A new year is a powerful occasion: It’s a time when we reflect on our gratitude for the past and our hopes for the future. And it’s a chance to welcome a fresh start to reinvigorate our enthusiasm for chasing goals and dreams.
May the new year bless you with health, wealth, and happiness. Have a happy and sparkling New Year!
Authored by Dmytro Filimonov*
Background: According to recent studies, thyroid hormones may have various effects on stroke severity, course and outcome, but underlying mechanisms of this association are still unclear.
Objective: The aim was to determine the relationship of thyroid hormones during stroke onset with stroke severity and outcome in clinical study.
Methods: In this study 168 adult patients with acute ischemic stroke were enrolled. Concentrations of free T3 (fT3), free T4 (fT4), TSH and basic stroke risk factors were assessed during 24h from symptoms onset. Neurological deficit was assessed by Scandinavian Stroke Scale (SSS). Disabling deficit was defined as mRs score ≥3 at 6 months after stroke.
Results: ANOVA showed that SSS scores were significantly higher in patients with fT3 level in 4th quartile (≥5.35 pmol/l) compared to 2-3rd quartile (SSS median 48 vs. 37, p=0,0481) and especially to 1st quartile (≤3,4050 pmol/l, SSS median 48 vs. 30, p=0,0018). In patients without prior stroke (n=124) baseline SSS-score was independently affected by fT3 (corrected R2 = 0.49, p < 0.0001). According to ROC-analysis, fT3 level <4,44 pmol/l was a predictor of disabling deficit (AUC = 0.727, specificity - 96.4%, sensitivity - 66.8%, p = 0.003). Univariate analysis showed association between poor outcome and low fT3, in multiple regression this association became insignificant only after correction for baseline SSS-score, but no other stroke risk factors
Conclusion: The study showed that a low serum free triiodothyronine level during stroke onset negatively affects the stroke severity in firsttime stroke patients and may be predictor of its unfavorable outcome. There was a trend for association between low free triiodothyronine and unfavorable stroke outcome after 6 months. Beneficial effects of additional fT3 supplement during stroke should be assessed in future studies.
Keywords: Ischemic stroke; Outcome; Thyroid hormones; Triiodothyronine
Abbreviations: AIS: Acute Ischemic Stroke; fT3: Free Triiodothyronine; fT4: Free Thyroxine; TSH: Thyroid-Stimulating Hormone; CRP: C-Reactive Protein; CI: Confidential Interval; ATP: Adenosine Diphosphate; SSS: Scandinavian Stroke Scale; mRs: Modified Rankin Scale
Currently, in most countries, stroke is one of the leading causes of death and disability [1]. Despite certain advances in the treatment and prevention of cerebrovascular diseases, stroke remains in second place in the world among the diseases leading to death. According to numerous clinical studies, the most effective treatment for acute ischemic stroke is the restoration of cerebral blood flow by reperfusion methods, such as intravenous or selective thrombolysis, or mechanical thrombectomy [2,3]. However, reperfusion therapy is possible only within a relatively narrow therapeutic window [4]. In cases where thrombolysis or thrombectomy is not indicated or there are no opportunities for its implementation, modern approaches to patient management during the acute period of stroke include both secondary prevention of cerebrovascular disease and an attempt to reduce the severity of neurological deficit by protecting ischemic (but potentially viable) brain tissue in penumbra zone [5]. Nevertheless, despite the diversity of neuroprotective drugs, different in their mechanism of action and effective in preclinical studies, none of them has enough clinical efficacy. In this regard, the search for new approaches of neuroprotection remains one of the most important tasks of modern neuropharmacology [5].
The survival of the brain tissue under ischemia depends on the intensity of metabolism, oxygen demand, as well as the ability to maintain the redox potential and support the synthesis of highenergy compounds (ATP, etc.). The mechanism of action of most neuroprotectors is based on the effects on these processes [6,7]. Over the past decades, special attention had been paid to the neuroprotective properties of endogenous molecules such as VEGF, erythropoietin, brain neurotrophic factor, etc. It is known that triiodothyronine, an active form of the thyroid hormone thyroxin, separates tissue respiration and oxidative phosphorylation. This process leads to disruption of the Krebs cycle, reduced ATP production, hyperthermia, and has a potentially negative effect in acute cerebral ischemia [8]. On the other hand, it is known that triiodothyronine has several neuroprotective effects - it contributes to the capture of neurotoxic glutamate by astrocytes, stimulation of the Na + / K + membrane channels in neurons, the restoration of intracellular pH [9]. Thus, selective therapeutic effect on thyroid metabolism (stimulation or inhibition of the function of thyroid hormones) may be promising potential target for new approaches in the treatment of stroke.
