Signs Of Weakness Research Articles

Enzyme replacement therapy (ERT) in pompe disease

Pompe disease (OMIM 232300) is an AR glycogenosis due to deficiency of the lysosomal enzyme alpha-glucosidase (GAA). As a result, glycogen storage occurs in muscles and patients present a wide clinical spectrum ranging from early onset severe cardiomyopathy (EOPD) to adult onset forms (LOPD). Severe loss of GAA activity correlates with early onset and severe phenotypes. Residual enzyme activity warrants later onset and a slowly progressive course, although a strict correlation is not always observed. Patients with Classic infantile Pompe disease show hypotonia, macroglossia, respiratory insufficiency and early death for cardiorespiratory failure. The availability of enzyme replacement therapy (ERT) with alglucosidase alfa ( human recombinant GAA) has changed the natural history of the disease allowing most children with EOPD a longer survival and a longer preserved muscle performance with increased quality of life in LOPD. The experience of the Regional referral Center for Metabolic Diseases, University of Catania, concerns 11 patients ( 9 months to 65 years at the time of the diagnosis). Their clinical and laboratory follow-up included eye tracking and Muscle MRI. EOPD, with a severe clinical picture since the first weeks of life and cardiomyopathy was observed in a newborn who died at age 4 months, despite early started and high dosage ERT. Another girl with EOPD is on ERT since the age of 9 months and, today, after 7 years of treatment shows only mild signs of muscle weakness and no cardiac involvement. Five more LOPD patients on ERT had a significant improvement of blood parameters including transaminases, LDH and CPK. No progression of muscle impairment was seen after 5 to 8 years of treatment, except for one 35 years old man, who was already severely compromised and did not show any benefit in terms of respiratory ventilation. In a recently performed Italian survey of classical Pompe disease treated with ERT, a substantial improvement in cardiac parameters and gross motor function was observed, even if residual muscle weakness still exist and gross motor function remain below age-appropriate levels. The different response to ERT depends on several factors mainly on timing of treatment (worse outcome if started later than 5 months of age) and cross reactive immune material (CRIM-negative status associated with less good response to ERT). Although some residual mild weakness is present in treated patients, ERT has demonstrated its effects on respiration, lowering nocturnal apneas and allowing patients a better quality of life.

O37: Unexpected benzodiazepine findings in three forensic toxicological cases

Introduction Three forensic cases with unexpected benzodiazepines are described. Case A involved a 41-year old man who was hospitalized with a severe head injury and died after four days of intensive treatment. In the autopsy samples, desalkylflurazepam was detected. In the samples collected at hospital admission, nor desalkylflurazepam nor one of its possible orally taken parent compounds (flurazepam or ethylloflazepate) were present. In case B, the urine of a 22 year old woman who was believed to be the victim of a drug facilitated sexual assault (DFSA) was confirmed positive for the presence of diazepam. The victim claimed not to have used diazepam. Case C involved a 20-month old toddler who was administered to the hospital with signs of weakness and sedation after a stay with the grandmother. Besides the presence of lorazepam in the urine, GC-MS analysis indicated the presence of delorazepam, which would be suggestive for the intake of cloxazolam. Methods All cases have undergone the Systematic Toxicological Analysis (STA) in our lab, which consists of screening procedures (immunological screening on urine, screening by GC-MS without and with derivatization on enzymatically hydrolyzed urine and blood, screening by HPLC-PDA on blood) and targeted analyses (ethanol by headspace-GC-FID, GHB and “classic” drugs of abuse by GC-MS). The libraries used for identification are both commercial (Maurer/Pfleger/Weber 4 th edition 2011, Rosner Designer Drugs 2013) and in-house built. Furthermore, most compounds identified by screening were quantified in blood using the most suitable inhouse technique (GC-MS, LC-MSMS or HPLC-PDA). Results In case A, no alcohol, pharmaceuticals or drugs of abuse were detected in the samples collected at hospital admission. In the hospital, the patient was administered atracurium, levetiracetam, lidocaine, midazolam, propofol, remifentanyl and thiopental. In the autopsy samples, all pharmaceuticals (mostly together with one or more metabolites) were detected by our STA, except for remifentanyl. Moreover, desalkylflurazepam, the metabolite of flurazepam and ethylloflazepate, was detected. This phenomenon could initially not be explained, since both pharmaceuticals are taken orally, and the patient became comatose soon after hospital admission. The presence of desalkylflurazepam could be explained by a recent paper of Vogt et al. (Drug Test. Analysis 2013, 5, 745-747) who unravelled that desalkylflurazepam is not a metabolite of midazolam, but an intermediate in the synthesis of midazolam which is sometimes still present in the formulation Dormicum®. In case B, laboratory analysis revealed the presence in urine of acetaminophen, aripiprazole, citalopram, diazepam, tetrazepam and valproic acid (most of them together with one or more of their metabolites). All parent compounds were also detected in blood, except for diazepam. The presence of diazepam in urine could be explained by the metabolism of tetrazepam and not by an (involuntary) consumption of diazepam itself. In case C, a positive benzodiazepine screening on urine was confirmed by the presence of lorazepam in urine. Only after injection of an acetylated extract in the GC-MS apparatus, a library hit for delorazepam appeared. Further chromatographic analysis revealed that this compound was not delorazepam (different retention time), but most probably a lorazepam (metabolite) artefact. Therefore, the possibility of administration of cloxazolam (which metabolizes quickly to delorazepam) could be ruled out. Conclusion In a forensic context, one has to take care in the interpretation of the origin of benzodiazepine findings. The presence of synthesis-intermediates in pharmaceutical formulations, minor metabolism pathways and GC-artefacts can significantly complicate elucidation of the events.

