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Biomedical subjects

K Nagai

Publications and source records attributed to K Nagai.

At least 145 records · Page 8Linked to original sources

Favorable and unfavorable morphological prognostic factors in peripheral adenocarcinoma of the lung 3 cm or less in diameter.

Many small adenocarcinomas can be detected as a result of recent advances in diagnostic radiology. Since the histological and biological heterogeneity of adenocarcinoma often makes it difficult to predict the outcome of operated patients, clarifying the morphological prognostic factors of the tumor is indispensable to the selection of appropriate treatment. We examined 200 cases of adenocarcinoma of the lung 3 cm or less in diameter (T1). Tumor size, tumor cell characteristics, growth pattern, characteristics of fibrosis, vessel and stromal invasion, and metastasis were evaluated to define favorable and unfavorable morphological prognostic factors by univariate and multivariate statistical analysis. There were no deaths in the 66 cases with more than a 75% of lepidic growth component defined as a region of tumor cells growing along alveolar walls and without stromal invasion, central focus of fibrosis 5 mm or less in maximum diameter, or no elastic fiber framework destruction by tumor cells. Multivariate analysis to investigate unfavorable factors revealed that vascular invasion (P<0.001) and a greater than 25% papillary growth component (P=0.043) were the most significant determinants of an unfavorable outcome. The favorable and unfavorable factors demonstrated in this study will be of great value in selecting the treatment of patients with small peripheral adenocarcinoma of the lung.

Adenocarcinoma↗

Increased cyclooxygenase 2 (COX-2) expression occurs frequently in precursor lesions of human adenocarcinoma of the lung.

A low incidence of lung carcinoma has been reported in cases of prolonged use of aspirin. Cyclooxygenase (COX) 2 expression is frequently seen in adenocarcinoma of the lung, but COX-2 expression in atypical adenomatous hyperplasia (AAH), a possible precursor lesion of adenocarcinoma of the lung, is not known. COX-2 expression was immunohistochemically evaluated in a cohort of 20 cuboidal cell hyperplasias (CCH), 81 atypical adenomatous hyperplasias (AAH), 18 bronchioloalveolar carcinomas (BAC), and 88 invasive adenocarcinomas (I-Ad). The relationship between COX-2 expression and clinicopathologic factors and survival was examined. COX-2 overexpression was detected in over 80% of CCH, AAH, BAC, and I-Ad. However, overexpression was diffuse in AAH (71.6%) and BAC (66.7%). No relationship was found between COX-2 expression and clinicopathological factors or survival. COX-2 expression was most frequently detected in AAH. These findings, taken with previous reports that treatment with COX-2 inhibitor suppresses human colon carcinogenesis, suggest that inhibition of COX-2 may reduce the incidence of human adenocarcinoma of the lung.

Adenocarcinoma↗

Impaired behavioral suppression by light in metabotropic glutamate receptor subtype 6-deficient mice.

The metabotropic glutamate receptor subtype 6 is localized on the dendrites of ON bipolar cells in mammalian retina, and is responsible for synaptic transmission from photoreceptors to ON bipolar cells. We have previously provided electrophysiological evidence that metabotropic glutmate receptor subtype 6-deficient mice have an impairment in the ON visual pathway. In this study, we compared, between metabotropic glutamate receptor subtype 6-deficient (n=9) and wild-type mice (n=7), their daily wheel-running activity in constant dark and light-dark cycle environments. There was no difference in their free-running rhythmicity in a constant dark environment nor in their ability to entrain their active/rest phase to the phase-shifted light-dark cycle environment, indicating that the circadian system in mutant mice was functioning normally. However, the wheel-running activity was suppressed immediately after light onset of the light-dark cycle in wild-type mice (suppressive effect), whereas that of mutant mice was prolonged for several hours in spite of light onset (very weak suppressive effect). The suppression of activity in wild-type mice is a "masking effect" of the endogenous circadian rhythm in response to light stimuli. The results indicate that the failure of mutant mice to suppress their activity upon light onset is not due to abnormality in their circadian system, but to their lack of response to light stimuli. This study clearly demonstrates that the dysfunction of the ON visual pathway in metabotropic glutamate receptor subtype 6-deficient mice impairs their behavioral responsiveness to light and yet preserves their circadian system.

