumbar rizopathies, Experientia, 24, 1195-6, 1968. Nachemson A: Intradiscal measurements of pH in patients with lumbar rhizopathies. Acta Orthop Scand, 40, 23-43, 1969. Keshari K R, Lotz J C, Link T M, Hu S, Majumdar S, Kurhanewicz J: Lactic acid and proteoglycans as metabolic markers for discogenic back pain, Spine, Vol. 33(3):312-317, 2008]. Average lactic acid concentration in painful lumbar disc  100  is about 14.5 mM, about 15 cc of fluid per disc (Diamant B, Karlsson J, Nachemson A: Correlation between lactate levels and pH of patients with lumbar rizopathies. Experientia, 24, 1195-1196, 1968). 
     Under anaerobic condition within the mid layer of the disc  100 , lactic acid  162  is produced and leaked from the nucleus  128  through fissures  121  to burn surrounding nerves  118  causing persistent back pain, as depicted in  FIGS. 4 and 5 . Colored drawings in the U.S. Provisional Application 61/400,223 entitled Alleviate Back Pain with Lactic Acid Inhibitor, filed on Jul. 23, 2010 by Jeffrey Yeung and Teresa Yeung, show superior and inferior diffusion zones near the calcified endplates and lactic acid zone in the mid layer of the degenerated disc. Similar black and white drawing is depicted in  FIG. 4 . 
     Some patients experience leg pain without visible spinal nerve impingement under MRI or CT. Lactic acid  162  can leak from the nucleus  128  through fissures  121  to spinal nerves  194 , causing leg pain as depicted in  FIG. 5 . Leg pain without visible impingement is commonly called chemical radiculitis. 
     Discography is a common diagnostic technique for identifying or confirming a painful disc  100  before surgical intervention. Intradiscal injection of an X-ray contrast flushes the lactic acid  162  from the nucleus  128  through fissures  121  to adjacent nerves  118 , causing instant and excruciating pain. For normal or non-painful discs, discography with mild injection pressure is nearly painless. 
     Composition Change of the Intervertebral Discs (approximation) 
                                             Normal Discs   Painful Discs   % Change from Normal Discs                   Glycosamino-   27.4 ± 2.4%   14.1 ± 1.1%   −48.5%       glycans                   Collagen   22.6 ± 1.9%   34.8 ± 1.4%     +54%       Water content   81.1 ± 0.9%   74.5 ± 1%    −8.1%       Acidity   pH 7.14   pH 6.65-5.70   [H + ]: +208% to +2,661%           [H + ]: 7.20 × 10 −8     [H + ]: 2.23 × 10 −7  to                   2.00 × 10 −6                      
(Reference: Kitano T, Zerwekh J, Usui Y, Edwards M, Flicker P, Mooney V: Biochemical changes associated with the symptomatic human intervertebral disk, Clinical Orthopaedics and Related Research, 293, 372-377, 1993. Scott J E, Bosworth T R, Cribb A M, Taylor J R: The chemical morphology of age-related changes in human intervertebral disc glycosaminoglycans from cervical, thoracic and lumbar nucleus pulposus and annulus fibrosus. J. Anat., 184, 73-82, 1994. Diamant B, Karlsson J, Nachemson A: Correlation between lactate levels and pH of patients with lumbar rizopathies, Experientia, 24, 1195-1196, 1968. Nachemson A: Intradiscal measurements of pH in patients with lumbar rhizopathies, Acta Orthop Scand, 40, 23-43, 1969.)
 
     Disc cells can survive without oxygen, but will die without glucose. The central area in the mid layer of the disc  100  is most vulnerable to glucose deficiency and cell death. Holes or vacuoles can be found during dissection of cadaveric discs  100 . Nuclei pulpos  128  of degenerated discs  100  are usually desiccated, with reduced swelling pressure and decreased capability to sustain compressive loads. The compressive load is thus transferred to the facet joints  129 , pressing the inferior articular processes  143  against the superior articular processes  142  of the facet joints  129 , causing strain, wear and/or pain (Dunlop R B, Adams M A, Hutton W C: Disc space narrowing and the lumbar facet joints, Journal of Bone and Joint Surgery—British Volume, Vol 66-B, Issue 5, 706-710, 1984). 
     A disc  100  with reduced swelling pressure is similar to a flat tire with flexible or flabby side walls. The vertebral body  159  above the soft or flabby disc  100  easily shifts or sways. This is commonly called segmental or spinal instability. The frequent or excessive movement of the vertebral body  159  strains the facet joints  129 , which are responsible for limiting the range of segmental mobility. Patients with spinal instability often use their muscles to guard or support their spines to ease facet pain. As a result, muscle tension and aches arise, but are successfully treated with muscle relaxants. Spinal motions, including compression, torsion, extension, flexion and lateral bending, were measured before and after saline injection into cadaveric discs. Intradiscal saline injections reduced all spinal motions in the cadaveric study (Andersson G B J, Schultz A B: Effects of fluid on mechanical properties of intervertebral discs, J. Biomechanics, Vol. 12, 453-458, 1979). 