In recent years, more publications appeared in the literature about the possible effect of thyroid hormones on the risk of development, severity and outcome of acute ischemic stroke. Nevertheless, the results of the published works are rather contradictory [10]. Finally, the nature of the influence of hyperor hypothyroidism on the course and outcome of a stroke is still unclear.
Aim of this study was to determine the relationship between markers of thyroid function and the severity of neurological and functional deficit in acute ischemic stroke.
This study was conducted at the single clinical and research center – V.K. Gusak Institute of Urgent and Reparative Surgery (Donetsk). 168 patients (women – 71, men – 97) aged 42 to 78 years with acute ischemic heterogeneous stroke were enrolled in this study. Patients with verified autoimmune thyroiditis or a malignancy were excluded from the study. Within 24 hours from stroke onset basic risk stroke factors were analyzed. Serum free triiodothyronine (fT3), free thyroxine (fT4) and the thyroid stimulator hormone (TSH) were determined using ELISA method (CHEMWELL EIA-analyzer with DRG-international assay kits). Blood sampling was performed during 24 hours from stroke onset. Neurological deficit was assessed using Scandinavian Stroke Scale (SSS). Poor stroke outcome was assumed as 3 or more points on the modified Rankin Scale (mRs) after 6 months from stroke onset. Thyroid hormones and TSH levels below 25 and above 75 percentiles were assumed as “low” and “high”, respectively.
Statistical analysis was performed using MedCalc v14 software. Continuous data with non-normal distribution is presented as median and 95% CI. For analysis of variation of neurological deficit ANOVA method was used and patients were divided to subgroups according to T3 levels: “hypothyroid” (T3 below 25-percentile), “euthyroid” (T3 in 25-75 percentile), “hyperthyroid” (T3 above 75 percentile). For determining impact of thyroid hormones on stroke outcome using logistic regression patient were dichotomized in subgroups with good outcome (mRs 0-2) and poor outcome (mRs 3-6).
Strokes in the carotid territory were the most frequent (79% of all patients), with the atherothrombotic subtype being the most common (64%). The leading basic risk factors were arterial hypertension (65%), smoking (42%), coronary heart disease (29%), atrial fibrillation (27%). 49 patients (28%) had previously history of TIA or ischemic stroke, 119 patients had the ischemic stroke developed for the first time. Demographic characteristics of the examined patients are presented in Table 1.
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May your Christmas be graced with peace, joy, and blessings! Hope this festive season will bring good luck and good health for you and your family. Wishing you a delightful Christmas.
Authored by Edda E Guareschi*
Poisoning by Tanax® is uncommon as a suicide method, and it is even more unusual for murder-suicides. Tanax® is a veterinary drug used for euthanasia in animals and, as such, poisoning by Tanax® is almost completely limited to veterinary workers. Its active components are embutramide, mebezonium iodide and tetracaine hydrochloride. It acts as a general and local anesthetic, and paralyses skeletal muscles by a curariform-like action. A literature review is provided with focus on embutramide and mebezonium concentrations detected in body fluids and solid organs of patients and victims. A unique case of murder-suicide by Tanax® poisoning is then detailed, leading to the medico-legal diagnosis of a complex suicide method following the murder. This case highlights the heterogeneity of information about lethal concentrations of embutramide and mebezonium in human body fluids and solid organs, the possible emergence of embutramide as a drug of abuse, and the delayed hepatotoxicity induced by dimethylformamide (DMF), contained in Tanax® as an organic solvent.
Keywords: Tanax®; Suicide; Abuse; Toxicology; Veterinary
Tanax® is a drug used in veterinary medicine for euthanasia in animals. It is a solution of three components dissolved in a mixture of the organic solvent dimethylformamide (DMF) and water. The components of Tanax® are embutramide, mebezonium iodide and tetracaine hydrochloride. Embutramide, which is exclusively used in Tanax® [1] is a general anesthetic with a strong narcotic action: it causes deep anesthesia by paralyzing the breathing centers in the central nervous system. Mebezonium iodide has a curariformlike action, paralyzing the skeletal muscles with fast respiratory collapse. Tetracaine hydrochloride is a local anesthetic, used to avoid pain at the injection site [2].
