Biomedical subjects

Ashok Kumar

Publications and source records attributed to Ashok Kumar.

At least 37 records · Page 2Linked to original sources

PubMed2003

Synthesis of newer indolyl/phenothiazinyl substituted 2-oxo/thiobarbituric acid derivatives as potent anticonvulsant agents.

2-Amino-5-(heteroarylmethylene)-1,3,4-oxadiazoles/thiadiazoles 7-10 were synthesized by cyclisation of 1-(heteroarylacetyl)semicarbazides/thiosemicarbazides 3-6. 5-(2'-Heteroarylmethylene-5'-aminomethylene-1',3,'4'- oxadiazol-2'-yl/thiadiazol-2'-yl)-2-oxo/thiobarbituric acids 11-18 were synthesized by condensation of compounds 7-10 at the 5th position of 2-oxo/thiobarbituric acids. The newly synthesized compounds showed anticonvulsant activity ranging from 50-90% (seizures protection). Compound 18 (5-(2'-phenothiazinylmethylene-5'-aminomethylene-1',3',4'-thiadiazol-2'- yl)-2-thiobarbituric acid) showed maximum activity being more potent than the reference drug phenytoin sodium (CAS 630-93-3).

Animals↗

PubMed2003

Newer substituted benzoxazepinyl-quinazolinones as potent antipsychotic and anticonvulsant agents.

3-Amino-[2'-substitutedaryl-3'-substitutedarylaminomethylene-2',3'- dihydro-1',5'-benzoxazepin-4'-yl]-2-methyl-quinazolin-4(3H)-ones 11-18 and 3-amino-[2'-substituted aryl-3'-substitutedaryl-azo-2',3'- dihydro-1',5'-benzoxazepin-4'-yl]-2-methyl-quinazolin-4(3H)-ones 19-26 were synthesized from 3-amino-[2'-substitutedaryl-2',3'-dihydro-1',5'- benzoxazepin-4'-yl]-2-methyl-quinazolin-4(3H)-ones 7-10 by Mannich's reaction and by diazotisation, respectively, on the 3rd position of the benzoxazepine ring of the compounds 7-10. The newly synthesized compounds showed potent antipsychotic and anticonvulsant activities.

Amphetamine↗

PubMed2003

Mechanical stress activates the nuclear factor-kappaB pathway in skeletal muscle fibers: a possible role in Duchenne muscular dystrophy.

The ex vivo effects of passive mechanical stretch on the activation of nuclear factor-kappaB (NF-kappaB) pathways in skeletal muscles from normal and mdx mouse, a model of Duchenne muscular dystrophy (DMD), were investigated. The NF-kappaB/DNA binding activity of the diaphragm muscle was increased by the application of axial mechanical stretch in a time-dependent manner. The increased activation of NF-kappaB was associated with a concomitant increase in I-kappaB (IkappaB) kinase activity and the degradation of IkappaBalpha protein. Pretreatment of the muscles with nifedipine (a Ca2+ channel blocker) and gadolinium(III) chloride (a stretch-activated channel blocker) did not alter the level of activation of NF-kappaB, ruling out involvement of Ca2+ influx through these channels. Furthermore, N-acetyl cysteine, a free radical inhibitor, blocked the mechanical stretch-induced NF-kappaB activation, suggesting the involvement of free radicals. Compared with normal diaphragm, the basal level of NF-kappaB activity was higher in muscles from mdx mice, and it was further enhanced in mechanically stretched muscles. Furthermore, activation of NF-kappaB and increased expression of inflammatory cytokines IL-1beta and tumor necrosis factor alpha in the mdx mouse precede the onset of muscular dystrophy. Our results show that mechanical stretch activates the classical NF-kappaB pathway and this pathway could be predominately active in DMD.

Acetylcysteine↗

PubMed2003

Radioprotective effect of Panax ginseng on the phosphatases and lipid peroxidation level in testes of Swiss albino mice.