Intestinal coccidiosis infection in domestic rabbits

The present study reports about the intestinal coccidiosis in a commercial rabbit farm. Seven New Zealand white rabbits were died in a commercial rabbit farm in Tirupati during the month of August. All the rabbits had signs of anorexia, diarrhea, dullness and weakness. Rabbits were necropsied and collected the intestinal contents for laboratory examination. Up on post mortem examination, hyperemic and oedematous intestinal mucosa was noticed. Oocysts of Eimeria spp. were detected in the faeces of all the rabbits. The collected oocysts were transferred into 2.5% aqueous potassium dichromate solution for sporulation. Faecal samples were examined by modified McMaster technique to determine oocyst counts which had ranged from 13,200 to 16,400. Keywords : Intestinal Coccidiosis, OPG, Rabbits, Sporulation.

Early-Onset Facioscapulohumeral Muscular Dystrophy Type 1 With Some Atypical Features

Facioscapulohumeral muscular dystrophy cases with facial weakness before the age of 5 and signs of shoulder weakness by the age of 10 are defined as early onset. Contraction of the D4Z4 repeat on chromosome 4q35 is causally related to facioscapulohumeral muscular dystrophy type 1, and the residual size of the D4Z4 repeat shows a roughly inverse correlation with the severity of the disease. Contraction of the D4Z4 repeat on chromosome 4q35 is believed to induce a local change in chromatin structure and consequent transcriptional deregulation of 4qter genes. We present early-onset cases in the Polish population that amounted to 21% of our total population with facioscapulohumeral muscular dystrophy. More than 27% of them presented with severe phenotypes (wheelchair dependency). The residual D4Z4 repeat sizes ranged from 1 to 4 units. In addition, even within early-onset facioscapulohumeral muscular dystrophy type 1 phenotypes, some cases had uncommon features (head drop, early disabling contractures, progressive ptosis, and respiratory insufficiency and cardiomyopathy).

How to live with a terminal illness.

For the past several years, my clinical focus has involved the application of the cognitive therapy model to patients with severe medical illness. Some people have reached the life stage that encompasses the end of life. Some of these patients have been diagnosed with cancer. To all I have said, “How you feel at this time will be determined by how you think.” In my job as a member of a palliative care team, my approach has been added to that of internal medicine aimed at easing the burden of ill and often dying patients. Established by the chief of the Department of Medicine of the Veterans Administration hospital in Charleston, South Carolina, this job underlines their commitment to providing palliative care to those patients in need. It came, therefore, as not a great surprise to be invited to join the health care team that works in the amyotrophic lateral sclerosis clinic in Charleston. Amyotrophic lateral sclerosis is a terminal illness that afflicts both young and old and both men and women and progresses through loss of function to death without hope of a cure. The staff recognized that adjustment to the progressive course of the illness would be aided by the addition of an approach to the emotional aspects of adaptation. And, after all, that is what I’ve been doing, albeit in other settings, for the past 4 years. Amyotrophic lateral sclerosis typically begins with signs of focal weakness.1 The disease progresses to involve muscle wasting and stiffness. Common symptoms include difficulty swallowing, difficulty speaking, and, eventually, difficulty breathing. Mobility is also typically affected. There may be physical pain, and pseudobulbar affect often occurs. Fine motor tasks (writing, dressing, personal hygiene) often become difficult.