Poisoning by Tanax® is a rare mode of suicide [3]. Murdersuicide is even less common, with only one case reported to date [4]. In addition to the effects of the three components, hepatotoxicity has been observed both in non-fatal and fatal human poisoning, and has been attributed to DMF [5,6]. The nature and use of the drugs almost completely confine self-poisoning by Tanax® to veterinary workers, who are at high risk of dying by suicide [7,8]. Literature case studies depict administration routes as oral ingestion, subcutaneous, intravenous and intracardiac injection [2] as well as analytical methods for embutramide and mebezonium detection [9]. To date, lethal concentrations in blood, urine, liver and kidney have been reported and are summarized in (Table 1) [1,3,10,11].
Here we report a unique case of murder-suicide by poisoning with Tanax®, where a veterinarian murdered his dog and himself using 50ml of Tanax®. According to published data, the concentrations of embutramide and mebenzonium in the veterinarian’s blood and urine were not lethal, and he would have survived if he had been promptly assisted and admitted into intensive hospital care.
In January 2012 the bodies of a man and his dog were found dead in a wood near Parma, in north-eastern Italy (Emilia-Romagna region). A passer-by spotted the human body from a distance, when he approached, he was surprised to discover a dog body lying next to it. The wood, a regional park of roughly 2,000 ha, has footpaths and is a popular destination for joggers, walkers and cyclists during the warmer months (Figure 1). The police, the forensic team and the recovery team easily reached the bodies on foot.
The bodies appeared close to one another and were scarcely strewn with leaf litter, the man was fully clothed, no insect colonization was observed on either body. No trauma to the bodies was evident at the scene, except a syringe with a clear liquid and a butterfly needle inserted within a vein in the man’s left ankle. The deceased man was promptly identified as a veterinary clinician, and the dog was positively identified as his. Three days before the bodies recovery, the veterinarian’s family had reported his disappearance to the local police. The prosecutors’ office decided that a criminal investigation would be conducted to determine the manner and time of death of both man and dog.
The purpose of the investigation was to ensure that the man’s cause of death was suicide, which was suspected based on the family reports about mental illness, depression and personality disorder, for which he was in the care of a psychiatrist.
At the death scene no traumatic findings were observed on either body (dog or man), except for a syringe with a butterfly needle inserted into a vein in the man’s left ankle, where the jeans trousers and the socks had been moved to expose the skin. The 60 mL syringe contained 23 mL of a clear transparent liquid. Next to the bodies some objects were recovered: a bottle of sparkling wine (70 cl, 12% alcohol) with a quarter remaining; a dog leash; a small backpack containing an empty bottle of Tanax® 50 mL; its paper box; and a 6 mL syringe containing six whole tablets and one half tablet of an unknown medication.
As agreed with the prosecutor, the forensic investigations started with the human body, and would later be extended to the dog body, if necessary. The external examination revealed a male, 30-35 years-old, of robust build (height 187 cm, weight 100 kg), with a needle puncture in the left ankle.
The autopsy showed cerebral oedema (1540g) and pulmonary bilateral oedema (1000g and 1050g), subpleural bilateral petechial hemorrhages, abundant mucus and foam in the bronchi lumen, light hypertrophy of the left ventricle (heart weight 440g), light hepatic steatosis, confirmed by histology, and surgical procedure of gastric binding, secured to the left rectus abdominis muscle. Toxicology analyses were performed on the human body biological samples by the Toxicology Section of the University of Milan, Italy, following a validated technique [12].
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Authored by John McEldowney*
Forensic science is pivotal to the working of the criminal justice system and the operation of the rule of law. Justice rests on the integrity and accuracy of evidence as well as its reliability and robustness. It is an area that is cross-cutting across from the world of science and proof to the world of law and probability- in fact, to establish evidence beyond a reasonable doubt in criminal cases. Trust lies at the heart of the system, for victims, juries, prosecutors and Judges. Historically, the Forensic Service in England and Wales was held in high esteem and provided the bulk of forensic provision. Today forensic services are divided between several private providers and the police. Currently, the Forensic providers are under strain. The Home Office and Ministry of Justice, the two government departments responsible have undergone considerable political and administrative changes. Forensic services have suffered. Budget cuts and re-organisation of structures within the Forensic Service providers have been problematic. The House of Lords Science and Technology Select Committee have published their 3rd Report (session 20i7-9), Forensic Science and the Criminal Justice System: A Blueprint for Change1.