The Panax ginseng has been used as traditional medicine for past several years among oriental people. The present investigation has been made to assess the radioprotective efficacy of ginseng root extract in the testicular enzymes of Swiss albino mice. The Swiss albino mice were divided into different groups. (i) Ginseng treated group: The animals were administered 10 mg/kg body weight ginseng root extract i.p. (ii) Radiation treated group: The animals were exposed to 8 Gy gamma radiation at the dose rate of 1.69 Gy/min at the distance of 80 cm. (iii) Combination group: Animals were administered ginseng extract continuously for 4 d and on 4th day they were irradiated to 8 Gy gamma radiation after 30 min of extract administration. The animals from above groups were autopsied on day 1, 3, 7, 14 and 30. Biochemical estimations of acid and alkaline phosphatases and Lipid peroxidation (LPO) in testes were done. In ginseng treated group acid and alkaline phosphatases activity and LPO level did not show any significant alteration. In irradiated animals there was a significant increase in acid phosphatase activity and LPO level. However, significant decline in alkaline phosphatase activity was observed. The treatment of ginseng before irradiation causes significant decrease in acid phosphatase and LPO level and significant increase in alkaline phosphatase activity. One of the cause of radiation damage is lipid peroxidation. Due to lipid peroxidation, lysosomal membrane permeability alters and thus results in release of hydrolytic enzymes. So, an increase in acid phosphatase was noticed after radiation treatment. The alkaline phosphatase activity is associated with membrane permeability and different stages of spermatogenesis. Due to membrane damage and depletion of germ cells of testes after irradiation the enzyme activity was decreased. Ginseng markedly inhibits lipid peroxidation. It acts in indirect fashion to protect radical processes by inhibition of initiation of free radical processes and thus reduces the radiation damages in testes of Swiss albino mice.

Animals↗

PubMed2002

Differential regulation of CD44 expression by lipopolysaccharide (LPS) and TNF-alpha in human monocytic cells: distinct involvement of c-Jun N-terminal kinase in LPS-induced CD44 expression.

Alterations in the regulation of CD44 expression play a critical role in modulating cell adhesion, migration, and inflammation. LPS, a bacterial cell wall component, regulates CD44 expression and may modulate CD44-mediated biological effects in monocytic cells during inflammation and immune responses. In this study, we show that in normal human monocytes, LPS and LPS-induced cytokines IL-10 and TNF-alpha enhance CD44 expression. To delineate the mechanism underlying LPS-induced CD44 expression, we investigated the role of the mitogen-activated protein kinases (MAPKs), p38, p42/44 extracellular signal-regulated kinase, and c-Jun N-terminal kinase (JNK) by using their specific inhibitors. We demonstrate the involvement, at least in part, of p38 MAPK in TNF-alpha-induced CD44 expression in both monocytes and promonocytic THP-1 cells. However, neither p38 nor p42/44 MAPKs were involved in IL-10-induced CD44 expression in monocytes. To further dissect the TNF-alpha and LPS-induced signaling pathways regulating CD44 expression independent of IL-10-mediated effects, we used IL-10 refractory THP-1 cells as a model system. Herein, we show that CD44 expression induced by the LPS-mediated pathway predominantly involved JNK activation. This conclusion was based on results derived by transfection of THP-1 cells with a dominant-negative mutant of stress-activated protein/extracellular signal-regulated kinase kinase 1, and by exposure of cells to JNK inhibitors dexamethasone and SP600125. All these treatments prevented CD44 induction in LPS-stimulated, but not in TNF-alpha-stimulated, THP-1 cells. Furthermore, we show that CD44 induction may involve JNK-dependent early growth response gene activation in LPS-stimulated monocytic cells. Taken together, these results suggest a predominant role of JNK in LPS-induced CD44 expression in monocytic cells.

Adult↗

PubMed2002

Impairment of cholinergic neurotransmission in adult and aged transgenic Tg2576 mouse brain expressing the Swedish mutation of human beta-amyloid precursor protein.