Medication Errors in the Intensive Care Unit

Medication Errors in the Intensive Care Unit

Expression of the Embryonic Cav1.1 Splice Variant in Adult Mice Alters Excitation-Contraction Coupling but Does not Cause Dystrophic Myotonia

CaV1.1e is the calcium channel splice variant of embryonic skeletal muscle. It functions as voltage sensor in EC coupling, but in contrast to the adult CaV1.1a variant it also supports sizeable calcium currents activating at the same membrane potential as SR calcium release. Mis-splicing of CaV1.1 results in elevated levels of the CaV1.1e variant in mature muscle that correlate with the severity of muscle weakness in patients suffering from dystrophic myotonia. Therefore we hypothesize that exclusive expression of CaV1.1e in exon 29 knockout mice will cause muscle weakness. In muscles of wildtype mice expression of CaV1.1e declines after birth. However, two weeks after sciatic nerve resection CaV1.1e transcript levels are upregulated in paralyzed muscles, indicative of an activity-dependent regulation of CaV1.1e splicing. Quantitative RT-PCR analysis demonstrates that exon 29 knockouts express exclusively the CaV1.1e splice variant at levels comparable to total CaV1.1 in wildtype muscle. Combined voltage clamp and fluorescence calcium recordings of isolated muscle fibers from exon 29 knockout mice revealed a substantial influx-dependent component of the calcium transient. This not only alters myoplasmic calcium handling, but is further expected to prolong the muscle action potential and consequently reduce the tetanic fusion frequency. Surprisingly, these severe alterations of the muscle fiber properties were not accompanied by a dystrophic myotonia phenotype in knockout mice. A battery of behavioral tests (home-cage activity, voluntary and forced running, grip strength and rotarod tests) revealed no signs of muscle weakness or altered motor activity compared to wildtype siblings. Thus, development of dystrophic myotonia may require the combinatorial action of several mis-spliced genes. Alternatively, strong compensatory mechanisms may cause the absence of the disease phenotype in exon 29 knockout mice. Support: FWF P23479, W1101, OTKA-NN107765, TAMOP-4.2.2./B.-10/1-2010-0024.

The Mstn-Cmpt Dl1Abc- Mice. A Mouse Model to Study Muscle Weakness, Fatigue and Soce

In our mouse model, a naturally occuring 12-bp deletion in the myostatin gene is considered responsible for the compact phenotype (Mstn(Cmpt-dl1Abc)) labeled by a tremendous increase in body weight along with signs of muscle weakness and easier fatigability.Western blot screenings showed significantly reduced endogenous STIM1 and Orai1 protein levels in the compact mouse muscle samples. As a consequence, we hypothesized that SOCE may be consequently altered. Enzymatically isolated fluo-8 AM loaded FDB fibers from wild type and Mstn(Cmpt-dl1Abc) mice were used. To elicit a massive SR Ca2+-release a RyR1 agonist (4-chloro-meta-cresol) was applied in a Ca2+ free medium and in the presence of the SR Ca2+ pump inhibitor (thapsigargin). The above cocktail triggered a deep transient store depletion which in turn switched on SOCE in a wild type cell. The peak of the Ca2+ transient (triggered by the entry of the external Ca2+ into the cytoplasm following the internal store depletion) was normalized to the peak of the SR Ca2+ release transient (1.06±0.11, n=17 vs 0.8±0.08, n=9). On isolated FDB fibers under voltage clamp, we found that the voltage dependence of the normalized fluorescence of the calcium transients in response to membrane depolarizations ranging between −60 and +30 mV, with a 10 mV increments were well fitted with a Boltzmann distribution (V0.5: −23.22±1.35 mV vs −24.15±0.77 mV with respective k values of 6.14±1.15 vs. 6.93±0.65). Fatigue inducing protocols are being currently tested. Collectively, these data point toward altered Ca2+ homeostasis in the compact mice. Understanding the mechanisms behind them may help developing new strategies in muscle atrophy, ageing and wasting diseases. To our knowledge, we are the first to employ Mstn(Cmpt-dl1Abc)mice and perform a comparative study to characterize their Ca2+ homeostasis in light of SOCE.