1 Paper 333. (1st May 2019)
The 2011 closure of the state run and mainly public financed Forensic Science Service (FSS) that used to be run by the Home Office, opened- up a niche for private sector providers. The result is that there is a mix of privately funded and publicly funded providers. This is an example of cost-sharing between the sectors. Private providers as well as the police are free to develop their own services. Regulating forensic scientists has to cut across both public and private entities and while there are opportunities tosup> develop new strategies, their co-ordination and organisation needs to be carefully monitored. The importance of uniform and fully accredited forensic services includes the need for proper resources, training, appropriate processes, and integrity in setting benchmarks and accreditation schemes. There is an International Standard ISO 17025 which sets the competence levels for testing and accreditation of laboratories. Since 2008 forensic science regulation has been in the hands of a single independent regulator, appointed since February 2008. The appointment of the regulator is run through the Home Office and is a public appointee whose main function is to ensure adequacy in the provision of forensic sciences services to the criminal justice system and that there is an appropriate regime of scientific quality standards. The regulator has no statutory powers. There is a separate and independent Forensic Science Society that is the professional body for forensic practitioners. It is largely supportive of the work of the regulator and operates a full range of related services. There is a Society’s Membership and Ethics Committee which applies strict criteria for membership, engages in supervising CPD activities and ensures that there is supervision of the Chartered Forensic Practitioner status. It holds workshops and conferences and seeks to enhance the education of forensic scientists. There is also considerable EU regulation over forensic science with an EU Framework Decision requiring DNA and fingerprint laboratories to conform to ISO/ IEC 17025. There are various drafts and guidance issued by the Regulator including the draft Codes of practice and Conduct for forensic science providers and practitioners in the criminal Justice system (2010) and various attempts to build into the regulatory structure the main components of ISO 17025 (2011).
2House of Commons, The Forensic Science Service, Science and Technology Committee (2011), para. 127
The Independent Forensic Science Regulator in her annual report has concluded that there is a need for “profound changes to funding and governance.3” This finding is consistent with the House of Lords Select Committee’s report. The major finding is that there is a “serious deficit of high-level leadership” between the Home Office and the Ministry of Justice. Current oversight and accountability are “piecemeal” and there should be a Forensic Science Board for the delivery of a new forensic science strategy for England and Wales. The current forensic science service is a market that is “dysfunctional” and is susceptible to market forces which may force some to go out of business. A further complication is the way each individual Police Authority (there are 43 in total) make decisions on how to deliver forensic services. This has resulted in a mixture of in-house provision and out-sourcing to private unregulated providers. The House of Lords Committee recommends that the Forensic Science Regulator should be given statutory powers to ensure that there is much needed trust in the delivery of forensic science. Defendants struggle with reductions in legal aid, especially when forensic evidence is in dispute. Additional challenges arise with the need for digital forensic evidence and the absence of substantial resources to tackle the growth in such evidence. There is also a need for legal practitioners to be better educated and experienced in this growing field of importance. The House of Lords Select Committee concluded that forensic science was “under-resourced ad uncoordinated.” Education and training are similarly neglected and requires attention. It is clear that the use of valuable police resources will be ineffective, unless fully supported by an adequate forensic science service.
3Forensic Service Regulator, Annual report November 2017-2018 (15th March 2019).
The House of Lords Select Committee has made a valuable contribution to the analysis of the delivery of forensic services. The Government responded in July 2019 , accepting many of the recommendations and a commitment to “giving statutory powers to the Regulator by bringing forward legislation at the first opportunity”. There is the possibility that this can be achieved by a government supported Bill or a Private Members Bill. It is accepted that there should be greater liaison with the private and public sectors including better funding of the service. It will remain to be seen whether the opportunity for improvements will be taken forward.