Animals↗

Antimicrobial susceptibilities and serotypes of Streptococcus pneumoniae in southwestern Japan and correlation of penicillin-binding protein 2b and 2x mutations in susceptibilities of penicillin G and cefotaxime.

MICs of penicillin G and other drugs and serotypes were determined for 218 strains of Streptococcus pneumoniae isolated from children in southwestern Japan. Twenty-one (9.6%) and 81 (37.2%) isolates were penicillin-resistant (MIC >/=2.0 microg/ml) and intermediate (MIC 0.13-1.0 microg/ml), respectively. Panipenem was most active parenteral agent against penicillin-intermediate (MIC(90) 0.125 microg/ml) and -resistant strains (MIC(90) 0.25 microg/ml). Among oral beta-lactam agents, cefditoren had good activity against penicillin-intermediate and resistant strains (MIC(90) 0.5/1.0 microg/ml). Serogroup 6 was the most prevalent (65/218) among all strains and 19F (44 strains) was the most prevalent among penicillin-intermediate and -resistant strains. Both pbp2b resistant and susceptible genes were found in penicillin-intermediate strains. Pbp2x resistant genes were found in 33 of 80 (41.3%) cefotaxime-susceptible strains. These results suggest that possible resistance mechanisms may occur even in drug susceptible strains and that drug susceptibility survey should be updated carefully in Japan.

Aminoacyltransferases↗

Carbon-monoxide poisoning presenting as an afebrile seizure.

A 1-year-old male who experienced an afebrile seizure and loss of consciousness caused by carbon-monoxide poisoning is reported. His blood gas analysis revealed an elevated carboxyhemoglobin level (up to 25%) and metabolic acidosis. A cranial computed tomography depicted diffuse swelling of the brain. He was promptly treated with hyperbaric oxygen. He recovered fully 8 hours after the onset of the illness. No neurologic deficit was evident during the 8 months of follow-up. Although seizures are generally regarded as a manifestation of severe and near-fatal carbon-monoxide poisoning, an early diagnosis and aggressive hyperbaric-oxygen therapy could result in a good clinical outcome. In a patient presenting with an afebrile seizure, carbon monoxide poisoning should always be considered as one of the etiologies.

Body Temperature↗

Human G-protein beta3 subunit variant is associated with serum potassium and total cholesterol levels but not with blood pressure.

The activity of a sodium-proton exchanger is enhanced in the patients with essential hypertension and regulated via G-protein, which is a signal transducer between receptors and intracellular effectors. A recent study has revealed that a novel variant (C825T) in exon 10 of the gene encoding the beta3 subunit of heterotrimetric G proteins (GNB3) is a genetic factor predisposing to hypertension in Caucasians. We examined the association between GNB3/ C825T and blood pressure, lipids, electrolytes, and other parameters in a Japanese population. Subjects (n = 352) were selected from the Ohasama Study, the population of which is regarded as from a rural community in Japan. To obtain precise clinical measurements, 24-h ambulatory blood pressure monitoring (ABPM), brain magnetic resonance imaging (MRI), and carotid ultrasonography (CUS) were conducted in this population. In addition, we recruited 762 subjects from outpatients at the Osaka University Medical School to carry out the association study between hypertension and GNB3. The GNB3 genotype distribution did not differ significantly between normotensives and hypertensives in either of the two studies. The T825 allele of GNB3 was not associated with the presence of hypertension, blood pressure level, the number of brain lacunae or carotid wall thickness. However, the serum potassium and total cholesterol levels were significantly higher in subjects with the T allele (P < .005). The T825 allele of GNB3 is associated with increased serum potassium and total cholesterol levels but not with blood pressure in a Japanese population.

Adult↗

Gene polymorphism of the renin-angiotensin system associates with risk for lacunar infarction. The Ohasama study.