Regional Alliances: A Political, Military, and Economic Strategy to Confront Hostile Regional Powers

IntroductionRussia and China have recently displayed aggressive actions that have steadily garnered international concern. The United States, as a country interested in preserving the existing international order, share apprehensions towards potential disruptions that could affect its interests. The intensifying nationalist sentiment of rising powers, their increasing military strength, demonstrable willingness to employ military aggression, and freshly invigorated territorial claims cause defenders of the status quo to worry that war is on the horizon. Will Russia and China make a bold attempt to seize what they claim as theirs? No fewer than two other regional powers give cause for concern. Neighbors of North Korea and Iran warily keep watch for aggressive actions from these rogue states. To what extent should threatened neighbors take precautions to protect their territorial integrity in the interests of national security? As seen in some recent signs of weakness from the threatened, a new generation of untested leaders and their respective populations must learn the lessons of peace through strength in order to protect themselves from possible aggression. Threatened countries should create, strengthen, and expand military alliances between mutually interested partners, grow military capability by ensuring adequate defense spending, and demonstrate the willingness to take military action against aggressors in order to lessen the threat of attack. Starting with an assessment of the present challenges, then examining how global powers should shield regional alliances during their formation, and lastly, analyzing the respective failure and success of alliances of World War I and the Cold War, this article proposes a strategy to thwart potentially hostile state-based regional powers. A nation or alliance facing a hostile regional power must match at least one-third of the potential aggressor's defense spending to discourage an aggressor, but should aim for matching two-thirds. Global powers should foster the formation of regional alliances in order to maintain the status quo.Russia: Returning to Grandeur of 19th Century Empire?The Russian Federation recently seized control of Crimea and poses a lasting threat to the territorial integrity of Ukraine. The international community has resoundingly condemned this action. Led by the United States in the form of sanctions, a number of countries have taken limited action to punish Russia. Although mostly symbolic, the U.S. has also exercised shows of military force consisting of small-force deployments in the region that demonstrate a level of resolve against further aggression. Ukraine offered very little resistance to the initial takeover of Crimea and stands little chance of successfully opposing a conventional invasion of their mainland. However, the country is now using military force to quell rebellion allegedly stoked by Russia.Many speculate about Russia's motives, but only Putin himself may comprehend the country's ultimate objective. Regardless of whether to reestablish the former greatness of czarist Russia, secure access to resources, or following through on face-value claims to secure ethnic Russians, the uncertainty of knowing obligates Russia's neighbors to make prudent hedges against the worst case scenario.In general, Russia's actions towards Ukraine have revealed some weaknesses in the West, but have also created an opportunity to renew Europe's interest in collective defense. Russia's nearby NATO members, Estonia, Latvia, Lithuania, and Poland have vocalized a need for greater strength. Former Warsaw Pact nations of Romania, Bulgaria, Hungary, the Czech Republic, and Slovakia fled the Eastern bloc after the fall of the Berlin Wall and have since achieved NATO membership, but surely Russia's new assertiveness must make them feel uneasy. However, these countries have not made sufficient effort to protect themselves against Russia, relied on the potential of other countries to augment their defensive capability, or primarily sought political alliances that rely more on the signature of documents rather than building their own military force. …

Evaluation of facial nerve following open reduction and internal fixation of subcondylar fracture through retromandibular transparotid approach

The objective of this study was to evaluate any damage to the facial nerve after a retromandibular transparotid approach for open reduction and internal fixation (ORIF) of a subcondylar fracture. We studied 38 patients with 44 subcondylar fractures (3 bilateral and 38 unilateral) treated by ORIF through a retromandibular transparotid approach. All patients were followed up for 6 months. Postoperative function of the facial nerve was evaluated within 24h of operation, and at 1, 3, and 12 weeks, and 6 months. Variables including type of fracture, degree of mouth opening, postoperative occlusion, lateral excursion of the mandible, and aesthetic outcome were also monitored. Nine of the 44 fractures resulted in transient facial nerve palsy (20%). Branches of the facial nerve that were involved were the buccal (n=7), marginal mandibular (n=2), and zygomatic (n=1). In the group with lateral displacement, 2/15 showed signs of weakness, whereas when the fracture was medially displaced or dislocated 7/23 showed signs of weakness. Of the 9 sites affected, 7 had resolved within 3 months, and the remaining 2 resolved within 6 months. The mean (range) time to recovery of function was 12 weeks (3–6 months). There was no case of permanent nerve palsy. The retromandibular transparotid approach to ORIF does not permanently damage the branches of the facial nerve. Temporary palsy, though common, resolves in 3–6 months. Postoperative occlusion, mouth opening, and lateral excursion of the mandible were within the reference ranges. We had no infections, or fractured plates, or hypertrophic or keloid scars.