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Authored by Baofa Yu*
Recent years cancer immunological therapy is getting very popular and many new drug have been approved by FDA like PD1 and PDl-1, however, in clinical practice of cancer treatment, it looks very limited efficacy for advanced cancer, so that physician started to use comprehensive plan by combination chemotherapy with PD1 as a novel strategy with a better clinical benefit. Since chemotherapy always produce the side effect like loss hair, vomit and neutropenia. Because of the extremely toxic side effects, many cancer patients cannot successfully complete a complete course of chemotherapy, and some even die from the side effects of chemotherapy due to a patient’s poor tolerance. The extreme side effects of anti-cancer drugs are often caused by the poor target specificity of such drugs regarding the tumor in the patient’s body. The drugs circulate through most normal organs of patients as well as the intended target tumors (less than 5% of the drug reach the tumor), while over 95% of the drug circulates through the whole body of the patient.
The more and more cancer patients do not like to choice to chemotherapy, it is pushing the oncologists to be in the embarrassed situation to suggest the therapy for the patient who lost surgery opportunity, in the fact for most late stages of cancer, how many choice our oncologists can give? a few choice, today I do like to introduce one treatment which is suitable for the most of latte stages of solid tumor with benefit, UMIPIC, ultra-minimum incision personalized intratumorally chemoimmunotherapy.
UMIPIC is a unique eclectic approach for cancer treatment utilizing the intratumorally injection of a combination of chemotherapy drugs (including Dox and Ara-C), coagulant agent oxidant to maintain the chemo agents at the injection site for a longer period of time, and a hapten for hapenation with intracellular tumor-associated antigens to stimulate the patient’s immune response while the tumor is been de-bulking like liquid surgery knife. Safer and more aggressive (higher dose) administration of toxic chemotherapy drugs that go directly into a tumor site with slow release, is an obvious and beneficial alternative to systemic treatment. The local retention afforded by intratumoral administration results in slowed and/or reduced entry of drug into the systemic circulation, minimizing exposure of distant tissues to the drug, and thus, resulting in a lower incidence of systemic side effects a more tumor killed. So far, there are 56 clinical trials found for intratumoral chemotherapy (ITCT) by visiting the website at the following: https://clinicaltrials.gov. But there is not one integrated with immune therapy and surgery knife to action like de-bulk.
In 1994, Dr. Yu developed the new concept of using the tumor itself as a drug carrier. Injection of anti-cancer drug ethanol saturated liquid into the tumor can generate a kind of intratumoral autologous therapeutic coagulum which can function as an antitumor drug depot. This autologous therapeutic coagulum can sustain or store anticancer drug in tumor and the surrounding tumor tissues to kill the tumor cells that have not been killed through ethanol coagulation treatment. It makes a fitting complement for the inadequacy of pure ethanol tumor treatment. A study of retaining drug in injected tumor demonstrated that the retention half-life of anticancer drug Ara-C in the tumor was 160 minutes following depot injection compared to only 6 minutes following intratumoral injection of Ara-C aqueous solution, thus increasing the drug retention by approximately 27 times [1]. The problem of using ethanol is that is is limited by the dosage for the patient and is also limited by tumor size (when the volume of tumor is large, it can dilute ethanol making it inefficient). Now Dr. Yu found oxidant is good role to replace the ethanol to coagulation of tumor as a drug carrier for slow releasing [2].
From 2003 to 2006, Dr. Yu also published many papers showing that the combination of intratumoral drug with hapten modification improves the immunogenicity of tumor cells, effectively inducing or activating body’s antitumor immune response and had 276 patients with cancer reported [3-5]. It indicates that when hapten is added to the UMIPIC, it plays an important role in stimulating immune response.
The UMIPIC is comprised of commercially available drugs for intratumoral injection which includes oxidant as coagulant, chemotherapy drugs and hapten. Intratumoral injection with UMIPIC, it produces its antitumor role in the following aspects:
The first aspect is coagulation by the oxidant. “Tumor coagulation” refers the process by which the blood clots to form solid masses, or clots, and their components and extracellular matrix are transformed into a kind of soft, semi-solid, or solid block. This transformation is induced by oxidation, which makes openings in the membrane of tumor cells. This creates higher permeability of membrane that allows the drugs to penetrate into tumor cells and eventually leads to the death of coagulated tumor cells and enhancement of the cancer drug entering agglomerated tumor cells.