The polymorphism of the angiotensin-converting enzyme gene is considered to be associated with increased risk for stroke, but there is a diversity in the results obtained. The genetic involvement of the renin-angiotensin system in stroke also remains unclear. To predict the genetic risk of lacunar infarction, we conducted an association study in an Ohasama population, which is the cohort in a rural region of northern Japan. A total of 134 subjects without major neurological, cardiovascular, or metabolic disorders were recruited. Using brain magnetic resonance imaging, the number of lacunae in each of four brain regions were calculated, and periventricular hyperintensity was classified into five grades. We used the following four candidate gene polymorphisms: angiotensin converting enzyme (ACE)/Insertion(I)-Deletion(D), angiotensinogen (AGT)/M235T, angiotensin II type 1 receptor (AT1)/ A1166C, type 2 receptor (AT2)/C3123A, to examine the association between polymorphisms and the severity of lacunar infarction. AGT/M235T was significantly associated with the number of lacunae in the brain stem, the basal ganglia (P < .05), and whole brain (P < .005) regions. The AT1 polymorphism was also significantly associated with the number of lacunae in the basal ganglia and whole brain regions (P < .05), and with periventricular hyperintensity grade (P < .005) in the younger population. However, ACE and AT2 polymorphisms failed to show an association with either the number of lacunae or the PVH grade. We concluded that AGT and AT1 polymorphisms are independent genetic risk factors for lacunar infarction.

Aged↗

Vanishing bile duct syndrome associated with chronic EBV infection.

We reported here an adult patient with vanishing bile duct syndrome due to chronic EBV infection. A 22-year-old male was admitted to a nearby hospital complaining of a sore throat and jaundice. He received a high dose of prednisolone for bile stasis of acute viral hepatitis. However, the hepatitis did not improve, and he was transferred to our hospital. He had exhibited jaundice for one year as well as hemophagocytic syndrome and intestinal perforation. Subtotal intestinal resection was successfully performed. Three follow-up biopsied liver specimens indicated vanishing bile duct syndrome. Positive results of EBV-DNA in his serum and mRNA of EBV by in situ hybridization of his liver indicated that massive doses of prednisolone caused chronic EBV infection and vanishing bile duct syndrome.

Adult↗

FD-891, a structural analogue of concanamycin A that does not affect vacuolar acidification or perforin activity, yet potently prevents cytotoxic T lymphocyte-mediated cytotoxicity through the blockage of conjugate formation.

FD-891 belongs to a group of 18-membered macrolides, and is a structural analogue of a specific inhibitor of vacuolar type H+-ATPase, concanamycin A (CMA). In our previous work, we have shown that CMA specifically inhibits perforin-dependent cytotoxic T lymphocyte (CTL)-mediated cytotoxicity through the degradation and inactivation of perforin, although CMA does not affect Fas ligand (FasL)-dependent cytotoxicity. Here, we show that FD-891 potently prevents not only perforin-dependent but also FasL-dependent CTL-mediated killing pathways by blocking CTL-target conjugate formation. In contrast to CMA, FD-891 was unable to inhibit vacuolar acidification and only slightly decreased the perforin activity in lytic granules. FD-891 blocked granule exocytosis in response to anti-CD3, mainly owing to the lack of CTL binding to immobilized anti-CD3. The conjugate formation was markedly inhibited only when effector cells were pretreated with FD-891. Consistent with these observations, fluorescence-activated cell sorter (FACS) analysis for cell surface receptors revealed that FD-891 significantly reduced the expression of the T-cell receptor (TCR)/CD3 complex. These data suggest that the blockage of conjugate formation and subsequent target cell killing might be at least partly owing to FD-891-induced down-regulation of the TCR/CD3 complex.

Animals↗

In vivo rapid reduction of alloantigen-activated CD8+ mature cytotoxic T cells by inhibitors of acidification of intracellular organelles, prodigiosin 25-C and concanamycin B.

Prodigiosin (PrG) 25-C and concanamycin B (CMB) are immunosuppressants that specifically inhibit the induction of cytotoxic T cells (CTL) without affecting the function of B cells and helper T cells in vivo. Both compounds inhibit acidification of intracellular organelles and induce destruction of cytotoxic granules and degradation of perforin in vitro. Here we show that a single intraperitoneal (i.p.) injection of PrG 25-C, and of CMB, into mice eliminates cytotoxic activity 7 days after alloantigen stimulation (when mature CTL activity has been detected in control mice), with minimal effect on the alloantigen-specific antibody titre in serum. FK506 did not suppress the cytotoxic activity with this administration schedule. Suppression was accompanied by a decrease in the CD8+ population and in perforin expression of spleen cells induced by alloantigen stimulation. The suppression of CTL activity and decrease in CD8+ cell number was detected as early as 7 hr after the injection of compounds. These results suggest that inhibitors of acidification of intracellular organelles suppress CTL activity in vivo by reducing the number of mature CD8+ CTL.