     Molecular bonds of collagen and proteoglycans of the disc matrix are vulnerable in acidic conditions, which may lead to matrix decomposition and fissure  121  of the disc  100 . Decomposition of the disc matrix leads to disc flattening and spinal instability. 
     Especially under anaerobic conditions, overall chemical equilibrium between pyruvate and L-lactate  162  strongly favors L-lactate  162  formation with large negative standard free-energy=−25.1 kJ/mol, catalyzed by lactate dehydrogenase and driven by oxidization of NADH to NAD+ as shown in  FIG. 6 . Through reduction-oxidation reaction, NAD+ is reduced back to NADH by 2 electrons and 2 protons as shown in  FIG. 7 . 
     Formation of lactic acid  162  can be inhibited by lactic inhibitors  163 . The lactic inhibitor  163  can be irreversible, reversible, competitive, non-competitive, un-competitive or mixed inhibitor  163 , as indicated in  FIG. 8 . The lactic acid inhibitor  163  can be called the lactate dehydrogenase inhibitor  163 ; lactate dehydrogenase is an enzyme that converts pyruvate to lactic acid. In this patent application, lactic inhibitor  163 , lactic acid inhibitor  163  and lactate dehydrogenase inhibitor  163  can be used interchangeably. 
     The lactic acid inhibitor  163  can be fluoropyruvic acid, fluoropyruvate, levulinic acid, levulinate, oxamic acid, N-substituted oxamic acids, oxamate, oxalic acid, oxalate, beta-bromopropionate, beta-chloropropionate, malonate, sodium formaldehyde bisufite, chloroacetic acid, alpha-chloropropionate, alpha-bromopropionate, beta-iodopropionate, acrylate, acetoin, malic acid, glycolate, diglycolate, acetamide, acetaldehyde, acetylmercaptoacetic acid, alpha ketobutyrate, thioglycolic acid, nicotinic acid, alpha-ketoglutarate, butanedione, hydroxypyruvic, chloropyruvic, bromopyruvic, 2,3-dihydroxy-6-methyl-4-(1-methylethyl)-1-naphthoic acid, diethyl pyrocarbonate, hexyl N,N-diethyloxamate, 3-acetylpyridine adenine dinucleotide, 7-p-Trifluoromethylbenzyl-8-deoxyhemigossylic acid, dihydroxynaphthoic acids, N-substituted oxamic acids, gossypol, gossylic iminolactone, derivatives of gossypol, dihydroxynaphthoic acid, 2,3-dihydroxy-6-methyl-4-(1-methylethyl)-1-naphthoic acid, blue dye, reactive blue dye #2 (Cibacron Blue 3G-A) urea, methylurea and hydantoic acid, glyoxylate, hydroxybutyrate, 4-hydroxyquinoline-2-3 carboxylic acids, sodium bisulfite, dieldrin, L-(+) beta monofluorolactic acid, fluoro-lactic acid, tartronic acid, mesotartarate, sesquiterpene 8-deoxyhemigossylic acid (2,3-dihydroxy-6-methyl-4-(1-methylethyl)-1-naphthoic acid), or analogues of these chemicals. The lactic acid inhibitor  163  can be dissolved, dispensed or dispersed in aqueous or organic liquid, as a solution or dispersion. 
     The lactic inhibitor  163  can also be NADH dehydrogenase inhibitor  163 . The NADH dehydrogenase inhibitor  163  includes gossypol, polyphenol, dihydroxynaphthoic acids, adenosine diphosphate ribose, rotenone, rotenoid, phenoxan, aureothin, benzimidazole, acetogenin, nitrosothiols, peroxynitrite, carvedilol, arylazido-beta-alanyl NAD+, piericidin A, annonin VI, phenalamid A 2 , aurachins A and B, thiangazole, fenpyroximate, adriamycin, 4-hydroxy-2-nonenal, pyridine derivatives, 2-heptyl-4-hydroxyquinoline N-oxide, dicumarol, o-phenanthroline or 2,2′-dipyridyl or others, that block conversion of pyruvate to lactic acid  162 , causing chronic back pain. 
     Adenosine triphosphate, ATP, is the high-energy compound essential for driving or energizing biochemical reactions, including the biosynthesis of the water retaining glycosaminoglycans for sustaining compressive loads on the disc  100 . Under anaerobic conditions, metabolism of each glucose molecule produces only two ATP and two lactic acids  162 , which irritate adjacent nerves  118 . By inhibiting conversion of two pyruvates to two lactic acids  162 , thirty-six ATP can be produced from each glucose molecule through glycolysis, citric acid cycle and electron transport chain under aerobic conditions to energize disc regeneration and alleviate back pain. Thereby, preservation of pyruvate by inhibiting lactic acid  162  production can reduce back pain and form additional ATP for disc regeneration. 