The second aspect is the concentration and sustainability of the drugs, the two key elements: Drug dosage and amount of time for destruction of cancer cells. Tumor coagulation also creates a “drug depot” which not only increases local drug action concentration (dozens or even hundreds of times more than the normal concentration by intravenous chemotherapy) to kill the tumor, but also retains the drugs within the tumor and gradually releases them from inside to the outside to kill residual tumor cells around tumor tissue. This “drug depot” not only extends drug action time in the tumor, but also prevents the leakage of anti-cancer drugs from the tumor, and lowers systemic drug concentration, toxicity and side effects.
The third aspect is stimulation of immune response. Tumor cells killed by the tumor coagulation effect and the chemotherapeutic agents could release intracellular proteins including tumorassociated antigens, which may already interact with hapten in that active reaction with tumor oxidation. The tumor antigens induce a personalized systemic immune response and the haptenation of tumor antigens could further stimulate immune response, thereby eliminating recurring or metastatic tumor cells.
The schematic diagram is shown with the function of components in UMIPIC and the Procedure of UMIPIC: Guided by CT, find the optimal route and angle for introducing the needle intratumoral, the needle is inserted into the tumor, connected to the inflator, the regimens of UMIPIC were slowly delivered into the tumor; a high pressure supplied by the inflator; the solution (UMIPIC) can penetrate into the extracellular matrix of tumor and facilitate forced diffusion. Same injection could be repeated to same tumor or other tumor several times according to evaluating by CT and physician or investigator brochures [6-9].
In the past years, UMIPIC treated lung cancer, median overall survival was 11.23 months in the UMIPIC (test) group and 5.62 months in the ITCT (control) group (P<0.01). The 6-month and 1-year survival rates of the UMIPIC and ITCT groups were 76.36% versus 45.23% (P<0.01) and 45.45% versus 23.81% (P<0.05), respectively. Two cycles of UMIPIC treatment (N=19) conferred a significant survival benefit compared with two cycles of ITCT (N=29); significant benefits in survival time were also found with UMIPIC (N=20) compared with ITCT (N=13) when both were utilized without hapten treatment.
Also UMIPIC for liver cancer with good result: the benefit rates (complete response + partial response + stable disease) were 78.68% and 81.52% in the UMIPIC and ITCT groups, respectively, with no statistically significant difference; however, the median overall survival was 7 months for UMIPIC (test) and 4 months for ITCT (control), respectively (P<0.01). The 6-month and 1-year survival rates for UMIPIC and ITCT were 58.88% vs 32.3% and 30.37% vs 13.6%, respectively (P<0.01). Single and multiple UMIPIC revealed significant improvement in overall survival compared to that of ITCT.
In the past years, UMIPIC treated pancreatic cancer, for single drug, median survival was 6.45 months for UMIPIC-S vs 4.98 months for ITCT-S, (P<0.05), one-year survival rate was 28% for UMIPIC-S vs 5% for ITCT-S (P<0.05). For double drugs, median survival was 15.5 months for UMIPIC-D vs 3 months in ITCT-D (P<0.01). The 6-month survival rate was 76.67% for UMIPIC-D vs 18.18% for ITCT-D (P<0.01) and 1-year survival rate for 56.67% UMIPIC-D vs 9.09% ITCT (P<0.01).
UMIPIC is a simple, clinically effective drug for a broad spectrum of tumors with minimal side effects through ultra-minimal invasive surgery under the guide of CT or ultrasound. In conclusion, UMIPIC provides a new method of decreasing tumor mass while boost the patient’s own immunological power to fight against micro tumor cells in a specific and innovative manner, which is one of its advantages over any treatment. Another advantage is that it is not limited in terms of tumor size, number, or location in the lung, liver, pancreatic or any location of tumor. In future, it is possible that UMIPIC may overtake in the treatment of all stages of tumor in the lung, liver, pancreatic or any location of tumor. UMIPIC can take the place of surgery and chemotherapy or radiation therapy in patients who are not suited for surgery or chemotherapy. We hope to continue to investigate UMIPIC therapy with double cytotoxic drugs with double hapten under clinical study to improve effectiveness.
Today, it is time to think how to replace the surgery, chemotherapy and radiation therapy which produce a damage of patient with cancer, we believe UMIPIC has provided a new eclectic approach for the treatment of primary all solid tumor at anywhere of body, even pre surgery and during of operation. UMIPIC is safe, easy to operate, and reproducible with good benefit for all solid tumor.