Animals↗

A diminished activation capacity of the interferon-inducible protein kinase PKR in human T lymphocytes.

The double-stranded (ds) RNA activated protein kinase PKR is an interferon (IFN)-inducible serine/threonine protein that regulates protein synthesis through the phosphorylation of the alpha subunit of translation initiation factor 2 (eIF-2alpha). PKR activation in cells is induced by virus infection or treatment with dsRNA and is modulated by a number of viral and cellular factors. To better understand the mechanisms of PKR action we have analyzed and compared the mode of PKR activation in a number of cell lines of different histological origin. Here we show that PKR activation and phosphorylation of eIF-2alpha are both diminished in various virus-transformed and nontransformed human T cells. Priming of T cells with IFN does not restore PKR activation. In vitro kinase assays show that the diminished PKR activation in T cells correlates with the presence of a 60-kDa (p60) phosphoprotein coimmunoprecipitated with PKR. P60 is absent from PKR immunoprecipitates from non T cells. Incubation of active PKR with T cell extracts results in inhibition of PKR autophosphorylation, which is proportional to the amount of phosphorylated p60 in the kinase reactions. Treatment of T cells with proteasome inhibitors or incubation of PKR immunoprecipitates with phosphatase inhibitors does not restore PKR activation. However, phosphorylation of p60 is enhanced upon treatment with the phosphatase inhibitor microcystin. These data show that the impaired activation capacity of PKR in human T cells is exerted at the post-translational levels in a manner that is independent of cell transformation or virus infection.

Adult↗

Identification of tudor repeat associator with PCTAIRE 2 (Trap). A novel protein that interacts with the N-terminal domain of PCTAIRE 2 in rat brain.

PCTAIRE 2 is a Cdc2-related kinase that is predominantly expressed in the terminally differentiated neuron. To elucidate the function of PCTAIRE 2, proteins that associate with PCTAIRE 2 were screened by the yeast two-hybrid system. A positive clone was found to encode a novel protein that could bind to PCTAIRE 2 in vitro as well as in vivo, and was designated as Trap (tudor repeat associator with PCTAIRE 2). The overall structure of Trap shows no significant homology to any proteins, but contains five repeated domains (the tudor-like domain), conserved in Drosophila tudor protein. Trap associates with the N-terminal domain of PCTAIRE 2 through its C-terminal domain, which contains two tudor-like domains. PCTAIRE 1, but not PCTAIRE 3, can also associate with Trap. Trap is predominantly expressed in brain and testis, and gradually increases during brain development throughout life, consistent with the expression pattern of PCTAIRE 2. Immunoreactivities for PCTAIRE 2 and Trap were colocalized to the mitochondria in COS 7 cells. Immunohistochemical analyses showed that PCTAIRE 2 and Trap were distributed in the same cell layer of the cerebral cortex and cerebellum. These findings suggest that Trap is a physiological partner of PCTAIRE 2 in terminally differentiated neurons.

Amino Acid Sequence↗

Sepsis in children.

BACKGROUND: Sepsis remains lethal to children. At our institution, we have noted that approximately 2% of all hospitalized patients have had sepsis. In the present study, we analyzed episodes of sepsis that occurred in our ward. METHODS: Sepsis that occurred in our institution between January 1984 and December 1998 was reviewed and analyzed. RESULTS: Three hundred and sixty-six episodes of sepsis in 244 admitted patients were analyzed. Sepsis occurred in approximately 2% of all hospitalized patients. Forty-three of 244 patients were under 1 year of age. Eighty-seven percent (212/244) of cases had underlying diseases. Hematologic disorders or neoplasms were the most common underlying disease, comprising 55% of all patients (133/244). Two-hundred and fifty-one of 366 episodes of sepsis were acquired during hospitalization. We identified 409 causative agents. There were 25 polymicrobial infections (25/366; 7%). Gram-positive bacteria comprised 68% of all organisms (280/409). Staphylococcus aureus was the most common organism, comprising 18% of causing agents (75/409). Sixty-six organisms came from the insertion of a central venous catheter. Eighty-one patients experienced recurrent episodes of sepsis. In terms of complications, respiratory distress was the most common complication (36 episodes) and there were 15 episodes of shock. Thirty-seven patients died of sepsis. Sepsis caused by Gram-negative bacteria showed significantly higher mortality than Gram-positive bacteria (11/43 (26%) vs 15/146 (10%); P= 0.053). CONCLUSIONS: In our institution, approximately 20% of septic patients were under 1 year of age and 90% had underlying diseases. The causative agents of sepsis affected the outcome.