To address the question of whether beta-amyloid peptides also affect cholinergic neurotransmission in vivo, brain tissue from transgenic Tg2576 mice with Alzheimer plaque pathology at ages ranging from 7 to 24 months were examined by immuno- and histochemical staining for choline acetyltransferase (ChAT) and acetycholinesterase (AChE), by assaying cholinergic enzyme activities and high-affinity choline uptake as well muscarinic and nicotinic cholinergic receptor binding levels by quantitative autoradiography. Cortical and hippocampal activities of AChE and ChAT were not different between transgenic mice and non-transgenic littermates regardless of the postnatal ages examined. However, high-affinity choline uptake was reduced in the hippocampus of 21-month-old transgenic mice. In brains of 8-month-old transgenic mice which do not yet demonstrate cortical beta-amyloids, reduced binding levels of cortical and hippocampal M1-muscarinic cholinergic receptors were observed, which were still reduced in 17-month-old transgenic mouse brains with high plaque load as compared to non-transgenic littermates. M2-muscarinic cholinergic receptor binding was hardly affected in brains from 8-month-old transgenic mice, but in 17-month-old transgenic mice reduced cortical and hippocampal binding levels were observed as compared to non-transgenic controls. Decreased cortical nicotinic cholinergic receptor binding was detected in 17-month-old transgenic mice. The development of changes in cholinergic synaptic markers in transgenic Tg2576 mouse brain before the onset of progressive plaque deposition provides in vivo evidence of a modulatory role of soluble beta-amyloid on cholinergic neurotransmission and may be referred to the deficits in learning and memory also observed in these mice before significant plaque load.

Acetylcholinesterase↗

PubMed2002

Distinct signaling pathways are activated in response to mechanical stress applied axially and transversely to skeletal muscle fibers.

In the diaphragm muscle we tested the hypothesis that MAP kinase signaling pathways are activated by mechanical stress and such signaling pathways are dependent on the direction in which mechanical stress is applied. Although equal magnitudes of mechanical stress were applied axially and transversely a greater level of activation of ERK1/2, p38, Raf-1, p90 RSK, Elk-1, and the DNA binding activity of AP-1 transcription factor was produced when the muscle was stretched transversely than when stretched axially. A significant up-regulation in protein tyrosine phosphorylation was observed in axially or transversely loaded diaphragm muscles and the activation of ERK1/2 was completely inhibited by genistein (protein-tyrosine kinase inhibitor). Pretreatment of muscles with wortmannin (phosphoinositide 3-kinase inhibitor), TMB-8 (antagonist of intracellular calcium release), GF109203X (PKC inhibitor), or PD98059 (MEK1/2 inhibitor) blocked the activation of ERK1/2 kinases in response to axial but not to transverse loading. On the other hand, pretreatment of muscles with protein kinase A inhibitors H-7 and KT5720 completely suppressed the activation of ERK1/2 in response to transverse loading only. Taken together with the alterations of MAP kinases and the findings of elevations of downstream transcription targets, our data are consistent with two distinct MAP kinase signal transduction pathways in response to mechanical stress.

Animals↗

PubMed2002

Angiotensinogen gene polymorphism at -217 affects basal promoter activity and is associated with hypertension in African-Americans.

Hypertension is a serious health problem in Western society, in particular for the African-American population. Although previous studies have suggested that the angiotensinogen (AGT) gene locus is involved in human essential hypertension, the molecular mechanisms involved in hypertension in African-Americans remain unknown. We show that an A/G polymorphism at -217 in the promoter of the AGT gene plays a significant role in hypertension in African-Americans. The frequency of the -217A allele was increased significantly in African-American hypertensive subjects compared with normotensive controls. We also show that the nucleotide sequence of this region of the AGT gene promoter bound strongly to CAAT/enhancer-binding protein (C/EBP) family transcription factors when nucleoside A was present at -217. In addition, we show that reporter constructs containing the human AGT gene promoter with nucleoside A at -217 had increased basal transcriptional activity upon transient transfection in HepG2 cells compared with reporter constructs with nucleoside G at -217. Finally, we show that interleukin-6 treatment in the presence or absence of overexpressed C/EBPbeta increased the promoter activities of reporter constructs containing nucleoside A at -217 compared with reporter constructs containing nucleoside G at -217. Because the AGT gene is expressed primarily in liver and adipose tissue, and C/EBP family transcription factors play an important role in gene expression in these tissues, we propose that increased transcriptional activity of the -217A allele of the human AGT gene is associated with hypertension in African-Americans.