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Authored by Matiss Mezals*
Low back pain is one of the leading causes of disability worldwide. Nevertheless, there is no consensus regarding recommendations for usage of lumbar supports for patients with low back pain which was demonstrated by asking opinions to different health care specialists. Thus, this confusion decreases trust in health care professionals and compliance of the patients for the treatment. Evidence is scarce and conflicting therefore making it difficult for medical experts to give firm recommendations. We do not have evidence-based answer to what type or material lumbar supports should be used. Nevertheless, manufactures claim that every kind of lumbar supports are safe and effective. In our opinion lumbar supports can be effective if used in conjunction with other treatment modalities especially exercise. Further studies are necessary to develop consensus among health care professionals and restore trust in the eyes of patients.
Keywords: Lumbar orthosis; Low back pain
Abbrevations:: LBP- Low Back Pain
Low back pain is one of the leading causes of disability and work absenteeism worldwide [1]. It’s treated by various types of health care professionals starting from general physicians till surgeons. Therefore, it is crucial that patients receive correct, similar and evidence-based information from health care specialists. Unfortunately, too often we see patients who have received contradictory information from various health care specialists which results in low patient compliance and reduced trust in health care system in general. In our daily practice we see that there is a relative consensus regarding pharmacological treatment of LBP among health care professionals, but there are vast differences in approach to patients with LBP in non-pharmacological treatment. One of the most contradictory topics lately have been usage of lumbar supports for LBP patients therefore we would like to state our opinion and urge for further research and discussion.
We asked opinion about lumbar support to the leading health care professionals in Latvia, who most commonly encounter patients with low back pain: general practitioners, neurologists and physiatrists. Views about usage of lumbar support for LBP varied vastly among them ranging from denial of utility of such supports till possible usage of the most part of the day. Deciding whether to use lumbar supports as treatment option, general practitioners based their opinion on patients’ profession and amount of physical activity in the work. However, physiatrists and neurologists tended to consider the diagnosis as primary criteria. This can easily confuse the patient as there are vast variations in recommendations from different specialists. Confusion continues also among medical experts because some research of LBP treatment state that it is possible to use lumbar supports for LBP prevention [2,3] and some state that it is not proven to be effective to use lumbar support for patients with LBP [5,6] and some guidelines even do not mention lumbar supports as a treatment option [7]. In either case strong evidence is lacking to support or reject usage of lumbar supports. In addition, guidelines do not specify type (soft\semi rigid\rigid) and material of lumbar support which is recommended and suits best. Also, it is not clear for how long period lumbar supports should be used. Other important questions that arise are whether lumbar supports decrease work absenteeism and increase participation and quality of life. As for the most treatments we need to take into consideration possible side effects which seem to be few [8], but still psychological dependence to lumbar supports can develop. Nevertheless, the most manufactures claim that lumbar supports treat back pain of various causes without enough evidence [9]. All these questions need to be investigated in order to reach consensus. Although we do not have strong evidence, based on our daily experience we recommend lumbar supports for short time period during the day if patients feel pain relief or stability in addition to other treatment methods especially exercise. We do not recommend using them alone.
Opinions about usage of lumbar supports for LBP are contradictory between health care professionals. Furthermore, research about lumbar supports are scare and evidence for recommendations are not strong enough. Further studies are needed to confirm or reject usage of lumber supports for low back pain hence health care professionals can reach consensus and improve quality of care for their patients.
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Authored by Jenna Herman*
Diabetes mellitus is a common, chronic, and complex metabolic disorder with two distinct types [1]. Almost 10% of the United States population, or 30.3 million people have diabetes. Nearly 25% of individuals with diabetes are undiagnosed. In 2012, the overall cost for treatment of diabetes patients was nearly $250 billion. On average $8,000 is spent annually on medical expenditures directly related to diabetes per diagnosed individual, which is more than twice the cost for their nondiabetic counterparts [2]. Diabetes type 1 is the result of autoimmune extermination of pancreatic islet cells. Onset is frequently abrupt and is influenced by genetics and certain environmental risk factors that appear to be unrelated. Presenting symptoms may be subacute with polydipsia, polyphagia, polyuria, malaise and weight loss, or more acute with symptoms such as visual disturbances and ketoacidosis. It is more often diagnosed in childhood but, may occur at any age [3].