Cognitive and Noncognitive Spectrum Mental Impairments in First-Degree Relatives of Patients with Alzheimer’s Disease

Cognitive and noncognitive spectrum impairments were studied in first-degree relatives of patients with Alzheimer’s disease (AD). A total of 134 relatives (mean age 47.6 years) were studied, of which 110 were children of probands and 24 were sisters or brothers. A high incidence of cognitive and noncognitive spectrum mental impairments was found in relatives of AD patients, and this was greater than the incidence in the control group (22 people who did not have relatives with AD). The relatives group showed twice the incidence of mild cognitive impairment (difficulty assimilating new information and impaired concentration of attention on tiring) than controls, with a 1.4-fold greater incidence of difficulty recalling distant events. Alzheimer’s phobia, and signs of irritable weakness were significantly more frequent. Signs of constitutional cognitive deficit were present in the history 2–4 times as commonly; signs of two or three different types of cognitive deficit were present 3–4 times more frequently. There was a 3.4-fold increase in combinations of signs of communicating hydrocephalus with MRI signs of cerebrovascular pathology. Information on these mental impairments of the cognitive and noncognitive spectra in first-degree relatives of AD patients may be of value as the basis of corrective and rehabilitative measures for the prophylaxis of progressive cognitive deficit.

Steroid myopathy in patients with chronic respiratory diseases

BackgroundCorticosteroid-induced myopathy is a well known clinical entity, and experimental studies showed decreased rate of protein synthesis and increased rate of protein breakdown in muscles of chronically treated animals. ObjectiveThe present observational study was aimed to evaluate skeletal muscle functions in asthmatics and patients with other chronic respiratory diseases treated by inhaled or oral corticosteroids. MethodsThirty six patients with respiratory diseases were included into the study. The physician-rated peripheral motor deficits scale, stepper test and ankle/wrist index were used for assessment of muscle functions. The effects of length of glucocorticoids intake on muscle functions were evaluated. ResultsSixty five per cent of patients using corticosteroids daily during 1year and longer reported weakness in legs, and 20% of these patients demonstrated objective signs of the muscle weakness. The performance on the stepper test was significantly worse in patients chronically using corticosteroids in comparison with the control group (10.9±3.4 steps vs 16.1±2.4 steps per 10s, respectively; F=21.6, p<0.001). In addition, a proportion of patients using corticosteroids for at least 18months were characterized by muscle hypotrophy at a dominant leg. ConclusionChronic intake of inhaled corticosteroids induces clinically significant decrease of muscle functions at least after 1-year of daily treatment.

A pilot randomized crossover trial comparing the effect of two exercise based management protocols on multidirectional instability of the glenohumeral joint: A research protocol