Adult↗

PubMed2002

Normalization of natural killer cell function and phenotype with effective anti-HIV therapy and the role of IL-10.

OBJECTIVES: Natural killer (NK) cell function is likely to be important in controlling HIV infection and opportunistic pathogens. We therefore evaluated NK function and phenotype over the course of antiretroviral therapy (ART) and examined the potential mechanisms of altered NK activity in HIV infection. METHODS: We measured NK cell percentage, NK cytolytic activity (both by flow cytometry) and plasma IL-10 concentrations (by enzyme-linked immunosorbent assay) in 10 HIV-seropositive patients before and over one year of effective ART. To examine potential mechanisms of altered NK activity, we measured NK receptor expression in ART treated and untreated HIV-positive individuals by flow cytometry. As IL-10 enhances NK activity, we studied the effect of IL-10 on NK receptor expression and activity in peripheral blood mononuclear cells (PBMC) from HIV-seronegative individuals. RESULTS: NK cytolytic activity was elevated in HIV infection and decreased with ART to levels observed in HIV-negative individuals. A greater proportion of NK cells from untreated HIV-positive individuals expressed the NK receptors CD158a and CD161 than either HIV-negative volunteers or effectively treated HIV-positive patients. NK cells from PBMC incubated with IL-10 demonstrated increases in CD158a, CD161 and CD94 expression and increases in cytolytic activity. The treatment-associated decrease in NK activity paralleled a decrease in IL-10 production. CONCLUSION: The observation that IL-10 alters NK receptor expression similar to that observed in HIV infection, and the fact that NK receptor expression and activity normalize in parallel with ART-induced reduction of circulating IL-10 levels supports a role for IL-10 in NK cell activity and HIV immunopathogenesis.

Anti-HIV Agents↗

PubMed2002

Distinct role of p38 and c-Jun N-terminal kinases in IL-10-dependent and IL-10-independent regulation of the costimulatory molecule B7.2 in lipopolysaccharide-stimulated human monocytic cells.

The costimulatory molecule B7.2 (CD86) plays a vital role in immune activation and development of Th responses. The molecular mechanisms by which B7.2 expression is regulated are not understood. We investigated the role of mitogen-activated protein kinases (MAPK) in the regulation of B7.2 expression in LPS-stimulated human monocytic cells. LPS stimulation of human monocytes resulted in the down-regulation of B7.2 expression that could be abrogated by anti-IL-10 Abs. Furthermore, SB202190, a specific inhibitor of p38 MAPK, inhibited LPS-induced IL-10 production and reversed B7.2 down-regulation, suggesting that LPS-induced B7.2 down-regulation may be mediated, at least in part, via regulation of IL-10 production by p38 MAPK. In contrast to human promonocytic THP-1 cells that are refractory to the inhibitory effects of IL-10, LPS stimulation enhanced B7.2 expression. This IL-10-independent B7.2 induction was not influenced by specific inhibitors of either p38 or p42/44 MAPK. To ascertain the role of the c-Jun N-terminal kinase (JNK) MAPK, dexamethasone, an inhibitor of JNK activation, was used, which inhibited LPS-induced B7.2 expression. Transfection of THP-1 cells with a plasmid expressing a dominant-negative stress-activated protein/extracellular signal-regulated kinase kinase 1 significantly reduced LPS-induced B7.2 expression, thus confirming the involvement of JNK. To study the signaling events downstream of JNK activation, we show that dexamethasone did not inhibit LPS-induced NF-kappaB activation in THP-1 cells, suggesting that JNK may not be involved in NF-kappaB activation leading to B7.2 expression. Taken together, our results reveal the distinct involvement of p38 in IL-10-dependent, and JNK in IL-10-independent regulation of B7.2 expression in LPS-stimulated monocytic cells.