Adolescent↗

Clinicopathologic analysis of lymph node metastasis in surgically resected superficial cancer of the thoracic esophagus.

We examined lymph node metastasis clinicopathologically in 236 cases of superficial cancer (T1, Tis) of the thoracic esophagus surgically resected at our department without adjuvant treatment. Mucosal cancer was observed in 112 cases (47%) and submucosal cancer in 124 cases (53%). Lymph node metastasis was present in 3% of mucosal cancer cases and 41% of submucosal cancer cases. By the recent pathologic subclassification of the extent of the cancerous invasion in superficial esophageal cancer, mucosal cancer and submucosal cancer were each divided into three subtypes according to the extent of invasion, i.e. m1, m2, m3, sm1, sm2 and sm3 cancers. There was no case of lymph node metastasis in m1 and m2 cases, but it was observed in 8% of m3 cases, in 11% of sm1 cases, in 30% of sm2 cases and in 61% of sm3 cases. The number of involved nodes was three or less in m3 and sm1 cases, however four or more involved nodes were observed in 14% of sm2 cases and in 24% of sm3 cases. Positive lymph nodes were found only in the mediastinum in m3 and sm1 cases. On the contrary, they were found extensively in the mediastinum, the abdomen and the neck and in two or more regions in 27% of sm2 cases and in 38% of sm3 cases. Considering the location of positive nodes, the recurrent nerve lymph nodes were most frequently involved, followed by the cardiac lymph nodes. A similar tendency was observed in cases with single node metastasis. The 5-year survival rate of cases from m1 to sm1 was similar. That of sm3 cases was significantly worse than that of other groups. Based on the clinical results, the therapeutic guidelines for superficial cancer of the thoracic esophagus are considered to be as follows: (i) in m1 and m2 cancer, endoscopic mucosal resection is generally indicated in principle, although transhiatal esophagectomy may be indicated in some cases; (ii) in m3 and sm1 cancer, endoscopic mucosal resection is performed initially, then subsequent treatment is selected if necessary; (iii) in sm2 and sm3 cancer, conventional transthoracic esophagectomy with systematic lymph node dissection is indicated.

Adult↗

Light-induced tyrosine phosphorylation of BIT in the rat suprachiasmatic nucleus.

Circadian changes of protein tyrosine phosphorylation in the hypothalamic suprachiasmatic nucleus have been studied using rats maintained under 12-h light/ 12-h dark cycles as well as constant dark conditions. We found that tyrosine phosphorylation of BIT (brain immunoglobulin-like molecule with tyrosine-based activation motifs), a transmembrane glycoprotein of 90-95 kDa, was higher in the light period than in the dark period and was increased after light exposure in the dark period. Similar changes in tyrosine phosphorylation were observed under constant dark conditions, but its amplitude was weaker than that in 12-h light/12-h dark cycles. As the tyrosine-phosphorylated form of BIT is able to bind to the Src homology 2 domain of a protein tyrosine phosphatase, SHP-2, we examined association of these proteins in suprachiasmatic nucleus extracts and found that SHP-2 was coprecipitated with BIT in parallel with its tyrosine phosphorylation. These results suggest that tyrosine phosphorylation of BIT might be involved in light-induced entrainment of the circadian clock.

Animals↗

The role of computed tomographic scanning in diagnosing mediastinal node involvement in non-small cell lung cancer.