of the brachial plexus. Initial symptoms of insidious onset, severe upper limb pain, non-dermatomal and non-mechanical in nature, was not relieved by analgesia. Exclusion of potential differential diagnoses, such as mass lesions, cervical disc herniation, foraminal stenosis andadhesive capsulitiswas confirmedwith imaging. There were no initial signs of mobility loss, muscle weakness or atrophy, however weakness in the right upper limb was evident within 3 weeks, limiting active range of shoulder movement, with maintenance of passive range. In particular, weakness of serratus anterior, deltoid, supraspinatus, infraspinatus and triceps was noted, implicating involvement of the axillary, long thoracic and suprascapular nerves. Discussion: A comprehensive literature review, cadaveric anatomical dissection and video images of the case report were examined. Common peripheral nerves affected in ParsonageTurner Syndromeare the long thoracic nerve arising fromtheupper trunk (C5 and C6 nerve roots), long thoracic nerve arising from the upper and middle trunks (C5, C6, C7 nerve roots) and the axillary nerve arising from the posterior cord (C5, C6 nerve roots). Insidious onset or following viral illness, trauma, surgery and vaccination have been reported as possible causes, however Parsonage-Turner Syndrome can be a diagnostic challenge for the clinician. Diagnosis is based on thorough history, physical examination, exclusion of co-morbidities and confirmed with electromyography (EMG) and nerve conduction studies (NCS). A key diagnostic clue is evidence of muscle weakness and atrophy in different peripheral nerves rather than dermatomal or myotomal pattern. The male athlete demonstrated loss of active shoulder range within 3 weeks of initial onset, with neurological examination demonstrating normal sensation and reflex testing but reduced isometricmuscle strength tests. At this stage EMG andNCS demonstrated denervation in the axillary, long thoracic and suprascapular nerves which when repeated at 9 months revealed re-innervation signs. Physiotherapy was undertaken in early stages to maintain mobility and muscle strength of unaffected musculature. Once re-innervation had been established, a graduated strengthening program was instituted with single muscle activation, muscle patterning and motor retraining. Active elevation was achieved by 18 months, with residual strength deficits resolving. Physiotherapy played a crucial role in facilitating an early diagnosis via onward referral for EMG andNCS confirmation, early pain management, education, prevention of secondary loss of mobility and further muscle atrophy, followed by implementation of targeted muscle and motor pattern retraining and subsequent sport specific rehabilitation.

The First Case of Angioinvasive Pulmonary Aspergillosis in a Himalayan Griffon Vulture (Gyps Himalayensis)

We present the first case of angioinvasive pulmonary aspergillosis caused by Aspergillus fumigatus in a Himalayan Griffon vulture ( Gyps himalayensis). We describe in detail the clinical, gross, histopathological and mycological findings. Clinical signs of weakness, emaciation, dyspnea, incoordination, and inability to fly were observed in this bird before succumbing to the illness, despite supportive care. Grossly, several yellowish circumscribed, raised, miliary nodules were observed on the surface of lungs, air sac membranes, trachea, pericardium, aorta, pulmonary artery and kidneys. Histologically, granulomatous pneumonia and airsacculitis, and angioinvasion of fungal hyphae were noticed. Aspergillus fumigatus organism was isolated from the lungs and air sacs of the bird. This seems to be the first report of angioinvasive pulmonary aspergillosis in birds of prey, and a rare finding in avian species.

Motor protein function in skeletal abdominal muscle of cachectic cancer patients

Cachexia presents with ongoing muscle wasting, altering quality of life in cancer patients. Cachexia is a limiting prognostic factor for patient survival and health care costs. Although animal models and human trials have shown mechanisms of motorprotein proteolysis, not much is known about intrinsic changes of muscle functionality in cancer patients suffering from muscle cachexia, and deeper insights into cachexia pathology in humans are needed. To address this question, rectus abdominis muscle samples were collected from several surgical control, non-cachectic and cachectic cancer patients and processed for skinned fibre biomechanics, molecular in vitro motility assays, myosin isoform protein compositions and quantitative ubiquitin polymer protein analysis. In pre-cachectic and cachectic cancer patient samples, maximum force was significantly compromised compared with controls, but showed an unexpected increase in myofibrillar Ca2+ sensitivity consistent with a shift from slow to fast myosin isoform expression seen in SDS-PAGE analysis and in vitro motility assays. Force deficit was specific for ‘cancer’, but not linked to presence of cachexia. Interestingly, quantitative ubiquitin immunoassays revealed no major changes in static ubiquitin polymer protein profiles, whether cachexia was present or not and were shown to mirror profiles in control patients. Our study on muscle function in cachectic patients shows that abdominal wall skeletal muscle in cancer cachexia shows signs of weakness that can be partially attributed to intrinsic changes to contractile motorprotein function. On protein levels, static ubiquitin polymeric distributions were unaltered, pointing towards evenly up-regulated ubiquitin protein turnover with respect to ubiquitin conjugation, proteasome degradation and de-ubiquitination.