Antigens, CD↗

PubMed2002

Radiosensitizing effects of neem (Azadirachta indica) oil.

Radiosensitization by neem oil was studied using Balbc/3T3 cells and SCID cells. Neem oil enhanced the radiosensitivity of the cells when applied both during and after x-irradiation under aerobic conditions. Neem oil completely inhibited the repair of sublethal damage and potentially lethal damage repair in Balbc/3T3 cells. The cytofluorimeter data show that neem oil treatment before and after x-irradiation reduced the G(2) + M phase, thus inhibiting the expression of the radiation induced arrest of cells in the G(2) phase of the cell cycle. However, SCIK cells (derived from the SCID mouse), deficient in DSB repair, treated with neem oil did not show any enhancement in the radiosensitivity. There was no effect of neem oil on SLD repair or its inhibition in SCIK cells. These results suggest that neem oil enhanced the radiosensitivity of cells by interacting with residual damage after x-irradiation, thereby converting the sublethal damage or potentially lethal damage into lethal damage, inhibiting the double-strand break repair or reducing the G(2) phase of the cell cycle.

3T3 Cells↗

PubMed2002

Modulation of serum phosphatases activity in Swiss albino mice against gamma irradiation by Mentha piperita Linn.

The modulatory influence of mentha oil (Mentha piperita Linn.) against a lethal dose (8.0 Gy) of gamma irradiation on the activities of serum phosphatases in Swiss albino mice was studied at various post-irradiation intervals between 6 h and 30 days. Mentha oil (40 microL/animal/day) given orally for 3 consecutive days prior to whole-body irradiation (8.0 Gy) showed a modulation of activity of serum phosphatases. The values of acid phosphatase activities were significantly higher in the irradiated groups throughout the experiment compared with the mentha treated unirradiated animals. However, the acid phosphatase activity of mentha treated irradiated animals showed a significant decline over untreated irradiated animals at all autopsy intervals, which attained the normal value on day 5. On the contrary, a marked decrease in serum alkaline phosphatase activity was noted in both irradiated groups but in the mentha treated irradiated group the values of alkaline phosphatase activity were found to be significantly higher than the respective control during the period of study being normal at day 5 post-irradiation and onwards.

Acid Phosphatase↗

PubMed2002

Leukemia in infants.

OBJECTIVE: Acute Leukemia is rare in infants. It is characterized by non-specific symptomatology requiring a high index of suspicion on the part of a pediatrician for referral and diagnosis. It has peculiar biological features, unresponsiveness to treatment and poor prognosis. METHODS: Eighteen infants with acute leukemia were seen during 1994 to 2001 and were analyzed on the basis of clinical and laboratory data. There were 13 cases of Acute Lymphoblastic Leukemia (ALL), 4 cases of Acute Myeloid Leukemia (AML) and one case remained unclassifiable, as the surface markers could not be done. Morphologically 9/13 cases of ALL were of FAB L1 type and remaining of L2 subtype, and 2/4 cases of AML were of FAB M1 type and remaining of M2 subtype. RESULT: Clinical data was available completely only in 11 cases. Hyperleucocytosis was present in 4 cases, organomegaly in 8 cases and lympadenopathy in 5 cases. One patient presented with a chloroma in the retrorbital region although there was no parenchymal involvement of the brain. Immunophenotyping could be done in 13 cases, where 7 cases were diagnosed as CALLA positive-ALL (HLADR+, CD19+, CD10+), 2 cases as Early Pre-B ALL (HLADR+, CD19+, CD10 negative), one as T ALL (cCD3+, CD2+, CD7+) and 3 cases as AML (CD13+, CD33+, HLADR+). None of our patients received treatment.