     The method of intra-discal injection of lactic inhibitor  163  is similar to the method for discography. Guided by anterior/posterior and lateral views of fluoroscopy, a spinal needle  276 B punctures into the painful disc  100 . A syringe  276 A with a plunger is loaded with lactic inhibitor  163  and connected to the spinal needle  276 B for intra-discal injection, as shown in  FIG. 9 . 
     The spinal needle  276 B has a distal beveled Quincke or Chiba tip to minimize potential damage to nerves during insertion into the patient. L5-S1 lumbar disc  100  is shielded by the iliac. The needle  276 B can be elastically curved, capable of resiliently straightened within a straight needle. The straight needle is inserted over the iliac to the outer surface of L5-S1 disc. The curved needle  276 B is then deployed from the straight needle, curving into the nucleus  128  of L5-S1 lumbar disc  100  for lactic inhibitor  163  injection. After injection, the curved needle  276 B is withdrawn into the straight needle before withdrawing both curved and straight needles from the patient. 
     Generally, nerves are not found within the intervertebral disc  100 , but nerves are found at the endplate  105  within the vertebral body  159 , which can cause back pain. High lactic acid  162  concentration within the disc  100  can permeate through the porous endplate  105  to irritate and burn the nerves at the endplate  105 . The lactic acid inhibitor  163  can be delivered through intra-vertebral body injection to alleviate back pain, as shown in  FIG. 13 . The needle  276 B for injecting lactic acid inhibitor  163  can be elastically curved, and can be resiliently straightened within a straight needle. The straight needle punctures through the pedicle, and the curved needle  276 B is then deployed from the straight needle toward the endplate  105  to inject lactic inhibitor  163  within the vertebral body  159 . Lactic inhibitor  163  can also be delivered by intravenous injection or oral ingestion to alleviate back pain, caused by burning of lactic acid  162  within the vertebral body  159 . 
     The lactic inhibitor  163  stops or reduces production of lactic acid  162  within the anaerobic and avascular disc  100 . However, the lactic acid  162  within the disc can be flushed out during intra-discal injection of lactic inhibitor  163 , thus causing excruciating pain to the patient, as shown in  FIG. 10 . For patient comfort, antacid, alkaline or buffering agent  122  can also be loaded with the lactic inhibitor  163  into the syringe  276 A, and slowly injected into the painful disc  100  through the spinal needle  276 B, as shown in  FIG. 11 . Before being flushed out the disc  100 , the antacid, alkaline or buffer agent  122  instantaneously neutralizes the lactic acid  162  into pH neutral lactate, to avoid burning the surrounding nerves  118 . The antacid, alkaline or buffering agent  122  and lactic inhibitor  163  can be intra-discal sequentially injected to neutralize the lactic acid  162 , and then inhibit the production of the lactic acid  162 . 
     Disc shunt  126  is a wick or conduit, capable of drawing blood plasma containing nutrients, oxygen and pH buffering solute  131  from muscle  193  and/or superior  106 A and/or inferior  106 B diffusion zones within the disc  100  into the mid-layer of the disc  100 , as shown in  FIG. 12 . Sodium bicarbonate is a pH buffering solute  193  in blood plasma capable of neutralizing lactic acid  162  within the disc  100 . Intra-discal injection of the lactic acid inhibitor  163  reduces or prevents conversion of pyruvate into lactic acid  162  within the disc  100 . In the presence of oxygen through the disc shunt  126 , pyruvate can be metabolized into carbon dioxide, generating many more adenosine triphosphate (ATP) to energize disc regeneration by building new disc matrix. 
     The disc shunt  126  can also be coated with lactic inhibitor  163  before implanting into the disc  100 . In addition, the lactic inhibitor  163  can be injected near the disc shunt  126  within the muscle  193 , so that the disc shunt  126  can draw the lactic inhibitor  163  from bodily circulation into the disc  100 . 
     The rate of sulfate incorporation for biosynthesizing glycosaminoglycans is pH sensitive. The maximum rate of sulfate incorporation is with pH 7.2-6.9. The rate of sulfate incorporation drops about 32-40% in acidic pH within the disc [Ohshima H, Urban J P: The effect of lactate and pH on proteoglycan and protein synthesis rates in the intervertebral disc. Spine, September:17(9), 1079-82, 1992]. Hence, pH normalization with lactic inhibitor  163  will likely increase production of the water-retaining glycosaminoglycans and swelling pressure of the disc  100 . 
     It is to be understood that the present invention is by no means limited to the particular chemicals or constructions disclosed herein and/or shown in the specification and drawings, but also includes any other chemical, analogues, modification, changes or equivalents within the scope of the claims. Any one or more of the chemicals or features described may be added to or combined with any of the other chemicals or embodiments to create alternative combinations of chemicals and embodiments. 
     It should be clear to one skilled in the art that the current chemicals, embodiments, materials, constructions, methods, tissues or injection sites are not the only uses for which the invention may be used. Different chemicals, analogues, materials, constructions, methods or device designs for introducing lactic inhibitor  163  can be substituted and used. Nothing in the preceding description should be taken to limit the scope of the present invention. The full scope of the invention is to be determined by the appended claims. 
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