Hemolytic anemia after ingestion of the natural hair dye Lawsonia inermis (henna) in a dog

AbstractObjectivesTo describe the clinical presentation and case management of a dog that developed hemolytic anemia and evidence of renal tubular dysfunction after ingestion of a natural hair dye containing Lawsonia inermis (henna). To review cases of henna toxicity reported in the human literature.Case SummaryAn 8‐year‐old female spayed Border Collie was presented 5 days after ingestion of a box of natural hair dye. The dog was showing signs of lethargy, vomiting, diarrhea, and weakness. A serum biochemistry profile, complete blood count, and urinalysis demonstrated evidence of renal tubular dysfunction and a regenerative anemia without spherocytosis. The dog was treated with a transfusion of packed RBCs and IV fluids, resulting in significant clinical improvement. Repeat diagnostics showed resolution of the anemia and no lasting evidence of tubular dysfunction.New or Unique Information ProvidedTo the authors’ knowledge, this is the first reported case in the veterinary literature of toxicity following ingestion of Lawsonia inermis (henna). Henna ingestion was associated with the development of hemolytic anemia and acute kidney injury.

An Empirical Study on Financial Performance of 'The Tirupati Cooperative Bank Limited', Tirupati

The study mainly focused attention to study the financial performance of Urban Cooperative banks with reference to Tirupati Town Co-Operative Bank Limited in Tirupati, which were covered under schedule II of RBI Act. In this regard, schedule II of RBI Act consists of 55 Urban Cooperative Banks. The researcher aims to analyze the financial performance of UCBs with reference to Tirupati Town Co-Operative Bank Limited. Survival and success in competitive markets demand performance through continuous improvement and learning. In a regime of planned development, sound cooperative banking movement is an instrument, which while retaining some of the advantages of decentralisation and local initiative, will yet serve willingly and readily the overall purposes and directives of the developmental plans of the government in the identified sectors. It is an indispensable instrument of planned economic action in a democracy. Urban Cooperative Banks (UCBs) figure among the vital segments of the banking industry of the country. They essentially cater to the credit needs of persons of small means. Though some UCBs have performed creditably in the recent years, a large number of them have shown discernible signs of weakness. The operational efficiency is unsatisfactory and characterized by low profitability, ever-growing Non-Performing Assets (NPAs) and relatively low capital base. It is therefore imperative to judge their relative performance and understand the best practices for better survival. In this context, this paper makes an attempt to examine the working and financial performance of the UCBs. The study is based on secondary data and other information provided by the bank in its published annual reports from 2006-07 to 2009-10, that is for 4 years, apart from the records of various financial institutions, including the RBI reports, manuals for UCBs and Bulletins, Reports of different committees and federations. In addition, various manuals, official circulars, and auditors reports have also been consulted to the study the different banking variables of the study. To make the analysis simpler and presentable, the author takes up The Tirupati Co-operative Bank Ltd, one of the leading UCBs Chittoor District of Andhra Pradesh. The objective of the study is to identify and analyze the trend, progress and to throw light on the problems of the bank and to offer some meaningful suggestions for improving the efficiency and effectiveness.

Hepatic Schistosomiasis - A case report

Purpose: We present the case of a 53 yr old female with mild right upper quadrant abdominal pain as well as signs of mild weakness 6 months after holidays on the Philippines.

IMAGING DIAGNOSIS—HYPOGLYCEMIA ASSOCIATED WITH CHOLANGIOCARCINOMA AND PERITONEAL CARCINOMATOSIS IN A HORSE

An 8-year-old Thoroughbred mare presented for decreased appetite, ataxia, and weakness. Abdominal ultrasound revealed a large volume of anechoic fluid along with multiple masses involving the spleen, liver, and diaphragm. Pleural fluid was identified via ultrasonography and thoracic radiography. Thoracic radiographs also identified pulmonary interstitial nodules, an undulant dorsal diaphragmatic margin and enlargement of tracheobronchial lymph nodes. Clinical signs of weakness and mild seizures were concurrent with hypoglycemic episodes. The final diagnosis was cholangiocarcinoma with extensive metastasis. Clinical signs of weakness, ataxia, and seizures were attributed to a paraneoplastic syndrome of tumor-associated hypoglycemia that has been infrequently reported in horses.

Diagnostic Exercise

Within a 24-hour period, 7 out of 200 three- to four-week-old pastured Katahdin lambs died after showing clinical signs of hemoglobinuria, red-tinged feces, weakness, and recumbency. One of the lambs that was examined clinically before natural death also had abdominal pain, trembling, tachycardia, and severe anemia with a packed cell volume of 4%. Pathologic findings included icterus, hemoglobinuric nephrosis, dark red urine, pulmonary edema, hydrothorax, splenomegaly, and acute centrilobular to midzonal hepatocellular degeneration and necrosis with cholestasis. The differential diagnoses and diagnostic workup to achieve the diagnosis are briefly discussed.