Female↗

PubMed2002

Newer N-substituted anthranilic acid derivatives as potent anti-inflammatory agents.

The new 5-bromo-N-[2'-amino(1"-acetyl-5"substitutedaryl-2"-pyrazolin-3"-yl)-1',3',4'-oxadiazol-5'-ylmethyl]anthranilic acids 7a-7e and N-[2'-amino-(1"-acetyl-5"-substiutedaryl-2"-pyrazolin-3"-yl)-1',3',4'-thiadiazol-5'-ylmethyl]anthranilic acids 6'a-6'c have been synthesised from 5-bromo-N-(2'-aminosubstituedbenzylideneacetyl-1',3',4'-oxadiazol-5'-ylmethyl)anthranilic acids 6a-6e and N-(2'-aminosubstitutedbenzylideneacetyl-1',3',4'-thiadiazol-5'-ylmethyl)anthranilic acids 5'a-5'e, respectively. All these compounds have been screened in vivo for their anti-inflammatory and acute toxicity. Compounds 7b and 6'b were found to be potent member of this series, which showed 50.66 and 47.56%, respectively, inflammation inhibitory activity at a dose of 50 mg kg(-1) p.o., while standard drug, phenylbutazone, exhibited 45.52% anti-inflammatory activity at the same dose. However, 5-bromo-N-[2'-amino-[1"-acety1-5"-(para-methoxyphenyl)-2"-pyrazolin-3"-yl]-1',3',4'-oxidiazol-5'-ylmethyl]anthranilic acid (7b) was found to be the most active and less ulcerogcnic compound than the standard drag mid rest of the compounds of this series. The structures of these compounds have been established by IR, 1H-NMR spectroscopic data and elemental analyses.

Administration, Oral↗

PubMed2002

Synthesis of newer thiadiazolyl and thiazolidinonyl quinazolin-4 3H-ones as potential anticonvulsant agents.

A series of 3-[[5-(alkylbenzylideneamino)-1,3,4-thiadiazol-2-yl]methylamino-2]-methyl-6-monosubstitutedquinazolin-4(3H)-one (4a-4l) have been synthesized via condensation of 3-[(5-amino-1,3,4-thiadiazol-2-yl)methylamino]-2-methyl-6-monosubstitutedquinazolin-4(3H)-one (3a-3b) with various aromatic aldehydes. Cycloaddition of thioglycolic acid with 4a-4l yielded 3-([4-[2-(alkylphenyl)-4-oxo-1,3-thiazolidin-3-yl]-1,3,4-thiadiazol-2-yl]methylamino)-2-methyl-6-monosubstitutedquinazolin-4(3H)-one (5a-5l). The compounds were screened for their anticonvulsant activity and were compared with the standard drugs, phenytoin sodium, lamotrigine and sodium valproate. Out of the 30 compounds the most active compound was 3-([4-[2-(m-methoxy-p-hydroxyphenyl)-4-oxo-1,3-thiazolidin-3-yl]-1,3,4-thiadiazol-2-yl]methylamino)-2-methyl-6-bromo-quinazolin-4(3H)-one (5l).

Animals↗

PubMed2002

Calcineurin as a potential contributor in estradiol regulation of hippocampal synaptic function.

Estradiol influences Ca(2+) regulation and Ca(2+)-dependent synaptic plasticity, suggesting estrogenic effects on Ca(2+)-dependent enzymes that regulate synaptic plasticity may mediate hormonal influences on cognition. In ovariectomized female rats, injections of estradiol benzoate (EB, 10 microg) reduced hippocampal cytosolic activity of serine/threonine protein phosphatases, calcineurin and protein phosphatase 1 (PP1). The decreased activity was rapid and recovered substantially over a 24-h period. Decreased calcineurin activity was associated with a decreased level of calcineurin in the cytosol. In contrast, expression of PP1 was not altered suggesting that the level of calcineurin activity regulated PP1 activity. EB application to hippocampal slices rapidly decreased cytosolic phosphatase activity, which was not blocked by the estrogen receptor antagonist, ICI 182780. Decreased phosphatase activity was associated with an increase in CA3-CA1 synaptic transmission. In addition, EB application shifted synaptic plasticity, blocking the induction of long-term depression and facilitating the establishment of long-term potentiation. The reduction in calcineurin activity and shift in synaptic plasticity were mimicked to a lesser extent by 17-alpha-estradiol. From these results we suggest that EB can act to rapidly influence Ca(2+) signaling pathways including the activity of Ca(2+)-regulated phosphatases involved in synaptic plasticity.