OBJECTIVES: The reliability of computed tomographic scanning in evaluating mediastinal node involvement is controversial because of the high false result rate. We attempted to identify significant factors responsible for false-positive and false-negative scans. METHODS: From August 1992 through April 1997, 401 patients with lung cancer who underwent major lung resection and systematic lymph node dissection were enrolled in this study. We retrospectively examined mediastinal node size, tumor location, maximum tumor dimension, the presence or absence of obstructive pneumonia, atelectasis, pulmonary fibrosis, and lymph node calcification on contrast-enhanced computed tomographic scans. We identified clinical and radiologic factors responsible for the false results by using univariate and multivariable analysis. RESULTS: Central tumor location proved to be a significant factor of false-positive scans. Elevated carcinoembryonic antigen level and larger tumor dimension were significant factors of false-negative scans. In patients with a peripheral tumor smaller than 40 mm and normal levels of serum carcinoembryonic antigen, sensitivity, specificity, positive predictive value, and negative predictive value were 6%, 93%, 8%, and 90%, respectively. The reliability of computed tomographic scanning in this low-risk subgroup was high in detecting N0-1 disease but low in diagnosing N2 disease. CONCLUSION: It is not possible to accurately diagnose N2 disease by using lymph node size on computed tomographic scanning alone, especially in patients with a central tumor, an elevated serum carcinoembryonic antigen level, or a tumor of 40 mm or larger. A preoperative invasive staging procedure is indicated in these populations and may not be indicated in the population with normal computed tomographic scan results without any of these risk factors.

Aged↗

Results of surgical treatment of lung cancer involving the diaphragm.

OBJECTIVES: Lung cancers with diaphragmatic invasion are categorized as T3 lesions, but the surgical results have not been well known. We retrospectively surveyed patients with resected primary lung cancers involving the diaphragm. METHODS: A total of 16,771 patients underwent surgical resection for lung carcinoma between 1986 and 1995 at 31 institutions of the Lung Cancer Surgical Study Group in Japan. By investigating the database, we identified 63 patients (0. 38%) who underwent resection of T3 lung cancer invading the diaphragm. These patients constituted the study population, and their clinical and pathologic records were retrospectively analyzed. RESULTS: Tumor invasion to the diaphragm was diagnosed before operation only in 17 patients (27.0%). Complete resections of the primary lung tumors with the invaded diaphragm were performed in 55 patients (87.3%), of whom 26 had T3 N0 M0 diseases and 29 had T3 Nl-2 M0 diseases. The operative mortality was 1.6% in all patients. The 5-year survival of patients with complete resection was 22.6%, but there was no 4-year survivor in patients with incomplete resection (P =.024). The survivals of patients with completely resected T3 N0 M0 and T3 N1-2 M0 tumors were 28.3% and 18.1%, respectively (P =.013). In those patients, the depth of diaphragmatic involvement significantly affected the prognosis. The 5-year survival of the patients with shallow invasion (parietal pleura or subpleural tissue involvement) was 33.0%, whereas that of the patients with deep invasion (muscle or peritoneal infiltration) was 14.3% (P =.036). CONCLUSIONS: In selected patients with lung carcinoma and diaphragmatic invasion, combined resection of the lung and diaphragm offers the prospect of cure with acceptable mortality. However, primary lung tumors with diaphragmatic invasion, especially invasion of the muscle layer or deeper tissue, are not considered to be T3 lesions, because these cancers are generally technically resectable but oncologically almost incurable.

Aged↗

A novel carbohydrate binding activity of annexin V toward a bisecting N-acetylglucosamine.

A bisecting GlcNAc-binding protein was purified from a Triton X-100 extract of a porcine spleen microsomal fraction using affinity chromatography, in conjunction with an agalacto bisected biantennary sugar chain-immobilized Sepharose. Since the erythroagglutinating phytohemagglutinin (E-PHA) lectin preferentially binds to sugar chains which contain the bisecting GlcNAc, during purification the binding activity of the protein was evaluated by monitoring the inhibition of lectin binding to the N-acetylglucosaminyltransferase III (GnT-III)-transfected K562 cells which express high levels of the bisecting GlcNAc. The molecular mass of the purified protein was found to be 33 kDa, as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. By sequencing analysis, the isolated protein was identified as annexin V. Flow cytometric analysis showed that fluorescein-labeled annexin V binds to the GnT-III-transfected cells but not to mock cells, and that the binding was not affected by the addition of phospholipids. Furthermore, surface plasmon resonance measurements indicated that annexin V binds to the agalacto bisected biantennary sugar chain with a K(d) of 200 microM while essentially no binding was observed in the case of the corresponding non-bisected sample. These results suggest that annexin V has a novel carbohydrate binding activity and may serve as an endogenous lectin for mediating possible signals of bisecting GlcNAc, which have been implicated in a variety of biological functions.

Acetylglucosamine↗