Insulin resistance as well as alpha and beta cell dysfunction in the pancreatic islets of Langerhans characterize diabetes type 2. Onset is more subtle and gradual than type 1 [4]. Obesity, smoking, sedentary lifestyle, high blood pressure, hyperlipidemia, and hyperglycemia are known risk factors [2]. Presenting symptoms may be similar to diabetes type 1 with polydipsia, polyphagia, polyuria, and lethargy. However, sometimes diabetes type 2 may be discovered because of signs and symptoms related to complications, or as an incidental lab finding of elevated blood glucose or glycosuria. Diagnosis is often made in adulthood but, can also happen at any age [4].
Treatment for diabetes is wide-ranging. While insulin is required for type 1, a variety of interventions are available for type 2. Lifestyle modifications including diet and exercise are important. However, if not controlled with diet and exercise alone, many medication options, including oral and subcutaneous glucose lowering agents exist for patients to try before the need for insulin [5].
Diabetes complications may include ischemic heart disease, stroke, lower extremity amputation and diabetic ketoacidosis and is the seventh leading cause of death in the United States. Nearly 15 million emergency department visits were completed and over 7 million hospitalizations occurred in 2014 related to diabetes. About 250,000 of visits were for hypoglycemia [2]. Hypoglycemia in those with diabetes is generally defined as a BG level low enough to cause signs and symptoms or have the potential to cause harm. Although there is no standard definition, for many patients this generally occurs when BG concentration is less than 70mg/dL [5].
Laura is a 28-year-old female brought in by her co-worker. She reports that about 30 minutes ago they were chatting about their plans for the weekend when suddenly Laura became pale, diaphoretic and verbally incoherent. Her co-worker transported Laura to the local clinic because the nearest hospital is an hour away and indicated that she does not know much about Laura’s medical history. Laura has not exhibited these symptoms during the three years they have worked together in the same office.
What are your priority actions?
• Answer: Checking her blood sugar would be an important first step. While her symptoms could be caused by a variety of conditions, hypoglycemia should be high on the list of initial considerations as it is more dangerous than other potential differentials. Giving her 15g of carbohydrates (4oz soda or juice, hard candy) would also be appropriate.
• Case study continuation: A glucose meter confirms her blood sugar is 58mg/dL and after consuming four ounces of orange juice, Laura is able to tell you a bit more history. She does not recall the events her co-worker described but, has been not feeling well for about a week with increased urinary frequency, urgency, and fatigue. Laura has been diagnosed with two urinary tract infections in the last year and has successfully treated her symptoms with more fluids. This time, however, despite drinking a gallon of water her symptoms have not abated. Laura had initially planned on making an appointment at the clinic after work. Laura has no past medical history, takes no medications, and has no allergies. She has no fever, chills, nausea or vomiting, or systemic symptoms. Her body mass index (BMI) is 35; otherwise, her vitals and physical exam are unremarkable.
What is your initial diagnosis for Laura’s presentation? Any diagnostic testing you would like to complete?
• Answer: Given the hypoglycemic episode, urinary symptoms, and fatigue, Laura has pre-diabetes or undiagnosed diabetes. It would be prudent to draw a hemoglobin A1C (HgbA1C) and have her return for a fasting blood sugar as part of a comprehensive metabolic panel. A complete blood count and lipid panel should also be considered at the next visit.
• Case study continuation: Laura declined to have an HgbA1C drawn that first day after stating she would return the next day for all recommended lab work. Her pertinent positive lab work results at her follow up visit are below. All other lab work was negative.
i. HgbA1C: 7.3%
ii. FBS: 132
At her follow up visit, the following week Laura states she has had no further episodes of hypoglycemia and is anxious about her new diabetes type II diagnosis. She is motivated to lose weight.
What treatment would you recommend for Laura?
• Answer: Treatment for diabetes type II can be as unique as the disease process itself. The overall goals to treat diabetes are to keep quality of life, improve symptoms, reduce long-term complications, and decrease the risk of early mortality. Laura should start checking her blood sugar at home before meals, documenting her levels, and receive training on the symptoms of hypoglycemia. Lifestyle modifications in conjunction with possible medication would be suitable for Laura. Discussion of diet rich in fruit, vegetables, and lean protein in conjunction with moderate intense exercise 30 minutes/ minimum of five times per week would be appropriate. The provider may consider prescribing a first line medication such as metformin. An adequate starting dosage would be 500mg by mouth twice daily. Laura would need to be instructed on how to take the medication and informed of adverse effects [4].
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