Animals↗

PubMed2002

Early gallbladder cancer.

BACKGROUND: The majority of patients with gallbladder cancer (GBC) have advanced disease at the time of diagnosis and are unresectable. Longterm survival is usually seen in a subset of patients with early GBC (EGBC)-cancer confined to the mucosa (pT1a) and muscularis (pT1b). Management guidelines of EGBC are not yet defined and are controversial. The purpose of this article is to evaluate the diagnostic aspects and effects of resectional procedures on survival outcome in patients with EGBC. STUDY DESIGN: EGBC was defined as cancer confined to the mucosa (pT1a) or muscularis (pT1b) according to the TNM classification. Clinicopathological details and survival data of 14 patients who had EGBC were analyzed. There were 9 women and 5 men, with a mean age of 60 years. RESULTS: A definite preoperative diagnosis was possible in only three patients and three patients were diagnosed at operation; the majority of patients were diagnosed incidentally after cholecystectomy for associated gallstones. Two patients underwent extended cholecystectomy and 12 patients underwent simple cholecystectomy. Two patients had pT1a and 12 had pT1b lesions. Mean (SD) survival was 71.5 (12.2) months and median survival was 42 months. There were five treatment failures with locoregional recurrence and death; all with pT1b tumors were treated by simple cholecystectomy. Cumulative 1-, 3-, and 5-year survival was 92%, 68%, and 68% respectively [corrected]. CONCLUSIONS: Simple cholecystectomy is an adequate treatment only for mucosal GBC. Patients with pT1b tumors require extended cholecystectomy. Incidental GBC extending up to the muscularis merits early reoperation for completion of extended cholecystectomy, which offers the only chance of cure.

Adult↗

PubMed2002

Pancreatic abscess: 10 years experience.

BACKGROUND: Secondary infections of pancreatic and peripancreatic necrosis account for most of the deaths following acute pancreatitis. These infections occur in the form of 'infected pancreatic necrosis' and 'pancreatic abscess'. The latter is a rare complication of acute pancreatitis in comparison with the former. METHODS: Twenty-one patients with pancreatic abscess were managed over a 10-year period at a tertiary care centre in Northern India. The present report details the clinical profile, investigations performed and management strategy (surgery and intervention radiology) of these patients. The role of surgery and percutaneous catheter drainage (PCD) in the management of pancreatic abscess is discussed, with emphasis on the successful outcome seen in a properly selected group of patients managed by PCD. RESULTS: Of the 21 patients, 12 were managed by percutaneous intervention, nine were managed surgically (of these, two had a prior PCD) and two patients were managed conservatively. The overall mortality was 9.5% (2/21). Thus, percutaneous management was suitable for 57% patients, was successful in 83.3%, with a mortality of 8.3%. Surgical therapy alone was offered to 33% of patients, was successful in 85.7%, with a mortality of 14.2%. Complications were seen in four of the nine patients managed by percutaneous drainage alone and eight of the nine patients managed surgically. CONCLUSIONS: Pancreatic abscess is a potentially lethal complication in patients recovering from acute pancreatitis. Early diagnosis and prompt intervention with careful selection of patients based on computed tomography imaging for surgical or percutaneous radio-logical management, is met with a successful outcome in a majority of patients. The roles of surgery and PCD are complementary.

Abscess↗